Brain and Behaviour

<drug-watch-international@googlegroups.com> on behalf of Maggie Petito – mlp3@starpower.net – 09 January 2026 13:47

This reportage derives from a UK newspaper item – published in the The London Telegraph on 09 January 2026 – -by Charles Hymas Home Affairs Editor and Meike Eijsberg Data journalist      

Starmer accused of ignoring more significant safety issue while planning to cut drinking limit for motorists

Drugs are now a bigger factor in road deaths than alcohol, official figures show.

The number of deceased drivers who tested positive for drugs increased by 78 per cent, from 106 to 189, in the decade to 2023, according to the Department for Transport (DfT) and police data.

By contrast, the number of dead motorists with alcohol proved to be present in their system rose by 5 per cent in the same period, from 162 to 171.

Sir Keir Starmer, the Prime Minister, now stands accused of ignoring the bigger problem of drug-driving while planning to reduce the drink-driving limit, which critics fear will “strangle” struggling pubs.

The Government’s proposals have prompted a backlash from MPs and publicans, who say the move will put pubs under more pressure following an increase in business rates.

Britain lost an average of one pub each day in 2025, and industry bosses have warned that rising tax bills and wages, on top of higher energy costs, will drive hundreds more out of business.

The Telegraph has launched a campaign to save the nation’s pubs, calling on Labour to stop its assault on Britain’s locals, and to cut tax and red tape.

Ministers are now expected to announce a climbdown, saying they are working on relief measures to be announced in the coming days. But the about-turn relates to jumps in business rates for landlords, not the new drink-drive limit.

DfT figures show that the percentage of fatal collisions in which drink-driving was involved has been relatively stable over the past 10 years, at 13 per cent.

However, the proportion in which drug-driving played a role has doubled from 5 per cent in 2014 to 10 per cent in 2023.

While drug-driving convictions rose by 13.5 per cent in 2024 to 27,000, the number of drivers convicted of drink-driving offences fell by 6 per cent to 36,415.

Meanwhile, injuries from drink-driving incidents have significantly decreased since 1980, from around 20,000 annually to about 5,000 since 2020.

Despite this, the Government’s new road strategy proposes “taking tougher action on drink-driving” by reducing the legal limit of 80mg of alcohol per 100ml of blood to 50mg, or around a pint.

It would be the most significant reform to road safety laws since 1967, when the blood alcohol limit was first introduced.

Chris Philp, the shadow home secretary, said: “Labour are now proposing even more measures that will endanger country pubs.

“At the same time, the Government is completely failing to do more to address a more rapidly growing road safety issue – drug-driving. More drivers killed in a collision had drugs in their system than alcohol.

“The Government should prioritise toughening up on drug-drivers above measures which will strangle struggling country pubs.”

‘Further pressure’ on pubs

The British Beer and Pub Association warned that any toughening of measures on drink-driving would harm rural pubs in areas without public transport or reliable taxi services.

A spokesman said: “The pub sector continues to face huge challenges, so any additional policy measures that further impact trade will be of real concern to licensees, especially those in rural areas.”

Drug-drivers face similar penalties as those caught drinking, including a minimum 12-month driving ban and up to six months in prison for serious or repeat offences.

Limits for illegal drugs such as cannabis, cocaine, ketamine and heroin are set at extremely low levels, but not at zero, to account for accidental exposure.

However, Government-funded research has suggested that dangerous drug-drivers have been escaping prosecution – and putting lives at risk – because some police forces ration the number of testing kits issued to officers to just one a day.

The study, by the Parliamentary Advisory Council for Transport Safety, found there was a “geographical lottery” where the best-performing forces were catching 10 times more drug-drivers per head of population than the worst.

Drivers can also escape justice because of delays of four to five months in processing blood tests. Officers have only six months to prosecute. Dangerous driving penalties to be reviewed

The Government’s new road safety strategy proposes that there should be a review of penalties and mandatory training for drink and drug-driving offences.

It has also pledged to explore alternative processing and evidence collection for drug-driving to “improve speed of results, supporting more robust enforcement outcomes.”

A DfT spokesman said the strategy would “save thousands of lives by targeting the root causes of deaths, including the impact of both alcohol and drugs”.

They added: “We’re determined to crack down on drug-driving, and the strategy includes new measures to modernise how we tackle it, including new testing methods, and powers to suspend driving licenses for those caught under the influence.

“We do not expect the new limit to harm pubs; experience in Scotland shows such changes have minimal impact on local businesses while making roads safer.”

Source: Maggie Petito – mlp3@starpower.net

By Press Advantage – January 01, 2026

Muse Treatment Alcohol & Drug Rehab Los Angeles has published a new educational resource examining how opioid tolerance develops and why it plays a significant role in substance use disorder progression and treatment planning. The article, titled “How Does Opioid Tolerance Develop”, provides research-informed context for patients, families, and healthcare professionals seeking a clearer understanding of opioid-related risk, dependence, and recovery pathways.

According to the National Institute on Drug Abuse, opioid tolerance occurs when repeated exposure to opioids reduces the body’s response to the drug, leading people to require higher doses to achieve the same effect. This physiological adaptation is a central driver of escalating use and overdose risk. The Centers for Disease Control and Prevention reports that opioids remain a major contributor to drug-related mortality in the United States, with tolerance and dose escalation frequently cited in toxicology findings. Peer-reviewed research published in journals such as The New England Journal of Medicine further confirms that tolerance alters brain chemistry and reward pathways, making cessation more complex without structured treatment support.

The newly published resource outlines how tolerance develops at the cellular and neurological level, emphasizing that it is not a failure of willpower but a predictable biological response. This distinction is supported by guidance from the Substance Abuse and Mental Health Services Administration, which frames substance use disorders as chronic medical conditions requiring evidence-based care. By presenting opioid tolerance through a clinical lens, the article reinforces the importance of early intervention and medically appropriate treatment selection.

This educational release aligns with the clinical services at the Los Angeles location, where inpatient treatment programs are designed around evidence-based frameworks used in accredited addiction treatment facilities. Program information is available at Muse Treatment Los Angeles. Services include medically supervised care models that address alcohol and opioid use disorders through structured programming, including intensive outpatient alcohol rehab and partial hospitalization alcohol rehab. These levels of care reflect standards outlined by SAMHSA, which identifies continuity of care and treatment intensity matching as key predictors of positive outcomes.

Patients seeking care often come from across Los Angeles and surrounding communities, reflecting the regional need for accessible, medically grounded addiction treatment. People searching for drug rehab near me in LA frequently include residents from West LA, where proximity and flexible treatment scheduling influence engagement. Downtown LA is also represented among patients accessing services, highlighting the demand for structured care models that integrate clinical oversight with community-based recovery. East LA similarly relies on nearby treatment options that support consistent participation without extended travel.

The reach of care extends into neighborhoods such as Glendale,Westwood and Westwood Village, where patients often seek programs that balance privacy with evidence-based clinical support. Little Holmby and Holmby Hills are included as well, underscoring the role of localized treatment availability when families evaluate the best alcohol rehab centers and related services. Bel Air shows similar patterns, reinforcing the importance of geographically relevant care when people decide whether to initiate treatment and follow through.

National outcome data support the treatment approaches discussed in the article. The National Institute on Drug Abuse reports that relapse rates for substance use disorders are comparable to those of other chronic conditions, such as diabetes and hypertension, emphasizing that effective care focuses on long-term management rather than short-term detoxification alone. Programs offering partial hospitalization alcohol rehab and intensive outpatient alcohol rehab are well-positioned to support patients as they transition between levels of care, particularly when tolerance and withdrawal symptoms complicate recovery.

The article also contributes to broader public health education around opioid risk. The CDC notes that tolerance can lower perceived risk while increasing physiological danger, as higher doses strain respiratory and cardiovascular systems. Understanding this dynamic is critical for patients and families evaluating treatment options, particularly in regions with sustained opioid exposure.

Accreditation standards further inform the clinical framework reflected in the services described. Organizations such as The Joint Commission emphasize medication management, patient safety, and evidence-based treatment protocols as benchmarks for quality addiction care. Independent analyses have shown that accredited programs demonstrate stronger adherence to clinical guidelines and improved coordination between medical and behavioral health services.

As healthcare search trends continue to show rising interest in opioid tolerance, overdose prevention, and structured treatment pathways, educational resources grounded in third-party research play a critical role in informed decision-making. By publishing this article and integrating it within a broader continuum that includes intensive outpatient alcohol rehab and partial hospitalization alcohol rehab services, Muse Treatment reinforces the role of education as a foundation of effective addiction treatment.

The resource serves as a reference point for patients, families, and healthcare professionals seeking clarity on how opioid tolerance develops, while supporting broader efforts to reduce preventable harm and improve recovery outcomes through evidence-based care across Los Angeles and surrounding communities.

Source: https://markets.financialcontent.com/wral/article/pressadvantage-2026-1-1-opioid-tolerance-explained-in-new-educational-resource-published-by-muse-treatment

It isn’t just people — when given the chance rats may also use cannabis to cope with stress, according to a study by researchers at Washington State University.

Published in the journal Neuropsychopharmacology, the study was designed to examine cannabis-seeking behavior and found that rats with higher natural stress levels are far more likely to self-administer the popular recreational drug.

“We ran rats through this extensive battery of behavioral and biological tests, and what we found was that when we look at all of these different factors and all the variables that we measured, stress levels seem to matter the most when it comes to cannabis use,” said Ryan McLaughlin, associate professor in WSU’s College of Veterinary Medicine.

Looking at traits ranging from social behaviors to sex, cognition, reward, and arousal, McLaughlin and his team of undergraduate and graduate student researchers created a behavioral profile for each rat. Then, over the course of three weeks, rats were observed for one hour daily as they were given the option to self-administer cannabis by poking their nose in a vapor port to release a three-second dispersal of cannabis vapor in an air-tight chamber.

During that one-hour period, student researchers tracked the number of “nose-pokes” by each rat and found a direct correlation to the number of nose-pokes and baseline stress hormone levels.

By measuring the stress hormone corticosterone in the rodents, the equivalent to the stress hormone cortisol in humans, the team found rats with higher natural stress hormone levels were far more likely to self-administer cannabis.

“If you want to really boil it down, there are baseline levels of stress hormones that can predict rates of cannabis self-administration, and I think that only makes sense given that the most common reason that people habitually use cannabis is to cope with stress,” McLaughlin said.

He said it’s important to note that it was a rat’s resting baseline stress levels that were associated with cannabis self-administration, not stress that fluctuates in real time with exercise or mentally challenging tasks. Stress hormone levels were also calculated after exposure to a stressor and showed no significant link to cannabis-seeking behavior.

There were also significant relationships between rates of cannabis self-administration and measures of “cognitive flexibility”, which is our ability to adapt to changing rules.

“Animals that were less flexible in shifting between rules, when we tested them in a cognitive task, tended to show stronger rates of cannabis-seeking behavior,” he said. “So, animals that rely more heavily on visual cues to guide their decision making, those rats, when we tested their motivation to self-administer cannabis vapor, were also very highly motivated rats.”

The study also identified a link between high morning corticosterone and low endocannabinoid levels to cannabis self-administration, although not as strongly as baseline stress.

‘Our findings highlight potential early or pre-use markers that could one day support screening and prevention strategies’ – Ryan McLaughlin, associate professor, Washington State University

Endocannabinoids are compounds produced on demand to help the body maintain a state of physiological balance, or homeostasis.

“There’s some thought behind why people might be more prone to use cannabis, and that maybe THC serves as a reasonable substitute for endocannabinoids in individuals that have lower endocannabinoid levels,” McLaughlin said. “So, perhaps there’s more of a drive to supplement that with cannabis.”

With more and more states decriminalizing cannabis and legalizing recreational cannabis, McLaughlin said it’s critical to understand the effects of the drug and the grips of drug abuse.

“Our findings highlight potential early or pre-use markers that could one day support screening and prevention strategies,” McLaughlin said. “I could certainly envision a scenario where having an assessment of baseline cortisol might provide some level of insight into whether there’s an increased propensity for you to develop problematic drug use patterns later in life.”

Media Contacts

  • Ryan McLaughlin and Josh  Babcock, WSU Department of Integrative Physiology and Neuroscience

Source:https://news.wsu.edu/press-release/2025/12/11/rats-may-seek-cannabis-to-cope-with-stress-wsu-research-finds/

By  CLAIRE RUSH, Associated Press –


November 17, 2025

PORTLAND, Ore. (AP) — A federal judge on Monday ruled there would be no prison time for a former Alaska Airlines pilot who had taken psychedelic mushrooms days before he tried to cut the engines of a passenger flight in 2023 while riding off-duty in the cockpit.

U.S. District Court Judge Amy Baggio in Portland, Oregon, sentenced Joseph Emerson to time served and three years’ supervised release, ending a case that drew attention to the need for cockpit safety and more mental health support for pilots.

Federal prosecutors wanted a year in prison, while his attorneys sought probation.

“Pilots are not perfect. They are human,” Baggio said. “They are people and all people need help sometimes.”

Emerson hugged his attorneys and tearfully embraced his wife after he was sentenced.

Emerson was subdued by the flight crew after trying to cut the engines of a Horizon Air flight from Everett, Washington, to San Francisco on Oct. 22, 2023, while he was riding in an extra seat in the cockpit. The plane was diverted and landed in Portland with more than 80 people.

Emerson told police he was despondent over a friend’s recent death, had taken psychedelic mushrooms about two days earlier, and hadn’t slept in over 40 hours. He has said he believed he was dreaming and was trying to wake up by grabbing two red handles that would have activated the fire suppression system and cut fuel to the engines.

He spent 46 days in jail and was released pending trial in December 2023, with requirements that he undergo mental health services, stay off drugs and alcohol, and keep away from aircraft.

Attorney Ethan Levi described his client’s actions as “a product of untreated alcohol use disorder.” Emerson had been drinking and accepted mushrooms “because of his lower inhibitions,” Levi said.

Emerson went to treatment after jail and has been sober since, he added.

Baggio said the case is a cautionary tale. Before she sentenced him, Emerson said he regretted the harm he caused.

“I’m not a victim. I am here as a direct result of my actions,” he told the court. “I can tell you that this very tragic event has forced me to grow as an individual.”

The judge sentenced Emerson to time served (46 days) and put him on probation for 3 years, with some restrictions. 

Source: Claire Rush – Associated Press

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Addendum by John Coleman Ph D, President, Drug Watch International

From: John J. Coleman. PhD <john.coleman.phd@gmail.com>
Sent: 19 November 2025 13:21
To: ndpa@drugprevent.org.uk
Subject: RE: Question about Psilocybin

It is now known that his employer, Horizon Airlines, terminated him as soon as his arrest was reported. Feelings here are very mixed over this outcome and some thought he should have been given some additional prison time. Had he been drunk on alcohol, things would have been different and he likely would have wound up in prison. In John Coleman’s opinion, being under the influence of psychedelics is even worse because the person can appear normal, as this fellow did, and still pose a serious risk to self and others.

Coleman  wrote the judge a letter and recommended she include several thousand hours of community service in the form of lecturing school children and young adults on the dangers of psychedelics, but she apparently didn’t consider it. 

Here’s what Coleman advised the judge:

November 11, 2025 to The Hon. Amy M. Baggio – United States District Judge – District of Oregon

In re: Sentencing of Joseph David Emerson, defendant in case #3:25-cr-00306, USA v. Emerson

Dear Judge Baggio,

Please forgive me for using an email to send this letter to you. I’m afraid regular mail would be too slow to get from one side of the country to the other.

On Monday, November 17, 2025, I believe you have scheduled a sentencing hearing for the defendant, Joseph David Emerson, who, in 2023, while under the influence of psilocybin, a Schedule I controlled substance, attempted to cause the destruction of an Alaska Airlines flight containing 84 passengers and crew, including himself. Emerson has admitted to the charge, among others, of interfering with a flight and flight crew (Title 49, United States Code, Section 46504). He has signed a plea agreement, and media reports indicate that the federal prosecutor has agreed to recommend a sentence of one year, along with restitution for costs incurred in the emergency landing and the rebooking of stranded passengers.

On a personal note, I served 33 years as a special agent for the Drug Enforcement Administration and headed several offices, including that of Assistant Administrator for Operations, the top non-appointed position in the agency. During the course of my long career, especially when working as a street agent in New York City, Chicago, Washington, D.C., Newark, and Boston, I was often asked what the most dangerous drug a drug abuser could take. My answer, your honor, was always the same: psilocybin. Over the years, I witnessed hundreds of people severely addicted to opiates and stimulants (like amphetamines and cocaine), and after completing treatment, they would bounce back and be productive members of society again. Some today are famous people, even high-level government officials, people I knew when they were hitting the bottom of the proverbial barrel. Many, indeed, most, rebounded in ways that I can only say were inspiring for me and my fellow officers.

The sole exception for which recovery never seemed possible involved those using psilocybin, especially chronic users of the drug. I was told by someone who would know that in street parlance, “psilocybin burns out the brain cells.” Some of the most bizarre crimes I ever encountered – people cutting off their own limbs and the heads of their spouses and children – were more often than not the result of taking psilocybin. Some were just too gruesome for words. My colleagues and I, in such instances, would suspect long before the tox or autopsy reports came in that psilocybin was the causative agent.

In closing, I would ask that, whatever you decide to do with Mr. Emerson as a result of his imprudent use of psilocybin, you consider including several thousand hours of directed community service in which he is accepted by an appropriate state or federal department, on behalf of which he will make presentations to school audiences and others about the dangers of using psychedelic drugs, especially psilocybin. Mr. Emerson was a commercial pilot, someone who even now might draw a considerable amount of attention. His personal experiences, given in a format of educating others, would surely go a long way toward keeping this and other dangerous drugs away from vulnerable people. And it might even go a long way toward helping him to deal with his own mental health issues.

Thank you for considering this suggestion, and thank you for your service to our nation.

Sincerely, – J. Coleman – [signed]

Source: John J. Coleman, PhD. President – Drug Watch International, Inc.

News Article by US News ReporterDec 01, 2025

There is “insufficient” evidence supporting the use of cannabis or cannabinoids for most medical purposes, a new review has concluded.

“We reviewed the totality of the evidence—over a thousand studies with emphasis on randomized trials, meta-analyses, and systematic reviews,” Dr Kevin Hill, one of the review authors, and director of addiction psychiatry at Beth Israel Deaconess Medical Center, and a professor of psychiatry at Harvard University, told Newsweek.

He said that “beyond the FDA-approved indications, the evidence for cannabis and cannabinoids as a medical treatment is limited.”

The review was published online in the peer-reviewed medical journal JAMA Network on November 26.

Why It Matters

There has been increasing use of cannabis and cannabinoids for medical treatment in recent years. It has gained popularity among cancer patients, for managing nausea, pain and reduced appetite, and it is favored among patients with chronic pain for its analgesic properties.

However, its use medically has gathered some concern, as while certain patients may experience benefits, some medical professionals have said that there is not enough research to determine if the positives outweigh any future negatives.

After the Senate passed its funding package to end the U.S. government shutdown, which included a measure that will lead to the banning of many THC products, the issue of cannabis use has been in the spotlight.

What The Review Found

The review found that 27 percent of adults from the U.S. and Canada have used cannabis for medical purposes, while 10.5 percent of Americans report using cannabidiol (CBD) for therapeutic purposes.

“Cannabis and cannabinoids like CBD have a broad range of effects, so, with so many people suffering from medical problems, it is not hard to see why they might consider cannabis and cannabinoids as treatments,” Hill said.

However, he said that “the evidence is not strong” for their use medically.

While doctors may “consider cannabis and cannabinoids as third-line treatments in various clinical scenarios,” Hill said, “the lack of evidence coupled with significant risks means that, most often, the risks outweigh the benefits.”

The review found that almost a third of adult users of medical cannabis go on to develop a cannabis use disorder—a complex condition that is a type of substance use disorder, where a patient can experience a problematic pattern of cannabis use that causes them distress or impairs their life.

It also found that daily inhaled cannabis use compared to nondaily use was associated with higher risks of coronary heart disease, heart attack, and stroke,

“The adverse effects of cannabis upon one’s physical health are becoming more well-defined,” Hill said.

He said that the purpose of this review was to provide clinicians and patients with “better information with which to have sensible, evidence-based conversations,” conversations about medical treatment which he said should take place between doctors and patients, and “not between budtenders and customers in dispensaries.”

What Other Experts Think

Jonathan Caulkins, a professor of operations research and public policy at Carnegie Mellon University, who was not involved in the review, told Newsweek that while there is “high-quality evidence supporting certain very specific medical uses,” most medical use is “predicated on much less evidentiary basis, and below what is expected for FDA approval.”

He said that what is “important” about this review is that it helps “counter the messaging from cannabis treatment advocates, who promote the good news, and the hopes, without balance or caution.”

“The actual situation is nuanced, and more gets written that pushes for an overly optimistic view of cannabis’ medical value,” he said.

Yasmin Hurd, chair of translational neuroscience and the director of the Addiction Institute at Mount Sinai, also told Newsweek that the findings are “notable” because it “confirms what has been previously published from other reviews and consensus reports like those from the National Academies, noting that there is insufficient evidence for the use of cannabis to treat most medical conditions.”

While the authors have “done a very comprehensive and in my view very useful review of this topic,” Dr Igor Grant, a professor of psychiatry and director of the HIV Neurobehavioral Research Program and Center for Medicinal Cannabis Research, at the University of California, San Diego, told Newsweek, “it is clear from the way the article is written that the authors have significant concerns about the use of medicinal cannabis, and as such have tended to emphasize many of the negatives, including potential side effects.”

He said that this “does not mean that the side effects are not there, nor does it negate the fact that evidence for efficacy of medicinal cannabis is weak in many areas. But there does seem to be a definite slant.”

He also said that while this review highlights cardiovascular risks, other research has also shown there is “actually no statistically reliable evidence to suggest that cannabis users suffer more cardiovascular risk, including no effect on hypertension, myocardial infarction, and presence of coronary atherosclerosis.”

What People Are Saying

Caulkins told Newsweek: “We customarily expect medicinal drugs to be produced in a way that guarantees consistency from dose to dose. Every pill in a bottle of pills that is prescribed by a physician, manufactured by a pharmaceutical company and distributed by a licensed pharmacy should have essentially the exact same dose. With the exception of the FDA-approved and regulated cannabinoids (which account for a tiny share of all consumption that is described or understood to be “medical cannabis”), there is not that same quality control for medical cannabis.”

He added: “Cannabis smoke contains known carcinogens. Sometimes good medical practice exposes patients to carcinogenic risk, notably radiation treatment does. But we do that carefully and knowingly, because the risk of untreated cancer is greater than the risk that radiation therapy will create new cancer. But given that in many cases the upside benefit of medical cannabis is not well established, it is striking how cavalier the system is with respect to known carcinogens present in cannabis smoke. For most categories of consumer products, the presence of known carcinogens is sufficient to have that product taken off the shelves, even if there are not epidemiological studies documenting effects on cancer rates at the population level. For whatever reason or reasons, we collectively seem surprisingly unconcerned about that risk regarding smoked cannabis, medical or non-medical.”

Hurd told Newsweek: “There remain numerous concerns about cannabis for medical use since there is so little known about whether it works, what particular conditions it might be helpful to treat and what dose and dosing regime for clinicians to recommend. In addition, there are also concerns that individuals will use ‘medicinal cannabis’ obtained from sources where the contents are not verified and cannabis with high THC concentration has well known significant side effects. Cannabis should be used with caution in medical settings. As such, like many medicines, especially where there is very limited information available, it is best to start low dose and go slow. Also, cannabis should not be the first line therapy and instead used only for conditions where conventional therapies have failed.”

She added: “It is important that the public also begins to better understand that cannabis is a very complex plant with hundreds of chemicals whereas ‘medicine’ is normally a product that has specific, well studied components. Also, cannabis is different from specific cannabinoids, like cannabidiol (CBD), which has FDA approval for the treatment of certain epilepsy conditions.”

Grant told Newsweek: “While I agree that physicians who are counseling patients about potential use of cannabis for various indications need to both warn patients about lack of evidence in many cases, the possibility of side effects, and certainly evaluate a patient in the event they have major psychiatric or substance use disorder, there are, as they note protocols for doing this, and in some ways, assuring safety. I believe also that the risk of people who use medicinal cannabis, who are often people who are older with various kinds of chronic conditions, is rather low that they will systematically increase their use to the point of developing a cannabis use disorder. Cannabis use disorder is real, and a concern, but very unlikely to be a problem in the clinical setting. The article tends at times to conflate recreational and medicinal use: that’s a bit like using data from opioid addiction to comment on appropriate use of opioids in a clinical setting.”

Source: https://www.newsweek.com/does-cannabis-actually-have-medical-benefits-11118810

Story by Camilla Jessen – Received by DWI: 02 December 2025 
Cannabis users warn of painful syndrome linked to long-term use

A growing number of regular cannabis users in the U.S. are coming forward with accounts of a severe and little-known disorder linked to long-term marijuana use.

The condition, now officially recognized by global health authorities, has led some people to hospital with pain so intense they describe it as unbearable.

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Troubling symptoms

As of 2023, roughly 17% of Americans reported using cannabis, with 24 states legalizing recreational use.

But while the drug is widely used for its therapeutic and recreational effects, doctors are increasingly treating patients who present with repeated vomiting, severe abdominal pain and dehydration.

The pattern has been identified as cannabis hyperemesis syndrome (CHS), a disorder seen primarily in people who use cannabis daily or near-daily over long periods.

UW Medicine says symptoms often appear within 24 hours of the most recent use and can persist for days.

The syndrome is sometimes nicknamed “scromiting,” a blend of “screaming” and “vomiting,” due to the intensity of the episodes.

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Users speak out

Many who have experienced CHS have shared their stories online.

One TikTok user described the onset as “the worst physical pain I’ve ever experienced… and I birthed a 9-pound baby.”

Another said she “almost died,” explaining she couldn’t keep food or water down for a week.

Despite the episodes, some users admitted they continued smoking, which only worsened the symptoms. One woman, now six months sober, said quitting was the only way to stop the cycle.

“Smoking nearly killed me,” she said.

Medical uncertainty

Doctors still do not fully understand why the condition occurs.

The Cleveland Clinic says one leading theory is that chronic use overstimulates cannabinoid receptors in the body’s endocannabinoid system, disrupting normal digestive regulation.

The World Health Organization has listed CHS in its International Classification of Diseases, allowing clinicians to formally track cases for the first time.

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Researchers say the new designation will provide more reliable data on cannabis-related health problems.

Calls for more awareness

Beatriz Carlini of the University of Washington School of Medicine said the classification will help quantify a growing issue.

“A new code for cannabis hyperemesis syndrome will supply important hard evidence on cannabis-adverse events,” she noted.

Sources: UW Medicine; Cleveland Clinic; WHO ICD, Unilad

Source: https://www.msn.com/en-au/health/other/cannabis-users-warn-of-painful-syndrome-linked-to-long-term-use/ar-AA1Rya8d?

Dr. Smita Das often hears the same myth: You can’t get hooked on pot .

And the misconception has become more widespread as a growing number of states legalize marijuana . Around half now allow recreational use for adults and 40 states allow medical use.
But “cannabis is definitely something that someone can develop an addiction to,” said Das, an addiction psychiatrist at Stanford University.
It’s called cannabis use disorder and it’s on the rise, affecting about 3 in 10 people who use pot, according to the U.S. Centers for Disease Control and Prevention.
Here’s how to know whether you or a loved one are addicted to marijuana — and what kinds of treatment exist.
How to identify signs of cannabis use disorder

If pot interferes with your daily life, health or relationships, those are red flags.

“The more that somebody uses and the higher potency that somebody uses, the higher the risk of that,” Das said.

It’s become more common as cannabis has gotten stronger in recent years. In the 1960s, most pot that people smoked contained less than 5% THC, the ingredient that gets you high. Today, the THC potency in cannabis flower and concentrates in dispensaries can reach 40% or more, according to the National Institute on Drug Abuse.

Cannabis use disorder is diagnosed the same way as any other substance use disorder — by looking at whether someone meets certain criteria laid out in the latest version of the Diagnostic and Statistical Manual of Mental Disorders, the main guide for mental health providers.

These include needing more of the drug to get the same effect, having withdrawal symptoms and spending a lot of time trying to get or use it.

“When we break it down into these criteria that have to do with the impacts of their use, it’s a lot more relatable,” Das said.

What the different levels of addiction are

If you’ve met just two of the criteria for cannabis use disorder in the last year, doctors say you have a mild form of the condition. If you meet six or more, you have a more severe form.

According to the latest version of the National Survey on Drug Use and Health, 7% of all people 12 or older had cannabis use disorder in 2024 and most had a mild form. About 1 in 5 had a severe form.
People can be dependent on and addicted to substances. Dependence is physical, while addiction involves behavior changes.

Where people can get help for cannabis use disorder

Many marijuana users first come to Das for help coping with something else, like alcohol use disorder. Later, she said, they’ll often come back and mention a struggle with cannabis.

She assures them that there are effective treatments for the disorder.

One is called motivational interviewing, a goal-oriented counseling style that helps people find internal motivation to change their behavior. Another is cognitive behavioral therapy or CBT, a form of talk therapy that helps people to challenge negative thought patterns and reduce unhelpful behaviors.
Twelve-step programs like Marijuana Anonymous can also be helpful, Das said. But whether someone chooses to join a group or not, even being able to lean on a community of people who aren’t using pot is an important part for recovery.

Dave Bushnell, a retired digital executive creative director, started a Reddit group 14 years ago for people who, like him, had developed an addiction or dependency to cannabis and wanted help recovering. Its discussion forum has 350,000 members and continues to grow.

Bushnell, 60, said peer support is essential to recovery and some people feel more comfortable chatting online than in person. “This is potheads taking care of potheads,” he said.

Doctors urged people who need help to get it, whether it’s with a professional or in a peer group.

As with alcohol, “just because something’s legal doesn’t mean that it’s safe,” Das said.

___

Associated Press reporter Leah Willingham in Boston contributed to this story.

Source: https://www.washingtonpost.com/health/2025/11/22/pot-cannabis-use-disorder-marijuana-addiction/dcfff9a4-c7ac-11f0-be23-3ccb704f61ac_story.html

Opening Statement by NDPA:

This research provides useful information which is relevant to study of prevention of health-compromising behaviours, such as drug misuse.

 

Image source,Monty Rakusen/Getty

by James Gallagher  – BBC Health and science correspondent – 25 November 2025The brain goes through five distinct phases in life, with key turning points at ages nine, 32, 66 and 83, scientists have revealed.

Around 4,000 people up to the age of 90 had scans to reveal the connections between their brain cells.

Researchers at the University of Cambridge showed that the brain stays in the adolescent phase until our early thirties when we “peak”.

They say the results could help us understand why the risk of mental health disorders and dementia varies through life.

The brain is constantly changing in response to new knowledge and experience – but the research shows this is not one smooth pattern from birth to death.

Instead, these are the five brain phases:

  • Childhood – from birth to age nine
  • Adolescence – from nine to 32
  • Adulthood – from 32 to 66
  • Early ageing – from 66 to 83
  • Late ageing – from 83 onwards

“The brain rewires across the lifespan. It’s always strengthening and weakening connections and it’s not one steady pattern – there are fluctuations and phases of brain rewiring,” the lead author of the research, Dr Alexa Mousley, told the BBC.

Some people will reach these landmarks earlier or later than others – but the researchers said it was striking how clearly these ages stood out in the data.

These patterns have only now been revealed due to the quantity of brain scans available in the study, which was published in the journal Nature Communications.

The five brain phases

Childhood – The first period is when the brain is rapidly increasing in size but also thinning out the overabundance of connections between brain cells, called synapses, created at the start of life.

The brain gets less efficient during this stage. It works like a child meandering around a park, going wherever takes their fancy, rather than heading straight from A to B.

Adolescence – That changes abruptly from the age of nine when the connections in the brain go through a period of ruthless efficiency. “It’s a huge shift,” said Dr Mousley, describing the most profound change between brain phases.

This is also the time when there is the greatest risk of mental health disorders beginning.

Unsurprisingly adolescence starts around the onset of puberty, but this is the latest evidence suggesting it ends much later than we assumed. It was once thought to be confined to the teenage years, before neuroscience suggested it continued into your 20s and now early 30s.

This phase is the brain’s only period when its network of neurons gets more efficient. Dr Mousely said this backs up many measures of brain function suggesting it peaks in your early thirties, but added it was “very interesting” that the brain stays in the same phase between nine and 32.

Adulthood – Next comes a period of stability for the brain as it enters its longest era, lasting three decades.

Change is slower during this time compared with the fireworks before, but here we see the improvements in brain efficiency flip into reverse.

Dr Mousely said this “aligns with a plateau of intelligence and personality” that many of us will have witnessed or experienced.

Early ageing – This kicks in at 66, but it is not an abrupt and sudden decline. Instead there are shifts in the patterns of connections in the brain.

Instead of coordinating as one whole brain, the organ becomes increasingly separated into regions that work tightly together – like band members starting their own solo projects.

Although the study looked at healthy brains, this is also the age at which dementia and high blood pressure, which affects brain health, are starting to show.

Late ageing – Then, at the age of 83, we enter the final stage. There is less data than for the other groups as finding healthy brains to scan was more challenging. The brain changes are similar to early ageing, but even more pronounced.

Dr Mousely said what really surprised her was how well the different “ages align with a lot of important milestones” such as puberty, health concerns later in life and even the pretty big social shifts in your early 30s such as parenthood.

‘A very cool study’

The study did not look at men and women separately, but there will be questions such as the impact of menopause.

Duncan Astle, professor of neuroinformatics at the University of Cambridge and part of the team responsible for the research, said: “Many neurodevelopmental, mental health and neurological conditions are linked to the way the brain is wired. Indeed, differences in brain wiring predict difficulties with attention, language, memory, and a whole host of different behaviours.”

The director of the centre for discovery brain sciences at the University of Edinburgh, Prof Tara Spires-Jones, who did not work on the research paper, said: “This is a very cool study highlighting how much our brains change over our lifetimes.”

She said the results “fit well” with our understanding of brain ageing, but cautioned “not everyone will experience these network changes at exactly the same ages”.

Source: https://www.bbc.co.uk/news/articles/cgl6klez226o.amp

Identifying early neural vulnerabilities in adolescence could help guide prevention before substance abuse begins.
Credit: Neuroscience News

from neurosciencenews.com – November 21, 2025 

Key Facts:

  • Distinct Neural Patterns: Girls at risk showed higher transition energy in default-mode networks, while boys showed lower transition energy in attention networks.
  • Risk Before Substance Use: Differences appeared at ages 9–11, indicating early vulnerability unrelated to drug exposure.
  • Tailored Prevention: Findings point toward sex-specific early interventions targeting rumination in girls and impulse control in boys.

Source: Weill Cornell University

The roots of addiction risk may lie in how young brains function long before substance use begins, according to a new study from Weill Cornell Medicine.

The investigators found that children with a family history of substance use disorder (SUD) already showed distinctive patterns of brain activity that differ between boys and girls, which may reflect separate predispositions for addiction.

The research, published Nov. 21, in Nature Mental Health, analyzed brain scans from nearly 1,900 children ages 9 to 11 participating in the National Institutes of Health’s Adolescent Brain Cognitive Development (ABCD) Study. 

“These findings may help explain why boys and girls often follow different paths toward substance use and addiction,” said senior author Dr. Amy Kuceyeski, professor of mathematics and neuroscience in the Department of Radiology and the Feil Family Brain & Mind Research Institute at Weill Cornell. “Understanding those pathways could eventually help guide how we tailor prevention and treatment for each group.”

Tracking Neural Energy Shifts

To explore these neural differences, the researchers used a computational approach called “network control theory” to measure how the brain transitions between different patterns of activity during rest.

 “When you lie in an MRI scanner, your brain isn’t idle; it cycles through recurring patterns of activation,” said first author Louisa Schilling, doctoral candidate in the Computational Connectomics Laboratory at Weill Cornell.

“Network control theory lets us calculate how much effort the brain expends to shift between these patterns.” This transition energy indicates the brain’s flexibility, or its ability to shift from inward, self-reflective thought to external focus.

Disruptions in this process have been observed in people with heavy alcohol use and cocaine use disorder, and when under the influence of psychedelics.

Opposing Patterns in Boys and Girls

The study found that girls with a family history of SUD displayed higher transition energy in the brain’s default-mode network, which is associated with introspection. Compared with girls without such a family history, this elevated energy suggests their brains may work harder to shift gears from internal-focused thinking.

“That may mean greater difficulty disengaging from negative internal states like stress or rumination,” Schilling said.

“Such inflexibility could set the stage for later risk, when substances are used as a way to escape or self-soothe.”

In contrast, boys with a family history showed lower transition energy in attention networks that control focus and response to external cues.

“Their brains seem to require less effort to switch states, which might sound good, but it may lead to unrestrained behavior,”  Dr. Kuceyeski said.

“They may be more reactive to their environment and more drawn to rewarding or stimulating experiences.”

Put simply, she said, “Girls may have a harder time stepping on the brakes, while boys may find it easier to step on the gas when it comes to risky behaviors and addiction.” Since the brain differences appeared before any substance use, they may indicate inherited or early-life environmental vulnerability rather than the effects of drugs.

Toward More Personalized Prevention

The researchers emphasize the need to analyze data from boys and girls separately, since averaging results across both groups masked the contrasts. Separate analyses revealed distinct patterns, underscoring the importance of sex as a biological variable in brain and behavioral research.

The findings mirror what clinicians see in adults: women are more likely to use substances to relieve distress and progress more quickly to dependence, while men are more likely to seek substances to feel euphoria or excitement. Identifying early neural vulnerabilities in adolescence could help guide prevention before substance abuse begins.

“Recognizing that boys and girls may travel different neural roads toward the same disorder can help tailor how we intervene,” Dr. Kuceyeski said. “For example, programs for girls might focus on coping with internal stress, while for boys the emphasis might be on attention and impulse control.”

Key Questions Answered:1

Q: How does family history of substance use disorder affect young brains?

A: It is linked to distinct patterns of neural transition energy before any substance use begins.

Q: Why do boys and girls show different addiction risk pathways?

A: They display opposing neural flexibility patterns in attention and introspection networks.

Q: How can this research guide prevention?

A: It suggests tailored early interventions targeting stress coping for girls and impulse control for boys.

Source: https://neurosciencenews.com/neurodevelopment-addiction-sex-differences-29965/

Contact: Keila DePape – Organization: Media Relations, McGill University

Published: 18 November 2025

Researchers using brain imaging gain rare insight into how prenatal exposure to modern, high-THC cannabis affects brain development into adulthood

McGill University researchers at the Douglas Research Centre have found evidence that heavy cannabis use during pregnancy can cause delays in brain development in the fetus that persist into adulthood.

Using advanced MRI techniques, the team tracked the effects of prenatal cannabis exposure in mice across key developmental stages.

While public health agencies caution against cannabis use during pregnancy, most supporting evidence from humans is observational. The findings add biological evidence showing how heavy use can disrupt brain growth from early development to adulthood.

Published in Molecular Psychiatry, a Nature Portfolio journal, the preclinical study also reflects the higher-potency cannabis available today, helping to fill a gap in understanding its potential risks.

“Since cannabis legalization is relatively recent, we don’t yet have long-term human data on newer THC products,” said senior author Mallar Chakravarty, Full Professor in the Department of Psychiatry and researcher at the Douglas. “Our findings offer an early glimpse of possible outcomes a decade or two down the line.”

Tracking brain development over time

The average THC potency in dried cannabis has risen from about three per cent in the 1980s to roughly 15 per cent in 2022, with some strains reaching 30 per cent, according to Health Canada.

To model heavy use, researchers simulated daily exposure equivalent to one or two joints containing more than 10 per cent THC during a stage comparable to the first trimester of human pregnancy.

They observed developmental changes across three life stages:

  1. Late pregnancy: Embryos exposed to THC had smaller bodies and larger brain ventricles that signal abnormal brain development.
  2. Early life: Newborns gained weight faster, but their brains developed more slowly, suggesting a mismatch or delay.
  3. Adolescence to adulthood: Smaller brain volumes persisted, especially in females, who also showed more anxiety-like behaviours.

“The good news is that many of these developmental delays are subtle and could likely be offset with a supportive environment,” said Chakravarty.

3D model of the neonatal brain showing regions of reduced growth (blue) and increased growth in the ventricles (red). (Source: Lani Cupo)

A rare look across the lifespan

The methods used provided a level of detail not often achieved in preclinical studies, the researchers explain.

“That’s partly because this type of research is incredibly resource intensive,” said first author Lani Cupo, who carried out the work over six years during her PhD at McGill. “We used live brain imaging to follow development across the lifespan, which isn’t commonly done in mice.”

Collaborators at the University of Victoria later used ultra-high-resolution microscopy to examine how brain cells changed after THC exposure.

Supporting informed choices

The researchers note that some people use cannabis before realizing they are pregnant, while others use it to manage nausea or to cope with anxiety and depression, conditions that can also affect pregnancy outcomes.

“There is no ‘ideal’ pregnancy,” said Chakravarty. “This isn’t about what is good or bad, it’s about giving people the information they need to make informed decisions.”

A follow-up study will explore whether other forms of cannabis, such as edibles, vaping and CBD products affect the brain differently.

About the study

“Impact of prenatal delta-9-tetrahydrocannabinol exposure on mouse brain development: a fetal-to-adulthood magnetic resonance imaging study” by Lani Cupo and Mallar Chakravarty et al., was published in Molecular Psychiatry. It was supported by the Canadian Institutes of Health Research.

by Herschel Baker –  24 November 2025 

The Taskforce has been making many submission over a number of years to all States and Federal Government the increase danger of Illicit drugs on Australian roads. But our so-called experts do not recognize overseas research data.

Now The Taskforce at last has some Australian evidence see below.

National Data reveals drug driving is now responsible for more deaths on Australian roads than drink driving.

Drug driving is now responsible for more deaths on Australian roads than drink driving. National crash data shows that between 2010 and 2023, fatal crashes involving drugs, including cannabis, methamphetamine, MDMA and cocaine, more than doubled to 16-point-8 percent. At least one of those drugs is being detected in about 1 in 5 motorcycle deaths. Over the same 13-year period, crashes linked to drink driving decreased significantly Continuing a long-term downwards trend. There were ten times more random breath tests last year than roadside drug tests, but a drug test was ten times more likely to yield a positive result. Testing for drugs using a saliva swab is more complicated and more expensive than a breath test but states and territories have been incorporating more of them into their testing regimes. 

Source: https://drugprevent.org.uk/ppp/?p=20329&preview=true.

LAKELAND, Fla. — Officials are warning young people about the risks of an opioid-related ingredient increasingly added to energy drinks.

In her 25 years with InnerAct Alliance, a youth substance abuse prevention organization, Angie Ellison has witnessed the emergence of various drugs.

“We watch those things and try to let the community know about them because when it starts with college kids, it trickles down to high school and middle school,” said Ellison.

Ellison said energy drinks made with the synthetic form of kratom, known as 7-hydroxymitragynine (7-OH) are now widely available at gas stations, smoke shops and online.

“We’re just trying to make sure that everybody is aware of it, especially parents. Because a lot of times those drinks just look like maybe something to help you stay awake, but it could have very addictive traits to it,” said Ellison.

“It is a substance that can be dangerous when taken too much. It can cause dependence and addiction and when stopped, it can cause a pretty serious withdrawal syndrome,” said Dr. Eric Shamas, ER physician with Orlando Health Bayfront Hospital.

At the Crisis Center of Tampa Bay, they are seeing more college students experiencing withdrawal from the kratom byproduct.

“They get told to buy this kratom energy drink because it helped me get through studying for the finals. They start drinking it and then they get hooked. That’s when we find out it wasn’t containing natural kratom,” said Cameron Pelzel, community paramedic manager for Crisis Center of TampaBay.

Although Florida has recently made it illegal to sell 7-OH products, Pelzel said the ingredient can still be found in energy drinks, gummies and supplements.

“A lot of manufacturers are finding other synthetic compounds that mimic the 7-OH part, and they are adding it into it to get passed all the loopholes in the legal system so they can keep people buying these drinks. So we’re getting a lot of people that are solely addicted to it,” Pelzel said.

Source: https://www.tampabay28.com/news/region-polk/experts-raising-awareness-on-addiction-associated-with-energy-drinks-containing-kratom

The number of people admitted to hospital in Scotland with alcohol-related brain damage has reached a 10-year high.

A total of 661 people required treatment for brain injury after alcohol misuse between 2016-17, the equivalent of nearly two people a day.

Alcohol-related brain damage can lead to problems with memory and learning.

NHS Greater Glasgow and Clyde had the most admissions at 230, followed by 99 in NHS Lothian.

The figures were released in response to a parliamentary question by the Scottish Conservative health spokesman Miles Briggs.

He said it was worrying that the statistics were continuing to rise despite efforts to combat alcohol misuse.

He said: “Scotland already has one of the worst records in Europe for alcohol consumption and, despite increased awareness, the problem only seems to be getting worse.”

He added: “The decision by SNP ministers to cut funding for alcohol and drug partnerships was wrong, and has clearly impacted on the delivery of services to support people addicted to alcohol.”

Mr Briggs called for more emphasis on recovery programmes and pilot schemes for new treatments.

The Scottish government said it had invested £746m to tackle alcohol and drug abuse in the past 10 years and would be delivering an additional £20m a year to further improve services.

‘Alcohol services’

A spokesman added: “We’ve recently implemented Minimum Unit Pricing to tackle the cheap, high strength alcohol that causes so much damage to families and communities across the country.

“We also provide funding to NHS boards to treat local health needs, including people with alcohol-related brain injury.

“We expect alcohol services, mental health services and social services to work jointly in these cases to ensure those injured receive the help they need to recover and any underlying mental health issues are addressed.”

The Government’s new mandate to carry out random oral-fluid roadside drug testing marks a milestone in New Zealand’s road safety policy

Under recently passed laws, police can now stop any driver, at any time, to screen with an oral swab for four illicit substances: THC (cannabis), cocaine, methamphetamine and MDMA (ecstasy).

Police will begin the rollout in Wellington in December, with nationwide coverage expected by mid next year.

Drivers will face an initial roadside swab taking a few minutes; a positive result triggers a second test. If confirmed, the driver will face an immediate 12-hour driving ban and have their initial sample sent to a lab for evidential testing.

With nearly a third of all road deaths involving an impairing drug, moves like this are clearly aimed at a serious problem.

Efforts by the previous Labour-led government stalled because no commercially available oral-fluid device met the evidentiary standards required at the roadside.

The government now appears to have what it needs to begin roadside testing. But it remains unclear whether this policy will achieve its goal of preventing truly impaired driving.

The science behind cannabis and driving

The research on cannabis and driving impairment is mixed. Many studies show an associative rather than causal link: people who use cannabis more often tend to report more crashes, but not whether those crashes happened while they were impaired.

Unlike alcohol – where blood-alcohol concentration closely tracks impairment – no such relationship exists for THC. Cannabis is fat-soluble, so traces linger in the body and appear in saliva long after any intoxicating effect has passed, making saliva testing a relatively poor proxy for impairment.

For the other targeted drugs – the stimulants methamphetamine, cocaine and MDMA – the connection to driving impairment is also unclear. At lower doses, stimulants can even improve certain motor skills. The risks are instead tied to perceptual shifts or lapses in attention, which a saliva test cannot detect.

Because cocaine and meth remain illegal globally, it is difficult to conduct the controlled studies needed to link presence and impairment.

The policy’s focus on just four illicit drugs also raises questions of scope. In practice, these are among the easiest and most visible substances to target: the low-hanging fruit.

Yet impairment from prescription medications such as sedatives or painkillers is far more common and remains largely self-policed.

Responsibility falls to individuals and their doctors to decide when it is safe to drive – a much bigger problem than many realise.

Police expect to conduct about 50,000 tests a year – around 136 a day nationwide – compared with more than four million alcohol breath tests annually.

While that’s a modest number, the introduction of roadside breath testing in the 1980s proved transformative. Alcohol consumption, which had been rising for decades, peaked around 1980 and then began to fall after the combined impact of breath testing and public awareness campaigns.

Whether the new drug-testing programme can produce a similar deterrent effect – without that level of visibility or education – remains to be seen.

Even if it does, the overall impact may be small. Drug use and drug-driving are far less common than alcohol use ever was, so the scope for large behavioural change is limited.

The problem of lingering traces

Another pressing question is what happens when the test detects traces of cannabis long after impairment has passed. THC can remain detectable in regular users for up to 72 hours, even though its intoxicating effects last only a few.

That means a medicinal cannabis patient who took a prescribed dose the night before – or a habitual user with high baseline levels – could therefore test positive while driving safely.

Although the law provides for a medical defence, there is still no clear procedure for proving a prescription at the roadside. Few people carry that documentation, and it’s uncertain whether digital GP records would be accepted.

In practice, some law-abiding drivers will inevitably be caught up in the process simply because of residual traces that pose no safety risk. Conversely, an inexperienced cannabis user may feel heavily impaired yet return a low reading.

This uncertainty reflects a deeper flaw in the system. When the previous government first designed the policy, it intended to test for impairment.

Because no devices could meet the evidentiary standard, the law was amended to test only for presence.

Perhaps the resulting regime’s relatively low-level penalties – such as a $200 fine and 50 demerit points for the confirmation of one “qualifying” substance – will help it withstand legal scrutiny, but they also highlight its scientific limitations.

Other jurisdictions have taken a different path. Many have returned to behavioural assessments of impairment – the traditional field-sobriety approach of observing coordination, balance and attention.

In the United States, for instance, officers often rely on such behavioural indicators because the law there still centres on proving a driver was impaired, not simply that they had used a substance.

In the end, a test that measures presence rather than impairment risks confusing detection with prevention – and may do little to make New Zealand’s roads any safer.

Author: Joseph Boden, Professor of Psychology, Director of the Christchurch Health and Development Study, University of Otago

Source: https://www.1news.co.nz/2025/11/17/will-drug-testing-drivers-really-make-nz-roads-safer/

Cannabis use directly increases the risk for psychosis in teens, new research suggests.

A large prospective study of teens shows that “in adolescents, cannabis use is harmful” with respect to psychosis risk, study author Patricia J. Conrod, PhD, professor of psychiatry, University of Montreal, Canada, told Medscape Medical News.

The effect was observed for the entire cohort. This finding, said Conrod, means that all young cannabis users face psychosis risk, not just those with a family history of schizophrenia or a biological factor that increases their susceptibility to the effects of cannabis.

“The whole population is prone to have this risk,” she said.

The study was published online June 6 in JAMA Psychiatry.

Rigorous Causality Test

Increasingly, jurisdictions across North America are moving toward cannabis legalization. In Canada, a marijuana law is set to be implemented later this year.

With such changes, there’s a need to understand whether cannabis use has a causal role in the development of psychiatric diseases, such as psychosis.

To date, the evidence with respect to causality has been limited, as studies typically assess psychosis symptoms at only a single follow-up and rely on analytic models that might confound intraindividual processes with initial between-person differences.

Determining causality is especially important during adolescence, a period when both psychosis and cannabis use typically start.

For the study, researchers used random intercept cross-lagged panel models (RI-CLPMs), which Conrod described as “a very novel analytic strategy.”

RI-CLPMs use a multilevel approach to test for within-person differences that inform on the extent to which an individual’s increase in cannabis use precedes an increase in that individual’s psychosis symptoms, and vice versa.

The approach provides the most rigorous test of causal predominance between two outcomes, said Conrod.

“One of the problems in trying to assess a causal relationship between cannabis and mental health outcomes is the chicken or egg issue. Is it that people who are prone to mental health problems are more attracted to cannabis, or is it something about the onset of cannabis use that influences the acceleration of psychosis symptoms?” she said.

The study included 3720 adolescents from the Co-Venture cohort, which represents 76% of all grade 7 students attending 31 secondary schools in the greater Montreal area.

For 4 years, students completed an annual Web-based survey in which they provided self-reports of past-year cannabis use and psychosis symptoms.

Such symptoms were assessed with the Adolescent Psychotic-Like Symptoms Screener; frequency of cannabis use was assessed with a six-point scale (0 indicated never, and 5 indicated every day).

Survey information was confidential, and there were no consequences of reporting cannabis use.

“Once you make those guarantees, students are quite comfortable about reporting, and they become used to doing it,” said Conrod.

Marijuana Use Highly Prevalent

The first time point occurred at a mean age of 12.8 years. Twelve months separated each assessment. In total, 86.7% and 94.4% of participants had a minimum of two time points out of four on psychosis symptoms and cannabis use, respectively.

The study revealed statistically significant positive cross-lagged associations, at every time point, from cannabis use to psychosis symptoms reported 12 months later, over and above the random intercepts of cannabis use and psychosis symptoms (between-person differences). The statistical significances varied from P < .001 to P < .05.

Cannabis use, in any given year, predicted an increase in psychosis symptoms a year later, said Conrod.

This type of analysis is more reliable than biological measures, such as blood tests, said Conrod.

“Biological measures aren’t sensitive enough to the infrequent and low level of use that we tend to see in young adolescents,” she said.

In light of these results, Conrod called for increased access by high school students to evidence-based cannabis prevention programs.

Such programs exist, but there are no systematic efforts to make them available to high school students across the country, she said.

“It’s extremely important that governments dramatically step up their efforts around access to evidence-based cannabis prevention programs,” she said.

Currently, marijuana use in teens is “very prevalent,” she said. Surveys suggest that about 30% of older high school students in the Canadian province of Ontario use cannabis.

“I’d like to see governments begin to forge some new innovative policy that will address this level of use in the underaged,” Conrad said.

Reducing access to and demand for cannabis among youth could lead to reductions in risk for major psychiatric conditions, she said.

A limitation of the study was that cannabis use and psychosis symptoms were self-reported and were not confirmed by clinicians. However, as the authors note, previous work has shown positive predictive values for such self-reports of up to 80%.

Unique Research

Commenting on the findings for Medscape Medical News, Robert Milin, MD, child and adolescent psychiatrist, addiction psychiatrist, and associate professor of psychiatry, University of Ottawa, said the study is at “the vanguard” of major research investigating cannabis use in adolescents over time that is being carried out by that National Institute on Drug Abuse in the United States.

“The study is at the forefront because it is specifically looking to measure psychosis symptoms and cannabis use in adolescents, and the model they are using strengthens the study,” said Milin.

That model uses “refined measures or improved measures to look at causality, vs what we call temporal associations,” he said.

The fact that the study investigated teens starting at age 13 years is unique, said Milin. In most related studies, the starting age of the participants is 15 or 16 years.

He emphasized that the study examined psychosis symptoms and not psychotic disorder, although having psychotic symptoms increases the risk for a psychotic disorder.

The study was supported by grants from the Canadian Institutes of Health Research. Dr Conrod and Dr Milin have disclosed no relevant financial relationships.

JAMA Psychiatry. Published online June 6, 2018Abstract

Source: https://www.medscape.com/viewarticle/898120#vp_1 June 2018

by Mark Gold M.D. –  Reviewed by Michelle Quirk –  –

Key points

  • We screen and intervene early for hypertension, type 2 diabetes, and cancer; we can do the same for addiction.
  • Preaddiction thinking supports early engagement, attacks denial, and normalizes a harm-reducing mindset.
  • Delaying treatment increases risks and harms, contradicting outcomes research and ethical medical practice.

Raising “rock bottom” with early diagnosis and intervention in substance use.

The mistaken belief that people with substance use disorders (SUDs) must “hit rock bottom” has shaped addiction care for decades. This model contrasts with how medicine manages chronic illnesses, where early detection and proactive treatment are normal. The “bottom” in addiction is a moment of maximum despair and hopelessness. It also may be a life-changing event like getting fired, losing a relationship, or facing legal charges. It could mean a moment between considering changing one’s life or suicide.

For more than 30 years, I have proposed that addiction treatment must “move up the bottom” to reduce harm and have a better chance of working. Applying preaddiction logic holds promise for lowering SUD-related suffering, illness, and mortality. Denying early diagnosis and treatment may primarily stem from addiction stigma.

“Let them hit bottom” was (and is) the refrain in addiction care; suffering supposedly must crescendo before people with an SUD accept the need to stop using drugs. Whether arising from fear of people gaming the system and seeking opioids for fake injuries or the inherent austerity of public institutions, this belief still shapes policy and practice.

In the early 1970s, I encountered this idea as a medical student. People who came to the emergency room with overdoses were not admitted. Medicine had little to offer and might undermine a person’s journey toward readiness; a person might feel ready for treatment, but someone else decided they’d not hit bottom. How ridiculous is this?

But when physicians misuse substances, then early intervention, long-term monitoring, and structured support are considered necessary. These practices, codified in physicians’ health programs (PHPs) across the United States, help most physicians, yielding an excellent return-to-work rate and resumed function. The message is clear: The “rock bottom” model is neither ethical nor clinically efficient.

National Institute on Drug Abuse Director Nora Volkow has called the belief that someone must “hit rock bottom” before treatment “a myth that can have dire consequences.” While the rock-bottom narrative offers psychological neatness—drama, surrender, catharsis—it lacks scientific grounding. Substance use disorders rarely emerge overnight; they evolve with “use,” then “risky use,” often in adolescence or early adulthood. By the time someone meets all criteria for severe SUD, the hijacked brain is adept at finding and using drugs, and not getting caught or sent to treatment. The longer SUD continues, the more complex and complicated the reversal is.

Ethically, “waiting” is untenable. Delayed intervention amplifies harm, entrenches bad behavior, and puts family, friends, and others at risk of harm. An earlier intervention and treatment might prevent loss of friends, family, and job, as well as halt the addiction from becoming entrenched.

We don’t withhold antihypertensives until catastrophic bleeds occur. We don’t wait for myocardial infarction to begin statins. Medicine emphasizes upstream prevention and treatment. While many perceive addiction as a choice, impaired MDs will tell you they wish someone had intervened and helped them earlier.

The directors of the National Institute on Drug Abuse and the National Institute on Alcohol Abuse and Alcoholism proposed, in 2022, earlier identification and intervention for substance use and its consequences. Volkow, Koob, and McLellan introduced this preaddiction concept by paralleling prediabetes. These researchers used mild to moderate Diagnostic and Statistical Manual of Mental Disorders, 5th Edition, SUD criteria to help define pre-addiction, allowing early detection, brief treatment, or intervention before addiction-related neurobehavioral and psychosocial collapses occurred.

Research shows that at mild to moderate levels of SUD severity, patients often retain executive function, can reassert control over drugs, and may still re-engage and preserve intact relationships, work roles, and decision-making. At this preaddiction point, brief interventions, outpatient treatment, or educational measures have great potential to resolve the preaddiction. Sometimes, treatment might comprise advice and education rather than weeks in a treatment facility. In addition, early interventions may not require anti-craving medications, detoxification, opioid treatment medications, hospitalization, or extensive monitoring.

Preaddiction thinking supports early engagement, attacks denial, and normalizes a preventive mindset. Preaddiction communicates risk while preserving agency, as with prediabetes. It gives clinicians a structured rationale to screen, counsel, and refer before severe illness.

Early Intervention Works

Nowhere is “raising the bottom” more visible than in PHPs. These state-based programs often identify impaired doctors from anonymous reports of patients, staff, or other providers. They protect patients from impaired physicians by managing them through structured evaluation, mandated treatment, regular toxicology testing, workplace monitoring, and ongoing recovery support—often for five or more years.

This model is widely celebrated, even though its success depends partly on external leverage: Physicians are often told noncompliance may result in license suspension and loss of professional status. In a five-year, multi-state study, DuPont and colleagues found that more than 70 percent of the doctors returned to practice, sustaining functional recovery. The model used early identification, accountability, structured care, serial urine testing, and long-term follow-up. It’s preventive, continuous, and outcome-driven.

The PHP system contradicts the “hitting bottom” mantra. It’s a real-life demonstration of what addiction care could be: long-term, hopeful, and outcome-driven, but with accountability. The limited application of such systems beyond professional circles reflects a profound inequity—not a clinical limitation.

Physician colleagues have moral, ethical, and legal obligations to report coworkers whose impairment threatens patients. Avoiding “punishment” and promoting sharing, shame reduction, and physicians helping each other in camaraderie while in treatment is critical to the success of physician programs.

When structured and ethical, coercion may paradoxically enhance autonomy by restoring capacity. Treat coercion as a clinical tool—not punishment. Integrate preaddiction into medical education, focusing on prevention, brain changes, and ethical duties.

“Bottom” need not be the destination just before treatment. Waiting or delaying intervention until full disorder or voluntary self-referral risks disease progression, more entrenched brain/behavior changes, worse prognosis, and higher costs.

Summary

To align addiction with other chronic medical conditions, SUD screening must be routine for every healthcare, clinic, or emergency department visit. Duration, age of initiation at use, and severity should be assessed. The preaddiction concept provides a teachable inflection point rather than the binary “normal vs addicted,” and intervention may change the trajectory. Brief interventions may be the only treatment needed if interventions start early enough.

Medicine should abandon the myth that people with SUDs must earn the right to be helped by suffering “enough.” Medicine has shown numerous benefits of early screening, intervention, and assisting patients in changing. If we can intervene early for hypertension, for type 2 diabetes, and for breast and colon cancer, we can do the same for addiction. What’s holding us back?

Source: https://www.psychologytoday.com/us/blog/addiction-outlook/202511/preaddiction-intervention-could-save-lives

The New England Journal of Medicine is again promoting failed progressive public policies. This time, it is “harm reduction.” From “The Erosion of Harm Reduction,” by Joshua Barocas, M.D.

Unlike the targets of many other recent attacks on public health and medicine in the United States, harm reduction is not a formal bureaucracy, but a philosophy and an approach to health care. As defined by the Drug Policy Alliance, it is “a set of ideas and interventions that seek to reduce the harms associated with both drug use and punitive drug policies.” Harm reduction is embodied in syringe-services programs (SSPs), naloxone distribution, overdose education, overdose-prevention centers [i.e. “safe injection sites”], and decriminalization of drugs.

Barocas decries the Trump Administration’s executive order that limits such policies:

Perhaps most concerning, an executive order focused on homelessness and civil commitment issued on July 24, 2025, prohibits federal SAMHSA discretionary grants from being used to fund harm-reduction activities, proposes a freeze on federal funding to organizations that provide “drug paraphernalia,” and threatens legal action against harm-reduction organizations. The executive order states that these approaches “only facilitate illegal drug use and its attendant harm.”

The Streets of San Francisco

My wife, the Las Vegas Review-Journal columnist Debra J. Saunders, covered San Francisco’s harm reduction drug policies extensively back when she worked for the San Francisco Chronicle. It started with “needle exchange,” which she initially supported as a means of preventing the spread of HIV. The idea was for addicts to “exchange” dirty needles — a prime source of HIV transmission — for clean ones. The rule was: no used needle, no free clean replacement. Unfortunately, the program led to greater drug abuse. “Harm reduction” zealots eventually dropped the exchange requirement, which resulted in dangerous used needles littering San Francisco’s sidewalks and even children’s playgrounds.

Debra noticed the decay and decided to investigate. I’ll let her describe it. From a 2019 Review-Journal column:

In 2015, I learned that San Francisco had abandoned the “needle exchange” model — clinics would dispense one new needle in exchange for each used needle — in favor of needle “access.” Which means free needles.

So I walked into a downtown clinic and walked out with a “starter kit” of 20 needles in a paper bag filled with other paraphernalia meant to make it safer to shoot up. It was that easy.

You see, it had become too much to expect the city’s many junkies to return used needles to get free needles. (It also was too much to expect drug users to buy their own needles, which had been legalized.)

Instead the Special City, as some call it, put out drop boxes in the hope that the civic-minded would use them. How did that work out? Just look at the sidewalks. It’s not working.

Can You Imagine?

San Francisco was allowing harm reducers to give away “starter kits” to people so they could begin injecting drugs! That’s harm causation.

Policies have consequences. Those of San Francisco’s homelessness “harm reduction” protocols were dire. Human feces befouled the streets, to the point that a “poop map” was published to warn people about unsanitary messes. The downtown commercial center imploded. Once-thriving shopping hubs closed. Union Square became a ghost town. Squalor ruled blocks of Market Street. A total “harm reduction” catastrophe.

The Good Doctor Barocas

But don’t tell that to the good doctor Barocas, who concludes his NEJM piece thusly:

Harm reduction is evidence-based health care that is rooted in public health principles. There is no single best form of harm reduction — this model depends on the availability of an array of services that meet patients where they are. Undermining harm reduction and cutting related programs isn’t merely a funding decision; it is an assault on an approach to health care that prioritizes evidence, compassion, and dignity — values that are central to the medical profession. Such actions are in keeping with other moves by the federal government that encroach on clinical practice and the professional judgment of clinicians and undermine the autonomy of patients. Like many other aspects of public health and medical care, harm reduction is being dangerously and rapidly eroded.

I don’t think that “personal autonomy” and “human dignity” entail shooting up harmful substances, defecating in public, living (and dying) on the streets, or engaging in the many other behaviors associated with drug abuse (and mental illness) that have ruined too many of America’s formerly world-class cities.

Helping drug abusers as well as we can is an ethical imperative. The question therefore becomes: Do we love our addicted countrymen enough to insist that they diligently engage in programs to restore themselves to lives of dignity and self-respect? Harm reduction isn’t that. Indeed, the more we take that path, the worse things get. Facilitating drug abuse — which is what “harm reduction” does — causes terrible harm, often to the people it purports to help and certainly to the communities in which they reside.

Wesley J. Smith – Chair and Senior Fellow, Center on Human Exceptionalism

Wesley J. Smith is Chair and Senior Fellow at Discovery Institute’s Center on Human Exceptionalism. Wesley is a contributor to National Review and is the author of 14 books, in recent years focusing on human dignity, liberty, and equality. Wesley has been recognized as one of America’s premier public intellectuals on bioethics by National Journal and has been honored by the Human Life Foundation as a “Great Defender of Life” for his work against suicide and euthanasia. Wesley’s most recent book is Culture of Death: The Age of “Do Harm” Medicine, a warning about the dangers to patients of the modern bioethics movement.

Source: https://scienceandculture.com/2025/11/harm-reduction-harms-the-homeless/


Opening Statement from NDPA:

Commentary on psychiatry and its interaction with drug problems: Whilst this article sometimes includes CCHR’s campaigning rhetoric (and CCHR do much good work) there is also much of generic interest and usefulness on this specific subject – both in the article text and in the sources listed. For this reason, we include this in NDPA’s archive. (CCHR’s background and work can be reviewed via info@cchr.org.uk)

LOS ANGELES, Calif., Nov. 3, 2025 (SEND2PRESS NEWSWIRE) — Each May and October, millions are urged to “raise awareness” for mental health through national and international campaigns, including World Mental Health Day in October. Yet, according to the mental health industry watchdog, Citizens Commission on Human Rights International (CCHR), many of the advocacy campaigns driving these observances are dominated by pharmaceutical interests and a biomedical model reliant on psychotropic drugs, electroshock, and even psychosurgery. The outcome has been catastrophic: more than 76 million Americans take psychiatric drugs, and an estimated 100,000—including children as young as five—are electroshocked annually.

CCHR warns that modern mental-health awareness campaigns are not about understanding the mind but promoting psychiatry’s drug-driven model of “treatment.” Since its founding in 1969, the organization has used these awareness months to expose psychiatric abuse and coercion—particularly the drugging, electroshocking, and violent restraint of children in behavioral facilities. Working with parents, doctors, and lawmakers, CCHR has helped establish hundreds of laws globally to protect against psychiatric harm, including the first U.S. bans on electroshock for minors in California (1976) and Texas (1993), and the 1983 prohibition of Deep Sleep Treatment in Australia following 48 patient deaths—now a criminal offense to administer it in New South Wales and Western Australia.

CHALLENGING DRUG-INDUCED VIOLENCE

CCHR has documented the tragic outcomes of psychiatry’s drug-based approach, including its potential links to acts of senseless violence. It testified before the first inquest into the deaths of eight victims of a Kentucky mass shooting in 1989, where the perpetrator’s psychiatrist acknowledged that the antidepressant Prozac (fluoxetine) potentially contributed to the crime. A decade later, CCHR obtained confirmation that Columbine ringleader Eric Harris had the antidepressant Luvox in his system—despite clinical trials showing the drug could “form of psychosis characterized by exalted feelings, delusions of grandeur…and overproduction of ideas.”[1]

The watchdog’s efforts led to a 1999 Colorado government hearing on psychiatric drugs and violence, with the chair, State Rep. Penn Pfiffner, stating: “There is enough coincidence and enough professional opinion from legitimate scientists to cause us to raise the issue and to ask further questions.”[2] Working with Patricia Johnson, then-member of the Colorado State Board of Education, CCHR helped obtain a precedent-setting resolution urging academic—not chemical—solutions for classroom issues.[3]

CCHR also joined with medical experts and parents to press the U.S. Food and Drug Administration to issue its 2004 “black box” warning that antidepressants can cause suicidal behavior in children, which was later expanded in 2007 to include young adults up to age 24. Today, studies confirm that 46–71% of antidepressant users experience emotional blunting, dulling empathy, and increasing detachment—a factor present in numerous violent tragedies.[4]

Further reforms followed. In 2004, CCHR helped secure the federal Prohibition of Mandatory Medication amendment, banning schools from forcing children to take psychotropic drugs as a condition of education. Three years later, language CCHR helped introduce into the FDA reform bill required pharmaceutical ads to direct consumers to report drug side effects, causing adverse drug reporting to increase by 33 percent.[5]

CCHR’s investigations have also helped expose corruption and abuse in the psychiatric hospital and “troubled teen treatment” industry. Working with whistleblowers and journalists, it uncovered coercive admissions and insurance fraud within major private psychiatric hospital chains, leading to multiple state and federal investigations, criminal penalties, and closure of hundreds of abusive facilities. New laws were enacted to prohibit “bounty hunter” practices used to capture insured individuals for involuntary commitment and billing exploitation.[6]

Raising awareness, CCHR emphasizes, means parents can make better-informed choices and seek non-invasive, evidence-based help for their children. One expert has described the psychiatric polypharmacy trend as creating “a generation of child guinea pigs.” As The New York Times reported, “many psychiatric drugs commonly prescribed to adolescents are not approved for people under 18. And they are being prescribed in combinations that have not been studied for safety or for their long-term impact on the developing brain.”[7]

In 2013, nearly 8.4 million American children were taking psychiatric drugs.[8] By 2020, the IQVIA Total Patient Tracker Database showed that number had dropped to 6.1 million[9]—a notable decline that CCHR attributes in part to heightened public awareness, stronger warnings, and parental advocacy. However, millions of children remain drugged, underscoring that while progress has been made, the systemic overreliance on psychotropic drugs continues.

In addition to its feature-length documentaries, CCHR produces short educational videos on its YouTube channel to inform the public about mental health abuses and their prevention. Working alongside doctors, whistleblowers, parents, consumers, and civil and human rights organizations, CCHR continues to supply legislators and government agencies with documentation exposing psychiatric abuses and driving legislative reform to safeguard consumer and patient rights.

Today, both the World Health Organization (WHO) and United Nations agencies are calling for an end to coercive psychiatric practices—particularly those inflicted on children. Yet much of the mental-health establishment, including “patient-advocacy” groups with deep pharmaceutical ties, remains silent—endorsing mass drugging instead of confronting its documented dangers.

For more than five decades, CCHR International, which was originally established by the Church of Scientology and eminent professor of psychiatry, Dr. Thomas Szasz, has been a catalyst for reform, exposing human-rights violations in psychiatry and helping to achieve legislative and cultural change that has already begun to reduce child drugging and public acceptance of coercion. Its continuing campaigns seek a mental-health system based on transparency, informed consent, and respect for human dignity—affirming that lasting mental health will come not through drugs or shocks, but through compassion, truth, and accountability.

To learn more, visit: https://www.cchrint.org/2025/10/31/cchr-exposes-harms-behind-todays-mental-health-awareness-campaigns/

Sources:

[1] https://www.cchrint.org/2023/01/16/school-mental-health-programs-questioned-after-6-year-old-shot-teacher/

[2] https://www.cchrint.org/2023/01/16/school-mental-health-programs-questioned-after-6-year-old-shot-teacher/; Kelly P. O’Meara, “A Different Kind of Drug War,” Insight Magazine, 13 Dec. 1999

[3] https://www.cchrint.org/2023/01/16/school-mental-health-programs-questioned-after-6-year-old-shot-teacher/; “Resolution: Promoting the Use of Academic Solutions to Resolve Problems with Behavior, Attention, and Learning,” Colorado State Board of Education, 11 Nov. 1999

[4] https://www.cchrint.org/2022/09/05/the-travesty-of-6-million-youths-on-psychotropics-a-expert-calls-it-a-generation-of-child-guinea-pigs/https://www.verywellmind.com/can-antidepressants-make-you-feel-emotionally-numb-1067348

[5] https://www.cchrint.org/about-us/cchr-accomplishments/

[6] https://www.cchrint.org/about-us/cchr-accomplishments/

[7] https://www.cchrint.org/2022/09/05/the-travesty-of-6-million-youths-on-psychotropics-a-expert-calls-it-a-generation-of-child-guinea-pigs/https://nypost.com/2022/08/29/the-ny-times-suddenly-discovered-were-giving-kids-dangerous-drugs/https://www.nytimes.com/2022/08/27/health/teens-psychiatric-drugs.html

[8] https://www.cchrint.org/2016/11/30/cchr-launches-parents-know-your-rights-campaign/

[9] https://www.cchrint.org/psychiatric-drugs/children-on-psychiatric-drugs/

Source: https://www.yourvalley.net/stories/cchr-warns-mental-health-awareness-masking-drug-and-shock-abuse,630679

Opening statement by NDPA:

Why are we addressing ‘gambling’ in a drug prevention website? We address it because gambling is but one of other behaviours which some professionals address under what they term a ‘family of compulsive behaviours’ – others in this ‘family’ will include, for example, sexual behaviour which may have become compulsive rather than ‘the norm’ (whatever that means in that context!)

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by Franny Lazarus – Ohio State News – Oct 212025

The ‘problem gambling’ issue can be devastating for college students

Since opening at The Ohio State University in 2015, the Higher Education Center for Alcohol and Drug Misuse Prevention and Recovery (HECAOD) has been developing college campus professionals who support alcohol and drug misuse prevention.

Beginning in 2023, HECAOD expanded its portfolio to focus on a new campus issue: gambling.

“The idea that college students are at higher risk of experiencing harms from gambling is not a new idea,” said Cindy Clouner, managing director. “Folks doing work in the community gambling space have known that for a long time. But on campuses, it’s not been on our radar.”

HECAOD established the Collegiate Problem Gambling Workgroup in 2023 to better learn what campuses are facing.

“It was necessary to understand quickly if we were going to do this work well,” said Jim Lange, the center’s executive director. “We invited all the people that we could find. It began to snowball – people were bringing other folks they knew. It’s been really helpful.”

One of the reasons that gambling can be a hard problem to track is that it’s not an obvious one.

“It’s a quieter issue,” Clouner said. “When students are experiencing harm from alcohol, they may be throwing up, being loud and obnoxious, vandalizing things. It can be easier to identify someone who may be impaired by substances. With the advent of online gambling, though, a student could be gambling on their phone, and no one would know.”

Gambling’s long-term impacts can be crippling, Lange said.

“We see that financial stress is a barrier to completing a college degree,” he said. “A gambling issue can be a risk factor for suicidal ideation and attempts. When you get to that extreme, it is literally deadly.”

HECAOD works closely with the Office of Student Life’s Student Wellness Center.

“Many campuses aren’t resourced like we are,” Clouner said. “We’re lucky at Ohio State. We have a large wellness center with multiple staff.”

Helping other schools develop resources is how HECAOD will use a $40,000 Agility Grant from the National Council on Problem Gambling, which the center received last year. HECAOD partners with the National Consortium of State Coalitions (NCSC) to reach campuses across the country.

“That group is made up of more than 30 statewide coalitions,” Clouner said. “They all operate differently and have different goals, but they bring together campus professionals who are focused on health and well-being initiatives.”

HECAOD will provide a turnkey training on collegiate gambling to NCSC members, who will then be able to deliver the training at their member institutions. Clouner said their goal is to reach 1,000 campuses.

“There may be one person doing all the wellness work at a university,” she said. “Putting something else on their plate is unrealistic. This way, we’ve established a go-to person in a region that multiple campuses can work with to develop knowledge and skills, provide resources and more.”

And these resources aren’t just for students worried about their own gambling.

“Sometimes a friend is seeking help,” Lange said. “They have a relationship with someone and they’re concerned about that person. That’s been identified as a really important component of the training of students.”

“If you’re concerned about yourself or someone else’s behavior,” Clouner said, “there are trained people who can help you get connected with resources.”

Source: https://news.osu.edu/ohio-state-center-leading-charge-against-problem-gambling/

pubmed logo
by: Madeline E CrozierLorenzo LeggioMehdi Farokhnia

Abstract

Background: The Behavioral Inhibition System (BIS) and the Behavioral Approach System (BAS) are two core motivational systems linked to addictive behaviors. Understanding the biobehavioral mechanisms and correlates of Alcohol Use Disorder (AUD), including BIS/BAS, could lead to improved strategies for prevention, diagnosis, and treatment.

Methods: Using baseline data from five clinical studies, we conducted secondary analyses to explore the link between BIS/BAS and alcohol-related outcomes in people with AUD (N = 94). We hypothesized that lower BIS and higher BAS scores would be associated with more severe alcohol use, obsessive thoughts, and compulsive behaviors toward alcohol. In additional post-hoc analyses, we also explored the mediating effects of anxiety and depression in this regard.

Results: Higher BIS scores were associated with higher severity of alcohol use and more obsessive-compulsive drinking behaviors, as respectively measured by the Alcohol Use Disorder Identification Test (AUDIT) and the Obsessive-Compulsive Drinking Scale (OCDS). Anxiety (Spielberger State-Trait Anxiety Inventory) and depression (Montgomery-Asberg Depression Rating Scale) significantly mediated the positive associations between BIS scores and AUDIT/OCDS. No significant associations were found between BAS scores and alcohol-related measures.

Conclusions: These findings suggest that, in this sample of middle-aged people with AUD, a heightened BIS leads to more severe alcohol use, and this relationship is mediated by anxiety and depressive symptoms. Further prospective research in adults with AUD and varying levels of alcohol use is necessary to better understand the relationship between BIS/BAS and alcohol-related outcomes.

Dear friends,

We wanted to make sure you had seen four key studies from the past week:

  • groundbreaking study in The Lancet found that marijuana use over four years actually made it harder for patients to cope with chronic pain, and did not reduce their use of opioids
  • A study in Frontiers in Psychiatry found that increasing self-exposure to non-medical marijuana was a predictor of greater odds of opioid dependence diagnosis.
  • A study in the International Review of Psychiatry found an increased rate of serious mental illness in states that had legalized medical marijuana.
  • In JAMA: “(The) associated acute and long-term psychoactive effects on brain function (of marijuana) are…known. Expanding use of cannabis among pregnant and lactating women (as likely will occur with legalization) may lead to increased risk from fetal and child exposures if the teratogenic potential of cannabis remains underappreciated.”

Additional Resources on Link Between Marijuana and Opioids

These articles follow other warnings from medical professionals: the recent editorial published in the Journal of the Society for the Study of Addiction, which cautions against drawing policy conclusions from population studies, and the editorial comment from the American Society of Addiction Medicine on February 20, 2018. And don’t forget NIDA’s rigorous study showing pot users are twice as likely to have abused opioids and have an opioid use disorder than non-marijuana users

SAM has published a one-pager describing the overwhelming link between marijuana and opioid abuse. While not every marijuana user will go on to use heroin, nearly all heroin users previously abused marijuana. We need smart policies that discourage use, get people back on their feet, and restore people to participate in and contribute to society. States that have legalized marijuana, by contrast, see increased drugged driving, increased arrests of minority youth, and increased emergency room visits. Colorado is experiencing the highest number of drug overdoses in its history. Legalization is a failed experiment.

Please visit learnaboutsam.org to learn about a smarter approach.

Sincerely,

  Kevin Sabet

  President, Smart Approaches to Marijuana (SAM)

  Affiliated Fellow, Yale University

Source: Email from reply@learnaboutsam.org July 2018

Elsevier

International Journal of Drug Policy

Volume 145, November 2025, 105015 by Shane O’Mahony
International Journal of Drug Policy
Abstract
The brain disease model of addiction (BDMA) is a dominant, if highly contested, model of drug addiction globally. Over many decades, researchers have marshalled evidence from animal studies, neuroimaging scans, and genome wide association studies to argue that addiction is a brain disease. However, critics have argued that the model de-emphasises social and economic contexts, downplays the phenomenon of spontaneous or natural recovery, and over-interprets neuroscientific findings. Building on this critical tradition, the current paper asks a related question: Has the claim that addiction is a brain disease helped or harmed those experiencing drug-related harm epistemically? While no definitive answer to this question is offered, the current paper argues that overall, the claim that addiction is a brain disease advanced by proponents of the BDMA has harmed substance users already experiencing multiple disadvantages epistemically.
Drawing on the concept of epistemic injustice, the current paper argues that the category ‘drugs’ creates an artificial and harmful dichotomy between those who use licit medicines and experience harm and those who use illicit substances and experience harm. Furthermore, this artificial dichotomy is compounded by racist and colonial discourses central to the war on drugs, and a rigid biological reductionism that de-emphasises social, economic, and cultural harm. The paper concludes by sketching an alternative approach rooted in epistemic justice, and a discussion of the implications of this concept for research and theory.

Introduction

Academic literature has witnessed significant debate over the past thirty years concerning whether addiction is best thought of as a brain disease. While the framing of addiction as a disease has a much longer history (see Levine, 1978), the claim that addiction is specifically a brain disease and the debates around this claim began in earnest when Leshner (1997) categorically claimed that neuroscientific advances had shown that drug addiction is a chronic, relapsing disease resulting from the prolonged effects of drugs on the brain. This framing centres the illness or disorder firmly in the realm of the brain’s structure and functioning, as opposed to a lack of meaning and purpose (i.e. a spiritual disease/malady) as per proponents of AA’s spiritual disease model (see O’Mahony, 2019), a disease of the will as per Benjamin Rush (see Seddon, 2010), or a highly heterogeneous disorder from which more homogeneous, qualitatively distinct subtypes might be derived, only some of which constitute a disease, as E.M. Jellinek and colleagues have argued (see Kelly, 2018).
Despite multiple sustained critiques of the BDMA from criminologists (O’Mahony, 2019), anthropologists (Bourgois, 2009), psychologists (Alexander, 2008), and some within neuroscience (Heilig, 2021, Kalant, 2014) have reiterated that, despite valid criticism, the claim that addiction has a firm neurobiological basis remains strongly supported by the best scientific evidence. Most recently, Heather et al. (2022) have produced a volume evaluating the BDMA through contributions from supporters, opponents, and undecided scholars. While the editors entertain arguments from many different perspectives and models, they argue that addiction is undergoing a revolutionary change—from being considered a brain disease to a disorder of voluntary behaviour (Heather et al., 2022)—though this is contested by advocates of the BDMA (see Heilig, 2021).
While some have examined the emergence of the BDMA from a social constructionist perspective (Keane et al., 2014), and criticised its relative ignorance of social and cultural context (Reinarman, 2005), the current paper asks a different question: has the claim that addiction is best thought of as a brain disease helped or harmed those suffering from harmful substance use epistemically? While critical scholars have approached this question from many angles, there has been little reflection among supporters of the model, where it is often assumed that framing addiction as a brain disease will reduce stigma, increase access to treatment, and lead to better outcomes in general for those experiencing harmful drug use (see Volkow & Koob, 2010). Yet many critical scholars argue that disease understandings commit people to a lifetime of reduced autonomy (Hart, 2021), as they are perceived—by themselves and others—to lack control and free will in important ways. This, in turn, can stigmatise them as disordered and constitutionally different from others. Moreover, clinical treatment providers appear ambiguous in their support of the BDMA. While some believe it can reduce stigma, others argue it may foster hopelessness within clients (Barnett et al., 2018).
Similarly, while access to treatment has increased in many countries, this has not always been due to the adoption of the BDMA or any disease model. For example, Ireland has expanded treatment access in the 21st century (see Butler, 2007), yet never explicitly adopted disease understandings. Sweden’s approach, while complex, accommodates both social and brain-based understandings of drug-related harm (Grahn et al., 2014). Meanwhile, the Islamic Republic of Iran has recently increased access to treatment despite its lack of commitment to disease framings (see Mirzaei et al., 2022). While one might argue that these increases were compelled by growing rates of drug-related harm, the case remains: representing addiction as a brain disease has not, in and of itself, played a decisive role in facilitating treatment access in these diverse contexts. This is not to say that the BDMA cannot support access, but that many culturally diverse countries have achieved this end without adopting it. Ultimately, the choice is not between viewing addiction as a moral failing or a brain disease, there are diverse ways to frame addiction to achieve stigma reduction and treatment uptake ends.
While much debate exists within the academic literature, the BDMA currently represents a dominant way addiction is understood in the United States (Barnett et al., 2018) and that the model is influential in Europe (see SStorbjörk, 2018; O’Mahony, 2019) and Australia (Keane et al., 2014). Given this position of influence, the current paper asks whether the model helps or harms those experiencing drug-related harm epistemically. That is, does the claim that they are suffering from a brain disease help them understand themselves and their experiences of drug-related harm and/or enable them to communicate this to others—or is it harmful in these respects? Before turning to this question, let us briefly examine the relevant literature.

Section snippets

Background

The brain disease model of addiction has been championed for several decades by the US based National Institute of Drug Abuse (NIDA). While the model contains many complexities, at its most basic, the claim is that persistent drug use changes the brain’s structure and function to such an extent as to ‘hijack’ the brain’s motivational reward circuitry. Koob and Simon (2009) argue, for example, that a key element of drug addiction is how the brain’s reward system changes throughout the course of

Epistemic injustice

Epistemic injustice is a form of injustice ‘done to someone specifically in their capacity as a knower’ (Fricker, 2007: p.1). Put simply, an injustice that harms a person’s ability to know things and be seen by others to know things. Fricker (2007) distinguishes between two different forms of epistemic injustice: (1) Testimonial injustice (TI); and (2) Hermeneutical injustice (HI). TI occurs when a hearer’s prejudices about a person’s identity led them to treat what the person says more

The concept of drugs and hermeneutical injustice

The first issue relevant to this paper is the category of ‘drug’ itself. The question is whether this category—central to the Brain Disease Model of Addiction (BDMA)—is rooted in hermeneutic injustice. A useful starting point is the work of British drug historian Porter (1996). In a paper tracing the historical origins of the “drug problem” in Britain, Porter argues that the concept of a drug is historically contingent:

“If you had talked about the ‘drug problem’ two hundred years ago, no one

The war on drugs and hermeneutic injustice

The previous section argued that the concept of “drugs” is rooted in hermeneutic injustice (HI). This section demonstrates that, cross-culturally, the prohibition and criminalisation of certain types of substance use have been selective regarding which substances are targeted. Put simply, evidence from several jurisdictions indicates that substances used by marginalised populations are disproportionately criminalised. We begin with examples from the United States.
In a landmark study on the

Biological reductionism and epistemic injustice

The previous section demonstrated that substance use among marginalised groups is often labelled drug use, stigmatised and criminalised, while use among powerful groups often escapes these labels and is treated more benignly. This section will show how this tendency also obscures the social, cultural, historical, and economic forces underpinning harmful drug use among marginalised Indigenous populations. This occurs through the biological reductionism at the heart of the Brain Disease Model of

An alternative frame: epistemic justice

This paper argued that the influence of the BDMA (though heavily contested) leads to multiple instances of epistemic injustice (specifically hermeneutic injustices). If this is the case, it is plausible to ask how we might move away from this harmful framing of substance-related problems to a more epistemically just approach. Epistemic justice has been defined as ‘the proper inclusion and balancing of all epistemic sources’ (Geuskens, 2018: 2). Firstly, if we are to move towards a context where

Conclusion and discussion

The current paper asked the following question: Does the claim that addiction is a brain disease put forth by supporters of the BDMA help or harm those who are currently experiencing drug-related harm epistemically? The answer that has been developed is that the BDMA causes harm as it leads to various instances of epistemic injustice. The first instance of epistemic injustice relates to the concept of ‘drugs’ itself. Put simply, built into the very foundations of the concept ‘drugs’ is the

CRediT authorship contribution statement

Shane O’Mahony: Writing – review & editing, Writing – original draft, Visualization, Validation, Supervision, Software, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization.
Source:  https://www.sciencedirect.com/science/article/abs/pii/S0955395925003111

Source: https://learnaboutsam.org/wp-content/uploads/2017/09/27Sep2017-opioids-one-pager.pdf September 2017

 

The UK government has launched a new campaign to alert young people to the dangers of ketamine, counterfeit medicines and adulterated THC vapes.
  • New campaign to alert young people to the dangers of ketamine, counterfeit medicines and adulterated THC vapes
  • Ketamine use and drug poisonings highest on record with 8 times more people seeking treatment since 2015
  • Government investing £310 million into drug treatment services alongside awareness campaign

Young people are being warned that they risk irreparable bladder damage, poisoning and even death if they take ketamine, synthetic opioids or deliberately contaminated THC vapes, as part of a new anti-drugs campaign.

Launching today (16 October 2025), the campaign, which includes online films, will target 16 to 24 years olds and social media users, following a worrying rise in the number of young people being harmed by drugs. There has been an eight-fold increase in the number of people requiring treatment for ketamine since 2015.

Supported by £310 million investment in drug treatment services, this initiative directly supports the government’s Plan for Change mission to create safer streets by reducing serious harm and protecting communities from emerging drug threats.

Health Minister Ashley Dalton said:

Young people don’t always realise the decision to take drugs such as ketamine can have profound effects. It can destroy your bladder and even end your life.

We’ve seen a worrying rise in people coming to harm from ketamine as well as deliberately contaminated THC vapes and synthetic opioids hidden in fake medicines bought online.

Prevention is at the heart of this government’s approach to tackling drugs and this campaign will ensure young people have the facts they need to make informed decisions about their health and safety, so they think twice about putting themselves in danger.

As part of the campaign, experts will highlight particular risks, including the:

  • potentially irreparable damage ketamine can cause to your bladder
  • dangers of counterfeit medicines containing deadly synthetic opioids purchased online
  • risks from so-called ‘THC vapes’ that often contain dangerous synthetic cannabinoids like spice rather than THC

Resources will be available for schools, universities and local public health teams with content available on FRANK, the drug information website.

There are growing concerns about novel synthetic opioids, particularly nitazenes, which are increasingly appearing in counterfeit medicines sold through illegitimate online sources. Users purchasing these products are typically younger and more drug-naïve.

Reports of harms from THC vapes have also increased, with many products containing synthetic cannabinoids (commonly known as ‘spice’) that have higher potency and unpredictable effects.

Katy Porter, CEO, The Loop, said:

The Loop welcomes the further investment in evidence-based approaches and support to reduce drug-related harm.

Providing accurate, non-judgemental information equips and empowers people to make safer choices and can help reduce preventable harms.

Drug poisoning deaths reached 5,448 in England and Wales in 2023, the highest number since records began in 1993. The campaign emphasises that while complete safety requires avoiding drug use altogether, those who may still use substances should be aware of the risks and know how to access help and support.

The campaign underlines that ketamine’s medical applications do not make illicit use safe, with urologists increasingly concerned about young people presenting with severe bladder problems from recreational ketamine use.

Resources will be distributed to local public health teams, drug and alcohol treatment services, youth services, schools and universities. The campaign provides clear information on accessing help and support for those experiencing drug-related problems or mental health issues.

This year the Department of Health and Social Care is also providing £310 million in additional targeted grants to improve drug and alcohol treatment services and recovery support in England, including specialist services for children and young people.

For information and support on drug-related issues, visit www.talktofrank.com or call the FRANK helpline on 0300 123 6600.

Background information

How to watch this YouTube videoThere’s a YouTube video on this page. You can’t access it because of your cookie settings.You can change your cookie settings or watch the video on YouTube instead:Ket: while each high lasts minutes, for some the damage to their bladder could last forever

How to watch this YouTube videoThere’s a YouTube video on this page. You can’t access it because of your cookie settings.You can change your cookie settings or watch the video on YouTube instead:Synthetic opioids: what are they and why are they so dangerous?

Additional resources for professionals and educators will be available through local public health networks.

The £310 million additional funding for drug treatment services is separate from the public health grant.

Source: https://www.gov.uk/government/news/young-people-given-stark-warning-on-deadly-risks-of-taking-drugs

 

Adolescence is a critical stage of growth, a time when young people begin to make their own independent choices in preparation for adulthood. However, it is also a time of vulnerability, especially when it comes to exposure to drugs and other harmful substances.

Because the brain is still developing, particularly in areas that control decision-making and impulse regulation, adolescents face unique risks that can affect their health and overall well-being. 

It is a well-established fact that the human brain does not fully mature until around the age of 25, leaving adolescents and young adults more vulnerable to the harmful effects of harmful substances. When exposure occurs during these critical years of development, it can cause both immediate harm and long-term consequences that may follow individuals well-into adulthood. 

One of the key reasons for this vulnerability lies in the development of the brain itself. According to the Harvard Health article “Adolescence: A high-risk time for substance use disorders” by Sharon Levy and Siva Sundaram, “the adolescent brain is ‘deliberately’ set up for risk-taking.” 

Areas such as the prefrontal cortex, a part of the brain which plays a central role in judgment, impulse control, and decision-making, are still “under construction” during adolescence. Because of this, younger individuals are more likely to engage in risky behaviors, including experimenting with drugs, often without fully understanding the dangers. The earlier drug use begins, the greater the potential for lasting harm. 

Substance use during this developmental period primes the brain for addiction and chronic health problems. Addiction occurs when the brain’s pleasure receptors are overstimulated, creating an artificial “reward system” that encourages repeated drug use.

For adolescents, this effect is magnified due to their still-developing neural pathways. With a heightened sensitivity to pleasure and a weaker ability to assess long-term consequences, teens are more likely to fall into cycles of use and dependency. 

What further exacerbates this issue is the limbic system, the part of the brain that processes emotions and rewards. Unlike the prefrontal cortex, the limbic system matures earlier, meaning teens often experience intense emotional responses and a stronger drive for immediate gratification.

Drugs offer that instant burst of dopamine, which quickly reinforces use through a “use-reward-repeat” pattern. 

Over time, this can disrupt the brain’s natural ability to feel pleasure, making ordinary activities less satisfying and increasing reliance on substances. 

The health risks tied to early drug use extend far beyond the brain. Adolescents who use drugs, as noted in the article “Teen drug abuse: Help your teen avoid drugs” published by Mayo Clinic, face heightened risks of heart attacks, strokes, organ damage, and worsening mental health conditions. 

Early experimentation can also serve as a gateway to more harmful substances, escalating the risks over time. Adding to the concern, research published in Neuropharmacology reports that patterns of substance use can pass down genetically, making future generations more susceptible to addiction as well.

Ultimately, drug use during adolescence is not just a temporary risk, but one that can set the stage for a lifetime of consequences. By understanding the unique vulnerabilities of the developing brain, it becomes clear why prevention and education are important. 

Protecting adolescents from early exposure to drugs is not only about safeguarding their present, but about preserving their future health as well. 

Source: https://www.pleasantonweekly.com/alameda-county/2025/10/06/how-drugs-alter-the-developing-brain-priming-adolescents-for-risk-and-dependency/

In a world where alcoholic drinks are seemingly ever-present and sold by even the makers of Sunny D and Mountain Dew, it can seem like a daunting task to raise kids who can withstand the societal pressures and avoid the harms of substance use disorder. 

But a recent speaker in the GPS Parent Series broke down the science of prevention and offered tips parents can use to help their children grow up to be competent, engaged, and sober. 

Jessica Lahey, an author, educator, and substance use prevention expert, shared best practices from her research, focusing on risk factors for substance use disorder and ways parents can use a basic understanding of the adolescent brain to help young people steer clear. 

“Risk and prevention is like the scales of justice,” Lahey said. “If your risk is really heavy, then your protections will have to be heavier to zero those out.”

Risk factors for substance use disorder

While there is no single “addiction gene,” Lahey — who has been in recovery from alcohol use disorder for the past 10 years — said genetics accounts for between 50 and 60% of a person’s risk for developing substance use disorder. Another major risk factor is occurrences known as ACEs, or adverse childhood experiences — things like neglect, abandonment, physical or sexual abuse, trauma, violence, separation, or divorce. 

But Lahey also pointed out several lesser-known risk factors, including early childhood aggression, under-managed learning differences, academic failure, social ostracism or identifying as LGBTQ+. Certain time periods can bring about higher risk as well, such as transitional phases like summers, moves between schools, or the weeks and months when a divorce is taking place. 

Prevention tips to raise sober kids

Lahey’s talks to the GPS audience, including several groups hosting watch parties, were full of proven prevention tactics that help youth not only avoid alcohol and drugs — but protect their developing brains in the process. Here are five of the top strategies she shared: 

Start early: As early as preschool, parents can start talking about substance safety with things like toothpaste and adult medicines to help children learn “to be safe about what you’re eating, and what you’re not putting in your body,” Lahey said.

Understand the adolescent brain: “The adolescent brain is wired for novelty,” Lahey said. So when a risk factor occurs, such as moving or starting a new school, parents can reframe this to meet their teen’s need for encountering new things. This allows teens to feel “hits of dopamine, mastery and competence that give a boost to their brain,” Lahey said. 

Know that drinking is different for adolescents: Because brain development is still taking place until the early 20s, youth brains are wired to weigh the potential positives of a situation more heavily than the risks. Research proves teens are more likely to engage in risky behavior if they believe their peers are watching, Lahey said. And they’re less likely to understand how impaired they are if they do start drinking. This can be a dangerous mix, but parents can counteract it by emphasizing the value of brain development. “Your brain is too important to mess with,” Lahey said.

Have a clear and consistent message: Delaying drug or alcohol use can allow ample time for healthy brain development, and Lahey said this results in a major decrease in lifelong risk for substance use disorder. So, the message from parents should be, “I just need you to delay,” she said. This can help create a family culture in which drinking isn’t an option until it’s legal. If teens don’t like that rule because it feels arbitrary, Lahey encourages parents to try this line about drinking: “No. Not until your brain is done developing.” 

Be preventive, not permissive: Behaviors that create a permissive culture around alcohol, such as allowing children and teens to take sips of alcoholic beverages in the home, or hosting parties where young people are allowed to drink, have been proven to increase risk for substance use disorder — not encourage moderation, Lahey said. “It is not inevitable that kids are going to drink,” she said. “Permissiveness results in kids with much higher levels of substance use disorder.” 

Parenting with the science of prevention

Jordan Esser, Project Coordinator of the DuPage County Prevention Leadership Team, introduced Lahey before the free online talks she gave on Sept. 25 and thanked her for sharing “the science of motivation, parenting and substance abuse prevention — because we as adults have the power to help our kids become more competent and fulfilled.”

Source: https://www.nctv17.org/news/how-to-raise-sober-kids-outweigh-risks-with-prevention-expert-says/

By Neuroscience – September 21, 2025

The findings were significant, Thanos explains, because not only did the HIIT animals exhibit a preference for the saline chamber, they exhibited a clear aversion to the cocaine chamber. Credit: Neuroscience News

Summary: A new study shows that high-intensity interval training (HIIT) is more effective than moderate exercise at protecting adolescent lab animals from cocaine use. Animals exposed to HIIT developed a preference for non-drug environments and an aversion to cocaine, linked to increases in ΔFosB, a molecular switch involved in addiction.

These results suggest exercise intensity matters in shaping the brain’s reward system and its response to drugs. The findings may inform new strategies for using exercise as a personalized tool in substance use disorder prevention and treatment.

Key Facts

  • HIIT Impact: High-intensity exercise made animals avoid cocaine and prefer safe environments.
  • Molecular Mechanism: HIIT raised ΔFosB levels, a transcription factor tied to addiction pathways.
  • Personalized Tool: Exercise may act as dose-dependent medicine for addiction prevention.

Source: University at Buffalo

People with substance use disorder who participate in recovery running programs have shown improved success in maintaining their sobriety and reducing their risk for relapse.

Those observations led Panayotis Thanos, a University at Buffalo neuroscientist who studies the brain’s reward system, to try to figure out the brain mechanisms behind that phenomenon.

In a new study published today in PLOS One, Thanos, PhD, senior research scientist in the Clinical and Research Institute on Addictions in the Jacobs School of Medicine and Biomedical Sciences at UB, and co-authors reveal that high-intensity interval training (HIIT) was more effective than moderate exercise in making adolescent lab animals avoid cocaine.

The researchers used adolescent lab animals because this is the age when most people who develop substance use disorder begin their exposure. The study focused on male rats only because previous observations have revealed some gender differences in drug-seeking behaviors between males and females. The researchers plan a future study on how HIIT affects females with regard to cocaine. 

HIIT as personalized medicine

“The study shows that HIIT exercise, rather than moderate exercise, during adolescence may protect against cocaine abuse,” says Thanos, a faculty member in the Department of Pharmacology and Toxicology in the Jacobs School.

The findings provide evidence that HIIT could become a personalized medicine tool in drug abuse intervention.

“The key take-home is that not all exercise is created equal in terms of outcome,” Thanos says. “Exercise is not a binary therapeutic tool but rather we need to think about exercise as dose-dependent, the way we think of medicine as dose-dependent.”

In the study, rats exposed to HIIT exercise on a treadmill were compared to rats exposed to moderate treadmill exercise. Both groups then underwent a behavioral test called cocaine place preference, which trains the animal to discriminate between two chambers: one where they can access cocaine and one where they can access saline. Cocaine preference is when the animal spends more time in the cocaine chamber, while cocaine aversion is when the animal chooses to spend more time in the saline chamber.

The findings were significant, Thanos explains, because not only did the HIIT animals exhibit a preference for the saline chamber, they exhibited a clear aversion to the cocaine chamber.

Increase in a molecular switch for addiction

“We believe that the increase in aversion to cocaine happens in the HIIT animals,” Thanos says, “because of this exercise dose-dependent effect on the brain’s reward circuit that involves an increase we observed in ΔFosB.” ΔFosB is a transcription factor commonly referred to as a molecular switch for addiction and known to boost sensitivity to drugs of abuse.

“Our study showed that HIIT increased ΔFosB levels causing an aversion to consuming cocaine,” he adds.

The findings reveal new avenues that Thanos and his colleagues plan to explore, including how HIIT may affect brain metabolism.

“We know from recent studies in our lab with steady, moderate treadmill running that compared to sedentary animals, exercise decreased metabolism in the somatosensory cortex of the brain while activating other brain regions involved in planning and decision,” he says. “That activation may help dampen various aspects of cocaine abuse and relapse.”

The paper also discusses the need to better understand gender differences in preference for cocaine. “Future studies need to explore how HIIT affects cocaine preference in female rats,” Thanos says, adding that the literature in the field includes evidence that females seem to be more vulnerable to certain phases of addiction.

UB co-authors are Teresa Quattin, MD, UB Distinguished Professor in the Department of Pediatrics and senior associate dean for research integration in the Jacobs School; Nikki Hammond, a former graduate student; and Nabeel Rahman and Sam Zhan, former undergraduate students in Thanos’ lab. Other co-authors are from Washington University School of Medicine and Western University of Health Sciences.

Source: https://neurosciencenews.com/hiit-exercise-addiction-neuroscience-29715/

Outdated views of addiction hurt patients. Dr. Roger Starner Jones, Jr. and others are working to change that.

Despite decades of medical research, public awareness campaigns, and growing national concern, many people still see addiction through a distorted lens. “Addict” remains a pejorative label. Misconceptions persist that addiction is a choice, a character flaw, or the result of bad parenting. These outdated ideas don’t just misinform—they actively harm. They delay care, deepen stigma, and make recovery even more complicated to reach.

But addiction is not a moral failing. It is a complex brain disease, and understanding it as such is crucial to saving lives.

A Medical Diagnosis, Not a Personal Weakness

Addiction, clinically known as substance use disorder (SUD), alters brain chemistry in ways that impact decision-making, impulse control, and the experience of pleasure and reward. According to the National Institute on Drug Abuse (NIDA), addiction is a chronic, relapsing disorder characterized by compulsive drug seeking, continued use despite harmful consequences, and long-lasting changes in the brain.

Yet societal attitudes lag behind the science. More than three-quarters of Americans surveyed believe that substance use disorder (SUD) is not a chronic medical illness, and more than half said they believe SUD is caused by bad character or lack of moral strength, according to findings from the 2024 Shatterproof Addiction Stigma Index Report. This belief system creates barriers to treatment by fueling shame, encouraging secrecy, and often leading families and employers to distance themselves rather than lean in with support.

The Real Risks of Misunderstanding

Misconceptions don’t just alienate people—they endanger them. Fear of judgment keeps many individuals from seeking help until their condition worsens. Delayed treatment can lead to job loss, relationship breakdowns, homelessness, overdose, and even death.

“Shame is one of the biggest enemies of recovery,” says Dr. Roger Starner Jones, Jr., a board-certified emergency and addiction medicine physician based in Nashville. “When patients think they’ll be judged instead of treated, they wait too long. They spiral. By the time they reach us, their situation is often much more severe than it needed to be.”

Dr. Jones has seen this pattern play out thousands of times. After a decade in emergency medicine, he pursued a fellowship in addiction medicine at Vanderbilt University Medical Center, driven by both clinical experience and personal history. Starner Jones’ father, who once faced 11 DUIs in seven years, found lasting sobriety after being committed to a state hospital and undergoing physician-led detox. That experience changed the course of both their lives—and led Dr. Jones to dedicate his career to compassionate, customized addiction care.

Rewriting the Narrative: Care That Meets Patients Where They Are

Through his practices—Nashville Addiction Recovery and Belle Meade AMP—Starner Jones delivers concierge-level, judgment-free care. His model includes in-home detox, private hotel suite treatment, and office-based services designed to remove as many barriers as possible between a patient and their recovery. His focus is on meeting patients where they are, not where the system dictates they should be.

“There’s no one-size-fits-all in addiction treatment,” Dr. Jones says. “Some people need a quiet, safe space to detox privately. Others need a highly structured plan for relapse prevention. What they don’t need is bureaucracy or blame.”

Starner Jones’s approach is part of a broader shift happening in the addiction medicine field. More physicians are advocating for low-threshold treatment models—services that reduce wait times, eliminate unnecessary paperwork, and avoid rigid abstinence requirements. According to the Substance Abuse and Mental Health Services Administration (SAMHSA), these models have been shown to increase engagement and retention in care, particularly among people with co-occurring mental health conditions.

While not a clinician in the traditional sense today, Dr. Gabor Maté is one of the most influential voices advocating for a trauma-informed approach to addiction. His book, In the Realm of Hungry Ghosts, explores how early childhood trauma, not moral weakness, underpins most substance use. He argues that addiction is not the problem itself, but rather a misguided attempt to solve internal pain. His philosophy underpins many treatment programs worldwide.

The Hazelden Betty Ford Foundation is one of the most established names in addiction treatment and has evolved to embrace an integrated model that combines medical detox, medication-assisted treatment (MAT), therapy, and mental health services. They openly reject the idea of addiction as a character flaw and emphasize long-term support and relapse prevention, rooted in compassion, not control.

Dispelling Common Myths

Several deeply ingrained myths continue to distort how addiction is viewed and treated. Let’s set the record straight:

  • Myth: Addiction is a choice.
    Reality: While the initial decision to use a substance may be voluntary, the progression to addiction is driven by changes in brain circuitry, not moral weakness.

  • Myth: You have to hit “rock bottom” to recover.
    Reality: Early intervention improves outcomes. Waiting for someone to “bottom out” can be fatal, especially in the era of fentanyl-laced street drugs.

  • Myth: Medication-assisted treatment is trading one addiction for another.
    Reality: FDA-approved medications like buprenorphine and methadone reduce cravings and withdrawal, allowing patients to stabilize their lives. They’re widely considered best practice in treating opioid use disorder.

  • Myth: Recovery is rare.
    Reality: Millions of Americans are living in recovery today. In the United States, 9.1%, or 22.35 million adults have reported resolving a substance use problem.

Compassion Is Evidence-Based

What ultimately works in addiction care isn’t punishment or shame—it’s connection. “When you treat addiction like the disease it is, you empower people to get better,” Dr. Starner Jones says. “You stop asking ‘What’s wrong with you?’ and start asking ‘What happened to you?’”

At Nashville Addiction Recovery, the ethos of compassion is baked into every interaction. From discreet intake to 24/7 physician supervision, the patient experience is defined by dignity and respect. Many of the patients Dr. Jones sees are high-profile professionals—athletes, musicians, executives—whose careers demand confidentiality. But the underlying need is universal: to be seen, respected, and supported through one of the most complex challenges a person can face.

A Call for Better Understanding

Changing how society views addiction won’t happen overnight, but it starts with how we talk about it. Swapping judgment for empathy, punishment for treatment, and generalizations for science can change not just conversations—but lives.

Source: https://www.bbntimes.com/science/what-most-people-get-wrong-about-addiction

 A new non-opioid pain reliever developed in Japan shows early success in clinical trials, offering hope for safer pain management.
If  effective, it could help curb the opioid crisis by providing a powerful alternative. Credit: Stock

The discovery of a new painkiller offers relief with fewer side effects.

Morphine and other opioids are commonly used in medicine because of their strong ability to relieve pain. Yet, they also pose significant risks, including respiratory depression and drug dependence. To limit these dangers, Japan enforces strict rules that allow only specially authorized physicians to prescribe such medications.

In contrast, the United States saw widespread prescribing of the opioid OxyContin, which fueled a rise in the misuse of synthetic opioids like fentanyl. By 2023, deaths from opioid overdoses had exceeded 80,000, marking the escalation of a nationwide public health emergency now known as the “opioid crisis.”

A new analgesic approach

Opioids may soon face competition. Researchers at Kyoto University have identified a new analgesic, named ADRIANA, that provides pain relief through a completely different biological pathway. The drug is now moving through clinical development as part of an international research collaboration.

“If successfully commercialized, ADRIANA would offer a new pain management option that does not rely on opioids, contributing significantly to the reduction of opioid use in clinical settings,” says corresponding author Masatoshi Hagiwara, a specially-appointed professor at Kyoto University.

Targeting adrenoceptors for safer pain relief

The researchers drew their initial inspiration from compounds that imitate noradrenaline, a chemical released during life-threatening situations that activates α2A-adrenoceptors to reduce pain. While effective, these compounds carry a high risk of destabilizing cardiovascular function. By examining the relationship between noradrenaline levels and α2B-adrenoceptors, the team proposed that selectively blocking α2B-adrenoceptors could increase noradrenaline activity, stimulate α2A-adrenoceptors, and provide pain relief without triggering cardiovascular instability.

  Mechanism of pain relief by ADRIANA. Credit: KyotoU / Hagiwara lab

To test this idea, the scientists used a specialized method called the TGFα shedding assay, which allowed them to measure the function of different α2-adrenoceptor subtypes. Through compound screening, they succeeded in identifying the world’s first selective α2B-adrenoceptor antagonist.

Promising clinical results and future trials

After success in administering the compound to mice and conducting non-clinical studies to assess its safety, physician-led clinical trials were conducted at Kyoto University Hospital. Both the Phase I trial in healthy volunteers and the Phase II trial in patients with postoperative pain following lung cancer surgery yielded highly promising results.

Building on these outcomes, preparations are now underway for a large-scale Phase II clinical trial in the United States, in collaboration with BTB Therapeutics, Inc, a Kyoto University-originated venture company.

As Japan’s first non-opioid analgesic, ADRIANA has the potential not only to relieve severe pain for patients worldwide but could also play a meaningful role in addressing the opioid crisis — a pressing social issue in the United States — and thus contribute to international public health efforts.

“We aim to evaluate the analgesic effects of ADRIANA across various types of pain and ultimately make this treatment accessible to a broader population of patients suffering from chronic pain,” says Hagiwara.

Reference: “Discovery and development of an oral analgesic targeting the α2B adrenoceptor” by Masayasu Toyomoto, Takashi Kurihara, Takayuki Nakagawa, Asuka Inoue, Ryo Kimura, Isao Kii, Teruo Sawada, Takashi Ogihara, Kazuki Nagayasu, Takayuki Kishi, Hiroshi Onogi, Dohyun Im, Hidetsugu Asada, So Iwata, Jumpei Taguchi, Yuto Sumida, Suguru Yoshida, Junken Aoki, Takamitsu Hosoya and Masatoshi Hagiwara, 7 August 2025, Proceedings of the National Academy of Sciences.
DOI: 10.1073/pnas.2500006122

Funding: Japan Society for the Promotion of Science, Japan Science and Technology Agency, Japan Agency for Medical Research and Development

Source:  https://scitechdaily.com/the-end-of-opioids-new-drug-could-change-the-way-we-treat-severe-pain/

by Kevin Sabet  August 22, 2025 

In 2018, 27-year-old Bryn Spejcher, an inexperienced marijuana smoker in California, killed her boyfriend Chad O’Melia by stabbing him 108 times, a crime the local district attorney described as “horrific” and “one of the worst our medical examiner has ever seen.” A jury found Spejcher guilty of involuntary manslaughter, but she received only probation at sentencing because of a compelling presentation of her defense of cannabis-induced psychosis. Prior to the violent incident, Spejcher had taken two hits of legal marijuana from a bong, and claimed that she began “seeing things that weren’t there” and lost touch with reality. She also stabbed herself repeatedly in the neck, and stabbed her own dog. Law enforcement agents called to the scene had to break her arm with a metal baton to get her to let go of the knife; multiple Taserings had no effect. 

Cases like Spejcher’s illustrate the stakes involved in the federal reclassification of marijuana. If President Trump follows through with such a move, the drug would remain illegal on the federal level, but would receive an imprimatur of being safer and face fewer restrictions, with significant commercial and social implications.  

Yet voices across public discourse persist in asking: why should anyone care if President Trump does just that? 

Celebrities like Mike Tyson and Joe Rogan and hedge-fund bosses like Andrew Lahde tell us that marijuana is no big deal. Numerous states have already legalized it for medical and recreational usage, and they claim to be regulating it well. If we are to believe the advocates, marijuana is a miracle cure for PTSD, anxiety, depression, and bipolar disorder — not to mention an unbeatable salve for the pain suffered by cancer patients.

So what sense does it make for this drug to sit in the same federal category as PCP and heroin? Isn’t marijuana’s placement in Schedule I, the most serious category, merely a relic of discredited thinking from the bad old days of the War on Drugs? It isn’t. To understand why it isn’t, and why a Trump move to reclassify weed would risk unmitigated harm to American health and safety, it’s first important to clear up some common misunderstandings around how and why drugs end up classified as they do.  

Under the Controlled Substances Act of 1971, a five-part schedule was established for classification of potentially dangerous drugs. This schedule is emphatically not an index either of a drug’s “hardness” or a kind of unofficial charging and sentencing guide for prosecutors and judges. Placement is earned specifically through consideration of a drug’s accepted medical use and its abuse risk. Drugs with no accepted medical use and a high risk of abuse get placed in Schedule I.  

That’s the commonality between marijuana and heroin; under federal law, the relevant agencies necessarily view them that way.  

Neither has an accepted medical use, though both drugs have approved medicines derived from them that remain in lower schedules (the medicine dronabinol, for example, is synthesized THC, the active ingredient in marijuana, and is in Schedule III). Both have high risks of abuse. The argument that one is a “hard” drug and the other is not  — which is debatable, especially given today’s ultra-high-potency weed — simply doesn’t come into play.  

Nor does the criminal-justice question. Keeping marijuana in Schedule I isn’t, as critics have it, a carceral strategy; conversely, moving it into Schedule III isn’t a de-carceral one. Under a move to Schedule III, the drug would remain federally illegal, still subject to the enforcement power of the Drug Enforcement Administration and the Department of Justice. No low-level offender would see his sentence commuted. This is sort of beside the point anyway, since most low-level marijuana users never receive a sentence for anything. 

But how can it be, another objection runs, that the drug has no medical use? Most US states currently allow doctors to recommend it. 

That, again, is technically correct. But the decisions those states made to allow doctors (and in some cases, “designated caregivers”) to recommend marijuana to treat pain and other issues were political decisions, not medical or scientific ones. Voters stated a preference; that has no effect on how federal agencies are required by current law to view the question. The facts of just how those recommendations get handed out drive home that political aspect. In 2022, Pennsylvania saw some 132,000 medical-marijuana certifications, a third of the state’s total for that year, issued by only 17 doctors.

Those decisions, taken in the aggregate, don’t constitute an accepted medical use. Or at least, they didn’t until October 2022. That was the month the Biden administration directed its Department of Health and Human Services to look into a possible reclassification of the drug.  

“This schedule is emphatically not an index either of a drug’s ‘hardness’ or a kind of unofficial charging and sentencing guide.”

Again, history is important here. Before the Biden process, the federal government had used an eight-factor test to determine how to schedule various drugs. Those factors focus on what the current and historical patterns of its abuse look like, as well as what that means for individual users, what risk it presents to public health, how likely it is to cause dependence (either physical or psychological), the state of the science around the drug and its pharmacology, and whether it’s a chemical precursor or “analogue” of another controlled substance.  

By these metrics, marijuana is precisely where it belongs in Schedule I. The best science shows that it isn’t an effective medical treatment. One of the most frequent conditions it’s used to treat is chronic pain. But the 2017 study cited to prove its efficacy there has seen dozens of subsequent meta-analyses and reviews fail to support its conclusions; a 2022 study of a decade’s worth of surgical records from a Cleveland hospital even found that using marijuana actually increases pain after surgery. 

The data also demonstrate that marijuana poses a significant risk of dependency: addiction rates are around 30% of all users and rising. Addiction in this case means exactly what it does for other substances: inability to quit, a need for ever more of the drug to achieve the same effect, and even withdrawal symptoms. Given the recent avalanche of data cataloguing marijuana’s harms specifically to cardiac and mental health — like a June British Medical Journal review  connecting it to a two-fold risk of cardiovascular death or the massive Danish study from 2023 suggesting that as much as 30% of schizophrenia cases among men between 21 and 30 were linked to cannabis-use disorder — its wider public-health risks are glaringly clear.  

The Biden administration supplanted the eight factors with a new system seemingly designed to push the drug into a less restrictive schedule. The Biden recommendation — likely a political compromise between the status quo and full legalization, timed just before Joe Biden’s re-election bid — also incorporated the shaky argument that because so many states have made political decisions to allow medical marijuana, that constitutes an accepted medical use.

An incisive article in JAMA Neurology, by the Harvard addiction scientist Bertha Madras, took a hard look at the process and found disturbing evidence of politicization. This included the fact that a high-ranking Biden DOJ official, Acting Assistant Attorney General Peter Hyun, argued that “cannabis has not been proven in scientific studies to be a safe and effective treatment for any disease or condition” — six months before the rescheduling directive appeared. Yet the science Hyun cites certainly had not changed in the interim.  

The federal government has long held the position Hyun laid out. Under the Obama administration, Jay Inslee and Gina Raimondo — then the governors of Washington and Rhode Island, respectively — petitioned the federal government to reclassify marijuana. The administration’s response made clear that federal drug schedules reflect what the science says, not “danger” or “severity.” Obama’s then-DEA chief, Chuck Rosenberg, announcing the denial of the petition, used language Hyun would later echo: “This decision isn’t based on danger. This decision is based on whether marijuana, as determined by the FDA, is a safe and effective medicine . . . and it’s not.”

Suggested reading

I have seen the damage cannabis does

By Peter Hurst

But let’s assume, for the sake of argument, that Trump reverses years of federal precedent to follow the logic of the rescheduling argument. What happens then? 

The truth: no one knows.  

It’s clear that the marijuana industry believes that rescheduling will be an enormous benefit to its shareholders. In one sense, that’s likely correct. Businesses selling substances in Schedule I face severe commercial restrictions under the tax code. A provision of the tax code prevents any such business from taking normal deductions at tax time on expenses like advertising. Lifting those restrictions seems sure to provide an enormous boost to revenues and reach for businesses selling marijuana products.

The impact on society is a different matter. The available evidence suggests that this will be a significant negative for society, especially given the research around how the young start using the drug: data published in June by researchers from the University of Southern California and Rutgers University show that exposure to marijuana social-media content plays a huge role in teens initiating use.  

But there are other externalities in play.  

If marijuana moves into Schedule III, it will be the only substance there without Food and Drug Administration approval. Will that play out in a similar way to the case of opium-poppy straw (i.e., the entirety of the plant, as it exists prior to the processes that turn it into heroin or opium)? Poppy straw is listed in Schedule II, but it also lacks an FDA approval — and it’s regularly seized by drug and border authorities, with a massive shipment grabbed up just in May. Though weed entrepreneurs clearly expect smooth sailing after a reclassification, they may well be in for a rough ride.

Then there’s the fact that substances listed in Schedule III face additional regulatory and enforcement power: Not only from the DEA and DOJ, but also from the FDA. There are strict rules around what sellers of Schedule III substances can and can’t say in advertisements. They’re forbidden from advertising off-label uses — and since marijuana lacks an FDA approval, all therapeutic uses are off-label. It’s easy to imagine another operator in the Schedule III space filing a lawsuit demanding precisely that kind of enforcement. 

In other words, rescheduling opens the door to regulatory chaos, even as it seems certain to add commercial firepower to an industry whose products, on the evidence, are extraordinarily harmful. How this combination will produce the benefits promised by proponents of rescheduling also remains unclear. 

The federal government shouldn’t signal to the American people that a drug that lacks medical or scientific imprimatur somehow possesses such approval. Others disagree — and vocally. They have a lot of money riding on it. But we should be crystal clear about what their preferred policy would  actually mean for American society — nothing good. 

Kevin Sabet, a former three-time White House senior drug-policy adviser, is president of Smart Approaches to Marijuana.

Source:  https://unherd.com/2025/08/the-illusion-of-safe-marijuana/?edition=us?

CHARLES CITY COUNTY, Va. (WRIC) — The Charles City County Elementary School will soon re-introduce a program focused on drug prevention and awareness for the 2025-26 academic year.

According to a release from the sheriff’s office, the program, DARE — Drug Abuse Resistance Education program — will come to the elementary school for the upcoming school year.

SRO Corporal Tramayne Mayo, who developed a curriculum to teach the program, reportedly attended a two-week training course as required by DARE to instruct.

“We are excited to get this program back into our school system,” said Jayson Crawley, Sheriff of Charles City County. “We feel that early education of the dangers of drugs should be taught to our youths and can have a significant positive impact on the decisions they make when faced with drugs. This is just part of our continued efforts to deter illegal drug activity in our county.”

Opioid settlement money awarded to all jurisdictions in the Commonwealth from a reported lawsuit filed against prescription drug companies will help fund the program, per the sheriff’s office.

8News previously reported that, in June, Virginia joined all other states and some U.S. territories in agreeing to sign a $7.4 billion settlement with Purdue Pharma and members of the Sackler family who own the company for their part in perpetuating the opioid crisis.

As a result, the state will receive as much as $103.8 million from this settlement over the next 15 years — funding which will go toward local prevention, treatment and recovery efforts, as previously reported by 8News.

Source:  https://www.wric.com/news/local-news/charles-city-county/dare-program-charles-city-elementary-2025-2026/

OPINION: Eric Adams is right 
Charles Fain Lehman is a fellow at the Manhattan Institute and senior editor of City Journal.

Can New York clean up its public drug-use problem?

Mayor Eric Adams aims to try: On Thursday, he called on the state Legislature to allow clinicians and judges to compel people into treatment when their drug use is hurting them and the city.

“We must help those struggling finally get treatment, whether they recognize the need for it or not,” Adams said at an event hosted by the Manhattan Institute (where I work).  

“Addiction doesn’t just harm individual users; it tears apart lives, families and entire communities, and we must change the system to keep all New Yorkers safer.”

Adams’ proposed state law, the Compassionate Interventions Act, may face an uphill battle in Albany, as “harm reduction” advocates assail it as coercive and dangerous.

But involuntary treatment should be a tool in New York’s arsenal for dealing with the public drug use that has plagued it for years.

Last year it reported nearly 4,000 homeless residents with a history of chronic substance use — probably an undercount, as such people are less likely to be identified by the city’s annual late-night census.

Regardless, it’s not hard to find people shooting up on New York’s streets — just visit the Hub in The Bronx or Washington Square Park in Manhattan.

Such behavior makes whole swaths of the city unlivable.

Public drug use hurts both users — there were more than 2,100 overdose deaths in the five boroughs last year — and the places where they use.

It deters commerce, and creates environments conducive to more serious crime.

Too often the city has responded to these situations with benign neglect, exemplified by its two “supervised consumption sites,” which give people a place to use with Narcan-wielding staff standing by.

These sites continue to operate, in spite of the fact that they don’t work and violate federal law.

Leaving people free to abuse drugs, it turns out, doesn’t save lives.

 

 

 

 

Involuntary treatment, by contrast, tries to correct the behavior that drives drug users to hurt both themselves and others.

That’s why 37 other states already permit it — and why New York under Adams’ plan would join them.

Critics will insist that involuntary drug treatment doesn’t work, and that people have to want to change.

But the balance of the evidence suggests that involuntary treatment performs as well as voluntary treatment.

That’s backed up both by older research on California’s involuntary-treatment scheme, and by strong indications that drug courts, which route drug offenders into treatment instead of prison, can reduce recidivism.

Opponents will also say that it’s immoral to compel people to get treatment they don’t want, and that it violates their “bodily autonomy.”

But there’s no right to shoot up in public spaces, or to ruin your body with fentanyl. And New Yorkers should have the right to expect their public spaces to be free from disorder, including public drug use.

The biggest challenge for Adams, though, may be the state’s limited treatment capacity.

New York state as a whole has only 134 long-term residential treatment facilities.

As of 2023, the most recent available data, they were serving 2,935 clients — fewer than the city’s tallied homeless drug-addict population.

Implementing the Compassionate Interventions Act will almost certainly require more funding for treatment beds, much as Adams’ previous efforts to institutionalize the seriously mentally ill did. That will have to be part of any ask in Albany.

But the mayor’s proposal will also allow diversion to outpatient treatment programs, including a new $27 million investment in contingency management therapy — an evidence-based intervention that has been shown to help treat drug addiction.

What happens if Albany says no to Adams’ proposal? Or if Adams is out of the mayoralty come the next legislative session?

The NYPD can still work to clear encampments. And the city can still try to divert drug users into its drug-courts system, which, while useful, faces administrative problems and lacks transparency.

But actually getting drug users the help they need, rather than just cycling them through the city’s jails, will be hard — much as the administration struggled to handle the seriously mentally ill before it had the power to compel them into treatment.

SOURCE: https://nypost.com/2025/08/14/opinion/involuntary-treatment-can-solve-the-public-drug-scourge/

Physical activity emerges as a powerful ally in exercise addiction recovery, offering hope and healing for those struggling with substance dependency. Recent groundbreaking research reveals how structured exercise programmes can reshape both body and mind, providing a natural pathway to wellness that supports long-term recovery goals.

The Science Behind Exercise Addiction Recovery

Two comprehensive studies from leading institutions demonstrate the remarkable impact of physical activity on individuals recovering from substance dependency. Research involving 90 participants in opioid substitution treatment and 43 individuals in drug rehabilitation centres reveals compelling evidence for physical activity recovery benefits.

Neurohormonal Changes Through Exercise

Exercise creates profound changes in the brain’s chemistry that directly counteract the damage caused by substance abuse. When individuals engage in regular moderate-intensity aerobic exercise, their bodies experience:

Increased β-endorphin production: These natural “feel-good” chemicals help restore the brain’s reward system, reducing cravings and improving mood without relying on substances.

Reduced cortisol levels: Exercise helps normalise stress hormone production, which is typically elevated during early recovery phases. This reduction helps manage anxiety, insomnia, and psychological distress.

Enhanced immune function: Regular exercise addiction recovery programmes boost white blood cell and neutrophil counts, strengthening the body’s natural defence systems weakened by substance abuse.

Physical Transformations Supporting Recovery

Body Composition Improvements

Research participants following structured exercise programmes showed remarkable physical changes after 24 weeks:

  • Significant reduction in body fat percentage
  • Increased skeletal muscle mass
  • Improved overall body composition
  • Enhanced physical strength and endurance

These improvements aren’t merely cosmetic—they represent fundamental changes that support sustained recovery by improving self-esteem and physical capability.

Fitness and Functional Capacity

Physical activity recovery programmes deliver measurable improvements across multiple fitness domains:

Cardiovascular health: Participants experienced substantial increases in vital capacity and overall cardiovascular function, supporting better oxygen delivery throughout the body.

Strength and endurance: Upper body and core muscle strength showed significant improvements, enabling individuals to engage more fully in daily activities and work responsibilities.

Flexibility and balance: Enhanced balance control and flexibility reduce injury risk whilst improving quality of life and confidence in physical activities.

Mental Health Benefits of Exercise Addiction Recovery

Anxiety and Depression Relief

The research demonstrates that structured exercise provides substantial mental health benefits:

  • 20% reduction in anxiety scores within 12 weeks
  • Significant decrease in depression symptoms sustained throughout the programme
  • Improved emotional regulation and stress management
  • Enhanced self-confidence and body awareness

The Mind-Body Connection

Exercise programmes that emphasise mind-body integration, such as Pilates, show particular promise. These activities combine physical movement with breath control and mental focus, helping individuals:

  • Develop greater body awareness
  • Learn effective stress management techniques
  • Build emotional resilience
  • Establish healthy coping mechanisms

Types of Exercise for Addiction Recovery

Aerobic Exercise

Moderate-intensity aerobic exercise performed at approximately 70% of maximum heart rate proves most effective for exercise addiction recovery. Activities include:

  • Treadmill walking or running
  • Cycling
  • Swimming
  • Group fitness classes

The key lies in consistency—training three times per week for 20-minute sessions produces measurable neurohormonal improvements.

Mind-Body Practices

Research specifically highlights the benefits of Pilates training for individuals in recovery:

  • Progressive intensity programmes that adapt to improving fitness levels
  • Emphasis on core strength and stability
  • Integration of breathing techniques with movement
  • Low injury risk suitable for deconditioned individuals

Creating Sustainable Exercise Addiction Recovery Programmes

Professional Supervision

Successful physical activity recovery requires proper oversight:

  • Medical clearance before beginning exercise
  • Trained supervision during sessions
  • Heart rate monitoring to ensure appropriate intensity
  • Progressive programme design that prevents overexertion

Long-Term Commitment

The research emphasises that benefits accumulate over time. Participants showed:

  • Initial improvements within 4-6 weeks
  • Significant changes by 12 weeks
  • Maximum benefits achieved after 24 weeks of consistent training

Integration with Comprehensive Care

Exercise works best as part of a holistic recovery approach that includes:

  • Professional counselling and therapy
  • Medical support as needed
  • Peer support networks
  • Structured daily routines

Practical Implementation Strategies

Starting an Exercise Programme

For individuals beginning their recovery journey, successful exercise addiction recovery programmes typically include:

Foundation PhaseWeek 1-4:

  • Low-intensity activities focusing on movement quality
  • 40-50% maximum heart rate
  • Emphasis on learning proper techniques

Development PhaseWeek 5-12

  • Moderate intensity training
  • 60-70% maximum heart rate
  • Increased session duration and frequency

Maintenance PhaseWeek 13-24

  • Sustained moderate-intensity exercise
  • Focus on long-term habit formation
  • Integration of preferred activities

Monitoring Progress

Successful programmes track multiple indicators:

  • Physical fitness improvements (strength, endurance, flexibility)
  • Mental health assessments (anxiety and depression scales)
  • Body composition changes
  • Adherence to exercise schedule

The Role of Exercise in Long-Term Recovery

Preventing Relapse

Physical activity recovery programmes address key relapse triggers:

  • Providing healthy stress relief mechanisms
  • Improving mood naturally through endorphin release
  • Building structured daily routines
  • Enhancing self-efficacy and confidence

Social Benefits

Group exercise activities offer additional advantages:

  • Peer support and accountability
  • Shared goals and achievements
  • Reduced isolation and loneliness
  • Development of healthy social connections

Building Support Networks

Family and Friends

Loved ones play crucial roles in supporting exercise addiction recovery:

  • Encouraging consistent participation
  • Participating in activities together when possible
  • Celebrating milestones and achievements
  • Understanding the importance of exercise in recovery

Professional Support Teams

Effective programmes involve multidisciplinary teams:

  • Exercise physiologists or qualified fitness professionals
  • Mental health counsellors familiar with addiction recovery
  • Medical professionals monitoring overall health
  • Peer support specialists with recovery experience

Evidence-Based Outcomes

The research provides compelling evidence for physical activity recovery effectiveness:

  • 96% programme adherence rates in supervised settings
  • Significant improvements in all measured physical parameters
  • Sustained mental health benefits throughout intervention periods
  • Strong correlations between physical improvements and psychological wellbeing

These outcomes demonstrate that exercise isn’t merely an adjunct therapy—it’s a fundamental component of comprehensive recovery strategies.

Moving Forward with Exercise Addiction Recovery

The evidence overwhelmingly supports integrating structured exercise addiction recovery programmes into comprehensive treatment approaches. By addressing both physical and mental health simultaneously, exercise provides a natural, sustainable foundation for long-term recovery success.

For individuals and families affected by substance dependency, understanding the transformative power of physical activity offers hope and practical steps towards healing. The journey may be challenging, but with proper support, professional guidance, and commitment to consistent exercise, lasting recovery becomes not just possible but probable.

The path to recovery through exercise requires dedication, but the rewards—improved physical health, enhanced mental wellbeing, and sustained freedom from substance dependency—make every step worthwhile.

OPENING STATEMENT BY NDPA

We repeat this 2004 article by Stanton Peele as a useful position statement for us all.  Peele’s classic 1975  text ‘Addiction and Love’ (Peele and Brosky – Published: Taplinger, New York) is also well worth reading in this context.

>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>>

By Stanton Peele Ph.D. published May 1, 2004

More people quit addictions than maintain them, and they do so on their own. People succeed when they recognize that the addiction interferes with something they value—and when they develop the confidence that they can change.

Change is natural. You no doubt act very differently in many areas of your life now compared with how you did when you were a teenager. Likewise, over time you will probably overcome or ameliorate certain behaviors: a short temper, crippling insecurity.

For some reason, we exempt addiction from our beliefs about change. In both popular and scientific models, addiction is seen as locking you into an inescapable pattern of behavior. Both folk wisdom, as represented by Alcoholics Anonymous, and modern neuroscience regard addiction as a virtually permanent brain disease. No matter how many years ago your uncle Joe had his last drink, he is still considered an alcoholic. The very word addict confers an identity that admits no other possibilities. It incorporates the assumption that you can’t, or won’t, change.

But this fatalistic thinking about addiction doesn’t jibe with the facts. More people overcome addictions than do not. And the vast majority do so without therapy. Quitting may take several tries, and people may not stop smoking, drinking or using drugs altogether. But eventually they succeed in shaking dependence.

Kicking these habits constitutes a dramatic change, but the change need not occur in a dramatic way. So when it comes to addiction treatment, the most effective approaches rely on the counterintuitive principle that less is often more. Successful treatment places the responsibility for change squarely on the individual and acknowledges that positive events in other realms may jump-start change.

Consider the experience of American soldiers returning from the war in Vietnam, where heroin use and addiction was widespread. In 90 percent of cases, when GIs left the pressure cooker of the battle zone, they also shed their addictions—in vivo proof that drug addiction can be just a matter of where in life you are.

Of course, it took more than a plane trip back from Asia for these men to overcome drug addiction. Most soldiers experienced dramatically altered lives when they returned. They left the anxietyfear and boredom of the war arena and settled back into their home environments. They returned to their families, formed new relationships, developed work skills.

Smoking is at the top of the charts in terms of difficulty of quitting. But the majority of ex-smokers quit without any aid––neither nicotine patches nor gum, Smokenders groups nor hypnotism. (Don’t take my word for it; at your next social gathering, ask how many people have quit smoking on their own.) In fact, as many cigarette smokers quit on their own, an even higher percentage of heroin and cocaine addicts and alcoholics quit without treatment. It is simply more difficult to keep these habits going through adulthood. It’s hard to go to Disney World with your family while you are shooting heroin. Addicts who quit on their own typically report that they did so in order to achieve normalcy.

Every year, the National Survey on Drug Use and Health interviews Americans about their drug and alcohol habits. Ages 18 to 25 constitute the peak period of drug and alcohol use. In 2002, the latest year for which data are available, 22 percent of Americans between ages 18 and 25 were abusing or were dependent on a substance, versus only 3 percent of those aged 55 to 59. These data show that most people overcome their substance abuse, even though most of them do not enter treatment.

How do we know that the majority aren’t seeking treatment? In 1992, the National Institute on Alcohol Abuse and Alcoholism conducted one of the largest surveys of substance use ever, sending Census Bureau workers to interview more than 42,000 Americans about their lifetime drug and alcohol use. Of the 4,500-plus respondents who had ever been dependent on alcohol, only 27 percent had gone to treatment of any kind, including Alcoholics Anonymous. In this group, one-third were still abusing alcohol.

Of those who never had any treatment, only about one-quarter were currently diagnosable as alcohol abusers. This study, known as the National Longitudinal Alcohol Epidemiologic Survey, indicates first that treatment is not a cure-all, and second that it is not necessary. The vast majority of Americans who were alcohol dependent, about three-quarters, never underwent treatment. And fewer of them were abusing alcohol than were those who were treated.

This is not to say that treatment can’t be useful. But the most successful treatments are nonconfrontational approaches that allow self-propelled change. Psychologists at the University of New Mexico led by William Miller tabulated every controlled study of alcoholism treatment they could find. They concluded that the leading therapy was barely a therapy at all but a quick encounter between patient and health-care worker in an ordinary medical setting. The intervention is sometimes as brief as a doctor looking at the results of liver-function tests and telling a patient to cut down on his drinking. Many patients then decide to cut back—and do!

As brief interventions have evolved, they have become more structured. A physician may simply review the amount the patient drinks, or use a checklist to evaluate the extent of a drinking problem. The doctor then typically recommends and seeks agreement from the patient on a goal (usually reduced drinking rather than complete abstinence). More severe alcoholics would typically be referred out for specialized treatment. A range of options is discussed (such as attending AA, engaging in activities incompatible with drinking or using a self-help manual). A spouse or family member might be involved in the planning. The patient is then scheduled for a future visit, where progress can be checked. A case monitor might call every few weeks to see whether the person has any questions or problems.

The second most effective approach is motivational enhancement, also called motivational interviewing. This technique throws the decision to quit or reduce drinking—and to find the best methods for doing so—back on the individual. In this case, the therapist asks targeted questions that prompt the individual to reflect on his drinking in terms of his own values and goals. When patients resist, the therapist does not argue with the individual but explores the person’s ambivalence about change so as to allow him or her to draw his own conclusions: “You say that you like to be in control of your behavior, yet you feel when you drink you are often not in charge. Could you just clarify that for me?”

Miller’s team found that the list of most effective treatments for alcoholism included a few more surprises. Self-help manuals were highly successful. So was the community-reinforcement approach, which addresses the person’s capacity to deal with life, notably marital relationships, work issues (such as simply getting a job), leisure planning and social-group formation (a buddy might be provided, as in AA, as a resource to encourage sobriety). The focus is on developing life skills, such as resisting pressures to drink, coping with stress (at work and in relationships) and building communication skills.

These findings square with what we know about change in other areas of life: People change when they want it badly enough and when they feel strong enough to face the challenge, not when they’re humiliated or coerced. An approach that empowers and offers positive reinforcement is preferable to one that strips the individual of agency. These techniques are most likely to elicit real changes, however short of perfect and hard-won they may be.

Source:  https://www.psychologytoday.com/gb/articles/200405/the-surprising-truth-about-addiction

Cannabis dependence affects millions globally, with over 23 million people worldwide struggling with problematic use patterns. As treatment demand continues rising, understanding which psychological interventions for cannabis dependence work best has become increasingly important. This comprehensive guide examines the latest evidence on therapeutic approaches that help individuals overcome cannabis-related difficulties.

Understanding Cannabis Dependence and Treatment Needs

Cannabis use becomes problematic when it significantly interferes with daily life, relationships, and responsibilities. The World Health Organisation recognises that whilst brief interventions may help casual users, those with established dependence require specialised psychological treatments for cannabis problems.

Recent statistics reveal the growing need for effective interventions:

  1. Treatment admissions in Europe increased by 30% between 2010 and 2019
  2. Young adults aged 20-24 show the highest rates of problematic use
  3. Cannabis is now the most frequently cited substance among those entering treatment programmes

Evidence-Based Psychological Interventions for Cannabis Users

A major systematic review from the University of Bristol analysed 22 clinical trials involving over 3,300 participants, providing crucial insights into which therapeutic approaches demonstrate real effectiveness.

Cognitive-Behavioural Therapy with Motivational Enhancement

The most extensively researched approach combines cognitive restructuring with motivation-building techniques. This integrated therapy helps individuals:

  1. Identify triggers and high-risk situations
  2. Develop practical coping strategies
  3. Build internal motivation for change
  4. Master skills to prevent relapse

Research demonstrates this approach can increase abstinence rates nearly threefold compared to no intervention, establishing it as a cornerstone of evidence-based care.

Third-Wave Therapies: DBT and ACT Approaches

Newer psychological interventions for cannabis problems incorporate mindfulness and acceptance-based strategies. These therapies teach:

  1. Mindfulness skills for managing cravings
  2. Emotional regulation techniques
  3. Distress tolerance without substance use
  4. Values clarification and committed action

Studies show these approaches can quadruple abstinence rates when compared to basic psychoeducation alone.

Community Reinforcement Strategies

This approach restructures the individual’s environment to support recovery through:

  1. Leveraging community resources
  2. Building substance-free social networks
  3. Creating natural reinforcements for positive change
  4. Addressing multiple life domains simultaneously

Effectiveness of Psychological Treatments for Cannabis Dependence

The research reveals important findings about treatment outcomes:

Abstinence Achievement

Structured psychological interventions significantly improve abstinence rates. Individuals receiving cognitive-behavioural therapy are 18 times more likely to achieve abstinence compared to those awaiting treatment.

Reducing Use Frequency

For individuals not ready for complete abstinence, certain therapies effectively reduce consumption patterns. Acceptance-based approaches can decrease usage frequency by approximately 60%.

Treatment Duration and Structure

Effective programmes typically include:

  1. 6-52 sessions (average of 14)
  2. Weekly meetings over 2-6 months
  3. Individual or group formats
  4. Structured, manualised approaches

Key Components of Successful Psychological Interventions for Cannabis

Research identifies several critical elements that enhance treatment effectiveness:

Skills Training

Teaching practical techniques for managing triggers, cravings, and high-risk situations proves essential for lasting change.

Motivational Enhancement

Building intrinsic motivation through personalised feedback and collaborative goal-setting improves engagement and outcomes.

Relapse Prevention

Comprehensive planning for potential setbacks helps maintain gains achieved during active treatment.

Environmental Modification

Addressing social and environmental factors that maintain problematic use patterns enhances long-term success.

Challenges in Delivering Effective Treatment

Despite proven effectiveness, several challenges affect treatment delivery:

Engagement and Retention

Maintaining participant engagement throughout treatment remains challenging, with completion rates varying significantly across different approaches.

Individual Differences

Treatment response varies based on:

  1. Severity of dependence
  2. Co-occurring mental health conditions
  3. Social support availability
  4. Personal motivation levels

Access to Services: Many individuals face barriers accessing evidence-based psychological treatments for cannabis problems, including geographical limitations and resource constraints.

Future Directions for Cannabis Treatment Research

As cannabis potency increases and use patterns evolve, treatment approaches must adapt accordingly. Priority areas include:

  1. Developing age-specific interventions for adolescents
  2. Creating culturally adapted treatments
  3. Integrating technology-enhanced delivery methods
  4. Addressing co-occurring conditions simultaneously

Implications for Treatment Seekers

For individuals considering treatment, research suggests:

  1. Evidence-based psychological interventions offer genuine hope for recovery
  2. Different approaches suit different individuals
  3. Professional assessment helps match treatment to personal needs
  4. Persistence often proves necessary, as initial attempts may not succeed

The growing evidence base confirms that specialised psychological interventions for cannabis dependence can produce meaningful, lasting change when properly implemented and tailored to individual needs.

Conclusion: Current research provides strong support for several psychological approaches in treating cannabis dependence. Whilst cognitive-behavioural therapy with motivational enhancement shows the most consistent evidence, acceptance-based therapies and community reinforcement approaches also demonstrate effectiveness. As our understanding grows, these evidence-based treatments offer real pathways to recovery for those struggling with cannabis-related problems.

Source: https://nobrainer.org.au/index.php/resources/i-need-to-stop-this-help/1471-psychological-interventions-for-cannabis-dependence-latest-research-on-effective-therapies?

by The Daily Telegraph, London, UK –

Sadiq Khan wants to decrim­in­al­ise the Class-B drug, but fam­il­ies and doc­tors warn that smoking it is ‘play­ing Rus­sian roul­ette with your brain’. By Gwyneth Rees

For retired char­ity dir­ector Terry Ham­mond, 78, the issue of can­nabis-induced psy­chosis has come to dom­in­ate his life. About 25 years ago, his teen­age son Steven, now 42, began smoking skunk – a highly potent strain of the drug – at friends’ houses, without his par­ents know­ing.

For retired char­ity dir­ector Terry Ham­mond, 78, the issue of can­nabis-induced psy­chosis has come to dom­in­ate his life. About 25 years ago, his teen­age son Steven, now 42, began smoking skunk – a highly potent strain of the drug – at friends’ houses, without his par­ents know­ing.

“He was like so many young boys,” recalls Ham­mond from his home in Leicester­shire. “He was binge­ing on it in secret and thought it would be fine.” But around six months later, in the autumn of 1999, Steven sud­denly became para­noid. “We were watch­ing the BBC news, and he turned to me and accused me of ringing them. He was con­vinced the presenters were talk­ing about him.”

The psy­chosis didn’t stop there. “He began to think ali­ens had taken over every­body,” adds Ham­mond. “Then he began mum­bling in an incom­pre­hens­ible lan­guage, shout­ing at the walls and lock­ing him­self in his room. He was a boy gripped by abso­lute fear and ter­ror, and his beau­ti­ful mind had just been des­troyed.”

The psy­chosis didn’t stop there. “He began to think ali­ens had taken over every­body,” adds Ham­mond. “Then he began mum­bling in an incom­pre­hens­ible lan­guage, shout­ing at the walls and lock­ing him­self in his room. He was a boy gripped by abso­lute fear and ter­ror, and his beau­ti­ful mind had just been des­troyed.”

At 21, and with no fam­ily his­tory of men­tal health prob­lems, Steven was dia­gnosed with para­noid schizo­phrenia – psy­chosis that con­tin­ues indef­in­itely. He spent three months in the depart­ment of psy­chi­atry at the Royal South Hants Hos­pital in Southamp­ton, where he was put on the anti­psychotic drug Olan­za­pine and given talk­ing ther­apy. But even now – two dec­ades on – Steven, who lives in a stu­dio flat in his par­ents’ garden, is still affected by his early drug use.

At 21, and with no fam­ily his­tory of men­tal health prob­lems, Steven was dia­gnosed with para­noid schizo­phrenia – psy­chosis that con­tin­ues indef­in­itely. He spent three months in the depart­ment of psy­chi­atry at the Royal South Hants Hos­pital in Southamp­ton, where he was put on the anti­psychotic drug Olan­za­pine and given talk­ing ther­apy. But even now – two dec­ades on – Steven, who lives in a stu­dio flat in his par­ents’ garden, is still affected by his early drug use.

At 21, and with no fam­ily his­tory of men­tal health prob­lems, Steven was dia­gnosed with para­noid schizo­phrenia – psy­chosis that con­tin­ues indef­in­itely. He spent three months in the depart­ment of psy­chi­atry at the Royal South Hants Hos­pital in Southamp­ton, where he was put on the anti­psychotic drug Olan­za­pine and given talk­ing ther­apy. But even now – two dec­ades on – Steven, who lives in a stu­dio flat in his par­ents’ garden, is still affected by his early drug use.

“He can­not work and struggles socially,” says Ham­mond, who has Steven’s per­mis­sion to share his story and has also writ­ten a book, Gone to Pot, to help oth­ers in sim­ilar cir­cum­stances. “He is still on anti­psychotic drugs but con­tin­ues to hear voices, although he now has the skills to ration­al­ise them.

“He can­not work and struggles socially,” says Ham­mond, who has Steven’s per­mis­sion to share his story and has also writ­ten a book, Gone to Pot, to help oth­ers in sim­ilar cir­cum­stances. “He is still on anti­psychotic drugs but con­tin­ues to hear voices, although he now has the skills to ration­al­ise them.

“It has com­pletely ruined his life, and as par­ents we have had to suf­fer the bereave­ment of los­ing our son. Fun­da­ment­ally, it has dam­aged his brain for good. Young people need to know smoking can­nabis is play­ing Rus­sian roul­ette with brain dam­age.”

It is a har­row­ing story. But the issue of how to tackle the grow­ing prob­lem of ever-more potent can­nabis on our streets divides those in power. Sir Sadiq Khan, Lon­don’s mayor, has backed a report by the Lon­don Drugs Com­mis­sion stat­ing that pos­ses­sion of small amounts of can­nabis should be decrim­in­al­ised. He said there was a “com­pel­ling, evid­ence­based case” for decrim­in­al­isa­tion.

It is a har­row­ing story. But the issue of how to tackle the grow­ing prob­lem of ever-more potent can­nabis on our streets divides those in power. Sir Sadiq Khan, Lon­don’s mayor, has backed a report by the Lon­don Drugs Com­mis­sion stat­ing that pos­ses­sion of small amounts of can­nabis should be decrim­in­al­ised. He said there was a “com­pel­ling, evid­ence­based case” for decrim­in­al­isa­tion.

But on July 7, Bri­tain’s lead­ing police chiefs rejec­ted this and urged their officers to crack down on the drug. Last month, David Sid­wick, the Con­ser­vat­ive police and crime com­mis­sioner for Dor­set, wrote a let­ter to the police min­is­ter Diana John­son – signed by 13 other police and crime com­mis­sion­ers – call­ing can­nabis a “chron­ic­ally dan­ger­ous drug” that is as harm­ful as cocaine and crack.

Evid­ence shows that can­nabisin­duced psy­chosis has sub­stan­tially increased in recent years. A 2019 study pub­lished in The Lan­cet by Prof Marta Di Forti shows that can­nabis is respons­ible for 30 per cent of first-time psy­chosis cases in south Lon­don (it is 50 per cent in Ams­ter­dam).

Evid­ence shows that can­nabisin­duced psy­chosis has sub­stan­tially increased in recent years. A 2019 study pub­lished in The Lan­cet by Prof Marta Di Forti shows that can­nabis is respons­ible for 30 per cent of first-time psy­chosis cases in south Lon­don (it is 50 per cent in Ams­ter­dam).

Fur­ther research, not yet pub­lished, by Dr Diego Quat­trone and Dr Robin Mur­ray, pro­fess­ors of psy­chi­at­ric research at King’s Col­lege Lon­don, reveals that can­nabis-induced psy­chosis in the

‘In Amer­ica, the THC con­tent is so strong, you can go psychotic in one night’

UK is three times more com­mon than in the 1960s. Their research sug­gests that 75 per cent of this increase is down to the use of skunk, which accounts for 94 per cent of can­nabis on the UK mar­ket.

“Viol­ence is also asso­ci­ated with psy­chosis, and of the psychotic people who go on to kill, 90 per cent are using either alco­hol or can­nabis,” says Mur­ray.

More experts are now link­ing can­nabis use to viol­ence, which they attrib­ute to a chem­ical com­pon­ent in the plant – tet­rahy­drocan­nabinol (THC) – which can trig­ger hal­lu­cin­a­tions and para­noid ideas in vul­ner­able indi­vidu­als. Wor­ry­ingly, THC levels in can­nabis have been rising sharply. In the 1960s, THC levels in “weed” were around 3 per cent. Today, most UK can­nabis has THC levels of 16 to 20 per cent. In Hol­land, the fig­ure is between 30 and 40 per cent, and in Cali­for­nia, where can­nabis is legal, levels can reach 80 per cent.

“It is not easy to get psy­chosis,” says Mur­ray. “Typ­ic­ally, someone may smoke skunk for five years before it kicks in. But in Amer­ica, the THC is so strong, you can go psychotic in one night. It will hit those who already have a his­tory of men­tal health prob­lems the worst. We are braced for an epi­demic of psy­chosis.”

Dr Niall Camp­bell, a con­sult­ant psy­chi­at­rist at the Roe­hamp­ton Pri­ory Clinic, believes looser can­nabis reg­u­la­tion com­bined with increased potency have led to more patients suf­fer­ing psy­chosis. “I don’t think this rise is that sur­pris­ing given how easy skunk is to buy online, and how ubi­quit­ous it has become,” he says.

“Psy­chosis often begins with young people smoking a few joints and feel­ing a bit para­noid. But if they don’t stop, over time they can reach a psychotic state which won’t go away, even if they stop smoking. Sadly, this psy­chosis may last a life­time and once people are told that they can get very depressed or sui­cidal.”

“Psy­chosis often begins with young people smoking a few joints and feel­ing a bit para­noid. But if they don’t stop, over time they can reach a psychotic state which won’t go away, even if they stop smoking. Sadly, this psy­chosis may last a life­time and once people are told that they can get very depressed or sui­cidal.”

Lin­sey Raf­ferty, 42, from Pais­ley near Glas­gow, is one of those to have exper­i­enced dam­age firsthand. She had three short psychotic epis­odes over the dec­ades she smoked, but in 2020, dur­ing the Covid lock­down, she suffered an extreme epis­ode. “I was hear­ing things and writ­ing all over the walls of my home,” she says. “I threw my phone away because I thought it had been tapped and was eat­ing out of bins. It all made total sense to me at the time, and I can under­stand why people go viol­ent.”

Lin­sey Raf­ferty, 42, from Pais­ley near Glas­gow, is one of those to have exper­i­enced dam­age firsthand. She had three short psychotic epis­odes over the dec­ades she smoked, but in 2020, dur­ing the Covid lock­down, she suffered an extreme epis­ode. “I was hear­ing things and writ­ing all over the walls of my home,” she says. “I threw my phone away because I thought it had been tapped and was eat­ing out of bins. It all made total sense to me at the time, and I can under­stand why people go viol­ent.”

Raf­ferty was sec­tioned and put on anti­psychot­ics. Five years on, she has stopped smoking.

“When I stopped smoking, the psy­chosis went away,” she says. “But still, the epis­ode was deep and long-last­ing, and the scars haven’t gone. I never real­ised it could make me so vul­ner­able. I used to think drugs should be leg­al­ised, but not any­more.”

Source: https://www.pressreader.com/uk/features/20250716/281548001918086?

by Hailey M. Warner and Kelly Corr

ESSAY — Volume 22 — July 17, 2025

Although cigarette use among high school students and adults has declined since its peak in 1997, in North Dakota, nearly 1 in 3 high school students instead use e-cigarettes, and approximately 1 in 5 adults continue to smoke (1). The prevalence of tobacco and nicotine dependence poses substantial public health challenges, especially in rural communities (2).

More than 480,000 people, equivalent to the average capacity of 8 professional football stadiums, die from cigarette smoking annually in the US (3). In North Dakota, 1,000 adult deaths annually are attributed to cigarette use (1). Of cancer-related deaths in North Dakota, approximately 1 in 4 are associated with smoking (1). Cigarette use results in a high economic burden: in 2018, it cost the US more than $600 billion, including $240 billion in health care spending and nearly $185 billion in lost productivity due to smoking-related illnesses and health conditions (4). In 2021, health care expenditures attributed to tobacco use in North Dakota totaled $326 million, approximately equivalent to spending $421 for each person living in the state that year (1). Annual smoking-related lost productivity equates to nearly $185 billion in the US and $233 million in North Dakota (1,4). It is clear why the Centers for Disease Control and Prevention cites cigarette smoking as the leading cause of preventable disease, disability, and death in the US (3).

Smoking is a behavior that can harm nearly every organ in the human body, increasing the risk of heart disease, stroke, lung disease, diabetes, and cancer, and resulting in a substantial impact on population health (3). This essay explores and promotes providing tobacco and nicotine dependence treatment in the community pharmacy setting to increase patient care opportunities and improve health outcomes, particularly in rural areas.

The Profession of Pharmacy

Pharmacists are highly accessible and trusted health care professionals (5). Community pharmacies are a key component of the health care system, especially in rural, medically underserved areas, and they present an opportunity to help people quit using tobacco and nicotine products (5). Our ethnographic graduate research focuses on piloting an education-based intervention to assist independent community pharmacies in North Dakota in addressing tobacco and nicotine use among their clients. Our preliminary research results support the concept that in smaller communities, people often have close relationships with each other, including their local pharmacist. In one of our research pilot sites, a pharmacy in a rural town, a staff pharmacist said, “We care about our patients, and we want the best for their health.” To expand their scope of practice and fill gaps in access to health care services, independent community pharmacies are increasingly offering clinical services and improving patient outcomes (6).

Tobacco and Nicotine Dependence Treatment

Smoking cessation, the process of quitting the use of cigarettes, is more formally called tobacco dependence treatment (7). To encompass cigarette use as well as use of other tobacco or nicotine products, we use the term “tobacco and nicotine dependence treatment.” The main components of this treatment are behavioral therapies and medications. Among the behavioral therapy options are cognitive behavioral therapy, motivational interviewing, mindfulness practices, and support from technology-based options such as telephone quitlines, text message communications, or online media platforms (7). Nicotine replacement therapy (NRT) products are offered in various formulations, including patches, gum, lozenges, and nasal spray. All NRT products are deemed equally effective and are estimated to increase treatment success by 50% to 70% (7). Multiple NRT products can be used concurrently and are thought to provide better relief of withdrawal symptoms and cravings (7). The US Food and Drug Administration (FDA) has approved bupropion and varenicline as oral tobacco cessation medications. Bupropion and NRT have been shown to be equally effective, and some studies suggest varenicline is more effective than bupropion alone or the use of a single form of NRT (7). Bupropion and varenicline can be used in combination with NRT, which allows prescribers to tailor a person’s tobacco and nicotine dependence treatment plan to their individual needs (7).

Implementing Tobacco and Nicotine Dependence Treatment in Community Pharmacies

The implementation of tobacco and nicotine dependence treatment in community pharmacies can bolster the clinical capabilities and public health impact of community pharmacies. As of March 2025, eighteen states had implemented legislation allowing pharmacists prescriptive authority to provide patients with tobacco and nicotine dependence treatment medications (8). Of these, 9 states allow pharmacists to prescribe all medications approved by the FDA for smoking cessation, and the other 9 allow NRT only (8). In 2021, pharmacists in North Dakota were granted the authority to independently prescribe all FDA-approved medications, including varenicline, bupropion, and NRT (9). In the following year, the state’s Medicaid program expanded their coverage to include tobacco and nicotine dependence counseling provided by pharmacists (10). This expanded coverage broadened the impact of pharmacists on the adult Medicaid population in North Dakota, whose prevalence of smoking is more than double the prevalence among all adults in the state (39.1% vs 17.4%) (10).

Other insurers permit pharmacists to become recognized as medical providers, which allows them to submit reimbursement claims for tobacco and nicotine dependence treatment consultations as well as for the medications and NRT products they prescribe (5). These additional incentives may increase the number of encounters between pharmacists and people who smoke and lead to a reduction in cigarette use. During an unstructured interview conducted as part of our ethnographic graduate research, a pharmacist offering tobacco and nicotine dependence treatment services said, “These people have control over it [their tobacco and nicotine use]. If we can get them to stop, they can have such a better life. I honestly . . . I feel very strongly about this.”

Some independently owned community pharmacies in North Dakota have become pioneers in offering tobacco and nicotine dependence treatment to their patients. They use Ask-Advise-Refer/Connect, a method that combines the approaches of Ask-Advise-Refer and Ask-Advise-Connect (11). Both approaches share the steps of engaging patients by asking about tobacco use and advising them to quit. The difference lies in what actions are taken in the last step. In Ask-Advise-Refer, the patient is given a referral to a resource for quitting, whereas in Ask-Advise-Connect, the patient is directly connected to a resource for quitting (11). A pharmacist using Ask-Advise-Refer/Connect can choose to make a referral or connect with the patient to provide treatment at the pharmacy, whichever the patient prefers (11). Referrals can be made to state quitlines or local public health units, which assist in providing behavioral counseling and free NRT products. Because pharmacists in North Dakota have the authority to prescribe tobacco and nicotine dependence treatment medications, patients who are ready to quit can be immediately connected to pharmacists and receive treatment at the pharmacy. Regardless of whether a patient is provided with a referral or a connection, the pharmacist should follow up with patients on their progress toward cessation during future pharmacy visits. The second author (K.C.) developed a flowchart describing how a patient progresses through a tobacco and nicotine dependence treatment support process.

Figure.
Basic pharmacy workflow for tobacco and nicotine dependence treatment in North Dakota. NDQuits is the state tobacco quitline. Over-the-counter (OTC) products refer to nicotine replacement products that can be acquired without a prescription. [A text version of this figure is available.]

Call to Action

Pharmacists are called to be public health professionals and capitalize on opportunities to provide tobacco and nicotine dependence treatment for their patients, especially in rural areas. This expansion of services necessitates strengthening knowledge of tobacco and nicotine dependence treatment medications, learning how to provide behavioral counseling, and completing the requirements to be recognized as a provider of tobacco and nicotine dependence treatment services by health insurers.

The training of pharmacy students should be studied to ensure they can take the initiative to offer new services, apply population health strategies, and as a result, better serve their patients’ health care needs. Practicing pharmacists may need to refresh their knowledge and skills to provide tobacco and nicotine dependence treatment. Continuing education is a professional requirement, and pharmacists should actively seek opportunities to learn about topics such as motivational interviewing, tobacco and nicotine dependence treatment counseling, and current trends in tobacco use. In states where tobacco and nicotine dependence treatment provided by pharmacists is not yet authorized, pharmacists are encouraged to work with their board of pharmacy and local pharmacy organizations to advocate for expanding patients’ access to clinical services in community pharmacy settings.

Billions of dollars and hundreds of thousands of lives are lost to cigarette smoking every year in the US. Promoting pharmacy services and ensuring future pharmacists’ readiness for success should be a top priority for the profession. The next step toward preventing the disease, disability, and death attributable to tobacco use lies with pharmacists implementing tobacco and nicotine dependence treatment in community pharmacies across the country.

Source: https://www.cdc.gov/pcd/issues/2025/25_0088.htm

by Journal of Substance Use & Addiction Treatment, 2025, 

Authors: Josh Aleksanyan, Zobaida Maria, Diego Renteria, Adetayo Fawole, Ashly E. Jordan, Vanessa Drury, … Charles J. Neighbors

Abstract:

Introduction: Transition-age (TA) adults, aged 18-25, have the highest prevalence of substance use disorder (SUD) among all age groups yet they are less likely to seek treatment and more likely to discontinue it than older adults, making them a high-priority treatment population. While structural barriers and varying expectations of recovery may affect treatment initiation, insights from providers working with TA adults can reveal what further impels and impedes treatment engagement.

Methods: We conducted two focus groups with 14 front-line treatment providers, representing urban and rural outpatient, residential, and inpatient SUD care settings across New York State. Providers were selected through stratified sampling using restricted-access treatment registry data. A semi-structured interview guide facilitated discussions, and transcripts were analyzed to identify key themes.

Results: Providers report that TA adults prefer briefer, innovative treatment approaches over traditional modalities like A.A./12-step recovery, driven by a desire to rebuild their lives through education and career. Post-pandemic social disruptions were cited as exacerbating engagement challenges and increasing the need for integrating mental health support. Providers highlighted the potential of technology to enhance treatment engagement, though expressed concerns regarding social isolation and the fraying of childhood safety nets and support systems (e.g., housing) undermining successful treatment outcomes and transitions to adulthood more broadly.

Conclusions: Providers report and perceive various challenges-unmet mental health needs, social alienation, and housing insecurity-that impede TA adults from successful SUD treatment. Understanding providers’ perceptions of the needs of young adults can inform patient and clinical decision-making, lead to the development of innovative treatment approaches tailored to TA adults and contribute to improved health outcomes over the life course.

To read the full text of this article, please visit the link below:

Source: https://drugfree.org/drug-and-alcohol-news/research-news-roundup-july-17-2025/

 

A police officer said that no motive is currently known and that Chesser was compliant at the time of her arrest. Police believe he was killed around midnight on Tuesday, June 17.

Australian Reality Star Charged With Murder After Boyfriend's Headless Body Found
Tamika Sueann-Rose Chesser, a 34-year-old former Australian reality TV star, has been charged with murdering her 39-year-old boyfriend, Julian Story. According to a report by The Telegraph, authorities discovered Mr Story’s headless body at their South Australia home in Port Lincoln on June 19, following a report of a small fire. The investigation led to Chesser’s arrest and murder charge after his dismembered remains were found at the apartment. Police are still searching for Mr Story’s severed head.

“It was a confronting scene for police and emergency services personnel as Julian’s body had been dismembered. Julian’s head had been removed during the dismemberment and, despite extensive searches, has not yet been located,” South Australia Police said in a statement Friday. 

Police believe he was killed around midnight on Tuesday, June 17.

A witness reported seeing smoke coming from the apartment and approached Chesser, who claimed she was doing nothing. She then took her dogs for a walk and locked the door. Police released surveillance footage showing a woman, believed to be Chesser, dressed in black and walking with three dogs, just hours after the alleged murder on June 17, around midnight. 

Police are urging residents to review their surveillance or dashcam footage to aid in the ongoing investigation.

“I can only imagine, and I want you to imagine, the grief this news is causing Julian’s family. Recovering Julian’s head to return it to his family so they can have a peaceful outcome, have a funeral and lay him to rest is a really important aspect for us,” Detective Superintendent Darren Fielke added. 

She was taken into custody after police found her in a catatonic and unresponsive state in the backyard of the crime scene, according to court documents. Mr Fielke said there was no obvious motive at this stage, and Chesser was cooperative at the time of the arrest, the ABC reported.

A spokesperson for Mr Story’s family said they were “navigating an unimaginable loss” as they thanked police and first responders for their “compassion and professionalism during this devastating time”.

“We are also deeply grateful to our family and friends and this extraordinary community, whose kindness and support have helped carry us through. Your prayers, presence, and quiet strength mean more than words can say,” the statement added. 

Chesser was the runner-up on the 2010 season of Beauty and the Geek and later modelled for men’s magazines including Playboy, Ralph and FHM. 

She remains in custody under a mental health detention order and due to appear in court again in December.

Sources:

India news: https://www.ndtv.com/world-news/australian-reality-star-charged-with-murder-after-boyfriends-headless-body-found-8795479

Australia news: https://www.aol.com/australian-reality-tv-star-charged-121626759.html

Los Angeles — Inside a bright new building in the heart of Skid Row, homeless people hung out in a canopy-covered courtyard — some waiting to take a shower, do laundry, or get medication for addiction treatment. Others relaxed on shaded grass and charged their phones as an intake line for housing grew more crowded.

The new Skid Row Care Campus offers homeless people health care and a place to rest, charge their phones, grab some

food, or even get connected with housing.Angela Hart / KFF Health News

 

The Skid Row Care Campus officially opened this spring with ample offerings for people living on the streets of this historically downtrodden neighborhood. Pop-up fruit stands and tent encampments lined the sidewalks, as well as dealers peddling meth and fentanyl in open-air drug markets. Some people, sick or strung out, were passed out on sidewalks as pedestrians strolled by on a recent afternoon.

For those working toward sobriety, clinicians are on site to offer mental health and addiction treatment. Skid Row’s first methadone clinic is set to open here this year. For those not ready to quit drugs or alcohol, the campus provides clean syringes to more safely shoot up, glass pipes for smoking drugs, naloxone to prevent overdoses, and drug test strips to detect fentanyl contamination, among other supplies.

As many Americans have grown increasingly intolerant of street homelessness, cities and states have returned to tough-on-crime approaches that penalize people for living outside and for substance use disorders. But the Skid Row facility shows Los Angeles County leaders’ embrace of the principle of harm reduction, a range of more lenient strategies that can include helping people more safely use drugs, as they contend with a homeless population estimated around 75,000 — among the largest of any county in the nation. Evidence shows the approach can help individuals enter treatment, gain sobriety, and end their homelessness, while addiction experts and county health officials note it has the added benefit of improving public health.

“We get a really bad rap for this, but this is the safest way to use drugs,” said Darren Willett, director of the Center for Harm Reduction on the new Skid Row Care Campus. “It’s an overdose prevention strategy, and it prevents the spread of infectious disease.”

Despite a decline in overdose deaths, drug and alcohol use continues to be the leading cause of death among homeless people in the county. Living on the streets or in sordid encampments, homeless people saddle the health care system with high costs from uncompensated care, emergency room trips, inpatient hospitalizations, and, for many of them, their deaths. Harm reduction, its advocates say, allows homeless people the opportunity to obtain jobs, taxpayer-subsidized housing, health care, and other social services without being forced to give up drugs. Yet it’s hotly debated.

Politicians around the country, including Gov. Gavin Newsom in California, are reluctant to adopt harm reduction techniques, such as needle exchanges or supervised places to use drugs, in part because they can be seen by the public as condoning illicit behavior. Although Democrats are more supportive than Republicans, a national poll this year found lukewarm support across the political spectrum for such interventions.

Los Angeles is defying President Trump’s agenda as he advocates for forced mental health and addiction treatment for homeless people — and locking up those who refuse. The city has also been the scene of large protests against Mr. Trump’s immigration crackdown, which the president has fought by deploying National Guard troops and Marines.

Mr. Trump’s most detailed remarks on homelessness and substance use disorder came during his campaign, when he attacked people who use drugs as criminals and said that homeless people “have no right to turn every park and sidewalk into a place for them to squat and do drugs.” Health and Human Services Secretary Robert F. Kennedy Jr. reinforced Mr. Trump’s focus on treatment.

“Secretary Kennedy stands with President Trump in prioritizing recovery-focused solutions to address addiction and homelessness,” said agency spokesperson Vianca Rodriguez Feliciano. “HHS remains focused on helping individuals recover, communities heal, and help make our cities clean, safe, and healthy once again.”

A comprehensive report led by Margot Kushel, a professor of medicine at the University of California-San Francisco, this year found that nearly half of California’s homeless population had a complex behavioral health need, defined as regular drug use, heavy drinking, hallucinations, or a recent psychiatric hospitalization.

The chaos of living outside, she said — marked by violence, sexual assault, sleeplessness, and lack of housing and health care — can make it nearly impossible to get sober.

Skid Row Care Campus

The new care campus is funded by about $26 million a year in local, state, and federal homelessness and health care money, and initial construction was completed by a Skid Row landlord, Matt Lee, who made site improvements on his own, according to Anna Gorman, chief operating officer for community programs at the Los Angeles County Department of Health Services. Operators say the campus should be able to withstand potential federal spending cuts because it is funded through a variety of sources.

Glass front doors lead to an atrium inside the yellow-and-orange complex. It was designed with input from homeless people, who advised the county not just on the layout but also on the services offered on-site. There are 22 recovery beds and 48 additional beds for mostly older homeless people, arts and wellness programs, a food pantry, and pet care. Even bunnies and snakes are allowed.

John Wright, 65, who goes by the nickname Slim, mingled with homeless visitors one afternoon in May, asking them what they needed to be safe and comfortable.

“Everyone thinks we’re criminals, like we’re out robbing everyone, but we aren’t,” said Wright, who is employed as a harm reduction specialist on the campus and is trying, at his own pace, to stop using fentanyl. “I’m homeless and I’m a drug addict, but I’m on methadone now so I’m working on it,” he said.

Nearby on Skid Row, Anthony Willis rested in his wheelchair while taking a toke from a crack pipe. He’d just learned about the new care campus, he said, explaining that he was homeless for roughly 20 years before getting into a taxpayer-subsidized apartment on Skid Row. He spends most of his days and nights on the streets, using drugs and alcohol.

The drugs, he said, help him stay awake so he can provide companionship and sometimes physical protection for homeless friends who don’t have housing. “It’s tough sometimes living down here; it’s pretty much why I keep relapsing,” said Willis, who at age 62 has asthma and arthritic knees. “But it’s also my community.”

Willis said the care campus could be a place to help him kick drugs, but he wasn’t sure he was ready.

Research shows harm reduction helps prevent death and can build long-term recovery for people who use substances, said Brian Hurley, an addiction psychiatrist and the medical director for the Bureau of Substance Abuse Prevention and Control at the Los Angeles County Department of Public Health. The techniques allow health care providers and social service workers to meet people when they’re ready to stop using drugs or enter treatment.

“Recovery is a learning activity, and the reality is relapse is part of recovery,” he said. “People go back and forth and sometimes get triggered or haven’t figured out how to cope with a stressor.”

Swaying public opinion

Under harm reduction principles, officials acknowledge that people will use drugs. Funded by taxpayers, the government provides services to use safely, rather than forcing people to quit or requiring abstinence in exchange for government-subsidized housing and treatment programs.

Los Angeles County is spending hundreds of millions to combat homelessness, while also launching a multiyear “By LA for LA” campaign to build public support, fight stigma, and encourage people to use services and seek treatment. Officials have hired a nonprofit, Vital Strategies, to conduct the campaign including social media advertising and billboards to promote the expansion of both treatment and harm reduction services for people who use drugs.

The organization led a national harm reduction campaign and is working on overdose prevention and public health campaigns in seven states using roughly $70 million donated by Michael Bloomberg, the former mayor of New York.

“We don’t believe people should die just because they use drugs, so we’re going to provide support any way that we can,” said Shoshanna Scholar, director of harm reduction at the Los Angeles County Department of Health Services. “Eventually, some people may come in for treatment but what we really want is to prevent overdose and save lives.”

Los Angeles also finds itself at odds with California’s Democratic governor. Newsom has spearheaded stricter laws targeting homelessness and addiction and has backed treatment requirements for people with mental illness or who use drugs. Last year, California voters approved Proposition 36, which allows felony charges for some drug crimes, requires courts to warn people they could be charged with murder for selling or providing illegal drugs that kill someone, and makes it easier to order treatment for people who use drugs.

Even San Francisco approved a measure last year that requires welfare recipients to participate in treatment to continue receiving cash aid. Mayor Daniel Lurie recently ordered city officials to stop handing out free drug supplies, including pipes and foil, and instead to require participation in drug treatment to receive services. Lurie signed a recovery-first ordinance, which prioritizes “long-term remission” from substance use, and the city is also expanding policing while funding new sober-living sites and treatment centers for people recovering from addiction.

“Harm encouragement”

State Sen. Roger Niello, a Republican who represents conservative suburbs outside Sacramento, says the state needs to improve the lives of homeless people through stricter drug policies. He argues that providing drug supplies or offering housing without a mandate to enter treatment enables homeless people to remain on the streets.

Proposition 36, he said, needs to be implemented forcefully, and homeless people should be required to enter treatment in exchange for housing.

“I think of it as tough love,” Niello said. “What Los Angeles is doing, I would call it harm encouragement. They’re encouraging harm by continuing to feed a habit that is, quite frankly, killing people.”

Keith Humphreys, who worked in the George W. Bush and Barack Obama administrations and pioneered harm reduction practices across the nation, said that communities should find a balance between leniency and law enforcement.

“Parents need to be able to walk their kids to the park without being traumatized. You should be able to own a business without being robbed,” he said. “Harm reduction and treatment both have a place, and we also need prevention and a focus on public safety.”

Just outside the Skid Row Care Campus, Cindy Ashley organized her belongings in a cart after recently leaving a local hospital ER for a deep skin infection on her hand and arm caused by shooting heroin. She also regularly smokes crack, she said.

She was frantically searching for a home so she could heal from two surgeries for the infection. She learned about the new care campus and rushed over to get her name on the waiting list for housing.

“I’m not going to make it out here,” she said, in tears.

Source:  https://www.cbsnews.com/news/los-angeles-harm-reduction-drugs-homelessness/

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF — the independent source for health policy research, polling, and journalism.

 

Opening Remark by NDPA:

This news item came from the website for a Kissimmee (Orlando, Fla) residents website for the Lindfields division.

The item is of general interest because although it is ostensibly limited to Florida, it introduces a tougher education course for new drivers, specifically including education on drinks/drugs and driving.

<<<<<<<<<<<<<<<<<<<<<<FLA>>>>>>>>>>>>>>>>>>>>>>

STATEMENT IN LINDFIELDS DIVISION RESIDENTS’ WEBSITE – JULY 2025

Florida is phasing out the old 4-hour course and introducing a new, more in-depth requirement for teen drivers under age 18. This affects anyone applying for a learner’s permit or first-time driver’s license. ????

Key Dates and What’s Required July 1 to July 31, 2025 (Transition Period) If you’re under 18 and applying for your learner’s permit or license: You may take either of the following: TLSAE/DATA: Traffic Law and Substance Abuse Education Also known as Drugs, Alcohol, Traffic Awareness A 4-hour course currently required for all new drivers in Florida DETS: Driver Education and Traffic Safety A new 6-hour course required for teen drivers beginning in 2025 August 1, 2025 and After Only DETS (Driver Education and Traffic Safety) will be accepted for drivers under 18 The TLSAE/DATA course will no longer be valid for minors applying for a learner’s permit Adults (18+) may still use TLSAE/DATA to meet the education requirement ????

What is DETS and Why the Change? The new 6-hour DETS course is designed to:

  • Strengthen defensive driving habits I
  • mprove hazard recognition
  • Cover DUI prevention and traffic laws in more detail
  • Reduce teen crash risks by offering a broader education experience

Summary:

  • Date Range Under-18 Requirements July 1–31, 2025 TLSAE/DATA or DETS accepted August 1, 2025 onward
  • Only DETS accepted Age 18+ Can continue using TLSAE/DATA.

Source:  LINDFIELDS DIVISION RESIDENTS’ WEBSITE – JULY 2025

  • by Oritro Karim (United Nations) – 

UNITED NATIONS, Jun 27 (IPS) – Since 1989, the United Nations (UN) has recognized June 26 as the International Day Against Drug Abuse and Illicit Trafficking in an effort to raise awareness around the global drug problem and foster a more compassionate world, free of drug abuse. Through this year’s campaign, “Break the Cycle. #StopOrganizedCrime”, the UN underscores the importance of addressing the root causes of global drug abuse and illegal drug trading, and investing in reliable systems that prioritize prevention, education, and health.

Concurrently, the United Nations Office on Drugs and Crime (UNODC) released its annual World Drug Report, in which it analyzed the current trends in global drug abuse amid a “new era of global instability”. In the report, UNODC emphasizes the wide ranging implications of drug use on the economy, the environment, global security, and human society.

According to the report, roughly 316 million people used drugs (excluding tobacco and alcohol) around the world in 2023. UNODC also estimates that nearly half a million people around the world die annually as a result of drug use disorders, indicating a “global health crisis”. Roughly 28 million years of life are lost annually from disabilities and premature deaths due to addiction. Furthermore, there is an overwhelming lack of healthcare and education resources for individuals with drug use disorders, as only one in twelve people are estimated to have received treatment in 2023.

Cocaine has been described as the world’s fastest growing illicit drug in terms of global usage, production, and seizures. In 2023, approximately 3,708 tons of cocaine were produced, marking a 34 percent increase from the previous year. Roughly 2,275 tons were seized in 2023, a 68 percent increase from 2019’s figures. Additionally, global usage of cocaine has inflated to 25 million users in 2023.

As nations began to implement harsher crackdowns on drug production, the use and transportation of synthetic drugs, such as fentanyl and methamphetamine, has reached record-highs, accounting for nearly half of all global drug seizures. Drug trafficking groups have found ways to chemically conceal these drugs, making distribution much easier.

UNODC Executive Director Ghada Fathi Waly states that organized drug trafficking groups around the world continue to exploit global crises, disproportionately targeting the most vulnerable communities. With worldwide synthetic drug consumption having surged in recent years, the UNODC forecasts that civilians displaced by armed conflicts face heightened risks of drug abuse and addiction.

Although the cocaine market was once contained in Latin America, trade has extended through to Asia, Africa, and Western Europe, with Western Balkans having greater shares in the market. This is a testament to the influence of organized crime groups in areas facing instability, natural disasters, and economic challenges.

According to the report, since the end of the Assad regime in Syria and the subsequent political transition, nationwide use of fenethylline — also known as captagon, a cheap, synthetic stimulant — has soared. Although the transitional government of Syria has stated that there is zero tolerance for captagon trade and consumption, UNODC warns that Syria will remain a significant hub for drug production.

Angela Me, the Chief of Research and Analysis at UNODC, states that captagon use in the Arabian peninsula was spurred by regional violence, with members of terrorist organizations using it on battlefields to stay alert. Due to its highly addictive properties, as well as its severe impacts on physical and mental health, the drug has seen widespread consumption over the past several years.

“These groups have been managing Captagon for a long time, and production is not going to stop in a matter of days or weeks,” said Me. “We see a lot of large shipments going from Syria through, for example, Jordan. There are probably still stocks of the substance being shipped out, but we’re looking at where the production may be shifting to. We’re also seeing that the trafficking is expanding regionally, and we’ve discovered labs in Libya.”

Global drug trafficking is estimated to generate billions of dollars per year. National budgets to combat drug trafficking, in terms of law enforcement and prosecution, cost governments millions to billions annually as well. Healthcare systems, which are often underfunded for addiction-related treatments, are overwhelmed by the vast scale of needs. Furthermore, damages related to theft, vandalism, violence, and lost productivity in the workplace have significant impacts on gross domestic products.

Additionally, increased rates of deforestation and pollution are linked with global drug cultivation. Additional adverse environmental impacts include ecosystem damage from drug waste, which yields notable costs in environmental restoration efforts.

It is imperative for governments, policymakers, and other stakeholders to invest in programs that disrupt illicit drug trafficking groups and promote increased security, especially along borders, which are critical hubs for transporting concealed substances. Furthermore, cooperation at an international level is instrumental for the transfer of information and promoting a joint and multifaceted approach.

“We must invest in prevention and address the root causes of the drug trade at every point of the illicit supply chain. And we must strengthen responses, by leveraging technology, strengthening cross-border cooperation, providing alternative livelihoods, and taking judicial action that targets key actors driving these networks,” said Waly. “Through a comprehensive, coordinated approach, we can dismantle criminal organizations, bolster global security, and protect our communities.”

Source:  https://www.globalissues.org/news/2025/06/27/40295

by Ingrid Fadelli, Phys.org – edited by Gaby Clark, reviewed by Robert Egan – The GIST – June 26, 2025

Omicron Limited’ 36 Hope Street, Douglas, IM1 1AR, Isle of Man

Cannabis, also known as marijuana or weed, is widely consumed worldwide, whether for recreational or medicinal purposes. Over the past decades, the use of cannabis has been fully legalized or decriminalized in various countries worldwide, including Canada, many U.S. states, the Netherlands, Germany, Spain and Portugal.

While some studies have found that cannabis and especially cannabidiol (i.e., the non-intoxicating compound contained in it) can have medicinal effects, others have linked the abuse of its psychoactive variations (i.e., containing tetrahydrocannabinol or THC) with a greater risk of being diagnosed with psychiatric disorders.

As many individuals worldwide use cannabis on a regular basis, understanding the mechanisms that could link its consumption with psychiatric disorders could be highly valuable, as it might help to identify factors that increase the risk of developing specific disorders.

In a paper published in Nature Mental Health, researchers at Yale University School of Medicine, the Veterans Affairs Connecticut Healthcare System and Washington University School of Medicine shed new light on the genetic associations between cannabis use, cannabis use disorder (CanUD) and various psychiatric disorders.

CanUD is a mental health disorder characterized by a continued use of cannabis, difficulties experienced when trying to cut down its consumption or cease using it altogether, and an interference of the substance with daily activities, relationships or responsibilities.

“Increasing prevalence of cannabis use and CanUD may increase risk for psychiatric disorders,” wrote Marco Galimberti, Cassie Overstreet and their colleagues in their paper. “We evaluated the relationships between these cannabis traits and a range of psychiatric traits, running global and local genetic correlations, genomic structural equation modeling, colocalization analyses and Mendelian randomization analyses for causality.”

Genomic-SEM. Genomic-SEM analyses of cannabis traits (CanUD and cannabis use) and
psychiatric disorders for a three-factor model. Credit: Galimberti et al.
(Nature Mental Health, 2025).

The researchers analyzed genetic, psychiatric and psychological data collected as part of earlier studies, using various statistical techniques. First, they tried to detect genetic patterns that linked cannabis use with specific psychiatric and personality traits, using a technique known as genomic structural equation modeling.

Subsequently, they ran colocalization analyses, a statistical analysis that allowed them to uncover instances where two traits shared the same underlying genetic variant. Finally, they used a technique called Mendelian randomization to uncover causal relationships between traits, or in other words, if a sporadic or problematic use of cannabis caused specific disorders via genetic factors and vice versa.

“Global genetic analyses identified significantly different correlations between CanUD and cannabis use,” wrote Galimberti, Overstreet and their colleagues. “A variant in strong linkage disequilibrium to one regulating CHRNA2 was significantly shared by CanUD and schizophrenia in colocalization analysis and included in a significant region in local genetic correlations between these traits. A three-factor model from genomic structural equation modeling showed that CanUD and cannabis use partially map together onto a factor with major depressive disorder and ADHD.”

Interestingly, the researchers found that although cannabis use and CanUD are in some ways related, they had different genetic relationships with psychiatric disorders. In fact, they found that variations in the regulation of the gene CHRNA2, which has also been linked to nicotine consumption and dopamine signaling, were common to both schizophrenia and CanUD, but not to casual or general cannabis use.

“In terms of causality, CanUD showed bidirectional causal relationships with most tested psychiatric disorders, differently from cannabis use,” wrote Galimberti, Overstreet and their colleagues. “Increasing use of cannabis can increase rates of psychiatric disorders over time, especially in individuals who progress from cannabis use to CanUD.”

Overall, the findings of this recent study suggest that there is a bi-directional genetic relationship between the abuse of cannabis, specifically CanUD, and various psychiatric disorders, including schizophrenia, ADHD, depression, and bipolar disorder. In other words, it appears that CanUD could increase the risk of developing mental health disorders, and being diagnosed with some psychiatric disorders could also prompt abuse of cannabis.

This recent work could potentially inform the development of public health interventions aimed at monitoring or limiting people’s consumption of cannabis early, to reduce the risk that they will later develop psychiatric disorders. In addition, the analyses could inspire other research groups to delve deeper into the genetic associations they uncovered, potentially by analyzing a wider pool of genetic, psychological and medical data.

Written for you by our author Ingrid Fadelli, edited by Gaby Clark , and fact-checked and reviewed by Robert Egan —this article is the result of careful human work. We rely on readers like you to keep independent science journalism alive. If this reporting matters to you, please consider a donation (especially monthly). You’ll get an ad-free account as a thank-you.

More information: Marco Galimberti et al, The genetic relationship between cannabis use disorder, cannabis use and psychiatric disorders, Nature Mental Health (2025). DOI: 10.1038/s44220-025-00440-4.

Journal information: Nature Mental Health

Source: https://medicalxpress.com/news/2025-06-explores-genetic-link-cannabis-psychiatric.html

By Dr. Nora Volkow – Nora’s Blog – June 17, 2025
In a recent commentary in The New England Journal of Medicine, my colleagues John Kelly, Howard Koh, and I likened the addicted brain to a house on fire—a crisis requiring urgent efforts to contain the damage and preserve life.1 The drug crisis in America has demanded a sustained focus to extinguish those fires by expanding treatment access and overdose prevention and reversal strategies—and encouragingly, data show that overdose fatalities have been declining since 2023. However, a house that has had its addiction fire extinguished still smolders and can readily burst into flames again. After an initial remission of substance use disorder (SUD) symptoms, it can take as much as 8 years and 4-5 engagements in treatment or mutual support groups to achieve sustained remission, and risk for meeting SUD criteria can remain elevated for several more years after that.2

As addiction clinicians and researchers, we have an obligation not only to improve our abilities at fighting the fires of active addiction, but also to enhance our ability to facilitate the processes of rebuilding in the aftermath, to reduce their future recurrence. Increasing the number of people achieving long-term recovery from SUDs is a national policy priority and a major goal of the research supported by NIDA—from basic neuroscience to understand how the brain rewires and recovers after addiction to an intensified focus on the supports and services that can help individuals thrive as they build healthier lives.3

Fortunately, the very same adaptability and neuroplasticity of the brain that makes it susceptible to developing addiction in the first place also enables it to heal, especially when internal and external conditions are supportive of recovery. The neurobiology underlying remission from SUDs has long been a focus of NIDA-funded research. Over two decades ago, as a NIDA grantee, I and my colleagues at Brookhaven National Laboratory and SUNY-Stony Brook used PET neuroimaging to show the recovery of lost dopamine transporters in the striatum of people with methamphetamine use disorder after prolonged abstinence.4 More recent longitudinal neuroimaging studies of people in SUD treatment show structural recovery in frontal cortical regions, insula, hippocampus, and cerebellum, and functional and neurochemical recovery in prefrontal cortical and subcortical regions.5

As the individual learns new behaviors, goals, and rewards, the learning process reshapes synaptic connectivity across a range of circuits, ultimately outcompeting drug-related memories and automatic behavioral patterns, which weaken over time.6 Among ongoing NIDA-funded projects is a study homing in on the circuits associated with medication adherence in patients with opioid use disorder (OUD) and those that predict return to opioid use during medication treatment. Another project is using biweekly neuroimaging of patients taking medications to treat OUD to characterize neural trajectories of remission.

NIDA has also made a major investment in research on services and supports that can make it easier for people in recovery to continue to choose non-drug rewards and thereby facilitate this neural rewiring. Such services may prove to be at least as important as treatment or overdose reversal in maintaining the recent gains made in reducing overdose deaths. A 2022 dynamic modeling study funded by the FDA projected that people returning to opioid use after a period of remission will account for an increasing proportion of OUD cases over the coming decade, compared to people newly developing OUD.7 Consequently, the authors found that, of 11 strategies to reduce OUD and fatal overdoses, services that help people stay in remission from OUD were likely to be among the most impactful.

Over the past few years, NIDA has funded several grants with the aim of building the infrastructure necessary to advance the science of recovery support. They included grants in 2020 and 2022 that supported the development of networks of recovery researchers working to establish key measures for the field, as well as clinical trial planning grants that establish the foundation necessary to conduct future large-scale clinical trials to understand the effectiveness of various recovery support services. NIDA is also supporting research on how to deliver services to groups like adolescents and young adults and people involved in the criminal-justice system, and to identify factors that are most predictive of recovery outcomes like recovery identity and meaningfulness.

One defining feature of recovery support services is the central role of peers who have lived or living experience of SUD. It can involve individual support by recovery coaches, living or working in settings with others in recovery such as recovery housing or recovery community centers, or mutual-aid groups like traditional 12-step programs and newer models like SMART Recovery. Among the many questions being addressed by NIDA grantees, therefore, are ways to support peers and their professional advancement to foster a more sustainable recovery workforce. NIDA is also working with startups to develop apps and other digital tools that can be used to facilitate connecting to peers, including mobile apps and digital peer-support platforms accessible in treatment settings for patients who are socioeconomically disadvantaged.

In whatever way recovery services are implemented, access and engagement over a longer duration of time than typical stints of addiction treatment can be crucial to help a person maintain remission and provide support when times get tough. Yet there is limited data on the optimal duration of recovery supports services, how the intensity or focus of services should change over the course of recovery, and, in the case of people taking medications for OUD, if and when medications can be safely discontinued. NIDA-funded recovery research is exploring the crucial question of optimal duration of medication treatment for people with OUD and developing discontinuation strategies for people who want to stop medication.

As we described in our New England Journal of Medicine commentary, the positive shift from punishing people experiencing addiction towards treating them in the clinic seen over the past four decades is now shifting into a new phase where the clinic is integrated with the community.  The integration of support in the community is giving nonclinicians, including peers, friends, and family, an increasingly important role in the care of people with SUDs, facilitating the continuity of care beyond treatment. NIDA recently solicited applications for research projects on the role played by loved ones and other support persons in SUD recovery, with the goal of incorporating them into individuals’ recovery process as well as developing interventions to give support to those who are supporting a loved one in recovery.

As more addiction fires are extinguished through public health measures at the national, state, and community levels, we must direct more scientific attention to the end goal of long-term health and wellness for all people whose lives have been affected by addiction.

Source: https://nida.nih.gov/about-nida/noras-blog/2025/06/advancing-recovery-research

While many of the conversations surrounding marijuana revolve around younger generations and their patterns of use, a growing body of research is starting to include older adults in the conversation. Two recent studies show an increase in the use of marijuana among older adults and a link to various health conditions.

 

The first study, out of the University of California, included data from 15,689 adults aged 65 and older. This study found a sharp increase in the prevalence of marijuana use over the past-month among this population – rising from 4.8% to 7.0%. This study identified a link between this rise and various factors, including residing in a state with legal medical marijuana, being a woman, and several health issues such as heart conditions, diabetes, hypertension, in addition to other sociodemographic and clinical outcomes.

 

The second study out of Ontario, Canada, where marijuana has been legal for recreational use since 2018, used health data from over 6 million individuals and focused on adults aged 45 and older over a 14-year period to assess whether marijuana use that led to an emergency department (ED) visit or hospitalization could be associated with future dementia diagnoses.

The study showed that between the years of 2008 to 2021, marijuana-related emergency care increased dramatically in adults aged 65 and older, with a 26.7-fold increase. Even among adults aged 45 to 64, the rate increased fivefold. This surge reflects both the growing normalization of marijuana and the growing number of older adults experimenting with or becoming dependent on its use. But as use has increased, so too has concern about its potential consequences for brain health.

 

This study found that those who required emergency care for marijuana-related reasons were significantly more likely to develop dementia. Within 5 years, 5% of marijuana-related acute care patients were diagnosed with dementia compared to 3.6% among individuals with other types of hospital visits, and just 1.3% in the general population.

 

Even after adjusting for factors like age, gender, chronic health conditions and mental health history, the elevated risk remained: Compared to peers hospitalized for any reason, marijuana users had a 23% higher risk of dementia. Compared to the general population, their risk was 72% higher. By 10 years, nearly one in five (18.6%) of those with marijuana-related hospital visits had developed dementia.

 

Although the specific biological mechanisms are still unknown, many studies have shown an association between heavy marijuana use and memory and cognitive decline, and this study adds to the concern that long-term use, heavy use or cannabis use disorder (CUD) may also accelerate long-term neurodegeneration. With chronic marijuana exposure possibly altering the brain structure, reducing cognitive reserve and interfering with key processes involved in memory and learning, this growing use is leaving older adults more vulnerable due to age-related changes in the brain and the possibility of unknown interactions with other health conditions or medications.

 

As marijuana use grows in this age group, targeted prevention and education strategies are urgently needed.

 

Source: Drug Free America Foundation | 333 3rd Ave N Suite 200 | St. Petersburg, FL 33701 US

OPENING REMARKS BY NDPA:

This book, and its review, engage with differing viewpoint s about addiction and addicts. Flanagan prefers to avoid the word ‘disease’ – characterising the condition as a behavioural ‘disorder’ – much in the way that Stanton Peele, in his classic 1975 text ‘Love and Addiction’ – (Peele and Brodsky – Pubd, Taplinger, New York) similarly views the condition. But in the professional field of today additional concepts have been introduced, what some might call ‘influencers’ – longest established is the notion of ‘harm reduction’ – this (in our opinion) has a valid purpose in limiting harm that users can experience, but it has also been ‘abused’ by campaigners who argue that ‘laws are harmful, so legalisation reduces harm’. More recently the notion of ‘stigma’ has become more prominent in the drug policy arena … and again, whilst there is a valid role for addressing gratuitous stigmatisation of users, the liberalising campaigners can be seen to abuse the notion, arguing that ‘all stigma is bad, therefore all stigma should be removed.’ In fact, society has long rationally deployed stigma where it can be seen as criticising an individuals drug abuse when this damages and jeopardises a healthful society, or threatens the health of people around the user … this is echoed in Flanagan’s text where, for example he says addicts are ‘… are by no means blameless just because they supposedly have a disease’. This dialogue will of course run and run, and NDPA will endeavour to maintain a balanced and rational journey through this jungle!

A new book looks at addiction through the lens of choice and responsibility.

 Reason Magazine – 

Owen Flanagan’s new book, What Is It Like To Be an Addict?, should be welcomed by anyone concerned with these issues. Despite its modest size, this is a work of large ambition and broad range informed not just by the author’s long career as a prominent philosopher but by his many years as a desperately addicted abuser of alcohol and sedatives.

“This is a deeply personal book,” he writes. “I was addicted to booze and benzos for twenty years on and off from the late 1970s until the early 2000s. The last years were especially ugly, requiring several hospitalizations, and involving constant self-loathing and suicidal despair.”

Unsurprisingly given his experience, Flanagan stresses that we should pay close attention to what the addicted have to tell us. And among the most important things addicts say is that they are by no means blameless just because they supposedly have a disease. On the contrary, many feel shame (for being an addict) and guilt (for behaviors that are slowly destroying them and harming their loved ones).

To Flanagan, these feelings are right and good. That stance may inspire horror from some people, who will see it as victim-blaming. But it’s consistent with Flanagan’s view that addicts can’t be reduced to flesh-and-blood automatons jerked about by their cravings. As he notes, even people who claim to believe this will then earnestly implore an addict to get help—a plea that could only be directed at someone presumed to have the ability to make choices. “Every treatment that works to unseat addiction,” he writes, “assumes that addicts are responsible and must participate in undoing their own addiction.”

Flanagan doesn’t even think addiction is a disease, exactly—more of a multifactorial disorder of enormous social, physical, psychological, and pharmacological complexity. Indeed, one of his book’s main points is that addiction cannot be seen as any one simple thing. But he doggedly insists that addicts retain some agency during their plight.

“Practices of compassion, forgiveness, and excusing are distinct from whether or not we hold the addict responsible,” he writes. “We hold addicts responsible in many respects and rightly so. Thus, the determination that addiction is a disease or mental disorder is much less consequential as far as holding addicts responsible goes than many suggest.”

Flanagan takes care to distinguish between unwilling addicts, willing addicts, and resigned addicts, helping us through these categories to think about what we mean by addiction and how best to mitigate it. Particularly notable are the minority who are willing addicts—he mentions as an example Keith Richards, who has said he was a longtime heroin user. At least some of these individuals are in control of the consequences of their habit and satisfied with their lives. Is their addiction any more meaningful than a coffee habit?

Unwilling addicts want to quit, and many will eventually succeed. And resigned addicts are those who wanted to quit, couldn’t, and just gave up, surrendering to hopelessness. They are in a sense beyond unwilling; by not trying to quit, they effectively acquiesce. Here, the author says, a kind of accommodation may help. One nonprofit in Europe helps resigned addicts to lead orderly lives through more disciplined consumption—in one methadone-like program, six pints of beer spread throughout the day—as well as suitable paid employment.

As for himself, the author credits Alcoholics Anonymous with saving his life by enabling his sobriety, but he also thinks it has a certain cultishness; like any good rationalist, he insists on “the distinction between the belief in a Higher Power having an effect and the Higher Power having an effect.”

Flanagan is also a capable researcher and reporter. Who knew that many addicts call the rest of us “earth people”? Or, more significantly, that there is so much overlap between addiction and other psychiatric disorders? “Twenty-five percent of individuals with severe mental illness, defined as a disorder that severely compromises normal functioning—schizophrenia with delusions or immobilizing depression—have a substance use disorder,” the author says. “In the other direction, 15 percent of individuals with a substance use disorder also have a severe mental illness.”

This book’s focus is substance abuse rather than, say, Facebook addiction, if such a thing exists. Flanagan is properly skeptical of the movement to medicalize all of life’s setbacks and sadnesses. He notes that men in most cultures are more likely than women to abuse alcohol and drugs, but that women are gaining. “There is no country where female alcoholism…rates are near 10 percent. But there are many countries in which the male alcoholism rate is above 10 percent and a few that top 13 percent: Russia (16.29 percent), Hungary (15.29 percent), Lithuania (13.35 percent), and South Korea (13.10 percent).”

He reminds us that while the war on drugs appears to be a costly failure, we can’t say for sure that many addictions wouldn’t be worse in its absence. And he notes some of the problems that have accompanied legalization initiatives. In Portugal, after a decade of good results, “substance use is on the rise, and fewer and fewer people in need are getting treatment. Recent data indicate that both overall drug use and drug overdose rates are up.” In Oregon, decriminalization Measure 110 “is being unwound” after evictions and fentanyl supplies surged. But he cautions: “The data do not mean, as some are quick to insist, that decriminalization, harm reduction, and treatment are not for the best.”

What Is It Like To Be an Addict? has its shortcomings, which largely stem from the author’s academic tribe. The book is not particularly well-organized or well-written; again and again, Flanagan tells us what he’s going to tell us, and then tells us the thing a couple more times to be on the safe side. And the book can be heavy on jargon. At one point, despite his professed sobriety, he writes: “When I report on the experiences of fellow addicts based on their autophenomenological reports, I am doing heterophenomenology.”

Particularly nettlesome is the author’s claim that, although addicts are responsible for their addiction, the rest of us are responsible too because of the woeful conditions we’ve allowed to persist. He wheels out the usual suspects including “social displacement,” poverty, inequality, racism, depression, “lack of good life options,” and other all-purpose woes that “are not caused by addicts.”

Blinkered by his ready-made list of villains, the author takes little account of other potential factors. Affluence in particular seems at least as likely a culprit as poverty. Today’s poor are often richer than middle-class Americans were in the middle of the last century, and today’s American middle class is extraordinarily affluent by historical and global standards. That means more of us can afford substance abuse of all kinds, not to mention addictions to shopping and other costly behaviors.

How about changes to family life or to levels of church attendance? Isn’t it possible that the religious and familial dimensions of A.A. are essential to its remarkable success? It’s noteworthy that the author’s own salvation came not from any arm of government but from a private, apolitical institution operating on a shoestring and making no attempt to end inequality or racism. Drunks come to A.A. and somehow get sober anyway.

But in truth, the author’s gestures toward collective responsibility feel more obligatory than emphatic. What he really wants is a humane, evidence-based approach to the problem of addiction consistent with individual agency, and that’s an approach fully in accord with a faith in human liberty. At the same time, we might as well recognize that voters will quickly lose their enthusiasm for legalizing drugs if they blame it for public chaos. Freedom always and everywhere relies on self-regulation. 

These are tough times for individual agency. Many philosophers and psychologists scoff at the notion of free will, which others seem to regard as the sole province of the “privileged.” A therapeutic culture and the nanny state give us all incentives to see ourselves as victims, helpless in the face of implacable forces of oppression. It is refreshing to read a book that refuses to dehumanize addicts by depriving them of responsibility or delegitimizing the shame they feel for their actions.

Source:  https://reason.com/2025/06/15/how-freedom-lovers-can-reckon-with-addicts-and-addiction/

#cannabisculture is undermining #MentalHealth in most demographics, adolescents hardest hit!


The conversation around marijuana and mental illness has taken a new, alarming turn. A systematic review published in the journal Biomolecules this March presents fresh evidence of a strong link between marijuana use and severe mental health issues, particularly schizophrenia and psychosis. Notably, the study highlights that adolescents are at a significantly higher risk, amplifying urgent questions about its impact on younger users.


The Risk of Psychosis and Schizophrenia: The Biomolecules review analysed data…which documented an association between marijuana use and an increased risk of developing schizophrenia or psychosis-like events…One staggering takeaway from the review is the calculated odds ratio. Individuals using marijuana had a 2.88 higher likelihood of developing psychosis-related conditions than those who abstained.
Adolescents who use marijuana, however, face an even greater threat. The study authors pointed to a “large age effect,” suggesting that the impact of marijuana on younger users is far more severe…


Why Adolescents Are at Greater Risk: One key hypothesis from the researchers is that marijuana affects adolescents in two major ways. First, it can cause acute psychotic sensations that resemble those triggered by hallucinogenic drugs, indicative of acute toxicity. Second, it disrupts synaptic plasticity during adolescence, leading to developmental changes in the brain that could contribute to long-term mental health issues.
The End of the Self-Medication Argument: For years, the “self-medication hypothesis” has been used to explain the relationship between marijuana and schizophrenia. It claimed that individuals with schizophrenia used cannabis as a coping mechanism to manage symptoms. However, the review pushes back strongly against this narrative, stating that in these cases, it’s the cannabis that comes first. Alison Knopf of Alcoholism and Drug Abuse Weekly emphasised that these findings mark a key step in resolving the “chicken-and-egg conundrum” around marijuana and mental illness. (Research: https://www.dalgarnoinstitute.org.au/…/2708-marijuana…)

Source:  https://www.dalgarnoinstitute.org.au/index.php/resources/cannabis-conundrum/2708-marijuana-and-mental-illness-what-the-latest-research-reveals?

by Shane Varcoe – Executive Director for the Dalgarno Institute


Why do people continue with behaviours or substances, such as alcohol or drugs, even when they openly wish to stop? This question cuts to the heart of understanding addiction. The disparity between intention and action reveals contradictions central to addiction behaviour, often oversimplified by two prevalent views.

For decades, addiction has been described through the lens of brain disease models, focusing on how substance use alters brain function to make drug use compulsive. While these models uncover meaningful insights, they are just one part of the story. On the other hand, some reduce addiction to an issue of morality or simple bad decisions, claiming people use substances solely out of selfish indulgence. Both these views highlight partial truths but fail to complete the picture.

Instead, a deeper understanding must combine these perspectives, recognising both the complex brain changes involved and the environmental and social factors that shape behaviour.

Paths to Recovery: Understanding addiction through the lens of decision-making opens new pathways for support. Instead of framing individuals as broken or helpless, this perspective views people in the context of their environment.
Encouragingly, it shows recovery is possible by increasing the availability, visibility, and value of non-drug alternatives. This may include offering accessible education, creating stable job opportunities, or fostering supportive communities. By making these changes, we shift focus away from stigma and towards empowering individuals to make better-informed choices.

While the psychology of addiction is undeniably complex, treating those impacted with empathy and focusing on promoting meaningful alternatives is the way forward. The path to recovery is not simple, but it’s one that can be supported through understanding human behaviour and its environmental influences. Source: https://nobrainer.org.au/…/1448-understanding-addiction… )

(Also a must read Research Report on this; Drug Use, Stigma & Proactive Contagions to Reduce Both https://nobrainer.org.au/…/364-drug-use-stigma-and-the… also containing Dealing with Addiction. Models, Modes, Mantras & Mandates – A Review of Literature Investigating Models of Addiction Management)
Source: Shane Varcoe – Executive Director for the Dalgarno Institute

Summary

This is the first systematic review of the safety of ketamine in the treatment of depression after single and repeated doses. We searched MEDLINE, PubMed, PsycINFO, and Cochrane Databases and identified 288 articles, 60 of which met the inclusion criteria. After acute dosing, psychiatric, psychotomimetic, cardiovascular, neurological, and other side-effects were more frequently reported after ketamine treatment than after placebo in patients with depresssion. Our findings suggest a selective reporting bias with limited assessment of long-term use and safety and after repeated dosing, despite these being reported in other patient groups exposed to ketamine (eg, those with chronic pain) and in recreational users. We recommend large-scale clinical trials that include multiple doses of ketamine and long-term follow up to assess the safety of long-term regular use.
Source: https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(17)30272-9/abstract January 2018
  • Arrests for drunk behaviour at airports and aeroplanes have rocketed this year
  • BBC1 Panorama collected information for 18 out of 20  airport police forces 
  • More than 387 passengers were arrested last year, a rise of 50% from 2015 

Arrests for drunken behaviour at airports and on aeroplanes have rocketed by half over the past year, a report shows.

It said 387 passengers were arrested last year for causing alcohol-fuelled disruption at airports or on aircraft – a rise of 50 per cent on 2015.

BBC1’s Panorama collected the information from 18 of the 20 police forces that cover Britain’s airports.

Licensing laws which affect pubs, bars and shops do not apply to ‘airside’ areas of airports, the zones in which passengers wait for flights after passing through security.

A House of Lords committee reported this spring that one airline – Jet2 – was faced with 536 disruptive incidents in the summer of 2016. It said that many offenders ‘had the opportunity to drink heavily at the airport before they get on the flight’.

Panorama said more than half the cabin crew staff who answered a survey said they had either experienced or witnessed verbal, physical or sexual abuse on a UK flight. One in five had been physically abused.

Former Virgin airlines crew manager Ally Murphy said: ‘People just see us as barmaids in the sky. They would touch your breasts, or they’d touch your bum or your legs … I’ve had hands going up my skirt before.’

Baroness Hayter, of Alcohol Concern, said of airports: ‘They are selling alcohol in front of children, they are selling it around licensing hours, they are selling it without asking how much people have already drunk. They are making it very, very readily available.’

Karen Dee, of the Airport Operators Association, said: ‘I don’t accept that the airports don’t sell alcohol responsibly.

‘The sale of alcohol per se is not a problem. It is the misuse of it and drinking to excess and then behaving badly.’

The Lords committee said rules that applied elsewhere should also be implemented airside.

The Home Office said ministers were considering the peers’ report.

Source: https://www.dailymail.co.uk/news/article-4787478/Drunk-air-passenger-arrests-soar-50-2016.html August 2017

by Pat Aussem, L.P.C., M.A.C., Vice President, Consumer Clinical Content Development – June 2025

Teen substance use trends are always changing, and staying informed can help parents have better conversations with their kids. The good news? Teen substance use is at an all-time low! According to the Monitoring the Future survey, fewer teens are drinking, vaping, or using drugs compared to previous years.1 So, the next time your teen says, “Everyone is doing it,” you can ask how they’re seeing substance use in their world and what their peers are saying. The truth is, most teens are making healthy choices.

That said, it’s still important to keep an eye on emerging trends. New products, shifting laws, and the influence of social media continue to shape how young people perceive and access substances. What was true when we were growing up may no longer apply today. This article breaks down the key trends for 2025—no scare tactics, just real information to help you guide and support your teen. Let’s explore what’s on the horizon together.

Trend #1: VAPING EVOLUTION

Vaping is not new, but it’s evolving. Today’s e-cigarettes are more discreet than ever, often resembling USB drives, pens, or even watches.

The biggest concerns? Flavors that mask the harshness of nicotine make it easier for first-time users. And nicotine concentrations have skyrocketed, as one pod can contain as much nicotine as an entire pack of cigarettes.

Signs of vape use can include increased thirst, sweet smells, unfamiliar tech devices, small cartridges or pods.

You can start a conversation with your child by asking, “Vaping devices keep changing. What are you seeing at school these days?”

Trend #2: NICOTINE POUCHES

Nicotine pouches are one of the fastest-growing nicotine products among young people. These small, tobacco-free pouches are placed between the lip and gum and contain nicotine powder delivered directly into the bloodstream.

Nicotine pouches come in small white pouches the size of Mentos or Chicklets gum. They are packaged in circular containers. In addition to seeing packaging, be aware of white stains on clothing and frequent spitting that are signs of use.

With flavors like mint and fruit, they’re designed to appeal to teens and young adults. In addition, because they’re tobacco-free, they face fewer regulations than traditional tobacco products.

If you see people using nicotine pouches or brands like Zyn on social media or TV shows, you could ask your child, “What have you heard about nicotine pouches?”

Trend #3: CANNABIS LANDSCAPE

With more states legalizing adult use of marijuana (cannabis), many people no longer see it as being risky. But today’s cannabis is not what it was decades ago.

Modern strains can have THC levels more than 3-4 times higher than in the 1990’s. And the ways to use it have expanded beyond smoking with options like edibles, vapes, drinks, salves and concentrates.

Marijuana use during adolescence has been linked to negative impacts on brain development and mental health problems like depression, anxiety, suicidal thinking and psychosis. And at the age when teens are becoming new drivers, remember that driving under the influence of marijuana is illegal, not to mention extremely dangerous.  It can impact a person’s ability to make split-second decisions, even to stay in their lane without weaving.

You can talk about safety with your child by offering options should they be in a situation where the driver is impaired. For example, you can come up with an emoji symbol that they can text you to let you know they need to be picked up with no questions asked until the next day.

Trend #4: ALCOHOL AWARENESS

Even today, alcohol is still the most commonly used substance among teens. While overall use has declined in recent years, the way teens consume alcohol has changed dramatically.

Today’s alcohol landscape is dominated by sweet, flavored options that mask the taste of alcohol, like hard seltzers, alcopops and coolers, and spirit-based ready-to-drink cocktails. Many teens don’t even consider these to be “real alcohol.” And social media-driven drinking games and challenges have made dangerous drinking patterns like binge drinking more normalized.

You may be able to use yourself as a way to open a conversation. Think back to when you first tried alcohol or share a situation you experienced with alcohol. Ask about what types of alcohol kids your age are talking about.

Trend #5: PRESCRIPTION DRUG MISUSE

Prescription medications—particularly ADHD stimulants like Adderall—continue to be misused, often for studying or weight loss.  School pressure can be intense, and some teens see these medications as performance enhancers rather than drugs of misuse.

Parents should secure medications, count pills regularly, and be aware of “study drug” culture. Teens often consider these medications “safe” because doctors prescribe them. But no one should take medication unless it is prescribed to them.

You may consider asking: “I’ve heard about students using medications to help with studying. What’s that like at your school?”

Trend #6: FENTANYL CRISIS

Fentanyl—a lab-made opioid 50 times stronger than heroin—is being found in counterfeit pills and mixed with other drugs like heroin and methamphetamine. These fake pills are flooding the U.S. and can look nearly identical to prescription medications like Xanax and Oxycontin.  Even one counterfeit pill can be fatal.

One way to support your child is by practicing or role playing with them how to manage peer pressure and how to decline a potential offer of any pills.

Trend #7: SOCIAL MEDIA INFLUENCE

Social media has transformed how substances are marketed and normalized. Content providers can push content making substance use look fun and cool, and teens are often exposed to misinformation.

What’s concerning? “Challenges” (like the Benadryl challenge) involving substances can go viral, and influencers may promote alcohol brands or cannabis products.

It’s helpful to stay familiar with your teen’s social platforms. Follow some of the same accounts they do. Create a family social media plan that includes critical thinking about sponsored content.

A conversation starter can be: “I noticed some of those social media videos show people partying with certain drinks or substances. Do you and your friends ever talk about whether that stuff is real or staged?”

Practical Tips:

What can you actually do with this information?

  1. Build trust through ongoing conversations, by finding opportunities to talk about substance misuse and risk – not just one big “drug talk”
  2. Focus on health and safety, not just rules
  3. Always stay curious, not judgmental
  4. Educate yourself on warning signs of substance use and mental health symptoms
  5. Roleplay scenarios involving peer pressure, saying “no” and planning an exit plan
  6. Identify trusted adults that your child can go to if you’re not available

The reality is that young people are going to encounter substances. Your goal isn’t to create fear around substance use, but to build trust and communication. With honest dialogue and good information, you’re giving them the tools to make better decisions.

 

Source:  https://drugfree.org/article/top-7-teen-substance-use-trends-parents-need-to-know-in-2025/

by Robert Colonna a,* , Zuha Pathan a , Anupradi Sultania a , Liliana Alvarez b

a Health and Rehabilitation Sciences, Western University, London, Canada

b School of Occupational Therapy, Western University, London, Canada

ARTICLE INFO:
Keywords:
Cannabis
Driving under the influence of cannabis
young drivers
systematic review
impaired driving

ABSTRACT:
Background: With recreational cannabis legalized across Canada, concerns persist about youth driving under the
influence of cannabis (DUIC). However, the extent of DUIC education and prevention efforts aimed at young
Canadians remains unclear. This systematic review examines recent Canadian initiatives (2017 onwards) focused
on reducing DUIC among youth. Specifically, we investigate (1) the types of initiatives and target audiences, (2)
content and delivery methods, (3) sustainability, and (4) evidence of impact.

Methods: A comprehensive search was conducted across MEDLINE, PsycINFO, CINAHL, SCOPUS, and EMBASE
(January 1, 2017–July 10, 2023), along with various grey literature sources. Initiatives were included if they
targeted DUIC behaviour among youth aged 16 to 24, were developed and delivered in Canada by reputable
organizations or individuals with institutional support, and aimed to address DUIC behaviour or its enabling
conditions. Data extraction and quality appraisal were performed.

Results: Fifteen Canadian initiatives were identified: seven educational programs and eight awareness campaigns,
encompassing national and regional levels. Delivery methods included in-person workshops, digital tools, online
programs, and smartphone applications. While some initiatives increased awareness and influenced perceptions
of DUIC, evidence of behaviour change remained limited. Challenges related to sustainability, particularly
concerning long-term funding and digital platform maintenance, were noted.

Conclusions: This research highlights the progress made in addressing youth DUIC in Canada. Examining current
DUIC educational initiatives is crucial for refining strategies, shaping policy, and allocating resources to prioritize the safety of young Canadians. Future efforts should focus on assessing behavioural impacts and ensuring financial sustainability and program longevity.

To access the full document:

  1. Click on the ‘Source’ link below.
  2. An image  – the front page of the full document will appear.
  3. Click on the image to open the full document.

 

Source:   Stoned on the road

This is an Email – Sent: 24 May 2025 – from Stuart Reece: stuart.reece@bigpond.com

To: Ms. Erika Olson, Chargé d’Affaires, Embassy of the United States of America, Canberra, Australia. (askembassycanberra@state.gov)

Dear Chargé d’Affaires Olson,

It has been reported in several news pieces lately that President Trump is becoming concerned about exponential autism epidemic in USA which particularly affects boys.  We and many other research have demonstrated beyond reasonable doubt that this epidemic is driven by cannabis as you can see in this paper, this 2,500 page book, this video and the attached references.

Even worse that the exponentiating USA autism epidemic is the epidemic of holes in the heart (atrial septal defect) which is growing hyper-exponentially as you can see in the attached unpublished report.  This is also driven by cannabis.

Cannabinoid genotoxicity has long been known.  As you can see in the attached references its implications across diverse domains including aging, birth defects, cancers, and mental retardation are clinically significant and impose a vast burden on public health and health infrastructures internationally.

Cannabinoid genotoxicity is due to all the cannabinoids as they all share the genotoxic chemical moiety, known as olivetol on their C-ring.

Cannabinoid genotoxicity and epigenotoxicity (their toxic effects on the epigenetic regulatory machinery which controls gene expression) acts for three to four generations.  The subject is covered at length in our recently published book.

Contamination of the food chain as is happening in several places in USA, including Kentucky, Tennessee, Mississippi, Missouri and possibly Louisiana, means that the whole community is exposed without their knowledge or consent.

Breast cancer is the commonest cancer of all.  Please find below graphs showing that both breast cancer and cannabis use increased across both Europe and USA together in coordinated fashion across space and time which strongly implicates cannabis in this commonest of cancers in a casual manner.  Note where the graphs turn pink where both covariates increase at the same time in the same place.  The “pinking of Europe”  is clearly demonstrated.  Similar changes albeit less well developed are clearly seen in USA.

Videos which explain these issues may be found as follows:

  1. Cannabis and Autism – https://www.youtube.com/watch?v=x8bDLzEInWA
  2. Cannabis and babies born limbless https://www.youtube.com/watch?v=EOQpy69HIEw&t=60s
  3. Cannabis and birth defects https://www.youtube.com/watch?v=aLQFvY-Z19g&t=19s
  4. Cannabis – effect on genome and epigenome https://www.youtube.com/watch?v=CEKdLD60TcE&t=4s
  5. Cannabis and cancers https://www.youtube.com/watch?v=4T_RKFbkNFo
  6. Cannabis and aging https://www.youtube.com/watch?v=JyyUG2A6RnE
  7. Cannabis summary https://www.youtube.com/watch?v=j0HwgyOfSEQ
  8. Cannabis and hole in the heart https://www.youtube.com/watch?v=zIg0gHg4HmA

I have also included a recent review on cannabinoid teratogenicity prepared for the EU for your benefit.

Thank you for your assistance.

Yours sincerely,

Professor Dr Stuart Reece, University of Western Australia, Edith Cowan University.

Source: Email from stuart.reece@bigpond.com Sent: 24 May 2025

by Dave Evans – Senior Counsel, Cannabis Industry Victims Educating Litigators (CIVEL)

via Drug Watch International <drug-watch-international@googlegroups.com>  24 May 2025

Subject: We need information on psychedelics.

Dr. Casey Means, the Trump Surgeon General pick, praised unproven psychedelic therapy and said mushrooms helped her find love. Her brother, Calley Means, an entrepreneur who now works in the Trump administration as a health adviser and has said he invested in biopharmaceutical companies that specialize in psychedelics.

https://www.msn.com/en-us/health/other/trump-surgeon-general-pick-praised-unproven-psychedelic-therapy-said-mushrooms-helped-her-find-love/ar-AA1EMtjb?ocid=BingNewsSerp

We also just heard that attorney Matt Zorn who was representing the pro-marijuana side at the DEA marijuana rescheduling hearing was just appointed as Deputy General Counsel at HHS to focus on streamlining psychedelics reform.

David G. Evans, Esq.

 

Source:  Dave Evans – 24 May 2025

 

There is a video to illustrate this information. To see the video, go to the Source at the foot of this article, then press the ‘play’ button as indicated.

BACKGROUND AND OBJECTIVE

Youth overdose deaths have remained elevated in recent years as the illicit drug supply has become increasingly contaminated with fentanyl and other synthetics. There is a need to better understand fatal drug combinations and how trends have changed over time and across sociodemographic groups in this age group.

METHODS

We used the National Vital Statistics System’s multiple cause of death datasets to examine trends in overdose deaths involving combinations of synthetic opioids with benzodiazepine, cocaine, heroin, prescription opioids, and other stimulants among US youth aged 15 to 24 years from 2018 to 2022 across age, sex, race and ethnicity, and region.

RESULTS

Overdose death counts rose from 4652 to 6723 (10.85 to 15.16 per 100 000) between 2018 and 2022, with a slight decrease between 2021 and 2022. The largest increases were deaths involving synthetic opioids only (1.8 to 4.8 deaths per 100 000). Since 2020, fatal synthetic opioid–only overdose rates were higher than polydrug overdose rates involving synthetic opioids, regardless of race, ethnicity, or sex. In 2022, rates of synthetic-only overdose deaths were 2.49-times higher among male youths compared with female youths and 2.15-times higher among those aged 20 to 24 years compared with those aged 15 to 19 years.

CONCLUSIONS

Polydrug combinations involving synthetic opioids continue to contribute to fatal youth overdoses, yet deaths attributed to synthetic opioids alone are increasingly predominant. These findings highlight the changing risks of the drug supply and the need for better access to harm-reduction services to prevent deaths among youth.

Source:  https://publications.aap.org/pediatrics/article-abstract/doi/10.1542/peds.2024-069488/201955/Changes-in-Synthetic-Opioid-Involved-Youth?redirectedFrom=fulltext

by Lisa O’Mary – works for WebMD – contributor to Medscape, LinkedIn, int. al – April 21, 2025

Forwarded by Herschel Baker <hmbaker1938@hotmail.com> 14 May 2025 04:45

A newly published large-scale study has cast serious doubt on the long-term safety of cannabis. Based on data from more than 6 million Canadians, the research shows that adults who had used cannabis and been hospitalized or visited an emergency room were up to four times more likely to develop dementia within five years, compared to non-users.

The findings have sparked concern among researchers and public health experts, especially given the sharp rise in cannabis-related hospital visits in recent years.

“The data is too compelling to ignore” – they recommend that one shouldAdd cannabis to the list of things now linked to a heightened risk of dementia.” the study’s authors said, according to WebMD.

Cannabis users who visited the emergency room or were hospitalized were up to four times as likely as people in the general population to be diagnosed with dementia within five years, according to a large new study.

 

Is Marijuana Safe for Teens?

How does it affect their grades, their mental health, and more?

While the study can’t say that cannabis use causes dementia – a progressive disease that affects memory, thinking, and language, along with emotions and behavior – its findings are compelling enough to capture attention from both the public and the medical community.

Here’s what to know about those findings, what’s still being investigated, and why it matters to you.

What the Study Found

The most well-known biological feature of dementia is the presence of brain plaques that kill neurons. Age is the biggest risk factor, but strong links have also been made to things like high blood pressure, diabetes, poor diet, heart and sleep problems, and lack of physical activity.

Published in JAMA Neurology, the study found that:

  • Cannabis users who went to the ER were 23% more likely to be diagnosed with dementia within five years, compared with nonusers who also went to the ER.
  • Among hospital patients, those who used cannabis had a 72% greater risk of dementia within five years, compared with cannabis abstainers.
  • The rate of people seeking ER or hospital care with documented cannabis use skyrocketed between 2008 and 2021, increasing five-fold. The rate among people ages 65 and older increased nearly 27-fold.

Does This Research Apply to You?

The study only included Canadian adults ages 45 and older who had no prior dementia diagnosis. It’s garnered a lot of respect in medical circles because of its size – more than 6 million people’s health data was included, making the results more reliable than past, smaller marijuana studies.

Marijuana Addiction and Abuse

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Is Marijuana Addictive?

Addiction is more common in drugs like alcohol or cocaine. But it’s possible to get hooked on marijuana, also known as cannabis. That means you can’t stop using it, even if you want to. Studies show about 1 in 10 adults who use marijuana can get addicted. Your chances go up to 1 in 6 if you use it before age 18.

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What Is Cannabis Use Disorder (CUD)?

You might have this condition if smoking marijuana causes physical, emotional, or social problems. It’s also called marijuana use disorder. CUD can range from mild to severe.

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How Do You Know If You Have CUD?

Do you use marijuana every day or almost every day? Have you tried to quit but can’t? Do you get unwanted symptoms when you stop, like anxiety, crankiness, or trouble sleeping? Do those go away when you use marijuana again? Do you have a strong urge, or craving, to use it? Do you keep using it even though bad things happen, like problems at work, school, or with friends and family? If you answered yes to any of these, you may have CUD.

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Problems Linked to CUD

Marijuana use can make it hard to think, learn, or pay attention. If you drive while high, you’re more likely to have a car wreck. If you already have mental health problems, CUD can worsen them. People who use marijuana a lot are more likely to be jobless and not happy with life. If you use it every day, you might get withdrawal symptoms a day or two after stopping. These include insomnia, mood problems, or cravings you can’t control.

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Who Gets CUD?

Early use may lead to marijuana problems. Genes and environment also play a role. You’re more likely to get CUD if you misuse other drugs, like alcohol. Your chances also go up if you use marijuana a lot and by yourself. Mental health issues, like an anxiety or a mood disorder, can raise your chances, too.

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How Does CUD Happen?

Marijuana has THC, or tetrahydrocannabinol as the primary psychoactive ingredient. It triggers receptors in your brain called endocannabinoid receptors. When you use addictive drugs like marijuana a lot, you can change circuits in your brain. Over time, you become less sensitive to the chemicals in marijuana. You might make less endocannabinoid, which your body produces on its own. That means you may need to use more of the drug to feel “normal,” or you may feel stressed out when you’re not using it.

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How to Avoid CUD

The only sure way to stop CUD from happening is to never use marijuana. Not using drugs when you’re young might lower your chances. If you have children, make sure they know marijuana can be harmful. Keep a close eye on your kids if you get divorced, move, or have to send them to a different school. Teenagers tend to use drugs when faced with uncertain changes or stressors.

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How to Treat CUD

Most people with CUD don’t seek treatment. But you may get better if you try psychotherapy, or talk therapy. That includes cognitive behavioral therapy (CBT), motivational enhancement therapy (MET), and contingency management (CM). These can help you change thoughts and behaviors that make it hard to quit. You could also try to set limits such as only using marijuana  on certain days of the week, like the weekends. If you have trouble sticking to self imposed limits, it may indicate a problem. Meditation or other stress relieving activities may also help you use less.

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Treatment for Teens with CUD

Psychotherapy can help young people too. But they may do better when loved ones are involved in treatment. That’s how multidimensional family therapy (MDFT) works. If you’re a caregiver, you can go to MDFT with your teen.

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Can Medicine Help With CUD?

If you’re dependent on cannabis, you could go through withdrawal for weeks or relapse after you quit. That’s why experts are studying how medicine can ease withdrawal symptoms like bad mood, anxiety, restlessness, and sleep issues. They’re looking at antidepressants, cannabinoid agonists, mood stabilizers, and insomnia medication, but there are no FDA-approved meds for CUD. Some of these may treat mental health problems that worsen CUD.

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Marijuana Abuse and Sleep

You may use cannabis to help you doze off at night. But in the long run, marijuana can do a lot of harm to your sleep. And heavy use may cause a lot of problems when you try to quit. You might have nightmares, insomnia, or bad sleep quality. If this happens to you, talk to your doctor about how to treat these symptoms.

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CUD and Pregnancy

Experts aren’t sure how cannabis affects your baby. But animal studies show it may change how their brain grows. More research is needed to know what’ll happen after they’re born. But if they’re exposed to marijuana daily, they may have a hard time learning or paying attention when they get older. If you’re pregnant or want to be, ask your doctor for help on how to give up cannabis

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How to Use Medical Marijuana

In some states, doctors can prescribe cannabis. There’s research into its health benefits. It’s used to treat pain that doesn’t go away and may help with symptoms of Parkinson’s disease, multiple sclerosis, or glaucoma. Write down what type of cannabis you use. (For example, is it an edible, a joint, or an oil?) Keep track of how it makes you feel. Tell your doctor about any bad side effects. They may be able to recommend a different kind or dose or whether you should be using it at all.

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Medical Marijuana and Pregnancy

You may have heard that marijuana helps with morning sickness. But there’s no scientific evidence this is safe. If you’re pregnant, you shouldn’t use medical marijuana unless your doctor says it’s OK.

Next

Medically Reviewed by Poonam Sachdev on October 11, 2023

But there are some important limitations and context to consider:

  • Most people in the study were included for comparison purposes, and the number of cannabis users was only about 16,000. The average age among users was 55, and their age varied a lot. About 60% were men.
  • The cannabis users were getting medical care for reasons related to their cannabis use – including mental and behavioral illness due to cannabis use, poisoning or adverse effects of cannabis or its derivatives, and cannabis addiction.
  • About 5% of cannabis users in the study were diagnosed with dementia within five years, compared to 3.6% of people who went to the ER or hospital for other reasons. The rate of dementia in a general population comparison group was 1.3%.
  • Looking 10 years after the ER or hospital visit, 19% of users were diagnosed with dementia, compared to 15% of nonusers who got the same level of medical care.
  • Cannabis use was linked to a 31% lower risk of dementia within five years, compared to people who were treated in the ER or hospital due to alcohol use, the researchers found.
  • Related:Binge Drinking: How Much Is Too Much?

What’s Still Being Investigated

There’s still a lot we don’t understand about the possible link between dementia and cannabis use. What researchers still don’t know:

  • Whether the link still exists for people who use cannabis without needing medical care
  • How the complex interaction of genetics, lifestyle, and other health conditions combine with cannabis use to increase a person’s risk of having dementia

The Bigger Picture

This is just the latest in a string of recent studies shedding long-awaited light on the health impacts of cannabis use.

How Marijuana Affects Your Body

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It Makes You High

Let’s be honest: This is why most people use marijuana. THC is what causes the high. When you smoke marijuana, THC goes from your lungs to your bloodstream and then makes its way to your brain. There it connects to parts of certain cells called receptors. That’s what gives you those pleasant feelings. You can also get marijuana in things like cookies, gummies, and brownies. These are called edibles. They get into your blood through your digestive system.

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Brain

You might find it harder to focus, learn, and remember things when you use marijuana. This short-term effect can last up to 24 hours after you stop smoking. Long-term use, especially in your teens, may have more permanent effects. Imaging tests that take pictures of the brain show fewer connections in areas linked to alertness, learning, and memory. Tests show lower IQ scores in some people.

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Lungs

Marijuana smoke can inflame your lungs. If you’re a regular user, you could have the same breathing problems as a cigarette smoker. That means a cough, sometimes long lasting, or chronic. It might produce colored mucus, or phlegm. You could also be more likely to get lung infections. Inflamed lung tissue is part of the reason, but THC also seems to affect the way some people’s immune systems work.

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Heart

Your normal heart rate of 50 to 70 beats per minute can rise by 20 to 50 beats or more for up to 3 hours after you use marijuana. Scientists think that this, along with tar and other chemicals in the drug, may raise your chance of a heart attack or stroke. The risk could go up further if you’re older or you already have heart problems.

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Mental Health

Anxiety and paranoia are common complaints among marijuana users. Clinical anxiety and depression are also more likely, but scientists aren’t yet sure exactly why. The drug can make symptoms of more serious mental illness like psychosis and schizophrenia worse. It’s also linked to a higher likelihood of substance abuse. These effects could be worse if your genes make you more likely to get a mental illness or an addiction.

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Appetite

Regular marijuana users often refer to this as the munchies.  Some reports suggest this increased appetite might help you gain weight lost to illnesses like AIDS or cancer, or because of treatment for those diseases. Scientists are still studying when and if the treatment works or if it’s safe.

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Stomach

By itself, THC (marijuana’s active ingredient) seems to ease nausea, especially if your symptoms are from chemotherapy treatment for cancer. Some people say the stomach-settling effects work better when you use marijuana instead of THC alone. This may be because other chemicals enhance the effects of THC. But long-term marijuana use can have the opposite effect and cause more vomiting. Cannabinoid hyperemesis syndrome can occur in regular users and leads to frequent vomiting.

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Eyes

Some evidence suggests that marijuana, or chemicals in it, can lower the eye pressure that’s a main symptom of glaucoma. The problem is the effect only lasts 3 to 4 hours. To keep it low, you’d have to get the drug into your bloodstream 6-8 times a day. Doctors have yet to come up with a form of the drug that’s safe to use as a glaucoma treatment. And though marijuana does seem to lower eye pressure, it also might reduce the blood supply to your eye, which could make glaucoma worse.

9/12

Chronic Pain

Both marijuana and a pill version of THC called dronabinol seem to help relieve pain by attaching to parts of brain cells called cannabinoid receptors. Some studies suggest CBD oil could ease pain from arthritis, nerve damage (neuropathy), and muscle spasms, among other causes. Scientists continue to study how and when and if this works in people.

10/12

Multiple Sclerosis

A version of THC that you spray up your nose called nabiximols is available in Canada, the U.K., and other countries. It seems to help calm muscle spasms, lessen nerve pain, and improve sleep for many people with multiple sclerosis. It may also help with other illnesses, like cancer. The FDA is working to test the drug for use in the U.S.

11/12

Inflammation

Though smoking marijuana can inflame your lungs, substances called cannabinoids seem to lessen the swelling in certain other tissues. Cannabidiol may be a good choice because it doesn’t cause the same high as THC. In animal tests, it shows some promise in the treatment of rheumatoid arthritis and conditions that inflame the digestive tract, like ulcerative colitis and Crohn’s disease.

12/12

Seizures

There’s good evidence that marijuana, or drugs made from it, may help lessen seizures in some people with epilepsy. The FDA has even approved a drug made with cannabidiol for that purpose (Epidiolex). But the agency only recommends it for two rare forms of childhood epilepsy called Lennox-Gastaut syndrome and Dravet syndrome.

Next

Medically Reviewed by Jabeen Begum, MD on March 16, 2024

A lack of scientific research has led many people to form their understanding of marijuana’s health effects based on limited evidence from their own or others’ experiences. Medical experts have long warned that the true health impacts of marijuana are largely unknown, and in recent years, some of the first rigorous studies have offered new information, including links between cannabis and:

  • Cardiovascular problems, like strokes and heart attacks
  • Early death
  • Reduced brain function during tasks that involve mental skills

Those risks are along with the already well-established understanding that cannabis use is particularly risky among youths and young adults, whose brains are still developing. The American Psychiatric Association says there’s evidence that cannabis use can speed up the start of mental illness, particularly in young adulthood. People with depression who use cannabis are at an increased risk of suicidal thoughts or attempts. Risks increase based on how much and how long a person uses.

Source: https://www.webmd.com/mental-health/addiction/news/20250421/new-study-links-cannabis-and-dementia-heres-what-that-means

 

by Dr Max Pemberton (The Mind Doctor) in the Daily Mail on 17 March 2025

Source: Daily Mail – 17 March 2025

Scott Strode and his company have an active take on recovery and sobriety.

Wall Street Journal    Andy Kessler         March 23, 2025

It wasn’t hard to find Scott Strode when we first met. He was the big guy in a black T-shirt with the word “SOBER” splashed across it. Mr. Strode is founder of the Phoenix, a national “sober active” community. Addiction statistics in the U.S. are sobering. According to Mr. Strode’s book, “Rise. Recover. Thrive,” one-third of Americans have substance-abuse issues or mental disorders.

When drinking, Mr. Strode felt valued. “People wanted to spend time with me. And I found community,” he says. “It’s just what we were building it around wasn’t healthy.” Alcohol. Cocaine. Dependency. Until one night he finally hit bottom. “I couldn’t imagine someone having to tell my mom this is how I died.”

The road to sobriety wasn’t easy for Mr. Strode, but he found solace in physical challenges. “I saw a poster for ice climbing,” he said. “It gave me something to strive for, and that led me into the boxing gym and triathlons and racing Iron Mans.” But it wasn’t enough. “I realized when I took other people with me, I felt lifted in a different way.”

I wasn’t sure what he meant. “Getting into recovery is like getting out of a burning building,” he said. “But there are other people in there, so you have to reach back in to help get them out. By using my passion to help others, it filled a void. That was really what the Phoenix was born from.”

The Phoenix Multisport active recovery community, its original name, started in Boulder, Colo., roughly 20 years ago. It was funded by friends and a few grants—no fees. Others might have been content with helping one community. Not Mr. Strode. After a few years, he started helping active-duty service members and many others in Colorado Springs and set up a location in Denver.

What’s the magic? “Your life gets so much bigger, and you start to realize what’s possible. You connect somewhere where you feel valued, accepted and loved.” Climbing. Hiking. Running. Yoga. A fellow rider and Phoenix member, Ben Cort, told him, “I got sober because I didn’t want to die. I stayed sober because I wanted to live.”

A mother who heard about the Phoenix approached Mr. Strode and offered him $200,000 to expand to San Diego to help her son. Sadly, her son passed away before they could get there, but the idea of scaling to other communities kicked in for Mr. Strode. Maybe people’s desire to help others could be leveraged and help the Phoenix scale. “We opened up this opportunity on our website for folks to raise their hand to become volunteers,” Mr. Strode said. “We thought we’d get a few. We got 700.” Over the next 10 years, they were in 28 locations.

In 2016 the Phoenix received some funding from the philanthropic organization Stand Together. One of their pillars is to help solve addiction. They discussed scaling, and Mr. Strode told them that for each location, “it starts with a man and a bike.” In January 2020 they mutually agreed on $50 million in funding with a goal of “serving one million people impacted by substance use” in five years. A stretch, for sure. But it had to go from push to pull—“stimulating volunteers in places where we can’t reach.”

What started in Boulder with a deal with CrossFit is now in every state—almost 200 communities with more than 5,000 volunteers. “We have served over 800,000 since Phoenix started.” It scales because it works—83% of Phoenix participants stay sober after three months, compared with an average of 40% to 60% from other programs.

That’s the power of volunteers. And technology. The Phoenix has a mobile app called NewForm. Anyone can have a profile. The Phoenix isn’t in your community? Start one yourself. The app links to other nonprofits, such as SeekHealing, that help people overcoming trauma, a potential cause of addiction. The Phoenix also sets up sober supportive spaces at concerts and festivals—the app can reveal “thousands of other sober people in those spaces.”

“We distribute tablets in prisons across the country, so you can come to Phoenix virtually,” Mr. Strode says. “We joke that we’re the sober Peloton in prisons.” Smart. Plus, “you don’t have to turn to those old cellphone numbers in your phone when you return home. You can actually find new connections and community to help support you on your healing journey.”

What about other addiction programs? “At the Phoenix, we’re really focused on helping people with what’s possible in their recovery. So it’s very forward-looking. We start to dream of what’s possible in our sober life. In the 12-step community, people often identify as their disease. ‘I’m Scott, I’m an addict, I’m an alcoholic.’ But I always say, ‘I’m Scott, I’m in recovery, I’m an ice climber and so much more.’ We see everybody for their intrinsic strength, not a problem to be fixed.”

The Phoenix should hit its goal of one million people helped later this year. I’m convinced after talking to Mr. Strode that 10 million is a reachable goal.

Source: https://www.wsj.com/opinion/a-new-approach-to-addiction-phoenix-fitness-community-mental-health-a3591f99

This video illustrates findings of research by LHSC Canada, showing a potential biological link between cannabis use and psychosis – this can be seen by clicking the link shown below:

by Raminta Daniulaityte – College of Health Solutions, Arizona State University, Phoenix, AZ, United States et al.

“I don’t know how you can overdose smoking them:” 

Highlights

  • Smoking was viewed as protective against overdose compared to other routes of use.
  • Beliefs about inconsistency of blues drove concerns about the overdose risks.
  • Some believed that the quality of blues improved recently, and they became safer.
  • Many aimed to avoid the fentanyl in powder form to reduce their overdose risks.
  • Dosing-related strategies emphasized personal responsibility and victim blaming.

Abstract

Aims

Illicitly manufactured fentanyl (IMF) remains the primary driver of overdose mortality in the US. Western states saw significant increases in IMF-laced counterfeit pain pills (“blues”). This qualitative study, conducted in Phoenix, Arizona, provides an in-depth understanding of how overdose-related risks are viewed and experienced by people who use “blues.”

Methods

Between 11/2022–12/2023, the study recruited 60 individuals who used “blues” using targeted and network-based recruitment. Qualitative interviews were recorded, transcribed, and analyzed using NVivo.

Results

The sample included 41.7 % women, and 56.7 % whites. 55.3 % had prior overdose, but most (62.2 %) rated their current risk as none/low. Risk perceptions centered on a multi-level calculus of drug market conditions, individual vulnerabilities, and behavioral factors. Smoking was considered a “normative” way of using “blues”, and most viewed it as protective against overdose in comparison to injection and other routes of use. Drug market conditions and the unpredictability of “blues” were emphasized as important factor of overdose risk. However, some believed that over time, the quality/consistency of “blues” improved, and they became less risky. Many also expressed fears about the emerging local availability of powder fentanyl and its risk. Views about safer dosing, polydrug use, tolerance, and health emphasized personal responsibility and individual vulnerability to overdose risks. Discussions of protective behaviors, including take-home naloxone, varied bases on the perceptions of overdose risks.

Conclusions

The findings emphasize the need for close monitoring of local IMF markets and design of comprehensive interventions and risk communication strategies to address perceptions that minimize IMF-laced counterfeit pill risks.

Introduction

Illicitly manufactured fentanyl (IMF) remains a critical driver of overdose mortality in the US (Spencer et al., 2024), and there are emerging concerns about its proliferation in other regions of the globe (Friedman & Ciccarone, 2025; Piatkowski et al., 2025). The spread of IMF in the local drug markets in the US has shown increasing complexity with notable regional differences in the types of IMF products available, and associated contamination risks (Kilmer et al., 2022). While powder IMF has been the predominant form in the Eastern part of the US, western states, including Arizona, have seen significant increases in the availability of IMF in counterfeit pill form, most commonly 30 mg oxycodone, referred to as “blues” or “M30s” (Daniulaityte et al., 2022; O’Donnell et al., 2023; Palamar et al., 2022, 2024). For example, between 2017 and 2023, the total number of IMF pill seizures in the US increased by 8509.7 %, and the increase was the steepest in the West (an 11,266.7 % increase) (Palamar et al., 2024). Increases in IMF pill presence have been especially dramatic in Arizona with retail-level seizures of IMF pills increasing from about 1000 in 2017, to 18,004 in 2019, and 155,572 pills in 2020 (Mully et al., 2020). In 2023, Arizona had the highest number of IMF pill seizures in the country (n = 1638), and the second highest in the total number of IMF pills seized (n = 36,525,410) (Palamar et al., 2024).
Along with the increasing availability of IMF in counterfeit pill form, Arizona experienced significant rise in overdoses. Overdose deaths in Arizona increased from 1532 in 2017 to 2550 in 2020, and 2664 in 2022 (Centers for Disease Control & Prevention, 2022). Available data on seized drugs in Arizona indicate that in 2022 seized counterfeit pills contained 2.5 mg of fentanyl on average, with a range of 0.03 to 5.0 mg/tablet (Drug Enforcement Administration, 2024). Nationally, in 2022, an estimated 6 in 10 seized counterfeit pills were found to contain at least 2 mg of fentanyl, which is considered a potentially lethal dose (Glidden et al., 2024). Arizona currently does not have community-based drug checking programs, and there is limited up-to date information on the changes in potency of counterfeit pills or on the types of other substances that may be present in them. Data from other regions suggest that besides fentanyl, the pills may contain other fentanyl analogs, acetaminophen, and other drugs (Wightman et al., 2024).
Prior studies have identified a broad range of behaviors and conditions that are associated with an increased likelihood of opioid overdose. Some of these established risk factors include prior overdose experiences, concurrent use of benzodiazepines or alcohol, returning to high doses after losing tolerance (e.g., individuals recently released from prison or inpatient drug treatment), and physical and mental health comorbidities (Carlson et al., 2020; Darke & Hall, 2003; Darke et al., 2014; Kline et al., 2021; Park et al., 2016). However, established frameworks and “expert knowledge” that guide overdose prevention interventions may not align with the perceptions and experiences of people who use drugs (Chang et al., 2024; Moallef et al., 2019). Risk assessment is not an objective and value free enterprise, but it is embedded in the individual histories and experiences, underlying socio-cultural values, and broader structural and environmental conditions (Agar, 1985; Rhodes, 2002). There is a need for qualitative studies to help increase the understanding of how people who use IMF view, experience and judge their overdose-related risks.
Several prior qualitative studies have examined overdose risks in the era of IMF spread, aiming to characterize how people who use drugs (PWUD) experience IMF risks, what harm reduction strategies they employ, and how broader social and structural factors contribute to the local environments of risk (Abadie, 2023; Bardwell et al., 2021; Beharie et al., 2023; Ciccarone et al., 2024; Collins et al., 2024; Fadanelli et al., 2020; Gunn et al., 2021; Lamonica et al., 2021; Latkin et al., 2019; Macmadu et al., 2022; Victor et al., 2020). Many of the prior studies on IMF-related overdose risk perceptions and experiences were conducted at the initial stages of IMF spread, and primarily focused on overdose risks associated with inadvertent exposures to IMF contaminated heroin or other drugs (Abadie, 2023; Ataiants et al., 2020; Carroll et al., 2017; Lamonica et al., 2021; Latkin et al., 2019; Stein et al., 2019; Victor et al., 2020). More research is needed to understand the perceptions of IMF-related overdose risks in the context of high market saturation with IMF, and among individuals who intentionally seek and use IMF-containing drugs. Further, most prior studies were conducted in the regions where IMF is primarily available in powder form and as a contaminant of or replacement for heroin Carroll et al. (2017); Ciccarone et al. (2024, 2017); Latkin et al. (2019); Mars et al. (2018); Moallef et al. (2019). A few recent studies conducted in California described an increasing trend of individuals who use opioids switching from injection to smoking route of using IMF in powder form. These emerging studies have highlighted health-related benefits that were linked to this transition, including potential reduction in overdose risks (Ciccarone et al., 2024; Kral et al., 2021; Megerian et al., 2024). In the context of these important findings, there remains a lack of data on overdose risk perceptions related to the use of IMF in a counterfeit pill form. This qualitative study, conducted in Phoenix, Arizona, aims to address these key gaps and provide an in-depth understanding of how overdose-related risks are viewed and experienced by people who intentionally seek and use IMF-laced counterfeit pain pills (blues).

Section snippets

Methods

This paper draws on data collected for a study on counterfeit drug use in Phoenix, Arizona. Semi-structured, qualitative interviews were completed between 11/2022–12/2023. To qualify for the study, individuals had to meet the following criteria: 1) at least 18 years of age; 2) currently residing in the Phoenix, Arizona, metro area; and 3) use of illicit and/or counterfeit/pressed opioid and/or benzodiazepines in the past 30 days. The study was approved by the Arizona State University (ASU)

Participant characteristics and patterns of drug use

Out of 60 study participants, 58.3 % were men, and the age ranged from 22 to 66-years-old, with a mean of 39.0 (SD 11.2). More than half reported that they were unemployed, and 90 % had lifetime experiences of homelessness. Most (90 %) reported having health insurance, and 65 % had experiences of accessing local harm reduction services in Arizona (Table 1).
Most participants reported their first use of blues about 2–3 years ago (mean years since first use 2.7, SD 1.5) (Table 1). All participants

Discussion

Participants who use IMF pills reported deploying a range of calculated tactics to reduce their overdose risk. Many shared attitudes that tended to minimize the risks and reinforce a sense of personal invulnerability. Some of the contextual and behavioral factors of risk that were emphasized by the study participants align with the prior studies conducted in other regions of the US (Abadie, 2023; Beharie et al., 2023; Ciccarone et al., 2024; Collins et al., 2024; Fernandez et al., 2023; Victor

Role of funding source

This study was supported by the National Institute on Drug Abuse (NIDA) Grant: 1R21DA055640-01A1 (Daniulaityte, PI). The funding source had no further role in the study design, in the collection, analysis and interpretation of the data, in the writing of the report, or in the decision to submit the paper for publication.

Declaration of ethics

The study received ethics approval from the Arizona State University Institutional Review Board.

CRediT authorship contribution statement

Raminta Daniulaityte: Writing – original draft, Validation, Supervision, Resources, Project administration, Methodology, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization. Kaylin Sweeney: Writing – review & editing, Project administration, Formal analysis, Data curation. Patricia Timmons: Writing – review & editing, Project administration, Formal analysis, Data curation. Madeline Hooten: Writing – review & editing, Project administration, Formal analysis,

Declaration of competing interest

All authors declare that there are no conflicts of interest.
Source: https://www.sciencedirect.com/science/article/abs/pii/S0955395925001070

    Delegation of the European Union to the International Organisations in Vienna

Statement by Press and information team of the Delegation to UN and OSCE in Vienna:

It is an honour to be here and to speak on behalf of the European Union and its Member States. Albania, Andorra, Bosnia and Herzegovina, Georgia, Iceland, Montenegro, North Macedonia, Republic of Moldova, San Marino and Ukraine align themselves with this statement.

Mr Chair,

We remain committed to strengthening the global cooperation to address drug-related challenges in accordance with an evidence-based, integrated, balanced and comprehensive approach. We acknowledge the important role of UNODC in monitoring the world drug situation, developing strategies on international drug control and recommending measures to address drug-related challenges.

As we meet today, conflicts and violence are unfolding in numerous parts of the world. The EU and its Member States call for the full respect for the UN Charter andinternational law, including international humanitarian law, whether in relation to Russia’s war of aggression against Ukraine, or the ongoing conflicts in the Middle East, Sudan, Ethiopia, DRC and elsewhere.

Drug trafficking controlled by organised crime groupsthreatens public health, our security, our economies and prosperous development worldwide, and even our democratic institutions and the rule of law. This is an important security challenge that Europe is currently facing. As demonstrated by the European Drug Report 2024, as a consequence of the high availability of drugs, large-volume trafficking and competition between criminal groups in Europe, some countries are experiencing an increase in violence and other forms of criminality linked to the operation of the drug market.

To address this concern, last November the EU hosted the European Conference on Drug-related Violenceas part of the implementation of the EU Roadmap to combat drug trafficking and organised crime. At the conference, the EU Drugs Agency called for action on drug-related violence, to encourage and support efforts to enhance safety and security across all sectors of society with measures to anticipate, alert, respond and learn from the growing complexities of drug-related violence. This initiative reflects our collective determination to address the increasing violence linked to drug trafficking.

In line with the pledge of the Global Coalition to address Synthetic Drug Threats that the EUcommitted to in September 2024, we are currently closely monitoring the risks of a potential increase in the supply and demand for synthetic opioids in Europe. This possible shift could represent unique challenges for public health systems and law enforcement.

Among such challenges is the growing number of illegal laboratories that produce synthetic drugs. Considering the threat they pose, Poland – on behalf of the EU – has tabled a resolution that draws attention to the protection of all those that are at the forefront of dismantling drug laboratories. Our aim is to set the ground for global standards in ensuring the safety of law enforcement officers, and we count on your support for this important resolution.

The EU and its Member States also call for greater consideration of development-oriented drug policies and alternative development measures, as well as the environmental damage linked to the direct and indirect impact of illicit drug crop cultivation, drug production and manufacture and drug policy responses. Conscious of the realities that shape our world, a resolution addressing the environmental impact of drugs has been tabled by France on behalf of the EU. This is atopic that needs more engagement from all of us, and we hope that you will back this resolution as well.

The EU and its Member States continue to emphasise that States are obliged to protect, promote and fulfilhuman rights, including when they develop and implement drug policies. All human beings are born free and equal in dignity and rights, and the EU and its Member States recall that the death penalty should be abolished globally. We condemn the use of capital punishment at all times and under all circumstances, including for drug-related offences. Additional measures should be taken for people in vulnerable and marginalised situations and to reduce stigma and discrimination. We underline that substance use disorders are a health issue requiring compassionateand evidence-based interventions. Stigmatisation and criminalisation of individuals with substance use disorders should be replaced with a health-centredapproach to reduce risks and harm.

Addressing drug-related harm also remains an important pillar of EU drug policy and the EU Drugs Strategy. The EU and its Member States are implementing a human rights-based approach with a range of measures in compliance with the three international drug conventions. The aim is to reduce drug supply and to take prevention, treatment, care and recovery measures, to reduce risk and harm to society and to the individual. We also ensure a meaningful involvement of scientific experts, civil society and affected communities. We urge the international community to further embrace pragmatic measures aimed at reducing the health and social harms, both for the individual and for society, associated with drug use. From needle and syringe exchange programmes to opioid agonist therapies, such evidence-based initiatives are essential for safeguarding public health and dignity. Prevention, treatment, care and recovery measures, risk and harm reduction must be expanded, adequately resourced, and firmly rooted in respect for human rights, as also set out in last year’s CND resolution 67/4 [on preventing and responding to drug overdose through prevention, treatment, care and recovery measures, as well as other public health interventions, to address the harms associated with illicit drug use as part of a balanced, comprehensive, scientific evidence-based approach].

In the context of current global drug-related challenges, it is important to stress that effective solutions can only be achieved through a balanced and whole-of-society approach as well as by engaging all relevant stakeholders, including health-care personnel, who provide critical support to those affected by substance use disorders; law enforcement officers, who risk their lives in targeting organised crime groups involved in drug production and trafficking; academia, which contributes with evidence-based research and innovative solutions; civil society organisations, which play an important role in prevention, and in risk and harm reduction initiatives. International cooperation is also indispensable to tackle the global drugs phenomenon and we count on the close involvement ofall relevant United Nations entities, including human rights bodies, to foster coordinated international action and inter-agency cooperation.

As set out in the high-level declaration by the CND on the 2024 mid-term review, we stress the urgent need for further ambitious, effective, improved and decisive actions as well as for more proactive, scientific evidence-based, comprehensive, balanced approaches to address drug-related challenges.

For that, we emphasise the critical importance of thorough data collection, monitoring, and scientific research. The European Union Drugs Agency is therefore key in developing Europe’s capacity to react to both current and future drug-related challenges, and we have made a concrete pledge in this regard at last year’s High-level segment of the CND.

Mr. Chair, to conclude,

Continuous drug-related challenges require our united front and cooperation to address them in the most effective and sustainable manner, and we count on global efforts to do so together. The EU and its Member States reaffirm their own commitment to fostering a comprehensive, inclusive, and balanced approach to addressing the world drug situation. We call on all Member States and stakeholders to join us in prioritising health, dignity, and human rights in all aspects of drug policy.

Thank you.

SOURCE: https://www.eeas.europa.eu/delegations/vienna-international-organisations/eu-statement-general-debate-68th-session-commission-narcotic-drugs-10-march-2025_en

Arizona State University


Children seen from behind sit next to each other with their arms around each other while looking out at a large body of water.

Over the past 20 years, science-based interventions and treatments using a statistical method called mediation analysis have contributed to reduced rates of smoking and drinking among teenagers and young adults in the U.S. Research from Arizona State University has developed these statistical techniques, which save time and money and are now used widely in psychology, sociology, biology, education and medicine. Many of available medical treatment options are the result of clinical trials that used mediation to figure out what worked.

Image by Duy Pham/Unsplash

by Kimberlee D’Ardenne –

Smoking rates among teenagers today are much lower than they were a generation ago, decreasing from 36% in the late 1990s to 9% today. The rates of alcohol consumption among underage drinkers have also decreased. At the turn of the century, people aged 12–20 years drank 11% of all the alcohol consumed in the U.S. Today, they only drink 3%.

These decreases are in part the result of science-based interventions that were designed to prevent substance use. But these interventions would not have been possible without statistical methods, including a statistical method called mediation analysis that lets researchers understand why an intervention or treatment succeeds or fails. Mediation analysis also identifies how aspects of a substance use reduction program or medical treatment cause its success.

About this story

There’s a reason research matters. It creates technologies, medicines and other solutions to the biggest challenges we face. It touches your life in numerous ways every day, from the roads you drive on to the phone in your pocket.

The ASU research in this article was possible only because of the longstanding agreement between the U.S. government and America’s research universities. That compact provides that universities would not only undertake the research but would also build the necessary infrastructure in exchange for grants from the government.

That agreement and all the economic and societal benefits that come from such research have recently been put at risk.

Prevention makes our lives better — and it saves money. Though smoking and drinking rates among adolescents are on the decline, there is still room for mediation analyses to save the U.S. more money. According to the National Institute on Alcohol Abuse and Alcoholism, misusing alcohol costs the U.S. $249 billion. The Centers for Disease Control and Prevention report that cigarette smoking costs the U.S. around $600 billion, including $240 billion in health care spending and over $300 billion in lost productivity from smoking-related deaths and illnesses.

David MacKinnon, Regents Professor of psychology at Arizona State University, has been studying and using mediation analyses for the past 35 years because of the many practical applications — and because they work really well.

“I like using science and math to address serious health problems like smoking, drug abuse and heart disease,” MacKinnon said. “Mediation analyses let us extract a lot of information from data and have the promise of identifying mechanisms by which effects occur that could be applicable to other situations.”

Unlike a third wheel, third variables are crucial — and causal

There are many paths to a teenager ending up struggling with substance abuse. They might struggle with impulsivity in general — or they might have parents who fight often, or maybe their friends get drunk most weekends.

Because there is more than one way to connect risk factors to substance use, scientists often have to take an indirect path that considers variables like parenting style or peer influences.

“Most research looks at the relationship between two variables — like risk-taking and substance use — but there can be a lot happening in between, and those ‘third variables’ can cause the outcome,” MacKinnon explains.

Long-lasting impacts

Adolescents who experiment with drugs and alcohol at a young age are more likely to develop lifelong substance abuse problems. A psychology department research team led by Nancy Gonzales, executive vice president and university provost, used mediation to create a program that decreases alcohol use in teenagers who started drinking at a young age.

The program brought families to their child’s school for a series of interactive sessions. Each session taught a skill, such as good listening practices or strategies for talking about difficult topics, and parents and students practiced as a family. Just spending 18 hours in the program produced protective effects against teenage alcohol misuse that lasted at least five years. By their senior year, kids who had participated in the program as seventh graders were drinking less.

This reduced alcohol consumption is important because even small reductions in adolescent drinking can have a cascade effect on other public health problems like alcoholism and drug abuse disorders, risky sexual behavior and other health problems.

Helping children of divorce

Close to half of all marriages in the U.S. end in divorce, affecting over 1 million children each year. These children are at an increased risk of struggling in school, experiencing mental health or substance use problems and engaging in risky sexual behavior. Mediation analyses have shown that a lot of these risks stem from conflict between divorced or separated parents, which creates fear of abandonment in children and contributes to future mental health symptoms.

Prevention scientists working in ASU’s Research and Education Advancing Children’s Health Institute leveraged decades of work using mediation to create an online parenting skills program for separated or divorced couples. The program reduces interparental conflict and decreases children’s anxiety and depression symptoms.

The answers to ‘why’ and ‘how’ questions save time and money

How much do school-based prevention programs decrease teen vaping rates? Why do monetary incentives and mobile clinics increase local vaccination rates?

Answering “how” and “why” questions like these require scientists to figure out what exactly caused a decrease in teen vaping or the reasons that caused more people to roll up their sleeves and get vaccinated. Causation can happen in many ways and can even be indirect, and mediation can accurately find the cause.

Mediation analysis strategies MacKinnon has developed are now used widely, in medicine, psychology, sociology, biology and education. And, many of the treatment options our doctors can offer us are possible because of clinical trials that used mediation to figure out what worked.

Mediation analysis lets researchers pull more information from scientific studies, which is why the National Institutes of Health recommends research proposals include a section evaluating why and how treatments or interventions work.

Source: https://news.asu.edu/20250304-science-and-technology-asu-research-helps-prevent-substance-abuse-mental-health-problems

Dangerous but common misconceptions can prevent crucial early addiction treatment.

Key points:

  • Misconceptions and the ignoring of research-based evidence prevent crucial early treatment of addiction.
  • Drugs of abuse cause health, life, and relationship problems with many long-lasting effects.
  • Teen and young adult drug prevention is necessary and needs funding.

Research published in high-quality peer-reviewed journals reveals key information on the realities of addiction, exposing pervasive myths and misconceptions, as in these examples.

False Belief 1: Drug experimentation is normal for teens and shouldn’t alarm parents.

Drug use and experimentation among teens often is ignored by many—even parents, who then may be unaware that any use places adolescent brains in jeopardy. For today’s teens, life often feels overwhelming, but avoiding alcohol, tobacco, marijuana, and other drugs is their one best choice to promote continued healthy physical and mental development. Preventing or delaying all teenage substance use not only reduces their current risks for depression, psychosis, and school/learning problems, but it also significantly decreases their probability of addiction as adults.

Harvard’s Sharon Levy, MD, MPH, and founding National Institute of Drug Abuse Director Robert DuPont, MD, strongly advocate a zero-tolerance approach to youth substance use. They emphasize that no amount of drug use is safe for young people. They promote the One Choice initiative encouraging adolescents to avoid substance use: alcohol, tobacco, marijuana, and other drugs.

It’s now known that THC in marijuana interferes with the developing brain circuits responsible for regulating behavior, leading to increased risk-taking and poor decision-making. Even infrequent teen use can impede judgment, increasing the probability of risky behaviors and accidents. Adolescents also are more likely than adults to develop cannabis use disorder (CUD) due to their heightened neuroplasticity during this developmental stage. The resulting impairment may lead to academic underperformance and problematic interpersonal relationships.

False Belief 2: Addiction is a personal weakness.

Addiction is not about people being weak-minded. It’s far more complicated. Becoming addicted depends on the drug used, dose, route, frequency, and risk factors like ages of users. Also, the same drug at the same dose affects people differently because of personal differences, as well as the presence/absence of traumatic past life experiences.

Yale’s Joel Gelernter identified genetic variants associated with vulnerability to addictions. However, genetic characteristics themselves interact with environmental factors in developing substance use disorders (SUDs). As Nora Volkow, director of NIDA, has said, “Addiction is a complex disease of a complex brain; ignoring this fact will only hamper our efforts to find effective solutions …”

False Belief 3: People must hit “rock bottom” to recover from addiction.

No, no, and no! Roadside alcohol testing has prevented thousands of deaths and helped many people with alcohol use disorders (AUD) obtain help, sometimes by coercion of courts. About 50 percent of those arrested for DUI have an AUD. Users often deny they have a problem with drugs or alcohol and believe they are truthful. But they are lying to themselves.

Addiction is a chronic, relapsing condition driven by changes in brain circuitry, particularly in areas controlling reward, stress, and decision-making. While some people seek help after suffering dire consequences, others are compelled into treatment by the courts, based on a past offense. Waiting to hit “rock bottom” increases major risks of harming the person’s relationships, job, and health—and strengthens the hold of the drug over the person.

False Belief 4: Addiction treatment never works.

Researchers from the University of British Columbia and Harvard Medical School recently analyzed survey data from nearly 57,000 participants in 21 countries over 19 years, providing clear data. They discovered that the number-one barrier to treatment was addicted people themselves: Most were in denial and did not recognize they needed treatment.

Alcoholics Anonymous is often successful, non-judgmentally providing new members a roadmap, role models, hope, and social connections. Successful people actively involved in AA complain that their friends kept asking them why they “weren’t cured yet” since they went to so many meetings. But going to meetings is what works.

Even among experts, there’s no consensus on what constitutes successful treatment. To some, success is that the person is still alive and hasn’t been rushed to the emergency room because of an overdose in the past 6 months or year. To others, it is taking treatment medications. And to still others, only abstinence and a full resumption of all family and work obligations counted as success.

Another issue is that most people with SUDs have multiple addictions. Even when they overdosed, most took multiple drugs. It’s also true that many people come to treatment also needing treatment for other medical, addiction, and psychiatric problems. Yet only rarely are patients evaluated and treated for all issues.

False Belief 5: Overdoses of drugs don’t cause brain damage.

Drugs of abuse can harm the brain. Overdose survivors may suffer from undetected brain damage and hypoxic brain injury caused by opioid-induced respiratory depression. As a society, we better understand hypoxia as associated with drowning or choking than its much more common occurrence in drug overdoses with loss of consciousness.

Recent studies estimate that at least half of people using opioids have illicitly experienced a non-fatal overdose or witnessed an overdose. People who regularly use drugs are at elevated risk of brain injury due to accidents, fights, and overdoses. A single fentanyl overdose could cause hypoxia, brain injury, and memory and concentration problems.

Overdoses with counterfeit pills, cocaine, methamphetamine, xylazine, or heroin usually also include fentanyl, making neurologically compromising overdoses more common.

Summary

Myths and misconceptions increase stigma and decrease the likelihood that someone with an addictive illness will receive prompt, effective treatment. We need early intervention and treatment during the preaddiction phase. Bottom line: Preventing teen and young adult use is crucial.

Mark Gold M.D.

Mark S. Gold, M.D., is a pioneering researcher, professor, and chairman of psychiatry at Yale, the University of Florida, and Washington University in St Louis. His theories have changed the field, stimulated additional research, and led to new understanding and treatments for opioid use disorders, cocaine use disorders, overeating, smoking, and depression.

Source: https://www.psychologytoday.com/intl/blog/addiction-outlook/202502/5-common-false-beliefs-about-drug-use-users-and-addiction

(1)    Use of Alternative Payment Models for Substance Use Disorder Prevention in the United States: Development of a Conceptual Framework

Journal: Substance Abuse Treatment, Prevention, and Policy, 2025, doi: 10.1186/ s13011-025-00635-z

Authors: Elian Rosenfeld, Sarah Potter, Jennifer Caputo, Sushmita Shoma Ghose, Nelia Nadal, Christopher M. Jones, … Michael T. French

Abstract:

Background: Alternative payment models (APMs) are methods through which insurers reimburse health care providers and are widely used to improve the quality and value of health care. While there is a growing movement to utilize APMs for substance use disorder (SUD) treatment services, they have rarely included SUD prevention strategies. Challenges to using APMs for SUD prevention include underdeveloped program outcome measures, inadequate SUD prevention funding, and lack of clarity regarding what prevention strategies might fit within the scope of APMs.

Methods: In November 2023, the Substance Abuse and Mental Health Services Administration (SAMHSA), through a contract with Westat, convened an expert panel to refine a preliminary conceptual framework developed for utilizing APMs for SUD prevention and to identify strategies to encourage their adoption.

Results: The conceptual framework agreed upon by the panel provides expert consensus on how APMs could finance a variety of prevention programs across diverse populations and settings. Additional efforts are needed to accelerate the support for and adoption of APMs for SUD prevention, and the principles of health equity and community engagement should underpin these efforts. Opportunities to increase the use of APMs for SUD prevention include educating key groups, expanding and promoting the SUD prevention workforce, establishing funding for pilot studies, identifying evidence-based core components of SUD prevention, analyzing the cost effectiveness of APMs for SUD prevention, and aligning funding across federal agencies.

Conclusion: Given that the use of APMs for SUD prevention is a new practice, additional research, education, and resources are needed. The conceptual framework and strategies generated by the expert panel offer a path for future research. SUD health care stakeholders should consider ways that SUD prevention can be effectively and equitably implemented within APMs.

To read the full text of the article, please visit the publisher’s website.

(2)     Quitline-Based Young Adult Vaping Cessation: A Randomized Clinical Trial Examining NRT and mHealth

Journal: American Journal of Preventive Medicine, 2025, doi: 10.1016/j.amepre.2024 .10.019

Authors: Katrina A. Vickerman, Kelly M. Carpenter, Kristina Mullis, Abigail B. Shoben, Julianna Nemeth, Elizabeth Mayers, & Elizabeth G. Klein

Abstract:

Introduction: Broad-reaching, effective e-cigarette cessation interventions are needed.

Study design: This remote, randomized clinical trial tested a mHealth program and nicotine replacement therapy (NRT) for young adult vaping cessation.

Setting/participants: Social media was used from 2021 to 2022 to recruit 508 young adults (aged 18-24 years) in the U.S. who exclusively and regularly (20+ days of last 30) used e-cigarettes and were interested in quitting.

Intervention: All were offered 2 coaching calls and needed to complete the first call for full study enrollment. Participants were randomized to one of 4 groups in the 2×2 design: mailed NRT (8 weeks versus none) and/or mHealth (yes versus no; stand-alone text program including links to videos and online content).

Main outcome measures: Self-reported 7-day point prevalence vaping abstinence at 3 months.

Results: A total of 981 participants were eligible and randomized; 508 (52%) fully enrolled by completing the first call. Enrolled participants were 71% female, 31% non-White, and 78% vaped daily. Overall, 74% completed the 3-month survey. Overall, 83% in the mailed NRT groups and 24% in the no-mailed NRT groups self-reported NRT use. Intent-to-treat 7-day point prevalence abstinence rates (missing assumed vaping) were 41% for calls only, 43% for Calls+mHealth, 48% for Calls+NRT, and 48% for Calls+NRT+mHealth. There were no statistically significant differences for mailed NRT (versus no-mailed NRT; OR=1.3; 95% CI=0.91, 1.84; p=0.14) or mHealth (versus no mHealth; OR=1.04; 95% CI=0.73, 1.47; p=0.84).

Conclusions: This quitline-delivered intervention was successful at helping young adults quit vaping, with almost half abstinent after 3 months. Higher than anticipated quit rates reduced power to identify significant group differences. Mailed NRT and mHealth did not significantly improve quit rates, in the context of an active control of a 2-call coaching program. Future research is needed to examine the independent effects of coaching calls, NRT, and mHealth in a fully-powered randomized control trial.

To read the full text of the article, please visit the publisher’s website.

(3)     The Alcohol Exposome

Journal: Alcohol, 2025, doi: 10.1016/j.alcohol.2024.12.003

Authors: Nousha H. Sabet, & Todd A. Wyatt

Abstract:
Science is now in a new era of exposome research that strives to build a more all-inclusive, panoramic view in the quest for answers; this is especially true in the field of toxicology. Alcohol exposure researchers have been examining the multivariate co-exposures that may either exacerbate or initiate alcohol-related tissue/organ injuries. This manuscript presents selected key variables that represent the Alcohol Exposome. The primary variables that make up the Alcohol Exposome can include comorbidities such as cigarettes, poor diet, occupational hazards, environmental hazards, infectious agents, and aging. In addition to representing multiple factors, the Alcohol Exposome examines the various types of intercellular communications that are carried from one organ system to another and may greatly impact the types of injuries and metabolites caused by alcohol exposure. The intent of defining the Alcohol Exposome is to bring the newly expanded definition of Exposomics, meaning the study of the exposome, to the field of alcohol research and to emphasize the need for examining research results in a non-isolated environment representing a more relevant manner in which all human physiology exists.

To read the full text of the article, please visit the publisher’s website.

(4)     Neural Variability and Cognitive Control in Individuals with Opioid Use Disorder

Journal: JAMA Network Open, 2025, doi: 10.1001/jamanetworkopen.2024.55165

Authors: Jean Ye, Saloni Mehta, Hannah Peterson, Ahmad Ibrahim, Gul Saeed, Sarah Linsky, … Dustin Scheinost

Abstract:

Importance: Opioid use disorder (OUD) impacts millions of people worldwide. Prior studies investigating its underpinning neural mechanisms have not often considered how brain signals evolve over time, so it remains unclear whether brain dynamics are altered in OUD and have subsequent behavioral implications.

Objective: To characterize brain dynamic alterations and their association with cognitive control in individuals with OUD.

Design, setting, and participants: This case-control study collected functional magnetic resonance imaging (fMRI) data from individuals with OUD and healthy control (HC) participants. The study was performed at an academic research center and an outpatient clinic from August 2019 to May 2024.

Exposure: Individuals with OUD were all recently stabilized on medications for OUD (<24 weeks). Main outcomes and measures: Recurring brain states supporting different cognitive processes were first identified in an independent sample with 390 participants. A multivariate computational framework extended these brain states to the current dataset to assess their moment-to-moment engagement within each individual. Resting-state and naturalistic fMRI investigated whether brain dynamic alterations were consistently observed in OUD. Using a drug cue paradigm in participants with OUD, the association between cognitive control and brain dynamics during exposure to opioid-related information was studied. Variations in continuous brain state engagement (ie, state engagement variability [SEV]) were extracted during resting-state, naturalistic, and drug-cue paradigms. Stroop assessed cognitive control.

Results: Overall, 99 HC participants (54 [54.5%] female; mean [SD] age, 31.71 [12.16] years) and 76 individuals with OUD (31 [40.8%] female; mean [SD] age, 39.37 [10.47] years) were included. Compared with HC participants, individuals with OUD demonstrated consistent SEV alterations during resting-state (99 HC participants; 71 individuals with OUD; F4,161 = 6.83; P < .001) and naturalistic (96 HC participants; 76 individuals with OUD; F4,163 = 9.93; P < .001) fMRI. Decreased cognitive control was associated with lower SEV during the rest period of a drug cue paradigm among 70 participants with OUD. For example, lower incongruent accuracy scores were associated with decreased transition SEV (ρ58 = 0.34; P = .008). Conclusions and relevance: In this case-control study of brain dynamics in OUD, individuals with OUD experienced greater difficulty in effectively engaging various brain states to meet changing demands. Decreased cognitive control during the rest period of a drug cue paradigm suggests that these individuals had an impaired ability to disengage from opioid-related information. The current study introduces novel information that may serve as groundwork to strengthen cognitive control and reduce opioid-related preoccupation in OUD.

To read the full text of the article, please visit the publisher’s website.

Source: https://drugfree.org/drug-and-alcohol-news/research-news-roundup-february-13-2025/

A study of nearly 10,000 adolescents funded by the National Institutes of Health (NIH) has identified distinct differences in the brain structures of those who used substances before age 15 compared to those who did not. Many of these structural brain differences appeared to exist in childhood before any substance use, suggesting they may play a role in the risk of substance use initiation later in life, in tandem with genetic, environmental, and other neurological factors.

This adds to some emerging evidence that an individual’s brain structure, alongside their unique genetics, environmental exposures, and interactions among these factors, may impact their level of risk and resilience for substance use and addiction. Understanding the complex interplay between the factors that contribute and that protect against drug use is crucial for informing effective prevention interventions and providing support for those who may be most vulnerable.”

Nora Volkow M.D., Director of NIDA

Among the 3,460 adolescents who initiated substances before age 15, most (90.2%) reported trying alcohol, with considerable overlap with nicotine and/or cannabis use; 61.5% and 52.4% of kids initiating nicotine and cannabis, respectively, also reported initiating alcohol. Substance initiation was associated with a variety of brain-wide (global) as well as more regional structural differences primarily involving the cortex, some of which were substance-specific. While these data could someday help inform clinical prevention strategies, the researchers emphasize that brain structure alone cannot predict substance use during adolescence, and that these data should not be used as a diagnostic tool.

The study, published in JAMA Network Open, used data from the Adolescent Brain Cognitive Development Study, (ABCD Study), the largest longitudinal study of brain development and health in children and adolescents in the United States, which is supported by the NIH’s National Institute on Drug Abuse (NIDA) and nine other institutes, centers, and offices.

Using data from the ABCD Study, researchers from Washington University in St. Louis assessed MRI scans taken of 9,804 children across the U.S. when they were ages 9 to 11 – at “baseline” – and followed the participants over three years to determine whether certain aspects of brain structure captured in the baseline MRIs were associated with early substance initiation. They monitored for alcohol, nicotine, and/or cannabis use, the most common substances used in early adolescence, as well as use of other illicit substances. The researchers compared MRIs of 3,460 participants who reported substance initiation before age 15 from 2016 to 2021 to those who did not (6,344).

They assessed both global and regional differences in brain structure, looking at measures like volume, thickness, depth of brain folds, and surface area, primarily in the brain cortex. The cortex is the outermost layer of the brain, tightly packed with neurons and responsible for many higher-level processes, including learning, sensation, memory, language, emotion, and decision-making. Specific characteristics and differences in these structures – measured by thickness, surface area, and volume – have been linked to variability in cognitive abilities and neurological conditions.

The researchers identified five brain structural differences at the global level between those who reported substance initiation before the age of 15 and those who did not. These included greater total brain volume and greater subcortical volume in those who indicated substance initiation. An additional 39 brain structure differences were found at the regional level, with approximately 56% of the regional variation involving cortical thickness. Some brain structural differences also appeared unique to the type of substance used.

While some of the brain regions where differences were identified have been linked to sensation-seeking and impulsivity, the researchers note that more work is needed to delineate how these structural differences may translate to differences in brain function or behaviors. They also emphasize that the interplay between genetics, environment, brain structure, the prenatal environment, and behavior influence affect behaviors.

Another recent analysis of data from the ABCD study conducted by the University of Michigan demonstrates this interplay, showing that patterns of functional brain connectivity in early adolescence could predict substance use initiation in youth, and that these trajectories were likely influenced by exposure to pollution.

Future studies will be crucial to determine how initial brain structure differences may change as children age and with continued substance use or development of substance use disorder.

“Through the ABCD study, we have a robust and large database of longitudinal data to go beyond previous neuroimaging research to understand the bidirectional relationship between brain structure and substance use,” said Alex Miller, Ph.D., the study’s corresponding author and an assistant professor of psychiatry at Indiana University. “The hope is that these types of studies, in conjunction with other data on environmental exposures and genetic risk, could help change how we think about the development of substance use disorders and inform more accurate models of addiction moving forward.”

Journal reference:

Miller, A. P., et al. (2024). Neuroanatomical Variability and Substance Use Initiation in Late Childhood and Early Adolescence. JAMA Network Opendoi.org/10.1001/jamanetworkopen.2024.52027.

Source: https://www.news-medical.net/news/20241230/Structural-brain-differences-in-adolescents-may-play-a-role-in-early-initiation-of-substance-use.aspx

The findings are still valid as to why marijuana should not be rescheduled as determined in the Denial of Petition To Initiate Proceedings To Reschedule Marijuana, by the Drug Enforcement Administration (DEA), 81 FR 53767-01(August 12, 2016)

Human Physiological and Psychological Effects of Marijuana

MARIJUANA AND MENTAL ILLNESS

Recent studies show a connection between marijuana use and mental illness. In 2017, the National Academy of Sciences (NAS) concluded after a review of over 10,000 peer-reviewed academic articles, that marijuana use is connected to mental health issues (like psychosis, social anxiety, and thoughts of suicide). [1]

A study discussed in an October 2017 Scientific American shows that people who had consumed marijuana before age 18 developed schizophrenia approximately 10 years earlier than others. The more marijuana you take – and the higher the potency – the greater the risk. [2]

A November 2017 report on a study found that marijuana use in youth is linked to bipolar symptoms in young adults. [3]

References

[1] Health Effects of Cannabis and Cannabinoids: Current State of Evidence and Recommendations for Research.
http://nationalacademies.org/hmd/~/media/Files/Report%20Files/2017/Cannabis-Health-Effects/Cannabis-chapter-highlights.pdf

[2] https://www.scientificamerican.com/article/link-between-adolescent-pot-smoking-and-psychosis-strengthens/

[3] http://www.newswise.com/articles/view/685947/?sc=dwtn November 2017

THERE IS A LINK BETWEEN MARIJUANA USE AND OPIATE USE

Marijuana use is associated with an increased risk for substance use disorders. [1] Marijuana use appears to increase rather than decrease the risk of developing nonmedical prescription opioid use and opioid use disorder. [2] In 2017, the National Academy of Sciences (NAS) landmark report written by top scientists concluded after a review of over 10,000 peer-reviewed academic articles, that marijuana use is connected to progression to and dependence on other drugs, including studies showing connections to heroin use. [3]

New research suggests that marijuana users may be more likely than nonusers to misuse prescription opioids and develop prescription opioid use disorder. The investigators analyzed data from more than 43,000 American adults. The respondents who reported past-year marijuana use had 2.2 times higher odds than nonusers of meeting diagnostic criteria for prescription opioid use disorder. They also had 2.6 times greater odds of initiating prescription opioid misuse. [4]

References

[1] JAMA Psychiatry. 2016 Apr;73(4):388-95. doi: 10.1001/jamapsychiatry.2015.3229.
Cannabis Use and Risk of Psychiatric Disorders: Prospective Evidence From a US National Longitudinal Study. Blanco C1, Hasin DS2, Wall MM2, Flórez-Salamanca L3, Hoertel N4, Wang S2, Kerridge BT2, Olfson M2. https://www.ncbi.nlm.nih.gov/pubmed/26886046

Cadoni C, Pisanu A, Solinas M, Acquas E, Di Chiara G. Behavioural sensitization after repeated exposure to Delta 9-tetrahydrocannabinol and cross-sensitization with morphine. Psychopharmacology (Berl). 2001;158(3):259-266. Available from: https://www.researchgate.net/publication/11640927_Behavioral_sensitization_after_repeated_exposure_to_D9-tetrahydrocannabinol_and_cross-sensitization_with_morphine

[2] Cannabis Use and Risk of Prescription Opioid Use Disorder in the United States, Mark Olfson, M.D., M.P.H., Melanie M. Wall, Ph.D., Shang-Min Liu, M.S., Carlos Blanco, M.D., Ph.D. Published online: September 26, 2017at: https://doi.org/10.1176/appi.ajp.2017.17040413

[3] Health Effects of Cannabis and Cannabinoids: Current State of Evidence and Recommendations for Research. See: http://nationalacademies.org/hmd/~/media/Files/Report%20Files/2017/Cannabis-Health-Effects/Cannabis-chapter-highlights.pdf

[4] https://www.drugabuse.gov/news-events/news-releases/2017/09/marijuana-use-associated-increased-risk-prescription-opioid-misuse-use-disorders

MARIJUANA USE BEFORE, DURING OR AFTER PREGNANCY CAN CAUSE SERIOUS MEDICAL CONDITIONS

Prenatal marijuana use has been linked with:

1. Developmental and neurological disorders and learning deficits in children.
3. Premature birth, miscarriage, stillbirth.
4. An increased likelihood of a person using marijuana as a young adult.
5. The American Medical Association states that marijuana use may be linked with low birth weight, premature birth, behavioral and other problems in young children.
6. Birth defects and childhood cancer.
7. Reproductive toxicity affecting spermatogenesis which is the process of the formation of male gamete including meiosis and formation of sperm cells.

References

Volkow ND, Compton WM, Wargo EM. The risks of marijuana use during pregnancy. JAMA. 2017;317(2):129-130.

https://www.drugabuse.gov/publications/research-reports/marijuana/letter-director

https://www.acog.org/Clinical-Guidance-and-Publications/Committee-Opinions/Committee-on-Obstetric-Practice/Marijuana-Use-During-Pregnancy-and-Lactation

Source: Email from Dave Evans to Drug Watch International April 2018

10Sep2024

In this special episode of the Pathways 2 Podcast, recorded live at the National Prevention Network (NPN) Conference, we bring you two insightful conversations with leaders who are making a significant impact in the field of prevention.

First, we sit down with Ben Stevenson, who oversees prevention and harm reduction services for Montgomery County, Maryland, and also runs his own consulting firm, Bess Consulting LLC. Ben shares his innovative approach to integrating youth empowerment with harm reduction, his journey in building a successful Youth Ambassador Program, and the challenges of overcoming stigma and navigating county government to drive meaningful change.

Next, we hear from Steve Miller, a prevention champion, podcaster, and man in long-term recovery. Steve takes us through his personal and professional journey, highlighting the powerful role music has played in his recovery and prevention work. He discusses how music serves as a muse, guiding his work and helping others find their path in prevention.

Whether you’re a prevention professional, a community leader, or simply interested in stories of resilience and innovation, this episode is packed with practical insights, inspiration, and a deep dive into what it takes to make a lasting impact in our communities.

Key Takeaways:

  • The power of youth-led initiatives in prevention and harm reduction.
  • Strategies for overcoming stigma and building community buy-in.
  • How music can influence behavior and serve as a tool for prevention.

Transcript:

Welcome back to another episode of the Pathways to Prevention podcast, where we shine a light on the people stories and strategy’s making a difference in the field of prevention. I’m your host, Dave Closson and today I am excited to bring you to insightful conversations recorded live from the National Prevention Network Conference, where the theme was shining a light on prevention.

In this episode, you’ll hear from two exceptional leaders who are driving impactful change in their communities and beyond. First, we have Ben Stevenson from Maryland who oversees prevention and harm reduction services in Montgomery county. We’ll also running his own consulting firm. Ben shares his experiences, challenges and successes in empowering youth. And integrating prevention with harm reduction in innovative ways. Then. I had the opportunity to sit down with Steve Miller. A true prevention champion. Long-term recovery advocate and fellow podcaster. Steve takes us on a journey through his work in prevention. The powerful role that music has played in his life and in his recovery. And how it continues to inspire his mission to help others. These conversations are full of wisdom, practical insights, and inspiration for anyone involved in prevention work. So let’s dive in. And hear from these incredible prevention leaders.

The Vision, a world where all people live free of the burden of drug abuse. This is the Drug Free America Foundation’s Pathway to Prevention podcast, where we are committed to developing strategies that prevent drug use and promote sustained recovery. Thank you for not only tuning in, but your continued support and efforts to help make this world a better place.

We hope you enjoy this episode.

Alright, so, first off, coming to folks here from the National Prevention Network Conference, would love for you to just introduce yourself.

Okay. All right. So I’m Ben Stephenson from Maryland. So I work in, oversee, prevention of harm reduction services for Montgomery County, Maryland and then I also own a best consulting LLC. All right, rock. And so tell me a little bit about the work that you do, whether it be through your consulting company or the harm reduction work, what do you do?

Sure. So, on the prevention side, oversee, all of our prevention, education and awareness efforts. So that includes community awareness campaigns, efforts around drug take back. Also oversee a youth ambassador program. So, we have used, we pretty much empower young people to use their voice to educate about the dangerous substances, mental health, wellness, and in advocacy, we train them in advocacy.

And then on the harm reduction side, oversee our Narcan training and distribution efforts. A syringe services program as well as our efforts to distribute, fentanyl test strips, xylazine test strips, currently working on expanding harm reduction services into vending machines, and other avenues to try to, you know, meet people where they are and support people until they’re ready to pursue their treatment and recovery.

And then on the consulting side, I’m a SAPS trainer, so I was a part of the consultants that, update the SAPS curriculum. So, now it’s the SPF application for prevention success training versus the substance abuse prevention skills training. I also, also an ethics trainer, and then I also do, you know, conference presentations.

But this week, I decided I just want to be a participant. So, you know, participating in the NPN. Taking it all in. Yeah. All right. You got a lot of work. You’re doing. I can only imagine that through doing that work, getting it started, maintaining, sustaining, growing that work. You’ve encountered some, some challenges or barriers.

What are a couple that come to mind? Yeah, I think that the main challenges you can think of are related to maybe stigma, still stigma around substance use. So people not necessarily understanding, how prevention or how harm reduction works. How they can be married together in a sense to build a stronger system.

I think it’s been a lot of like education on my end and my team’s end to try to educate people on how this, how it could look, how it could work together versus, hey, you have this funding. They have that funding and then you don’t really, you know, communicate. Then of course, you know, me working in county government, sometimes you have some extra hoops and hurdles to work through.

To overcome. Which is of course, you know, a challenge within itself. But, you know, you just still, you get up every day. You fight the good fight and the, and the joy of prevention is that it’s always changing. It’s never the same. So you just adapt to the times and figure out how you can be innovative and help your community.

What are some of those successes that you’ve seen? I think for me as of late, so, we’re moving into our fourth year of having a youth ambassador program. in totality, I’ve been with the county for 10 years. It’s something I’d always wanted to do because I knew the power of the youth voice.

So giving them that space, I think has been very rewarding for me. You know, working with adults, you can kind of burn yourself out, but working with kids, they energize you, right? So I think this past couple of years, you know, the youth really were in tune with, You know, what we’ve been experiencing as a country around opioids and overdose deaths and wanted to do something.

So, you know, I worked with a group of young people who wanted to change policy within the within the school system so that you could carry Narcan within school. So you, you can carry Narcan in our school system without feeling as if they’re going to get punished. Right. Then also all of the schools have are equipped with Narcan all the way down to the elementary school.

Then this past year, youth wanted to actually train their peers on identifying the signs and symptoms of an overdose, how to respond, and how to administer Narcan. So, we trained 11 of our youth ambassadors to train other, their peers, and they trained about 300 youth last year and adults. So, I think, you know, that has been a, a major success because now the school system has seen it and they’re like, Hey, we want to make sure that you have youth ambassadors from every high school in the county where there’s 26 high schools and I’ve had representatives from maybe 11 of them.

So trying to get across the entire county and then build up the infrastructure to where you build a pipeline of those youth having that same message from the middle school level all the way to the high school. So once the high school situation gets solidified, we can filter it down to the middle school level.

I’ll call it a 10 year journey that you’ve been on and still are on to get the youth ambassador program to where it is today What might be some tips or some things you’ve learned that you can share with our listeners? Yeah, I think one challenge that I ran into initially was trying to establish smaller youth ambassador chapters at each school Which of course in those situations Me being in such a large jurisdiction Those situations is hard because you got to have a sponsor at the school to oversee that.

So that was a challenge within itself. So I realized, okay, maybe I need to just pull it back and just do something countywide. knowing that, okay, you got youth from all over the county. How do you want to make sure they have the ability to meet without having to drive somewhere? So, luckily zoom has been, you know, or, you know, I think Google meets all kinds of platforms we use initially.

Have been phenomenal because it helps to keep youth engaged. but then also giving them the power to control it to not just having the voice, but they it’s their baby and let them know that, hey, we’re only going to be successful based off of you. I’m just here to support you and to put some fiscal, you know, money or put something behind you to support the strategies and initiatives you want to do.

So, I think having that youth co-chair model, Having youth officers, them leading the meetings, them pretty much recruiting, doing all those different things has been, you know, phenomenal. I just, I just sit back and just kind of watching it manifest, you know? Yeah, yeah. Well, I heard what sounded like a pretty good piece of wisdom, but you kind of just rolled right off your tongue.

You had a vision, the local chapter’s vision, but then you realized that that wasn’t the right path forward and you, you adjusted course. All still within that grander big picture vision of the youth advisory that not afraid to pivot. Right. Of course. And I think I learned that, from, you know, experiences with like larger organizations like CADCA and then seeing other organizations within my state that were doing youth initiatives that were maybe that jurisdiction wasn’t at the size of mine, but saying, Hey, They can do it.

We can do it too. and then just getting, you know, upper leadership to believe that it could be done. And now that they’re seeing it, they’re like, wow, how can we be a part? What can we do to support? Like, what do you need and things like that? And so, I think that has, you know, being able to put prevention in a place of prominence is important.

because you know, we have the, what the Institute of Medicine’s continuum of care. But sometimes people still don’t understand prevention because it’s not providing those immediate results. Right. And so, if you can see, if you can show some, some of those mild substance moments, you know, from, you know, kids sharing their experiences in the program from them sharing what they learn, to, you know, county leadership, seeing them present and articulate themselves in a way that they’re just like, wow, these are some and even trying to get, you know, to the kids who might be on the fence of if I want to use or not, Hey, this seems pretty cool.

And I can get community service hours and, you know, writing recommendation letters for college. And we’ve gotten to a place of giving honor cords for graduating seniors that could wear graduation. So when other kids are seeing it, they’re like, Hey, I want to be a part of that. I think that kind of speaks to.

The importance of like, not only addressing risk factors in our community, but also addressing those protective factors. So that positive opportunity to belong is important because I, I mean, I can see it, you know, I can see the importance of it, right? Yes. So I’ve got, I’ll say I’ve got four questions left.

Okay. You touched on two things that I hear from folks in the prevention field all the time as far as barriers, challenges, or how the heck are we supposed to do that? Yeah. One getting upper leadership on board, but then also the, the buy in and the, the youth taking ownership. Yeah. What kind of insights or experience could you share there for our listeners?

Yeah. So, I learned a lot from, you know, just some time working with, with CADCA and a really good friend of mine oversaw like the youth leadership initiative and that mantra of youth, youth led, but adult guided. And I really believed in that because. I could see how like the, like the youth that were working with, with CACA in those spaces, they were, they were very bright, phenomenal, and they were leading educational sessions, things like that.

And I was like, I know I have kids in my, or youth in my, in my county that can do that same thing. I just have to find them. it’s, it’s initially it kind of happened organically, but then, you know you started reaching out, Hey, I’m doing this project on such and such. And it’s related to fentanyl or whatever.

And I’m like, well, why are you not in my program? Like, what have you been doing? And then they’ll sign on and they like, Hey, I don’t know why I haven’t been here, but I’m happy to be here now. Right. Yeah. So I think really just understanding that it’s not going to happen overnight. You got to just continue to just keep, keep fighting a good fight.

Eventually those things that you want to change and manifest in your community will happen. Like Rich Lucey from DEA says prevention is about the long game. Yes. 10 years running. Yeah. I’m curious if you have a, a good story that really shows the impact of your work with the youth and stigma, whatever it may be. Just a story that talks about the, the impact. Yeah. So I used to get requests to, do presentations at high schools, right? And you never really know, you never really know the impact of those presentations because you might be presenting to like a parent group or something like that.

Right. And so, we eventually got to a place of wanting to train all of our bus operators in the lock zone administration so that they can have Narcan on the bus and things like that. Just in case overdose happens on the bus. Well, not knowing that one of the administrators or one of the managers of supervisors over the transit system was in one of my presentations at the high school because their daughter was a student at the high school.

it was a full circle moment because he basically said to me, he was like, a lot of the things you share that night helped me and my wife because our daughter eventually dealt with substance use disorder. But we knew what to do to help support her and navigate her through that space.

So that really like it was a real like aha moment to me that, you know, what we’re doing is working. And yes, if someone does go down that path, you still want to make sure you give them those tools and maybe you can help bring them back in and keep them safe and keep them alive.

Right. So, I think that was just, I mean, there’s been a lot of moments, literally you thought it gave me goosebumps. I can feel that, one last question, one last, but I promise, I promise, you mentioned earlier, you said it so eloquently about putting prevention in a prominent place.

The theme of this conference is shining a light on prevention. So can you give us, you know, a description of what does that, what does that mean to you? Yeah. I, I really feel like there’s a lot of opportunities for prevention out here, whether it’s through not only, you know, pursuit of grant fund is, but I think that’s mobilizing to say, Hey, you know, block grant funds haven’t changed in the past 20 years.

What? Maybe we need to advocate, you know, to get that shift. But I think making sure that we’re at the tables. of those who are in control of funding, right? And so, I think for me, I’ve been fortunate enough to be at some of those tables where, you know, we are gaining access to some of the, like the opioid abatement funds to build up the infrastructure of prevention in the county and to build up harm reduction in the county and things like that, which, you know, you know, treatment services and crisis services and other service areas, they’ve always had money to do the things that they needed to do.

But prevention never really had that. So I think, you know, continuing to, you know, do the work, advocate, you know, show, you know, positive results and get to those tables is important to help us get to that prominent level that, hey, we’re part of the continuum or the spectrum of services as well. We need to be funded in a way so that we can prevent all those people from having to go to treatment to him and experience recovery.

Right. So I think Not only, you know, advocating for ourselves, but also building up those allies to help us advocate, to show the power of prevention because it’s definitely a place for us. and, you know, we’re all in the same business of trying to, you know, promote optimal wellbeing in our communities, right?

The themes that I heard were persistence, perseverance. together. Yeah. And, and I would say a twofold listening and learning. Yes, of course. Cause I mean, we might be the experts on the process, but of course we’ve got to connect with those and collaborate with those people in the community because they’re the experts on the, on the story of that community.

We can’t really, you know, talking to a lot of my colleagues, we, we talk about shifting from being implementers to coaches or mentors so that, you know, you can sustain some of the efforts and outcomes that are in the communities, you know, so, so that’s the hope and goal, right? Yeah. All right.

What would be one final takeaway call to action to leave our listeners with? Yeah. I’ll just say that, you know, my experience in this field is that It’s important to network because you can always learn from somebody else. Something innovative, something creative that somebody else has done in another part of the country that you could maybe implement in your, your area.

and then always just, just making sure you stay abreast and up on top of, you know, language and evidence based practices and all those different things. Because I’ve only been in the field for 18 years and it’s changed exponentially over the course of that time. So. Just saying, staying abreast of that and staying engaged, mentors, having a mentor, I have multiple.

And if you feel burnt out, make sure you take care of yourself. Mom’s always said, if you don’t take care of yourself, you can’t take care of somebody else. So All right. Folks. That was, was an enlightening conversation with Ben. Who’s truly leading the way. In integrating prevention and harm reduction in his community. And I just loved hearing about his work with youth and this commitment to breaking down barriers is, is inspiring and really does offer us some valuable lessons for, for everyone in the prevention field.

But now we’re shifting gears to another powerful voice in prevention. Steve Miller is not only a longterm recovery advocate, but also someone who’s found a unique way. To incorporate his passion for music into his prevention work. Steve’s insights on the role of music and shaping behavior. And his own journey through recovery are both thought provoking and motivating. So let’s dive into my conversation with Steve Miller.

All right, folks, bringing you another conversation from the NPN conference. Where the theme is shining a light on prevention, and I’m honored to be hanging out here with the one and only Steve Miller, who is a prevention champion, prevention podcaster, man in long term recovery and is sharing his voice, his story, his wisdom to help make positive change in this world.

So without further ado, Steve, great to be talking to you again. Hey, thanks, Dave. I’m glad to be here. Yeah. Oh, all right. So we’re jumping right in. We’re jumping right in. I don’t want to, to really tell your background and why you work in prevention now, but I’m hoping you might be able to, to give us, we’ll say a cliff notes version of highlights real of.

What led you to working in prevention? That’s always an interesting question, Dave. And one of the things that I’ve realized, and this has been in the last couple of years, that I would have said, oh, there’s just been so many random things that have happened in my life. And then when I sat down and kind of looked at them on a timeline, I realized it was actually a straight line.

And it wasn’t something that was so haphazard. It was actually what was intended all along for me to be doing. And, and part of that is, is the natural evolution. As you said, I am a person in, in long term recovery. And so I’ve been working in either the treatment field or some variation of prevention for three decades now.

And so that’s really been my life’s focus is my own recovery. And, and then what I’ve learned in that journey is how do I kind of. Find my work through who I, who I really am. And one of the common denominators through all of this, before I was in recovery, since I’ve been in recovery and now in the prevention field has been this.

I call it the muse leading me through song, if you will, and I had to learn the prevention field. I didn’t know it existed. I didn’t know there was a science. I just kind of fit the description of what they were looking for as a new staff member. And I thought, Oh, I could do that. And it didn’t take me long to figure out that.

My guiding force through prevention is believing that by finding, we find our work through ourselves and when we do that kind of strengthens our commitment to do this kind of work, but it also strengthens the workforce because just like you, you’ve kind of found a path that leads you in the work that you’re doing.

But you started in prevention and I found a path by starting in prevention, learning the science, learning how the strategic prevention framework operates, all that kind of stuff. Then I stood back and I thought, does music belong in? And lo and behold, that’s kind of the answer has been, Oh yeah, it does.

Because it’s been such a powerful force in my life. I thought it’s got to be added into what I’m doing in prevention, added into your story, because like you said, it, it’s been a muse behind that straight line to prevention. So let’s just talk about that. Let’s, let’s go right there and talk about. Music.

You say it’s been your muse. What do you mean by that? How has it been your muse? People ask me when I talk about it, they go, so what instrument do you play? And I’m like, I play the radio really well. And if I want to, I can put a record on the turntable, but I am not a musician. I have been someone who has been an avid consumer of music like a lot of people since I was an adolescent.

And I tell a whole story through a training that I do about how music shaped my life, but how it shapes our lives. And then I just overlay that in the, into the prevention field, because there’s a lot of research that shows how music influences our choices. And when we’re adolescents and we’re trying to figure out who we are and what we want out of life and where we’re going to go, we’re very susceptible to outside stimulus and peer pressure is really what that comes down to.

And music can be a part of that music. Plays a part in helping us form our identity because we have such this creative bond with music. Everybody can think for themselves, what was that song that was the soundtrack to your life as an adolescent? Did you dance to? Who’d you fall in love to? Who’d you hang out with your buddies?

You know, what was the, what was playing in the background? And we all kind of have that somewhere inside of us. My choices happen to be very detrimental and that was a part of my addiction. And then when I found myself in a recovery process, it was music again, that kind of just woke me up and made me realize there are messages in all of these songs that are beneficial to who I am at this particular point in my life.

So that we’re kind of a meditative process. But then when I got into prevention, I started thinking, how could, how could my experience And how could the research that supports my experience be beneficial to a message that would target an audience that’s either adolescents, or I talk about how music is a part of the workforce development in my life, music, really.

I start my day with it and I probably end with it, but I start most days with a song. And I mean, to prove that to you this morning, I woke up with a song in my head. And I sat down in the, before I even really get out of bed, I write kind of a journal entry about that song and what it means to me and how it kind of feels like it’s guiding me for the day, what that intention would happen to be.

And I’ve just followed it because it’s fun. I feel like I’m kind of the only one that does it. I’ve shared these ideas with other people, but been very insightful for me. And, and, I still provide training and technical assistance through prevention to lots of audiences, but there’s this little niche that I talk about where the music kind of fits right in there, I’d like to, to zoom in and.

Wanna really. Invite you to share a great example of, of how music played a part in your addiction. You said you kind of, it kind of kicked you off and had a prominent role there. Can you give us that, that kind of that, that clear example, like what happened? I mean, think, and I was trying to get, we were talking about this for the, for the audience to kind of.

I was how to Get this in their mindset as well. If you think about a song that you hear and when you hear it, you’re kind of transported to a time and place in your life. Now, I have a song that always takes me to exactly the same memory and it’s, it’s uncanny that I actually, it was, it’s, it’s a song by ACDC and it takes me to the lake outside of the town I grew up in.

And it’s not just the song and the, and, and the association of that time in my life. I actually, I’m telling you right now, it’s almost like I can feel the air around the lake on my skin. It, it’s like, It’s being transported to that memory and reliving it again. And that’s how powerful music is. So I ask people all the time, what is that song for you?

And why do you have such a strong association with it? Maybe it’s because you fell in love, you know, that kind of thing. Maybe it’s the first dance you ever had, because I have that story as well. But there was a time in my life when if you’d have said, Oh, Steve, you’ll smoke cigarettes, or you’ll drink alcohol, or you’ll use some kind of substance.

I would have thought you’re, you’re crazy. Cause I was like any other kid that I grew up with. I played sports, hung out with my friends. We rode our bikes everywhere. I grew up in the 1970s. Anybody that’s listening probably knows what that was like. And one day, I mean, I know that it was a Saturday. I know that it was eight minutes after nine o’clock in the morning and an older brother To one of my friends came into the room and put on a song and in that moment, everything about what I thought life was changed.

And the song to me was rock and roll. And I thought it was about something that I wanted to pursue. And it was really about. In that moment, to me, it was about using drugs and alcohol. Now, I had some experience with it before then, but after that moment, everything changed. I mean, it was like a slipper slide.

It went downhill quick. And then years later, when I got curious about this topic we’re talking about, I got to looking at that specific song. And I realized that song is not a pro drug use anthem that I thought it was. It’s actually a very thought provoking message to one of the singer’s bandmates because he was concerned about his own health and his own life because of his substance use.

And I, so I point out to the audience that as adolescents, we kind of make a lot of things up based upon what we want to hear, because we’re looking for that, that identity, who are we, where are we going? How do I feel those kinds of things? And a song can slip right in there. And I’m not unique in that fashion.

I have talked to several people in the last 10 plus years that have told me stories about how they heard a song and made a decision in the moment. And sometimes I’ve stood back and said, you did what, and then they explain it to me and it makes perfect sense because of the time of their life, what they were experiencing, those kinds of things.

And so that song really impacted my life. In a very detrimental way, some people, it impacts their lives in a very positive. And I’ve talked to some that it, a song shaped their life in a way. It is very financially rewarding. So I think it’s across the board. The question is, is do we ever, do we ever really listen to what that song is actually saying to us or how we feel about it or what it means to us?

And I think that’s the key is really being in the moment and aware enough to know that this song may say one thing, but I may take it another way. And then when we’re adolescents, it might behoove us to ask someone, an adult or someone we trust. This is what I hear this song saying, as opposed to this is what I think this song is saying.

So getting some of that feedback and checking that out before I make some sort of a critical life decision. And that’s basically, we talk in prevention about media literacy. So that could be printed or television ads or radio or social media, whatever that looks like. I just put it under the heading of it’s really about music literacy and understanding the impact it has in our lives.

You just made me kind of understand about myself. There’s a lot of songs that I love and they make me feel a way when I hear them and they take me back to those moments like you talked about, but I can’t say I know all the lyrics. I may only know just the chorus or one line, but I love these songs because of the memories I have, the feelings I have associated to them, like the, for my, my wedding.

I asked for a, I call it a secret first dance. I wanted to dance a specific song before we went into the actual like dinner afterwards. And so it was just my wife and I, and the photographer and that’s it. And I don’t know the lyrics to that song. I know the title of it and the artist, but that’s it.

But I love it whenever I hear it. Come on. It takes me right back to that moment. We’re having our moment. Yeah. Yeah. But I don’t know the lyrics. And what’s interesting is I watched it was. A reel on one of the social media channels just in the last couple of days. And it was something that said as a Gen Xer actually listens to the song and, and you can see ’em kind of keying into what the message is and being like, oh, I didn’t realize that’s what that song was saying.

Right? Mm-Hmm. . Mm-Hmm. . And, and that, that fits the bill. Some of us know that hook and some of us know just the, the feeling that we get. That’s associated with the song, but there’s a lot of research out there that says, even if we’re not consciously aware of the lyrics, some part of our brain is picking up on the messaging of that.

Now, whether that’s detrimental or whether that’s inspiring or whatever that looks like is different for the individual. No two songs are the same. But like I said, I hear a song and, and the song I heard this morning is one that I really only know the hook to, like you just said, so I Googled the whole lyrics and then I sat down and wrote a little passage about it, but I have had experiences where I woke up and I had that same thought, you know, some, some, some statements going through my head and I’m like, I don’t even know if that’s a song and then I’ll say, I’ll Google lyric and then whatever it is I’m thinking, and if it comes up as a song and I yeah.

I’m amazed. There’s been times when I’ve done that and I swear to you, I have no recollection of ever hearing that song in my life. Now, where did I pick it up? Why did it come to me in my sleep? I don’t know. But I am fascinated by the fact that when I’ve been led to understanding that there’s some something stuck in my subconscious, if you will, and it ekes out when I wake up in the morning and it’s a song that I picked up somewhere along the way, I just don’t know where or when or why, but that’s why the why is like, well, why is this showing up?

And then I try to kind of analyze it, kind of meditate on it, gives me a way to set my intention for the day. And sometimes I might share that with other people if I find it a profound insight in some way or another, I’m going to draw a connection that might not be there or not, but I’m reaching for it.

And I know and trust that you’ll be like, ah, Dave, there’s no connection there. But I talk a lot about the power of storytelling and prevention, treatment, and recovery, both for the, the listeners, but then also for the actual storyteller themselves, but songs. They have the story element, they have the story factor too.

So wouldn’t that be sort of one in the same? I think so. I’ve, I’ve heard people talk about that songwriting really is a gift because I’ve seen interviews with artists or authors that have written books and they’re like, they can tell a story in three and a half, four minutes that takes me a chapter or two to tell, but they can synthesize it down in a way.

And that’s the part like that led up to anything really being, you know, like understanding how music impacts me emotionally as an adolescent, because my parents played music when I was growing up, but the songs that stick with me to this day are the ones that tell a very vivid story. And so I’m kind of a storyteller of sorts myself, but I like a song that tells a really powerful story.

So as an example, The first song that I really can remember, I wanted that song so bad. And it was a, it’s a singer named Jim Croce. And the song is bad, bad Leroy Brown. And I was a nine year old boy. And I mean, bad, bad Leroy Brown was the baddest man in the whole damn town. Badder than old King Kong and meaner than a junkyard dog.

And to a nine year old boy, it’s like. I want to be, you know, like to me, it was like the he’s respected and, you know, he’s a tough guy and, you know, kind of things that as a nine year old boy, you’re playing G. I. Joe and playing army with your buddies. You know, you’re kind of wanting to be that masculine kind of identity.

And that was what bad, badly Roy Brown was. But it’s a very vivid story song. And a lot of Jim’s work is story songs. And so I’ve always sought those out. I like all kinds of music. I don’t pick a genre, but the ones that seem to rise to the top are the ones that tell me a story about something that I don’t understand.

And I’m, as I’m explaining this, I watched a documentary about a group and, and they had on there as a guest, he was a professor of music of some sort from a university. And he said, I had a student that did a, master’s thesis on this particular subject. And he spent all semester long or all year long, however long that takes and wrote this thesis.

And he said, this singer captured the same essence in three and a half minutes. That’s the power of a song. And if you can deliver that and people can really kind of onboard that, it can be powerful in a lot of ways, or it can be, like I said, it can be, it can be harmful in ways. So it just depends on the listener and how you.

How you perceive it, how you receive it and, and how you may or may not act on it. I want to ask about a powerful song that if I remember correctly, as part of your journey as to where you are today. So if I, if I throw out the Beatles song help, where does that take you to in your life? Well, that’s the turning point.

I’ve actually written a short story for a friend of ours that’s doing a collection of legacy stories. And I kind of tell the story through two things, the, the song that was kind of the gateway into substance misuse. And then it was the song by the Beatles help that was kind of the book into it. And it was the one that really kind of illustrated to me that songs spoke to people in very unique ways.

And it was a Catholic priest that was talking about the fact that, the lyrics of a popular song could be the catalyst to get someone’s attention about their addiction. And I remember thinking in that moment, wow, I wonder if that would happen for me. Now, when I look back, the surprise is it was happening to me, right?

But that’s the desperation of, of that point when you’re asking for help in recovery and the Beatles song help is, was the song he illustrated. And if you look at those lyrics. Makes perfect sense. When I was much younger, so much younger than today, I never needed anybody’s helping. Well, here I am in a institution asking for help and realizing that someone has captured that essence of what I’m going through and put it in a song and it kind of planted that seed like, well, what other songs are in my life that might be signposts and.

Those kinds of things. And, and I was a huge consumer still lamb, but I had more time on my hands when I was younger. I was a huge consumer of music and I worked in television at the time and the general manager’s assistant just one day casually said to me, Steve, how long has it been since you listened to any music?

And I said, it’s kind of a strange question. And she said, your personality is different when you don’t listen to music for a period of time. And that’s another point in my life when I was like. What, what is this all about, you know, and I started at that point, not just listening to like a popular song that I liked, I started like listening to entire albums, like what’s being portrayed here and I read an article and, and the author had said that if you really want to understand The author that writes popular novels or something like that, read everything that they’ve ever written, and you’ll have some understanding of who they are as a person.

And so I started that through the lens of music and started thinking about some of the artists that I was enamored with and started listening to their entire albums and their entire catalogs, just to kind of seek out, like, What has been the path for this person and, and lo and behold, after doing that for years on end, it found its way into the prevention work.

To me, it’s really about following the muse, if you will, or following your own life’s path. And in prevention, that’s kind of where I started in, in prevention. If you stick around here and you find some attraction to it. I think you have to put yourself into the work at some. It has to start becoming a reflection of who you are.

You have to be vulnerable enough to really say, this is this is kind of who I am. And this thing that I do kind of all merged together because for me, prevention and my recovery, but. Prevention is really about people. Somebody I know says prevention is better together, and together we are stronger. And that says everything about prevention.

Because it doesn’t happen in a vacuum. You can’t go in and change a community’s rate of underage alcohol consumption just by telling the chief of police or having an article in the newspaper. You have to get people together in a concerted effort. Effort to make a difference. And that’s why I do the work that I do.

And that’s why I’m passionate about bringing the music into it, because I think we all, whether we’re as active in their consumption of music as I am, I think we all have been touched by music or love music in some form or fashion. And if I can just help people to see that maybe those songs are speaking to them about something, then, then that’s, that’s kind of how it’s played out in my life.

I say that I practice a two way communication with music. I listened to the song and then I asked the song, what is it that you want me to hear from this? And then I try to write about it. So I know we could talk for hours. But we’ve got a conference to get back to, so I want to just throw one more thing your way before we wrap up this chat as a to be continued.

But I’m curious, what’s final takeaway if you’re going to leave with one thing, what’s it going to be or call to action for our listeners from around the globe? Well, I love the call to action and it is think about that song. What is that song that stops you in your tracks and takes you to that moment?

And why is it so? Unbelievably powerful in your life. And, and like I’ve already said, think about what it might be saying to you, because it’s unique. I heard Dave Grohl, he’s the lead singer for the band Foo Fighters, and others might know him as the drummer from Nirvana, but he said, the amazing thing is, is he said, I can stand on stage and I know that I am singing this song to 80, 000 people.

But the beauty of music is. 80, 000 people are singing back their own interpretation of that song. To me, that really personalizes all of this in that I think music is a very powerful presence in our lives and it must serve some greater purpose because a question I’ll often ask is. Music doesn’t have to exist, but it does.

Think for a moment that music no longer is a part of your life. And I’ve never met anybody say, well, I won’t miss it. Most people are like, wow, that means there’s, there’s no soundtrack at the movie, the commercials are just talking heads. You don’t even know that birds chirp because that’s music. If all of that was gone from our lives, what a different world it would be.

So I turn it around and say, this must mean that there’s something here. And I would always challenge people just to ask themselves, what is the value that music plays? And with that listeners do some thinking, do some listening and have a conversation with some songs. Steve, thanks for taking time to chat.

Always, always, always a pleasure. Thanks, Dave. Always glad to be here.

That concludes this episode. Thanks for tuning in. Be sure to hit the subscribe button and share this episode with a friend before you leave. And we look forward to seeing you on social media because prevention is better together. Together, we are stronger.

 

Source: Drug Free America Foundation

The recently released National Drug Control Strategy (2022) from the White House Office of National Drug Control Policy (ONDCP) lays out a comprehensive plan to, not only enhance access to treatment and increase harm reduction strategies, but also increase implementation of evidence-based prevention programming at the community level. Furthermore, the Strategy provides a framework for enhancing our national data systems to inform policy and to evaluate all components of the plan. However, not only are there several missing components to the Strategy that would assure its success, but there is a lack of structure to support a national comprehensive service delivery system that is informed by epidemiological data, and trains and credentials those delivering evidence-based prevention, treatment, and harm reduction/public health interventions within community settings. This paper provides recommendations for the establishment of such a structure with an emphasis on prevention. Systematically addressing conditions known to increase liability for behavioral problems among vulnerable populations and building supportive environments are strategies consistently found to avert trajectories away from substance use in general and substance use disorders (SUD) in particular. Investments in this approach are expected to result in significantly lower rates of SUD in current and subsequent generations of youth and, therefore, will reduce the burden on our communities in terms of lowered social and health systems involvement, treatment needs, and productivity. A national strategy, based on strong scientific evidence, is presented to implement public health policies and prevention services. These strategies work by improving child development, supporting families, enhancing school experiences, and cultivating positive environmental conditions.
Appeared originally in Clin Child Fam Psychol Rev 2023; 26:1–16
Source: https://psychiatryonline.org/doi/10.1176/appi.focus.24022020

Source: https://static1.squarespace.com/static/599a426ee45a7ccab72c77d2/t/5f3ad99ce4a6280272c97cb6/1597692318766/Marijuana_%2BA%2Bman%2Bmade%2Bdisaster.pdf April 2018

In the 50 years since its establishment, the National Institute on Drug Abuse has made significant investment and strides toward improving individual and public health. Epidemiology serves as the foundation for understanding the how many, why, how, where, and who of drug use and its consequences, and effective epidemiology research and training are geared toward actionable findings that can inform real-world responses. Epidemiologic findings enhance clinicians’ ability to provide ongoing care by incorporating information about the patterns and outcomes of drug use that their patients may experience. The goal of this article is to provide a context for epidemiology of substance use as a foundation for prevention, with examples of how epidemiology can provide targets for prevention, and to set the stage for addressing the importance of prevention in clinical settings.
Source: https://psychiatryonline.org/doi/10.1176/appi.focus.20240018 

Our research on the adverse effects of cannabis contributed to a major public debate and Government campaign to inform teenagers about the potential risks of cannabis.

Research led by Professors Terrie Moffitt, Avshalom Caspi, Philip McGuire, Sir Robin Murray, Louise Arseneault & Drs Paul Morrison & Marta Di Forti

Our research on the adverse effects of cannabis contributed to a major public debate and Government campaign to inform teenagers about the potential risks of cannabis.

Cannabis is the most widely used drug in the world, but its effect on mental health has only recently been uncovered.

Research led by Professors Terrie Moffitt and Avshalom Caspi demonstrated that the earlier people start using cannabis, the more likely they are to have symptoms of psychosis as a young adult. A study of 1,000 men and women in New Zealand showed that people who had been regular cannabis users at 15 were about four times more likely to have psychotic symptoms by the time they were 26 than their abstaining peers. The research also identified genetic variations that made people more vulnerable to the harmful effects of cannabis.

Further work led by Dr Marta Di Forti showed that people who smoke a potent form of cannabis (skunk) regularly are much more likely to develop psychosis than those who use traditional cannabis resin (hash) or old-fashioned grass.

Research led by Dr Paul Morrison helped explain why, by investigating the effects of the two main constituents of cannabis: THC (delta-9-tetrahydrocannabinol), the psychoactive ingredient that produces the ‘high’, and CBD (cannabidiol), which seems to moderate the effect of THC. Skunk contains much more THC than hash or old-fashioned grass and virtually no CBD. Our research illustrated that an injection of pure synthetic THC can induce transient symptoms of psychosis in people who have no experience of mental health problems.

‘Overall, our research in this area had a major impact on the perception of the risks of cannabis use on mental health,’ says Philip McGuire, Professor of Psychiatry and Cognitive Neuroscience.

In the wake of these studies and other evidence from around the world linking cannabis use with psychosis, the Home Secretary asked the UK Advisory Council on the Misuse of Drugs to review the legal classification of cannabis in 2007. Professor Murray submitted written evidence to this review and Dr Morrison, spoke at a review meeting about the effects of THC and CBD.

In 2008, the ACMD reported that the majority of its members thought cannabis should remain as a class C drug, but confirmed that the drug, particularly skunk, can damage people’s mental health, especially if young people start to use it an early age.

Despite the recommendation, the Government decided to tighten the law and in 2009 the Misuse of Drugs Act cannabis was amended and cannabis was re-classified from class C (considered the least harmful), to class B, making it illegal to possess cannabis, give to friends or sell it.

Following reclassification, the Department of Health launched a major TV, radio and online campaign to demonstrate the role cannabis can play in the development of mental health problems. The ‘Talk to Frank’ television adverts, aimed at young people, illustrated how cannabis can contribute to paranoia and damage mental health.

Although cannabis is still the most widely used illicit drug in Britain, its use has been steadily declining. The 2011/12 Crime Survey for England and Wales showed that 15.7 per cent of young people said they had used cannabis in the previous year, the lowest level since measurement began in 1996, when 26 per cent of young people said they had taken cannabis.

Additionally, our research into the effects of CBD and THC has also led to a partnership with the pharmaceutical industry to develop a new antipsychotic medication based on CBD.

Source: https://www.kcl.ac.uk/news/spotlight/uncovering-the-link-between-cannabis-and-psychosis

BY Lindsey Leake

August 27, 2024
While the modern marijuana consumer may be shedding that lazy stoner stereotype, new research shows that employees who use and abuse the drug are more likely to miss work.

The findings were published Monday in the American Journal of Preventive Medicine.

Work absences included days missed due to illness or injury in addition to skipped days when employees “just didn’t want to be there.” Respondents were a majority or plurality white (62%), male (57%), ages 35 to 49 (35%), married (52%), had at least a college degree (42%), and had an annual household income exceeding $75,000 (55%). About 16% of employees had reported using cannabis within the last month, with about 7% of whom meeting CUD criteria (mild: 4%; moderate: 2%; severe: 1%).

People who said they had never used cannabis missed an average 0.95 days of work in the past 30 days due to illness/injury and skipped 0.28 days. Cannabis users, by comparison, recorded the following absences:

  • Past-month use: 1.47 illness/injury, 0.63 skipped
  • Mild CUD: 1.74 illness/injury, 0.62 skipped
  • Moderate CUD: 1.69 illness/injury, 0.98 skipped
  • Severe CUD: 2.02 illness/injury, 1.83 skipped

The results also showed that people who used cannabis most frequently skipped the most work. For instance, those who consumed it once or twice per month skipped 0.48 days, while those who consumed it 20 to 30 days per month skipped 0.7 days. People who used cannabis three to five days per month had the highest prevalence of missed days due to illness/injury (1.68). Cannabis use longer than a month ago had no bearing on employee absence.

“These findings highlight the need for increased monitoring, screening measures, and targeted interventions related to cannabis use and use disorder among employed adults,” researchers wrote. “Moreover, these results emphasize the need for enhanced workplace prevention policies and programs aimed at addressing and managing problematic cannabis use.”

Researchers said that while their latest work supports much of the existing literature on cannabis use and workplace absenteeism, it also contrasts with other studies. One previous study, for example, showed a decline in sickness-related absences in the wake of medical marijuana legislation, while another found no link between the two.

One limitation of the new study, the authors note, is that it relied on participants’ self-reported answers. In addition, the data don’t reflect whether cannabis was used for medicinal or recreational purposes, whether it was consumed during work hours, or address other factors that may have affected a person’s cannabis use patterns.

What are the signs of cannabis use disorder?

That marijuana isn’t addictive is a myth. People with CUD are unable to stop using cannabis even when it causes health and social problems, according to the Centers for Disease Control and Prevention (CDC). Cannabis consumers have about a 10% likelihood of developing CUD, a disorder impacting nearly a third of all users, according to previous research estimates. At higher risk are people who start using cannabis as adolescents and who use the drug more frequently.

The CDC lists these behaviors as signs of CUD:

  • Continuing to use cannabis despite physical or psychological problems
  • Continuing to use cannabis despite social or relationship problems
  • Craving cannabis
  • Giving up important activities with friends and family in favor of using cannabis
  • Needing to use more cannabis to get the same high
  • Spending a lot of time using cannabis
  • Trying but failing to quit using cannabis
  • Using cannabis even though it causes problems at home, school, or work
  • Using cannabis in high-risk situations, such as while driving a car
  • Using more cannabis than intended

In addition to interfering with everyday life, CUD has been linked to unemployment, cognitive impairment, and lower education attainment. People with CUD often have additional mental health problems, including other substance abuse disorders. In this study, for example, 14% of respondents reported having alcohol use disorder within the past year.

 

Source:  https://fortune.com/well/article/marijuana-abuse-cannabis-use-disorder-workplace-absenteeism-sick-days/

October 1, 2024

This blog was originally posted on the The BRAIN Blog.

The BRAIN Initiative is marking a milestone—10 years of advancing neuroscience and neurotechnology research by funding innovative projects. As part of a rotating series of blog posts, the directors of the BRAIN Initiative-partnering Institutes and Centers share their voice and perspectives on the impact BRAIN has made on their respective missions—and vice versa.

This year marks the 50th anniversary of the National Institute on Drug Abuse (NIDA). The research NIDA has funded and conducted over five decades has greatly advanced the biomedical understanding of addiction as a treatable condition involving brain systems governing reward, emotion, stress, and self-control. NIDA research has helped pave the way for effective prevention, treatment, and harm reduction approaches, and opened up new pathways to recovery.

NIDA has been a key player in the BRAIN Initiative, as our Institute continues to apply these new tools and emerging knowledge to inform research about the science of drug use and addiction. As the United States continues to face a devastating overdose epidemic fueled in recent years by an influx of illicit fentanyl, NIDA’s scientific efforts are ever more important. Central to those efforts is our significant investment in basic neuroscience research. Since its launch a decade ago, the BRAIN Initiative has greatly aided and accelerated that research. Tools developed through the BRAIN Initiative are catalyzing scientists’ ability to precisely monitor and manipulate brain activity at multiple scales, giving us an ever more fine-grained understanding of the brain mechanisms underpinning drugs’ effects and suggesting potential avenues for mitigating, preventing, or reversing those effects to heal the brain.

The BRAIN initiative has transformed neuroscience research at many levels. It has created a culture of team science that has led to development and dissemination of new tools that have been used to characterize gene expression with cellular resolution across multiple species, tools that allow visualizing and manipulating neural circuits, as well as new approaches to data science and computational modeling. Our staff who work on BRAIN Initiative program teams get a unique exposure to these approaches and technologies that will critically shape our Institute’s research in future years.

Advances made possible through the BRAIN Initiative will transform translational research by improving the validity and innovation of the models we use to probe mechanisms underlying substance use and use disorders—enriching our research community’s capacity to innovate. NIDA participation in the BRAIN Initiative provides opportunities to accelerate the application of these advances among the researchers who focus on these questions. And it enables NIDA to promote areas of focus where our Institute has been at the forefront, including investigation of non-neuronal cells (glia) and developmental studies that dovetail with the Adolescent Brain Cognitive Development (ABCD) study.

How has NIDA participated in the NIH BRAIN Initiative?

Several of NIDA’s scientific staff are members of BRAIN Initiative program teams, and our Institute leads or co-leads some key BRAIN projects. NIDA co-leads the team that is managing the Data Science and Informatics project, which is creating the informatics infrastructure needed for storing, sharing, and interpreting the vast quantities of data gathered by the BRAIN Initiative. NIDA also co-leads the Tools and Technologies for Brain Cells and Circuits research program, which is creating brain cell atlases of the neuronal and glial cells in the brain. This fundamental knowledge will be used to build viral vectors to monitor and manipulate brain function at the cellular level.

We are also a major supporter of the Brain Behavior Quantification and Synchronization Program (BBQS). This uniquely transdisciplinary program, which was just launched in 2022, is supporting the development and validation of novel tools and methods for quantifying complex behaviors and simultaneously recording brain activity. This program promises to transform behavioral and cognitive neuroscience by supporting research that will generate high-resolution tools for analyzing behavior and new computational and theoretical approaches for understanding behavior as a complex system. NIDA leads the BBQS emphasis area on organismal behavior.

Although it was just launched two years ago, the BRAIN BBQS concept has influenced multiple NIDA initiatives, including Translating Socioenvironmental Influences on Neurocognitive Development and Addiction Risk (TransSINDA), Mechanistic Studies on Social Behavior in Substance Use Disorder (in both humans and animal models), and the NIDA Animal Genomics Consortium. These initiatives support research that identifies cause-and-effect relationships between socioenvironmental factors and brain function that guide behavior.

Toward advancing the emergence of common marmosets as a promising animal model in neuroscience, NIDA has also played a leadership role in BRAIN’s transgenic marmoset initiative. This set of projects is aimed at developing novel tools and techniques for marmoset genome editing and male germline editing to facilitate research on genetic underpinnings of brain health and disease, as well as assisted reproduction techniques to increase the efficiency of these procedures.

What major BRAIN-funded scientific advancements or conversations has NIDA been a part of?

As one of the Institutes co-leading the BRAIN Initiative’s Tools and Technologies for Brain Cells and Circuits research program, NIDA has been closely involved in shaping and supporting the inventory and molecular mapping of cell classes across the whole mouse brain, and there are ongoing plans to accomplish the same in human and nonhuman primate brains.

A component of this program is the Cell Census Network, and among the brain regions of central interest in this project are the basal ganglia. The basal ganglia comprise the reward pathway and other circuits that play a major role in substance use disorders. Scientific staff at NIDA and several NIDA-funded grantees are participating in the effort to create a systematic map of this region to enhance our knowledge of its cellular and molecular architecture. This research could potentially lead to tools that could selectively target the basal ganglia’s cellular constituents, which would be a game changer for NIDA science.

Through BRAIN Initiative programs like BBQS mentioned above, NIDA has been co-leading discussions about advancing cause and effect relationships in human neuroscience research. We now have large neurocognitive datasets that can be mined and analyzed using large-scale network approaches, such as those generated by the Human Connectome Project and the ongoing ABCD study. These databases have enabled novel insights about fundamental brain function and neurocognitive dysfunction. For instance, ABCD is deepening our understanding of how environmental exposures affect neurocognition including revealing factors like economic disadvantage and social discrimination that can be targeted in prevention efforts. But while these datasets are excellent for identifying associations between network structure/function and behavior, they generally cannot help us establish causal relationships, leaving a gap in our ability to translate findings to clinical application.

Data derived from new methods and approaches like systematic circuit perturbation in combination with neural recordings in a behavioral context hold potential to fill this gap and significantly advance our understanding of these important cause and effect relationships in human neuroscience.

How has the BRAIN Initiative advanced or shaped NIDA’s mission?

Many tools developed through the BRAIN Initiative are helping NIDA scientists understand how drugs affect the brain, from cellular to circuit levels. For example, NIDA’s BRAIN-inspired research programs are already producing exciting findings. One of them is NIDA Single Cell Opioid Response in the Context of HIV, or SCORCH, which is applying single-cell sequencing-based approaches to inventory the cellular targets of drugs and the changes in those targets that drugs induce. A NIDA-funded team has recently identified a group of neurons in the dorsal peduncular nucleus, a brain region central to emotional regulation, reward, and motivation, that act as a master regulator of opioid reward.

Another NIDA initiative inspired by BRAIN is the Neural Ensembles and Used Substances (NExUS) Collaboratory, which seeks to integrate molecular information from cell taxonomies with measurement of neuronal population dynamics in behaving animals. NExUS aims to decipher how activity within the mosaic of brain cells “encode” particular properties of misused substances, such as the analgesic versus addictive properties of opioids. A NIDA-funded team has also recently used a mouse model to identify a brain circuit that mediates placebo pain relief.

In its 10 years, the BRAIN initiative has provided tools to visualize, monitor, and manipulate brain activity from molecular to network levels and has led to an exponential growth in understanding of how the brain functions. NIDA has been a key player in this effort, and our Institute continues to apply these new tools and emerging knowledge to inform research on urgent questions under its mission to advance the science of drug use and addiction.

Source: https://nida.nih.gov/about-nida/noras-blog/2024/10/brain-10-view-national-institute-drug-abuse

Photo: © Francis Odeyemi

Torrential rains last week caused a dam to collapse and flood north-east Nigeria, affecting more than four million people in 14 countries. Over 550,000 hectares of cropland were flooded, compounding an existing food security crisis.

“I have never in my life experienced a disaster as terrible as this,” writes Yakura*, a UN Office on Drugs and Crime (UNODC) Youth Peace Champion.  Youth Peace Champions are a network of young leaders dedicated to promoting prevention, rehabilitation and reintegration for children affected by adversity.

Yakura is one of tens of thousands of young people taking action in their communities, organizing rescue efforts and distributing essential food and water supplies.

“So many souls lost, so many properties destroyed. But one thing we still have is our resilience. Our resilience shines through even in the face of adversity,” she continues.

But where do resilience and adaptability come from? How can we unlock brain science to leverage the powers of youth creativity and cooperation and overcome the multiple crises faced by Yakura’s community and millions of other young people?

The European Brain Council and partner organizations, including UNICEF and UNODC, are joining forces to explore the ways in which brain health and brain science can reshape and improve policy and practice to support the advancement of humanity and the planet. The two entities are co-sponsoring a two-day summit, held from 19 to 20 September at the 79th UN General Assembly, on adolescent brain development and systemic policy change.

A series of UNODC-UNICEF papers being launched at the summit combine neuroscience and mental health research with data; exploration of community-driven innovations; and voices of youth such as Yakura’s from the frontline of climate change, violence and inequality. The papers highlight the potential that scientific understanding of the adolescent brain has for advancing policy change and protecting and uplifting vulnerable children and adolescents.

As Dr. Joanna Lai, Health Specialist at UNICEF explains: “Adolescents are full of potential but at the same time uniquely vulnerable, especially when faced with adverse experiences. To uplift them, we are advocating for policy and practice change across sectors that is based on a deep understanding of their development, ensuring timely, empathetic, and empowering intervention.”

Support in adversity

As noted by Alexandra Martins, Global Team Leader, END Violence Against Children at UNODC and co-panelist at the joint session, such research is needed now more than ever: “Hundreds of millions of children and adolescents are not able to grow up in an environment that supports healthy development and protection1. Every seven minutes, an adolescent dies as a result of violence. 15 to 19 year-olds are three times more likely to die violently than 10 to 14-year-olds. 15 million girls are victims of rape in their lifetime. At least 130 million adolescents, between the ages of 13 and 15, endure bullying in school. And we are not even accounting for the trauma being endured by young people affected by climate change and forced displacement.”

Chronic stress and violence can profoundly affect the development of the human brain, particularly during early childhood and teenage years. It may disrupt the developmental stages of neural networks; cause physical health degradation and brain aging; and modify learning and social connectedness. In the context of criminal justice and community safety, we know that children and adolescents who offend are disproportionately more likely to have experienced victimization and trauma.

But the adolescent brain, UNODC and UNICEF contend, is not only vulnerable to adversity and violence; it is also resilient, creative and flexible.

Adaptive and resilient – with the right support

As the UNODC-UNICEF papers highlight, adolescents’ brains are adaptive and young people are resilient problem-solvers when provided with the proper social support.Adolescents – be they survivors of adversity, violence or crime – can be co-authors and creative agents of policy change and innovation.

It is not only important to build awareness of the way in which adversity, violence and trauma negatively alter adolescent brain development but also to understand that the brain – especially the adolescent brain – is neither a static organ nor a fixed story. Science tells us that the adolescent brain has a unique and adaptive ability to rewire itself on the basis of its environment. A young person’s brain is particularly well-designed to rapidly forge new circuitry and behavioral pathways for resilience if health, education and justice systems provide the appropriate support.

Mohammed*, another Nigerian UNODC Youth Peace Champion, recently took part in an innovative peacebuilding training programme that combined neuroeducation with capacity building on the relationship between brain development, chronic stress, adversity and violence. “I was limited and could not see outside the box, but now I’m more open-minded and see things in better proportion,” he says. “I can now understand their [children’s] challenges and come up with a solution for them to be resilient and overcome their challenges and low self-esteem”.

“My rehabilitation and reintegration skills have been improved,” he continues. “I’m confident that within the context of insecurity, I can play a significant role in engaging with victims.”

 

Source: https://www.unodc.org/unodc/frontpage/2024/September/unlocking-the-science-of-adolescence-to-promote-effective-policy-and-practice.html

Abstract

Background

Youth in disadvantaged socio-economic circumstances in South Africa face significant risks to their physical and mental well-being due to exposure to harmful behaviours. More than 50% of the global disease burden is attributed to non-communicable diseases linked to such behaviours. While interventions have been initiated to address these risks, the limited reduction in risky behaviour necessitates closer examination and the exploration of more targeted or innovative approaches for effective mitigation.

Objectives

To explore existing health risk behaviour prevention/intervention programmes targeting youth, focusing on decreasing risky behaviour engagement and to discuss the success of the intervention used.

Methods

Three electronic databases were searched from 2009 until November 2023. Studies specifically reported using an intervention programme in youth or adolescents aged 9 to 19 were included. Data extracted included age, grade, sample size, targeted risky behaviour, and outcome.

Results

A total of 1072 articles were screened across three major databases, and of the nine included studies, n = 7 yielded mild to moderate intervention success results. The use of incentives yielded unsuccessful results. The most successful intervention strategy identified was school-based intervention programmes targeting multiple risky behaviours.

Conclusion

School interventions combining counselling, electronic screening, and personalized feedback effectively modified behaviour, while incentive-based programs had minimal impact. This underscores the importance of targeted interventions to discourage risky behaviour among young people.

Clinical implications

Effective intervention and prevention programs targeting health risk behaviours in youth are essential in safeguarding their mental and physical well-being. A clear link between risky behaviour engagement and the potential development of non-communicable diseases or trauma should be emphasised.
The full article can be accessed by clicking on the Source link below:
Source: https://www.springermedizin.de/health-risk-behaviour-prevention-intervention-programmes-targete/27472880

   Youth Today magazine

Summary

“The Youth Risk Behavior Survey Data Summary & Trends Report provides data on health behaviors and experiences of high school students in the United States. Data highlight students’ behaviors and experiences in 2023, changes from 2021 to 2023, and 10-year trends. The report focuses on six key areas:

  1. Sexual behavior
  2. Substance use
  3. Experiences of violence
  4. Mental health
  5. Suicidal thoughts and behaviors
  6. Other important issues, like social media use

Key Findings

  • In 2023, female students and LGBTQ+ students experienced more violence, signs of poor mental health, and suicidal thoughts and behaviors than their male and cisgender and heterosexual peers.
  • From 2021 to 2023, there were early signs that adolescent mental health is getting better. There were also concerning increases in students’ experiences of violence at school.
  • From 2013 to 2023, 10-year trends were similar to what data showed in 2021. There were decreases in students’ use of substances. There were increases in students’ experiences of violence, signs of poor mental health, and suicidal thoughts and behaviors. Students’ sexual activity decreased, but so did their protective sexual behaviors, like condom use.”

Read Full Report →

[Related report: 2024 U.S. national survey on the mental health of LGBTQ+ young people]

[Related: As more youth struggle with behavior and traditional supports fall short, clinicians are partnering with lawyers to help

Source: https://youthtoday.org/2024/08/youth-risk-behavior-survey-2013-2023/

Written by Ania Wellere, Master of Public Health Candidate, UNC Gillings School of Global Public Health.

As many know, drinking alcohol in a licensed premise under the age of 18 is against the law in the UK, however those aged 16 or 17 and accompanied by an adult can drink but not buy beer, wine, or cider with a meal. However, with relatively high alcohol use among children and young people in the UK, is the flexibility of this law one of many factors contributing to heavy episodic drinking among this population?

Youth drinking

According to Truque et al. (2023), 25% of adolescents in Europe begin to consume alcohol as early as the age of 13, and depending on region and gender, the prevalence of weekly alcohol consumption from adolescents is anywhere from 2%-33%. In 2021, NHS England found that the proportion of 15-year-olds who reported drinking at least once a month was 36%, with 14% saying at least weekly. Specifically in England, the World Health Organization found that the proportion of 13-year-olds who had consumed alcohol was far higher than the Health Behaviour in School-aged Children (HBSC) average – which covers 44 countries – and in Scotland and Wales.

Several factors influence children and young people’s alcohol use. One of the primary reasons young people give for why they drink at a young age is because of their peers. Drinking interest stems from failure to miss out, pressure to drink, and an attempt to improve their social status.

There are also some non-consensual factors, particularly outdoor advertising, but also advertising in magazines and television, that could be fuelling underage drinking because of its appeal to younger audiences. Children and young people do not ask to be exposed to these advertisements, and they cannot always filter the advertisements that they see through these mediums.

Despite regulatory efforts and codes that have been in place to protect children from alcohol marketing, researchers believe that attempts to protect children through the regulatory system and codes are failing. Several councils across the UK have taken the initiative to establish local policies that restrict advertisements of unhealthy commodities, including alcohol. If more local authorities follow suit in creating policies to restrict alcohol advertising, it would protect children and young people from exposure and potential alcohol-related harms.

Effect on the adolescent brain

Although youth drinking is slowly decreasing across the UK, heavy episodic drinking and its health impact is still a concern amongst adolescents, especially the effect alcohol has on the adolescent brain. Research on the effect alcohol has on the adolescent brain is limited. Research has typically focused on the impact alcohol has on the adult brain and the relationship between alcohol dependence and increased risk of dementia and other chronic diseases.

Before diving into the specific impact alcohol has on adolescent brains, it is important to lay out the process of how alcohol even travels through the body. So envision this: you take your first sip, and the alcohol makes its way through the stomach and into your bloodstream through the walls of your small intestine, where the blood will take the alcohol throughout the rest of your body. Alcohol then makes its way quickly to your brain, kidneys, lungs, and liver via the bloodstream. The way these parts of the body act is also contingent on the amount of alcohol that is in the bloodstream. For the brain, alcohol can impact your thought processes, emotions, memory, and coordination.

For an adolescent, alcohol moves through the body and breaks down slower than other age groups. The brains of adolescents have an increased likelihood of being negatively impacted compared to adult brains, according to the National Institute on Alcohol Abuse and Alcoholism. For young heavy episodic drinkers, brain development, structure, and function could possibly be altered compared to young non-heavy episodic drinkers, as seen through neuroimaging.

This impact on the brain has been noted to significantly affect the executive function of the adolescent brain. Executive function is defined as the mental processes that help an individual set and carry out their goals. Scientific evidence shows that weakened executive functions cause young people to make more errors and struggle with their shifting abilities (i.e., the ability to adapt). In the long run, this can follow young heavy episodic drinkers to adulthood.

In more technical terms, adolescent heavy episodic drinking is associated with a greater risk of reductions in grey matter during adolescence and disrupts white matter integrity, impacting neurocognitive functioning, according to Chikritzhs et al. (2024). In simple terms, the brain’s grey matter that helps individuals control movement, memory, and emotions is reduced, and white matter that allows the brain to exchange information and gives the ability to concentrate and learn is disrupted.

With these types of tissues being impacted by alcohol at a young age, there is research that has highlighted some of the risk factors that have come to disturb the lives of young heavy episodic drinkers when they become adults. A study including about 488,000 Swedish men found that heavy episodic drinking in adolescence was one of the strongest risk factors for developing early-onset dementia in adulthood.

As adolescence is a critical phase of development, more protective measures are put in place to reduce alcohol use among adolescents and, as a result, reduce alcohol-related harm to their brains. These protective measures usually include regulation of youth’s access to alcohol and alcohol advertising.

As we know, alcohol marketing is causally linked to young people drinking more and at an earlier age, and much of this marketing is non-consensual. To protect children’s rights, ‘the state must do all it can, through passing legislation and creating administrative systems, to promote and protect children’s rights’, according to the United Nations Convention on the Rights of the Child.

The brain is a vital organ to the body, and adolescent brain health is critical. With alcohol being accessible to children and young people in the UK, a ban on alcohol marketing should be taken into consideration. In addition, the normalisation of alcohol use among young people has to be put to an end, and that may start in the home with parents reshaping how they communicate alcohol use with their children and not encouraging drinking behaviour. Furthermore, future research should look at the differences between light to moderate and heavy drinking among adolescents to see if the effects on the brain are drastically different.

Source: https://www.ias.org.uk/2024/08/01/alcohol-and-its-impact-on-the-adolescent-brain/

Background: Most violent crimes (52 %) are committed by adults aged 18-34, who account for 23 % of the US population and have the highest prevalence of cannabis use and cannabis use disorder (CUD). We examined whether and how associations of cannabis use, use frequency, and CUD with violent behavior (i.e., attacking someone with the intent to harm seriously) vary by sex in U.S. young adults.

Methods: Data were from 113,454 participants aged 18-34 in the 2015-2019 US National Surveys on Drug Use and Health, providing nationally representative data on cannabis use, CUD (using DSM-IV criteria), and violent behavior. Descriptive analyses and bivariate and multivariable logistic regression analyses were conducted.

Results: Among U.S. adults aged 18-34, 28.9 % (95 % CI = 28.5-29.2 %) reported past-year cannabis use (with/without CUD), including 20.5 % (95 % CI = 20.2-20.8 %) with non-daily cannabis without CUD, 4.7 % (95 % CI = 4.5-4.8 %) with daily cannabis use without CUD, 2.1 % (95 % CI = 1.9-2.2 %) with non-daily cannabis use and CUD, and 1.7 % (95 % CI = 1.5-1.8 %) with daily cannabis use and CUD. Past-year adjusted prevalence of violent behavior was higher among males with daily cannabis use but without CUD (2.9 %, 95 % CI = 2.4-2.7 %; adjusted prevalence ratio (PR) = 1.7, 95 % CI = 1.3-2.2) and males with daily cannabis use and CUD (3.1 %, 95 % CI = 2.3-4.0 %; adjusted PR = 1.8, 95 % CI = 1.3-2.4) than males without past-year cannabis use (1.7 %, 95 % CI = 1.6-1.9 %). Adjusted prevalence of violent behavior was higher among females with cannabis use regardless of daily cannabis use/CUD status (adjusted prevalence = 1.6-2.4 %, 95 % CIs = 0.9-3.2 %; adjusted PRs = 1.6-2.4, 95 % CI = 1.3-3.2) than females without past-year cannabis use (1.0 %, 95 % CI = 0.9-1.1 %).

Conclusions: Research is needed to ascertain the directionality of the associations between cannabis use and violent behavior and underlying sex-specific mechanism(s). Our results point to complex sex-specific relationships between cannabis use frequency, CUD, and violent behavior and highlight the importance of early screening for and treatment of CUD and of preventive interventions addressing cannabis misuse.

Keywords: Attacking someone with the intent to seriously hurt them; Cannabis use; Cannabis use disorder; Violent behavior.

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Source: https://pubmed.ncbi.nlm.nih.gov/38677161/

BY JULIA MARNIN –  AUGUST 02, 2024

 

A New Jersey man caused the diversion of a flight due to his dangerous behavior and was arrested when the plane landed, feds say. Jan Rosolino via Unsplash An American Airlines passenger forced a Dallas-bound flight to land in a different city because of his “violent” and dangerous behavior, including repeated attempts to open the plane’s doors and his assault on a flight attendant, federal prosecutors said. The flight crew and passengers had to restrain Eric Nicholas Gapco’s hands and feet with flexible restraints until the flight from Seattle landed in Salt Lake City on July 18, according to the U.S. Attorney’s Office for the District of Utah. Gapco, 26, of Delanco, New Jersey, was arrested when the flight landed, according to prosecutors. Gapco continued “to engage in violent and erratic behavior” at the Salt Lake City International Airport, where he smashed the glass door of a holding cell, court documents say. He denied consuming illegal drugs or prescription medication, but later told his arresting officers he ate “approximately ten marijuana edibles,” according to a motion for his detention. Gapco said he didn’t know how much THC, a psychoactive component of the cannabis plant, was in each edible, the motion says. Gapco was indicted July 31 on charges of interference with a flight crew and attempted damage to an aircraft, the U.S. Attorney’s office said in a news release. His federal public defender didn’t immediately respond to McClatchy News’ request for comment on Aug. 1. On the July 18 flight, prosecutors said Gapco wouldn’t stay in his seat, tried to take a flight attendant’s seat, “propositioned a flight attendant for sex,” was loud, yelling, vaping and disrupting others. He also locked himself in a plane bathroom, went on to try to open the flight’s doors and is accused of trying to hand another passenger a bag of pills, according to prosecutors. Gapco “assaulted and intimated a flight attendant and aircraft crew members,” prosecutors said. “The safety and security of our customers and team members is our top priority,” American Airlines told McClatchy News in a statement on Aug. 1. “We thank our team members for their professionalism and our customers for their understanding.” American Airlines didn’t immediately respond to McClatchy News’ request for comment on Aug. 1. After Gapco broke a glass door at the Salt Lake City airport following his arrest, Gapco was taken to a hospital to be medically evaluated, according to prosecutors. “He continued to be belligerent” and “combative with medical staff and the police,” prosecutors wrote in the motion for his detention. “At one point, he spat on an officer.” Galco’s temporary detention was granted on July 23, court records show. He is due to appear for his initial appearance in court the afternoon of Aug. 1, prosecutors said.

Source: https://www.sacbee.com/news/nation-world/national/article290654789.html

 

Suicide rate among Native American population is second-highest in the state

UPDATED: 

In 2020, Assemblymember James C. Ramos, D-San Bernardino, celebrated the creation of the state’s new Office of Suicide Prevention.

Four years later, more work remains to be done, he and other Native American leaders say.

Despite making up only 3.6% of Californians in 2020, American Indians or Alaskan Natives made up 9.8% of those who killed themselves that same year, according to the California Department of Public Health. Nationally, Native American populations are more than twice as likely as Black or White populations to die due to deaths of “despair” — suicidedrug overdoses and alcoholic liver disease — according to a UCLA Health survey released in April.

On Wednesday, July 17, Ramos — author of  Assembly Bill 2112, which created the Office of Suicide Prevention — gathered with representatives of Inland Empire tribes at the Morongo Band of Mission Indians’ Tribal Council Chambers in a roundtable to discuss the need for more help preventing suicide among Native Americans.

“We’ve had incidents where young members have taken their lives,” said Soboba Band of Luiseno Indians Chairperson Isaiah Vivanco. “Life is so precious, and when we have young ones taking their own lives, it has to be (a warning), it has to be an issue.”

Tribal leaders said that, too often, health professionals don’t understand native culture, and end up pushing those who need help away.

“Culture is healing as well,” said Soboba tribal secretary Monica Herrera. “Sometimes (mental health) facilities don’t recognize that (patients) are Native American and that sweat lodge or praying or some type of cultural healing is not encouraged. ‘We can’t take you to the sweat lodge; it’s against our policies.’ “

California health officials vowed to do better at the meeting.“Our traditional behavioral health system has woefully failed Native American populations,” California Health and Human Services Deputy Secretary of Behavioral Health Stephanie Welch told the tribal leaders. “There are high rates of suicide, there are high rates of self-harm as I have heard in the room, and there are high rates of drug misuse and overdose.”

Native communities aren’t using existing mental and behavioral health resources, state officials reported.

“When I see statistics around low utilization of behavioral health services, that’s on us,” Welch said. “Behavioral health services has not traditionally reflected the acceptance of (the) cultural, linguistic and geographical diversity that’s needed to address the needs of Native Americans communities.”

The department knows that it isn’t reaching many groups that need its mental health services and has embarked on a new initiative, “Mental Healthcare for All,” she said.

“And that truly means all of us and it needs to be inclusive of California Native Americans,” Welch said. “Everybody should have access to affordable, equitable, and most importantly, culturally responsive mental health and substance use disorder (treatment).”

As part of the effort, the state is investing in mobile clinics to bring services directly to tribal communities.

Within five years, Welch said, her agency hopes to have culturally appropriate mental health counselors available on mental health crisis lines in the state. In the meantime, her team is examining gaps in existing services when it comes to meeting the needs of California’s Native American population, along with identifying barriers that prevent the community from accessing healthcare options.

More mental health resources should be on the way.

Voters approved Proposition 1 in the March 5 primary election this year, authorizing a nearly $6.4 billion bond for facilities for mental health or substance abuse treatment.

“We want to make sure that California’s first people are not left out of that equation,” Ramos said.

Source: https://www.eastbaytimes.com/2024/08/04/california-needs-to-do-more-to-prevent-suicide-among-native-americans-tribal-leaders-say/

How can modern psychedelic research and traditional approaches integrate to address substance use disorders and mental health challenges?

A recent study published in the Journal of Studies on Alcohol and Drugs discusses the history and current state of psychedelic research for the treatment of substance abuse disorders (SUDs).

Psychedelics

Psychedelics are consciousness-altering drugs, some of which include lysergic acid diethylamide (LSD), dimethyltryptamine (DMT), psilocybin, and mescaline. Methylenedioxymethamphetamine (MDMA) and ketamine are also considered psychedelics; however, these drugs have different mechanisms of action.

Although psychedelics have been exploited for centuries to induce altered states of consciousness, their use, as opposed to their abuse, has largely been unexplored in modern medicine. In fact, several studies have indicated the potential utility of psychedelics for individuals who have mental illness due to traumatic experiences, false beliefs, and unhealthy behavioral patterns, such as posttraumatic stress disorder (PTSD) and depression.

The recent coronavirus disease 2019 (COVID-19) pandemic led to global changes in the use of methamphetamine, alcohol, and cannabis, as well as a significant increase in opioid overdoses in the United States. Thus, another promising application of psychedelics is their potential use for treating SUDs.

However, restrictive policies, poor funding, lack of equitable and diverse recruitment and access, as well as the multiplicity of small-scale psychedelic research programs have prevented researchers from effectively investigating the effects of psychedelics in the treatment of SUDs.

Overview

Over the past seven decades, researchers have become increasingly interested in examining the potential use of psychedelics in traditional medicine. Despite federal policies banning recreational drug use, researchers have elucidated some of the biological effects of psychedelics on the central nervous system (CNS) and their potential role in the treatment of SUDs. Nevertheless, there remains a lack of well-controlled multi-center trials and systematic reviews in this area.

As researchers continue to examine the pharmacological potential of these drugs, it is crucial to address their addiction and abuse potential, the legalization of recreational drugs, and the attempts of pharmaceutical companies to introduce high-selling psychedelics as therapies for mental illness.

History and current use of psychedelics

Psychedelics like ayahuasca, Peyote, and psilocybin-containing mushrooms have been used throughout history by traditional healers and indigenous communities for both spiritual and health purposes. By recognizing these contributions, researchers can benefit from the potential benefits of traditional usage patterns while investigating the use of these drugs for treating SUDs and other mental health disorders.

For example, a hybridized SUD therapy program in Peru utilizes ayahuasca to treat alcohol and drug use. At one year following treatment, reduced depression and anxiety, higher quality of life, and reduced severity of addiction have been reported.

One notable contribution is the acknowledgment that key experiences of treatment participants might provide more insight than the search for putative “active ingredients” of interventions as complex as psychedelic-assisted treatment.”

Purging in psychedelic treatment

Psychedelic use, specifically ayahuasca use, is closely linked to vomiting as a means of purging the body. This is reported to have spiritual, Amazonian, and clinical benefits.

Conclusions

The optimal approach to psychedelic-assisted treatment involves mutual respect for and recognition of the value of both traditional and modern applications. Thus, mixed-methods research is crucial, as traditional approaches may help identify a better therapeutic agent or program than traditional approaches to identifying and isolating active ingredients.

However, it is essential to evaluate and quantify the success rates of traditional approaches to psychedelic use, as well as elucidate the biological mechanisms that may contribute to their therapeutic effects. Researchers must recognize and credit traditional history and practices throughout these efforts to protect these cultures from being exploited, ignored, and suppressed by pharmaceutical industries.

The rush to patent processes in psychedelic treatments of addiction and other psychiatric conditions reflects the enormous greed of private commercial entities to benefit financially from vulnerable patients in need of effective therapies.

Thus, regulatory control of psychedelic therapies is vital to establish rigorous research standards that can lead to the generation of sufficient evidence in this area. Without this type of overview, private corporate interests may seek to exploit governmental support for crucial research needed to address these mental health issues.

Source:  https://www.news-medical.net/news/20240828/Psychedelics-A-new-hope-for-substance-abuse-treatment.aspx

How much should we worry?

American parents have been warning teenagers about the dangers of marijuana for about 100 years. Teenagers have been ignoring them for just as long. As I write this, a couple of kids are smoking weed in the woods just yards from my office window and about a block and a half from the local high school. They started in around 9 A.M., just in time for class.

Exaggerating the perils of cannabis—the risks of brain damage, addiction, psychosis—has not helped. Any whiff of Reefer Madness hyperbole is perfectly calibrated to trigger an adolescent’s instinctive skepticism for whatever an adult suggests. And the unvarnished facts are scary enough.

We know that being high impairs attention, memory and learning. Some of today’s stronger varieties can make you physically ill and delusional. But whether marijuana can cause lasting damage to the brain is less clear.

A slew of studies in adults have found that nonusers beat chronic weed smokers on tests of attention, memory, motor skills and verbal abilities, but some of this might be the result of lingering traces of cannabis in the body of users or withdrawal effects from abstaining while taking part in a study. In one hopeful finding, a 2012 meta-analysis found that in 13 studies in which participants had laid off weed for 25 days or more, their performance on cognitive tests did not differ significantly from that of nonusers.

But scientists are less sanguine about teenage tokers. During adolescence the brain matures in several ways believed to make it more efficient and to strengthen executive functions such as emotional self-control. Various lines of research suggest that cannabis use could disrupt such processes.

For one thing, recent studies show that cannabinoids manufactured by our own nerve cells play a crucial role in wiring the brain, both prenatally and during adolescence. Throughout life they regulate appetite, sleep, emotion, memory and movement—which makes sense when you consider the effects of marijuana. There are “huge changes” in the concentration of these endocannabinoids during the teenage years, according to neurologist Yasmin Hurd of the Icahn School of Medicine at Mount Sinai, which is why she and others who study this system worry about the impact of casually dosing it with weed.

Brain-imaging studies reinforce this concern. A number of smallish studies have seen differences in the brains of habitual weed smokers, including altered connectivity between the hemispheres, inefficient cognitive processing in adolescent users, and a smaller amygdala and hippocampus—structures involved in emotional regulation and memory, respectively.

More evidence comes from research in animals. Rats given THC, the chemical that puts the high in marijuana, show persistent cognitive difficulties if exposed around the time of puberty—but not if they are exposed as adults.

But the case for permanent damage is not airtight. Studies in rats tend to use much higher doses of THC than even a committed pothead would absorb, and rodent adolescence is just a couple of weeks long—nothing like ours. With brain-imaging studies, the samples are small, and the causality is uncertain. It is particularly hard to untangle factors such as childhood poverty, abuse and neglect, which also make their mark on brain anatomy and which correlate with more substance abuse, notes Nora Volkow, director of the National Institute on Drug Abuse and lead author of a superb 2016 review of cannabis research in JAMA Psychiatry.

To really sort this out, we need to look at kids from childhood to early adulthood. The Adolescent Brain Cognitive Development study, now under way at the National Institutes of Health, should fill the gap. The 10-year project will follow 10,000 children from age nine or 10, soaking up information from brain scans, genetic and psychological tests, academic records and surveys. Among other things, it should help pin down the complex role marijuana seems to play in triggering schizophrenia in some people.

But even if it turns out that weed does not pose a direct danger for most teens, it’s hardly benign. If, like those kids outside my window, you frequently show up high in class, you will likely miss the intellectual and social stimulation to which the adolescent brain is perfectly tuned. This is the period, Volkow notes, “for maximizing our capacity to navigate complex situations,” literally building brainpower. On average, adolescents who partake heavily wind up achieving less in life and are unhappier. And those are things a teenager might care about.

Source: https://www.scientificamerican.com/article/what-pot-really-does-to-the-teen-brain/ December 2017

Abstract

Studies examining lifestyle and cognitive decline often use healthy lifestyle indices, making it difficult to understand implications for interventions. We examined associations of 16 lifestyles with cognitive decline. Data from 32,033 cognitively-healthy adults aged 50-104 years participating in prospective cohort studies of aging from 14 European countries were used to examine associations of lifestyle with memory and fluency decline over 10 years. The reference lifestyle comprised not smoking, no-to-moderate alcohol consumption, weekly moderate-plus-vigorous physical activity, and weekly social contact. We found that memory and fluency decline was generally similar for non-smoking lifestyles. By contrast, memory scores declined up to 0.17 standard deviations (95% confidence interval= 0.08 – 0.27) and fluency scores up to 0.16 standard deviations (0.07 – 0.25) more over 10 years for those reporting smoking lifestyles compared with the reference lifestyle. We thus show that differences in cognitive decline between lifestyles were primarily dependent on smoking status.

Source: https://www.nature.com/articles/s41467-024-49262-5 June 2024

More than 178 000 people died from excessive alcohol use in the US during 2020 to 2021, surpassing deaths from the overdose epidemic.1 Excessive drinking is now the leading cause of preventable death in the US.1 Alcohol use disorder (AUD) most commonly begins during adolescence, although rarely is it identified and treated at this age.2 We urgently need interventions that allow us to better identify those young people at risk of developing AUD and alcohol-related complications later in adulthood. In their study of alcohol use among youths with a chronic medical condition (CMC), Weitzman et al3 describe a novel approach for alcohol prevention in a population of youths with medical vulnerability. Youths with a CMC are particularly susceptible to the effects of alcohol and warrant particular attention. Although the rate of alcohol use among these youths is similar to that of their peers, youths with a CMC have higher rates of progression to heavy alcohol use and AUD.4 Weitzman et al3 found that high-risk alcohol use occurred in more than 1 of 10 youths (aged 14-18 years) with a CMC seen in the specialty clinics included in their study. These youths also have an increased risk of treatment nonadherence and potential medication reactions with alcohol as a result of the underlying disease, worsening the potential effects of high-risk alcohol exposure in this population.4

Given these disparities, Weitzman et al3 designed a randomized clinical trial aimed at evaluating the effects of the Take Good Care (TGC) alcohol use prevention intervention over 12 months among youths with a CMC. In the specialty clinic setting, youths in the intervention group received a brief, personalized intervention consisting of a self-administered slide deck on an electronic tablet. Slides were disease tailored, and they included specific effects of alcohol use on disease processes, treatment safety, and efficacy as well as motivational information on health-protecting decisions and behaviors. Although there was no change among youths reporting no or minimal (low-risk) alcohol use, there was a 40% relative reduction in self-reported frequency of alcohol use among those receiving the TGC intervention who reported high-risk alcohol use at baseline compared with those who received treatment as usual.

The study by Weitzman et al3 highlights the potential importance of brief interventions in changing youth behavior, particularly among a group of youths who are medically vulnerable. Although a shocking 11.5% of youths with a CMC in this study reported high-risk alcohol use at baseline, nationally only a quarter of pediatricians report using validated screening tools to assess alcohol use among adolescents and only 11% of pediatricians correctly use the Screening, Brief Intervention, and Referral to Treatment (SBIRT) tool recommended by the American Academy of Pediatrics.5 Despite growing evidence supporting the benefit of SBIRT for pediatric populations, barriers to implementation include insufficient time and need for clinician training5; both of these barriers are ameliorated with the use of the self-administered, electronic intervention described by Weitzman et al.3 This study adds to the growing database highlighting the effectiveness of SBIRT in identifying and intervening in instances of substance use among youths. It presents a tool easily adopted by clinicians, with an impact on those youths at greatest risk of developing problematic alcohol use.

Considering the prevalence of alcohol use among youths with CMCs, an important aspect of the study by Weitzman et al3 is its low-touch intervention that can be easily adapted and implemented in a variety of clinical settings. Weitzman et al3 show the value of even simple, low-touch interventions in changing youth behavior. From the patient perspective, the use of an electronic tablet enhances privacy when answering questions and allows for flexibility in time spent on each piece of content. From the clinician perspective, the use of an electronic tablet requires minimal additional effort or training, standardizes the content provided, and allows for intervention completion outside of face-to-face appointment time. Yet despite its simplicity, the low-touch TGC intervention has been shown to exert a substantial effect on adolescent behavior. At 12 months, the reduction in alcohol use frequency among youths with a CMC and high-risk alcohol use represents not only a meaningful behavioral change but also an enduring one.

In contrast with traditional fear-based messages around alcohol prevention, Weitzman et al3 demonstrate the impact of a strengths-based model that engages the normal adolescent quest for independence and the examination of choice in larger contexts. The TGC intervention educated youths with a CMC on disease-specific processes, treatments, and effects of alcohol, thereby encouraging reflection around alcohol-related choices. In presenting this information for youths to consider, the intervention relayed respect for patients’ ability to engage in their own health care and health behaviors. Additionally, disease-tailored content paired with motivational information on health-protecting behaviors encouraged patients’ sense of autonomy and independence. The statistically significant effects of this approach suggest that personalized intervention resonates with youths with CMCs and is an effective tool for behavioral change. Furthermore, this delivery model allows for content to be tailored based on disease or other aspects of youths’ lived experience. Content adjusted to the needs of specific subpopulations of youths creates interventions that they connect with and are thus most greatly affected by, in both depth and longevity of impact.

Finally, key to the study by Weitzman et al3 is the intervention location; utilization of the specialty care setting for an alcohol use prevention intervention is novel and effective. Many youths with a CMC receive the majority of their care in the specialty care setting and, accordingly, often develop stronger therapeutic relationships with their specialty care physician than their primary care physician. In 41.3% of visits to their specialists, youths with a CMC present for routine preventative care,6 yet specialists screen for substance use at alarmingly low rates compared with their primary care counterparts (self-reported 8% vs 38%, respectively).7 Interventions within the specialty clinic space allow for greater potential to reach more youths with CMCs at critical moments in their health journeys, thereby curbing heavy alcohol use, its associated medication nonadherence, and potential interaction with medications. By doing so, this method of intervention may decrease disease-associated complications and mortality in addition to alcohol-associated complications and mortality among youths with CMCs, and by extension, the adults that they become. The TGC intervention and its broader application represent an exciting new paradigm for future practice.

Source: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2820973 July 2024

Source: Email from Ed Moses to Drug Watch International drug-watch-international@googlegroups.com August 2017

This is The Drug Report’s Friday Fact report – The rate of violent behavior in daily marijuana users aged 18-34 was nearly twice the violent behavior rate of non-users

The study “Associations of cannabis use, use frequency, and cannabis use disorder with violent behavior among young adults in the United States” was recently published by Nora D. Volkow and the team at NIDA. The study found that the rate of violent behavior in daily marijuana users aged 18-34 was nearly twice the violent behavior rate of non-users.

The study consisted of 113,434 participants, aged 18 to 34, and relied on data from the 2015-2019 National Surveys on Drug Use and Health (NSDUH).

The datasets provided information on the rates of daily marijuana use, whether the participants had Cannabis Use Disorder, and violent behavior. The study found:

The violence behavior rates for both males and females who were daily marijuana users and had Cannabis Use Disorder were close to doubling that of males and females who were non-marijuana users.

Source: Email from Smart Approaches to Marijuana (SAM) reply@learnaboutsam.org May 2024

Bertha Madras, a leading expert on weed, outlines the science linking it to psychiatric disorders, permanent brain damage, and other serious harms.

Young people who smoked marijuana in the 1960s were seen as part of the counterculture. Now the cannabis culture is mainstream. A 2022 survey sponsored by the National Institutes of Health found that 28.8% of Americans age 19 to 30 had used marijuana in the preceding 30 days—more than three times as many as smoked cigarettes. Among those 35 to 50, 17.3% had used weed in the previous month, versus 12.2% for cigarettes.

While marijuana use remains a federal crime, 24 states have legalized it and another 14 permit it for medical purposes. Last week media outlets reported that the Biden administration is moving to reclassify marijuana as a less dangerous Schedule III drug—on par with anabolic steroids and Tylenol with codeine— which would provide tax benefits and a financial boon to the pot industry.

Bertha Madras thinks this would be a colossal mistake. Ms. Madras, 81, is a psychobiology professor at Harvard Medical School and one of the foremost experts on marijuana. “It’s a political decision, not a scientific one,” she says. “And it’s a tragic one.” In 2024, that is a countercultural view.

Ms. Madras has spent 60 years studying drugs, starting with LSD when she was a graduate student at Allan Memorial Institute of Psychiatry, an affiliate of Montreal’s McGill University, in the 1960s. “I was interested in psychoactive drugs because I thought they could not only give us some insight into how the brain works, but also on how the brain undergoes dysfunction and disease states,” she says.

In 2015 the World Health Organization asked her to do a detailed review of cannabis and its medical uses. The 41-page report documented scant evidence of marijuana’s medicinal benefits and reams of research on its harms, from  cognitive impairment and psychosis to car accidents.

She continued to study marijuana, including at the addiction neurobiology lab she directs at Mass General Brigham McLean Hospital. In a phone interview this week, she walked me through the scientific literature on marijuana, which runs counter to much of what Americans hear in the media.

For starters, she says, the “addiction potential of marijuana is as high or higher than some other drug,” especially for young people. About 30% of those who use cannabis have some degree of a use disorder. By comparison, only 13.5% of drinkers are estimated to be dependent on alcohol. Sure, alcohol can also cause harm if consumed in excess. But Ms. Madras sees several other distinctions.

One or two drinks will cause only mild inebriation, while “most people who use marijuana are using it to become intoxicated and to get high.” Academic outcomes and college completion rates for young people are much worse for those who use marijuana than for those who drink, though there’s a caveat: “It’s still a chicken and egg whether or not these kids are more susceptible to the effects of marijuana or they’re using marijuana for self medication or what have you.”

Marijuana and alcohol both interfere with driving, but with the former there are no medical “cutoff points” to determine whether it’s safe to get behind the wheel. As a result, prohibitions against driving under the influence are less likely to be enforced for people who are high. States where marijuana is legal have seen increases in car accidents.

One of the biggest differences between the two substances is how the body metabolizes them. A drink will clear your system within a couple of hours. “You may wake up after binge drinking in the morning with a headache, but the alcohol is gone.” By contrast, “marijuana just sits there and sits there and promotes brain adaptation.”

That’s worse than it sounds. “We always think of the brain as gray matter,” Ms. Madras says. “But the brain uses fat to insulate its electrical activity, so it has a massive amount of fat called white matter, which is fatty. And that’s where marijuana gets soaked up. . . . My lab showed unequivocally that blood levels and brain levels don’t correspond at all—that brain levels are much higher than blood levels. They’re two to three times higher, and they persist once blood levels go way down.” Even if people quit using pot, “it can persist in their brain for a while.”

Thus marijuana does more lasting damage to the brain than alcohol, especially at the high potencies being consumed today. Levels of THC—the main psychoactive ingredient in pot—are four or more times as high as they were 30 years ago. That heightens the risks, which range from anxiety and depression to impaired memory and cannabis hyperemesis syndrome—cycles of severe vomiting caused by long-term use.

There’s mounting evidence that cannabis can cause schizophrenia. A large-scale study last year that examined health histories of some 6.9 million Danes between 1972 and 2021 estimated that up to 30% of young men’s schizophrenia diagnoses could have been prevented had they not become dependent on pot. Marijuana is  worse in this regard than many drugs usually perceived as more dangerous.

“Users of other potent recreational drugs develop chronic psychosis at much lower rates,” Ms. Madras says. When healthy volunteers in research experiments are given THC—as has been done in 15 studies—they develop transient symptoms of psychosis. “And if you treat them with an antipsychotic drug such as haloperidol, those symptoms will go away.”

Marijuana has also been associated with violent behavior, including in a study published this week in the International Journal of Drug Policy. Data from observational studies are inadequate to demonstrate causal relationships, but Ms. Madras says that the link between marijuana and schizophrenia fits all six criteria that scientists use to determine causality, including the strength of the association and its consistency.

Ms. Madras says at the beginning of the interview that she was operating on three hours of sleep after crashing on scientific projects. Yet she is impressively lucid and energized. She peppers her explanations with citations of studies and is generous in crediting other researchers’ work.

Another cause for concern, she notes, is that more pregnant women are using pot, which has been linked to increased preterm deliveries, admissions of newborns into neonatal intensive care units, lower birth weights and smaller head circumferences. THC crosses the placenta and mimics molecules that our bodies naturally produce that regulate brain development.

“What happens when you examine kids who have been exposed during that critical period?” Ms. Madras asks. During adolescence, she answers, they show an increased incidence of aggressive behavior, cognitive dysfunction, and symptoms of ADHD and obsessive-compulsive disorders. They have reduced white and gray matter.

A drug that carries so many serious side effects would be required by the Food and Drug Administration to carry a black-box warning, the highest-level alert for drugs with severe safety risks. Marijuana doesn’t—but only because the FDA hasn’t cleared it.

The agency has selectively approved cannabis compounds for the treatment of seizures associated with Lennox-Gastaut or Dravet syndrome, nausea associated with chemotherapy for cancer, and anorexia associated with weight loss in AIDS patients. But these approved products are prescribed at significantly less potent doses than the pot being sold in dispensaries that are legal under state law.

What about medicinal benefits? Ms. Madras says she has reviewed “every single case of therapeutic indication for marijuana—and there are over 100 now that people have claimed—and I frankly found that the only one that came close to having some evidence from randomized controlled trials was the neuropathic pain studies.” That’s “a very specific type of pain, which involves damage to nerve endings like in diabetes or where there’s poor blood supply,” she explains.

For other types of pain, and for all other conditions, there is no strong evidence from high-quality randomized trials to support its use. When researchers did a “challenge test on normal people where they induce pain and tried to see whether or not marijuana reduces the pain, it was ineffective.”

Ms. Madras sees parallels between the marketing of pot now and of opioids a few decades ago. “The benefits have been exaggerated, the risks have been minimized, and skeptics in the scientific community have been ignored,” she says. “The playbook is always to say it’s safe and effective and nonaddictive in people.”

Advocates of legalization assert that cannabis can’t be properly studied unless the federal government removes it from Schedule I. Bunk, Ms. Madras says: “I have been able to study THC in my research program.” It requires more paperwork, but “I did all the paperwork. . . . It’s not too difficult.”

Instead of bankrolling ballot initiatives to legalize pot, she says, George Soros and other wealthy donors who “catalyzed this whole movement” should be funding rigorous research: “If these folks, these billionaires, had just taken that money and put it into clinical trials, I would have been at peace.”

It’s a travesty, Ms. Madras adds, that the “FDA has decided that they’re going to listen to that movement rather than to what the science says.” While the reclassification wouldn’t make recreational marijuana legal under federal law, dispensaries and growers would be able to deduct their business expenses on their taxes. The rescheduling would also send a cultural signal that marijuana use is normal.

Ms. Madras worries that “it sets a precedent for the future.” She points to the movement in states to legalize psychedelic substances, for whose medicinal benefits there also isn’t strong scientific evidence. Meantime, she says it makes no sense that politicians continuously urge more spending on addiction treatment and harm reduction while weakening laws that prevent people from becoming addicted in the first place.
Her rejoinder to critics who say the war on drugs was a failure? “This is not a war on drugs. It’s a defense of the human brain at every possible age from in utero to old age.”

Ms. Finley is a member of the Journal’s editorial board.

Source: https://www.wsj.com/articles/what-you-arent-reading-about-marijuana-permanent-brain-damage-biden-schedule-iii-9660395e May 2024

Foreword
The National Institute on Drug Abuse (NIDA) is pleased to publish in its Research Monograph series the proceedings of the 48th Annual Scientific Meeting of the Committee on Problems of Drug Dependence, Inc. (CPDD). This meeting was held at Tahoe City, Nevada, in June 1986.

The scientific community working in the drug abuse area was saddened by the untimely death of one of its very productive and active leaders: Joseph Cochin, M.D., Ph.D. Joe was a talented scientist who was greatly admired by his students and colleagues. For the past five years, Joe had served as the Executive Secretary of the CPDD. This monograph includes papers from a symposium on “Mechanisms of Opioid Tolerance and Dependence,” dedicated to his memory. These papers were presented by many of his friends and colleagues, who took the opportunity to express their high esteem for Joe.
The CPDD is an independent organization of internationally recognized experts in a variety of disciplines related to drug addiction. NIDA and the CPDD share many interests and concerns in developing knowledge that will reduce the destructive effects of abused drugs on the individual and society. The CPDD is unique in bringing together annually at a single scientific meeting an outstanding group of basic and clinical investigators working in the field of drug dependence. This year, as usual, the monograph presents an excellent collection of papers. It also contains progress reports of the abuse liability testing program funded by NIDA and carried out in conjunction with the CPDD. 

This program continues to represent an example of a highly successful government/private sector cooperative effort. I am sure that members of the scientific community and other interested readers will find this volume to be a valuable “state-of-the art” summary of the latest research into the biological, behavioral, and chemical bases of drug abuse.

Charles R. Schuster, Ph.D.
Director
National Institute on Drug Abuse

For the full contents, please go to: 

Source: https://babel.hathitrust.org/cgi/pt?id=ien.35557000188076&seq=11 This version September 2023

US DRUG CZAR EXPLAINS CAUSES AND RSDT TOOL TO PREVENT TEEN DRUG USE AND OVERDOSE DEATH INTERVIEW WITH U.S. DRUG CZAR JOHN WALTERS

Introduction:  In response to recent news of a huge increase in drug overdose deaths and arrests for drug trafficking among Fairfax County youths, Fox News TV5 reporter Sherri Ly interviewed U.S. Drug Czar John Walters for his expert views on the cause and potential cure for these horrific family tragedies.  Following is a transcript of that half-hour interview with minor editing for clarity and emphasis added.  The full original interview is available through the 11/26/08 Fox5 News broadcast video available at link:

WALTERS:  Well, as this case shows, while we’ve had overall drug use go down, we still have too many young people losing their lives to drugs, either through overdoses, or addiction getting their lives off track.  So there’s a danger.  We’ve made progress, and we have tools in place that can help us make more progress, but we have to use them

Q 1:  You meet with some of these parents whose children have overdosed.  What do they tell you, and what do you tell them?

WALTERS:  It’s the hardest part of my job; meeting with parents who’ve lost a child.  Obviously they would give anything to go back, and have a chance to pull that child back from the dangerous path they were on.  There are no words that can ease their grief.  That’s something you just pray that God can give them comfort.  But the most striking thing they say to me though is they want other parents to know, to actAnd I think this is a common thing that these terrible lessons should teach us.

Many times, unfortunately, parents see signs: a change in friends, sometimes they find drugs; sometimes they see their child must be intoxicated in some way or the other.  Because it’s so frightening, because sometimes they’re ashamed – they hope it’s a phase, they hope it goes away – they try to take some half measures.  Sometimes they confront their child, and their child tells them – as believably as they ever can – that it’s the first time.  I think what we need help with is to tell people; one, it’s never the first time.  The probability is low that parents would actually recognize these signs – even when it gets visible enough to them – because children that get involved in drugs do everything they can to hide it.  It’s never the first time.  It’s never the second time.  Parents need to act, and they need to act quickly.  And the sorrow of these grieving parents is, if anything, most frequently focused on telling other parents, “Don’t wait: do anything to get your child back from the drugs.”

Secondly, I think it’s important to remember that one of the forces that are at play here is that it’s their friends.  It’s not some dark, off-putting stranger – it’s boyfriends, girlfriends.  I think that was probably a factor in this case.  And it’s also the power and addictive properties of the drug.  So your love is now being tested, and the things you’ve given your child to live by are being pulled away from them on the basis of young love and some of the most addictive substances on earth.  That’s why you have to act more strongly.  You can’t count on the old forces to bring them back to safety and health.

Q 2:  When we talk about heroin – which is what we saw in this Fairfax County drug ring, alleged drug ring – what are the risks, as far as heroin’s concerned?  I understand it can be more lethal, because a lot of people don’t know what they’re dealing with?

WALTERS:  Well it’s also more lethal because one, the drug obviously can produce cardiac and respiratory arrest.  It’s a toxic substance that is very dangerous.  It’s also the case that narcotics, like heroin – even painkillers like OxyContin, hydrocodone, which have also been a problem – are something that the human body gets used to.  So what you can frequently get on the street is a purity that is really blended for people who are addicted and have been long time addicted.  So a person who is a new user or a naïve user can more easily be overdosed, because the quantities are made for people whose bodies have adjusted to higher purities, and are seeking that effect that only the higher purity will give them in this circumstance.  So it’s particularly dangerous for new users.  But we also have to remember, it almost never starts with heroin.  Heroin is the culmination here.  I think some of the – and I’ve only seen press stories on this — some of these young people may have gotten involved as early as middle school.

We have tools so that we don’t have to lose another young woman like this– or young men.  We now have the ability to use Random Student Drug Testing (RSDT) because the Supreme Court has, in the last five years, made a decision that says it can’t be used to punish.  It’s used confidentially with parents.  We have thousands of schools now doing it since the president announced the federal government’s willingness to fund these programs in 2004.  And many schools are doing it on their own.  Random testing can do for our children what it’s done in the military, what it’s done in the transportation safety industry– significantly reduce drug use.

First, it is a powerful reason not to start.  “I get tested, I don’t have to start.”  We have to remember, it’s for prevention and not a “gotcha!”  But it’s a powerful reason for kids to say, even when a boyfriend or girlfriend says come and do this with me, “I can’t do it, I get tested.  I still like you, I still want to be your friend; I still want you to like me, but I just can’t do this,” which is very, very powerful and important.  And second, if drug use is detected the child can be referred to treatment if needed.

Q 3:  Is the peer pressure just that much that without having an excuse, that kids are using drugs and getting hooked?

WALTERS:  Well one of the other unpleasant parts of my job is I visit a lot of young people in treatment; teenagers, sometimes as young as 14, 15, but also 16, 17, 18.  It is not uncommon for me to hear from them, “I came from a good family.  My parents and my school made clear what the dangers were of drugs.  I was stupid.  I was with my boyfriend (or girlfriend) and somebody said hey, let’s go do this.  And I started, and before I knew it, I was more susceptible.

We have to also understand the science, which has told us that adolescents continue to have brain development up through age 20-25.  And their brains are more susceptible to changes that we can now image from these drugs.  So it’s not like they’re mini-adults.  They’re not mini-adults.  They’re the particularly fragile and susceptible age group, because they don’t have either the experience or the mental development of adults.  That’s why they get into trouble, that’s why it happens so fast to them, that’s why it’s so hard for them to see the ramifications.

So what does RSDT do?  It finds kids early–­ if prevention fails.  And it allows us to intervene, and it doesn’t make the parent alone in the process.  Sometimes parents don’t confront kids because kids blackmail them and say “I’m going to do it anyway, I’m going to run away from home.”  The testing brings the community together and says we’re not going to lose another child.  We’re going to do the testing in high school – if necessary, in middle school.  We’re going to wrap our community arms around that family, and get those children help.  We’re going to keep them in school, not wait for them to drop out.  And we’re certainly not going to allow this to progress until they die.

Q 4:  And in a sense, if you catch somebody early, since you’re saying the way teenagers seem to get into drug use is a friend introduces it to a friend, and then next thing you know, you have a whole circle of friends doing it.  Are you essentially drying that up at the beginning, before it gets out of hand?

WALTERS:  That is the very critical point.  It’s not only helping every child that gets tested be safer, it means that the number of young people in the peer group, in the school, in the community that can transfer this dangerous behavior to their friends shrinks.  This is communicated like a disease, except it’s not a germ or a bacillus.  It’s one child who’s doing this giving it behaviorally to their friends, and using their friendship as the poison carrier here.  It’s like they’re the apple and the poison is inside the apple.  And they trade on their friendship to get them to use.  They trade on the fact that people want acceptance, especially at the age of adolescence.  So what you do is you break that down, and you make those relationships less prone to have the poison of drugs or even underage drinking linked to them.  And of course we also lose a lot of kids because of impaired driving.

Q 5:  And how does the drug testing program work, then, in schools– the schools that do have it.  Is it completely confidential?  Are you going to call the police the minute you find a student who’s tested positive for heroin or marijuana or any other illicit drug?

WALTERS:  That’s what is great about having a Supreme Court decision.  It is settled – random testing programs cannot be used to punish, to call law enforcement; they have to be confidential.  So we have a uniform law across the land.  And what the schools that are doing RSDT are seeing is that it’s an enormous benefit to schools for a relatively small cost.  Depending on where you are in the country, the screening test is $10-40.  It’s less than what you’re going to pay for music downloads in one month for most teenage kids in most parents’ lives.  And it protects them from some of the worst things that can happen to them during adolescence.  Not only dying behind the wheel, but overdose death and addiction.

 Schools that have done RSDT have faced some controversy; so you have to sit down and talk to people; parents, the media, young people.  You have to engage the community resources.  You’re going to find some kids and families that do have treatment needs.  But with RSDT you bring the needed treatment to the kids.

I tell, a lot of times, community leaders – mayors and superintendents, school board members – that if you want to send less kids into the criminal justice system and the juvenile justice system, drug test — whether you’re in a suburban area or in an urban area.

What does the testing do?  It takes away what we know is an accelerant to self-destructive behavior: crime, fighting in school, bringing a weapon, joining a gang.  We have all kinds of irrefutable evidence now – multiple studies showing drugs and drinking at a young age accelerate those things, make them worse, make them more violent, as well as increasing their risks of overdose deaths and driving under the influence.  So drug testing makes all those things get better.  And it’s a small investment to make everything else we do work better.

Again, drug testing is not a substitute for drug education or good parenting or paying attention to healthy options for your kid.  It just makes all those things work better.

Q 6:  And I know you’ve heard this argument before, but isn’t that big brother?  Aren’t there parents out there who say to you, “I’m the parent: why are you going to test my child for drugs in school; that’s my job?” 

WALTERS:  I think that is the critical misunderstanding that we are slowly beginning to change by the science that tells us substance abuse is a disease.  It’s a disease that gets started by using the drug, and then it becomes a thing that rewires our brain and makes us dependent.  So instead of thinking of this as something that is a moral failing, we have to understand that this is a disease that we can use the kind of tools for public health – screening and interventions – to help reduce it.

Look, let me give you the counter example.  It’s really not big brother.  It’s more like tuberculosis.  Schools in our area require children to be tested for tuberculosis before they come to school.  Why do they do that?  Because we know one, they will get sicker if they have tuberculosis and it’s not treated.  And we can treat them, and we want to treat them.  And two, they will spread that disease to other children because of the nature of the contact they will have with them and spreading the infectious agent.  The same thing happens with substance abuse.  Young people get sicker if they continue to use.  And they spread this to their peers.  They’re not secretive among their peers about it; they encourage them to use them with them.  Again, it’s not spread by a bacillus, but it’s spread by behavior.

If we take seriously the fact that this is a disease and stop thinking of it as something big brother does because it’s a moral decision that somebody else is making, we can save more lives.  And I think the science is slowly telling us that we need to be able to treat this in our families, for adults and young people.  We have public health tools that we’ve used for other diseases that are very powerful here, like screening – and that’s really what the random testing is.  We’re trying to get more screening in the health care system.  So when you get a check up, when you bring your child to a pediatrician, we screen for substance abuse and underage drinking.  Because we know we can treat this, and we know that we can make the whole problem smaller when we do. 

Q 7:  You have said there were about 4,000 schools across the country now that are doing this random drug testing.  What can we see in the numbers since the Supreme Court ruling in 2002, as far as drug use in those schools, and drug use in the general population?

WALTERS:  Well, what a number of those schools have had is of course a look at the harm from student drug and alcohol use.  Some of them have put screening into place, random testing, because they’ve had a terrible accident; an overdose death; death behind the wheel.  What’s great is when school districts do this, or individual schools do this, without having to have a tragedy that triggers it.  But if you have a tragedy, I like to tell people, you don’t have to have another one.  The horrible thing about a tragic event is that most people realize those are not the only kids that are at risk.

There are more kids at risk, obviously, in our communities in the Washington, DC area where this young woman died.  We know there’s obviously more children who are at risk of using in middle school and high school.  The fact is those children don’t have to die.  We cannot bring this young lady back.  Everybody knows that.  But we can make sure others don’t follow her.  And the way we can do that is to find, through screening, who’s really using.  And then let’s get them to stop – let’s work with their families, and let’s make sure we don’t start another generation of death.  So what you see in these areas is an opportunity to really change the dynamic for the better.

Q 8:  Now, although nationally drug use among our youth is going down – what does it say to you – when I look at the numbers specific to Virginia, the most recent that I could find tells me that 3% of 12th graders, over their lifetime, have used a drug like heroin?  What does it say to you?  To me, that sounds like a lot.

WALTERS:  Yeah, and it’s absolutely true.  I think the problem here is that when you tell people we are taking efforts that are making progress nationwide, they jump to the conclusion that that means that we don’t have a problem anymore.  We need to continue to make this disease smaller.  It afflicts our young people.  It obviously also afflicts adults, but this is a problem that starts during adolescence — and pre-adolescence in some cases — in the United States.  We can make this smaller.  We not only have the tools of better prevention but also better awareness and more recognition of addiction as a disease.  We need to make that still broader.  We need to use random testing.  If we want to continue to make this smaller, and make it smaller in a permanent way, random testing is the most powerful tool we can use in schools.

We want screening in the health care system.  We have more of that going on through both insurance company reimbursement and public reimbursement through Medicare and Medicaid for those who come into the public pay system.  That needs to grow.  It needs to grow into Virginia, it’s already being looked at in DC; it needs to grow into Maryland and the other states that don’t have it.  We are pushing that, and it’s relatively new, but it’s consistent with what we’re seeing – the science and the power of screening across the board.

We need to continue to look at this problem in terms of also continuing to push on supply.  We’re working to reduce the poisons coming into our communities, which is not the opposite of demand; that we have to choose one or the other.  They work together.  Keeping kids away from drugs and keeping drugs away from kids work together.  And where we see that working more effectively, we’ll save more lives.  So again, we’ve seen that a balanced approached works, real efforts work, but we need to follow through.  And the fact that you still have too many kids at risk is an urgent need.  Today, you have kids that could be, again, victims that you have to unfortunately tell about on tonight’s news, that we can save.  It’s not a matter we don’t know how to do this.  It’s a matter of we need to take what we know and make it reality as rapidly as possible.

Q 9:  Where are these drugs coming from?  Where’s the heroin that these kids allegedly got coming from?

WALTERS:  We do testing about the drugs to figure out sources for drugs like heroin.  Principally, the heroin in the United States today has come from two sources.  Less of it’s coming out of Colombia.  Colombia used to be a source of supply on the East Coast, but the Colombian government, as a part of our engagement with them on drugs, has radically reduced the cultivation of poppy and the output of heroin.  There still is some, but it’s dramatically down from what it was even about five years ago.  Most of the rest of the heroin in the United States comes from Mexico.  And the Mexican government, of course, is engaged in a historic effort to attack the cartels.  You see this in the violence the cartels have had as a reaction.  So we have promising signs.  There are dangerous and difficult tasks ahead, but we can follow through on that as well.

Most of the heroin in the world comes from Afghanistan; 90% of it.  And we are working there, of course, as a part of our effort against the Taliban and the forces of terror and Al Qaeda, to shrink that.  The good news is that last year we had a 20% decline in cultivation and a 30% decline in output there.  Most of that does not come here, fortunately.  But it has been funding the terrorists.  It’s been drained out of most of the north and the east of the country.  It’s focused on the area where we have the greatest violence today, in the southwest.  We’re working now – you see Secretary Gates talking to the NATO allies about bringing the counter-insurgency effort together with the counter-narcotics effort to attack both of these cancers in Afghanistan.  We have a chance to change heroin availability in the world in a durable way by being successful in Afghanistan.  We’ve started that path in a positive way.  Again, it’s a matter of following through as rapidly as possible.

Q 10:  Greg Lannes, the father of the girl in Fairfax County who died, told me that one of his main efforts, as you imagined, was to let people know that those drugs, they’re coming from where it is produced, outside our country; that they’re getting all the way down to the street level and into our neighborhoods– something that people don’t realize.  So when you hear that they busted a ring of essentially teenagers who have been dealing, using and buying heroin, what does that say to you as the man in charge of combating drugs in our country?

WALTERS:  Well again, we have tools that can make this smaller.  But we have to use those tools.  And we have multiple participants here.  Yes we need to educate.  And we need to make sure that parents know they need to talk to their children, even when their children look healthy and have come from a great home.  Drugs – we’ve learned, I think, over the last 25 years or more, drugs affect everybody; rich or poor, middle class, lower class or upper class.  Every family’s been touched by this, in my experience, by alcohol or drugs.  They know that reality– we don’t need to teach them that.

What we need to teach them is the tools that we have that they can help accelerate use of.  Again, I think – there is no question in my mind that had this young woman been in a school, middle school or high school that had random testing – since that’s where this apparently started, based on the information I’ve seen in the press – she would not be dead today.  So again, we can’t go back and bring her to life.  But we can put into place the kind of screening that makes the good will and obvious love that she got from her parents, the obvious good intentions that I can’t help but believe were a part of what happened in the school, the opportunities that the community has to have a lot of resources that she didn’t get when she needed them.  And now she’s dead.  Again, we can stop this: we just have to make sure we implement that knowledge in the reality of more of our kids as fast as possible.

Q 11:  Should anyone be surprised by this case?  And that such a hardcore drug like heroin is being used by young people?

WALTERS:  We should never stop being surprised when a young person dies.  They shouldn’t die.  They shouldn’t die at that young age, and we should always demand of ourselves, even while we know that’s sometimes going to happen today, that every death is a death too many.  I think that it is very important not to say we’re going to accept a certain level.  Never accept this.  Never!  That’s my attitude, and I know that’s the president’s  attitude as well here.  Never accept that heroin’s going to get into the lives of our teenagers.  Never accept that our children are going to be able to use and not be protected.  It’s our job to protect themThey have a role, also, obviously in helping to protect themselves.  But we need to give them the tools that will help protect them.

When I talk to children and young adults in high school or college, they know what’s going on among their peers.  And in some ways, when you get them alone and they feel they can talk candidly, they tell us they don’t understand why we, as adults who say this is serious, don’t act.  They know that we see children who are intoxicated; they know that we must see signs of this, because as kid’s lives get more out of control, they show signs of it.  They want to know why we don’t act.

We can use the tools of screening, and we can use the occasion of a horrible event like this to bring the community together and say it’s time for us to use the shock and the sorrow for something positive in the future.  I haven’t met a parent of a child who’s been lost who doesn’t say I just want to use this now for something positive.  And that’s understandable, and I think we ought to honor that wish.

Q 12:  Well, I guess I’m not asking should we accept that this is in our schools, but is it naïve for people not to understand or realize that these hardcore drugs are in our schools, and in our communities, and in our neighborhoods. 

WALTERS:  Yeah.  Where it is naïve, I think, is to not recognize the extent and access that young people have to drugs and alcohol.  I think we sometimes think that because they come from a home where this isn’t a part of their lives now, that it’s not ever going to be part of their lives.  Look, your viewers should go on the computer.  Type marijuana into the Google search engine and see how many sites encourage them to use marijuana, how to get marijuana, how to grow marijuana, the great fun of marijuana.  Go on YouTube and type in marijuana, and see how many videos come up using marijuana, joking around about marijuana.  And then when you start showing one, of course the system is designed to show you similar things.  Type in heroin.  See what kind of sites come up, and see what kind of videos come up on these sites.  Young people spend more time on these sites than they do, frequently, watching television.  Remember, there is somebody telling your children things about drugs.  And if it’s not you, the chances are they’re telling them things that are false and dangerous.  So there is a kind of naiveté about what the young peoples’ world, as it presents itself to them, tells them about these substances.  It minimizes the danger, it suggests that it’s something that you can do to be more independent, not be a kid anymore. 

We, from my generation — because I’m a baby boomer — unfortunately have had an association of growing up in America with the rebellion that’s been associated with drug use.  That’s been very dangerous, and we’ve lost a lot of lives.  We have to remember that it’s alive and well, and has become part of the technological sources of information that young people have.  I also see young people in treatment centers who got in a chat room and somebody offered them drugs or offered them to come and buy them alcohol and flattered them, and got them involved in incredibly self-destructive behavior.  The computer brings every predator and every dangerous influence into your own child’s home – into their bedroom in some cases, if that’s where that computer exists.  You wouldn’t let your kids go out and play in the park with drug dealers.  If you have a computer and it’s not supervised, those drug dealers are in that computer.  Remember that.  And they’re only a couple of keystrokes away from your child.

Q 13:  And you talk about the YouTube and the computers and all those things.  What about just the overall societal image?  Because we have this whole image with heroin, of heroin chic.  How much does that contribute to the drug use, and how difficult does it make your job, when a drug is being made out to be cool in society by famous people?

WALTERS:  There are still some elements of that.  It was more prominent a number of years ago.  I would say you see less of that now glamorized in the entertainment industry, or among people who are celebrities in and out of entertainment.  You see more cases of real harm.  But it’s still out there.  The one place that I think is replacing that, just to get people ahead of the game here, is prescription pharmaceuticals.  Those have been marketed to kids on the internet as a safe high.  They falsely suggest that you can overcome the danger of an overdose because you can predict precisely the dosage of OxyContin, hydrocodone, Vicodin.  And there are sites that suggest what combination of drugs to use.  We’ve seen prescription drug use as the one counter example of a category of drug use going up among teens.  We’re trying to work on that as well, but that’s something that’s in your own home, because many people get these substances for legitimate medical care.  Young people are going to the medicine cabinet of family or friends, taking a few pills out and using those.  And those are as powerful as heroin, they’re synthetic opioids, and they have been a source of overdose deaths. 

So let’s not forget – while this Fairfax example reminds us of the issues of heroin chic and of the heroin that’s in our communities, the new large problem today is a similar dangerous substance in pill form in our own medicine cabinets.  Barrier to access is zero.  They don’t have to find a drug dealer; they just go find the medicine cabinet.  They don’t have to pay a dime for it because they just take it and they share that with their friends.  We need to remember, that’s another dimension here.  Keep these substances out of reach – under our control when we have them in our home.  Throw them away when we’re done with them.  Make sure we talk to kids about pills.  Because people, again, are telling them that’s the place to go to avoid overdose death, is to take a pill.

Q 14:  When you see a lot of these celebrities checking in and out of rehab, does it sort of glamorize it for kids?  And teach them hey, you can use, you can check into rehab, you can come back, you can – you know.  Is there a mixed message there?

WALTERS:  There is.  Some young people interpret it the way you describe; of it’s something you do and you can get away with it by going into rehab.  We do a lot of research on young people’s attitudes for purposes of helping shape prevention programs in the media, as well as in schools and for parents.  We do a lot with providing material to parents.  I would say that compared to where we’ve been in the last 15 or 20 years, there’s less glamorization today.

I think we should also remember the positive, because we reinforce that.  A lot of young people – obviously not all or we wouldn’t have this death – believe that taking drugs makes you a loser.  They’ve seen that a lot of those celebrities are showing their careers going down the toilet because they can’t get away from the pills and the drugs and the alcohol.  And I think they see that even among some of their peers.  That’s a good thing.  We should reinforce that as parents: teaching our kids that drug and alcohol use may be falsely presented to you as something you do that would make you popular, make you seem like you should have more status in society generally.  But actually, look at a lot of these people; they’ve had enormous opportunities, enormous gifts, and they can’t stop themselves from throwing them away.  And they may not stop themselves from throwing away their lives. 

I think you could use these events as a teachable moment.  It can go two ways.  Help your child understand what the truth is here.  And I tell young people – and I think parents have to start this more directly – this is the way this is going to come to you:  Somebody you really, really want to like you; somebody you really, really like; someone you may even love — or think you love — they’re going to say come and do this with me.  If you can’t find any other reason to not do this with them, say, “Before we do this, let’s go to a treatment center.  Let’s go talk to people who stood where we stood and said it’s not going to happen to me.”  If everybody, when they got the chance to start, thought of an addict or somebody who was dead, they wouldn’t start.  The fact is that does not enter their mind. 

Many people in treatment centers understand that part of the task of recovery is helping other people avoid this.  So they’re willing to talk about it.  In fact, that’s part of their path of staying clean and sober, which not many kids are going to be able to do on their own.  But it makes them think that what presents itself as something overwhelmingly attractive has behind it a horrible dimension, for their friends as well as for themselves.  And more and more, I think kids understand this.

We can use the science of this as a disease, and the experience of many families.  Remember, uncle Joe didn’t used to be like this.  Especially Thanksgiving, when we have families getting together and all of a sudden mom’s going to get loaded and become ugly in the corner.  We also have to remember we have an obligation to reach out to those people, and to get them help.  We can treat them.  Nobody gets sober, in my experience, by themselves.  They have to take responsibility.  But you have to overcome the pushback, and addiction and alcoholism have, as a part of the disease, denial.  When you tell somebody they have a problem, they get angry with you.  They don’t say hey thanks, I want your help.  They don’t hit bottom and become nice.  That’s a myth.  They need to be grabbed and encouraged and pushed.  Almost everybody in treatment is coerced – by a family member, by an employer, sometimes by the criminal justice system.

So remember that, when you find your child using and they want to lie to you up down and sideways saying, “It’s the first time I’ve ever done it.”  No, no, no, no, no, that’s the drugs talking.  That shows you, if anything, you have a bigger problem than you realized and you need to reach out, get some professional help.  But don’t wait!

Source:    National Institute of Citizen Anti-drug Policy (NICAP)

DeForest Rathbone, Chairman, Great Falls, Virginia, 703-759-2215, DZR@prodigy.net

Abstract

Background

Previous research suggests an increase in schizophrenia population attributable risk fraction (PARF) for cannabis use disorder (CUD). However, sex and age variations in CUD and schizophrenia suggest the importance of examining differences in PARFs in sex and age subgroups.

Methods

We conducted a nationwide Danish register-based cohort study including all individuals aged 16–49 at some point during 1972–2021. CUD and schizophrenia status was obtained from the registers. Hazard ratios (HR), incidence risk ratios (IRR), and PARFs were estimated. Joinpoint analyses were applied to sex-specific PARFs.

Results

We examined 6 907 859 individuals with 45 327 cases of incident schizophrenia during follow-up across 129 521 260 person-years. The overall adjusted HR (aHR) for CUD on schizophrenia was slightly higher among males (aHR = 2.42, 95% CI 2.33–2.52) than females (aHR = 2.02, 95% CI 1.89–2.17); however, among 16–20-year-olds, the adjusted IRR (aIRR) for males was more than twice that for females (males: aIRR = 3.84, 95% CI 3.43–4.29; females: aIRR = 1.81, 95% CI 1.53–2.15). During 1972–2021, the annual average percentage change in PARFs for CUD in schizophrenia incidence was 4.8 among males (95% CI 4.3–5.3; p < 0.0001) and 3.2 among females (95% CI 2.5–3.8; p < 0.0001). In 2021, among males, PARF was 15%; among females, it was around 4%.

Conclusions

Young males might be particularly susceptible to the effects of cannabis on schizophrenia. At a population level, assuming causality, one-fifth of cases of schizophrenia among young males might be prevented by averting CUD. Results highlight the importance of early detection and treatment of CUD and policy decisions regarding cannabis use and access, particularly for 16–25-year-olds.

Source: Association between cannabis use disorder and schizophrenia stronger in young males than in females | Psychological Medicine | Cambridge Core May 2023

Summary

Background

Adolescence represents a crucial developmental period in shaping mental health trajectories. In this study, we investigated the effect of the COVID-19 pandemic on mental health and substance use during this sensitive developmental stage.

Methods

In this longitudinal, population-based study, surveys were administered to a nationwide sample of 13–18-year-olds in Iceland in October or February in 2016 and 2018, and in October, 2020 (during the COVID-19 pandemic). The surveys assessed depressive symptoms with the Symptom Checklist-90, mental wellbeing with the Short Warwick Edinburgh Mental Wellbeing Scale, and the frequency of cigarette smoking, e-cigarette use, and alcohol intoxication. Demographic data were collected, which included language spoken at home although not ethnicity data. We used mixed effects models to study the effect of gender, age, and survey year on trends in mental health outcomes.

Findings

59 701 survey responses were included; response rates ranged from 63% to 86%. An increase in depressive symptoms (β 0·57, 95% CI 0·53 to 0·60) and worsened mental wellbeing (β −0·46, 95% CI −0·49 to −0·42) were observed across all age groups during the pandemic compared with same-aged peers before COVID-19. These outcomes were significantly worse in adolescent girls compared with boys (β 4·16, 95% CI 4·05 to 4·28, and β −1·13, 95% CI −1·23 to −1·03, respectively). Cigarette smoking (OR 2·61, 95% CI 2·59 to 2·66), e-cigarette use (OR 2·61, 95% CI 2·59 to 2·64), and alcohol intoxication (OR 2·59, 95% CI 2·56 to 2·64) declined among 15–18-year-olds during COVID-19, with no similar gender differences.

Interpretation

Our results suggest that COVID-19 has significantly impaired adolescent mental health. However, the decrease observed in substance use during the pandemic might be an unintended benefit of isolation, and might serve as a protective factor against future substance use disorders and dependence. Population-level prevention efforts, especially for girls, are warranted.

Funding

Icelandic Research Fund.
Source: Depressive symptoms, mental wellbeing, and substance use among adolescents before and during the COVID-19 pandemic in Iceland: a longitudinal, population-based study – The Lancet Psychiatry June 2021

Highlights

  • Alcohol intake is associated with smaller grey matter volumes across the brain.
  • It is also associated with lower FA and increased functional connectivity
  • Binge drinking steepens association between alcohol and total grey matter volume.
  • Findings suggest even 7–14 units of alcohol weekly may be associated with brain differences.

Abstract

Moderate alcohol consumption is widespread but its impact on brain structure and function is contentious. The relationship between alcohol intake and structural and functional neuroimaging indices, the threshold intake for associations, and whether population subgroups are at higher risk of alcohol-related brain harm remain unclear. 25,378 UK Biobank participants (mean age 54.9 ± 7.4 years, 12,254 female) underwent multi-modal MRI 9.6 ± 1.1 years after study baseline. Alcohol use was self-reported at baseline (2006–10). T1-weighted, diffusion weighted and resting state images were examined. Lower total grey matter volumes were observed in those drinking as little as 7–14 units (56–112 g) weekly. Higher alcohol consumption was associated with multiple markers of white matter microstructure, including lower fractional anisotropy, higher mean and radial diffusivity in a spatially distributed pattern across the brain. Associations between functional connectivity and alcohol intake were observed in the default mode, central executive, attention, salience and visual resting state networks. Relationships between total grey matter and alcohol were stronger than other modifiable factors, including blood pressure and smoking, and robust to unobserved confounding. Frequent binging, higher blood pressure and BMI steepened the negative association between alcohol and total grey matter volume. In this large observational cohort study, alcohol consumption was associated with multiple structural and functional MRI markers in mid- to late-life.

Source: Alcohol consumption and MRI markers of brain structure and function: Cohort study of 25,378 UK Biobank participants – ScienceDirect May 2022

 

Aaron Hernandez was supposed to be the epitome of the American Dream—overcoming childhood setbacks to earn a spot in the NFL on the New England Patriots. Millions of kids across America wish they could be so lucky. But the 2020 documentary on Netflix, “Killer Inside: The Mind of Aaron Hernandez,” takes a deep dive into his life to investigate how his dream unraveled into a nightmare. Convicted of murdering his friend Odin Lloyd and accused of killing two other men (but found not guilty), Hernandez took his own life in a prison suicide in 2017. He was only 27.
The compelling docuseries explores many of the factors that could have contributed to the tragic end of such a promising life—childhood abuse, unstable parenting, hidden bisexuality. And then there was his brain. The docuseries delivers a fascinating look at his troubled brain, but it misses one key factor that may have contributed to Hernandez’ brain dysfunction.

The Brain of Aaron Hernandez
After Hernandez’s death, his brain was delivered to Boston University, where researchers made razor-thin slices for examination. Their findings? His brain was “riddled” with Stage 3 chronic traumatic encephalopathy (CTE). This neurodegenerative disease, which has 4 stages, has been found in athletes like football players, boxers, and soccer players who endure repeated concussions and other blows to the head. It has been associated with memory loss, cognitive dysfunction, and suicidal thoughts and behavior.
A Boston University publication reported that Ann McKee, director of BU’s Chronic Traumatic Encephalopathy Center, said that his brain was the worst case of CTE ever seen in someone so young. “Especially in the frontal lobes, which are very important for decision-making, judgment, and cognition, we could see damage to the inner chambers of the brain,” she said. The frontal lobes are also involved in impulse control, empathy, and learning from past experiences.
The documentary focuses heavily on CTE and the significant role it likely played in Hernandez’ downfall, and for good reason. The filmmakers also hone in on another aspect of his life that may have contributed to his troubles—cannabis use. It is reported that the football player began smoking marijuana regularly in high school and continued to smoke throughout his pro career. The docuseries calls him a “chainsmoker” with a serious habit, but it neglects to connect the dots between marijuana use and brain dysfunction.

Marijuana and the Brain
A growing body of evidence shows that marijuana use impairs brain activity. In the largest known brain imaging study, which appeared in the Journal of Alzheimer’s Disease, scientists from Amen Clinics, Google, Johns Hopkins University, UCLA, and the UC San Francisco evaluated 62,454 brain SPECT scans of more than 30,000 individuals (ages 9 months to 105 years) to investigate factors that accelerate brain aging. SPECT (single-photon emission computed tomography) is a brain imaging technology that measures brain activity and blood flow. The study found that a number of brain disorders and behaviors predicted accelerated aging. Of all the disorders and behaviors analyzed, cannabis abuse ranked as the second-highest brain ager, topped only by schizophrenia.
The study, which included brain scans from 1,000 cannabis users, 25,168 non-cannabis users, and 100 healthy controls, showed reduced cerebral blood flow among the cannabis users compared to non-users and healthy controls. A significant decrease in blood flow was noted specifically in the right hippocampus, an area of the brain that helps with memory formation. This part of the brain is severely affected in those that suffer from Alzheimer’s disease.


Healthy SPECT Scan

Marijuana Affected SPECT Scan

Other research has concluded that marijuana harms the teenage brain in numerous ways. For example, a 2019 review found that it increases the risk of depression and suicidal thoughts and behaviors. And marijuana use at a young age has also been associated with increased impulsivity.
Although pot promoters would argue that most people who smoke marijuana don’t become murderers and don’t die by suicide, it’s important to understand that in vulnerable people it may have negative impacts on brain function that contribute to unhealthy behaviors. Sadly, considering that Hernandez’s brain was so damaged by CTE, marijuana use was likely only making bad brain function worse.

You Can Change Your Brain
Unfortunately, this information is too late to help Hernandez, but it isn’t too late for other football players who have endured years of helmet-to-helmet tackles. A study at Amen Clinics on 30 retired professional football players who had suffered head trauma showed that after following a brain healthy program for 6 months, 80% showed significant improvement in blood flow to the frontal lobes, as well as improvements in overall cognitive functioning, processing speed, attention, reasoning, and memory. Hall of Fame quarterback Terry Bradshaw spoke openly about his own brain rehabilitation after suffering multiple concussions. 
Likewise, it isn’t too late for people who grew up in traumatic households. See how a man named Kevin overcame his traumatic upbringing to enhance his brain health using a variety of innovative therapies. And it isn’t too late for people who have been bad to their brain with drug use. Find out how Arnie broke free from the chains of addiction. It’s never too late to start enhancing brain function.
The world’s largest database of brain scans related to behavior—over 160,000 and growing —shows that when you adopt a brain health program, you can change your brain and change your life for the better.
At Amen Clinics, we take a unique brain-body approach that gets to the root cause of your symptoms. Our comprehensive evaluations include brain SPECT imaging, as well as laboratory testing and assessing other important factors that could be contributing to symptoms. By getting to the root cause of your symptoms, we can create a more effective, personalized treatment plan for you.
If you want to join the tens of thousands of people who have already enhanced their brain health, overcome their symptoms, and improved their quality of life at Amen Clinics, speak to a specialist today at 888-288-9834. If all our specialists are busy helping others, you can also schedule a time to talk.

Source: What the Aaron Hernandez Documentary Missed About His Brain | Amen Clinics Amen Clinics February 2020

One way to deter harmful recreational drug use by teenagers is to treat them like adults. Rather than simply tell them to “Just Say No” to alcohol, tobacco or illicit drugs, it may be more helpful to explain how these substances create unique risks for them risks that arise due to the changing state of the adolescent brain.

 

It’s an approach recommended by Dr. Robert DuPont, the first director of the National Institute of Drug Abuse, the second White House “drug czar” and the current head of the Institute for Behavior and Health.

 

Scientists have long recognized that people who use alcohol, tobacco, marijuana and other drugs while adolescents are far more likely to use more dangerous drugs in their 30s and 40s. Back in 1984, researchers writing in the American Journal of Public Health reported that “the use of marijuana is a good predictor of the use of more serious drugs only if it begins early” and that early drinking is a similar “predictor of marijuana use.”

 

It should come as no surprise, then, that Americans in their 30s and 40s who used recreational drugs as teenagers are the group most severely affected by opioid overdoses today.

 

Unfortunately, neither the media nor popular culture adequately informs young people about the neurological damage alcohol, nicotine, and marijuana can inflict on the brain. On the contrary, despite strong evidence that early recreational drug use increases the likelihood of future drug addiction, the media and today’s culture often describe marijuana use as an “organic,” “natural” approach to anxiety and stress management. Indeed, Northern Michigan University launched the nation’s first medicinal plant chemistry major, offering students the chance to focus on marijuana-related studies. What message does that send to the still-developing minds of college students?

 

One group is taking a non-traditional approach to convincing students otherwise.

 

One Choice is a drug prevention campaign developed for teenagers by the Institute for Behavior and Health. It relies on cutting-edge neuroscience to encourage young Americans to make decisions that promote their brain health.

 

Pioneered by Dr. DuPont, One Choice specifically advocates that adolescents make “no use of any alcohol, nicotine, marijuana or other drugs” for health reasons. The theory is that adolescents who make the decision not to use alcohol, nicotine, or marijuana at all that make “One Choice” to avoid artificial, chemical brain stimulation are far less likely to wind up addicted to drugs such as opioids later on.

 

The One Choice approach is evidence-based. In 2017, scientists at Mclean Hospital and Harvard Medical School published their findings on the impact of early substance use on cognitive development. They explained that the brains of teenagers are still developing and can be negatively impacted by substance use. Adolescent brains are still forming the communication routes that regulate motivation, stress and habit-formation well into adulthood. As such, it is easier for substances to hijack and alter those routes in developing brains than in adult brains.

 

Hindering the vital attributes of habit formation, stress management and motivational behavior can drastically affect a young person’s academic performance. Collectively, and in the long run, that can impair the competitiveness of a national economy. Thus, it is crucial that young Americans learn to prioritize brain health.

 

The timing for the innovative One Choice approach is propitious. Today’s young Americans are more interested in biology, psychology and health sciences than ever before. According to the National Center for Education Statistics, the field of “health professions and related programs” is the second most popular major among college students, with psychology and biological or biomedical sciences following as the fourth and fifth most popular, respectively. By explaining developmental neuroscience to teenagers, One Choice engages young people on a topic of interest to them and presents the reality of a pressing public health issue, instead of throwing moral platitudes and statistics at them.

 

Pro-marijuana legalization organizations, such as the Drug Policy Alliance, agree: “The safest path for teens is to avoid drugs, doing alcohol, cigarettes, and prescription drugs outside of a doctor’s recommendations.” And certainly honesty, along with scientific accuracy, is critical if we are to persuade adolescents not to use drugs.

 

Brain health is critical to the pursuit of happiness. And leveraging scientifically accurate presentations and testimonies to convince young Americans to prioritize their own brain health early on can prevent future substance abuse.

Source: Using Neuroscience to Prevent Drug Addiction Among Teenagers | The Heritage Foundation January 2019

Just one or two joints seem to change the structure of the brain, say researchers from universities around the world, led by senior author and University of Vermont professor of psychiatry Hugh Garavan, PhD, and first author and former UVM postdoctoral fellow Catherine Orr, PhD.
 
The study is part of a long-term European effort called IMAGEN, which has collected brain images from 2,000 children in Ireland, France, and Germany, starting when they were age 14 and continuing through age 23.
 
Researchers compared the brain images of 46 children age 14 who reported having used marijuana once or twice with those of children that age who had not used the drug. The images of the marijuana triers showed greater brain volume in areas with cannabinoid receptors. The biggest differences were in the amygdala, involved in fear and other emotions, and the hippocampus, the site of memory development and spatial abilities.
 
“You’re changing your brain with just one or two joints. Most people would likely assume that one or two joints would have no impact on the brain,” says Dr. Garavan.
 
It is unclear what the extra gray matter in these brain areas means. Normally at age 14, the brain is refining its synaptic connections to make it thinner, not thicker. Dr. Garavan says one possibility is that initial marijuana use in this age group may be disrupting that “pruning” process.
 
The new findings open a new area of focus for future research.
 
Read study abstract here.

Source:  The Marijuana Report  16.01.2019

There is evidence in both patients with psychotic disorders and the general population that cannabis use is associated with adverse effects of psychopathology and cognition.

RESEARCH UPDATE

Substance use comorbidity in schizophrenia has been described as “the rule rather than the exception.”1 The large Epidemiological Catchment Area study estimated that 47% of patients with schizophrenia also had a lifetime comorbid diagnosis of a substance use disorder.2 Substance use comorbidity is also often deleterious to the course of schizophrenia, including potential contributions to medication non-adherence and illness relapse.1 Cannabis (marijuana) is one of the most commonly used substances by patients with schizophrenia.

There is recent, renewed interest in the endocannabinoid system, which represents a novel potential treatment target in schizophrenia.3 Modulation of this system by the main psychoactive component in marijuana, Δ9-tetrahydro-cannabinol (THC), can induce acute psychosis and cognitive impairment. However, the non-psychotropic plant-derived agent cannabidiol (CBD) may decrease psychotic symptoms and improve cognitive function in schizophrenia.4-6

Presently, CBD oil is sold at numerous shops throughout the US, with purported benefits that include alleviation of symptoms such as depression, anxiety, insomnia, and pain. However, the purity and safety of CBD is not regulated by the US Food and Drug Administration. CBD may be “contaminated” with some amount of THC and/or other unknown ingredients. In the past decade, there have been a number of systematic reviews regarding associations between cannabis use and psychosis. Therefore, a review of systematic evidence for associations between cannabis use, risk of psychosis, and the clinical course of schizophrenia is of particular relevance to the practicing clinician.

Adverse effects of cannabis on psychosis and cognition

There is evidence from a quantitative review of 15 studies in healthy participants that a single administration of THC (intravenous, oral, or nasal) versus placebo induced positive, negative, and other psychopathology with large effect sizes (ESs).7 Furthermore, evidence from 69 studies, comprising 2152 adolescents and young adults who used cannabis and 6575 controls with minimal cannabis exposure, showed that frequent or heavy use was associated with significantly reduced cognitive functioning with a small-to-medium ES = -0.25, although these effects were diminished with abstinence for more than 72 hours.8

Cannabis use and risk of psychosis

Moore and colleagues9 performed a systematic review of 35 studies of cannabis use and risk of psychotic mental health outcomes. They found that individuals who had used cannabis had a significant, 1.4-fold increased risk of any psychotic outcomes, independent of potential confounding and transient intoxication effects. Findings also provided evidence for a dose-response effect, with even greater, 2.1-fold risk in individuals who used cannabis most frequently.

More recently, Marconi and colleagues10 performed a meta-analysis of 10 studies, including 66,810 individuals, that investigated the association between the degree of cannabis consumption and risk of psychosis. In all individual studies, higher levels of cannabis use were associated with increased risk of psychosis. They also found evidence for a dose-response relationship, with a 2-fold increase in risk for the average cannabis user, and a 4-fold increase in risk for the heaviest users, compared with non-users. Although these findings do not definitively establish a causal association between marijuana use and psychotic disorders, it nevertheless remains a replicated risk factor for psychosis with a clear dose-dependent relationship.

Cannabis use in patients with psychotic disorders

Koskinen and colleagues11 performed a quantitative review of the rates of cannabis use disorders (CUDs) in clinical samples of patients with schizophrenia. They identified 35 studies for inclusion in the meta-analysis. The median current rate of CUD was 16.0% (Interquartile Range [IQR] 8.6-28.6%), and the median lifetime rate of CUD was 27.1% (IQR=12.2-38.5). The rate of current/lifetime CUDs was markedly higher in first-episode (28.6%/44.4%) versus chronic schizophrenia (22.0%/12.2%), as well as in younger patient samples and samples with a high proportion of males. They concluded that approximately 1 in 4 patients with schizophrenia has a diagnosis of a comorbid CUD.

Hunt and colleagues12 more recently performed a systematic review of the prevalence of comorbid substance use in patients with schizophrenia spectrum disorders. They identified 69 studies, and the pooled estimate for current or lifetime CUD was 26.2%. Consistent with the review by Koskinen and colleagues,11 the prevalence was significantly higher in individuals with first-episode psychosis (35.6%) versus chronic schizophrenia (20.8%), but did not differ by study setting or patient clinical status.

The substantial prevalence of cannabis use also appears to extend to the psychosis prodrome. There is evidence from 30 studies, including 4205 individuals at ultra high risk (UHR) for psychosis, that there are high rates of current (26.7%) and lifetime (52.8%) cannabis use, and CUDs (12.8%).13 Compared with non-users, UHR cannabis users also had higher rates of suspiciousness and unusual thought content.

Furthermore, research suggests that people with substance-induced psychoses will later transition to a diagnosis of schizophrenia. Murrie and colleagues14 synthesized the results of longitudinal observations studies of transition from substance-induced psychosis to schizophrenia. Six studies with estimates of transition to schizophrenia among 3040 people with cannabis-induced psychosis were included. The risk of transition to schizophrenia in these individuals was 34% (95% CI 25-46%), which was the highest risk among all substances. They concluded that substance-induced psychoses are common reasons for seeking care, and these serious conditions are associated with substantial risk of transition to schizophrenia. Treatment of cannabis-induced psychoses should be considered in the same framework as that for other brief psychotic disorders (i.e., engagement, assessment, and care); this also may help decrease rates of transition to schizophrenia.

Impact of cannabis on psychotic disorders

Large and colleagues15 conducted a systematic review of the association between cannabis use and the age of onset of psychosis. They included 41 samples, finding that the age of onset of psychosis for those who used cannabis was 2.7 years younger than for non-users, corresponding to a small-to-medium effect size of 0.41. These findings are broadly consistent with a potential causal role for cannabis in the development of psychosis in some patients.

Bogaty and colleagues16 performed a meta-analysis of 14 studies of neurocognition in lifetime cannabis users and never-users in young patients with psychotic disorders (aged 15 to 45 years). They found that lifetime cannabis users performed significantly worse than never-users on several cognitive domains, including premorbid and current IQ, verbal learning and working memory, and motor inhibition. Effect sizes were small to medium for most domains (0.17-0.40), except for verbal working memory, which showed a large effect size (0.76). Interestingly, patients who use cannabis performed better on tests of conceptual set-shifting. Increasing age exacerbated the between-group differences.

Schoeler and colleagues17 conducted a systematic review and meta-analysis of the effect of continued versus discontinued cannabis use after the onset of psychosis. They identified 24 studies, including 16,565 patients with pre-existing psychosis and at least a 6 month duration of follow-up. They found that continued cannabis use was associated with a significant: increase in risk of relapse of psychosis compared with non-users (ES=0.36) and discontinued users (ES=0.28); longer hospital admissions than non-users (ES=0.36); and more severe positive, but not negative, symptoms. Krause and colleagues18 performed a meta-analysis of the efficacy, acceptability, and tolerability of antipsychotics in patients with schizophrenia and comorbid substance use. They included 8 randomized controlled trials in patients with cannabis use comorbidity. Clozapine was superior to other antipsychotics for reduction of substance use and negative symptoms in those who used cannabis. Risperidone was superior to olanzapine for reducing of drug cravings and weight gain.

Conclusions

Premorbid cannabis use is associated with a dose-dependent increased risk of developing a psychotic disorder. There is evidence in both patients with psychotic disorders and the general population that cannabis use is associated with adverse effects of psychopathology and cognition. Cannabis use and CUDs are highly prevalent throughout the clinical course of illness.

Cannabis use is associated with an earlier age of onset of psychosis and more severe impairments in neurocognition. Continued cannabis use after the onset of psychosis is associated with increased risk of illness relapse, longer hospitalizations, and more severe positive psychopathology. There is also evidence for superior efficacy of clozapine for reduction of substance use and negative symptoms in patients with schizophrenia and comorbid cannabis use. Targeted interventions for improved prevention, detection, and treatment are warranted to improve outcomes in this population.

Dr Miller is Professor, Department of Psychiatry and Health Behavior, Augusta University, Augusta, GA. He is the Schizophrenia Section Chief for Psychiatric Times.

The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

Source: https://www.psychiatrictimes.com/view/novel-insights-cannabis-psychosis July 2020

A new study recently published in Nature Medicine found a stunning association between prenatal THC exposure and development of autism. Using provincial birth registries, Canadian researchers analyzed all live births that occurred in Ontario between April 2007 and March 2012 for a total of 497,821 births.

Investigators found that infants who were prenatally exposed to THC were 57% more likely to develop autism spectrum disorder (ASD) and 35% more likely to develop intellectual disabilities and learning disorders. Previous studies of this type have been difficult to interpret due to polysubstance use among expectant mothers making it difficult to tease out the effects of THC exposure alone. In this study, researchers were able to directly compare unexposed infants to those whose mothers only used marijuana during their pregnancy. Thus, any effects observed in this study can be reliably attributed to prenatal THC exposure since no other substances were used. Results persisted even adjusting for other potential risk factors for ASD such as maternal age, education, psychiatric disorders, socioeconomic status, parity, and race.

The results of this study confirm that of previous research on the harms of prenatal THC exposure. Nevertheless, marijuana is routinely recommended to pregnant women by pot docs as well as dispensary employees with no medical training at all. Given the explosion in marijuana use among pregnant women in states like FL, lawmakers must take immediate action to fund education campaigns and ban marijuana recommendations for pregnant women. How many more lives need to be ruined so that Big Pot and their political allies can line their pockets?

Source:  https://www.dfaf.org/study-finds-link-between-prenatal-thc-exposure-and-autism/ 19.08.20

ABSTRACT

Parental cannabis use has been associated with adverse neurodevelopmental outcomes in offspring, but how such phenotypes are transmitted is largely unknown. Using reduced representation bisulphite sequencing (RRBS), we recently demonstrated that cannabis use is associated with widespread DNA methylation changes in human and rat sperm. Discs-Large Associated Protein 2 (DLGAP2), involved in synapse organization, neuronal signaling, and strongly implicated in autism, exhibited significant hypomethylation (p < 0.05) at 17 CpG sites in human sperm. We successfully validated the differential methylation present in DLGAP2 for nine CpG sites located in intron seven (p < 0.05) using quantitative bisulphite pyrosequencing. Intron 7 DNA methylation and DLGAP2 expression in human conceptal brain tissue were inversely correlated (p < 0.01). Adult male rats exposed to delta-9-tetrahydrocannabinol (THC) showed differential DNA methylation at Dlgap2 in sperm (p < 0.03), as did the nucleus accumbens of rats whose fathers were exposed to THC prior to conception (p < 0.05). Altogether, these results warrant further investigation into the effects of preconception cannabis use in males and the potential effects on subsequent generations.

KEYWORDS: Cannabis, sperm, DNA methylation, autism, heritability

Introduction

Cannabis sativa is the most commonly used illicit psychoactive drug in the United States (U.S.) and Europe [1]. In the U.S., 11 states and Washington D.C. have legalized the recreational use of cannabis and 33 states have legalized the use of medicinal cannabis [2,3]. Since 1995, cannabis potency (defined as the concentration of the psychoactive cannabis component delta-9-tetrahydrocannabinol, or THC, in the sample [4]) has consistently risen from ~4% to as high as 32% in some states [2,5,6]. Changes in cannabis potency have been accompanied by changes in attitudes about cannabis and patterns of cannabis use. Between 2002 and 2014, the percentage of adults in the U.S. who perceived cannabis use as risky declined from 50% to 33% [6]. During this same period, the percentage of U.S. adults who believed cannabis to have no risk rose from 6% to 15% [6]. According to a 2015 Survey on Drug Use and Health, 52.5% of men in the U.S. of reproductive age (≥18) have reported cannabis use at some point in their lives, making cannabis exposure especially relevant for potential future fathers [711].

Given the increased prevalence of cannabis use in the U.S., studies are beginning to focus on the effects of use on the health and development of offspring. Prenatal cannabis exposure via maternal use during pregnancy is associated with decreased infant birth weight, an increased likelihood to require the neonatal intensive care unit, and the potential for an impaired fetal immune system compared to those infants who are not exposed during gestation [1,12]. In rodent studies, rat pups born to parents who were both exposed to THC during adolescence had increased heroin-seeking behaviour later in life, a phenotype that was accompanied by epigenetic changes in the nucleus accumbens [1315]. These studies and others have begun to highlight the potential for intergenerational consequences of cannabis exposure [16]. Identifying the mechanism that underlies these changes is critical as cannabis use continues to increase across the U.S.

The environment impacts the integrity and maintenance of the epigenome such that it is now viewed as a molecular archive of past exposures [17]. While the majority of environmental epigenetic studies are focused on the impact of the inutero environment on the epigenome and health of the child, it has become apparent that the exposure history of the father must also be considered – specifically the impact of his exposures on the sperm epigenome. Studies have shown that exposure to phthalates, pesticides, nutritional deficiencies, and obesity can all induce potentially heritable changes in the sperm epigenome [1824]. It is likely that other common and emerging exposures, including cannabis, may also contribute to disruption of sperm DNA methylation in a similar fashion, and that such changes could be transmitted to the subsequent generation.

Using reduced representation bisulphite sequencing (RRBS) our group recently demonstrated that cannabis use in humans, and THC exposure in rats, is associated with decreased sperm concentrations and widespread changes in sperm DNA methylation [25]. Of the regions identified in humans, Discs-Large Associated Protein 2 (DLGAP2) exhibited significant hypomethylation in the sperm of cannabis-exposed men compared to controls (p < 0.05). DLGAP2, a membrane-associated protein located in the post-synaptic density of neurons, plays a key role in synapse organization and neuronal signaling [26]. Dysregulation of DLGAP2 is associated with various neurological and psychiatric disorders, such as autism spectrum disorder (ASD) and schizophrenia [2629]. In our prior screen, we identified 17 differentially methylated CpG sites within DLGAP2 in the sperm of cannabis-exposed men compared to controls. DLGAP2 was just one of 46 genes with greater than 10 CpG sites showing significantly altered DNA methylation in the sperm of cannabis users compared to controls, out of the 2,077 genes we identified as having altered DNA methylation. The first objective of this study was to validate our preliminary RRBS findings for DLGAP2 using quantitative bisulphite pyrosequencing. Our second objective was to determine the functional association between DNA methylation and gene expression of DLGAP2 to better understand how cannabis use might affect this relationship. To determine the possible intergenerational effects of paternal cannabis use, our third objective was to determine if Dlgap2 was differentially methylated in the sperm of rats exposed to THC versus controls, and if so, whether or not these changes were intergenerationally heritable.

Results

DLGAP2 is hypomethylated in sperm from cannabis users versus controls by Reduced Representation Bisulphite Sequencing (RRBS)

Our prior study [25] revealed 17 differentially methylated sites by RRBS in the sperm of cannabis users compared to controls for the DLGAP2 gene. Table S1 lists all 17 of these sites and their genomic coordinates. Figure 1a graphically demonstrates the significant hypomethylation of nine of these sites that are clustered together in the seventh intron of this gene. DLGAP2 is schematically shown in Figure 1b, including the exon-intron structure, position of CpG islands, transcription start site and the region of interest in intron 7 within the context of the gene body, with an inset showing the nucleotide sequence analysed in this study.

Validation of DLGAP2 RRBS methylation data

To confirm the methylation differences that were initially detected using RRBS, we designed a bisulphite pyrosequencing assay for the DLGAP2 intron 7 region (see Figure 1b) which captures 10 CpG sites, nine of which were identified as significantly differentially methylated using RRBS. We first validated pyrosequencing assay performance using defined mixtures of fully methylated and unmethylated human genomic DNAs. The measured levels of methylation by pyrosequencing showed good agreement between the amount of input methylation levels and the amount of methylation detected (r2 = 0.99 and p = 0.0003) (Figure 1c). These results confirmed the linearity of the assay in the ability to detect increasing amounts of DNA methylation at this region across the full range of possible methylation values, and indicate that the assay is suitable for use with biological specimens.

The DLGAP2 intron 7 region is not an imprinting control region (ICR)

DLGAP2 is paternally expressed in the testis, biallelically expressed in the brain, and has low expression elsewhere in the body [30]. Since DLGAP2 is known to be genomically imprinted in testis [30], and since the imprint control region for this gene has not yet been defined, we sought to determine if the region of interest in intron 7 is part of the DLGAP2 imprint control region (ICR). The methylation at ICRs is established during epigenome reprogramming in the primordial germ cells in embryonic development. Male and female gametes exhibit divergent methylation at ICRs, and this methylation profile is maintained through subsequent post-fertilization epigenetic reprogramming and in somatic cells throughout the life course. Therefore, we expected that if the DLGAP2 intron 7 region is an ICR, the diploid testis tissues from human conceptuses would exhibit approximately 50% methylation due to the complete methylation of one allele at this region and the complete lack of methylation at the other allele. Human conceptal testes tissues (n = 3) showed an average of 72.5% methylation at the DLGAP2 intron 7 region (Figure 1d). This finding, of higher than anticipated and variable levels of methylation, is inconsistent with ICR status.

Bisulphite pyrosequencing validates the RRBS methylation data in human sperm

We next performed quantitative bisulphite pyrosequencing on the same sperm DNA samples from cannabis users and controls as those used to generate the RRBS data to confirm the loss of methylation present at the intron 7 region of DLGAP2. All nine CpG sites that were hypomethylated in the cannabis users by RRBS were also found to be hypomethylated by bisulphite pyrosequencing, as well as an additional CpG site that was captured in the assay design (p < 0.05 for all 10 sites) (Figure 2). Following Bonferroni correction of the p value to adjust for multiple comparisons (p < 0.005), CpG sites 1,2,3,5,7,8,9, and 10 remained significant. From this pyrosequencing assay we observed methylation differences of 7–15% between the sperm of the cannabis users (n = 8) compared to controls (n = 7). Correlation of the RRBS and pyrosequencing data for each individual CpG site showed significant agreement at all sites analysed (p < 0.02 for all sites; Figure S1). All CpG sites showed a significant loss of methylation in accordance with the direction of change observed by RRBS for these same CpG sites.

Methylation of DLGAP2 intron 7 is inversely correlated with DLGAP2 expression

Given that we observed significant loss of intron 7 DLGAP2 DNA methylation in sperm of cannabis users relative to non-users, we next examined the relationship between DNA methylation and gene expression in the brain, where this gene’s function is critical. We used 28 conceptal brain tissues to examine the relationship between DNA methylation and mRNA expression. Expression levels were normalized to the lowest expressing sample, and the relationship between DNA methylation and mRNA expression was calculated with a Pearson correlation. We found that as methylation increased in this region, mRNA expression decreased significantly (p < 0.05) (Figure 3a). Knowing that there are sex differences in autism spectrum disorder (ASD), and that dysregulation of DLGAP2 is associated with ASD [26], we sought to determine if there were any sex differences in the methylation-expression relationship in these tissues. To investigate this, we ran the correlation for males (n = 15) and females (n = 13) independently. The inverse relationship between methylation and expression was evident for both males and females, but this relationship was significant only in females (p = 0.006) (Figure 3b, c).

Intergenerational inheritance of altered Dlgap2 DNA methylation

We next sought to investigate Dlgap2 using data obtained from our prior study [25] to determine if there was any differential methylation of Dlgap2 in THC versus control rats that was not initially identified using the imposed thresholds of that study. We were particularly interested in the potential for intergenerational transmission and to determine if route of THC exposure affected DNA methylation at this gene. The pilot study rats [25] were given THC via oral gavage (to mimic oral ingestion of drug) while subsequent studies dosed rats via intraperitoneal injection (to mimic inhalation of drug). From the rats administered THC via oral gavage versus controls, we identified a region of Dlgap2 that showed differential methylation by the RRBS analysis that contains eight CpG sites. This region is in the first intron of Dlgap2, in a CpG island that spans the first exon of this gene as well (schematic of the gene structure and sequence of this region shown in Figure 4a). We validated the rat Dlgap2 pyrosequencing assay using commercially available rat DNA of defined methylation status. The results showed good agreement between the input methylation and the amount of methylation detected by pyrosequencing (r2 = 0.92, p = 0.01) (Figure 4b).

We were able to demonstrate intergenerational inheritance of an altered DNA methylation pattern in Dlgap2. Comparing the average methylation for exposed and unexposed sperm for each CpG site revealed that sites 2,3,4 and 6 of the eight CpG sites analysed were significantly hypomethylated in the sperm of rats exposed via injection to 4mg/kg THC compared to controls (p = 0.03 to p = 0.005) (Figure 4c). CpG site 6 remained significant after Bonferroni correction (p < 0.006). The same region of Dlgap2 was then analysed in the hippocampus and nucleus accumbens of rats whose fathers were exposed to control or 4mg/kg THC. While CpG site 7 was significantly hypomethylated (p < 0.05) in the hippocampus of the offspring (Figure 5a), this site was not identified as differentially methylated in the sperm of THC exposed rats, and therefore we could not conclude that this change was transmitted as the result of changes present in the exposed sperm. In the nucleus accumbens, however, significant hypomethylation (p = 0.02) at CpG site 2 was detected in the offspring (Figure 5b), one of the same sites identified in the sperm of THC exposed rats. We also found that there was an inverse relationship between DNA methylation and expression of Dlgap2 in the nucleus accumbens, though not statistically significant likely due to the small sample size available in this study (n = 6 exposed, n = 8 unexposed; Figure S2).

Discussion

In this study, we examined the effects of regular male cannabis use on human sperm DNA methylation, at DLGAP2. Our RRBS study initially identified 17 CpG sites in DLGAP2 that were differentially methylated in the sperm of cannabis users compared to controls. Of the sites that were initially identified, nine of them all reside together in the seventh intron of this gene, though not in a defined CpG island. To first confirm the RRBS data, we performed quantitative bisulphite pyrosequencing for the nine clustered CpG sites. We were able to capture an additional CpG site with careful assay design for a total of ten CpG sites analysed via bisulphite pyrosequencing. We successfully validated the RRBS findings, confirming that there was significant hypomethylation among these ten sites with cannabis use. We confirmed a significant inverse correlation between methylation and expression at this region in human conceptal brain tissues.

To begin to determine whether or not the effects of cannabis on sperm are heritable, we analysed sperm from THC exposed and control male rats, as well as the hippocampus and nucleus accumbens from offspring of THC exposed and control males for changes in DNA methylation at Dlgap2. Rats exposed to THC were given a dose (4mg/kg THC for 28 days) that is pharmacodynamically equivalent to daily cannabis use to resemble frequent use in humans. We identified significant hypomethylation at Dlgap2 in the sperm of exposed rats as compared to controls. This hypomethylated state was also detected in the nucleus accumbens of rats born to THC exposed fathers compared to controls, supporting the potential for intergenerational inheritance of an altered sperm DNA methylation pattern. While the changes in the degree of methylation are small in the rats (0.5–0.7%), we previously reported that fractional changes in methylation can significantly influence the degree to which the gene’s expression is altered [31].

DLGAP2 is a member of the DLGAP family of scaffolding proteins located in the post-synaptic density (PSD) of neurons. The PSD is a protein-dense web that lies under the postsynaptic membrane of neurons and facilitates excitatory glutamatergic signaling in the central nervous system [26,32]. DLGAP2 functions to transmit neuronal signals across synaptic junctions and helps control downstream signaling events [26,32]. Due to its important role in PSD signaling, even small changes in the expression of DLGAP2 can have severe consequences [26,32]. Of particular relevance, DLGAP2 has been linked to schizophrenia and importantly, has been identified as an autism candidate gene [27,28,33,34]. Differential methylation of DLGAP2 is reported in the brain of individuals with autism, and has been linked to post-traumatic stress disorder in rats [27,35]. Knockout of Dlgap2 in mice results in abnormal social behaviour, increased aggressive behaviour, and learning deficits [36].

Studies are increasingly showing associations between cannabis use and various neuropsychiatric and behavioural disorders including anxiety, depression, cognitive deficits, autism, psychosis, and addiction [2,6,7,9,14,3739]. Research looking into the effects of THC exposure found that rat pups born to parents who were exposed to THC during adolescence showed increased effort to self-administer heroin compared to those born to unexposed parents [13]. This increase in addictive behaviour was driven by THC-induced changes in DNA methylation, occurring in the striatum, including the nucleus accumbens [14,15]. One of the genes whose methylation was altered by parental THC exposure was Dlgap2 [15]. Recently, a group from Australia analysed datasets from two independent cohorts to examine the relationship between cannabis legalization in the U.S. and ASD incidence. They determined there was a strikingly significant positive association between cannabis legalization and increased ASD incidence. Further, the study authors predicted that there will be a 60% increase in excess ASD cases in states with legal cannabis by 2030, and deemed ASD the most common form of cannabis-associated clinical teratology [40].

It is estimated that the ratio of boys with ASD to girls with ASD is 4:1 which led us to stratify our analysis looking at the relationship between DNA methylation and gene expression by sex [41,42]. The results of our methylation-expression analyses demonstrated a significant association in females but not males. While we don’t know the ASD status of these samples, there are several reasons why this may be the case. First, there are certain genes that confer a stronger ASD phenotype in girls compared to boys [41,42]. Thus, while we see the trend in both sexes, it is possible that dysregulation of this gene may manifest phenotypically more in girls. Alternatively, it may be that the regulatory relationship between methylation and expression is retained in females while altered methylation further exacerbates an already fragile relationship in males. Overall, this data confirms that the region of DNA methylation within DLGAP2 that was differentially methylated in the sperm of cannabis users compared to controls is functionally important in the brain.

DLGAP2 is an imprinted gene that exhibits paternal expression in the testis, biallelic expression in the brain, and low expression elsewhere in the body [30]. Because the methylation established at imprinted genes resists post-fertilization epigenetic reprogramming [4345], this supports the possibility that changes in methylation at DLGAP2 in sperm could be transmitted to the next generation. However, given that the region in intron 7 is not an ICR, it is unlikely that this would be a potential mechanism for intergenerational inheritance of an altered methylation pattern at this region. However, it has recently been discovered that a subset of genes termed ‘escapees’ are able to escape primordial germ cell (PGC) and post-fertilization reprogramming events [46,47], providing a mechanism for epigenetic changes incurred by sperm to be passed on to the subsequent generation.

Processes in the PSD are sensitive to endocannabinoids [26,4851], which suggests that these processes are potentially sensitive to exogenous cannabinoids, such as THC and cannabis. This is especially important as cannabis legalization and use are increasing dramatically across the U.S. It is estimated that 22% of American adults currently use cannabis, of which 63% are regular users (≥1–2 times per month) [710]. Among regular users 55% are males and over half of all men over 18 have reported cannabis use in their lifetime [710]. Importantly, this age range includes individuals of reproductive age. Since almost half of all pregnancies in the U.S. are unplanned, there is concern that many pregnancies may occur during a time when one, or both, parents are using or are exposed to cannabis [52].

Our results provide novel findings about the effects of paternal cannabis use on the methylation status of an ASD candidate gene, a disorder whose rates continue to climb, but whose precise aetiologies remain unknown. Studies are beginning to show that there is a potential for paternal intergenerational inheritance. In particular, epigenetic changes in umbilical cord blood of babies born to obese fathers were also found in the sperm of obese men. This study is the first to demonstrate that there are changes present in the sperm epigenome of cannabis users at a gene involved in ASD.

The results of this study have several limitations. The sample size was small, which might limit generalization of the study findings. However, even though our sample size was small, we were able to identify common pathways that were differentially methylated in both human and rat sperm, highlighting the potential specificity of these effects [25]. We did not account for a wide variety of potential confounders such as various lifestyle habits, sleep, diet/nutrition, exercise, etc, given that their influence on the sperm DNA methylome is largely unknown. Larger studies are required to confirm these findings. In the conceptal tissues we were only able to analyse whole brain, rather than the areas where DLGAP2 is most highly expressed such as the hippocampus and the striatum, which could have diluted the strength of the results.

Strengths of the study included that we used a highly quantitative method to confirm the methylation status that was measured by RRBS. This study was the first demonstration of the association between cannabis use and substantial hypomethylation of DLGAP2 in human sperm. Additionally, we are able to confirm a functional relationship between methylation and expression in a relevant target tissue, and have shown that the relationship between methylation and expression is weakened in males, which could bear relevance to the sexual dimorphism in the prevalence of autism. This is the first demonstration of potential heritability of altered methylation resulting from preconceptional paternal THC exposure. Given the increasing legalization and use of cannabis in the U.S., our results underscore a need for larger studies to determine the potential for heritability of DLGAP2 methylation changes in the human F1 generation and beyond. It will also be important to examine how cannabis-associated methylation changes relate to neurobehavioral phenotypes

Source:   Epigenetics. 2020; 15(1-2): 161–173.

Published online 2019 Aug 26. doi: 10.1080/15592294.2019.1656158

Highlights

  • Population-based longitudinal cohort study over 30 years spanning age 19/20 to 49/50
  • Cannabis use in adolescence predicted the occurrence of depression and suicidality in adulthood
  • Association between adolescent cannabis use and adult depression/suicidality hold when adjusted for various covariates, including time-varying pattern of substance abuse in adulthood
  • Younger age at first cannabis use and more frequent use in adolescence related to an particularly increased risk of adult depression

Abstract

  • Objective

    To examine the association between cannabis use in adolescence and the occurrence of depression, suicidality and anxiety disorders during adulthood.

  • Methods

    A stratified population-based cohort of young adults (n = 591) from Zurich, Switzerland, was retrospectively assessed at age 19/20 for cannabis use in adolescence. The occurrence of depression, suicidality and anxiety disorders was repeatedly assessed via semi-structured clinical interviews at the ages of 20/21, 22/23, 27/28, 29/30, 34/35, 40/41, and 49/50. Associations were controlled for various covariates, including socio-economic deprivation in adolescence as well as repeated time-varying measures of substance abuse during adulthood.

  • Results

    About a quarter (24%) reported cannabis use during adolescence; 11% started at age 15/16 or younger and 13% between the ages of 16/17 and 19/20. In the adjusted multivariable model, cannabis use during adolescence was associated with adult depression (aOR = 1.70, 95%-CI = 1.24–2.32) and suicidality (aOR = 1.65, 95%-CI = 1.11–2.47), but not anxiety disorders (aOR = 1.10, 95%-CI = 0.82–1.48). First use at age 15/16 and younger (as against first use between age 16/17 and 19/20 and no use) and frequent use in adolescence (as against less frequent use and no use) were associated with a higher risk of depression in adult life.

  • Conclusions

    In this longitudinal cohort study over 30-years, cannabis use during adolescence was associated with depression and suicidality in adult life. Young age at first use and high frequency of use in adolescence may particularly increase the risk of depression in adulthood. All associations were independent of cannabis abuse and other substance abuse during adulthood.

Introduction

An extensive body of evidence suggests that cannabis use in adolescence increases the risk of adult psychotic disorders (Arseneault et al., 2002, Moore et al., 2007, Rossler et al., 2012); based on Mendelian randomization studies it appears that this association may at least partly be causal (Gage et al., 2017, Vaucher et al., 2018). However, it is less clear whether adolescent cannabis use also predicts depression and other affective disorders (Moore et al., 2007). For instance, a recent 35-year longitudinal cohort study of male conscripts found a weak association between cannabis use and an increased risk for depression, but this association disappeared after adjustment for covariates (Manrique-Garcia et al., 2012).

Another prospective population-based study over 3 years including both male and female adults likewise found that cannabis use at baseline weakly increased the risk of depression and anxiety, but once again these associations disappeared after controlling for covariates (comprising alcohol and drug use, education level, and family climate) (Danielsson et al., 2016). In contrast, a longitudinal cohort study of 14-15 year-old students followed over seven years reported a remarkably strong association between early cannabis use and later depression and anxiety that persisted after adjustment for baseline covariates (Patton et al., 2002). Finally, a recent meta-analysis of longitudinal studies found that adolescent cannabis use predicts the development of depression (OR = 1.4), suicidal ideation (OR = 1.5) and suicide attempts (OR = 3.5), but not anxiety (OR = 1.2), in young adulthood (Gobbi et al., 2019).

The aim of the present work was to re-address the association between adolescent cannabis use and later mood and anxiety disorders. We extended previous research by focusing separately on mood disorders, anxiety disorders and suicidality. Moreover, we did not only control for baseline covariates, such as family climate and socio-economic background, but also for concomitant abuse of both alcohol and illicit drugs (including both cannabis and other substances) across the participants’ adult lives. Finally, with a total observation period of 30 years, the present longitudinal study is much longer than most research conducted thus far.

Section snippets

Participants and sampling procedure

The Zurich Study comprised a cohort of 4547 subjects (m = 2201; f = 2346) representative of the canton of Zurich in Switzerland, who were screened in 1978 with the Symptom Checklist 90-Revised (SCL-90-R) (Derogatis, 1977) when males were 19 and females 20 years old. Male and female participants were sampled with different approaches. In Switzerland, every man of Swiss nationality must undertake a military screening test at the age of 19. With the consent of the military authorities, but…

Results

Comprehensive dropout analyses of this cohort have been presented elsewhere (Eich et al., 2003, Hengartner et al., 2016). In short, dropouts appeared to be either extremely low or extremely high scorers on the SCL GSI, but except for a weak gender bias (men were more likely to drop out) there were no baseline characteristics that predicted early study termination. The frequencies of adolescent cannabis use and baseline socio-demographic characteristics are shown in Table 1. In total 143 of 586…

Discussion

In this 30-year longitudinal cohort-study we examined the associations between cannabis use in adolescence (i.e. before the age of 19/20 years) and the development of depressive disorders, severe suicidality and anxiety disorder during adulthood (i.e. between the ages of 20/21 and 49/50). Our results show that cannabis use in adolescence, independently of substance abuse in adulthood, is significantly related to the occurrence of depressive disorders and severe suicidality, but not to anxiety…

Funding

The Zurich Cohort Study was supported by the Swiss National Science Foundation (Grant number 32-50881.97). The donator/sponsor had no further role in the experimental design, the collection, analysis, and interpretation of data, the writing of this report, or the decision to submit this paper for publication…

Author contributions

MPH drafted the manuscript and conducted all statistical analyses; JA and WR contributed to design and conduct of the study, interpretation of the data and critical revision of the manuscript; VAG contributed to interpretation of the data and critical revision. All authors approved the final version of this manuscript…

Source: https://www.sciencedirect.com/science/article/abs/pii/S0165032719320919 May 2020

In what is sure to be a controversial finding among cannabis users and proponents, a review of existing research published this week in The Lancet Psychiatry suggests that a single dose of THC may induce a variety of psychiatric symptoms associated with schizophrenia and other psychiatric disorders.

According to a news release issued by The Lancet on March 17:

A single dose of the main psychoactive component in cannabis, tetrahydrocannabinol (THC), can induce a range of psychiatric symptoms, according to results of a systematic review and meta-analysis of 15 studies including 331 people with no history of psychotic or other major psychiatric disorders, published in The Lancet Psychiatry journal.

The study was funded by the Medical Research Council and was conducted by researchers from Kings College London, South London and the Maudsley NHS Foundation Trust, Imperial College London, Leiden University Medical Hospital, Yale University School of Medicine, Connecticut Mental Health Center, and VA Connecticut Healthcare System.

The study also notes that these psychiatric symptoms are not associated with cannabidiol (CBD), one of the other major active compounds in cannabis. The authors reviewed four studies examining CBD’s effects on the development of the same psychiatric symptoms, and no significant differences were found between the effects of CBD and the effects of a placebo. “In studies that focused on whether CBD counters THC-induced symptoms, one study identified reduced symptoms, using a modest sample, but three larger studies failed to replicate this finding.”

The aforementioned news release quotes King’s College professor Oliver Howes as saying, “As the THC-to-CBD ratio of street cannabis continues to increase, it is important to clarify whether these compounds can cause psychotic symptoms. Our finding that THC can temporarily induce psychiatric symptoms in healthy volunteers highlights the risks associated with the use of THC-containing cannabis products. This potential risk should be considered in discussions between patients and medical practitioners thinking about using cannabis products with THC. This work will also inform regulators, public health initiatives, and policy makers considering the medical use of THC-containing cannabis products or their legalisation for recreational use.” 

There’s an important distinction to note here. Although the researchers found that a dose of THC—which they say is roughly equivalent to a single joint—can induce symptoms that mimic those of certain psychiatric disorders, THC does not in fact cause said disorders in users. 

This will come as little surprise to cannabis users, who are well aware from decades of anecdotal evidence that smoking a joint can make some people a little paranoid, but it has certainly never made anyone schizophrenic.

To put things in perspective, consider that in a commentary he wrote for the Straight last August, author and activist Dana Larsen noted that “every analysis of relative drug harms lists cannabis as one of the safest psychoactive substances there is.”

You can read the paper, which is title “Psychiatric symptoms caused by cannabis constituents: a systematic review and meta-analysis”, at the Lancet Psychiatry website.

Source:  https://www.straight.com/cannabis/1374471/review-studies-suggests-thc-cannabis-could-induce-psychotic-symptoms-healthy-people  19th March 2020

A meta-analysis of all studies worldwide showing association between marijuana use and schizophrenia:

Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319–328.
http://dirwww.colorado.edu/alcohol/downloads/Cannabis_and_behavior.pdf

“There was an increased risk of any psychotic outcome in individuals who had ever used cannabis…with greater risk in people who used cannabis most frequently. There is now sufficient evidence to warn young people that using cannabis could increase their risk of
developing a psychotic illness later in life.”

The most recent study conducted in the United States (Columbia University, New York), showing a high risk (odds ratio, “OR”) for schizophrenia spectrum disorders, particularly in those who become cannabis-dependent:

Davis GP, Compton MT, Wang S, Levin FR, Blanco C. Association between cannabis use, psychosis, and schizotypal personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Schizophr Res. 2013 Dec;151(1-3):197-202.
“There was a similar dose-response relationship between the extent of cannabis use and schizotypal personality disorder (OR=2.02 for lifetime cannabis use, 95% CI 1.69-2.42; OR=2.83 for lifetime cannabis abuse, 95% CI 2.33-2.43; OR=7.32 for lifetime cannabis dependence, 95% CI 5.51-9.72). Likelihood of individual schizotypal features increased significantly with increased extent of cannabis use in a dose-dependent manner.”

Studies that corrected for general genetic background effects and many non-cannabis environmental variables by comparing siblings. The risk ratios are somewhat lower than general population studies, because genetic predisposition is more or less controlled for:

McGrath J, Welham J, Scott J, Varghese D, Degenhardt L, Hayatbakhsh MR, Alati R, Williams GM, Bor W, Najman JM. Association between cannabis use and psychosis-related outcomes using sibling pair analysis in a cohort of young adults. Arch Gen Psychiatry. 2010; 67(5):440-7.
“Longer duration since first cannabis use was associated with multiple psychosis-related outcomes in young adults… the longer the duration since first cannabis use, the higher the risk of psychosis-related outcomes…
Compared with those who had never used cannabis, young adults who had 6 or more years since first use of cannabis (i.e., who commenced use when around 15 years or younger) were twice as likely to develop a nonaffective psychosis…
This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.”

Giordano GN, Ohlsson H, Sundquist K, Sundquist J, Kendler KS. The association between cannabis abuse and subsequent schizophrenia: a Swedish national co-relative control study.
Psychol Med. 2014 Jul 3:1-8. [Epub ahead of print]
http://journals.cambridge.org/download.php?file=%2FPSM%2FS0033291714001524a.pdf&code=79f795824a92c8eead870197ef071dd8

“Allowing 7 years from initial CA registration to later diagnosis, the risk for schizophrenia in discordant full sibling pairs remained almost twofold….The results of this study therefore lend support to the etiologic hypothesis, that CA is one direct cause of later schizophrenia.”

Those diagnosed with schizophrenia who also use recreational drugs are much more likely to be violent, including those who use cannabis:

Fazel S, Långström N, Hjern A, Grann M, Lichtenstein P. Schizophrenia, substance abuse, and violent crime. JAMA. 2009 May 20;301(19):2016-23.
“The risk was mostly confined to patients with substance abuse comorbidity (of whom 27.6% committed an offense), yielding an increased risk of violent crime among such patients (adjusted OR, 4.4; 95% CI,3.9-5.0), whereas the risk increase was small in schizophrenia patients without substance abuse comorbidity (8.5% of whom had at least 1 violent offense; adjusted OR,1.2; 95% CI, 1.1-1.4; P<0.001 for interaction).”

Fazel S, Gulati G, Linsell L, Geddes JR, Grann M. Schizophrenia and violence: systematic review and meta-analysis. PLoS Med. 2009 Aug;6(8):e1000120. doi: 10.1371/journal.pmed.1000120. Epub 2009 Aug 11.
“The effect of comorbid substance abuse was marked with….. an OR of 8.9” (as compared to the general population)

Arseneault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin Study. Arch Gen Psychiatry. 2000;57(10):979-86.
“for having more than two of these disorders at once…..the OR (odds ratio for violence) was, …..for marijuana dependence plus schizophrenia spectrum disorder, 18.4”

Harris AW, Large MM, Redoblado-Hodge A, Nielssen O, Anderson J, Brennan J. Clinical and cognitive associations with aggression in the first episode of psychosis. Aust N Z J Psychiatry. 2010 Jan;44(1):85-93.
‘The use of cannabis with a frequency of more than fourfold in the previous month was the only factor that was found to be associated with serious aggression’

Self-report of psychotic symptoms by otherwise healthy users (12% to 15%):

Thomas H. A community survey of adverse effects of cannabis use. Drug Alcohol Depend. 1996 Nov;42(3):201-7.
“This survey estimates the frequency of various adverse effects of the use of the drug cannabis. A sample of 1000 New Zealanders aged 18-35 years were asked to complete a self-administered questionnaire on cannabis use and associated problems. The questionnaire was derived from criteria for the identification of cannabis abuse which are analagous to criteria commonly used to diagnose alcoholism. Of those who responded 38% admitted to having used cannabis. The most common physical or mental health problems, experienced by 22% of users were acute anxiety or panic attacks following cannabis use. Fifteen percent reported psychotic symptoms following use.”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%).”

Barkus EJ, Stirling J, Hopkins RS, Lewis S.. Cannabis-induced psychosis-like experiences are associated with high schizotypy Psychopathology 2006;39(4):175-8.
“In the sample who reported ever using cannabis (72%) the means for the subscales from the CEQ were as follows: ……Psychotic-Like Experiences (12.98%).”

Rates of psychotic symptoms in those with cannabis dependence as compared to non-dependent users and nonusers:

Fergusson DM, Horwood LJ, Swain-Campbell NR. Cannabis dependence and psychotic symptoms in young people. Psychol Med. 2003 Jan;33(1):15-21.
“Young people meeting DSM-IV criteria for cannabis dependence had elevated rates of psychotic symptoms at ages 18 (rate ratio = 3.7; 95% CI 2.8-5.0; P < 0.0001) and 21 (rate ratio = 2.3; 95% CI 1.7-3.2; P < 0.0001).”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“more than half of the respondents who were dependent on cocaine (80%), cannabis (63.5%), amphetamines (56.1%), and opiates (53.1%) reported psychotic symptoms. Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%)……. There was also a marked increase in the risk for psychotic symptoms when dependence became moderate or severe for cannabis (OR=25.1, OR=26.8; respectively).”

Studies on the psychotomimetic properties of THC administered to healthy individuals in the clinic:

D’Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH. The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis. Neuropsychopharmacology. 2004 Aug;29(8):1558-72.
“∆-9-THC (1) produced schizophrenia-like positive and negative symptoms; (2) altered perception;(3) increased anxiety; (4) produced euphoria; (5) disrupted immediate and delayed word recall, sparing recognition recall; (6) impaired performance on tests of distractibility, verbal fluency, and working memory (7) did not impair orientation; (8) increased plasma cortisol. These data indicate that D-9-THC produces a broad range of transient symptoms, behaviors, and cognitive deficits in healthy individuals that resemble some aspects of endogenous psychoses.”

Morrison PD, Nottage J, Stone JM, Bhattacharyya S, Tunstall N, Brenneisen R, Holt D, Wilson D, Sumich A, McGuire P, Murray RM, Kapur S, Ffytche DH. Disruption of frontal θ coherence by ∆9-tetrahydrocannabinol is associated with positive psychotic symptoms. Neuropsychopharmacology. 2011;;36(4):827-36.
“Compared with placebo, THC evoked positive and negative psychotic symptoms, as measured by the positive and negative syndrome scale (p<0.001)…… The results reveal that the pro-psychotic effects of THC might be related to impaired network dynamics with impaired communication between the right and left frontal lobes.”

Bhattacharyya S, Crippa JA, Allen P, Martin-Santos R, Borgwardt S, Fusar-Poli P, Rubia K, Kambeitz J, O’Carroll C, Seal ML, Giampietro V, Brammer M, Zuardi AW, Atakan Z, McGuire PK. Induction of psychosis by ∆9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing. Arch Gen Psychiatry. 2012 Jan;69(1):27-36. doi: 10.1001/archgenpsychiatry.2011.161.
“Pairwise comparisons revealed that 9-THC significantly increased the severity of psychotic symptoms compared with placebo (P<.001) and CBD (P<.001).”,

Freeman D, Dunn G, Murray RM, Evans N, Lister R, Antley A, Slater M, Godlewska B, Cornish R, Williams J, Di Simplicio M, Igoumenou A, Brenneisen R, Tunbridge EM, Harrison PJ, Harmer CJ, Cowen P, Morrison PD. How Cannabis Causes Paranoia: Using the Intravenous Administration of ∆9-Tetrahydrocannabinol (THC) to Identify Key Cognitive Mechanisms Leading to Paranoia. Schizophr Bull. 2014 Jul 15. pii: sbu098. [Epub ahead of print]
“THC significantly increased paranoia, negative affect (anxiety, worry, depression, negative thoughts about the self), and a range of anomalous experiences, and reduced working memory capacity.”

For data on dose-response (a very large study by Zammit et al., and another by van Os et al.) and the greater risk for psychosis posed by high strength marijuana (DiForti et al.):

Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G, 2002, Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ. 2002 Nov 23;325(7374):1199. http://www.bmj.com/content/325/7374/1199.full.pdf
“We found a dose dependent relation between frequency of cannabis use and risk of schizophrenia, with an adjusted odds ratio for linear trend across the categories of frequency of cannabis use used in this study of 1.2 (1.1 to 1.4, P < 0.001). The adjusted odds ratio for subjects with a history of heaviest use of cannabis ( > 50 occasions) was 3.1 (1.7 to 5.5)………………Cannabis use is associated with an increased risk of
developing schizophrenia, consistent with a causal relation. This association is not explained by use of other psychoactive drugs or personality traits relating to social integration.”

van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol. 2002 Aug 15;156(4):319-27.
“…..further evidence supporting the hypothesis of a causal relation is demonstrated by the existence of a dose-response relation.. between cumulative exposure to cannabis use and the psychosis outcome……. About 80 percent of the psychosis outcome associated with exposure to both cannabis and an established vulnerability to psychosis was attributable to the synergistic action of these two factors. This finding indicates that, of the subjects exposed to both a vulnerability to psychosis and cannabis use, approximately 80 percent had the psychosis outcome because of the combined action of the two risk factors and only about 20 percent because of the action of either factor alone.”

DiForti M, Morgan C, Dazzan P, Pariante C, Mondelli V, Marques TR, Handley R, Luzi S, Russo M, Paparelli A, Butt A, Stilo SA, Wiffen B, Powell J, Murray RM. High-potency cannabis and the risk of psychosis. Br J Psychiatry. 2009,195(6):488-91.
“78% (n = 125) of the cases group preferentially used sinsemilla (skunk) compared with only 31% (n = 41) of the control group (unadjusted OR= 8.1, 95% CI 4.6–13.5). This association was only slightly attenuated after controlling for potential confounders (adjusted OR= 6.8, 95% CI 2.6–25.4)………. Our most striking finding is that patients with a first episode of psychosis preferentially used high-potency cannabis preparations of the sinsemilla (skunk) variety…… our results suggest that the potency and frequency of cannabis use may interact in further increasing the risk of psychosis.”

DiForti M, Marconi A, Carra E, Fraietta S, Trotta A, Bonomo M, Bianconi F, Gardner-Sood P, O’Connor J, Russo M, Stilo SA, Marques TR, Mondelli V, Dazzan P, Pariante C, David AS, Gaughran F, Atakan Z, Iyegbe C, Powell J, Morgan C, Lynskey M, Murray RM. Proportion of
patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study. Lancet Psychiatry, online February 18, 2015, http://dx.doi.org/10.1016/S2215-0366(14)00117-5.
“In the present larger sample analysis, we replicated our previous report and showed that the highest probability to suffer a psychotic disorder is in those who are daily users of high potency cannabis. Indeed, skunk use appears to contribute to 24% of cases of first episode psychosis in south London. Our findings show the importance of raising awareness among young people of the risks associated with the use of high-potency cannabis. The need for such public education is emphasised by the worldwide trend of liberalisation of the legal constraints on cannabis and the fact that high potency varieties are becoming much more widely available.”

For data on percent of those with marijuana-induced psychosis who go on to receive a diagnosis of a schizophrenia spectrum disorder:

Arendt M, Mortensen PB, Rosenberg R, Pedersen CB, Waltoft BL. Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia. Arch Gen Psychiatry. 2008;65(11):1269-74. http://archpsyc.ama-assn.org/cgi/reprint/65/11/1269
“Approximately half of the subjects who received treatment of a cannabis induced psychosis developed a schizophrenia spectrum disorder within 9 years after treatment…… The risk of schizophrenia after a cannabis-induced psychosis is independent of familial predisposition……. cannabis-induced psychosis may not be a valid diagnosis but an early marker of schizophrenia……. Psychotic symptoms after cannabis
use should be taken extremely seriously.”

Niemi-Pynttäri JA, Sund R, Putkonen H, Vorma H, Wahlbeck K, Pirkola SP. Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. J Clin Psychiatry. 2013 74(1):e94-9.
“Eight-year cumulative risk to receive a schizophrenia spectrum diagnosis was 46% for persons with a diagnosis of cannabis-induced psychosis ….. chances for amphetamine-, hallucinogen-, opioid-, sedative- and alcohol-induced (schizophrenia spectrum diagnoses) were 30%, 24%, 21%, and 5% respectively.”

For cause and effect (which comes first: psychosis or marijuana use):
Arseneault L, Cannon M, Poulton R, Murray R, Caspi A, Moffitt TE, 2002, Cannabis use in
adolescence and risk for adult psychosis: longitudinal prospective study.BMJ. 2002 Nov 23;325(7374):1212-3.
“Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis. Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). Thirdly, risk was specific to cannabis use, as opposed to use of other drugs….”

Henquet C, Krabbendam L, Spauwen J, et al. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ. 2005;330:11–15. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC539839/pdf/bmj33000011.pdf
“Exposure to cannabis during adolescence and young adulthood increases the risk of psychotic symptoms later in life. Cannabis use at baseline increased the cumulative incidence of psychotic symptoms at follow up four years later…but has a much stronger effect in those with evidence of predisposition for psychosis……….Predisposition for psychosis at baseline did not significantly predict cannabis use four years later..”

and also:

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: d738 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021)…………There was no evidence for self medication effects, as psychotic experiences at T2 did not predict incident cannabis use between T2 and T3 (0.8, 0.6 to 1.2; P=0.3).”

For data on those who quit using when psychotic symptoms develop (further evidence against self-medication):

Fergusson DM, Horwood LJ, Ridder EM. Tests of causal linkages between cannabis use and psychotic symptoms. Addiction. 2005;100(3):354-66.

For degree of risk relative to other drugs:

Niemi-Pynttäri JA, Sund R, Putkonen H, Vorma H, Wahlbeck K, Pirkola SP. Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. J Clin Psychiatry. 2013 74(1):e94-9.
“Eight-year cumulative risk to receive a schizophrenia spectrum diagnosis was 46% for persons with a diagnosis of cannabis-induced psychosis ….. chances for amphetamine-, hallucinogen-, opioid-, sedative- and alcohol-induced (schizophrenia spectrum diagnoses) were 30%, 24%, 21%, and 5% respectively.”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“more than half of the respondents who were dependent on cocaine (80%), cannabis (63.5%), amphetamines (56.1%), and opiates (53.1%) reported psychotic symptoms. Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%)……. There was also a marked increase in the risk for psychotic symptoms when dependence became moderate or severe for cannabis (OR=25.1, OR=26.8; respectively).”

Another angle on the potential confound of self-medication: genetic predisposition for schizophrenia does not predict cannabis use:

Veling W, Mackenbach JP, van Os J, Hoek HW. Cannabis use and genetic predisposition for schizophrenia: a case-control study. Psychol Med. 2008 Sep;38(9):1251-6. Epub 2008 May 19.
“BACKGROUND: Cannabis use may be a risk factor for schizophrenia. RESULTS: Cannabis use predicted schizophrenia [adjusted odds ratio (OR) cases compared to general hospital controls 7.8, 95% confidence interval (CI) 2.7-22.6; adjusted OR cases compared to siblings 15.9 (95% CI 1.5-167.1)], but genetic predisposition for schizophrenia did not predict cannabis use [adjusted OR intermediate predisposition
compared to lowest predisposition 1.2 (95% CI 0.4-3.8)].”

For data on potential benefits of cessation:

González-Pinto A, Alberich S, Barbeito S, Gutierrez M, Vega P, Ibáñez B, Haidar MK, Vieta E, Arango C. Cannabis and first-episode psychosis: different long-term outcomes depending on continued or discontinued use. Schizophr Bull. 2011 May;37(3):631-9. Epub 2009 Nov 13. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080669/pdf/sbp126.pdf
“OBJECTIVE: To examine the influence of cannabis use on long-term outcome in patients with a first psychotic episode, comparing patients who have never used cannabis with (a) those who used cannabis before the first episode but stopped using it during follow-up and (b) those who used cannabis both before the first episode and during follow-up….. CONCLUSION: Cannabis has a deleterious effect, but stopping use after the first psychotic episode contributes to a clear improvement in outcome. The positive effects of stopping cannabis use can be seen more clearly in the long term.”

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“The finding that longer exposure to cannabis was associated with greater risk for persistence of psychotic experiences is in line with an earlier study showing that continued cannabis use over time increases the risk for psychosis in a dose-response fashion. This is also in agreement with the hypothesis that a process of sensitisation might underlie emergence and persistence of psychotic experiences as an indicator of liability to psychotic disorder.”

For data on marijuana use resulting in an earlier age of onset of schizophrenia (suggestive of causality), see Dragt et al. and a meta-analysis (see Large et al.,); also: a very extensive (676 schizophrena patients) and therefore more statistically powered analysis (see DeHert paper); two papers showing that the age-of-onset effect may be specific to those without a family history (see Scherr et al. and Leeson et al., papers); two studies that evaluate the age of onset specific to gender (Veen et al. and Compton et al. ) which is important because comparing across genders can be confounded by the greater tendency of males to engage in risky behavior (the conclusions are not the same in terms of gender; the gender distribution was slightly better in the Veen et al. study) and finally, two papers of relevance to specificity of age of onset effect to cannabis, a meta-analysis of published studies on age of onset that shows another drug of abuse (tobacco) is not associated with
a decreased age of onset (Myles et al.) and a study showing that ecstasy, LSD, stimulants, or sedatives did not have an effect to lower age of onset whereas cannabis use did (Barnes et al.) :

Large M, Sharma S, Compton MT, Slade T, Nielssen O. Cannabis Use and Earlier Onset of Psychosis: A Systematic Meta-analysis. Arch Gen Psychiatry. 2011 68(6):555-61. http://www.ncbi.nlm.nih.gov/pubmed/21300939
“The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.”

Dragt S, Nieman DH, Schultze-Lutter F, van der Meer F, Becker H, de Haan L, Dingemans PM, Birchwood M, Patterson P, Salokangas RK, Heinimaa M, Heinz A, Juckel G, Graf von Reventlow H, French P, Stevens H, Ruhrmann S, Klosterkötter J, Linszen DH; on behalf of the EPOS group.Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Acta Psychiatr Scand. 2011 Aug 29. doi: 10.1111/j.1600-0447.2011.01763.x. [Epub ahead of print]
“Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Objective: Numerous studies have found a robust association between cannabis use and the onset of psychosis. Nevertheless, the relationship between cannabis use and the onset of early (or, in retrospect, prodromal) symptoms of psychosis remains unclear. The study focused on investigating the relationship between cannabis
use and early and high-risk symptoms in subjects at clinical high risk for psychosis. Results: Younger age at onset of cannabis use or a cannabis use disorder was significantly related to younger age at onset of six symptoms (0.33 < r(s) < 0.83, 0.004 < P < 0.001). Onset of cannabis use preceded symptoms in most participants. Conclusion: Our results provide support that cannabis use plays an important role in the development of psychosis in vulnerable individuals.”

De Hert M, Wampers M, Jendricko T, Franic T, Vidovic D, De Vriendt N, Sweers K, Peuskens J, van Winkel R.Effects of cannabis use on age at onset in schizophrenia and bipolar disorder. Schizophr Res. 2011 Mar;126(1-3):270-6.

“BACKGROUND: Cannabis use may decrease age at onset in both schizophrenia and bipolar disorder, given the evidence for substantial phenotypic and genetic overlap between both disorders….RESULTS:… Both cannabis use and a schizophrenia diagnosis predicted earlier age at onset. There was a significant interaction between cannabis use and diagnosis, cannabis having a greater effect in bipolar patients….DISCUSSION:…. Our results suggest that cannabis use is associated with a reduction in age at onset in both schizophrenic and bipolar patients. This reduction seems more pronounced in the bipolar group than in the schizophrenia group: the use of cannabis reduced age at onset by on average 8.9 years in the bipolar group, as compared to an average predicted reduction of 1.5 years in the schizophrenia group.”

Scherr M, Hamann M, Schwerthöffer D, Froböse T, Vukovich R, Pit schel-Walz G, Bäuml J.. Environmental risk factors and their impact on the age of onset of schizophrenia: Comparing familial to non-familial schizophrenia. Nord J Psychiatry. 2011 Aug 31. [Epub ahead of print]
“Background and aims: Several risk factors for schizophrenia have yet been identified. The aim of our study was to investigate how certain childhood and adolescent risk factors predict the age of onset of psychosis in patients with and without a familial component (i.e. a relative with schizophrenia or schizoaffective disorder). Results: Birth complications and cannabis abuse are predictors for an earlier onset of schizophrenia in patients with non-familial schizophrenia. No environmental risk factors for an earlier age of onset in familial schizophrenia have been identified.”

Leeson VC, Harrison I, Ron MA, Barnes TR, Joyce EM. The Effect of Cannabis Use and Cognitive Reserve on Age at Onset and Psychosis Outcomes in First-Episode Schizophrenia. Schizophr Bull. 2011 Mar 9. [Epub ahead of print] http://schizophreniabulletin.oxfordjournals.org/content/early/2011/03/09/schbul.sbq153.full.pdf+html
“Objective: Cannabis use is associated with a younger age at onset of psychosis, an indicator of poor prognosis, but better cognitive function, a positive prognostic indicator. We aimed to clarify the role of age at onset and cognition on outcomes in cannabis users with first-episode schizophrenia as well as the effect of cannabis dose and cessation of use……Conclusions: Cannabis use brings forward the onset of psychosis in people who otherwise have good prognostic features indicating that an early age at onset can be due to a toxic action of cannabis rather than an intrinsically more severe illness. Many patients abstain over time, but in those who persist, psychosis is more difficult to treat.”

Veen ND, Selten JP, van der Tweel I, Feller WG, Hoek HW, Kahn RS. Cannabis use and age at onset of schizophrenia. Am J Psychiatry. 2004 Mar;161(3):501-6. http://ajp.psychiatryonline.org/cgi/reprint/161/3/501
“The results indicate a strong association between use of cannabis and earlier age at first psychotic episode in male schizophrenia patients.”

Compton MT, Kelley ME, Ramsay CE, Pringle M, Goulding SM, Esterberg ML, Stewart T, Walker EF. Association of pre-onset cannabis, alcohol, and tobacco use with age at onset of prodrome and age at onset of psychosis in first-episode patients. Am J Psychiatry. 2009 Nov;166(11):1251-7. Epub 2009 Oct 1. http://ajp.psychiatryonlie.org/cgi/reprint/166/11/1251
“Whereas classifying participants according to maximum frequency of use prior to onset (none, ever, weekly, or daily) revealed no significant effects of cannabis or tobacco use on risk of (editor’s note: “timing of”) onset, analysis of change in frequency of use prior to
onset indicated that progression to daily cannabis and tobacco use was associated with an increased risk of onset of psychotic symptoms. Similar or even stronger effects were observed when onset of illness or prodromal symptoms was the outcome. A gender-by-daily-cannabis use interaction was observed; progression to daily use resulted in a much larger increased relative risk of onset of psychosis in females than in males.”

Myles N, Newall H, Compton MT, Curtis J, Nielssen O, Large M. The age at onset of psychosis and tobacco use: a systematic meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2011 Sep 8. [Epub ahead of print]
“Unlike cannabis use, tobacco use is not associated with an earlier onset of psychosis.”

Barnes TR, Mutsatsa SH, Hutton SB, Watt HC, Joyce EM. Comorbid substance use and age at onset of schizophrenia. Br J Psychiatry. 2006 Mar;188:237-42. http://bjp.rcpsych.org/content/188/3/237.full.pdf+html
“Alcohol misuse and any substance use (other than cannabis use) were not significant in relation to age at onset….. those patients in the sample who reported that they had used cannabis had an earlier age at onset of psychosis than other patients who did not report cannabis use but who shared the same profile with regard to the other variables (e.g. comparing men who reported alcohol misuse and use of both cannabis and other drugs with men who had the same characteristics apart from the fact that they had not used cannabis).”

Data from other cultures

Sarkar J, Murthy P, Singh SP. Psychiatric morbidity of cannabis abuse. Indian J Psychiatry. 2003 Jul;45(3):182-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952166/pdf/IJPsy-45-182.pdf
“The paper evaluates the hypothesis that cannabis abuse is associated with a broad range of psychiatric disorders in India, an area with relatively high prevalence of cannabis use. Retrospective case-note review of all cases with cannabis related diagnosis over a 11 -year period, for subjects presenting to a tertiary psychiatric hospital in southern India was carried out. Information pertaining to sociodemographic, personal, social, substance-use related, psychiatric and treatment histories, was gathered. Standardized diagnoses were made according to Diagnostic Criteria for Research of the World Health Organization, on the basis of information available.Cannabis abuse is associated with
widespread psychiatric morbidity that spans the major categories of mental disorders under the ICD-10 system, although proportion of patients with psychotic disorders far outweighed those with non-psychotic disorders. Whilst paranoid psychoses were more prevalent, a significant number of patients with affective psychoses, particularly mania, was also noted.”

Rodrigo C, Welgama S, Gunawardana A, Maithripala C, Jayananda G, Rajapakse S. A retrospective analysis of cannabis use in a cohort of mentally ill patients in Sri Lanka and its implications on policy development. Subst Abuse Treat Prev Policy. 2010 Jul 8;5:16. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910013/pdf/1747-597X-5-16.pdf
”BACKGROUND: Several epidemiological studies have shown that cannabis; the most widely used illegal drug in the world, is associated with schizophrenia spectrum disorders (SSD)……. CONCLUSIONS: Self reported LTC (editor’s note: life time cannabis) use was strongly associated with being diagnosed with SSD (editor’s note: schizophrenia spectrum disorders”.

Population study showing change in incidence rate in young when drug laws are eased

Ajdacic-Gross V, Lauber C, Warnke I, Haker H, Murray RM, Rössler W. Changing incidence of psychotic disorders among the young in Zurich. Schizophr Res. 2007 Sep;95(1-3):9-18. Epub 2007 Jul 16.
“There is controversy over whether the incidence rates of schizophrenia and psychotic disorders have changed in recent decades. To detect deviations from trends in incidence, we analysed admission data of patients with an ICD-8/9/10 diagnosis of psychotic disorders in the Canton Zurich / Switzerland, for the period 1977-2005. The data was derived from the central psychiatric register of the Canton Zurich. Ex-post forecasting with ARIMA (Autoregressive Integrated Moving Average) models was used to assess departures from existing trends. In addition, age-period-cohort analysis was applied to determine hidden birth cohort effects. First admission rates of patients with psychotic
disorders were constant in men and showed a downward trend in women. However, the rates in the youngest age groups showed a strong increase in the second half of the 1990’s. The trend reversal among the youngest age groups coincides with the increased
use of cannabis among young Swiss in the 1990’s.”

Estimates of how many men aged 20-40 would have to avoid regular marijuana use for one year in order to prevent one case of schizophrenia in that same year (but for number relevant to a 20 year avoidance of schizophrenia by avoiding regular marijuana use during
20 years, divide by 20):

Hickman M, Vickerman P, Macleod J, Lewis G, Zammit S, Kirkbride J, Jones P. If cannabis caused schizophrenia–how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations. Addiction. 2009;104(11):1856-61.

“In men the annual mean NNP (number needed to prevent) for heavy cannabis and schizophrenia ranged from 2800 [90% confidence interval (CI) 2018–4530] in those aged 20–24 years to 4700 (90% CI 3114–8416) in those aged 35–39”.

Key studies interpreted to diminish the connection between marijuana and schizophrenia:

Proal AC, Fleming J, Galvez-Buccollini JA, Delisi LE. A controlled family study of cannabis users with and without psychosis. Schizophr Res. 2014 Jan;152(1):283-8.
“The results of the current study, both when analyzed using morbid risk and family frequency calculations, suggest that having an increased familial risk for schizophrenia is the underlying basis for schizophrenia in these samples and not the cannabis use. While cannabismay have an effect on theage of onset of schizophrenia it is unlikely to be the cause of illness.”

Rebuttal: Miller CL. Caution urged in interpreting a negative study of cannabis use and schizophrenia. Schizophr Res. 2014 Apr;154(1-3):119-20.
“The morbid risk reported for the relatives of the non-cannabis-using patients (Sample 3) was actually 1.4-fold higher than the cannabis using patients (Sample 4), but the study did not have enough power to statistically confirm or refute a less than 2-fold difference. An increase in sample size would be required to do so, and if the observed difference were to be confirmed, it would explain not only why the Sample 4 data fits poorly with a multigene/small environmental impact model but also would give weight to the premise that cannabis use significantly contributes to the development of this disease.”

Power RA, Verweij KJ, Zuhair M, Montgomery GW, Henders AK, Heath AC, Madden PA, Medland SE, Wray NR, Martin NG. Genetic predisposition to schizophrenia associated with increased use of cannabis. Mol Psychiatry. 2014 Jun 24. doi: 10.1038/mp.2014.51. [Epub ahead of print] http://emilkirkegaard.dk/en/wp-content/uploads/Genetic%20predisposition%20to%20schizophrenia%20associated%20with%20increased%20use%20of%20cannabis.pdf
“Our results show that to some extent the association between cannabis and schizophrenia is due to a shared genetic aetiology across common variants. They suggest that individuals with an increased genetic predisposition to schizophrenia are
both more likely to use cannabis and to use it in greater quantities.”

Rebuttal: Had this paper been titled “The causal genes for schizophrenia have been discovered” it would never have been published. In the absence of a consistent finding of genes of major effect size for schizophrenia, this study of inconsistently associated genes of low effect size is meaningless.

Buchy L, Perkins D, Woods SW, Liu L, Addington J. Impact of substance use on conversion to psychosis in youth at clinical high risk of psychosis. Schizophrenia Res 156 (2-3): 277–280.
“Results revealed that low use of alcohol, but neither cannabis use nor tobacco use at baseline, contributed to the prediction of psychosis in the CHR sample”.
Rebuttal: The study was small in size and the age range of their subjects at study onset was large (12 to 31) which included both subjects that had not reached the peak age of risk for schizophrenia even by the end of the study as well as subjects who were well past the peak age of onset of schizophrenia. The fact that the study screened out psychotic individuals was problematic for the latter group, in that those who were most vulnerable to the psychosis inducing effects of cannabis would already have converted to psychosis by that age.

Overview of Key Public Health Issues Regarding the Mental Health Effects of Marijuana

For the monetary cost of schizophrenia to the U.S. annually ($63 billion in 2002 dollars):

Wu EQ, Birnbaum HG, Shi L, Ball DE, Kessler RC, Moulis M, Aggarwal J. The economic burden of schizophrenia in the United States in 2002. J Clin Psychiatry. 2005 Sep;66(9):1122-9.

For the trends in adolescent drug, alcohol and cigarette use, showing an upward tick in marijuana use as medical marijuana has become more prevalent, and that the mind-altering drug legal for adults (alcohol) is still more commonly used by teens than is marijuana:

Johnston, L. D., O’Malley, P. M., Bachman, J. G., & Schulenberg, J. E. (2012). Monitoring the Future national results on adolescent drug use: Overview of key findings, 2011. Ann Arbor, MI: Institute for Social Research, The University of Michigan.

For a summary of Sweden’s drug law experience:
Hallam C., 2010, Briefing paper 20, The Beckley Foundation: What Can We Learn from Sweden’s Drug Policy Experience? www.beckleyfoundation.org/pdf/BriefingPaper_20.pdf
“in the case of Sweden, the clear association between a restrictive drug policy and low levels of drug use is striking. In his foreword to the article on Sweden’s Successful Drug Policy, Antonio Maria Costa is frank enough to confess that, “It is my firm belief that the generally positive situation of Sweden is a result of the policy that has been applied to address the problem”.

For data showing the relationship between drug enforcement policies in Europe and drug use, such that Sweden has a zero tolerance policy on drugs and has one of the lowest rates of “last month use” in Europe (1%), 4-fold lower than the Netherlands and 7-fold lower than Spain and Italy, two countries that have liberalized their enforcement policies so that marijuana possession carries no substantive penalty.

European Monitoring Centre for Drugs and Addiction, 2012 Annual report
http://www.emcdda.europa.eu/attachements.cfm/att_190854_EN_TDAC12001ENC_.pdf

Source: Microsoft Word – 2015- Summary of literature on marijuana and psychosis.doc (momsstrong.org) January 2016

Alex Azar
Secretary of Health and Human Services
US Department of Health and Human Services
200 Independence Avenue SW
Washington D.C, 20201
November 5, 2019

Dear Secretary Azar:
This letter is to bring to your attention a study underway at the University of Washington referred to as the “Moms and Marijuana Study” and granted under the title: “Olfactory Activation and Brain Development in Infants with Prenatal Cannabis Exposure.” The Office of Human Research Protections issued a decision against opening a case on this research, and we are asking you, as the Secretary of Health and Human Services, to overturn that decision based on the scientific concerns we outline in this letter.

Women who are in their first trimester of a pregnancy, who are frequent users of marijuana for morning sickness, are being recruited. The study seeks to assess the damage marijuana prenatal exposure may have on the babies by means of various testing, including an MRI scan of the infants at six months of age. The recruited women will receive $300.00 + for their participation. The study is solely funded by NIDA. This study calls into question serious issues over human rights and raises ethical questions, including mandatory reporting pertaining to substance abuse in pregnancy. This open letter seeks to gather support from you in seeing that this study is re-evaluated at the federal level. The study’s website is at the following link: https://depts.washington.edu/klab/infoMM.html

We are of the view that the Kleinhans study does not meet the requirements set forth by the Office of Human Research Protections (https://www.hhs.gov/ohrp/regulations-and-policy/regulations/45-cfr46/ ): “Subpart B presumption that pregnant women may be included in research, provided certain conditions are met. According to Subpart B, the permissibility of research with pregnant women hinges on a judgment of the potential benefits and risks of the research. Approval of proposed research carrying no “prospect of direct benefit” to the woman or fetus requires that the risk to the fetus be judged “not greater than minimal”. Fetal risk that exceeds that standard is permissible only when the proposed research offers a prospect of direct benefit to the pregnant woman, the fetus, or both.

Notably, if the proposed research does not fit within either of those two parameters, Subpart B offers an additional mechanism at the national level for approval by the Secretary of Health and Human Services.”

The federal definition of minimum risk reads: “That the magnitude and probability of harm or discomfort anticipated in the research are not greater in and of themselves than those ordinarily encountered in daily life or during the performance of routine physical or psychological examinations or tests.” Although the primary harm at issue is exposure to marijuana, the use of MRI or fMRI has not yet been proven safe for otherwise healthy infants, where an unknown risk would come with no benefit, as there is no diagnosis being sought. The UW study consent form reads on page 3:“There are no known side effects associated with MRI or fMRI when earphones are used to protect your hearing.” …. “There may be risks associated with the use of magnetic resonance which are not known at this time.” It is precisely questions about the potential for MRI risks that should be investigated in an animal model first. In principle, any study that recruits subjects and then tracks the consequences of drug transfer to a developing fetus should be carried out in animal models first, and not in humans until the animal results point towards safety. The evidence of decades of research on marijuana in pregnancy does not point to safety but rather to risk and harm.

Two basic principles in bioethics are relied upon to determine the merit of research that involves human subjects: Is the study necessary and can the research be done without the use of human subjects? There now exists a significant body of scientific evidence that warrants and justifies warning women not to use marijuana products at pre-conception, while pregnant, or breast-feeding. The University of Washington study is not necessary to conclude that marijuana use is associated with risk to the child (and also the mother). The National Academies, a lead authority, concluded in a scientific literature review in 2017: There is substantial evidence of a statistical association between maternal cannabis smoking and lower birth weight of the offspring. Studies have already shown that prenatal use is associated with a 50 percent increased likelihood of low birth weight. The Surgeon General’s advisory of August 29, 2019 is also relied upon here. What is the “necessity” that this study addresses? The conclusion has already been made by the findings of science – pregnant women should refrain from marijuana use in order to protect the life and health of their child.

Yet, in spite of existing scientific literature of concern, a highly misleading recruitment statement appears on the University of Washington study’s website introductory page: “We do not expect to find anything of medical concern during the infant MRI scans…If you’re interested in helping us learn more about whether cannabis is safe to use for morning sickness, click the Sign Up button and let us know!” Their lack of concern about the potential for adverse medical outcomes directly contradicts the findings of Grewen et al. (2015) which similarly evaluated postnatal outcomes using MRI scans on infants that had been exposed to marijuana in utero. As compared to controls, the exposed infants showed hypoconnectivity between brain regions: ” Marijuana-specific differences were observed in insula and three striatal connections: anterior insula–cerebellum, right caudate–cerebellum, right caudate–right fusiform gyrus/inferior occipital, left caudate–cerebellum. +MJ neonates had hypo-connectivity in all clusters compared with −MJ and CTR groups.” While an imperfect study because the cases included a proportion of women in the case group who used not only marijuana but also alcohol, tobacco, opiates and SSRIs, one of the two control groups was matched to the cases for use of those drugs, while the other was completely drug free. Notably, work in an animal model by Tortoriello et al. (2014) presents a plausible mechanism for the observed effect of marijuana seen between cases and controls. The combined evidence points towards harm, and confirmation could easily be sought in an animal model that parallels the intent of the University of Washington study.

Furthermore, the ethics are clearly different between the Kleinhans et al. and Grewen et al. studies, because unlike the protocol for the former, the study of Grewen et al. did not recruit women while the fetus was developing but recruited shortly before or after the time of birth. Being unaware of marijuana use until the time of birth, the researchers could not intervene to encourage abstinence for the sake of the fetus, whereas the University of Washington team could intervene, but their protocols do not allow them to. As a further point of distinction, the University of Washington protocol states that infants enrolled in the study will be screened and excluded if they have been in an NICU for 24 hours. This will, for obvious reasons, result in a biased outcome in reporting overall harm from marijuana use during pregnancy.

Typical morning sickness affects up to 91% of pregnancies (Castillo and Phillippi, 2015), and is regarded by many medical practitioners as being a reflex protecting against consumption of dangerous foods or beverages, as well as a sign of a healthy pregnancy because the absence of morning sickness is associated with a higher rate of miscarriage (reviewed by Sherman and Flaxman, 2002). The rare condition when morning sickness becomes pathologic, hyperemesis gravidarum, affects on average 1.1% of pregnancies, and is defined as a loss of 5% or more of the pre-pregnancy weight (Castillo and Phillippi, 2015). Maintenance of fluid and electrolyte balance may become problematic in this situation and pharmacologic intervention may become necessary, both for the health of the mother and the baby. To date, the serious documented outcomes include an increased risk for preterm births and low birth weight (Dodds et al., 2006).

Thus, if the Kleinhans study were to be proposing to recruit only those with hyperemesis gravidarum, the ethics might be more favorable. They would, however, have to exclude women whose marijuana use may have triggered the hyperemesis, which may occur in a subset of pregnant users (Alaniz et al., 2015). The study recruitment website is definitely remiss in not making that possibility clear to those interested in enrolling, and the research protocol describes no effort to ascertain if marijuana might be triggering hyperemesis in their study subjects.

In summary, there is already sufficient scientific evidence to answer the question as to whether or not marijuana is safe to use for typical morning sickness. That answer is no. Please see additional references for numerous research publications showing harm at the end of this letter.
Complaints have been filed with NIDA, The University of Washington, The World Medical Association regarding the Helsinki Declaration, The Office of Human Research Protections, and two doctors have filed a human rights complaint on behalf of the children involved. Complaint documents will be forwarded on request.

Thank you for your time in reviewing this serious situation.

Best regards,
Pamela McColl
Child Rights Activist
pjmccoll@shaw.ca

and

Christine L. Miller, Ph.D.
Neuroscientist
MillerBio
6508 Beverly Rd
Baltimore, Maryland 21239
cmiller@millerbio.com

et al.

Correspondence with the OHRP in regards to the University of Washington study began in September
of 2019. On October an email was received from the OHRP to Pamela McColl:
October 25, 2019

Hello,
OHRP has reviewed the study and will not be opening a case.
Sincerely,
Division of Compliance Oversight OHRP

September 25, 2019
“OHRP is now reviewing your complaint and this study. We are currently gathering the information about the research being conducted before a full review is started. Once OHRP completes a full review of the study, the research conducted and the study’s approval process, we will contact you with our findings. Please remember, this does not mean you can’t contact OHRP again before we finish the full review. You can contact us using this email address to update your complaint at any time.
Thank-you,
Division of Compliance Oversight (OHRP)

September 17, 2019
Thank you for contacting the Office for Human Research Protections (OHRP). OHRP has responsibility for oversight of compliance with the U.S. Department of Health and Human Services (HHS) regulations for the protection of human research subjects (see 45 CFR Part 46 at
www.hhs.gov/ohrp/regulations-and-policy/guidance/index.html

In carrying out this responsibility, OHRP reviews allegations of noncompliance involving human subject research projects conducted or supported by HHS or that are otherwise subject to the regulations, and determines whether to conduct a for-cause compliance evaluation. For further details see OHRP’s guidance, “Compliance Oversight Procedures for Evaluating Institutions,” at www.hhs.gov/ohrp/compliance-and-reporting/evaluating-institutions/index.html.

OHRP has jurisdiction only if the allegations involve human subject research (a) conducted or supported by HHS, or (b) conducted at an institution that voluntarily applies its Assurance of Compliance to all research regardless of source of support. Since this requirement appears to be met by the circumstances described in your email, OHRP appears to have jurisdiction.
Sincerely,
Division of Compliance Oversight
cc. Surgeon General Jerome Adams
cc. Director NIDA Dr. Nora Volkow

In-text citations:
Alaniz VI, Liss J, Metz TD, Stickrath E. Cannabinoid hyperemesis syndrome: a cause of refractory nausea and vomiting in pregnancy. Obstet Gynecol. 2015 Jun;125(6):1484-6.
Castillo MJ, Phillippi JC. Hyperemesis gravidarum: a holistic overview and approach to clinical assessment and management. J Perinat Neonatal Nurs. 2015;29(1):12-22.
Dodds L, Fell DB, Joseph KS, Allen VM, Butler B. Outcomes of pregnancies complicated by hyperemesis gravidarum. Obstet Gynecol. 2006;107(2, pt 1):285–292.
Grewen K, Salzwedel AP, Gao W. Functional Connectivity Disruption in Neonates with Prenatal Marijuana Exposure. Front Hum Neurosci. 2015;9:601.
Sherman PW, Flaxman SM. Nausea and vomiting of pregnancy in an evolutionary perspective. Am J Obstet Gynecol. 2002;186(5 Suppl Understanding):S190-7.
The National Academies of Sciences, Engineering, and Medicine, 2017, The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. National Academies Press, Washington, D.C. 20001
Tortoriello G, et al. Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway. EMBO J. 2014;33(7):668-85.

Additional references on specific neonatal outcomes:
Lower birth weight, animal studies
Benevenuto SG et al., Recreational use of marijuana during pregnancy and negative gestational and fetal outcomes: An experimental study in mice. Toxicology. 2017;376:94-101.
“Five minutes of daily (low dose) exposure during pregnancy resulted in reduced birthweight…..females from the Cannabis group presented reduced maternal net body weight gain, despite a slight increase in their daily food intake compared to the control group”

Lower birth weight, human studies
Gunn,JKL, Rosales CB, Center KE, Nunez A, Gibson SJ, Christ C, and Ehiri EJ. Prenatal exposure to cannabis and maternal and child health outcomes: A systematic review and meta-analysis. BMJ Open 2016; 6(4):e009986.
“Infants exposed to cannabis in utero had a decrease in birth weight (low birth weight pOR=1.77: 95% CI 1.04 to 3.01; pooled mean difference (pMD) for birth weight=109.42 g: 38.72 to 180.12) compared with infants whose mothers did not use cannabis during pregnancy. Infants exposed to cannabis in utero were also more likely to need placement in the neonatal intensive care unit compared with infants whose mothers did not use cannabis during pregnancy (pOR=2.02: 1.27 to 3.21).”
Brown SJ, Mensah FK, Ah Kit J, Stuart-Butler D, Glover K, Leane C, Weetra D, Gartland D, Newbury J, Yelland J. Use of cannabis during pregnancy and birth outcomes in an Aboriginal birth cohort: a crosssectional, population-based study. BMJ Open. 2016;6(2):e010286.
“Controlling for education and other social characteristics, including stressful events/social health issues did not alter the conclusion that mothers using cannabis experience a higher risk of negative birth outcomes (adjusted OR for odds of low birth weight 3.9, 95% CI 1.4 to 11.2).”
Fergusson, D. M., L. J. Horwood, and K. Northstone. 2002. Maternal use of cannabis and pregnancy outcome. British Journal of Obstetrics and Gynaecology 109(1):21–27.
“Over 12,000 women expecting singletons at 18 to 20 weeks of gestation who were enrolled in the Avon Longitudinal Study of Pregnancy and Childhood……the babies of women who used cannabis at least once per week before and throughout pregnancy were 216g lighter than those of non-users.”

Preterm birth, animal studies
Wang H, Xie H, Dey SK. Loss of cannabinoid receptor CB1 induces preterm birth. PLoS One. 2008;3(10):e3320.
“CB1 deficiency altering normal progesterone and estrogen levels induces preterm birth in mice…. CB1 regulates labor by interacting with the corticotrophin-releasing hormone-driven endocrine axis.”

Preterm birth, human studies
Luke S, Hutcheon J, Kendall T. Cannabis Use in Pregnancy in British Columbia and Selected Birth Outcomes. J Obstet Gynaecol Can. 2019;41(9):1311-1317.
“Using cannabis in pregnancy was associated with a 47% increased risk of SGA (adjusted OR 1.47; 95% CI 1.33–1.61), a 27% increased risk of spontaneous preterm birth (adjusted OR 1.27; 95% CI 1.14–1.42), and a 184% increased risk of intrapartum stillbirth (adjusted HR [aHR] 2.84; 95% CI 1.18–6.82).”
Corsi DJ, Walsh L, Weiss D, Hsu H, El-Chaar D, Hawken S, Fell DB, Walker M. Association Between Selfreported Prenatal Cannabis Use and Maternal, Perinatal, and Neonatal Outcomes. JAMA. 2019;322(2):145-152.
“In a cohort of 661 617 women…. The crude rate of preterm birth less than 37 weeks’ gestation was 6.1%among women who did not report cannabis use and 12.0% among those reporting use in the unmatched cohort (RD, 5.88% [95%CI, 5.22%-6.54%]). In the matched cohort, reported cannabis exposure was significantly associated with an RD of 2.98%(95%CI, 2.63%-3.34%) and an RR of 1.41 (95% CI, 1.36-1.47) for preterm birth. Compared with no reported use, cannabis exposure was significantly associated with greater frequency of small for gestational age (third percentile, 6.1% vs 4.0%; RR, 1.53 [95%CI, 1.45-1.61]), placental abruption (1.6%vs 0.9%; RR, 1.72 [95% CI, 1.54-1.92]), transfer to neonatal intensive care (19.3%vs 13.8%; RR, 1.40 [95%CI, 1.36-1.44]), and 5-minute Apgar score less than 4 (1.1% vs 0.9%; RR, 1.28 [95%CI, 1.13-1.45]).”
Saurel-Cubizolles MJ, Prunet C, Blondel B. Cannabis use during pregnancy in France in 2010. BJOG. 2014;121(8):971-7.
“Cannabis users had higher rates of spontaneous preterm births: 6.4 versus 2.8%, for an adjusted odds ratio (aOR) of 2.15 (95% CI 1.10–4.18).”
Leemaqz SY, Dekker GA, McCowan LM, Kenny LC, Myers JE, Simpson NA, Poston L, Roberts CT;

SCOPE Consortium. Maternal marijuana use has independent effects on risk for spontaneous preterm birth but not other common late pregnancy complications. Reprod Toxicol. 2016;62:77-86. “continued maternal marijuana use at 20 weeks’ gestation was associated with” spontaneous preterm birth “independent of cigarette smoking status [adj OR2.28 (95% CI:1.45–3.59)] and socioeconomic index (SEI) [adj OR 2.17 (95% CI:1.41–3.34)]. When adjusted for maternal age, cigarette smoking, alcohol and SEI, continued maternal marijuana use at 20 weeks’ gestation had a greater effect size [adj OR 5.44 (95% CI 2.44–12.11)].”

Impacts on the neonatal immune system, animal study
Zumbrun EE et al. Epigenetic Regulation of Immunological Alterations Following Prenatal Exposure to Marijuana Cannabinoids and its Long Term Consequences in Offspring. J Neuroimmune Pharmacol. 2015; 10(2):245-54.
“Data from various animal models suggests that in utero exposure to cannabinoids results in profound T cell dysfunction and a greatly reduced immune response to viral antigens

Impacts on cortical wiring and development, animal studies
Tortoriello G, et al. Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway. EMBO J. 2014;33(7):668-85.
“Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry….these data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis”
DiNieri JA, Wang X, Szutorisz H, Spano SM, Kaur J, Casaccia P, Dow-Edwards D, Hurd YL. Maternal cannabis use alters ventral striatal dopamine D2 gene regulation in the offspring. Biol Psychiatry. 2011 Oct 15;70(8):763-9.
“we exposed pregnant rats to THC and examined the epigenetic regulation of the NAc Drd2 gene in their offspring at postnatal day 2, comparable to the human fetal period studied, and in adulthood…. Decreased Drd2 expression was accompanied by reduced D2R binding sites and increased sensitivity to opiate reward in adulthood”
Rodríguez de Fonseca F, Cebeira M, Fernández-Ruiz JJ, Navarro M, Ramos JA. Effects of pre- and perinatal exposure to hashish extracts on the ontogeny of brain dopaminergic neurons. Neuroscience. 1991;43(2-3):713-23.
“Perinatal exposure to cannabinoids altered the normal development of nigrostriatal, mesolimbic and tuberoinfundibular dopaminergic neurons, as reflected by changes in several indices of their activity”.

Impacts on cortical wiring and development, human studies
Grewen K, Salzwedel AP, Gao W. Functional Connectivity Disruption in Neonates with Prenatal Marijuana Exposure. Front Hum Neurosci. 2015;9:601.

“+MJ (marijuana-exposed) neonates had hypo-connectivity in all clusters compared with –MJ (marijuana unexposed) and CTR (control) groups. Altered striatal connectivity to areas involved in visual spatial and motor learning, attention, and in fine-tuning of motor outputs
involved in movement and language production may contribute to neurobehavioral deficits reported in this at-risk group. Disrupted anterior insula connectivity may contribute to altered integration of interoceptive signals with salience estimates, motivation, decision-making, and later drug use.”
El Marroun H, Tiemeier H, Franken IH, Jaddoe VW, van der Lugt A, Verhulst FC, Lahey BB, White T. Prenatal Cannabis and Tobacco Exposure in Relation to Brain Morphology: A Prospective Neuroimaging Study in Young Children. Biol Psychiatry. 2016;79(12):971-9.
“prenatal cannabis exposure was associated with differences in cortical thickness….. it may be possible that the frontal cortex in cannabis-exposed children undergoes altered neurodevelopmental maturation (i.e., having differences in cortical trajectories) as compared with
nonexposed control subjects”
Wang X, Dow-Edwards D, Anderson V, Minkoff H, Hurd YL. In utero marijuana exposure associated with abnormal amygdala dopamine D2 gene expression in the human fetus. Biol Psychiatry. 2004; 56:909–915.
“Adjusting for various covariates, we found a specific reduction, particularly in male fetuses, of the D(2) mRNA expression levels in the amygdala basal nucleus in association with maternal marijuana use. The reduction was positively correlated with the amount of maternal marijuana intake during pregnancy.”

Received by email

I, Surgeon General VADM Jerome Adams, am emphasizing the importance of protecting our Nation from the health risks of marijuana use in adolescence and during pregnancy. Recent increases in access to marijuana and in its potency, along with misperceptions of safety of marijuana endanger our most precious resource, our nation’s youth.

BE PREPARED. GET NALOXONE. SAVE A LIFE.

Background

Marijuana, or cannabis, is the most commonly used illicit drug in the United States. It acts by binding to cannabinoid receptors in the brain to produce a variety of effects, including euphoria, intoxication, and memory and motor impairments. These same cannabinoid receptors are also critical for brain development. They are part of the endocannabinoid system, which impacts the formation of brain circuits important for decision making, mood and responding to stress.

Marijuana and its related products are widely available in multiple forms. These products can be eaten, drunk, smoked, and vaped. Marijuana contains varying levels of delta-9-tetrahydrocannabinol (THC), the component responsible for euphoria and intoxication, and cannabidiol (CBD). While CBD is not intoxicating and does not lead to addiction, its long-term effects are largely unknown, and most CBD products are untested and of uncertain purity.

Marijuana has changed over time. The marijuana available today is much stronger than previous versions. The THC concentration in commonly cultivated marijuana plants has increased three-fold between 1995 and 2014 (4% and 12% respectively). Marijuana available in dispensaries in some states has average concentrations of THC between 17.7% and 23.2%. Concentrated products, commonly known as dabs or waxes, are far more widely available to recreational users today and may contain between 23.7% and 75.9% THC.

The risks of physical dependence, addiction, and other negative consequences increase with exposure to high concentrations of THC and the younger the age of initiation. Higher doses of THC are more likely to produce anxiety, agitation, paranoia, and psychosis. Edible marijuana takes time to absorb and to produce its effects, increasing the risk of unintentional overdose, as well as accidental ingestion by children and adolescents. In addition, chronic users of marijuana with a high THC content are at risk for developing a condition known as cannabinoid hyperemesis syndrome, which is marked by severe cycles of nausea and vomiting.

This advisory is intended to raise awareness of the known and potential harms to developing brains, posed by the increasing availability of highly potent marijuana in multiple, concentrated forms. These harms are costly to individuals and to our society, impacting mental health and educational achievement and raising the risks of addiction and misuse of other substances.  Additionally, marijuana use remains illegal for youth under state law in all states; normalization of its use raises the potential for criminal consequences in this population. In addition to the health risks posed by marijuana use, sale or possession of marijuana remains illegal under federal law notwithstanding some state laws to the contrary.

Watch the Surgeon General Answer FAQs on Marijuana

https://youtu.be/OYZvUDbzUk8?si=_hDG7gAcem3esbvS

Marijuana Use during Pregnancy

Pregnant women use marijuana more than any other illicit drug. In a national survey, marijuana use in the past month among pregnant women doubled (3.4% to 7%) between 2002 and 2017. In a study conducted in a large health system, marijuana use rose by 69% (4.2% to 7.1%) between 2009 and 2016 among pregnant women. Alarmingly, many retail dispensaries recommend marijuana to pregnant women for morning sickness.

Marijuana use during pregnancy can affect the developing fetus.

  • THC can enter the fetal brain from the mother’s bloodstream.
  • It may disrupt the endocannabinoid system, which is important for a healthy pregnancy and fetal brain development
  • Studies have shown that marijuana use in pregnancy is associated with adverse outcomes, including lower birth weight.
  • The Colorado Pregnancy Risk Assessment Monitoring System reported that maternal marijuana use was associated with a 50% increased risk of low birth weight regardless of maternal age, race, ethnicity, education, and tobacco use.

The American College of Obstetricians and Gynecologists holds that “[w]omen who are pregnant or contemplating pregnancy should be encouraged to discontinue marijuana use. Women reporting marijuana use should be counseled about concerns regarding potential adverse health consequences of continued use during pregnancy”. In 2018, the American Academy of Pediatrics recommended that “…it is important to advise all adolescents and young women that if they become pregnant, marijuana should not be used during pregnancy”.

Maternal marijuana use may still be dangerous to the baby after birth. THC has been found in breast milk for up to six days after the last recorded use. It may affect the newborn’s brain development and result in hyperactivity, poor cognitive function, and other long-term consequences. Additionally, marijuana smoke contains many of the same harmful components as tobacco smoke. No one should smoke marijuana or tobacco around a baby.

Marijuana Use during Adolescence

Marijuana is also commonly used by adolescents, second only to alcohol. In 2017, approximately 9.2 million youth aged 12 to 25 reported marijuana use in the past month and 29% more young adults aged 18-25 started using marijuana. In addition, high school students’ perception of the harm from regular marijuana use has been steadily declining over the last decade. During this same period, a number of states have legalized adult use of marijuana for medicinal or recreational purposes, while it remains illegal under federal law. The legalization movement may be impacting youth perception of harm from marijuana. 

The human brain continues to develop from before birth into the mid-20s and is vulnerable to the effects of addictive substances. Frequent marijuana use during adolescence is associated with:

  • Changes in the areas of the brain involved in attention, memory, decision-making, and motivation. Deficits in attention and memory have been detected in marijuana-using teens even after a month of abstinence.
  • Impaired learning in adolescents. Chronic use is linked to declines in IQ, school performance that jeopardizes professional and social achievements, and life satisfaction.
  • Increased rates of school absence and drop-out, as well as suicide attempts.

Risk for and early onset of psychotic disorders, such as schizophrenia. The risk for psychotic disorders increases with frequency of use, potency of the marijuana product, and as the age at first use decreases. 

  • Other substance use. In 2017, teens 12-17 reporting frequent use of marijuana showed a 130% greater likelihood of misusing opioids23.

Marijuana’s increasingly widespread availability in multiple and highly potent forms, coupled with a false and dangerous perception of safety among youth, merits a nationwide call to action. 

You Can Take Action

No amount of marijuana use during pregnancy or adolescence is known to be safe. Until and unless more is known about the long-term impact, the safest choice for pregnant women and adolescents is not to use marijuana.  Pregnant women and youth–and those who love them–need the facts and resources to support healthy decisions. It is critical to educate women and youth, as well as family members, school officials, state and local leaders, and health professionals, about the risks of marijuana, particularly as more states contemplate legalization.

Science-based messaging campaigns and targeted prevention programming are urgently needed to ensure that risks are clearly communicated and amplified by local, state, and national organizations. Clinicians can help by asking about marijuana use, informing mothers-to-be, new mothers, young people, and those vulnerable to psychotic disorders, of the risks. Clinicians can also prescribe safe, effective, and FDA-approved treatments for nausea, depression, and pain during pregnancy. Further research is needed to understand all the impacts of THC on the developing brain, but we know enough now to warrant concern and action. Everyone has a role in protecting our young people from the risks of marijuana.

Information for Parents and Parents-to-be

You have an important role to play for a healthy next generation.

Information for Youth:

You have an important role to play for a healthy next generation.

Information for States, Communities, Tribes, and Territories:

You have an important role to play for a healthy next generation.

Information for Health Professionals:

You have an important role to play for a healthy next generation.

Source: Surgeon General’s Advisory: Marijuana Use & the Developing Brain | HHS.gov August 2019

 

 

  • Common Pattern.  The almost ubiquitous pattern in which medical cannabis is used today is to treat decades long cannabis addiction, with the other indications serving as mere “tickets” to engage whilst simultaneously avoiding legal censure.

 

  • Parallel Drug Approval Pathway.  It is obvious that whilst all other drugs are held to a strict approvals and regulatory pathway cannabis products are held to no serious control whatsoever with the industry in an effectively unregulated exponential growth phase.

 

  • Limited Benefits. Despite the international rhetoric of many governments and the  cannabis industry there is either nil or very poor evidence for the efficacy of the vast majority of cannabinoid products in the management of  most indications presenting to GPs  (Ref RACGP Review).

 

  • Known Harms.  Alternately, there is increasing direct and indirect evidence from cellular, mechanistic, case data and epidemiological studies of “likely” harm from cannabis, both within and across generations (epigenetics). This is supported by large epidemiological studies, confirming increased cancers and neonatal congenital abnormalities in areas of increased cannabinoid use, not dissimilar from those used to identify links between tobacco or alcohol and morbidities.  Numerous aging pathologies are also accelerated.

 

  • Further Harms.
    1. Gateway role – Into harder drugs and criminal lifestyle is now well established by studies in numerous countries.  Whilst few cannabis users progress to harder drugs, virtually all users of harder drugs have used cannabis, with much higher rates of drug and criminal progression amongst ever users of cannabis.
    2. Adult Brain – Most major psychiatric syndromes have been linked with cannabis viz: sedation, amotivational state, anxiety, PTSD, serious mental disorders, depression, psychosis, bipolar disorder, schizophrenia, suicidal thoughts and completed suicides.  Also linked with homicide and violence and over 70 mass shootings in USA thought to be linked with aggression (seen in both cannabis withdrawal and intoxication), impaired judgement and psychosis
    3. Child Brain – ADHD-like and autism-like features; extreme aggression; impaired cortical processing; learning difficulties; smaller brain; microcephaly; anencephaly (which causes death within hours)
    4. Chest disease – COPD, chronic bronchitis, emphysema, lung cysts, elevated residual volume, premalignant changes in upper and lower airways
    5. Immunomodulation – Both immunosuppression and immunostimulation are described mediated via T-cells, B-cells, NK Cells, T-reg cells, antibodies and cytokines
    6. Endocrinopathy – Central and peripheral hypogonadism, Prolactin elevated
    7. Cardiovascular  – accelerated coronary artery and atherosclerotic disease; strongly arrythmogenic (many tachyarrhythmias both atrial and ventricular)

 

  • Genetic Toxicity.  These include gestationally and neonatal congenital abnormalities, cancers both childhood and adult, and the occurrence of premature age-related morbidities, and powerful direct effects on the aging process etc.

 

  • Known Mechanisms.  These findings are underpinned by clear cellular mechanistic studies on how cannabinoids (both THC and CBD based) can cause the above by interfering  with normal cellular and body functions creating antecedents of disease. This of course is not surprising given the increasing understanding of the role of endogenous cannabinoids in normal development, body functioning, and cellular reproduction and maintenance, chromosomes, gene maintenance and control (epigenome) and that use of large doses or prolonged exogenous cannabinoids can significantly disrupt these functions.

 

  • “Do No Harm.”  Given the aforementioned, it is clear that caution needs to be applied to the medical use of cannabinoids, that although in the most positive interpretation may have a nominal impact managing morbidities, may in turn cause greater harm transgenerationally.

 

 

  • Rigorous Trials – Evidence Base.  It is therefore not only reasonable but essential that each cannabinoid product marketed should be assessed by the established international standards for pharmaceutical development, and to which all other pharmaceutical products, prior to being released and used in populations must conform.  There is need for a robust evidence base.  At present cannabis is not performing impressively in hundreds of clinical trials.  In the case of cannabinoids this must include rigorous and long term tests of genetic, epigenetic and epitranscriptomic toxicity including: genotoxicity, carcinogenicity, mutagenicity, teratogenicity and gametotoxicity in both sexes.

 

Source: https://pubmed.ncbi.nlm.nih.gov/

Methamphetamine, a well-known psychostimulant drugs of abuse is in a resurgence in people using opioids and others. While many treatment options exist for patients with opioid use disorders, alcohol use disorders, and even tobacco smokers, there are far fewer options for people trying to stop using methamphetamines. No known medical treatments exist for overdose, dependence, craving, relapse, or to reverse all of the effects of methamphetamine binges and dependence. Experts studying substance use disorders recognize that their effects from misuse, especially the misuse of methamphetamine, can linger even after periods of abstinence.

Patients treated for methamphetamine binges, or dependence, for example, often suffer from cognitive impairments, including psychosis. Some of the persistent problems may reflect underlying brain change or even damage. If overlooked, cognitive problems can limit the effectiveness of treatment. They can also create a dangerous hopelessness or relapse cycle. That’s one reason why it’s so important to understand how substances like methamphetamine may alter the brain’s structure.

How Long Do Methamphetamine Brain Changes Last?

Methamphetamine addiction is a growing epidemic worldwide, following on the heels of the opioid crisis. Chronic methamphetamine use has been shown to lead to neurotoxicity in both humans and animals.  Magnetic resonance imaging (MRI) studies in methamphetamine users have shown enlarged striatal volumes, and positron emission tomography (PET) studies have shown decreased brain glucose metabolism (BGluM) in the striatum of abstinent methamphetamine users.

Some features of the methamphetamine toxicity profile are puzzling as well as difficult to treat. In prior work, it’s been noted how psychosis can follow methamphetamine use and last into abstinence. Varying levels of methamphetamine use can induce psychosis, depending in part on an individual’s background, and it can develop quickly or after 20 years of use. This psychosis can be quite similar to Schizophrenia – in some cases, violent behaviors have been connected to methamphetamine psychosis as well.

A study of Japanese prisoners found that a subgroup of methamphetamine users experienced chronic psychosis. Lingering cognitive problems may cause other health complications, difficulty thinking or concentrating at work, and increasingly risky behavior, in addition to higher relapse rates. Furthermore, later-in-life stress can also revive psychotic symptoms. More research on methamphetamine and cognitive problems can help treatment providers understand these hidden tripwires for patients.

One study, by Thanos et. al., looked at brain changes in rats after long-term methamphetamine use. Researchers split rats into 3 groups and gave them methamphetamine daily for 4 months. They dissolved methamphetamine in a saline solution and gave one rat group high methamphetamine doses, one rat group low methamphetamine doses, and the remaining rat group saline. Subsequent testing showed significant changes in the rats’ brains, stemming from higher doses. They also detected changes in brain glucose metabolism across different areas of the brain. These changes affect sleep cycles, face sensory processing, navigation, and memory. Researchers additionally found increases in striatal volume, referring to a part of the brain with a key role in decisions and reward management.

These increases resemble the results of other research, an important part of the study. Cognitive problems in humans taking methamphetamine can exist before substance use. But Thanos et. al. observe that a combination of research on methamphetamine use and this part of the brain, involving humans, monkeys, and rats, all finds similar increases. Unfortunately, this combination indicates that some methamphetamine-induced problems in the brain are prolonged and significant.

Thanos et. al. also start the rats’ substance use in adolescence. They point out that studies of human use in adolescence and adulthood find similar brain problems, adding to the likelihood of long-term damage. Thanos has continued this work with NIDA Director Volkow, looking at damage produced in the brain by methamphetamine. These most current results from their group, corroborate clinical experiences and reports of toxicity and encourage us to further examine the mechanisms behind MA-induced neurotoxicity.

 Why Is This Important?

This kind of study is important because treatment and recovery providers need to understand the full spectrum of issues their patients face. Once the acute problems are resolved, many challenges may remain. Even in abstinence, brain problems after methamphetamine use may become substantial hurdles for patients in recovery.

Psychological and neuropsychological testing may help the clinical team understand what has been lost and what might be done to help. Thanos et. al. also suggest that methamphetamine use may trigger a direct brain injury that we suggested was similar to a concussion or traumatic brain injury. Thanos suggests that methamphetamine targets the dopamine rich pleasure system, undermines it and the residual brain inflammation is both the proof and the cause of the post-drug changes to the health of our dopamine systems. Determining long-term methamphetamine brain changes can be even more useful for setting goals and interventions designed to help patients. Some of the strategies currently used to treat traumatic brain injuries may be helpful, as may use of exercise, dance, and transcranial magnetic stimulation. Post drug abstinence psychoses may not be as reversible by medications used for naturally-occurring psychoses.

Many patients, for example, show subtle changes without clear signs of cognitive difficulties. Testing may reveal real problems. Others present with fears and anxiety or disordered thinking that may have there roots in changes to their brains. And untangling cause and effect can help us better understand when pre-existing cognitive problems, and not substance use, are the main culprits. As with many substance use disorders, we have to remember that a holistic approach based on individual needs is the best way to help.

With methamphetamine this is even more important as medication assisted therapies do not exist. Time of abstinence, rehabilitation with healthy thinking, eating, sleeping, and diet are easier to prescribe or advise than find. Time of abstinence is of the essence as it appears that methamphetamine induces a drug use disorder with binges, relapses and cravings but also with loss of brain function and evidence of something that looks like a traumatic brain injury. Treating it like a neurological injury in addition to traditional addiction treatment, may be an idea worth looking at too.

Source:https://www.addictionpolicy.org/blog/tag/research-you-can-use/examining-brain-health-could-help-fight-methamphetamine-use-disorder    1st  August 2019

Abstract:

Background: The relationship between cannabis and violence remains unclear, especially amid those with severe mental illnesses (SMI). The objective of this meta-analysis was to investigate the cannabis-violence association in a population of individuals with a SMI.

Method: A systematic search of literature using PubMed, PsychINFO, Web of Science and Google scholar was performed (any time-August 2018). All peer-reviewed publications assessing both cannabis use and the perpetration of violence in an SMI sample were included. Data on several key study characteristics such as the proportion of SMI in the sample as well as the number of cannabis users and violent participants were extracted. Odds ratios (OR) were likewise extracted and aggregated with random-effects models.

Results: Of the potential 2449 articles that were screened for eligibility, 12 studies were analyzed using a random-effect meta-analysis. Results showed a moderate association between cannabis use and violence (OR = 3.02, CI = 2.01–4.54, p = 0.0001). The association was significantly higher when comparing cannabis misuse (OR = 5.8, CI = 3.27–10.28, p = 0.0001) to cannabis use (OR = 2.04, CI = 1.36–3.05, p = 0.001).

Conclusion: These findings are clinically relevant for violence prevention/management and highlight the necessity of further investigations with methodologically-sound studies. Thus, longitudinal studies adjusting for important confounding factors (i.e., psychopathic traits and stimulant use) are warranted

Source: Cannabis use and violence in patients with severe mental illnesses: A meta-analytical investigation – PubMed (nih.gov) April 2019

In March 2014, the Colorado Department of Public Health and Environment (CDPHE) learned of the death of a man aged 19 years after consuming an edible marijuana product. CDPHE reviewed autopsy and police reports to assess factors associated with his death and to guide prevention efforts.

The decedent’s friend, aged 23 years, had purchased marijuana cookies and provided one to the decedent. A police report indicated that initially the decedent ate only a single piece of his cookie, as directed by the sales clerk. Approximately 30-60 minutes later, not feeling any effects, he consumed the remainder of the cookie.

 During the next 2 hours, he reportedly exhibited erratic speech and hostile behaviors. Approximately 3.5 hours after initial ingestion, and 2.5 hours after consuming the remainder of the cookie, he jumped off a fourth floor balcony and died from trauma.

The autopsy, performed 29 hours after time of death, found marijuana intoxication as a chief contributing factor. Quantitative toxicologic analyses for drugs of abuse, synthetic cannabinoid, and cathinones (“bath salts”) were performed on chest cavity blood by gas chromatography and mass spectrometry. The only confirmed findings were cannabinoids (7.2 ng/mL delta-9 tetrahydrocannabinol [THC] and 49 ng/mL delta-9 carboxy-THC, an inactive marijuana metabolite). The legal whole blood limit of delta-9 THC for driving a vehicle in Colorado is 5.0 ng/mL. This was the first reported death in Colorado linked to marijuana consumption without evidence of polysubstance use since the state approved recreational use of marijuana in 2012.

Source:  MMWR Morb Mortal Wkly Rep. 2015 Jul 24;64(28):771-2.

As with any addiction, alcoholism is closely connected with stress. And while plenty of people first started drinking as a way to cope with stress or even just wind down after a long day, developing an alcohol use disorder can end up causing significant stresses of its own. If you’re thinking about pursuing alcohol use disorder treatment for yourself or for a loved one, it can be helpful to understand how alcohol is connected to stress.

Present Stress That Can Lead to Alcohol Use

While stresses from your past can certainly contribute to alcoholism, plenty of people also start to develop alcohol use disorder as they struggle to cope with current stress. Often, people end up turning to alcohol in order to try to manage the stresses of day-to-day life. These can include pressure at work or at school, marriage, and divorce, moving, and financial issues.

Minority stress is also an important consideration. If you’re a minority (either in terms of race/ethnicity or sexual orientation), you face unique stresses. You might stress about being passed over for a promotion at work, and you also might fear harassment or becoming the victim of a hate crime.

It’s important to note that stress alone typically does not cause a substance use disorder. However, significant stresses may place you at higher risk of developing one, and high stress levels in sobriety can also make relapse more likely. High stress is a risk factor for alcoholism, along with the following:

Past Stress That Can Lead to Alcohol Use

Unfortunately, it isn’t just current stressful events that can predispose you to drink more. Stresses and traumas from your past can also play a role in alcoholism. Several studies point to childhood abuse and neglect as being a significant factor in the development of an alcohol use disorder. One study found that emotional abuse and neglect were most commonly seen in men and women seeking help for alcoholism. The severity of their alcoholism correlated with the severity of the abuse.

Past traumas, even if they were not experienced in childhood, may also make someone more likely to experience alcoholism. Many people with an alcohol use disorder also have PTSD. As with other mental health diagnoses, the relationship between alcoholism and PTSD becomes a vicious cycle. Alcohol use makes PTSD symptoms worse, and the PTSD symptoms make alcoholism worse.

If you have experienced trauma and are also struggling with alcohol use disorder, it’s easy to feel as though there is no hope. But at Granite Recovery Centers, we offer evidence-based therapies including trauma therapy. In therapy for trauma and PTSD, you will be able to process your trauma and develop healthier coping strategies to help you avoid self-destructive behaviors. With these therapies, you’ll be able to break the cycle of worsening symptoms and experience a greater quality of life.

How Can Alcohol Use Cause Stress?

While it might seem logical that alcohol use can cause stress, there’s also a good bit of biochemical evidence to explain, at least in part, how alcohol shapes your stress response. Even in the short term, alcohol consumption increases levels of cortisol. Cortisol is known as the stress hormone, and your body also releases it during periods of intense anxiety or fear. In the short term, a cortisol release can be helpful — it increases alertness and focus, which was helpful evolutionarily because it helped humans and animals get themselves out of dangerous situations.

However, having elevated cortisol over a long period of time can be detrimental, exhausting, and even dangerous. And in chronic heavy drinkers and those with alcohol use disorder, cortisol isn’t just elevated during intoxication — it stays elevated through withdrawal. In fact, one study even found that cortisol increased as intoxicated people started moving toward withdrawals. If you’ve ever experienced intense anxiety when withdrawing from alcohol, you’ve felt this cortisol surge firsthand.

Because most people with an alcohol use disorder go through a near-constant cycle of intoxication and withdrawal, cortisol can remain elevated for years on end. Chronically elevated cortisol can cause a number of ill health effects:

  • Slow healing (of wounds, broken bones, etc.)
  • Acne
  • Thinning skin
  • Weight gain
  • Extreme fatigue
  • Irritability
  • Trouble focusing
  • Muscle weakness
  • Headaches
  • Elevated blood pressure

Chronically elevated cortisol may cause other health problems as well, but more research is needed to determine exactly what these effects are. Of course, the physical stresses of elevated cortisol combined with chronic heavy drinking can mean your body is put through a lot of physical stress as well as emotional stress.

You already know that plenty of people use alcohol to alleviate stress, but over time, alcohol can cause its own significant stresses. As mentioned above, the elevated cortisol you experience while intoxicated and in withdrawal can cause significant emotional distress. When your body is under stress, and elevated cortisol is effectively causing a constant stress response, it becomes significantly more difficult to handle even everyday stresses.

And in some cases (like when you are intoxicated enough to experience blackouts or respiratory suppression), being intoxicated can be a stressful experience in itself. And for many people with an alcohol use disorder, that stressful experience is something they experience on a daily or near-daily basis. Some of the physical effects of heavy drinking — including dizziness, nausea, headaches, and dehydration — can compound the emotional stress you’re already feeling.

Many people also consciously or unconsciously use alcohol to self-medicate psychiatric disorders, including depression and bipolar disorder. However, in many cases, alcohol use worsens the symptoms of mental health issues, which can cause considerably more emotional distress on a daily basis. In some cases, heavy alcohol use can even contribute to the development of new mental health diagnoses.

If you’ve been using alcohol to help manage a mental health diagnosis (or to help manage a mental health issue that has not yet been diagnosed), Granite Recovery Centers’ dual diagnosis treatment program can help you. With this approach, medical and recovery professionals work with you to find better treatments and coping mechanisms for your mental health diagnosis while also helping you manage your alcohol use disorder. In many cases, this treatment approach will greatly improve your quality of life, as you’ll be much better equipped to manage both diagnoses.

Regardless of whether you have a mental health diagnosis or not, heavy alcohol use can begin to cause stress as it starts to affect the rest of your life. For example, you may constantly worry whether someone will smell alcohol on your breath at work, or you may worry about when you can take another drink. For many people with an alcohol use disorder, it can start to feel like leading a double life, which becomes exhausting and highly stressful over time. And as a person starts to drink more, they often become more socially isolated. Feeling isolated can increase stress, and the person may then continue drinking heavily to cope with that stress.

If you struggle with an alcohol use disorder or other substance use disorder, you already know just how stressful day-to-day life can become. If you have to drink to get rid of withdrawal symptoms and can’t control your drinking once you start, it’s easy to feel trapped, which is, of course, a major stress in itself. If you feel this way, you aren’t alone — taking the first steps to get help can free you from the seemingly unending cycle of alcohol use.

How Do I Know If I’ve Developed an Alcohol Use Disorder?

If you have started using alcohol as a way to cope with stress, it can be difficult to tell whether you have developed an alcohol use disorder or if you are beginning to develop one. While you’ll need to consult a medical professional if you’re looking for a definite diagnosis, you can look for some of the common signs:

  • Spending a lot of time both drinking and recovering from drinking
  • Not being able to control how much you drink once you start
  • Continuing to drink even when you experience negative consequences
  • Giving up on hobbies or responsibilities in order to drink
  • Developing an alcohol tolerance
  • Craving alcohol or becoming preoccupied with drinking when you can’t drink
  • Experiencing withdrawal symptoms when you don’t drink (or drinking to ensure you avoid these symptoms)
  • Using alcohol when it is dangerous to do so (like when you’re driving)

Binge drinking can also be a sign of a developing alcohol use disorder. Binge drinking is defined as consuming five or more standard drinks in two hours for men and consuming four or more standard drinks in two hours for women. On its own, binge drinking doesn’t necessarily indicate an alcohol use disorder, but it could be a sign that one is starting to develop.

It’s important to keep in mind that alcohol use disorders are on a spectrum. Milder cases tend to have fewer symptoms present, while more severe cases have more. Even if you think you only have a mild case, you can still benefit tremendously from treatment. Most cases of alcohol use disorder become progressively worse over time.

How Can Treatment Help?

If you’re unfamiliar with substance use disorder treatment, you may think residential treatment’s only benefit is preventing you from accessing your substance of choice. This couldn’t be further from the truth. A good residential treatment program takes a holistic approach to help you improve your life.

In most cases (and definitely in severe cases), a stay at a residential treatment center begins with a medical detox program. In medical detox, you’ll be supervised by a doctor and likely given medication to prevent seizures and other complications of alcohol withdrawal. Withdrawing from alcohol on your own can be very dangerous, and inpatient detox can ensure that you’re safe. Granite Recovery Centers provides medical detoxification for people who do not need immediate medical intervention, are not a danger to themselves, and are capable of self-evacuation in the event of an emergency.

Once you’re in treatment, you’ll work with counselors and medical professionals to help you identify issues that make you want to drink. These professionals will help you develop healthier coping mechanisms to deal with stress so you’ll be less likely to turn to alcohol in the future. You may get to participate in cognitive behavioral therapy and dialectical behavioral therapy, as well as trauma therapy if needed.

Nutritional deficiencies developed while drinking heavily can add to stress and feeling generally unwell, so residential rehabilitation includes healthy food and ample exercise opportunities. And if you have a co-occurring mental health condition, on-site professionals will help you develop an effective treatment plan.

Ready to Take the Next Step?

Alcohol is an easy answer to stress for many people. But if you have an alcohol use disorder, chances are good that alcohol only causes more stress and worsens the stress you already have. And if the prospect of quitting by yourself seems like too much, don’t worry—the professionals working with Granite Recovery Centers will be helping you every step of the way. If you’re ready to change your life, give us a call at 855-712-7784 today!

Source: https://www.graniterecoverycenters.com/resources/the-connection-between-stress-and-alcoholism/ April 2021

In the September/October 2020 Missouri Medicine, Polocaro and Vettraino raise the important issue of the transgenerational effects of prenatal cannabinoid exposure (PCE) on subsequent generations.1 The implications of multigenerational toxicity of cannabinoids is very far-reaching with major policy implications.

The picture presented by Polcaro and Vettraino relating to the mental health implications of PCE is correct if too conservative. As they observe the subject is deeply confounded with multiple other factors impacting post-natal neurological development. For these reasons the significant concordance between reports from five longitudinal studies of childhood development relating to impaired indices of concentration, startle, excitability, poor visuospatial processing and executive functioning including ADHD-like and autism-like features are of particular concern.26 Under a legalization paradigm the state effectively condones unlimited all day every day exposure to extremely high concentrations of THC, other cannabinoids and cannabis tars. What is especially concerning about this is that many of the neurotoxic and neurodevelopmental toxicities of cannabis exhibit threshold dose effects above which severe damage becomes commonplace.7 In the context of an increasingly solid consensus relating to the harmful impacts of adult and adolescent cannabis exposure8 the implications of PCE-neurotoxicity have not been carefully considered. It has been shown that nationwide autism rates are undergoing an exponential rise and indeed New Jersey has been shown to have 4.5% of 8-year-old boys who carry an autism spectrum disorder diagnosis.9,10 Our space-time and causal inference studies demonstrate that indeed cannabinoid exposure to THC and cannabigerol amongst other fractions of cannabis, is a principal driver of this nationwide epidemic (manuscript submitted).9,10

A very concerning consensus is now emerging relating to cannabis-induced teratogenesis, embryotoxicity and fetotoxicity. A 2007 Hawaiian study found that 21 birth defects including many cardiovascular defects, Downs syndrome, orofacial clefts, gastroschisis and arm and hand defects were elevated in offspring of women exposed only to cannabis gestationally with odds ratios up to 40-fold and upper confidence intervals to 123-fold.11 A report on Canada found that total congenital defects were three times more common in the northern territories where cannabis is smoked about three times as much.12,13 In October 2018 Colorado Health reported an excess of 20,152 total birth defects beyond their baseline expected 67,620 defects 2000–2013 across the period of cannabis legalization when the use of other drugs was falling, representing an elevation of 29.8% above background rates.14 In a high cannabis use area of Australia 13 defects were found to be elevated compared to Queensland, which for methodological reasons is a conservative estimate.15 Concerningly elevated rates of Downs syndrome in Colorado, Hawaii, Australia and Canada clearly indicate that heritable cannabis genotoxicity can occur at the hundred megabase chromosomal scale.11,12,14,15 A close association of atrial septal defect (secundum type) with rising patterns of cannabis use across space and time in the US was recently reported, suggesting that the list of known teratological associations of prenatal cannabis exposure is as yet incomplete.16 This epidemiological literature is closely concordant with studies in experimental animals.1719 Again an abrupt rise in genotoxicity with increasing cannabinoid exposure has been demonstrated for many cannabinoids and is of particular concern.2023

Links between cannabis and several paediatric cancers including acute lymphoid leukaemia (ALL), acute myeloid leukaemia, rhabdomyosarcoma and neuroblastoma suggest further implications of cannabinoid genotoxicity.2428 Since these tumours together encompass the common tumours of childhood, it is at least possible that cannabis is responsible for the 43% elevation in total childhood cancer across US 1975–2017.29 Indeed Downs syndrome is well known to be associated with a 2,000-fold elevated risk of childhood ALL from 2/100,000 to around 5/100.30,31

This diverse assemblage of highly congruent evidence of severe cannabis-related neurotoxicity and genotoxicity from varied locations can only be described as extremely concerning indeed. In view of its well described epigenetic and chromoanagenetic effects3234 and its clearly transgenerational-multigenerational impacts one can only conclude that if the evidence base is not admitted to the cannabis debate and access to fetotoxic and embryotoxic cannabinoids is not immediately restricted the community will inevitably pay a heinous price in terms of avoidable paediatric neurotoxicity, congenital birth defects, heritable cancerogenesis and multigenerational epigenotoxicity.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721409/ Nov-Dec 2020 in response to ‘Cannabis in Pregnancy and Lactation – A Review’ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723128/

Source: Preventing Marijuana Use Among Youth & Young Adults (getsmartaboutdrugs.gov) March 2017

Researchers have found that even occasional cigarette use is enough to affect the volume and connectivity of developing brains

After decades of educational programming and advertising, regular cigarette smoking and sales in the United States have declined to their lowest levels in 50 years. But doctors and parents are now racing to deal with another health crisis that has popped up in its place: the meteoric rise of electronic cigarettes (or e-cigarettes) among adolescents.

This nicotine electronic delivery device was originally introduced to the market as a promising tool to aid smoking cessation among already current smokers. Yet, the lack of federal regulations, the appealing flavors available, and perceptions that these devices were less harmful than regular cigarettes have led to a worrying spike in use among U.S. adolescents. One in five U.S. high school students and one in 20 middle school students currently use e-cigarettes.

E-cigarette use among youth has skyrocketed in the past few years

U.S. Surgeon General Jerome Adams has declared e-cigarettes an epidemic among youth, stressing that e-cigarette aerosols containing nicotine increase the risk of addiction to nicotine and other drugs, and impact brain development which can induce mood disorders and lower impulse control. Now, new research led by Dr. Bader Chaarani of the University of Vermont and published in the journal Biological Psychiatry: Cognitive Neuroscience and Neuroimaging has found adolescents that smoked only a few cigarettes had smaller and less connected brain areas than their peers who never smoked. This could mean that adolescent smokers’ brains will develop and function differently, which may affect decision-making and self-control in adulthood. 

Just like regular cigarettes, e-cigarettes contain nicotine, a neuroactive chemical and an addictive component whose main target is the brain. Nicotine acts upon receptors in our brains -through nicotinic acetylcholine receptors (nAChRs)- to promote the release of a neurotransmitter called dopamine. Dopamine is a feel-good chemical, triggering a pleasurable response in our brains. When linked with the action of smoking, it plays a fundamental role in nicotine addiction.

Adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired

Nicotine exposure among adults presents lower risks compared to adolescents. This is because our brains develop throughout our first three decades of life. During this maturation period, the brain circuits are being remodeled, especially those involved in reward function (dopamine) and cognitive function (acetylcholine). Therefore, adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired, making young people even more vulnerable to future addiction. 

Previous studies have shown that adolescent smokers have reduced neural activity and show symptoms of nicotine dependency at lower nicotine levels than adults, and that individuals that begin smoking during adolescence are more likely to develop nicotine dependence than individuals that start in their late 20′s.

Studies of smoking’s effects on the brain have largely focused on adults, not youth – until now

One big gap in research observing the effects of cigarette smoking on brain volume, connectivity, and function to date is that such studies have been mostly performed on adult smokers rather than adolescent smokers. The majority have also focused on daily and heavy smokers, yet have overlooked occasional smokers, which is relevant due to common experimentation behaviors during adolescence

The new research by Dr. Chaarani and their team finally addresses these gaps by looking at the brains of adolescent light smokers. They found that just a couple of cigarette puffs can potentially alter the development of adolescent brain. 

The research team recruited over 600 14-year-old adolescents and calculated a cigarette-smoking score for each participant based on how many times, during their lifetime, they had smoked cigarettes. Participants ranged from young people who had never smoked to those who have smoked more than 40 times.

Smoking even a few times is significantly linked to a decreased volume of the gray matter and neuronal connectivity

The researchers also looked at the brain of each of the participants using functional magnetic resonance imaging (fMRI). These images were used to estimate the brain gray matter volume corresponding to the neuron bodies where synapses occur, and white matter connectivity, meaning the “telephone wires” that connect neurons and brain areas by carrying electrical signals. 

Interestingly, Dr. Chaarani and their team found that smoking even a few times was significantly linked to a decreased volume of the gray matter and neuronal connectivity. And the more teens smoked, the more the gray matter volume at the ventromedial prefrontal cortex (vmPFC), and the connectivity at the corpus callosum of their brains was reduced. Scientists have previously linked alterations in the vmPFC volume with a reduction in reward and with an increased risk of anxiety disorders. 

Moreover, reduction in the connectivity could indicate that nicotine induces axonal damage, meaning it may be altering the communication between brain areas. These alterations in brain connection have also been reported in individuals with substance addiction and alcohol dependence. While the research only showed a link between low doses of cigarette smoking and brain alterations, rather than a causal effect, these type of consequences have been consistently reported in many studies on brains of adult smokers.

E-cigarettes may look harmless, but they have lasting effects on developing brains

Although this study focused on adolescents who smoked traditional cigarettes, scientists have demonstrated that such risks are applicable to teenagers who vape using the popular JUUL brand of e-cigarettes since the two methods deliver similar amounts of nicotine.

Researchers are still working to understand the impact of nicotine in the brain of young smokers, particularly now that e-cigarette use among youth has increased rapidly. This new study could play a critical role in educational campaigns, and spur regulatory agencies, parents, and teachers to take an active role in preventing this newest addiction. 

Source:  https://massivesci.com/articles/smoking-vaping-risks-adolescent-brain-function-development-addiction-nicotine/   June 2019

Summary

Background

Cannabis use is associated with increased risk of later psychotic disorder but whether it affects incidence of the disorder remains unclear. We aimed to identify patterns of cannabis use with the strongest effect on odds of psychotic disorder across Europe and explore whether differences in such patterns contribute to variations in the incidence rates of psychotic disorder.

Methods

We included patients aged 18–64 years who presented to psychiatric services in 11 sites across Europe and Brazil with first-episode psychosis and recruited controls representative of the local populations. We applied adjusted logistic regression models to the data to estimate which patterns of cannabis use carried the highest odds for psychotic disorder. Using Europe-wide and national data on the expected concentration of Δ9-tetrahydrocannabinol (THC) in the different types of cannabis available across the sites, we divided the types of cannabis used by participants into two categories: low potency (THC <10%) and high potency (THC ≥10%). Assuming causality, we calculated the population attributable fractions (PAFs) for the patterns of cannabis use associated with the highest odds of psychosis and the correlation between such patterns and the incidence rates for psychotic disorder across the study sites.

Findings

Between May 1, 2010, and April 1, 2015, we obtained data from 901 patients with first-episode psychosis across 11 sites and 1237 population controls from those same sites. Daily cannabis use was associated with increased odds of psychotic disorder compared with never users (adjusted odds ratio [OR] 3·2, 95% CI 2·2–4·1), increasing to nearly five-times increased odds for daily use of high-potency types of cannabis (4·8, 2·5–6·3). The PAFs calculated indicated that if high-potency cannabis were no longer available, 12·2% (95% CI 3·0–16·1) of cases of first-episode psychosis could be prevented across the 11 sites, rising to 30·3% (15·2–40·0) in London and 50·3% (27·4–66·0) in Amsterdam. The adjusted incident rates for psychotic disorder were positively correlated with the prevalence in controls across the 11 sites of use of high-potency cannabis (r = 0·7; p=0·0286) and daily use (r = 0·8; p=0·0109).

Interpretation

Differences in frequency of daily cannabis use and in use of high-potency cannabis contributed to the striking variation in the incidence of psychotic disorder across the 11 studied sites. Given the increasing availability of high-potency cannabis, this has important implications for public health.

Funding source

Medical Research Council, the European Community’s Seventh Framework Program grant, São Paulo Research Foundation, National Institute for Health Research (NIHR) Biomedical Research Centre (BRC) at South London and Maudsley NHS Foundation Trust and King’s College London and the NIHR BRC at University College London, Wellcome Trust.

Source: The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study – The Lancet Psychiatry March 2019

The study by Sadananda et al published in the current issue of the IJMR highlights the neurophysiological basis of altered cognition in subjects with opioid addiction. The study demonstrated aberrant network activity between the default mode network (DMN) and fronto-parietal attentional network (FAN) as a major cause for working memory deficits in drug addiction. Working memory is an important to retain the cognitive information essential for goal directed behaviours. Human beings are endowed with an efficient cognitive faculty of working memory, essential for efficient functioning of the executive network system of the brain. As working memory is the key to carry out any cognitive process involving attention, volition, planning, goal directed behaviour, etc., consciousness is linked largely to working memory processing. The importance of integrating neuroscience knowledge especially the executive functions of human brain in leadership has been taught in neuro-leadership programs as a mean to maximize the human capabilities, productivity, creativity, leadership, wellness, positive attitude.

Aberrant network activities and structural deficits in brain areas of executive functioning impede most of our intellect including mental flexibility, novel problem solving, behavioural inhibition, memory, learning, planning, judgement, emotion regulation, self-control and other social functioning. Deficits in working memory and attention owing to reduced fronto-parietal network (FPN) activity is reported in schizophrenia, autism, attention deficit hyperactive disorder (ADHD) and anxiety disorders. Opioid addiction is reported to impede such dynamicity of the executive system leading to a wide range of deficits in cognition. Opioid addiction alters the network integrity between DMN and FPN networks and weakens the cognitive information processing in cognitively challenging paradigms. Dysfunctional dynamics of DMN activity is believed to contribute to impaired self-awareness, negative emotions and addiction related ruminations. Aberrant DMN activity and reduced medial prefrontal cortical functions are common neural phenotypes of cognitive deficits in conditions like mental illness, drug addiction, sleep deprivation and neurodegenerative disorders. People with substance use disorders develop mental illnesses as a serious comorbidity that in turn, leads to severe behavioural impairments at the social, emotional and cognitive domains. Chronic sleep deprivation associated with drug addiction and substance abuse is another predisposing factor that worsen the behavioural impairments. Over all, drug addiction, substance abuse and the subsequent maladaptive behaviours including mental illness and sleep deprivation trigger a complex set of network instability in the domains of cognition and affect. The euphoria and hallucinating experience of drugs of abuse would soon lead to psychological distress and to cognitive and emotional behavioural impairments due to the disruption of various top down and bottom-up network dynamics.

Substance use disorders are an imminent socio-economic burden and have become a major public health concern worldwide. Despite knowing the harmful effects and consequences of drug use, reports say that the youth especially the adolescents have a tendency to continue the habit. There is a need to have effective measures in place such as educational programmes to improve the self-efficacy of parents and family members to help their children to develop the right behavioural attitude, enhance the capacity building in teachers to strengthen the self-esteem and wellness of students to organize substance use control awareness programmes in coordination with NGOs at educational institutions, involvement of television and other visual and social media platforms to organise substance abuse control programmes and for interactive opportunity for children/youth with educators, researchers and professionals, organization of knowledge dissemination programmes to the public/schools/colleges to highlight the adverse effects of drug abuse on mental health and cognition. Introduction to such knowledge sharing platforms such as the Virtual Knowledge Network (VKN) at NIMHANS, Bengaluru, provide interactive skill building opportunities to safeguard them from substance abuse and addiction. People should have easy access to such services and rehabilitation centers. Various behavioural intervention strategies such as cognitive retraining, psychotherapy, yoga therapy, mindfulness-based intervention programmes etc. are reported to improve cognitive abilities, regulation of negative emotions and restoration of motivational behaviours. A study on single night exposure to olfactory aversive conditioning during sleep helped to quit addiction to cigarette smoking temporarily. Such studies highlight the possibility of learning new behaviours during sleep and its positive impact on wake associated behaviours. Such approaches are quite useful, easily testable and cost-effective. Thanks to the incredible phenomenon of adult brain plasticity, it is possible to re-establish social intelligence, prosocial motivation among people with substance abuse.

Source: Drug addiction – How it hijacks our cognition & consciousness – PMC (nih.gov) October 2021

Abstract

Rates of cannabis use among adolescents are high, and are increasing concurrent with changes in the legal status of marijuana and societal attitudes regarding its use. Recreational cannabis use is understudied, especially in the adolescent period when neural maturation may make users particularly vulnerable to the effects of Δ-9-tetrahydrocannabinol (THC) on brain structure. In the current study, we used voxel-based morphometry to compare gray matter volume (GMV) in forty-six 14-year-old human adolescents (males and females) with just one or two instances of cannabis use and carefully matched THC-naive controls. We identified extensive regions in the bilateral medial temporal lobes as well as the bilateral posterior cingulate, lingual gyri, and cerebellum that showed greater GMV in the cannabis users. Analysis of longitudinal data confirmed that GMV differences were unlikely to precede cannabis use. GMV in the temporal regions was associated with contemporaneous performance on the Perceptual Reasoning Index and with future generalized anxiety symptoms in the cannabis users. The distribution of GMV effects mapped onto biomarkers of the endogenous cannabinoid system providing insight into possible mechanisms for these effects.

SIGNIFICANCE STATEMENT Almost 35% of American 10th graders have reported using cannabis and existing research suggests that initiation of cannabis use in adolescence is associated with long-term neurocognitive effects. We understand very little about the earliest effects of cannabis use, however, because most research is conducted in adults with a heavy pattern of lifetime use. This study presents evidence suggesting structural brain and cognitive effects of just one or two instances of cannabis use in adolescence. Converging evidence suggests a role for the endocannabinoid system in these effects. This research is particularly timely as the legal status of cannabis is changing in many jurisdictions and the perceived risk by youth associated with smoking cannabis has declined in recent years.

Discussion

We present evidence of GMV differences in adolescents associated with only one or two instances of cannabis use. Although novel, this work is consistent with reports of a dose–response effect of cannabis on behavioral and brain measures following heavier use (Lorenzetti et al., 2010Silins et al., 2014). We identified significantly greater GMV in adolescents who reported only one or two instances of cannabis use relative to cannabis naive controls in large medial temporal clusters incorporating the amygdala, hippocampus, and striatum, extending into the left prefrontal cortex. Significantly greater GMV was also observed in the lingual gyri, posterior cingulate, and cerebellum. The regions identified in this whole-brain, VBM approach replicated previous findings of differences in volume (Yücel et al., 2008Ashtari et al., 2011Schacht et al., 2012) and shape (Gilman et al., 2014Smith et al., 20142015) associated with cannabis use in ROI studies and with the spatial distribution of the eCB system (Burns et al., 2007). Although cannabis use has been associated with reduced brain volumes, studies typically report on adults with heavy substance use histories (cf. Ashtari et al., 2011). Gilman et al. (2014), however, have reported gray-matter density increases in the amygdala and nucleus accumbens of young adult recreational users and Medina et al. (2007) observed hippocampal enlargement in cannabis using adolescents. Our results are also consistent with the Avon Longitudinal Study of Parents and Children (French et al., 2015), which showed a trend for greater cortical thickness in male adolescents with <5 instances of cannabis use relative to THC-naive controls.

Converging evidence suggests that these effects may be a consequence of cannabis exposure. GMV differences could not be explained by group differences in demographic, personality, psychopathology, or other substance use factors. Examination of THC-naive 14-year-olds who later used cannabis showed no GMV differences, even using a more liberal ROI test, suggesting that the differences do not precede cannabis use and are not because of unidentified factors in those predisposed to use. Finally, the spatial distribution of GMV effects was associated with the eCB system, suggesting cannabis exposure may cause these findings.

The preclinical literature presents a number of possible mechanisms by which low levels of cannabis exposure could result in greater GMV relative to THC-naive controls. Adolescent rats treated with cannabinoid agonist showed altered gliogenesis in regions including the striatum and greater preservation of oligodendroglia relative to control animals (Bortolato et al., 2014). Zebra finches treated with cannabinoid agonist showed greater dendritic spine densities (Gilbert and Soderstrom, 2011); critically, these effects were observed in late-prenatal but not adult animals. Of particular relevance to this study, a single dose of Δ9THC transiently abolished eCB-mediated long-term depression (LTD) in the nucleus accumbens and hippocampus of adolescent mice (Mato et al., 2004). Suspension of LTD may interrupt maturation-related neural pruning and preserve gray matter. Future studies should assess whether these processes operate in human adolescents and whether they produce persisting alterations in GMV.

These findings should be interpreted in light of the study’s limitations. The IMAGEN sample is racially and ethnically homogenous so it remains to be determined whether the findings generalize to youth from more diverse backgrounds. Substance use was assessed using self-report and we do not have standard dose units of cannabis nor information on mode of use or a measure of drug metabolites. Combining images from different sites and imaging platforms remains controversial and is not completely controlled by including site as a covariate. Future studies should replicate the present results using images acquired at the same site on the same scanner or with equal numbers of cases and controls per scanner. We also note that the CNR1 gene expression (Hawrylycz et al., 2012) and CB1 receptor density (D’Souza et al., 2016) maps were generated in independent samples of adults and may not accurately represent the eCB system in our sample of adolescents. Although we report significant spatial associations between GMV effects and both CNR1 gene expression and CB1 receptor density, the effect sizes were small and any suggestion that these associations represent mechanisms for the effects we observe is speculative and requires further investigation.

We adopted a whole-brain, VBM approach to detect effects that were not limited by anatomical boundaries and to allow exploration of spatial relationships between GMV effects and the eCB system. There is evidence, however, that brain perfusion can influence VBM measures of local volume (Franklin et al., 20132015Ge et al., 2017; cf. Hawkins et al., 2018) so future studies should combine VBM with other measures of brain structure to provide confirmatory evidence. In particular, shape analysis has been shown to be sensitive to brain structural differences associated with cannabis use (Gilman et al., 2014Smith et al., 20142015Weiland et al., 2015). Moreover, combining morphometry metrics allows for testing of associations between them, which can identify different relationships between shape deformations and local volume (Gilman et al., 2014) providing evidence of further differences between cannabis users and controls.

One source of variability in the human findings on brain structural correlates of cannabis use may be comorbid substance use (Weiland et al., 2015Gillespie et al., 2018). Given recent evidence of different patterns of functional connectivity in groups using alcohol, nicotine, and cannabis alone and in combination (Vergara et al., 2018), it will be important to account for any possible interaction effects of cannabis with other psychoactive substances. This issue is particularly important considering the ways in which comorbid substance use has been addressed in two recent, widely cited studies. Gilman et al. (2014) covaried for alcohol and nicotine use and found gray-matter density increases and shape deformations associated with cannabis use. Weiland et al. (2015) matched groups on alcohol and nicotine use and reported no morphometric differences associated with cannabis use, concluding that previously reported differences associated with cannabis may instead be attributable to alcohol use. The participants in Weiland et al.’s (2015) study, however, were using alcohol and nicotine at higher levels than those in Gilman et al.’s (2014) study. It is possible that cannabis, alcohol, and nicotine have differential effects on brain morphometry; specifically, recreational cannabis use has been associated with volume increases, whereas alcohol has been associated with volume reductions. In the current study, we matched the groups on alcohol and nicotine use and, within the cannabis using group, neither alcohol nor nicotine use was associated with individual differences in GMV, suggesting that the GMV differences we report are associated with cannabis use.

We note individual differences in GMV effects: although regional GMV was greater at the group level for adolescents with low levels of cannabis exposure, the distributions showed a high degree of overlap such that many cannabis users had GMV equivalent to that of controls. None of the tested demographic, personality, or substance use factors stratified GMV in the cannabis users. We note evidence that an association between cannabis use and cortical thickness was stratified by genetic risk for schizophrenia (French et al., 2015) and that an association between cannabis use and hippocampal shape was stratified by dopamine-relevant genes (Batalla et al., 2018). Some adolescents may be vulnerable to GMV effects at extremely low levels of cannabis use and it will be critical to identify those at risk as these structural brain changes may be associated with individual risk for psychopathology and deleterious effects on mood and cognition.

Of the behavioral variables tested, only sensation seeking and agoraphobia differed between the cannabis users and controls and these factors were not related to GMV differences. In the cannabis using participants, GMV in the medial temporal clusters was associated with PRIQ and psychomotor speed such that greater GMV in these regions was associated with reduced performance. The finding that right medial temporal GMV predicted generalized anxiety symptoms at follow-up for those participants who had used cannabis should be interpreted with caution given the small sample size and that we were not able to identify factors that drove the individual differences in cannabis effects on GMV at baseline. These findings are notable, however, as panic and anxiety symptoms are frequently reported side effects by naive and occasional cannabis users (Hall and Solowij, 1998). We also note fMRI evidence of hypersensitivity of the amygdala to signals of threat in a partly overlapping sample of cannabis using adolescents (Spechler et al., 2015) and a relationship between adolescent cannabis use and future mood complaints (Wittchen et al., 2007), even with comparatively low levels of use (Cheung et al., 2010).

We have revealed greater GMV in adolescents with only one or two instances of cannabis use in regions rich in CB1 receptors and CNR1 gene expression. Critically, we were able to control for a range of demographic and substance use effects, to confirm that these structural brain effects were not associated with comorbid psychopathology, and to demonstrate that these effects were unlikely to precede cannabis use. The pattern of results is characterized by individual differences in GMV effects in the cannabis users; these individual differences were associated with PRIQ and with vulnerability to future symptoms of generalized anxiety. Given the increasing levels of cannabis use among adolescents today, we suggest that studying the effects of recreational use early in life is an area of particular importance that should be addressed in the future by large scale, prospective studies.

Source: Grey Matter Volume Differences Associated with Extremely Low Levels of Cannabis Use in Adolescence | Journal of Neuroscience (jneurosci.org) March 2019

This article is distilled from a paper given at the Recovery Plus conference in London on 26th June 2018 by Peter Stoker, Director of the National Drug Prevention Alliance.

References available on request.

Prevention, the word and meaning, comes from the Latin “praevenire” which means “to come before”. In other words, to act pre-the event – not during it or after it. Any action later than pre-the event is not prevention, it is repair. And both are required.

 

When it comes to funding, Prevention is the Cinderella service, and reasons why could include that Treatment has more workers with a resulting vigour; Treatment is easier to count, pleasing accountant-oriented funders; Prevention is (falsely) depicted as inhibiting Human Rights, and libertarian campaigners have always had deeper pockets that Prevention ever had.

INTERNATIONAL HISTORY

Early responses to the drug problem were characterised by being reactive rather than proactive, often with a legal or enforcement flavour.

There was also a tendency to focus on transmission of knowledge, sometimes coupled with a challenging of the users’ attitudes – unintended consequences could follow, for example:

  • if you give knowledge to a user you may produce a knowledgeable user, and
  • if you challenge a user’s attitude you may produce a knowledgeable user with an attitude.

In due course a more complete model was developed using the simple synonym – KAB, meaning you should address a mixture of Knowledge, Attitudes and Behaviour. (And focus on encouraging positive behaviour, rather than punishment).

Libertarians spotted the educational arena as fertile ground for their campaigns; their speculative allegation that the so-called ‘war on drugs’ was failing was the launchpad for harm reduction (HR1) – this was later augmented by inclusion of human rights (HR2). I witnessed all this being promoted vigorously at the 2009 UNGASS/CND conference in Vienna – we were emphasising ‘Whole Health’ as a goal, but throughout the proceedings there was an apparently innocuous and almost irresistible request from ACLU delegates that human rights should be included in all clauses. It wasn’t evident at this moment that they would later insist that using drugs was itself a “human right”, which therefore meant that prevention was, in effect, a breach of human rights. This activism was bankrolled by George Soros’ Open Society.

You can explore people’s thinking on this every day, in the Google Alerts, but remember what H.L.Mencken had to say: “For every complex problem there is a simple solution … and it doesn’t work”.

Exemplary practice can be observed in several initiatives. There are too many to cover them all, but here are some indicative examples and source materials:

DFAF – Drug Free America Foundation – www.dfaf.org – internationally active, establishing conferences in Europe and the Americas. Publishes a learned journal, and holds an enormous library.

NFIA – National Families In Action – Atlanta USA – www.nationalfamilies.org – countless years of detailed research and practice. Many learned papers. They have just published a very useful technical paper called ‘The MJ File’ – requires reading.

CADCA  – www.cadca.org – Community Anti-Drug Coalitions of America – until recently under direction of Major General Arthur Dean, US Army retired. CADCA is well-resourced; in 2016 alone it trained over 8,000 youth.

A very useful publication by NIDA/CSAP www.drugabuse.gov (Center for Substance Abuse Prevention) is ‘Preventing Drug Abuse’ – a slim volume, its first edition in 1997, revised in 2003 … about due for an update, one might say!

DARE – www.dare.org –  has suffered attacks in recent years but has survived, to the extent that it is signing new client organisations at the rate of about 200 a year even now.

DWI – Drug Watch International –  www.drugwatch.org a long-standing forum of experts in America and abroad. Membership by invitation only.

Straight – peer-led youth rehab service, now closed. Featured in the movie ‘Not My Kid’ starring George Segal and Stockard Channing.  Straight came in for criticism from the liberal left, and eventually closed, but not for this reason. I asked Bill Oliver, Chief Executive for many years, what caused the collapse of Straight. He told me “We were very good drug workers but lousy accountants”. A salutory comment!

SAM – Smart Approaches to Marijuana – www.sam.org . One of the most potent bodies in recent years, in the legalisation battle zone. Under the direction of Kevin  Sabet, a former policy adviser in the  US drug czar’s office. Senior staffers include former Congressman Patrick Kennedy. Their approach is soundly based on scientific evidence.

 And NDPA – National Drug Prevention Alliance – based in Slough, near Heathrow, and almost 30 years old. NDPA has provided support and training for parents, young people, drugs professionals and teachers. It has provided counselling and referral for users, and has done a large amount of work in the broadcast and print media,. It runs two websites – one for drugs professionals www.drugprevent.org.uk and one – more accessible in its presentation –  for parents – www.pinpoints.org.uk The websites include thousands of technical papers as well as other advisory publications. The websites are regularly visited internationally, several hundred thousand visits per year, and readers include our own Home Office.

EXAMPLES OF SUCCESS

Perhaps the earliest example was almost 40 years ago, in the late 1980s. Increased drug use sparked large numbers of parents to press academics into action, with the most memorable campaign being ‘Just Say No’ – under Ronald Regan’s wife Nancy. It was ridiculed by the left, but the campaign was very much more than a slogan, included detailed trainings for parents and youth, plus media activism, and the hard evidence is that it reduced prevalence by more than 60% – 11 million fewer users. Any other health-related campaign today would kill for such a result.

Perhaps the best example of this in recent years has been around the use of tobacco. Historically tobacco was used freely everywhere. Even doctors said it was good for you – it would soothe your throat, for example. Advertising sold it vigorously. Such protests as were made, were largely ignored. And if any people suggested that smoking had made them ill, the rest of us felt that that was their own fault and nothing to do with the us – they were getting what they deserved

Then, one day, the US Surgeon General announced that tobacco smoking by one person could give other persons cancer (through passive smoking). This was a game-changing announcement; we could no longer ignore what these drug users were doing – now it was affecting all of us. Anti-smoking articles and adverts appeared in the media; doctors advised strongly against it, schools told their pupils to avoid it, offices prohibited smoking in the premises, causing those who still were dependent on cigarettes to huddle in unpleasant external doorways, and the newly emerging Health and Safety brigade put in their six-pennorth. In due course the government reacted, producing new and influential legislation, banning smoking in many places. Before long the culture changed markedly, and in consequence so did the prevalence.

But if you want a bang up-to-date success, story you need look no further than Iceland. Comparing latest European figures with a couple of decades ago, teen drinkers have dropped from 42% to 5%, cannabis use has dropped from 17% to 7%, and tobacco smoking from 23% to 3%. The emphasis is on providing stimulating activities for youth, and on schooling parents in now to be more engaged with their families. Countries are following the Icelandic model, and research shows Risk factors and Protective Factors are pretty much the same everywhere.

There are localised examples of how to get ahead of the game – for example, one effective program was run in New York – called ‘Fixing Broken Windows’ the approach was to keep the streets and buildings clean and tidy – it reduced drug abuse and other social aspects.

In society as a whole, what promises the best results? In essence, the most effective  strategy will come from changing the culture.

Balanced prevention policy and strategy

I have yet to find a better definition what we should do than that written by a leading expert in the prevention field, based in Arizona – William Lofquist:

“We need to get beyond the notion that prevention is stopping something happening, to a more positive approach which creates conditions which promote the well-being of people”.

Lofquist found the importance of treating youth as resources, rather than objects or recipients of project work. He also emphasised that it should engage the whole of society, not in some rigid formulaic way but in a fluid, proactive approach which is alive to changes in society and always works to stay ahead of the game.

An assembly of this co-ordinated strategy and policy might include the following:

Government

Health

Education

Higher ed

Youth peers

Parents

Religions

Pharmacists

Businesses

Media

Volunteers

Sport

Leisure

Drugs services

–  specify, resource, oversee, evaluate and improve

–  address all health elements

–  focus on health promoting approaches

–  train teachers and youth workers in prevention

–  develop and utilise their potential

–  de-marginalise, train, resource, support

–  spiritual lead, network, interface working

–  more proactive, preventing, reducing harm

–  health promoting environments. EAPs, RDTs

–  educate and support editorial staff, no mixed messages

–  realise their potential, utilise more widely

–  health promoting environments, health image

–  widen education and training. Explore expansion

–  encourage plurality, with more emphasis on recovery

We can also learn much from the science of ‘Behaviour Modification’  – as practised by, inter all, Professor Brian Sheldon of the Royal Holloway University.

Constructive selfishness …

The tobacco example above describes what I mean by this expression. We should not shrink from recognising that selfishness is a powerful driving force across society. And since it is a powerful driving force, we should seek to drive it to our advantage.

We have yet to wake up to the potential of defining and communicating to society at large the various ways in which one person’s drug misuse adversely affects the rest of us.

Establishing readiness for prevention – CULTURAL CHANGE

What influences culture?

  • Peer group influence
  • Personal perceptions
  • Income versus cost of any action
  • Health issues
  • Moral structure
  • Spiritual structure
  • Family values
  • Attraction of risk-taking
  • Media
  • Mental state
  • Legislation
  • Economy – the well-off or the poor
  • Employment – job or no job

CSAP found in their comparison of practices that the best prevention results come through co-ordinated prevention efforts, offering multiple strategies, and providing multiple points of access.

*                 *                   *                 *                  *

This is but a quick canter through the jungle of Prevention. There is much more to it, but I hope I have whetted your appetite – and you may even see the sense in building prevention into your work spectrum. (As co-operators rather than competitors with other agencies).

Don’t fear that prevention will reduce your treatment client base – as treatment workers, you are going to be in demand for a long time yet! Whilst some will be prevented from drug and alcohol abuse, and some will manage to cure themselves, most people need expert help.

We are, after all, working towards the same objective.  I once saw a cartoon in which a drug worker was asking a guru how to solve the drug problem. ‘Why do people use drugs?’ asked the guru. ‘To escape reality’ said the worker. ‘Then the solution is obvious’. Said the guru. ‘Improve reality’

Abstract

Objectives: 

E-cigarette use has increased dramatically among adolescents in the past 5 years alongside a steady increase in daily use of marijuana. This period coincides with a historic rise in depression and suicidal ideation among adolescents. In this study, we describe the associations between e-cigarette and marijuana use and depressive symptoms and suicidality in a large nationally representative sample of high school students.

Methods: 

We used data from the 2 most recent waves (2015 and 2017) of the Youth Risk Behavior Survey. Our sample (n = 26,821) included only participants with complete information for age, sex, race/ethnicity, and exposure to e-cigarettes and marijuana (89.5% of survey respondents). We performed multivariate logistic regressions to explore the associations between single or dual use of e-cigarette and marijuana and depressive and suicidal symptoms in the past year adjusting for relevant confounders.

Results: 

E-cigarette-only use was reported in 9.1% of participants, marijuana-only use in 9.7%, and dual e-cigarette/marijuana use in 10.2%. E-cigarette-only use (vs no use) was associated with increased odds of reporting suicidal ideation (adjusted odds ratio [AOR]:1.23, 95% CI 1.03–1.47) and depressive symptoms (AOR: 1.37, 95% CI 1.19–1.57), which was also observed with marijuana-only use (AOR: 1.25, 95% CI 1.04–1.50 and AOR: 1.49, 95% CI 1.27–1.75) and dual use (AOR: 1.28, 95% CI 1.06–1.54 and AOR: 1.62, 95% CI 1.39–1.88).

Conclusions: 

Youth with single and dual e-cigarette and marijuana use had increased odds of reporting depressive symptoms and suicidality compared to youth who denied use. There is a need for effective prevention and intervention strategies to help mitigate adverse mental health outcomes in this population.

Source: Depressive Symptoms and Suicidality in Adolescents Using e-C… : Journal of Addiction Medicine (lww.com) Sept/Oct 2019

Three decades ago, I would have been over the moon to see marijuana legalized. It would have saved me a lot of effort spent trying to avoid detection, constantly looking for places to hide a joint. I smoked throughout my teens and early 20s. During this period, upon landing in a new city, my first order of business was to score a quarter-ounce. The thought of a concert or a vacation without weed was simply too bleak.

These days it’s hard to find anybody critical of marijuana.

The drug enjoys broad acceptance by most Americans — 63 percent favoured ending cannabis prohibition in a recent Quinnipiac poll — and legislators on both sides of the aisle are becoming more likely to endorse than condemn it. After years of loosening restrictions on the state level, there are signs that the federal government could follow suit: In April, Senate Minority Leader Charles E. Schumer (D-N.Y.) became the first leader of either party to support decriminalizing marijuana at the federal level, and President Trump (his attorney general notwithstanding) promised a Republican senator from Colorado that he would protect states that have legalized pot.

And why not? The drug is widely thought to be either benign or beneficial. Even many of those apathetic toward its potential health benefits are ecstatic about its commercial appeal, whether for personal profit or state tax revenue. Legalization in many cases, and for many reasons, can be a good thing. I’m sympathetic.

But I am also a neuroscientist, and I can see that the story is being oversimplified. The debate around legalization — which often focuses on the history of racist drug laws and their selective enforcement — is astoundingly naive about how the widespread use of pot will affect communities and individuals, particularly teenagers. In our rush to throw open the gate, we might want to pause to consider how well the political movement matches up with the science, which is producing inconveniently alarming studies about what pot does to the adolescent brain.

Marijuana for sale at a Colorado dispensary.    (Matthew Staver/Bloomberg Creative Photos)

I took a back-door route to the science of marijuana, starting with a personal investigation of the plant’s effects. When I was growing up in South Florida in the 1980s, pot was readily available, and my appreciation quickly formed the basis for an avid habit. Weed seemed an antidote to my adolescent angst and ennui, without the sloppiness of alcohol or the jaw-grinding intensity of stimulants.

Of the many things I loved about getting high, the one I loved best was that it commuted the voice in my head — usually peevish or bored — to one full of curiosity and delight. Marijuana transformed the mundane into something dramatic: family outings, school, work or just sitting on the couch became endlessly entertaining when I was stoned.

Like any mind-altering substance, marijuana produces its effects by changing the rate of what is already going on in the brain. In this case, the active ingredient delta-9-THC substitutes for your own natural endocannabinoids and mimics their effects. It activates the same chemical processes the brain employs to modulate thoughts, emotions and experiences. These specific neurotransmitters, used in a targeted and judicious way, help us sort the relentless stream of inputs and flag the ones that should stand out from the torrent of neural activity coding stray thoughts, urges and experience. By flooding the entire brain, as opposed to select synapses, marijuana can make everything, including the most boring activities, take on a sparkling transcendence.

Why object to this enhancement? As one new father told me, imbibing made caring for his toddler much more engrossing and thus made him, he thought, a better parent. Unfortunately, there are two important caveats from a neurobiological perspective.

As watering a flooded field is moot, widespread cannabinoid activity, by highlighting everything, conveys nothing. And amid the flood induced by regular marijuana use, the brain dampens its intrinsic machinery to compensate for excessive stimulation. Chronic exposure ultimately impairs our ability to imbue value or importance to experiences that truly warrant it.

In adults, such neuro-adjustment may hamper or derail a successful and otherwise fulfilling life, though these capacities will probably recover with abstinence. But the consequences of this desensitization are more profound, perhaps even permanent, for adolescent brains. Adolescence is a critical period of development, when brain cells are primed to undergo significant organizational changes: Some neural connections are proliferating and strengthening, while others are pared away.

Although studies have not found that legalizing or decriminalizing marijuana leads to increased use among adolescents, perhaps this is because it is already so popular. More teenagers now smoke marijuana than smoke products with nicotine; between 30 and 40 percent of high school seniors report smoking pot in the past year, about 20 percent got high in the past month, and about 6 percent admit to using virtually every day. The potential consequences are unlikely to be rare or trivial.

The decade or so between puberty and brain maturation is a critical period of enhanced sensitivity to internal and external stimuli. Noticing and appreciating new ideas and experiences helps teens develop a sense of personal identity that will influence vocational, romantic and other decisions — and guide their life’s trajectory. Though a boring life is undoubtedly more tolerable when high, with repeated use of marijuana, natural stimuli, like those associated with goals or relationships, are unlikely to be as compelling.

It’s not surprising, then, that heavy-smoking teens show evidence of reduced activity in brain circuits critical for  flagging newsworthy experiences, are 60 percent less likely to graduate from high school, and are at substantially increased risk for heroin addiction and alcoholism. They show alterations in cortical structures associated with impulsivity and negative moods; they’re seven times more likely to attempt suicide.

Recent data is even more alarming: The offspring of partying adolescents, specifically those who used THC, may be at increased risk for mental illness and addiction as a result of changes to the epigenome — even if those children are years away from being conceived. The epigenome is a record of molecular imprints of potent experiences, including cannabis exposure, that lead to persistent changes in gene expression and behavior, even across generations. Though the critical studies are only now beginning, many neuroscientists prophesize a social version of Rachel Carson’s “Silent Spring,” in which we learn we’ve burdened our heirs only generations hence.

Might the relationship between marijuana exposure and changes in brain and behavior be coincidence, as tobacco companies asserted about the link between cancer and smoking, or does THC cause these effects? Unfortunately, we can’t assign people to smoking and nonsmoking groups in experiments, but efforts are underway to follow a large sample of children across the course of adolescent development to study the effects of drug exposure, along with a host of other factors, on brain structure and function, so future studies will probably be able to answer this question.

In the same way someone who habitually increases the volume in their headphones reduces their sensitivity to birdsong, I followed the “gateway” pattern from pot and alcohol to harder drugs, leaping into the undertow that eventually swept away much of what mattered in my life. I began and ended each day with the bong on my nightstand as I floundered in school, at work and in my relationships. It took years of abstinence, probably mirroring the duration and intensity of my exposure, but my motivation for adventure seems largely restored. I’ve been sober since 1986 and went on to become a teacher and scholar. The single-mindedness I once directed toward getting high came in handy as I worked on my dissertation. I suspect, though, that my pharmacologic adventures left their mark.

Now, as a scientist, I’m unimpressed with many of the widely used arguments for the legalization of marijuana. “It’s natural!” So is arsenic. “It’s beneficial!” The best-documented medicinal effects of marijuana are achieved without the chemical compound that gets users high. “It’s not addictive!”  This is false, because the brain adapts to marijuana as it does to all abused drugs, and these neural adjustments lead to tolerance, dependence and craving — the hallmarks of addiction.

It’s true that a lack of benefit, or even a risk for addiction, hasn’t stopped other drugs like alcohol or nicotine from being legal, used and abused. The long U.S. history of legislative hypocrisy and selective enforcement surrounding mind-altering substances is plain to see. The Marihuana Tax Act of 1937, the first legislation designed to regulate pot, was passed amid anti-Mexican sentiment (as well as efforts to restrict cultivation of hemp, which threatened timber production); it had nothing do with scientific evidence of harm. That’s true of most drug legislation in this country. Were it not the case, LSD would be less regulated than alcohol, since the health, economic and social costs of the latter far outweigh those of the former. (Most neuroscientists don’t believe that LSD is addictive; its potential benefits are being studied at Johns Hopkins and New York University, among other places.)

Still, I’m not against legalization. I simply object to the astounding lack of scepticism about pot in our current debate. Whether or not to legalize weed is the wrong question. The right one is: How will growing use of delta-9-THC affect individuals and communities?

Though the evidence is far from complete, wishful thinking and widespread enthusiasm are no substitutes for careful consideration. Instead of rushing to enact new laws that are as nonsensical as the ones they replace, let’s sort out the costs and benefits, using current scientific knowledge, while supporting the research needed to clarify the neural and social consequences of frequent use of THC. Perhaps then we’ll avoid practices that inure future generations to what’s really important.

                                       By Judith Grisel,    May 25, 2018

Source:  https://www.washingtonpost.com/ posteverything/wp/2015/04/30/yes-pot-should-be-legal-but-it-shouldnt-be-sold-for-a-profit/   

Substance use has often been described as “bad learning” linked with impairments in reward processing and decision-making, but there is little substantial research to support this idea. A recent study by Byrne et al. suggests that substance misuse not only promotes harmful habit formation, which might undermine survival, but also makes it difficult to stop using.

Model-free vs. Model-based Learning

The “Dual Systems” theory of reinforcement learning defines two distinct systems:

  1. The model-based, or goal-directed system, where actions are planned and purposeful, and we learn about the connection between actions and outcomes, and how to modify our behavior to achieve the desired outcome. This system requires more cognitive processing and is more flexible and controlled.

  2. The model-free, or habit-based system, where learning is informed by reflexive responses to stimuli – like compulsive substance use and cravings. This system of learning is less flexible and is more controlled by automatic processing.

The differences between the two systems of learning have been highlighted by researchers in relation to harmful habitual behaviors such as substance use. One school of thought suggests that learning informed by the model-free system, with more of a focus on instinctual response to stimuli and less of a focus on conscious and informed decision-making, sets a person up to be more likely to engage in detrimental behaviors like substance use.

There is evidence that progressing from first use to misuse and addiction is paralleled by a shift from planned, purposeful, and goal-directed behavior to behavior that is habitual and reflexive. This progression and subsequent loss of control has been discussed by National Institutes on Drug Abuse Director Dr. Nora Volkow in her keynote speech at the APA and in her blog about free will. Model-free, conditioned learning means it is harder for a person to engage their frontal lobes, the part of the brain that helps us prioritize healthy, long-term and rational decisions. Repeated problematic substance use initiates a process where humans begin to respond more instinctually to the substance, wanting more and more of it over time. Use begets use, which leads to maladaptive behaviors centered around obtaining and using the substance to trigger the very same dopamine response that drives and reinforces model-free, habitual learning.

Substance Use and Reward Devaluation

Reward devaluation is a process that occurs in the brain where the value of a desirable outcome, like singing in a band, mentoring, or maintaining sobriety is reduced significantly. This process plays into why improving treatment outcomes can be so hard – treatment for addiction is not as “reinforcing” in the brain as substance use. Compulsive drug use is considered “highly pleasurable” by the parts of the brain that control decision-making when people are heavily addicted and feel as though they need the substance to survive. But treatment? not so much — long-term treatment is difficult to complete without continual support and a long-term treatment plan. Many patients stop attending treatment and/or support groups, and taking prescribed medications unless they are compelled to follow a set treatment plan and have adequate supports in place to help keep them on track.

Addiction is correlated to a considerable decrease in a person’s ability to devalue or disengage from habits learned through the model-free system. This means that problematic substance use affects our ability to make decisions and as the disorder progresses, we begin to put less value on long-term rewards and more value on immediately satisfying a need. Gradually, short term needs, like substance use, override long-term needs, like maintaining employment or investing in personal relationships.

Goals of Study

  1. To examine the associations between model-based and model-free learning with a wide array of substance use behaviors. The process used to determine this was measuring individual variations in eye-blink rate, an indirect proxy for dopamine functioning, a key neural process related to model-free learning.

  2. To assess whether problematic substance use predicted reward disengagement.

Why is This Important?

Patients with substance use disorders are driven to use despite harmful consequences, and although addiction is understood more and more as an acquired brain disease, many are still mystified as to why those suffering can’t manage to break their “habit.” This study helps foster a greater understanding of the mechanisms that explain why. Use may be thought of as “recreational” by the user, but it poses a challenge to the brain, reinforcement systems, and reward hierarchies, which can change a person quickly and in a way that is hard for those around them to understand. Once reward-outcome associations are well established— i.e., taking drugs makes a person “feel good”— individuals with substance use disorders have changed the most basic mechanisms in their brain, and will have more difficulty disengaging from the habitual tendencies. It is not clear how individual experiences, genetics, trauma, and other factors change the speed of these changes. That said, the results of this study are consistent with previous data depicting how alcohol dependence indicates a greater likelihood that a person has habit-based learning strategies over goal-directed strategies. The results do not, however, provide us with more information about whether biological recovery is possible, and how we could make recovery more likely and sustainable for patients.

Authors state that current findings highlight how problems with substance use go beyond the realms of habit formation: they also influence the process of disengaging or “breaking” habits by making it more difficult for individuals with substance use disorders to stop using substances. A better understanding of the mechanisms in the brain that take over once substance use becomes problematic may help us create more effective prevention campaigns and treatments once substance use progresses to a harmful habit.

Source: Why are habits so hard to break? (addictionpolicy.org) May 2019, updated October 2022

Tell Your Children:
The Truth About Marijuana, Mental Illness, and Violence

by alex berenson

free press, 272 pages, $26

The smoking of marijuana, with its careful preparation of the elements and the solemn passing around of the shared joint, was the unholy communion of the counterculture in the late 1960s, when our present elite formed its opinions. Many of them allowed their children to follow their bad examples, and resent that this exposes their young to a (tiny) risk of persecution and career damage. As a result, those who still disapprove of marijuana are much disliked. The book I wrote on the subject six years ago, The War We Never Fought, received a chilly reception and remains so obscure that I don’t think Alex ­Berenson, whose book has received much friendlier coverage, even knows it exists. As a writer who naturally covets readers and sales, I find this mildly infuriating.

But let me say through clenched teeth that it is of course very good news that a fashionable young metropolitan person such as Mr. ­Berenson is at last prepared to say openly that marijuana is a dangerous drug whose use should be severely discouraged. For, as ­Berenson candidly admits, he was until recently one of the great complacent mass of bourgeois bohemians who are pretty relaxed about it. He confesses in the most important passage in the book that he once believed what most of such people believed. He encapsulates this near-universal fantasy thus:

Marijuana is safe. Way safer than alcohol. Barack Obama smoked it. Bill Clinton smoked it too, even if he didn’t inhale. Might as well say it causes presidencies. I’ve smoked it myself, I liked it fine. Maybe I got a little paranoid, but it didn’t last. Nobody ever died from smoking too much pot.

These words are a more or less perfect summary of the lazy, ignorant, self-serving beliefs of highly educated, rather stupid middle-class metropolitans all over the Western world in such places as, let’s just say for example, the editorial offices of the New York Times. Thirty years from now (when it’s too late), they will look as crass and irresponsible as those magazine advertisements from the 1950s in which pink-faced doctors wearing white coats recommended certain brands of cigarettes. But just now, we are in that foggy zone of consciousness where the truth is known to almost nobody except those with a certain kind of direct experience, and can be ignored by everyone else.

One of the experienced ones, thank heaven, is Alex ­Berenson’s wife Jacqueline. She is a psychiatrist who specializes in evaluating mentally ill criminals. One evening, the Berensons were discussing one of her cases, a patient who had committed a terrible, violent act. Casually, Jacqueline remarked, “Of course he was high, been smoking pot his whole life.” Alex doubtfully interjected, “Of course?,” and she replied, “Yeah, they all smoke.” (She didn’t mean tobacco.) And she is right. They all do. You don’t need to be a psychiatrist to know this. You just have to be able to do simple Internet searches.

Most violent crime is scantily reported, since local newspapers lack the resources they once had. The exceptions are rampage mass killings by terrorists (generally in Europe) and non-political crazies (more common in the United States). These crimes are intensively reported, to such an extent that news media find things out they were not even looking for, such as the fact that the perpetrator is almost always a long-term marijuana user. Where he isn’t (and it is almost always a he), some other legal or illegal psychotropic, such as steroids or “antidepressants,” is ­usually in evidence. But you do have to look, and most people don’t. Then you have to see a pattern, one that a lot of important, influential people specifically do not want to see.

That husband-and-wife conversation in the Berenson apartment is the whole book in a nutshell, the epiphany of a former apostle of complacency from the college-­educated classes who suddenly discovers what has been going on around him for years. What he repeats over and over again is very simple: Marijuana can make you permanently crazy. (This is a long-term cumulative effect, not the effect of immediate intoxication.) And once it has made you crazy, it can make you violent, too.

You’ll only find out if you’re susceptible by taking it. It is not soft. It is not safe. It is one of the most dangerous drugs there is, and we are on the verge of allowing it to be advertised and put on open sale. Berenson has gotten into predictable trouble for asserting that the connection is pretty much proved. Alas, this is not quite so. But the correlation is hugely powerful. The chance that it is meaningful is great. Who would be surprised if a drug with powerful psychotropic effects turned out to be the cause of mental illness in its users? Correlation is not causation, but it is one of the main tools of ­epidemiology. Causation, ­especially in matters of the brain, is extraordinarily difficult to prove, and so we may have to base our actions, or our refusals to take action, on something short of total certainty.

Tell Your Children is filled with persuasive, appalling individual case histories of wild violence, including the abuse of small children. It also lists and explains the significance of powerful, large-scale surveys of Swedish soldiers and New Zealand students, which connect the drug to mental illness and lowered school performance. Berenson provides facts and statistics about violent crime in places where marijuana is widely available, and anecdotes so repetitive that they cease to be anecdotes. The puzzle remains as to why it is necessary to say all this repeatedly when a sensible person would listen the first time.

Perhaps it is because of the large, and very well-funded, campaigns for marijuana legalization described by Berenson. People who drink fair-trade coffee and eat vegan, who loathe other greed lobbies—such as pharmaceuticals, tobacco, fast food, or sugary drinks—smile on this campaign to make money from the misery of others.

Berenson shows how mental illness has grown in our midst without being noticed in public statistics. A comparable growth in, say, measles or tuberculosis would have shown up. But deteriorating mental health does not, thanks to privacy concerns, and to the fact that mental illness is not easily classified. It is also a sad truth that rich, advanced Western societies nowadays begrudge money for the mental hospitals needed to house and protect those who have overthrown their own minds. They are reluctant to record the existence and prevalence of the very real suffering that ought to be treated in the hospitals they have sold off, demolished, or never built.

Berenson also witheringly describes the propaganda devised by those who want to legalize the drug, from the mind-expanding zealots who view drug use as liberating to the hard-headed entrepreneurs and political professionals. Argue against them at your peril. Your audience may learn something, but your opponents will not. Wilful ignorance is the most powerful barrier to communication. It seals the human mind up like a fortress. You might as well read the works of Jean-Paul Sartre to a hungry walrus as try to debate with such people. I have attempted it. They don’t hear a word you say, but they hate you for getting in their way.

Berenson gives a fairly thorough account of the “medical marijuana” campaign, an almost comically absurd attempt to portray a poison as a medicine. This campaign is so bogus that it will vanish from the earth within days of full legalization, because in truth there is very little evidence that marijuana-based medicines are of much use. Berenson quotes one refreshingly candid marijuana defender as admitting, “Six percent of all marijuana users use it for medical purposes. Medical marijuana is a way of protecting a subset of society from arrest.”

In the U.S., legalizers are poised to win the modern civil war over the legalization of marijuana which has been dividing the country for half a century. It looks now as if marijuana will soon be legalized, on general sale, advertised and marketed and taxed. This worrying process has already begun in Canada. The United States has approached the issue sideways, conceding states’ rights in a way that would have delighted the Confederates.

The United Kingdom has taken a similar route: It pretends to maintain the law and, when asked, insists it has no plans to change it. But the police and the courts have gradually ceased to enforce it, so that it is now impossible to stroll through central London without nosing the reek of marijuana. Europe has gone the same way, with minor variations. Among the free law-governed nations, only Japan and South Korea still actively and effectively enforce their drug possession laws, and benefit greatly from it. But how long can they hold out?

The legalization campaigners are working like termites to undo the 1961 U.N. Convention that is the basis of most national laws against narcotics, using all the money and dishonesty at their command. They have plenty of both. So, besides the two disastrous, irrevocably legal poisons of alcohol and tobacco, we shall before long have a third—and probably a fourth and fifth not long afterward. If marijuana is legal, how will we keep cocaine and ecstasy illegal for long? Next will come heroin and LSD.

One reason for the default in favor of legalization and non-enforcement is the false association made by so many between marijuana and liberty. The belief that a dangerous, stupefying drug is an element of human liberty has taken hold of two, perhaps three generations. They should know better. Aldous Huxley warned in his much-cited but infrequently read dystopian novel Brave New World that modern men, appalled by the disasters of war and social conflict, would embrace a world where thinking and knowledge were obsolete and pleasure and contentment were the aims of a short life begun in a test-tube and ended by euthanasia. He predicted that they would drug themselves and one another to banish the pains of real life, and—worst of all—come to love their own servitude. In one terrible scene, the authorities spray protesting low-caste workers with the pleasure drug soma, and the workers end up hugging one another and smiling vaguely before returning to their drudgery. (Soma, unlike its real-life modern equivalents, is described as harmless, something easier to achieve in fiction than in reality.) What ruler of a squalid, wasteful, unfair, and ugly society such as ours would not prefer a stupefied, flaccid population to an angry one? Yet somehow, the freedom to stupefy oneself is held up quite seriously by educated people as the equal of the freedoms of thought, speech, and assembly. This is the way the world ends, with a joint, a bong, and a simper.

Whatever was wrong with my intense little segment of the 1960s revolutionary generation (and plenty was wrong with it), we believed that when we saw injustice we should fight it, not dope ourselves into a state of mind where it no longer mattered. But my tiny strand of puritan Bolsheviks was long ago absorbed into a giggling mass of cultural revolutionaries, who scrawled “Sex, Drugs, and Rock and Roll” on their banners instead of “Liberty, Equality, and Fraternity,” or even “Workers of All Lands, Unite!”

While Berenson’s facts are devastating, his own response to the crisis is feeble. He opposes marijuana legalization—and what intelligent person does not? He babbles of education and warning our children. But he declares that “decriminalization is a reasonable compromise.” Actually, it is not. It cannot be sustained. If matters are left as they are, legalization—first de facto and then de jure—will follow, because there will be no impetus to resist it. Unless the law decisively disapproves of and discourages the actual use of the drug, it is neither morally consistent nor practically effective.

The global drug trade would be nowhere without the dollars handed over to it by millions of individuals who are the end-users. We search for Mr. Big and never catch him. But we ignore or even indulge Mr. Small, regarding him as a victim, when in truth he keeps the whole thing going. In the end, the logic leads relentlessly to the stern prosecution and deterrent punishment of individual users. It is because I recognize this grim necessity that I remain a pariah. It is because he doesn’t that Alex Berenson is still just about acceptable in the part of the Western world that believes marijuana is a torch of ­freedom. 

Peter Hitchens is a columnist for The Mail on Sunday.

Source:  https://www.firstthings.com/article/2019/05/reefer-sadness

Kevin Sabet was a drug control policy adviser in the White House for both Republicans and Democrats

When most people talk about Canada’s impending legalization of marijuana, they talk about the future. When Kevin Sabet talks about it, he worries about history repeating. 

“There are huge misconceptions, I often feel like we’re living in 1918, not 2018,” he said.” When I say 1918, I mean 1918 for tobacco when everyone thought that smoking cigarettes was no problem and we had a new industry that was just starting.”

In 1918, soldiers returning home from the trenches of the First World War brought cigarettes home with them and unwittingly sowed the seeds of one of 20th century’s biggest health epidemics. 

“We hadn’t had tobacco related deaths before the 20th century because we hadn’t had a lot of cigarettes, which actually gave us the most deadly form of tobacco we’ve ever seen. I feel like we’re like that with marijuana.”

Kevin Sabet is the president of Smart Approaches to Marijuana, or SAM, a non-profit agency in the United States devoted to ‘preventing another big tobacco.’ (Smart Approaches to Marijuana)

A former drug control policy adviser to the White House under both the Democrats and Republicans, Sabet is the President and CEO of Smart Approaches to Marijuana, a public health organization opposed to marijuana legalization and commercialization in the United States. 

He said the sudden about-face by Ontario’s newly-elected Progressive Conservative government away from a public monopoly on marijuana sales to a mixed public-private is “a really bad move.” 

“When I see the government monopoly being tossed out the window in favour of a private program that really puts private profit over public health.. I worry about that,” he said. “I think it’s a really bad move.” 

“They are moving from a government monopoly to private retail and that’s going to open the door to all the marketing and promotion and normalization that already is a huge problem for our already legal drugs.”

“We’ve seen how that turned out for pharmaceuticals like opiates, which are highly dangerous and we’ve seen how that turned out for tobacco and alcohol.”

Big investors lining up to cash-in on pot

With legalization still months away, there are growing signs that marijuana and big business are starting to become best buds. (Nicolas Pham/Radio-Canada)

In fact, Sabet points out, some of the same players have already expressed their willingness to provide Canadians with legal marijuana on a massive scale. 

Constellation Brands, the maker of some of the most popular wines and beers in the world, has already paid $5 billion for Canopy Growth, the world’s largest publicly traded licensed producer of marijuana in Smith Falls, Ont. 

Several notable Canadian brands have also expressed an interest in legal bud, including Molson, which has mused publicly about a THC infused beer and Shopper’s Drug Mart, which hopes to branch out in sales of medical marijuana online. 

“We’re already seeing the private market salivating in Canada, waiting to be that next addiction for profit substance and I don’t see how that helps us.” 

‘Not your Woodstock weed’

Why that worries Sabet is the combination of savvy corporate marketing and increasingly intense levels of THC, or tetrahydrocannabinol, the active ingredient in marijuana. 

“Today’s marijuana is not your Woodstock weed,” he said. “I think there’s a wild misperception about what today’s marijuana experience really is.” 

There are signs too that marijuana sold on the street is stronger than it used to be. According to a 2017 report from the Hazelden Betty Ford Foundation, an American healthcare organization that helps people struggling with addiction, said the concentration of THC in marijuana has risen three-fold in the last two decades, from four per cent in 1994 to 12 per cent in 2014. 

Sabet notes that marijuana sold commercially in some states goes even further and is available in highly concentrated forms, such as hash, wax, or shatter with no rules or limits on the concentration of marijuana’s active ingredient. 

“It’s not four per cent THC, which is the ingredient that gets you high. It’s up to 99 per cent THC and there are no limits on THC,” he said. “I’m really concerned especially how today’s high potent marijuana is going to contribute to mental illness.” 

Potent pot and drug-induced psychosis

Anecdotally, one only has to look as far as the story of Mark Phillips, a lawyer from a prominent Toronto family, who pleaded guilty to assault causing bodily harm in April, after he attacked a St. Thomas family with a baseball bat, calling them terrorists. 

During Phillips’ court appearance, his lawyer and psychiatrist said he was suffering from a drug-induced psychosis.

His lawyer, Steve Kurka told Justice John Skowronski that Phillips, whose mental health had been declining in the months and weeks leading up to the December 2017 baseball bat attack, smoked three or four joints before driving to London and then nearby St. Thomas, getting into arguments with people he believed to be Muslims targeting him along the way.

“[It] doesn’t shock me,” Sabet said of the Phillips case. “Today’s highly potent THC can have an aggressive violent effect. I’m not going to say everybody is going to have a psychotic breakdown. We’re going to see stuff like this become more and more common.”

Despite his concerns about pot, Sabet said he doesn’t want to see Canada go back to the days of arresting people for simple pot possession, nor does he see a problem with people growing the plant at home on a small scale either. 

“I don’t care about that,” he said. “The issue is when you make this a legal market and advertise it and throw it to the forces who are in the business of promotion. They are in the business of advertising and commercialization and pot shops next to your kid’s school and billboards and coupons and products, that’s my worry.” 

Sabet believes the real Reefer Madness is giving private companies control of retail sales, where they can use marijuana as a tool in their pursuit of profit at the cost of public health. 

“I worry that Canada is following the example of the United States in terms of this new industry which promotes, recklessly advertises, makes wild claims, ignores all harms and absolutely focuses on advertising to kids.” 

Source: Ontario’s new retail pot plan ‘puts profit over public health’ says former Obama drug adviser | CBC News August 2018

  • Teenagers who smoke have thicker matter in certain parts of their brains
  • This was found in areas involved with emotions, memory, fear and panic
  • Adolescent brains are typically thinning and being refined during this period
  • Experts said ‘most people would assume one or two joints would have no impact’

Just one or two joints is enough to change the structure of a teenager’s brain, scientists have warned.

And the drug could cause changes affecting how likely they are to suffer from anxiety or panic, according to a study.

Researchers found 14-year-old girls and boys exposed to THC – the psychoactive chemical in cannabis – had a greater volume of grey matter in their brains.    

This means the tissue in certain areas is thicker, and it was found to be in the same areas as the receptors which marijuana affects.

Experts said thickening of brain tissue is the opposite of what usually happens during puberty, when teenagers’ brain matter gets thinner and more refined.

Researchers did scans of teenagers’ brains and discovered those who had been exposed to small amounts of marijuana (top row) had thicker regions of the brain (indicated by more orange and yellow tissue) than those who had never smoked cannabis (bottom row)

Researchers from the University of Vermont scanned the brains of teenagers from England, Ireland, France and Germany to study marijuana’s effects. 

They found differences in the volume of grey matter in the amygdala and the hippocampus.

These sections are involved with emotions, fear, memory development and spatial skills – changes to them suggests smoking cannabis could affect these faculties.    

Scientists said theirs is the first evidence to suggest structural brain changes and cognitive effects of just one or two uses of cannabis in young teenagers.

And it suggests as teenagers brains are still developing, they may be particularly vulnerable to the effects of THC.

THC, full name tetrahydrocannabinol, is the chemical in marijuana which makes people high and is what makes it illegal in the UK. 

‘Consuming just one or two joints seems to change grey matter volumes in young adolescents,’ said study author Professor Dr Hugh Garavan.

‘The implication is that this is potentially a consequence of cannabis use. You’re changing your brain with just one or two joints.

‘Most people would likely assume that one or two joints would have no impact on the brain.’

What changes the increased brain volume directly causes is unclear, but the researchers said it is important to understand cannabis’s effects in detail.

This is especially so in the US, where more states are legalising the drug and a view of it being harmless is spreading, they said.

Professor Garavan said cannabis use appears to produce the opposite effect on brain matter of what usually happens during puberty. 

He said a typical adolescent brain undergoes a ‘pruning’ process in which  it gets thinner, rather than thicker, as it refines its connections. 

‘One possibility is they’ve actually disrupted that pruning process,’ he said. 

Previous studies have focused on heavy marijuana users later in life and compared them against non-users. 

Few have looked at the effects of the first few uses of a drug.

Another of the study’s authors, Catherine Orr, now a lecturer at Swinburne University of Technology in Australia said: ‘Rates of cannabis use among adolescents are high and are increasingly concurrent with changes in the legal status of marijuana and societal attitudes regarding its use.

‘Recreational cannabis use is understudied, especially in the adolescent period when neural maturation may make users particularly vulnerable to the effects of THC on brain structure.’

The study, part of a long-term European project known as IMAGEN, involved 46 teenagers who used recreational marijuana once or twice by the age of 14.

They reported how many joints they had smoked and had brain scans.

It also involved 69 teenagers who used the drug at least 10 times between the ages of 14 and 16, and 69 who had not touched the drug by age 16.

Scientists also assessed them for signs of various mental disorders including ADHD, anxiety, depression and panic disorder.    

Dr Orr said: ‘Of the behavioural variables tested, only sensation seeking and agoraphobia differed between the cannabis users and controls. And these factors were not related to greater grey matter differences.’ 

The researchers said the area of the brain which cannabis interacts with is particularly important for brain development in adolescence, suggesting teenagers could be particularly affected by THC. 

Dr Orr concluded: ‘Almost 35 per cent of American 10th graders have reported using cannabis and existing research suggests that initiation of cannabis use in adolescence is associated with long-term neurocognitive effects.

‘We understand very little about the earliest effects of cannabis use, however, as most research is conducted in adults with a heavy pattern of lifetime use.

‘This study presents evidence suggesting structural brain and cognitive effects of just one or two instances of cannabis use in adolescence.’  

The study was published in The Journal of Neuroscience.

Source: Smoking weed just ONCE could change a teenager’s brain | Daily Mail Online January 2019

Abstract

Background: Normalisation of medicinal and recreational marijuana use has increased the importance of fully understanding effects of marijuana use on individual-and population-level health, including prenatal exposure effects on child development. We undertook a systematic review of the literature to examine the long-term effects of prenatal marijuana exposure on neuropsychological function in children aged 1-11 years.

Methods: Primary research publications were searched from Medline, Embase, PsychInfo, CINAHL EbscoHost, Cochrane Library, Global Health and ERIC (1980-2018). Eligible articles documented neuropsychological outcomes in children 1-11 years who had been prenatally exposed to marijuana. Studies of exposure to multiple prenatal drugs were included if results for marijuana exposure were reported separately from other substances. Data abstraction was independently performed by two reviewers using a standardised protocol.

Results: The eligible articles (n = 21) on data from seven independent longitudinal studies had high quality based on the Newcastle-Ottawa Scale. Some analyses found associations (P < 0.05) between prenatal marijuana exposure and decreased performance on memory, impulse control, problem-solving, quantitative reasoning, verbal development and visual analysis tests; as well as increased performance on attention and global motion perception tests. Limitations included concurrent use of other substances among study participants, potential under-reporting and publication biases, non-generalisable samples and limited published results preventing direct comparison of analyses.

Conclusions: The specific effects of prenatal marijuana exposure remain unclear and warrant further research. The larger number of neuropsychological domains that exhibit decreased versus increased psychological and behavioural functions suggests that exposure to marijuana may be harmful for brain development and function.

Keywords: attention; cannabis; intellect; intrauterine; memory; perception.

Source: Effects of prenatal marijuana exposure on neuropsychological outcomes in children aged 1-11 years: A systematic review – PubMed (nih.gov) November 2018

Radula complanata, a cannabinoid moss. Henri Koskinen/Shutterstock

Most of us know that the cannabis plant produces compounds that react with the human body. That’s because we have our own system that makes similar compounds, cannabinoids, that have a wide range of actions from appetite control to immune function. Cannabis contains a cannabinoid called THC that interacts with the brain, resulting in euphoria and relaxation, as well as increased hunger and anxiety. It was long thought that there was no other natural source of cannabinoids – and along with a long list of supposed medical uses the mythical power of cannabis, and the psychoactive properties of THC, has grown.

But as it turned out, another plant contains something similar: a compound that has the structural hallmarks for it to act on the brain in a similar way to THC. The discovery of this lost twin, called cis-PET (perrottetinene), or PET, was tucked away in specialist chemistry journals in papers published in 1994 and 2002, with no subsequent research confirming its biological activity. But in a new study, published in Science Advances, a group of Swiss scientists have delved into the mechanism by which PET may be acting on the brain.

The particular liverwort in question, Radula, is endemic to New Zealand and Tasmania and is used as a herbal medicine by the Maori people. Preparations using this plant are also sold as a THC-like legal high on the internet.

But while similar to THC, does PET actually produce the same effects that THC does at a cellular and molecular level? Does it mimic the physiological effects? And is it different in ways that could give it therapeutic advantage or disadvantage? Some 24 years after its first discovery, the team of chemists and biochemists behind the new study have teased some of the answers out.

Their research was no mean feat. It required a new synthesis method to produce enough PET to do meaningful experiments. Once this was achieved, the researchers looked at two mirror versions of the two compounds, cis (the version found in the liverwort) and trans (a version they artificially created in the lab). In chemistry, the cis and trans terms tell us which side of the carbon chain the functional groups are (the bit of the molecule that does the work).

The researchers wanted to find out if these two versions of PET were able to interact with the two receptors found in humans that mediate the psychoactive effects of cannaboids – CB1, the receptor that produces the “high” effect from THC, and CB2 – in the same way as THC (how strongly they bound and how much is needed to produce an effect).

The researchers found intriguing similarities between the two versions in PET and THC. For both PET and THC, the trans versions (the abundant THC version found in cannabis and the lab-synthesised version found in liverwort) bound to the CB1 receptor better than the cis versions.

THC and PET side by side. Oliver Kayser

What’s interesting about this is that while the levels of cis-PET found in the liverwort plant are too low to produce the “high” effects produced by THC (hence why smoking PET won’t produce a high), it could explain why PET might still have a medicinal effect (similar to the effect produced by lower dose THC). However, any methods to extract and concentrate the liverwort compound could lead to the same problems as THC.

But what about CB2, the other cannabinoid receptor? This receptor plays a role in immune responses. Here the Swiss scientists found that the cisversions of both THC and PET bound this receptor better than the transversions. The implications of this are yet to be explored, but it again hints at a potential medicinal benefit worth exploring further.

The authors of the study then went on to test whether the binding of the CB1 receptors in the brains of mice had the same recognisable THC effects. Usually when THC binds with this receptor it produces four key effects: reduced body temperature, muscle rigidity, reduced movement and decreased sensitivity to pain. In this behavioural test, all four effects were also achieved in the mice using cis-PET, albeit in a much bigger amount.

But there was one notable difference. Inflammation in the brain is mediated by molecules called prostaglandins that can be derived from metabolic pathways involving our own body cannabinoids or plant-derived trans-THC. In contrast, the production of these mediators was reduced by cis-PET. It remains to be seen whether this is a good thing or a bad thing.

So while the study is just a start in understanding the mechanisms and effects of PET on the brain, there’s much we still don’t know. What we do know now, however, is that the levels of PET that are found in the natural liverwort plant are too low to produce the recognised effects of THC, so smoking it is unlikely to lead to a high. But it is also interesting that this compound could well have medicinal benefits without the high – one of the key reasons that THC has previously been dismissed as a medicine. Illegal trading and cultivation has confounded much meaningful clinical research, but this is changing and this new compound will add to the treasure trove of plant-derived cannabinoids that we still have much to understand.

Source: https://theconversation.com/liverwort-could-have-medicinal-benefits-of-cannabis-thc-without-the-high  Oct.24th 2018

* Correspondence:

Albert Stuart Reece  

A leading perspectives piece in the New England Journal of Medicine recently observed the salience of assessing drug safety in children and emphasized that effects experienced in childhood can have long lasting impacts as they interfere with maturation and growth of the organism into later life.  Senior researchers from the National Institute of Drug Abuse have frequently drawn attention to the implications of adolescent cannabis exposure.  The effects of gestational exposure are even more far reaching.  These factors are given further urgency by studies showing 25% of Californian teenage mothers in California use cannabis.

Cannabis-related neuroteratology appears to clearly fall on a spectrum of deficits.

With the obvious caveats that many of the longitudinal studies of prenatal cannabis exposure (PCE) have been conducted in very different populations, that it is not easy to control for other sociodemographic factors frequently associated with drug use, and that the concentration of cannabis commonly used in the older studies was much lower, findings which together engender a fair degree of heterogeneity in the published reports, a remarkably consistent thread runs through the PCE literature.  Three major longitudinal studies have followed children exposed prenatally from white middle class Ottawa from the late 1970’s; from predominantly African-American Pittsburgh from 1982; and from the Netherlands from 2001.  Reductions in birth weight of 200-300g, slightly smaller head circumferences (2.8mm), and body length are reported in weekly users with several studies reporting dose-response effects.

In terms of neurobehavioural functioning increased neonatal startle response were seen, with specific cognitive defects in grade school, increased impulsivity, hyperactivity and depression at age 10, poor school achievement, adolescent delinquency, increased violence and aggression amongst girls, increased use of tobacco and cannabis in teens, and in the early 20’s in the longest running study, deficits in short term memory, visuospatial memory and motor impulse control.  These defects have been linked with ADHD and with autism.  Microcephaly was also noted in a large Hawaiian study.  Increased neonatal startle and later cognitive defects are also seen in rodents after PCE.

These findings are clinically significant, and may assume public health significance when one notes that autism is increasing in all USA states where it is measured, paralleling rising rates of cannabis use across the country.

Two reports from C.D.C. indicate an almost doubling of the rate of anencephaly following PCE R.R.=1.9 (95%C.I. 1.1-3.2).  In the context of the foregoing findings this major datum implies that cannabis has the unusual distinction of being a neurotoxin which interferes with brain development to the point of chemically amputating the forebrain.  Hence there is clear evidence of a graded spectrum of deficits following PCE from subtle ASD- and ADHD- like neurobehavioural defects, to smaller heads, to microcephaly and to anencephaly including foetal neurological and neonatal death.

In the context of indicative epidemiology consideration of pathophysiological mechanisms is pertinent to address the Hill principles of causality.

There are numerous compelling mechanisms by which PCE can be related to subsequent teratogenic outcomes.

Importantly the cerebellum, midbrain, diencephalon and forebrain express moderate to high levels of type 1 cannabinoid receptors (CB1R) from early in gestation.

It was recently powerfully demonstrated that opposing gradients of the ligand-receptor guidance pairs slit-Roundabout (robo) and the notch ligand dll control and determine mammalian corticogenesis in diverse organisms including snakes, birds, mice and human organoids by controlling the switch for cortical neurogenesis from directly via radial glia cells to a more indirect and proliferative pathway via intermediate progenitors (Figure 1).   Cannabinoids have been shown to reverse this natural gradient for dll, and acting via a 2AG / CB2R / slit2 / Robo1 / 2AG / CB1R / JNK / ERK pathway to stimulate robo.

Neurexin-neuroligin is a trans-synaptic ligand-receptor pair which directly induces and maintains synapse formation, and has been shown to be inhibited by cannabinoids.

Axon guidance is also controlled by robo-slit and by stathmin-induced tubulin polymerization, which are sensitive to cannabinoids.

White matter disconnection is well documented following adolescent and prenatal cannabis use, and in autism, and oligodendrocytes have CB1R’s and CB2R’s.

Mitochondria possess both CB1R’s and cannabinoid signal transduction machinery and are known to be highly sensitive to cannabinoids and interact with DNA maintenance pathways by several routes.

Cannabinoids have also been shown to alter signaling via the neurotransmitters: glutamate, GABA, opioids, dopamine, serotonin and enkephalin.

Cannabinoids have demonstrated intergenerational epigenetic effects on the medium spiny neurons of the nucleus accumbens and amygdala and also on immune cells which sculpt dendritic networks and prune synapses.

Acting via CB1R, GPR55, and vanilloid type 1 receptors cannabis has been linked with arteritis with likely downstream actions on neurogenic and other stem cell niches.

Endocardial cushions also carry high levels of CB1R’s and the American Academy of Pediatrics has a position statement noting the increased incidence of Ebstein’s syndrome and ventricular septal defect (VSD) after PCE.  Both syncytiotrophoblast and placental arteries carry high concentrations of CB1R’s and abnormalities of uterine blood flow have been documented.

Cannabinoids interfere with tubulin polymerization and mitotic spindle function and thereby act as indirect genotoxins. The implication of cannabis with four inheritable cancers implies malignant teratogenicity and genotoxicity.

Colorado reports dramatic rises of total congenital anomalies, microcephaly, VSD, ASD, Down’s syndrome and chromosomal defects, all of which are relatively straightforward to quantify.

Colorado legislators have also moved to declare a state of crisis related to an autism rate presently growing by 30% 2012-2014.  Similarly in northern California a coincident hotspot of cannabis use, gastroschisis and autism has been reported.  In New Jersey 4.5% of 8 year old boys are autistic.

The above findings comprehend both positive and negative association along with multiple plausible biological pathways linking causality.

As rising rates of community cannabis use augment rising cannabis concentrations and intersect often asymptotic cannabinoid dose-response genotoxicity curves, increased clinical teratogenesis is to be expected.  Of these anomalies the neurobehavioural teratology will likely be the most common, is arguably the most costly and severe, and is also most difficult to quantify.

Are we prepared?

Source:  Paper by Albert Stuart Reese sent to Elinore.Mccance-katz@samhsa.hhs.gov  2018

Abstract

Excessive alcohol use is extremely prevalent in the United States, particularly among trauma-exposed individuals. While several studies have examined genetic influences on alcohol use and related problems, this has not been studied in the context of trauma-exposed populations. We report results from a genome-wide association study of alcohol consumption and associated problems as measured by the alcohol use disorders identification test (AUDIT) in a trauma-exposed cohort. Results indicate a genome-wide significant association between total AUDIT score and rs1433375 [N = 1036, P = 2.61 × 10-8 (dominant model), P = 7.76 × 10-8 (additive model)], an intergenic single-nucleotide polymorphism located 323 kb upstream of the sodium channel and clathrin linker 1 (SCLT1) at 4q28. rs1433375 was also significant in a meta-analysis of two similar, but independent, cohorts (N = 1394, P = 0.0004), the Marine Resiliency Study and Systems Biology PTSD Biomarkers Consortium. Functional analysis indicated that rs1433375 was associated with SCLT1 gene expression and cortical-cerebellar functional connectivity measured via resting state functional magnetic resonance imaging. Together, findings suggest a role for sodium channel regulation and cerebellar functioning in alcohol use behavior. Identifying mechanisms underlying risk for problematic alcohol use in trauma-exposed populations is critical for future treatment and prevention efforts.

Keywords: AUDIT; alcohol consumption; alcohol use disorder; expression QTL; fMRI; genome-wide association study.

Source: Problematic alcohol use associates with sodium channel and clathrin linker 1 (SCLT1) in trauma-exposed populations – PubMed (nih.gov) September 2018

Abstract

Opioid use disorder is a highly disabling psychiatric disorder, and is associated with both significant functional disruption and risk for negative health outcomes such as infectious disease and fatal overdose. Even among those who receive evidence-based pharmacotherapy for opioid use disorder, many drop out of treatment or relapse, highlighting the importance of novel treatment strategies for this population. Over 60% of those with opioid use disorder also meet diagnostic criteria for an anxiety disorder; however, efficacious treatments for this common co-occurrence have not be established. This manuscript describes the rationale and methods for a behavioral treatment development study designed to develop and test an integrated cognitive-behavioral therapy for those with co-occurring opioid use disorder and anxiety disorders.

The aims of the study are (1) to develop and pilot test a new manualized cognitive behavioral therapy for co-occurring opioid use disorder and anxiety disorders, (2) to test the efficacy of this treatment relative to an active comparison treatment that targets opioid use disorder alone, and (3) to investigate the role of stress reactivity in both prognosis and recovery from opioid use disorder and anxiety disorders. Our overarching aim is to investigate whether this new treatment improves both anxiety and opioid use disorder outcomes relative to standard treatment. Identifying optimal treatment strategies for this population are needed to improve outcomes among those with this highly disabling and life-threatening disorder.

Source: Development of an integrated cognitive behavioral therapy for anxiety and opioid use disorder: Study protocol and methods – PubMed (nih.gov) July 2017

(Reuters Health) – Cannabis use by mothers or fathers during pregnancy, or even only before pregnancy, is associated with an increased risk of psychotic-like episodes in their children, a Dutch study suggests.

Because pot use by mothers and fathers carried similar risk, and a mother’s use before pregnancy had the same effect as use during pregnancy, the study team speculates that parental pot use is likely a marker for genetic and environmental vulnerability to psychotic experiences rather than a cause, and could be useful for screening kids at risk for psychosis later in life.

Babies exposed to cannabis in the womb do have an increased risk of being underweight and unusually small when they’re born and developing cognitive and behavior problems early in life, the researchers note in Schizophrenia Research. Cannabis can also cause hallucinations in adults, particularly with frequent use and at high doses, but less is known about the potential for infants exposed to the drug in the womb to develop psychotic-like symptoms.

For the study, researchers examined data from questionnaires asking 3,692 10-year-olds whether they had symptoms that are similar to what adults might experience with psychosis: hearing voices that nobody else detects, seeing things others don’t see, and having thoughts that others might find strange.

They also examined mothers’ reports on their own marijuana use as well as any use by their partners, and they also looked at lab tests for signs of cannabis in mothers’ urine.

When mothers used marijuana during pregnancy, children were 38 percent more likely to have these psychotic-like symptoms than the children of mothers who abstained from use during pregnancy, the study found. But children of mothers who used pot only before, but not during, pregnancy also had a 39 percent higher risk than the kids of mothers who didn’t use it.

Fathers’ cannabis use during pregnancy, meanwhile, was associated with a 44 percent greater likelihood of psychotic-like experiences in their kids.

“Some children with psychotic experiences are at increased risk to develop psychosis or other psychiatric disorders,” said lead study author Dr. Koen Bolhuis, a researcher at Erasmus Medical Center Rotterdam in the Netherlands.

“Unfortunately very little is known about how to treat psychotic experiences in children, or to prevent them from getting worse,” Bolhuis said by email.

Psychotic-like experiences aren’t disabling or frequent enough to be classified as psychosis, a severe mental health disorder in which patients’ thoughts and emotions are impaired on such a regular basis that they routinely experience delusions and hallucinations that make it impossible to know what’s real and what isn’t.

Psychosis can be caused by schizophrenia, and it can also happen as a result of some other medical conditions and as a side effect of certain prescription medications or illegal drugs.

In the current study, mothers who used cannabis during pregnancy were more likely than other women to smoke and drink during pregnancy, which can both independently influence the risk of emotional and behavioral health problems in children. They were also more likely to have partners who used cannabis while they were pregnant.

The study wasn’t a controlled experiment designed to prove whether or how cannabis exposure might directly cause psychotic experiences in children.

Researchers also lacked data on how much of infants’ cannabis exposure came from parent’s smoking versus ingesting pot.

With inhaled cannabis, it’s difficult to separate the impact of the drug itself from the effect of carbon monoxide also released in the smoke, noted Marcel Bonn-Miller of the University of Pennsylvania Perelman School of Medicine in Philadelphia.

“Carbon monoxide is a known toxicant which causes hypoxia, or oxygen deprivation, which has several well-known and well-studied detrimental effects on pregnancy and offspring development,” Bonn-Miller, who wasn’t involved the study, said by email.

Still, the current study results add to evidence that there’s no safe amount of cannabis exposure for babies in the womb, said Dr. Nathaniel DeNicola of George Washington University in Washington, D.C.

“We have sufficient data and biologic plausibility that marijuana use during pregnancy increases the risk of preterm birth and growth restricted babies,” DeNicola, who wasn’t involved the study, said by email. “The data is mixed on stillbirth, but still cause for concern.”

Source: Pot smoking by parents tied to risk of psychotic episodes in kids | Reuters August 2018

Abstract

Objectives To estimate the prevalence of fetal alcohol spectrum disorder (FASD) among young people in youth detention in Australia. Neurodevelopmental impairments due to FASD can predispose young people to engagement with the law. Canadian studies identified FASD in 11%–23% of young people in corrective services, but there are no data for Australia.

Design Multidisciplinary assessment of all young people aged 10–17 years 11 months and sentenced to detention in the only youth detention centre in Western Australia, from May 2015 to December 2016. FASD was diagnosed according to the Australian Guide to the Diagnosis of FASD.

Participants 99 young people completed a full assessment (88% of those consented; 60% of the 166 approached to participate); 93% were male and 74% were Aboriginal.

Findings 88 young people (89%) had at least one domain of severe neurodevelopmental impairment, and 36 were diagnosed with FASD, a prevalence of 36% (95% CI 27% to 46%).

Conclusions This study, in a representative sample of young people in detention in Western Australia, has documented a high prevalence of FASD and severe neurodevelopmental impairment, the majority of which had not been previously identified. These findings highlight the vulnerability of young people, particularly Aboriginal youth, within the justice system and their significant need for improved diagnosis to identify their strengths and difficulties, and to guide and improve their rehabilitation.

Source: https://bmjopen.bmj.com/content/8/2/e019605 February 2018

Abstract

Chronic alcohol abuse causes cognitive impairments associated with neurodegeneration and volume loss in the human hippocampus. Here, we hypothesize that alcohol reduces the number of granule cells in the human dentate gyrus and consequently contribute to the observed volume loss. Hippocampal samples were isolated from deceased donors with a history of chronic alcohol abuse and from controls with no alcohol overconsumption. From each case, a sample from the mid-portion of hippocampus was sectioned, immunostained for the neuronal nuclear marker NeuN, and counter stained with hematoxylin. Granule cell number and volume of granular cell layer in the dentate gyrus were estimated using stereology. We found a substantial reduction in granule cell number and also a significantly reduced volume of the granular cell layer of chronic alcohol abusers as compared to controls. In controls there was a slight age-related decline in the number of granule cells and volume of granular cell layer in line with previous studies. This was not observed among the alcoholics, possibly due to a larger impact of alcohol abuse than age on the degenerative changes in the dentate gyrus. Loss of neurons in the alcoholic group could either be explained by an increase of cell death or a reduced number of new cells added to the granular cell layer. However, there is no firm evidence for an increased neuronal death by chronic alcohol exposure, whereas a growing body of experimental data indicates that neurogenesis is impaired by alcohol. In a recent study, we reported that alcoholics show a reduced number of stem/progenitor cells and immature neurons in the dentate gyrus, hence that alcohol negatively affects hippocampal neurogenesis. The present results further suggest that such impairment of neurogenesis by chronic alcohol abuse also results in a net loss of granule cells in the dentate gyrus of hippocampus.

Keywords: Addiction; Alcohol abuse; Dentate gyrus; Granule cells; Hippocampus; Human; Neurogenesis; Neurons.

Source: Hippocampal granule cell loss in human chronic alcohol abusers – PubMed (nih.gov) December 2018

Free-marketeers are ignoring the devastating harm it can do as they champion consumer rights.

Four men had to be rescued last weekend from England’s highest mountain, Scafell Pike, after becoming “incapable of walking due to cannabis use”. Said Cumbria police: “Words fail us.”

Well, yes. Does everyone agree that these men placed an irresponsible burden on a public service? Apparently so. Does everyone agree that the use of cannabis should be discouraged to reduce its irresponsible burden on society? Well, no; quite the opposite.

Last week Prince William raised the “massive issue” of drug legalisation. Although he expressed no opinion, merely to raise it was inescapably to express one, since the only people for whom it is a “massive issue” are those who promote it.

At the Labour Party conference yesterday the comedian Russell Brand called for drugs to be decriminalised. At next week’s Conservative conference, the free-market Adam Smith Institute will be pushing for the legalisation of cannabis. Legalisation means more users. That means more harm, not just to individuals but to society. The institute, however, describes cannabis as “a low-harm consumer product that most users enjoy without major problems”. What? A huge amount of evidence shows that far from cannabis being less harmful than other illicit drugs, as befits its Class B classification, its effects are far more devastating. Long-term potheads display on average an eight-point decline in IQ over time, an elevated risk of psychosis and permanent brain damage.

Cannabis is associated with a host of biological ill-effects including cirrhosis of the liver, strokes and heart attacks. People who use it are more likely than non-users to access other illegal drugs. And so on.

Ah, say the autonomy-loving free-marketeers, but it doesn’t harm anyone other than the user. Well, that’s not true either. It can destroy relationships with family, friends and employers. Users often display more antisocial behaviour, such as stealing money or lying to get a job, as well as a greater association with aggression, paranoia and violent death. According to Stuart Reece, an Australian professor of medicine, cannabis use in pregnancy has also been linked to an epidemic of gastroschisis, in which babies are born with intestines outside their abdomen, in at least 15 nations including the UK.

Long-term potheads display on average an eight-point drop in IQ

The legalisers’ argument is that keeping cannabis illegal does not control the harm it does. Yet wherever its supply has been liberalised, its use and therefore the harm it does have both gone up. In 2001 Portugal decriminalised illegal drugs including cocaine, heroin and cannabis. Sparked by a report by the American free-market Cato Institute, which claimed this policy was a “resounding success”, Portugal has been cited by legalisers everywhere as proof that liberalising drug laws is the magic bullet to erase the harm done by illegal drugs.

The truth is very different. In 2010 Manuel Pinto Coelho, of the Association for a Drug Free Portugal, wrote in the BMJ: “Drug decriminalisation in Portugal is a failure . . . There is a complete and absurd campaign of manipulation of facts and figures of Portuguese drug policy . . .”

According to the Portuguese Institute for Drugs and Drug Addiction, between 2001 and 2007 drug use increased by 4.2 per cent, while the number of people who had used drugs at least once rose from 7.8 per cent to 12 per cent. Cannabis use went up from 12.4 per cent to 17 per cent.

The latest evidence about Portugal, a study by the Intervention Service for Addictive Behaviours and Dependencies, shows “a rise in the prevalence of every illicit psychoactive substance from 8.3 per cent in 2012 to 10.2 per cent in 2016-17”, with most of that rise down to increased cannabis use.

For free-marketeers, this evidence of devastating harm to individuals and society is irrelevant. Nothing can be allowed to dent their dogmatic belief that all human life is a transaction, market forces are a religion and the rights of the consumer are sacrosanct. Says the Adam Smith Institute about cannabis legalisation: “The object isn’t harm elimination, it’s not even harm reduction alone, it’s utility maximisation.” In other words, they want as many people as possible to be puffing on those spliffs.

Free-market libertarians are nothing if not consistent. They oppose policies to reduce social harm across the board. Smoking curbs, mandatory seat-belts, speed cameras, gambling restrictions, controls to end unmanageable immigration — they’ve been against them all.

Despite how they are viewed, there’s nothing conservative about the free-marketeers. Far from conserving legal or social constraints, they want to tear them down in the name of consumer choice. The classical political thinkers they quote in support of applying market principles to every aspect of society never in fact subscribed to such a doctrine. Far from putting the autonomous self on a pedestal, Adam Smith himself in his Theory of Moral Sentiments put personal rights last and the interests of others first.

The distortion of such thinking is why Russell Brand and the Adam Smith Institute are soul mates. In a fearful symmetry, both the left and the free-market right deny the importance of conserving the social good. One calls it paternalism, the other the nanny state. Both are radically irresponsible and destructive. The only difference is the gender. And even that, in our current lifestyle free-for-all, is now surely up for grabs.

Source: Thinking is warped on cannabis legalisation (thetimes.co.uk) September 2017

This Notice of Liability Memo and attached Affidavit of Harms give formal notification to all addressees that they are morally, if not legally liable in cases of harm caused by making toxic marijuana products legally available, or knowingly withholding accurate information about the multiple risks of hemp/marijuana products to the Canadian consumer.  This memo further gives notice that those elected or appointed as representatives of the people of Canada, by voting affirmatively for Bill C45, do so with the knowledge that they are breaching international treaties, conventions and law.  They do so also with the knowledge that Canadian law enforcement have declared that they are not ready for implementation of marijuana legalization, and as they will not be ready to protect the lives of Canadians, there may arise grounds for a Charter of Rights challenge as all Canadian citizens are afforded a the right to security of self.

Scientific researchers and health organizations raise serious questions about the safety of ingesting even small amounts of cannabinoids. Adverse effects include risk of harm to the cardio-vascular system, respiratory tract, immune system, reproductive and endocrine systems, gastrointestinal system and the liver, hyperemesis, cognition, psychomotor performance, psychiatric effects including depression, anxiety and bipolar disorder, schizophrenia and psychosis, a-motivational syndrome, and addiction.  The scientific literature also warns of teratogenicity (causing birth deformities) and epigenetic damage (affecting genetic development) and clearly establishes the need for further study. The attached affidavit cites statements made by Health Canada that are grounded in scientific evidence that documents many harms caused by smoking or ingesting marijuana.  

Putting innocent citizens in “harm’s way” has been a costly bureaucratic mistake as evidenced by the 2015 Canadian $168 million payout to victims of exposure to the drug thalidomide. Health Canada approved thalidomide in 1961 to treat morning sickness in pregnant women but it caused catastrophic birth defects and death.

It would be instructive to reflect on “big tobacco” and their multi-billion-dollar liability in cases of misinformed sick and dead tobacco cigarette smokers. Litigants won lawsuits for harm done by smoking cigarettes even when it was the user’s own choice to obtain and smoke tobacco. In Minnesota during the 1930’s and up to the 1970’s tobacco cigarettes were given to generally healthy “juvenile delinquents’ incarcerated in a facility run by the state.  One of the juveniles, now an adult, who received the state’s tobacco cigarettes, sued the state for addicting him. He won.

The marijuana industry, in making public, unsubstantiated claims of marijuana safety, is placing itself in the same position, in terms of liability, as the tobacco companies.
In 1954, the tobacco industry published a statement that came to be known during Minnesota’s tobacco trial as the “Frank Statement.” Tobacco companies then formed an industry group for the purposes of deceiving and confusing the public.

In the Frank Statement, tobacco industry spokesmen asserted that experiments linking smoking with lung cancer were “inconclusive,” and that there was no proof that cigarette smoking was one of the causes of lung cancer. They stated, “We believe the products we make are not injurious to health.” Judge Kenneth Fitzpatrick instructed the Minnesota jurors: “Jurors should assume in their deliberations that tobacco companies assumed a “special duty” by publishing the ad (Frank Statement), and that jurors will have to determine whether the industry fulfilled that duty.” The verdict ruled against the tobacco industry.

Effective June 19, 2009, marijuana smoke was added to the California Prop 65 list of chemicals known to cause cancer. The Carcinogen Identification Committee (CIC) of the Office of Environmental Health Hazard Assessment (OEHHA) “determined that marijuana smoke was clearly shown, through scientifically valid testing according to generally accepted principles, to cause cancer.”

Products liability and its application to marijuana businesses is a topic that was not discussed in the Senate committee hearings. Proposition 65, requires the State to publish a list of chemicals known to cause cancer, birth defects or other types of reproductive harm. Proposition 65 requires businesses to provide their customers with notice of these cancerous causing chemicals when present in consumer products and provides for both a public and private right of action.

The similarities between the tactics of “Big Tobacco” and the “Canadian Cannabis Trade Alliance Institute” and individual marijuana producers would seem to demand very close scrutiny. On May 23, a witness testified before the Canadian Senate claimed that marijuana is not carcinogenic. This evidence was not challenged.

The International Narcotics Control Board Report for 2017 reads: “Bill C-45, introduced by the Minister of Justice and Attorney General of Canada on 13 April 2017, would permit the non-medical use of cannabis. If the bill is enacted, adults aged 18 years or older will legally be allowed to possess up to 30 grams of dried cannabis or an equivalent amount in non-dried form. It will also become legal to grow a maximum of four cannabis plants, simultaneously for personal use, buy cannabis from licensed retailers, and produce edible cannabis products. The Board wishes to reiterate that article 4 (c) of the 1961 Convention restricts the use of controlled narcotic drugs to medical and scientific purposes and that legislative measures providing for non-medical use are in contravention of that Convention….

The situation pertaining to cannabis cultivation and trafficking in North America continues to be in flux owing to the widening scope of personal non-medical use schemes in force in certain constituent states of the United States. The decriminalization of cannabis has apparently led organized criminal groups to focus on manufacturing and trafficking other illegal drugs, such as heroin. This could explain why, for example, Canada saw a 32 per cent increase from 2015 to 2016 in criminal incidents involving heroin possession….The Canadian Research Initiative in Substance Misuse issued “Lower-risk cannabis use guidelines” in 2017. The document is a health education and prevention tool that acknowledges that cannabis use carries both immediate and long-term health risks.”

https://www.incb.org/documents/Publications/AnnualReports/AR2017/Annual_Report_chapters/Chapter_3_Americas_2017.pdf

Upon receipt of this Memo and Affidavit, the addressees can no longer say they are ignorant or unaware that promoting and/or distributing marijuana cigarettes for recreational purposes is an endangerment to citizens. Receipt of this Memo and Affidavit removes from the addressees any claim of ignorance as a defense in potential, future litigation.

Pamela McColl www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

 

AFFIDAVIT May 27, 2018

I, Pamela McColl, wish to inform agencies and individuals of known and potential harm done/caused by the use of marijuana (especially marijuana cigarettes) and of the acknowledgement the risk of harm by Health Canada. 

Marijuana is a complex, unstable mixture of over four hundred chemicals that, when smoked, produces over two thousand chemicals.  Among those two thousand chemicals are many pollutants and cancer-causing substances.  Some cannabinoids are psychoactive, all are bioactive, and all may remain in the body’s fatty tissues for long periods of times with unknown consequences. Marijuana smoke contains carcinogenic (cancer-causing) substances such as benzo(a)pyrene, benz(a)anthracene, and benzene in higher concentrations than are present in tobacco smoke.  The mechanism by which benzo(a)pyrene causes cancer in smokers was demonstrated scientifically by Denissenko MF et al. Science 274:430-432, 1996. 

Health Canada Consumer Information on Cannabis reads as follows:  “The courts in Canada have ruled that the federal government must provide reasonable access to a legal source of marijuana for medical purposes.”

“Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of cannabis for therapeutic purposes, or of marijuana generally, by Health Canada.”

“Serious Warnings and Precautions: Cannabis (marihuana, marijuana) contains hundreds of substances, some of which can affect the proper functioning of the brain and central nervous system.”

“The use of this product involves risks to health, some of which may not be known or fully understood. Studies supporting the safety and efficacy of cannabis for therapeutic purposes are limited and do not meet the standard required by the Food and Drug Regulations for marketed drugs in Canada.”

Health Canada – “When the product should not be used: Cannabis should not be used if you:-are under the age of 25 -are allergic to any cannabinoid or to smoke-have serious liver, kidney, heart or lung disease -have a personal or family history of serious mental disorders such as schizophrenia, psychosis, depression, or bipolar disorder-are pregnant, are planning to get pregnant, or are breast-feeding -are a man who wishes to start a family-have a history of alcohol or drug abuse or substance dependence Talk to your health care practitioner if you have any of these conditions. There may be other conditions where this product should not be used, but which are unknown due to limited scientific information.

Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of this product, or cannabis generally, by Health Canada.”

Prepared by Health Canada Date of latest version: February 2013, accessed May 2018. https://www.canada.ca/en/health-canada/services/drugs-health-products/medical-use-marijuana/information-medical-practitioners/information-health-care-professionals-cannabis-marihuana-marijuana-cannabinoids.html

A report published by survey company RIWI Corp. (RIWI.com) can be found at: https://riwi.com/case-study/measuringcanadians-awareness-of-marijuanas-health-effects-may-2018

The report measures Canadians’ awareness of marijuana’s health effects as determined by Health Canada and published on Health Canada’s website. RIWI data indicates: 1. More than 40% of those under age 25 are unaware that marijuana impacts safe driving. Further, 21% of respondents are not aware that marijuana can negatively impact one’s ability to drive safely. Health Canada: “Using cannabis can impair your concentration, your ability to make decisions, and your reaction time and coordination. This can affect your motor skills, including your ability to drive.” 2. One in five women aged 25-34 believes marijuana is safe during pregnancy, while trying to get pregnant, or breastfeeding. • RIWI: “For women of prime childbearing age (25-34), roughly one in five believe smoking marijuana is safe during pregnancy, planning to get pregnant, and breastfeeding.” • Health Canada: “Marijuana should not be used if you are pregnant, are planning to get pregnant, or are breastfeeding. … Long-term use may negatively impact the behavioural and cognitive development of children born to mothers who used cannabis during pregnancy.” 3. One in three Canadians do not think that marijuana is addictive. • Health Canada: “Long term use may result in psychological dependence (addiction).” 4. One in three Canadians believe marijuana aids mental health. • Health Canada: “Long term use may increase the risk of triggering or aggravating psychiatric and/or mood disorders (schizophrenia, psychosis, anxiety, depression, bipolar disorder).” 5. One in two males were unaware that marijuana could harm a man’s fertility • “Marijuana should not be used if you are a man who wishes to start a family.”

ClearTheAirNow.org, a coalition of concerned Canadians commissioned the survey.

Affiant is willing to provide further sources of information about the toxicity of marijuana.

Pamela McColl

www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

Source: From email sent to Drug Watch International May 2018

Damage is caused in several different ways.
BRAIN: Messages are passed from cell to cell (neurons) in the brain by chemicals called neurotransmitters which fit by shape into their own receptor sites on specific cells.
The neurotransmitter, anandamide, an endo-cannabinoid (made in body) whose job is to control by suppression the levels of other neurotransmitters is mimicked and so replaced by a cannabinoid (not made in body) in cannabis called THC (Tetrahydrocannabinol). THC is very much stronger and damps down more forcefully the release of other neurotransmitters. Consequently the total activity of the
brain decreases. Chaos ensues.

Neurotransmitters delivering messages to the hippocampus, the area for learning and memory don’t receive enough stimulation to reach it, so signals are lost for ever.
Academic performance plummets and IQs fall by about 8 points. Neurons can be lost permanently. This is brain damage. No child using cannabis even occasionally will achieve their full potential.
Because signalling is slowed down, reaction times increase. Driving becomes hazardous and fatal accidents are rising in legalised USA states. Alcohol plus cannabis in drivers is 16 times more dangerous.
Since THC is fat-soluble, it stays in cells for weeks, constantly ensuring this decrease in brain activity. In the sixties/seventies the THC content was around 1-3%, now in London only ‘skunk’ at 16-20% THC is available. Professor Sir Robin Murray has said that, ‘users will be in a state of low-grade intoxication most of the time’. The Dopamine neurotransmitter has no receptor sites for anandamide and so THC
doesn’t affect it. But the inhibitory Gaba neurotransmitter has. Gaba normally suppresses dopamine but since it is itself suppressed by THC, levels of dopamine quickly increase. Excess dopamine is found in the brains of psychotics, and even schizophrenics if they have a genetic vulnerability. Anyone taking enough THC at one sitting will suffer a psychotic episode which could become permanent. Aggression, violence, even homicides, suicides and murders have resulted from cannabis-induced psychosis. The first research paper linking THC with psychosis was published in 1845. Cannabis-induced schizophrenia costs the country around £2 billion/year. Some of these mentally ill people will spend the rest of their lives in psychiatric units.
THC also depletes the levels of the ‘happiness’ neurotransmitter Serotonin. This can cause depression which may lead to suicide. THC causes dependence. This will affect 1 in 6 using adolescents and 1 in 9 of the general population. Since THC replaces anandamide, there is no need for its production which reduces and eventually stops so the receptor sites are left empty.
Withdrawal then sets in with irritability, sleeplessness, anxiety, depression, even violence until anandamide production resumes. Rehab specialists have told us that adolescent pot addiction is the most challenging to treat.
Cannabis can also act as a gateway drug – it can ‘prime’ the brain for the use of other drugs. Professor David Fergusson (NZ) in longitudinal studies from birth found that ‘The use of cannabis in late adolescence and early adulthood emerged as the strongest risk factor for later involvement in other illicit drug use’.
THC inhibits the vomiting reflex. If a person has drunk too much alcohol, they are often sick and get rid of it. An overdose of alcohol can kill (respiratory muscles stop working) so using cannabis together with alcohol can be fatal.
The signalling of endo-cannabinoids is crucial in brain development. They guide the formation, survival, proliferation, motility and differentiation of new neurons. THC badly interferes with these essential processes. Chaos ensues among the confused brain signals and a cannabis personality develops. Users can’t think logically. They have fixed opinions and answers, can’t find words, can’t take criticism – it’s always someone else’s fault, and can’t plan their day. Families suffer from their violent mood swings – houses get trashed. Anxiety, panic and paranoia may ensue. At the same time users are lonely, miserable and feel misunderstood.

Respiratory System:
Cannabis smoke has many of the same constituents as tobacco smoke but more of its carcinogens – in cancer terms a joint equals 4/5 cigarettes. More tar is deposited in the lungs and airways. Coughing, wheezing, emphysema, bronchitis and cancers have been seen in the lungs.

Heart:
Heart rates rise and stay high for 3-4 hours after a joint. Heart attacks and strokes have been recorded. Some teenagers had strokes and died after bingeing on cannabis.

Hypothalamus:
The hypothalamus is a region of the brain known to regulate appetite. Endocannabinoids in this area send ‘I’m hungry’ messages. When you take THC, that message is boosted. This is called ‘the munchies’. Nabilone, (synthetic THC) can be used to stimulate the appetite in AIDS patients.

DNA and Reproduction:
THC affects the DNA in any new cells being made in the body. It speeds up the programmed cell death (apoptosis) of our defence white blood cells, so our immune system is diminished. There are also fewer sperm. Infertility and impotence have been reported as far back as the 1990s.
An Australian paper published in July 2016 explains this phenomenon. THC can disrupt the actual process of normal cell division mitosis and meiosis (formation of sperm and eggs). In mitosis, the chromosomes replicate and gather together at the centre of the cell. Protein strands (microtubules) are formed from the ends of the cell to pull half of the chromosomes to each end to form the 2 new cells. Unfortunately THC disrupts microtubule formation. Chromosomes can become isolated, rejoin other bits of chromosome and have other abnormalities. Some will actually be shattered into fragments (chromothripsis).
This DNA damage can also cause cancers. Oncogenes (cancer-causing genes) may be activated, and tumour suppressant genes silenced. Chromosome fragments and abnormal chromosomes are frequently seen in cancerous tissues. This would account for other cancers, leukaemia, brain, prostate, cervix, testes and bladder etc, reported in regions of the body not exposed to the smoke. Pregnant users see a 2-4
fold increase in the number of childhood cancers in their offspring. The DNA damage has also been associated with foetal abnormalities – low birth weight, pre-term birth, spontaneous miscarriage, spina bifida, anencephaly (absence of brain parts), gastroschisis (babies born with intestines outside the body) cardiac defects and shorter limbs. All these defects bear in common an arrest of cell growth and cell migration at critical development stages consistent with the inhibition of mitosis noted with cannabis.
DNA damage at meiosis results in fewer sperm as we have seen. Increased errors in meiosis have the potential for transmission to subsequent generations. The zygote (fertilised egg) death rate rises by 50% after the first division. In infants, birth weight is lower and they may be born addicted. Children may have problems with behaviour and cognitive functions as they grow. Childhood cancers are
more common. Intensive care for newborns doubles. The younger they start using cannabis, the more likely they are to remain immature, become addicted, suffer from mental illnesses or progress to other drugs. Average age of first use is 13. Regular cannabis users have worse jobs, less than average money, downward social mobility, relationship problems and antisocial behaviour.

References:
Cannabis Skunk Website www.cannabisskunksense.co.uk Cannabis: A survey of its
harmful effects by Mary Brett is available on DOWNLOADS. It is a 300+ page report
written in 2006 and kept up to date.

Chromothripsis and epigenomics complete causality criteria for cannabis- and
addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity

Book: Adverse Health Consequencies of Cannabis Use. Jan Ramstrom National Institute of Public Health Sweden www.fhi.se

Source: https://www.cannabisskunksense.co.uk/uploads/site-files/ty,Chromothripsis,CarcinogenicityandFetotoxicity,MR-FMMM.pdf March 2020

Abstract

The aim was to examine cross-sectional association between moderate alcohol consumption and total brain volume in a cohort of participants in early middle-age, unconfounded by age-related neuronal change. 353 participants aged 39 to 45 years reported on their alcohol consumption using the AUDIT-C measure. Participants with alcohol abuse were excluded. Brain MRI was analyzed using a fully automated method. Brain volumes were adjusted by intracranial volume expressed as adjusted total brain volume (aTBV). AUDIT-C mean of 3.92 (SD 2.04) indicated moderate consumption. In a linear regression model, alcohol consumption was associated with smaller aTBV (B = – 0.258, p < .001). When sex and current smoking status were added to the model, the association remained significant. Stratified by sex, the association was seen in both males (B = – 0.258, p = 0.003) and females (B = – 0.214, p = 0.011). Adjusted for current smoking, the association remained in males (B = – 0.268, p = 0.003), but not in females. When alcohol consumption increased, total brain volume decreased by 0.2% per one AUDIT-C unit already at 39-45 years of age. Moderate alcohol use is associated with neuronal changes in both males and females suggesting health risks that should not be overlooked.

Figure 1 

Association between AUDIT-C and aTBV. Association between alcohol consumption (AUDIT-C as a continuous variable) and total brain volume adjusted for intracranial volume in males and females. Points in the plot have been jittered to improve visibility of single cases.
Source: Moderate alcohol use is associated with decreased brain volume in early middle age in both sexes – PubMed (nih.gov) August 2020

Abstract

The molecular composition of the cannabinoid type 1 (CB1) receptor complex beyond the classical G-protein signaling components is not known. Using proteomics on mouse cortex in vivo, we pulled down proteins interacting with CB1 in neurons and show that the CB1 receptor assembles with multiple members of the WAVE1 complex and the RhoGTPase Rac1 and modulates their activity. Activation levels of CB1 receptor directly impacted on actin polymerization and stability via WAVE1 in growth cones of developing neurons, leading to their collapse, as well as in synaptic spines of mature neurons, leading to their retraction. In adult mice, CB1 receptor agonists attenuated activity-dependent remodeling of dendritic spines in spinal cord neurons in vivo and suppressed inflammatory pain by regulating the WAVE1 complex. This study reports novel signaling mechanisms for cannabinoidergic modulation of the nervous system and demonstrates a previously unreported role for the WAVE1 complex in therapeutic applications of cannabinoids.

Child Neglect and Violence by Marijuana Impaired Parents are the Leading Causes

As articles in popular magazines portray cannabis as the “it” drug, parents are being led to believe that a serving of marijuana is no more dangerous than a glass of beer or wine.”

— Dr. Ken Finn

WASHINGTON, DC, US, April 23, 2018 /EINPresswire.com/ — Parents Opposed to Pot (POP), a nonprofit dedicated to exposing the dangers of marijuana, counts 106 child abuse deaths related to marijuana since states voted to legalize it in November 2012. POP cautions that the normalization of marijuana should be a primary concern to parents and child protection agencies. April is Child Abuse Prevention Awareness Month, and April 25 is Child Abuse Prevention Awareness Day.

Parents Opposed to Pot found local newspaper reports of the incidents online, and the number of deaths could actually be much higher. Some states are more likely than other states to report when marijuana drug use is involved. The deaths have occurred in 30 states, and the counts are higher in states that have legalized pot. The problem is serious enough that when the National Alliance for Drug-Endangered Children ran a conference last summer, much of it focused on marijuana. Nationally, approximately 1700 child abuse deaths occur each year, and substance abuse is a major risk factor.

The earliest deaths after 2012 that POP recorded seemed to be from neglect: toddlers who drowned, died in fires, or infants who were left in hot cars when parents smoked pot and forgot about them. However, many deaths related to marijuana were caused by domestic violence, because parents became angry or psychotic from pot use and had paranoid delusions. The potency of marijuana is several times stronger than it was in the 1990s.The public has not been educated well about how marijuana can trigger psychosis and/or schizophrenia, as stated in the 2017 National Academy of Sciences report.

Shortly after Colorado commercialized marijuana in 2014, stories of three tragic deaths of toddlers related to their parents’ use of marijuana emerged. The month Washington legalized possession of marijuana, a two-year-old drank from his mother’s bong and died. After investigating, state officials determined that the toddler had ingested lethal amounts of both THC and meth, enough to kill an adult.

“As articles in popular magazines such as Cosmopolitan and Oprah Winfrey’s ‘O’ portray cannabis as the ‘it’ drug, parents are being led to believe that a serving of marijuana is no more dangerous than a glass of beer or wine,” explains Dr. Ken Finn, a medical advisor to PopPot.org. “However, three sets of twins died in fires when parents abandoned these toddlers for reasons related to their marijuana use.”

The promotion of marijuana as a way to relax is inappropriate for parents or caregivers of small children, and the promotion of marijuana for pregnant women with morning sickness is a dangerous trend.

Marijuana use impairs executive functioning — which led to poor judgement and forgetfulness in many of these deaths. Greater acceptance means more use, and more use means more addiction.

Eleven deaths occurred in Colorado, while 10 took place in California. In both states, at least one child died where butane hash oil (BHO) labs operated, and numerous children were injured in BHO fires. The two most recent deaths in Colorado occurred last summer when a mother followed a cult leader to a marijuana farm. No one knows how long the two girls had been dead when they were discovered locked in a car covered in tarp last September. They were starved to death. An unusual death in California occurred when a babysitter went to her cousin’s car to smoke pot, leaving a 16-month-old boy inside. The toddler eventually came outside and the visiting car ran over him.

Many ER treatments followed the accidental ingestion of marijuana candies and cookies. A medical journal reported last year that an 11-month-old baby suffered from an enlarged heart muscle and couldn’t be revived a few days after ingesting marijuana in Colorado. However, it’s usually not edibles that kill children, but other acts of neglect and violent behavior.

In Florida, three children drowned when parents or babysitters smoked pot and forgot about them. At least 10 deaths occurred when parents left small children in hot cars while they smoked cannabis. The most common forms of death by neglect when parents use cannabis are fires, 15, drownings, 10 and hot cars, 10.

During the intense debate over medical marijuana in Pennsylvania, the number of pot-related child abuse deaths seemed to increase. Much drama was used to discuss children with seizures, while five other children died due to adult pot use between April and December, 2016.

POP is not the only organization to notice the uptick in child deaths related to marijuana. Yvapil County District Attorney Sheila Polk reported that, in 2013, 62 deaths of children in Arizona were associated with cannabis , and that it was the substance most often related to accidental deaths in the state.

Nationally, parents cause about three quarters of child abuse deaths and most child abuse deaths occur because of neglect. When there’s marijuana in the picture, violence or violent neglect are just as likely to cause death. Boyfriends of the mothers caused 14 such deaths, most often from violence, with the moms in these instances often using pot too. One recent death was the beating death of a three-year-old. The stepfather, who was charged, kept marijuana in the house. Research shows that cannabis can trigger negative thoughts and violent behavior. But, we haven’t included this case our list because it’s not clear what role the drug played in this death.

In four cases, children died because babysitters’ neglected the child, while in four different instances a relative was responsible for the deaths.

POP published 18 blog articles on Child Endangerment that explain some of facts surrounding the deaths. A downloadable fact sheet available on the PopPot.org webpage simplifies the statistics.

Parents Opposed to Pot is a 501c3 nonprofit based in Merrifield, Virginia.

Source: Over 100 Child Abuse Deaths Found Related to Cannabis, with Rise of Commercial Industry (einpresswire.com) April 2018

Abstract

There is a strong association between cannabis use and schizophrenia but the underlying cellular links are poorly understood. Neurons derived from human-induced pluripotent stem cells (hiPSCs) offer a platform for investigating both baseline and dynamic changes in human neural cells. Here, we exposed neurons derived from hiPSCs to Δ9-tetrahydrocannabinol (THC), and identified diagnosis-specific differences not detectable in vehicle-controls. RNA transcriptomic analyses revealed that THC administration, either by acute or chronic exposure, dampened the neuronal transcriptional response following potassium chloride (KCl)-induced neuronal depolarization. THC-treated neurons displayed significant synaptic, mitochondrial, and glutamate signaling alterations that may underlie their failure to activate appropriately; this blunted response resembles effects previously observed in schizophrenia hiPSC- derived neurons. Furthermore, we show a significant alteration in THC-related genes associated with autism and intellectual disability, suggesting shared molecular pathways perturbed in neuropsychiatric disorders that are exacerbated by THC.

Conflict of interest statement

The authors declare that they have no conflict of interest.

Fig. 1. THC treatment regulates genes involved in mitochondrial and glutamate pathways. 

a RNA sequencing of hiPSC-derived neurons reveals 497 genes (acute) and 810 genes (chronic) are significantly changed following THC exposure, including. b genes involved in mitochondrial (e.g., COX7A2MT-CO1, and MT-CO3) and glutamate (e.g., GRID2) pathways (Quantitative RT–PCR (qRT–PCR); Ordinary one-way ANOVA with Tukey’s multiple comparisons test: *p < 0.05. n = 5 (see qRT–PCR, Ca–Ce, Supplementary Table S1)). Ingenuity pathway analysis shows that mitochondrial oxidative phosphorylation is strongly altered after both acute c and chronic d THC exposure

Fig. 2. Postsynaptic density and ion channel genes are regulated by THC treatment. 

ab Multiple postsynaptic density and ion channel genes are significantly altered in hiPSC-derived neurons following acute or chronic THC exposure, including the postsynaptic gene HOMER1 (Quantitative RT–PCR (qRT–PCR); Ordinary one-way ANOVA with Tukey’s multiple comparisons test: *p < 0.05. n = 5 (see qRT–PCR, Ca–Ce, Supplementary Table S1)). c Network analysis combining all THC-related genes from acute and chronic THC treatment shows broad changes to fundamental cellular functions such as RNA biology, chromatin regulation and development

Fig. 3. Genes altered by THC treatment in hiPSC-derived neurons are significantly associated with autism and intellectual disability. 

a Venn diagram showing the overlap between THC-related genes and autism, intellectual disability and schizophrenia. b THC-related genes are significantly related to autism and intellectual disability (p-value < 0.05)

Fig. 4. THC treatment results in neuronal hypo-excitability similar to observations using schizophrenia-associated neurons. 

a Venn diagram showing impaired transcriptional response following 50 mM KCl treatment for 3 h in THC exposure hiPSC-derived neurons. b A similar decrease in significantly regulated transcripts following 50 mM KCl for 3 h is observed in schizophrenia-associated hiPSC-derived neurons. c A cohort of 5 control (C1–5) and 4 schizophrenia-associated (SZ1-4) cases were used for (d) candidate qRT–PCR analysis investigating COX7A2GRID2 and HOMER1 following acute THC exposure. e Blunted effect of THC treatment can be seen in immediate early gene transcripts such as NR4A1 and (fFOSB following KCl-induced activation (Quantitative RT–PCR (qRT–PCR); Ordinary one-way ANOVA with Tukey’s multiple comparisons test: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. n = 5 controls (see qRT–PCR, Ca–Ce, Supplementary Table S1); n = 4 schizophrenia (see qRT–PCR, S1–S4, Supplementary Table S1))

Abstract

The recent demonstration that addiction-relevant neuronal ensembles defined by known master transcription factors and their connectome is networked throughout mesocorticolimbic reward circuits and resonates harmonically at known frequencies implies that single-cell pan-omics techniques can improve our understanding of Substance Use Disorders (SUD’s). Application of machine learning algorithms to such data could find diagnostic utility as biomarkers both to define the presence of the disorder and to quantitate its severity and find myriad applications in a developmental pipeline towards therapeutics and cure. Recent epigenomic studies have uncovered a wealth of clinically important data relating to synapse-nucleus signalling, memory storage, lineage-fate determination and cellular control and are contributing greatly to our understanding of all SUD’s. Epigenetics interacts extensively with glycobiology. Glycans decorate DNA, RNA and many circulating critical proteins particularly immunoglobulins. Glycosylation is emerging as a major information-laden post-translational protein modification with documented application for biomarker development. The integration of these two emerging cutting-edge technologies provides a powerful and fertile algorithmic-bioinformatic space for the development both of SUD biomarkers and novel cutting edge therapeutics.

Hypotheses: These lines of evidence provide fertile ground for hypotheses relating to both diagnosis and treatment. They suggest that biomarkers derived from epigenomics complemented by glycobiology may potentially provide a bedside diagnostic tool which could be developed into a clinically useful biomarker to gauge both the presence and the severity of SUD’s. Moreover they suggest that modern information-based therapeutics acting on the epigenome, via RNA interference or by DNA antisense oligonucleotides may provide a novel 21st century therapeutic development pipeline towards the radical cure of addictive disorders. Such techniques could be focussed and potentiated by neurotrophic vectors or the application of interfering electric or magnetic fields deep in the medial temporal lobes of the brain.

Source: Pathways from epigenomics and glycobiology towards novel biomarkers of addiction and its radical cure – PubMed (nih.gov) July 2018

Abstract 

Objectives

We aimed to describe and correlate the hospital panorama of psychotic disorders (PD) with cannabis use (CU) trends in all Portuguese public hospitals.

Methods

We conducted a retrospective observational study that analysed all hospitalizations that occurred in Portuguese public hospitals from 2000 to 2015. Hospitalizations with a primary diagnosis of PD or schizophrenia were selected based on Clinical Classification Software diagnostic single-level 659. Episodes associated with CU were identified by the International Classification of Diseases Version 9, Clinical Modification code 304.3/305.2 that correspond to cannabis dependence/cannabis abuse.

Results

The number of hospitalizations with a primary diagnosis of PD and schizophrenia associated with CU rose 29.4 times during the study period, from 20 to 588 hospitalizations yearly (2000 and 2015, respectively) with a total of 3,233 hospitalizations and an average episode cost of €3,500. Male patients represented 89.8% of all episodes, and the mean/median age at discharge were 30.66/29.00 years, respectively. From all hospitalizations with a primary diagnosis of PD or schizophrenia, the ones with a secondary diagnosis of CU rose from 0.87% in 2000 to 10.60% in 2015.

Conclusions

The increase on secondary diagnosis coding and the change on cannabis patterns of consumption in Portuguese population with an increasing frequency of moderate/high dosage cannabis consumers may explain the rise on PD hospitalizations

We note the report on the rising gastroschisis incidence 3.1 times 1995-2012

The 20-fold variation across California mirrors the ten-fold variation across Canada here the distribution pattern closely mirrors cannabis consumption, and from where cannabis-related adjusted O.R.= 3.54 (95%C.I. 2.22-5.63) has been reported .

Several clues suggest cannabis is likely involved also in California.  Statewide gastroschisis rose 2.84-fold 2005-2012, whilst last month cannabis use in northern California rose 2.56-fold from 8.41% to 21.55% 2006-2008 to 2014-2016 in the National Survey of Drug Use and Health.

Combining the midrange county rates supplied  with published birth, population and NSDUH data it can be shown that the gastroschisis rate in the NSDUH 1R northern 15 counties rose O.R.=2.33 (95%C.I. 1.91-2.83) compared to the rest of the state for the whole period 1995-2012.

Anderson found rurality was a risk factor for cannabis use which fits with the burgeoning cannabis industry.  Timber production was a probable surrogate marker, and the Federal parks are known to accommodate substantial cannabis plantations.

Moreover as various potent herbicides and rodenticides including carbofuran are used in commercial operations and contaminate the water table these also need to be considered as novel indirect toxins.

Gastroschisis follows cannabis use in many places including Australia, Canada, Mexico, North Carolina, and Washington state.  Mechanistically this is consistent with the appearance of cannabinoid type 1 receptors (CB1R) on the omphalovitelline vessels from the ninth week of gestation, and documented occurrence of cannabis arteritis .

The real possibility clearly needs to be considered that the global rise in cannabis use may underlie the dramatic rise in gastroschisis in many locations.  Indeed since heart and brain defects including anencephaly and brain impairments consistent with autistic deficits are also well described in the congenital cannabis exposure literature, together with Downs syndrome, it may be that a wide variety of defects could be related to the budding industry.

The potential link with the autism spectrum including cannabis-dependent, dose-related and rampant neurexin- neurologin-mediated synaptic dehiscence is of particular concern.  The rapidly growing autism epidemic in Colorado is matched by an autism hotspot in the northern cannabis zone of California which has likely become even hotter since that study was conducted.

Careful substance-spatiotemporal analyses of positive and negative correlation are indicated to investigate causal relationships.

The possibility of worldwide multiorgan cannabis-induced CB1R-mediated severe clinical teratology has not been widely canvassed.

Source:  email: stuart.reece@bigpond.com  

Abstract

Endocannabinoids regulate brain development via modulating neural proliferation, migration, and the differentiation of lineage-committed cells. In the fetal nervous system, (endo)cannabinoid-sensing receptors and the enzymatic machinery of endocannabinoid metabolism exhibit a cellular distribution map different from that in the adult, implying distinct functions. Notably, cannabinoid receptors serve as molecular targets for the psychotropic plant-derived cannabis constituent Δ(9)-tetrahydrocannainol, as well as synthetic derivatives (designer drugs). Over 180 million people use cannabis for recreational or medical purposes globally. Recreational cannabis is recognized as a niche drug for adolescents and young adults. This review combines data from human and experimental studies to show that long-term and heavy cannabis use during pregnancy can impair brain maturation and predispose the offspring to neurodevelopmental disorders. By discussing the mechanisms of cannabinoid receptor-mediated signaling events at critical stages of fetal brain development, we organize histopathologic, biochemical, molecular, and behavioral findings into a logical hypothesis predicting neuronal vulnerability to and attenuated adaptation toward environmental challenges (stress, drug exposure, medication) in children affected by in utero cannabinoid exposure. Conversely, we suggest that endocannabinoid signaling can be an appealing druggable target to dampen neuronal activity if pre-existing pathologies associate with circuit hyperexcitability. Yet, we warn that the lack of critical data from longitudinal follow-up studies precludes valid conclusions on possible delayed and adverse side effects. Overall, our conclusion weighs in on the ongoing public debate on cannabis legalization, particularly in medical contexts.

At the Tip of an Iceberg: Prenatal Marijuana and Its Possible Relation to Neuropsychiatric Outcome in the Offspring – PubMed (nih.gov) September 2015

Abstract

Evidence has accumulated over the past several decades suggesting that both exocannabinoids and endocannabinoids play a role in the pathophysiology of schizophrenia. The current article presents evidence suggesting that one of the mechanisms whereby cannabinoids induce psychosis is through the alteration in synchronized neural oscillations. Neural oscillations, particularly in the gamma (30-80 Hz) and theta (4-7 Hz) ranges, are disrupted in schizophrenia and are involved in various areas of perceptual and cognitive function. Regarding cannabinoids, preclinical evidence from slice and local field potential recordings has shown that central cannabinoid receptor (cannabinoid receptor type 1) agonists decrease the power of neural oscillations, particularly in the gamma and theta bands. Further, the administration of cannabinoids during critical stages of neural development has been shown to disrupt the brain’s ability to generate synchronized neural oscillations in adulthood. In humans, studies examining the effects of chronic cannabis use (utilizing electroencephalography) have shown abnormalities in neural oscillations in a pattern similar to those observed in schizophrenia. Finally, recent studies in humans have also shown disruptions in neural oscillations after the acute administration of delta-9-tetrahydrocannabinol, the primary psychoactive constituent in cannabis. Taken together, these data suggest that both acute and chronic cannabinoids can disrupt the ability of the brain to generate synchronized oscillations at functionally relevant frequencies. Hence, this may represent one of the primary mechanisms whereby cannabinoids induce disruptions in attention, working memory, sensory-motor integration, and many other psychosis-related behavioral effects.

Source: It’s All in the Rhythm: The Role of Cannabinoids in Neural Oscillations and Psychosis – PubMed (nih.gov) December 2015

Abstract

Background: Inconsistent findings exist regarding long-term substance use (SU) risk for children diagnosed with attention-deficit/hyperactivity disorder (ADHD). The observational follow-up of the Multimodal Treatment Study of Children with ADHD (MTA) provides an opportunity to assess long-term outcomes in a large, diverse sample.

Methods: Five hundred forty-seven children, mean age 8.5, diagnosed with DSM-IV combined-type ADHD and 258 classmates without ADHD (local normative comparison group; LNCG) completed the Substance Use Questionnaire up to eight times from mean age 10 to mean age 25.

Results: In adulthood, weekly marijuana use (32.8% ADHD vs. 21.3% LNCG) and daily cigarette smoking (35.9% vs. 17.5%) were more prevalent in the ADHD group than the LNCG. The cumulative record also revealed more early substance users in adolescence for ADHD (57.9%) than LNCG (41.9%), including younger first use of alcohol, cigarettes, marijuana, and illicit drugs. Alcohol and nonmarijuana illicit drug use escalated slightly faster in the ADHD group in early adolescence. Early SU predicted quicker SU escalation and more SU in adulthood for both groups.

Conclusions: Frequent SU for young adults with childhood ADHD is accompanied by greater initial exposure at a young age and slightly faster progression. Early SU prevention and screening is critical before escalation to intractable levels.

Keywords: ADHD; Attention deficit disorder; adolescence; drug abuse.

Conflict of interest statement

Conflict of Interest Disclosures: J.M.S. acknowledges research support, advisory board/speaker’s bureau and/or consulting for Alza, Richwood, Shire, Celgene, Novartis, Celltech, Gliatech, Cephalon, Watson, CIBA, UCB, Janssen, McNeil, Noven, NLS, Medice, and Lilly. J.T.M. received royalties from New Harbinger Press. L.E.A. received research funding from Curemark, Forest, Lilly, Neuropharm, Novartis, Noven, Shire, Supernus, and YoungLiving and consulted with or was on advisory boards for Gowlings, Neuropharm, Novartis, Noven, Organon, Otsuka, Pfizer, Roche, Seaside Therapeutics, Sigma Tau, Shire, and Tris Pharma and received travel support from Noven. L.H. received research support, served on advisory boards and was speaker for Eli Lilly, Glaxo/Smith/Kline, Ortho Janssen, Purdue, Shire and Ironshore. Other authors have no disclosures.

Source: https://www.ncbi.nlm.nih.gov/pubmed/29315559 June 2018

Legalization advocates and the weed industry can support necessary reforms while being honest about the risks of marijuana use, the study’s author says.

A large percentage of marijuana users around the world report signs of dependence, even as cannabis appears to be one of the safest and most commonly used drugs overall, according to the results of a survey released on Wednesday.

The findings are contained in the 2018 Global Drug Survey, a detailed questionnaire that compiled responses from more than 130,00 people in over 40 countries in the past year. One section of the survey used the “Severity of Dependence Scale,” or SDS, a popular tool that asks respondents five questions regarding impaired control over drug use and anxieties related to consumption and quitting.

Around 50,000 of the survey respondents reported having used marijuana in the last 12 months. Only alcohol and tobacco use were more common.

Of all cannabis users, 20.2 percent showed substantial signs of dependence, measured by affirmative answers to at least four of the five SDS questions. Crystal methamphetamine was the drug most closely associated with dependence, with nearly 25 percent of users scoring four or higher on the SDS.

A positive SDS score is not the same as a clinical diagnosis of dependence, Adam Winstock, a British addiction psychiatrist and founder of the Global Drug Survey, told HuffPost. But it does suggest that many marijuana users have considerable misgivings about their habits.

“You’ve got 20 percent of the people who are significantly worried about the impact of their use on their life,” said Winstock. “It’s a measure of subjective worry and concern, but those questions tap into things like how much you use, how often, your sense of control and your desire to stop.”

The responses to individual SDS questions offer a window into some of those feelings of dependence.

Cannabis was the substance most frequently associated with anxiety over the prospect of quitting, for example. Although nearly 74 percent of users said the idea of stopping “never or almost never” made them anxious, 19.7 percent said it “sometimes” did, with the rest reporting that it “often” or “always” did.

A total of 21.4 percent of marijuana users said it would be “quite difficult” for them to stop using, with 6.4 percent responding that it would be either “very difficult” or “impossible.” Around 72 percent said quitting would not be difficult.

Nearly 30 percent of cannabis users reported that their cannabis use was at least occasionally “out of control,” with 22.6 percent of respondents saying it was only “sometimes” an issue, 5.3 percent saying it was “often” an issue and 1.6 percent saying it was “always or nearly always” an issue.

The survey also sought to measure the overall safety of substances by asking respondents if they’d sought emergency medical treatment after using various drugs. Just 0.5 percent of all cannabis users reported seeking treatment after use, the second-lowest rate of any substance. Magic mushrooms appeared to be the safest recreational drug for the second year in a row, with just 0.2 percent of users saying they’d pursued medical intervention.

The cannabis dependence results were particularly surprising to Winstock, who said he would’ve expected to see around 10 to 15 percent of marijuana users report signs of dependence.

“You’re legalizing a drug that a fair number of people who use it have worries about themselves,” Winstock said. “The question is what do you do about that?”

The Global Drug Survey may hold some answers. Since 2014, the independent research company has partnered with medical experts and media groups to conduct an annual survey with the goal of making drug use safer through increased access to education and treatment resources.

Around 300,000 marijuana users have partaken in Global Drug Surveys over the years, said Winstock. Those respondents have consistently shown high levels of support for establishing government guidelines around safe marijuana use. Among cannabis users who have expressed a desire to use less frequently or quit entirely, many have said they’d like assistance in doing so. But very few end up seeking help.

Taken together, the surveys suggest elected officials and the marijuana industry should be engaging in a more honest discussion about the risks associated with cannabis use so they can better address issues that may arise as laws are liberalized, said Winstock.

That advice may be particularly salient in the U.S., where a number of states are considering legalizing recreational marijuana in the face of growing public opposition to prohibition. Eight states, as well as Washington, D.C., have already legalized weed.

“Clearly arresting someone and giving them a criminal record for smoking a joint is a futile and pointless exercise and … nothing I’m suggesting is me saying cannabis is a bad drug and the government made a mistake,” said Winstock.

“What I’m saying is that at the point they regulated cannabis, they should have mandated a whole bunch of things that allowed it to be easier for people to reflect on their cannabis use and how it impacted on them and how to control their use,” he went on. “There should have been mandated health warnings and advice and an index of harm for different products.”

Among the 3,400 U.S. marijuana users surveyed this year, just under 25 percent expressed a desire to use less ― compared to 29.3 percent of users globally. Just over 25 percent reported getting high more than 300 days out of the past year, though that may not be reflective of broader marijuana trends, because the survey didn’t randomly sample users nationwide.

Sixteen percent of the American marijuana users who said they wanted to cut back also responded that they’d like help doing so. Nearly 50 percent of all U.S. users said they’d attempted to quit at some point, with 67 percent of those saying they’d tried in the previous year.

Winstock says it makes sense to increase access to harm reduction tools in order to reach those who say they want help with their dependence on cannabis. But broad support for this sort of comprehensive approach requires people on all sides to confront the fact that marijuana, like pretty much any drug, can lead to dependence with some frequency.

Instead, the legalization debate has played out in a far more polarized fashion, with advocates often pushing back against decades of government anti-weed hysteria by claiming cannabis is a harmless drug, especially when compared to alcohol or tobacco.

In light of the cataclysmic failures of the nation’s war on drugs, there is plenty of reason to be tempted by that portrayal.

“It could just be that so many people are saying we’ve raised billions in taxes, saved thousands of hours of police time, saved loads of innocent young lives from having their careers ruined and being banged up in prison,” said Winstock. “Those are such huge wins that I could see people going, ‘That’s enough.’”

But just because the status quo has been so bad for so long and marijuana is less harmful than alcohol or tobacco ― legal drugs that kill more people each year than all illicit drugs combined ― doesn’t mean the push to legalize cannabis can’t learn from past mistakes.

For Winstock, it’s not too late for legal weed states and leaders in the marijuana industry to place more focus on public health.

“Stop for a moment and think about how you cannot become the tobacco industry or the alcohol industry,” said Winstock. “Be the best you can be, don’t just make the biggest profit. Be the most responsible industry you can, and that means be honest.”

Source: Marijuana Users Report High Rates Of Dependence In Global Drug Survey | HuffPost UK Health (huffingtonpost.co.uk) May 2018

Smoking during pregnancy has well-documented negative effects on birth weight in infants and is linked to several childhood health problems. Now, researchers at the University at Buffalo Research Institute on Addictions have found that prenatal marijuana use also can have consequences on infants’ weight and can influence behavior problems, especially when combined with tobacco use.

“Nearly 30 percent of women who smoke cigarettes during pregnancy also report using marijuana,” says Rina Das Eiden, PhD, RIA senior research scientist. “That number is likely to increase with many states moving toward marijuana legalization, so it’s imperative we know what effects prenatal marijuana use may have on infants.”

Through a grant from the National Institute on Drug Abuse, Eiden studied nearly 250 infants and their mothers. Of these, 173 of the infants had been exposed to tobacco and/or marijuana during their mothers’ pregnancies. None were exposed to significant amounts of alcohol.

Eiden found that infants who had been exposed to both tobacco and marijuana, especially into the third trimester, were smaller in length, weight and head size, and were more likely to be born earlier, compared to babies who were not exposed to anything. They also were more likely to be smaller in length and weight compared to babies exposed only to tobacco in the third trimester. The results were stronger for boys compared to girls.

“We also found that lower birth weight and size predicted a baby’s behavior in later infancy,” Eiden says. “Babies who were smaller were reported by their mothers to be more irritable, more easily frustrated and had greater difficulty calming themselves when frustrated. Thus, there was an indirect association between co-exposure to tobacco and marijuana and infant behavior via poor growth at delivery.”

Furthermore, women who showed symptoms of anger, hostility and aggression reported more stress in pregnancy and were more likely to continue using tobacco and marijuana throughout pregnancy. Therefore, due to the co-exposure, they were more likely to give birth to infants smaller in size and who were more irritable and easily frustrated. The infants’ irritability and frustration is also linked to mothers who experienced higher levels of stress while pregnant.

“Our results suggest that interventions with women who smoke cigarettes or use marijuana while pregnant should also focus on reducing stress and helping them cope with negative emotions,” Eiden says. “This may help reduce prenatal substance exposure and subsequent behavior problems in infants.”

The study appeared in the March/April issue of Child Development and was authored by Pamela Schuetze, PhD, Department of Psychology, Buffalo State College, with co-authors Eiden; Craig R. Colder, PhD, UB Department of Psychology; Marilyn A. Huestis, PhD, Institute of Emerging Health Professions, Thomas Jefferson University, Philadelphia; and Kenneth E. Leonard, PhD, RIA director.

Source: Prenatal marijuana use can affect infant size, behavior, study finds — ScienceDaily May 2018

They were the mind-altering drugs of the Sixties, but now lysergic acid diethylamide (better known as LSD), magic mushrooms and a range of other banned psychedelic drugs are making a comeback.

Not on the party scene, but as the focus of researchers who believe they could treat a variety of mental health problems, including depression.

British researchers are at the forefront of this renaissance of hallucinogenics. But, as Good Health can reveal, a key organisation funding their work is a pressure group with a parallel agenda.

In addition to supporting research into the potential therapeutic benefits of banned drugs, the Beckley Foundation — created by Amanda Feilding, a wealthy countess who’s spent a lifetime advocating the benefits of LSD — is working ‘to erode the pervasive taboo surrounding . . . recreational drug use’.
It would be wrong to dismiss the ‘Cannabis Countess’ (who’s previously advocated legalising the drug) as simply a colourful character.

For here we reveal the extent of her influence in this controversial area, both in funding the research and also actively participating ‘in the inception, design, and writing up’ of no fewer than 37 studies — despite the fact that she has no scientific qualifications.

In 2012, there were just 58 papers exploring the effects and possible medical benefits of LSD, psilocybin (the active ingredient in magic mushrooms) and ayahuasca, a mind-altering plant used in rituals by Amazon tribes. In the past year alone, there have been at least 135.

In the vanguard are researchers at Imperial College London. Known as the Psychedelic Research Group, they’re exploring the potential of banned drugs for treating conditions including depression and even for dealing with grief.

One of the key figures is David Nutt, the psychiatrist and professor of neuropsychopharmacology at Imperial who, in 2009, had to resign as the government’s chief drugs adviser after he said that LSD, ecstasy and cannabis were less harmful than alcohol.

Since then, Professor Nutt has collaborated with the Beckley Foundation and its founder Feilding — the two are co-directors of what is described by the foundation as the Beckley Imperial Research Programme. Despite lacking scientific qualifications, Feilding is co-author of 24 papers published by researchers at Imperial College London and is one of the 32‑member team of the Psychedelic Research Group, as is Professor Nutt.

Feilding’s involvement may raise a serious question about her foundation’s twin agendas.

On its website, it seeks donations to ‘support psychedelic research’, but also ‘drug policy reform’. Feilding herself insists that the war on drugs has failed and has campaigned tirelessly for reform.

In Jamaica, where Feilding has a house, the foundation played a role in the government’s decision to decriminalise cannabis.

At a conference in 2015, Feilding expressed the hope that ‘the United Kingdom will learn some lessons from Jamaica’s progress, and will at least begin by recognising the rights of those in need of access to cannabis for medicinal and religious purposes’.

But more disturbing, perhaps, is her support for ‘microdosing’, where small amounts of psychedelics are taken supposedly to achieve greater creativity; worryingly, some are reportedly using it to treat depression and anxiety.

At a psychedelics conference in the U.S. last year, Feilding spoke of her use of LSD when younger to ‘hit that sweet spot, where vitality and creativity are enhanced’, a practice she compared to ‘what people are now doing with microdosing’.

She added that microdosing ‘may indeed be the way we break down barriers, and make the psychedelic experience more accessible to people at large’.

Another member of the Beckley Imperial Research Programme with links to the countercultural aspects of psychedelic drugs is Dr Robin Carhart-Harris, a frequent co-author on papers with Feilding.

In 2016, he addressed a London conference of The Psychedelic Society, which ‘advocates the careful use of psychedelics as a tool for personal and spiritual development’ (such drugs, it says, are banned solely ‘on the basis of unsubstantiated health risks and tabloid hysteria’).

This isn’t the first time scientists have experimented with mind-altering drugs for mental health conditions. Between 1954 and 1965 psychiatrists at British hospitals used LSD to treat patients. This ended in 1966, when it was banned amid fears it caused delusions and suicidal thoughts.

But according to Professor Nutt, clinical use and studies before the ban showed that patients with disorders such as depression had ‘sometimes benefited considerably’ from the ability of ‘the classical psychedelic drugs . . . to “loosen” otherwise fixed, maladaptive patterns of cognition and behaviour, particularly when given in a supportive, therapeutic setting’.

He believes such drugs ‘may have a place in the treatment of neurotic disorders, particularly depressive disorder, anxiety disorders, addictions and in the psychological challenges associated with death’.

But for psychedelic treatment to become a reality, what’s needed are large-scale scientific trials. Now, thanks to the support of the Beckley Foundation, that’s about to happen.

Imperial’s Psychedelic Research Group has been recruiting patients with long-term depression for a major trial comparing the effects of a six-week course of the antidepressant escitalopram with a single dose of psilocybin. Dr Carhart-Harris, Professor Nutt and Feilding are the leading members of the research team.

Imperial wouldn’t say if funding is forthcoming from the Beckley Foundation for this study. But in a response to a Freedom of Information request we sent, it revealed that since 2009 it has received ‘a total of £108,519’ from the Foundation for ‘research projects’.

Public funding has also been provided for psychedelic research. In 2012, the Medical Research Council (MRC) gave Professor Nutt £500,000 for research into psilocybin to treat major depression.

The next year they gave him £250,000 for a study on psilocybin and schizophrenia. And the National Institute for Health Research, the research arm of the NHS, told us it funded ‘a small proportion’ of Professor Nutt’s salary.

The new trial follows on from a series of studies by Professor Nutt and colleagues at other UK institutions since 2010 involving psilocybin for depression.

Some involved healthy volunteers. But then, in 2016, a team from Imperial, University College London, Barts Health NHS Trust, King’s College and the Maudsley Hospital conducted the first trial with patients.

Involving just 12 people, it was designed to investigate the safety and feasibility of psilocybin for major long-term depression.

As The Lancet Psychiatry reported, eight of the patients were ‘depression-free’ one week after treatment; five were still clear after three months. But all experienced ‘transient anxiety’ and nine also reported ‘transient confusion or thought disorder’.

Last December, Compass Pathways, a new UK company whose expert advisers include Dr Carhart-Harris and Professor Sir Alasdair Breckenridge, former chair of the drug watchdog the Medicines and Healthcare products Regulatory Agency, announced a programme of clinical trials of psilocybin.

In the past few years, the Psychedelic Research Group has also looked at the potential use of drugs such as LSD.

But are yet more drugs, not least mind-altering psychedelic ones, really the solution for conditions such as depression?

In fact, the recommended treatment is psychological therapy. But as the British Medical Association found this year, thousands of patients with serious mental health problems were waiting up to two years for treatments such as cognitive behavioural therapy.

Too often ‘the only thing on offer to patients with depression is medication, which often has significant unwanted side-effects and does not help everyone’, says Anne Cooke, editor of the British Psychological Society report, Understanding Psychosis And Schizophrenia.

As for the use of psychedelics to treat mental health problems, Ms Cooke, a consultant clinical psychologist at Canterbury Christ Church University, adds: ‘My understanding is they could be used as an adjunct to psychological therapy, to try to help the person enter a frame of mind where they can make best use of the therapy.

‘But the same can sometimes be achieved by other means, such as relaxation methods. And, as we know, these drugs can also have adverse effects, so it’s important to exercise caution.’

Peter Kinderman, a professor of clinical psychology at the University of Liverpool and a member of the Council for Evidence-based Psychiatry, agrees drugs such as psilocybin ‘might help’ encourage ‘flexible thinking’.

He’s even advising a European research project looking at psilocybin for depression.

But he says it’s ‘important we’re very cautious with drugs such as psilocybin and LSD’ and says he’s ‘pretty sceptical’ generally about drug treatments for mental health: ‘I really worry that a lot of people in the mental health system have been prescribed too large quantities of too many drugs for too long.’

Amanda Feilding declined to comment.

I’m all for keeping an open mind about how drugs can be used. Even drugs that were once considered dangerous can, in certain circumstances, have benefits.

Thalidomide, banned after it was found to cause birth deformities, has made a comeback as an effective treatment for certain types of lung cancer, for example.

But I have profound reservations about this sudden interest in illegal drugs and fear it will erode our drug laws further. 

As a doctor who has worked in drug addiction, this makes me profoundly uneasy. Time and again I have seen the destruction these drugs can cause.

Yes, of course, substances such as alcohol are also very dangerous. But that’s not a reason to decriminalise other drugs, too.

It’s perfectly possible that illegal recreational drugs could have a medical use; a major analysis suggested LSD can help in alcoholism. But there are many other drugs that help and which don’t have the potential for abuse or psychiatric complications.

What makes me suspicious is that the resurgence of interest in recreational drugs for mental health conditions hasn’t sprung out of new research or a new discovery about how the brain works.

Why focus on recreational drugs and not on developing new antidepressants, for example? It seems more of a fishing expedition to find results that support a certain view, rather than being led by a solid, scientific reason to research these drugs. We’ve seen a similar thing with cannabis. There’s no doubt it can help some with conditions such as epilepsy. Which is why scientists are trying to identify the specific component responsible and turning it into a medication that can be prescribed to help patients.

That’s what usually happens in medicine. For instance, the key ingredient in aspirin is acetylsalicylic acid, which was originally derived from the leaves of the willow tree.

But when someone has a headache, we don’t give them a bit of tree to chew on. We’ve identified the chemical responsible for the useful property and produced it in a tablet, where the dose and purity can be consistent. But rather than identify the components, campaigners insist we should simply legalise cannabis for medicinal use.

To me, this is just a back-door attempt to make recreational use legal, too.

I’m not convinced LSD even has any benefits. I’ve never met someone who’s used it and said to myself: ‘Well, that’s solved all your problems.’ Rather, too often I’ve come across regular users, typically in their 60s or 70s, and thought how odd they were. I’ve also met many who have spent significant periods in hospital as a result of drug use.

Making illegal drugs medically acceptable is the first step in making them socially acceptable. If decriminalisation is what you really want, at least be honest about it. Don’t try to use medicine to push a social agenda.

The blue-blooded brains behind it – with NO science qualifications! 

One of the driving forces behind the research into psychedelic drugs is Amanda Feilding, the 75-year‑old Countess of Wemyss and March.

She stood unsuccessfully for Parliament on the platform that trepanation — drilling a hole in the head — should be available on the NHS to allow people to experience a higher state of consciousness.

In a speech she gave to a conference on psychedelic drugs last October, Feilding said she ‘learned the value’ of regular doses of LSD back in the Sixties. She was able to ‘live and work on LSD, and in my opinion to see much further and deeper . . .I grew to love this state’.

But it would be a mistake to dismiss Feilding as just eccentric.

She is a leading figure in the explosion of research into the ‘medicinal use’ of psychedelic drugs and a founder and co-director (with Professor David Nutt) of the Beckley Imperial Research Programme at Imperial College London, as well as working with other UK and international universities.

On the website of the Beckley Foundation, which she set up in 1996 as the Foundation to Further Consciousness, she is described as ‘the “hidden hand” behind the renaissance of psychedelic science’.

Since 2010, the foundation, which is based at Beckley Park — her spectacular stately home in Oxfordshire — has funded, or otherwise been involved in, the research for almost 60 papers published in scientific journals investigating the properties and therapeutic potential of illicit mind-altering drugs including LSD, ecstasy and psilocybin (the active ingredient in magic mushrooms).

‘None of it would have been possible without Amanda and the Beckley Foundation,’ Dr Robin Carhart-Harris, the head of Imperial’s Psychedelic Research Group, told a newspaper in 2015.

Good Health has learned that at least five British universities have accepted money from the foundation. Imperial College London has received £108,519 since 2009, while the University of Exeter received £11,488 for a study on cannabidiol (a component of cannabis).

The Institute of Psychiatry at King’s College London was given £4,000, also for cannabis studies, and Cardiff University says the foundation has agreed to give it £50,000 to investigate ecstasy for post-traumatic stress disorder.

University College London (UCL) says it has ‘no record of any philanthropic donations from the Beckley Foundation or Amanda Feilding’. But between 2012 and 2015 Feilding collaborated with Val Curran, a professor of psychopharmacology at UCL.

One 2012 paper on cannabis, on which Professor Curran and Feilding are co-authors, clearly states the study was part-funded by the Beckley Foundation. Another paper published in 2013 and co-authored by Feilding looking at ‘the harms and benefits’ of psychoactive drugs acknowledges as ‘a potential conflict of interest . . . the study was funded by the Beckley Foundation which seeks to change global drug policy’.

The Beckley Foundation has a lot of money at its disposal. Accounts filed with the Office of the Scottish Charity Regulator show that between 2013 and 2017 it had an income of £2.26 million.

Since 2009 the foundation has supported the Beckley Imperial Research Programme which aims ‘to develop a comprehensive account of how substances such as LSD, psilocybin [and] MDMA [ecstasy] affect the brain to alter consciousness, and how they produce their potentially therapeutic effects’.

Feilding’s involvement doesn’t stop at funding. Despite confirming to Good Health that she has ‘no formal qualifications’, she is credited as a co-author on 37 academic papers published in journals ranging from The Lancet Psychiatry to the Journal of Psychopharmacology (24 of these papers, exploring the potential clinical uses of drugs including psilocybin, LSD and ecstasy, have been published in collaboration with Imperial researchers, including Professor Nutt and Dr Carhart-Harris).

On almost all of these 37 papers on which Feilding is a co-author, her foundation is acknowledged as having funded the research. Yet on almost none is her dual role recognised as a potential conflict of interest.

A spokesperson for the Beckley Foundation said that Feilding had ‘actively participated in the inception, design, and writing up’ of all the papers where she was a co-author. All had been peer-reviewed, ‘which means that the scientific community at large is confident that these results speak for themselves, regardless of the author’s viewpoint or political position’.

But criticism of this unusual arrangement was voiced in January 2017 in a paper in the journal Therapeutic Advances in Psychopharmacology, which queried the merits of a paper on psilocybin published by the Beckley Foundation-funded Imperial College team in the British Journal of Psychiatry in March 2012.

It said: ‘Since detailed information on conflicts of interest has not been provided scepticism may arise as to the role of such foundations [i.e. Beckley] in study design and execution, potentially biasing the results.’

Feilding’s influence extends to the upper reaches of the scientific community. Members of the Beckley Foundation’s scientific advisory board include Sir Colin Blakemore, former chief executive of the Medical Research Council (MRC), which controls much of the public funding for medical research and which, since Sir Colin’s tenure ended, has funded Professor Nutt’s work with psilocybin to the tune of £750,000.

In its annual report for 2017, the Beckley Foundation celebrated the MRC’s backing as ‘the first time UK government funds have been allocated to a classic psychedelic study since before prohibition’.

Sir Colin has been a member of the board since 2001, including during his leadership of the MRC (from 2003 to 2007).

While still head of the MRC, Sir Colin was a co-author with Professor Nutt on a paper in The Lancet that challenged the classification of illegal drugs. ‘Some of the ideas developed in this paper,’ they wrote, ‘arose out of discussion at workshops organised by the Beckley Foundation.’

An MRC spokesperson told us: ‘Neither Colin nor the MRC saw his involvement with the Beckley Foundation as a conflict with his position at the MRC.’

Meanwhile, a spokesperson for the Beckley Foundation said it was ‘an inaccurate shortcut’ to suggest Feilding wanted banned drugs such as LSD legalised for recreational use. Rather, she believed ‘such drugs should be investigated thoroughly, both in terms of their safety and their therapeutic potential, and that their legal scheduling should be based on facts rather than ungrounded beliefs’.

Imperial College London, Amanda Feilding, Professor Nutt and Dr Carhart-Harris did not respond to requests for their comments.

Source: How you have paid to help legalise lethal party drugs | Daily Mail Online May 2018

As the federal government prepares to legalize the recreational use of marijuana, an Ontario judge has ruled that cannabis-induced psychosis led a man to a seemingly hate-filled attack on a family, in what appears to be the first case of its kind in Canadian criminal courts.

The man who committed the attack, Mark Phillips, is a Toronto lawyer with an otherwise clean record, and the great-grandson of Nathan Phillips, a former mayor after whom the civic square in front of Toronto City Hall is named. The 37-year-old pleaded guilty Tuesday to assault causing harm in the Dec. 7 incident in St. Thomas, in southwestern Ontario, in which he cracked a man’s rib with a baseball bat.

Sergio Estepa was with his wife, Mari, teenage son and a family friend, speaking Spanish in the parking lot of a St. Thomas mall when a stranger, Mr. Phillips, approached and told them to stop speaking French, according to evidence in court.

He then came at them with a baseball bat, repeatedly screaming “ISIS,” saying he was arresting the family, and calling for help. The family also called for help.

Ontario Court Justice John Skowronski said that, in ordinary circumstances, such an attack would call for a penitentiary sentence ­– that is, at least two years in federal prison. But he accepted the recommendation of defence lawyer Steven Skurka that Mr. Phillips be given a conditional discharge, on the condition that he complete three years of probation. A conditional discharge means that, once his probation is successfully finished, Mr. Phillips will not have a criminal record.

Addressing the family, whose members had told the court in emotional victim-impact statements about the nightmares and anxiety they had experienced, Justice Skowronski said he wanted them to know that what happened to them was an aberration for the country. “Canada is a country of immigrants, different nations, skin colours, accents, names,” he said, adding that his name had not come from this country.

“This is something that took place because of a mental illness.”

Although Crown prosecutor Lisa Defoe had urged a suspended sentence and probation, which would have left Mr. Phillips with a criminal record, she, too, had accepted the defence argument that the attack was caused by cannabis-induced psychosis.

“At first blush this may appear to be a hate crime,” she told Justice Skowronski, “but it’s important for the Crown not to react emotionally.”

Mr. Skurka had told the court that Peter Collins, a forensic psychiatrist at the Centre for Addiction and Mental Health in Toronto, had uncovered after several sessions with Mr. Phillips that he had been smoking marijuana heavily, including three or four joints earlier on the day of the attack.

With marijuana legalization on the horizon, the case raises questions about mental-health risks and new challenges for the legal system. According to Mr. Skurka, Dr. Collins warned that higher levels than in the past of tetrahydrocannabinol (THC), the active ingredient in cannabis, is creating a higher incidence of drug-induced psychosis.

Mr. Phillips’s parents said he had been having irrational fears about Nazis, Muslims and terrorists. In one incident the same day as the attack, he shouted about North Korea and was kicked out of Air Canada Centre in Toronto.

Dr. Collins ­found that Mr. Phillips’s actions were not those of a hate crime, but of cannabis-induced psychosis.

“In my professional opinion, Mark Aaron Phillips suffered from a drug-induced psychosis in and around the time of the event that led to his arrest,” he wrote in his report.

Mr. Skurka had also read to the court from a medical journal that said that paranoid and grandiose delusions similar to those caused by schizophrenia can also be caused by cannabis use.

“This is someone without any history of discrimination, racism or violence,” Mr. Skurka said in an interview outside the courtroom, after sentencing.

Mr. Estepa said in an interview that he could not understand how a man of Mr. Phillips’s education and training as a lawyer could have been unaware of the effects of marijuana before using it.

“I can’t believe that in 2018, people don’t know that marijuana can affect your mind-state,” he said.

When asked by Justice Skowronski whether he had anything to say, Mr. Phillips replied, “I’m very, very sorry for what happened.”

Mr. Phillips withdrew from his practice of personal injury law after the incident, but hopes to resume working as a lawyer. He will need the Law Society of Ontario’s approval to do so.

Mr. Estepa met his wife after they moved to Canada separately from Colombia in the early 2000s. In his victim-impact statement, he described the pain of hearing his son treated as an outsider.

“Here in his home country, someone told him, ‘You don’t belong here.’ ”

Source: Marijuana-induced psychosis behind Toronto lawyer’s bat attack, judge rules – The Globe and Mail April 2018

High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other.

The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found.

The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient.

Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity.

“If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts.

“The difference is there whether you have psychosis or not, and we think this is strictly related to the potency of the cannabis,” she added. Details of the study are reported in the journal Psychological Medicine.

The scans found that daily users of high-potency cannabis had a slightly greater – by about 2% – “mean diffusivity” in the corpus callosum. “That reflects a problem in the white matter that ultimately makes it less efficient,” Dazzan told the Guardian. “We don’t know exactly what it means for the person, but it suggests there is less efficient transfer of information.”

The study cannot confirm that high levels of THC in cannabis cause changes to white matter. As Dazzan notes, it is may be that people with damaged white matter are more likely to smoke skunk in the first place.

“It is possible that these people already have a different brain and they are more likely to use cannabis. But what we can say is if it’s high potency, and if you smoke frequently, your brain is different from the brain of someone who smokes normal cannabis, and from someone who doesn’t smoke cannabis at all,” she said.

But even with the uncertainty over cause and effect, she urged users and public health workers to change how they think about cannabis use. “When it comes to alcohol, we are used to thinking about how much people drink, and whether they are drinking wine, beer, or whisky. We should think of cannabis in a similar way, in terms of THC and the different contents cannabis can have, and potentially the effects on health will be different,” she said.

“As we have suggested previously, when assessing cannabis use, it is extremely important to gather information on how often and what type of cannabis is being used. These details can help quantify the risk of mental health problems and increase awareness of the type of damage these substances can do to the brain,” she added.

In February, Dazzan and others at the Institute of Psychiatry reported that the ready availability of skunk in south London might be behind a rise in the proportion of new cases of psychosis being attributed to cannabis.

Source: Smoking high-strength cannabis may damage nerve fibres in brain | Drugs | The Guardian November 2015

Yasmin L. HurdOlivier J. ManzoniMikhail V. PletnikovFrancis S. LeeSagnik Bhattacharyya and Miriam Melis

Abstract

The recent shift in sociopolitical debates and growing liberalization of cannabis use across the globe has raised concern regarding its impact on vulnerable populations, such as pregnant women and adolescents. Epidemiological studies have long demonstrated a relationship between developmental cannabis exposure and later mental health symptoms. This relationship is especially strong in people with particular genetic polymorphisms, suggesting that cannabis use interacts with genotype to increase mental health risk. Seminal animal research directly linked prenatal and adolescent exposure to delta-9-tetrahydrocannabinol, the major psychoactive component of cannabis, with protracted effects on adult neural systems relevant to psychiatric and substance use disorders. In this article, we discuss some recent advances in understanding the long-term molecular, epigenetic, electrophysiological, and behavioral consequences of prenatal, perinatal, and adolescent exposure to cannabis/delta-9-tetrahydrocannabinol. Insights are provided from both animal and human studies, including in vivo neuroimaging strategies.

Keywords: adolescence; cannabis; cognition; perinatal; psychiatric disorders; reward.

Source: Cannabis and the Developing Brain: Insights into Its Long-Lasting Effects – PubMed (nih.gov) October 2019

Judith Grisel

Occasionally during my love affair with marijuana I would experience perceptual disruptions profound enough to freak me out. One time I was driving along a crowded road when my car seemed a little wobbly and then listed towards the centre, an alarming thud-thud emanating from the back end. In the middle of a densely populated spot without a hard shoulder, I crept slowly across a few lanes of traffic and pulled to a stop. Concentrating very hard, I got out of the car to assess and hopefully change the flat tyre. I rarely got paranoid from smoking weed; neither did it typically make me sleepy. Instead, I was among the lucky ones, as the drug made everyday activities such as gardening, waiting on tables and talking to my family bearable if not interesting. So I was shocked and embarrassed to find, after a few minutes of close inspection amid the honking horns, that there was nothing wrong with the car.

At the time I took hallucinations as evidence of a good score. Now, as an ex-smoker and neuroscientist whose focus is addictive drugs, I know that my resilient response to this stressful experience was contingent on having a neurotypical brain. Neural pathways are forged by finely orchestrated signals for synapse growth and pruning; disruptions can result in atypical neural connections that increase the risk of psychosis. The liability may be unmasked by environmental conditions that can essentially be reduced to an ambiguous but well-recognised bogeyman: stress.

new study in the Lancet Psychiatry journal has attempted to shed light on the relationship between cannabis and psychosis. The authors assessed symptoms such as trouble telling the difference between real and unreal experiences, having false ideas about what is taking place, or who one is, nonsense speech, lack of emotion, and social withdrawal – all core features of the debilitating disorder schizophrenia. Replicating and extending earlier studies, the authors were able to connect cannabis use to increased risk for psychosis.

As anyone who has ever taken a general psychology course well knows, correlation does not mean causation. We would need an experiment to prove this link unequivocally – for example, taking a large group of people and randomly assigning them to using and non-using groups, following them for a number of years and then assessing them for psychotic symptoms. Obviously, that would be unethical. Nevertheless, this study strongly supports the notion that schizophrenia can be precipitated by consuming weed, with high-potency strains a particular concern.

This drug is an increasingly ubiquitous part of modern, socially liberal life. A majority of Americans think it is at least harmless, if not beneficial. The plant contains more than 100 pharmacologically active compounds, called cannabinoids. Of these, the two of primary interest to researchers and consumers are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).

In 1964 we learned that THC is responsible for the drug’s recreational high. Two key discoveries followed. First, THC produces its effects (perceptual distortions, changes in thinking and euphoria, for example) by interacting with a particular class of cell receptors. These CB1 receptors are present in virtually every synapse – the point at which brain cells convey information to each other. Such wide distribution indicates that they play a critical role in most, if not all, brain activity. That’s not because we evolved to enjoy smoking weed. It’s because those plants happen to mimic signalling molecules found in our bodies – endocannabinoids – just like morphine mimics our endorphins. It seems that one role of endocannabinoids is to help highlight especially important communication. When something meaningful happens, the release of these molecules helps ensure that relevant circuits in the brain take note.

The primary difference between THC and our brain’s own cannabinoids is dosing. Neurotransmission occurs in a targeted, local manner appropriate to specific demands. After using cannabis, all brain circuits are flooded with THC, so the process of sorting meaning from the mundane is disrupted. Everyday occurrences such as eating a meal, listening to music, watching television or driving a car become soaked with import. For someone with hearty neural connections who is resilient to stress, this can be a real treat, but for those whose ability to cope and sort is naturally less robust, including those with a susceptibility schizophrenia, it can be a threat.

Well designed, placebo-controlled studies on cannabis are still lacking. In particular, we need more research to distinguish between the effects of THC and those of CBD. The latter compound counteracts the effects of THC and has therapeutic promise for a number of health conditions. There seems no reason therefore not to make CBD widely available, but plenty to suggest careful consideration before embracing THC.

We are swept up in a backlash against overly restrictive and unscientific regulation of cannabis. While it is well past time to loosen restrictions, promote research and consider the data that emerges, the Lancet study provides evidentiary warning about the inherent dangers – to some – of our quest to mitigate reality.

Most societies take it upon themselves to provide appropriate assistance for those with disability; they ought also to take reasonable measures to prevent those disabilities occurring, when possible. Addiction and psychosis are similar in that they are the result of biological vulnerability combined with a stressful environment. Some are more predisposed than others, and this should provoke ethical and moral obligation – particularly from those of us who are not at risk – to protect the unlucky ones for whom the use of cannabis may be permanently detrimental.

  • Judith Grisel is a behavioural neuroscientist and author of Never Enough: The Neuroscience and Experience of Addiction

Source: Can we all chill out about cannabis? Not quite yet | Judith Grisel | The Guardian 24th March 2019

Abstract

Importance: Despite studies showing that repeated cannabis use may worsen depressive symptoms, the popular media increasingly presents cannabis as beneficial to mental health, and many members of the public view cannabis as beneficial for depression. Therefore, cannabis use among individuals with depression may be becoming more prevalent.

Objective: To examine the association of depression with past-month cannabis use among US adults and the time trends for this association from 2005 to 2016.

Design, setting, and participants: This repeated cross-sectional study used data from 16 216 adults aged 20 to 59 years who were surveyed by the National Health and Nutrition Examination Survey, a national, annual, cross-sectional survey in the United States, between 2005 and 2016. Data analysis was conducted from January to February 2020.

Exposures: Survey year and depression, as indicated by a score of at least 10 on the Patient Health Questionnaire-9.

Main outcomes and measures: Any past-month cannabis use (ie, ≥1 use in the past 30 days) and daily or near-daily past-month cannabis use (ie, ≥20 uses in the past 30 days). Logistic regression was used to examine time trends in the prevalence of cannabis use, depression, and the association between cannabis use and depression from 2005 to 2016.

Results: The final analysis included 16 216 adults, of whom 7768 (weighted percentage, 48.9%) were men, 6809 (weighted percentage, 66.4%) were non-Hispanic White participants, and 9494 (weighted percentage, 65.6%) had at least some college education. They had a weighted mean age of 39.12 (95% CI, 38.23-39.40) years. Individuals with depression had 1.90 (95% CI, 1.62-2.24) times the odds of any past-month cannabis use and 2.29 (95% CI, 1.80-2.92) times the odds of daily or near-daily cannabis use compared with those without depression. The association between cannabis use and depression increased significantly from 2005 to 2016. The odds ratio for depression and any past-month cannabis use increased from 1.46 (95% CI, 1.07-1.99) in 2005 to 2006 to 2.30 (95% CI, 1.82-2.91) in 2015 to 2016. The odds ratio for depression and daily or near-daily past-month cannabis use increased from 1.37 (95% CI, 0.81-2.32) in 2005 to 2006 to 3.16 (95% CI, 2.23-4.48) in 2015 to 2016.

Conclusions and relevance: The findings of this study indicate that individuals with depression are at increasing risk of cannabis use, with a particularly strong increase in daily or near-daily cannabis use. Clinicians should be aware of these trends and the evidence that cannabis does not treat depression effectively when discussing cannabis use with patients.

Conflict of interest statement

Conflict of Interest Disclosures: None reported.

Cannabis Use and Health 2014
Introduction

Cannabis is a group of substances from the plant cannabis sativa. Cannabis is used in three main forms: flowering heads, cannabis resin (hashish) and cannabis oil. There are more than 60 psycho-active chemicals in cannabis, including the cannabinoids:
 delta-9 tetrahydrocannabinol (THC), which is found in the resin covering the flowering tops and upper leaves of the female plant and which alters mood and produces the feeling of a ‘high’;
and
 cannabidiol, which can offset the effects of THC.

Cannabis is usually smoked, either in a hand-rolled cigarette (a ‘joint’) containing the leaf, heads or resin of the plant, or through a water-pipe (a ‘bong’) where water is used to cool the smoke before it is inhaled. In Australia, cannabis is also commonly known as gunja, yarndi, weed and dope.

Patterns of Cannabis Use in Australia and its Public Health Impacts

In 2010, cannabis was the most commonly used illicit drug in Australia. Over one third of Australians (35.4%, approximately 6.5 million) aged 14 years and over had used cannabis at least once in their lifetime, and 1.9 million of these had used cannabis recently (i.e., in the last 12
months). Recent cannabis use among those 14 years and older has increased from 9.1% in 2007 to 10.3% in 2010, though daily users decreased from 14.9% in 2007 to 13% in 2010. In 2010, approximately 247,000 Australians 14 years and over used cannabis daily. For most cannabis users, use is relatively light. Most young people have used it once or twice. However, the younger people start using cannabis, and the greater the frequency with which they use it, the greater the risk of harm.
Based on current use patterns, alcohol abuse and tobacco pose much greater harms to individual and public health in Australia than cannabis. Cannabis-related psychosis, suicide, road-traffic crashes and dependence were estimated to account for 0.2% of the total disease burden in Australia in 2003. This compares to 7.8% of the total burden attributable to tobacco use and 2.3% attributable to alcohol use. In 2004-05, the estimated social costs of cannabis use (including health, crime, road crash and labour costs) was $3.1 billion. Ninety percent of this cost was due to dependent cannabis use. In comparison, the health, crime, road-crash and labour costs of alcohol use in 2004-05 are estimated to be more than three times as much ($9.4 billion).

The Health Effects of Cannabis Use

There is a dose-response relationship between cannabis use and its effects, with stronger effects
expected from larger doses.
 Intoxicating effects occur within seconds to minutes and can last for three hours;
 Effects last longer with larger doses;
 Effects on cognitive function and coordination can last up to 24 hours;
 Short-term memory impairment may last for several weeks; and
 A single dose in a chronic user can take up to 30 days for the metabolites to be excreted.

Short-term effects of small doses
The most common short-term effects of using cannabis are:
 a feeling of euphoria or ‘high’ – with a tendency to talk and laugh more than usual;
 impaired balance, reaction time, information processing, memory retention and retrieval, and perceptual-motor coordination;
 increased heart rate;
 decreased inhibitions such as being more likely to engage in risky behaviour, e.g. unsafe
sexual practice; and
 if smoked, increased respiratory problems including asthma.

Short-term effects of large doses
The most common short-term effects of a large dose can include:
 hallucinations and changed perceptions of time, sound, colour, distance, touch and other sensations;
 panic reactions;
 vomiting;
 loss of consciousness; and
 restlessness and confusion.

The severity of these short-term effects depend on a person’s weight, tolerance to the drug, amount taken, interactions with other drugs, circumstances in which the drug is taken, and the mode of administration.

Long-term effects
The evidence associating regular cannabis use with specific long-term health conditions and adverse effects is of variable quality. Cannabis use is highly correlated with use of alcohol, tobacco and other illicit drugs, all of which have potential adverse health effects. There is sufficient evidence, however, to indicate that cannabis is a risk factor for some chronic health effects and conditions.

Regular and prolonged cannabis use may cause:
 cannabis dependence, characterised by impaired control over its use and difficulties in ceasing use; increased tolerance (meaning more of the drug is needed to produce the same effect) and possible withdrawal symptoms, including anxiety, insomnia, appetite disturbance, and
depression;
 increased risk of myocardial infarction in those who have already had a myocardial infarction;
and
 deficits in verbal learning, memory and attention (in heavy users).

While not conclusive, there is evidence that regular cannabis use can cause chronic bronchitis and impaired immunological competence of the respiratory system. Occasional cannabis use however, is not associated with adverse effects on pulmonary function. Cannabis smoke contains many carcinogens, but there is variable evidence concerning the relationship between cannabis smoking and lung cancer.

Evidence supporting an association between cannabis use and sexual and reproductive effects is weak. However, some studies show an association between cannabis use and increased risk of testicular cancer.
Daily consumption of large quantities of cannabis may lead to the neglect of other important personal and social priorities such as relationships, parenting, careers and community responsibilities.

Pregnant women
Cannabis is the most commonly used illicit drug in women of child-bearing age. Cannabis use during pregnancy has been consistently associated with lower birth-weight babies and pre-term birth, but does not appear to increase the risk of miscarriage or birth abnormalities. Some studies suggest that children exposed to cannabis in utero may have slight impairment in higher cognitive processes such as perceptual organisation and planning. There is insufficient evidence of an association between prenatal cannabis use and postnatal behaviour.

Accidental ingestion by young children
Accidental ingestion of cannabis can cause coma in young children. Cannabis ingestion can be confirmed by positive urine screening for cannabinoids. Cannabis ingestion needs to be considered in toddlers and children with impaired consciousness.

Driving under the influence of cannabis
Cannabis slows reaction time and increases the risk of having a car crash. Other risk factors are blurred vision, poor judgement and drowsiness which can persist for several hours. The effects are increased by alcohol.

Dependence and tolerance
Cannabis dependence is usually defined as impaired control over continued use and difficulty ceasing despite the harms of continued use.19 Dependence can negatively affect personal relationships, education, employment and many other aspects of a person’s life. Data from Australia and other countries indicates that demand for professional help related to cannabis is increasing. Cannabis dependence is the most frequent type of substance-dependence in Australia after alcohol and tobacco. It has been estimated that cannabis dependence will affect around one in ten cannabis users, and around half of those who use it daily. Animal and human studies demonstrate that tolerance to many of the psychological and behavioural responses to cannabis occurs with repeated exposure to the drug. The symptoms of withdrawal from cannabis appear similar to those associated with tobacco, but less severe than withdrawal from alcohol or opiates.

There is a view that the cannabis being used today has a higher THC content and potency than in the past. This may be a perception caused by changes in the mode of use (i.e. through ‘bongs’ rather than ‘joints’, and with more consumption of the heads of the cannabis plant). However, there is some independent evidence that cannabis used today can be of a higher potency. The cannabis in recent street-level seizures in Sydney and the North Coast of NSW has been shown to have a high potency, with around 15% THC, with little or no cannabidiol.

Cannabis as a Gateway Drug
The gateway hypothesis is that cannabis use may act as a causal ‘gateway’ to the use of other illicit drugs such as cocaine and heroin. It is a controversial hypothesis with proponents arguing that because the use of so-called harder drugs is almost always preceded by cannabis use, this means that cannabis use physiologically and/or psychologically causes people to progress to harder drugs. The alternative theory is known as the ‘common cause’ theory whereby a person’s use of cannabis and their later use of other illicit drugs are both seen as effects of common causes such as personal or socio-economic factors, or exposure to illicit drug distribution networks. Evidence for the gateway hypothesis is inconclusive given the difficulties in disentangling the effect of other potential influences in drug use progression. Meta-analyses suggest that the progression in use that has been observed is likely to be due partially to the influence of independent common
causes.

Cannabis and Mental Health

Cannabis and psychosis
Cannabis use is associated with poor outcomes in existing psychosis and is a risk factor for developing psychosis. For those with existing psychosis, using cannabis can trigger further episodes of psychosis, worsen delusions, mood swings, hallucinations and feelings of paranoia, as well as contributing to poor compliance with medication regimes. The research base on cannabis and psychosis has expanded in recent years with studies showing a consistent association between early-aged onset of cannabis use, regular use and a later diagnosis of schizophrenia. Meta-analyses have noted a doubling of the risk of psychotic outcomes in regular cannabis users, and earlier onset (by 2.7 years) among cannabis users who develop psychosis.
There is increasing evidence that the association between cannabis and onset of psychosis is not due to other co-occurring factors. The most plausible view is that cannabis use is a ‘contributory cause’ of psychosis in vulnerable individuals, and that it is one of a number of potential factors that can bring on psychosis (including genetic predisposition)’

Cannabis and depression
The association between cannabis use and depression is weak and insufficient to establish a causal connection. Studies that have found an association are likely to have been affected by confounding variables such as family and personality factors, other drug use and marital status.
There is currently insufficient evidence available to conclude whether cannabis use is associated with suicide. Research is made difficult by confounding factors such as the stresses of an illicit drug-dependent life and pre-existing poor mental health.

Cannabis and anxiety
There is emerging evidence associating cannabis use with anxiety disorders. However, the current level of evidence is not yet sufficient to establish a causal relationship.

Medical Uses Of Cannabis
In addition to psychoactive compounds, cannabis has constituents with other pharmacological effects, including antispastic, analgesic, anti-emetic, and anti-inflammatory actions. These constituents may have therapeutic potential.

Cannabis extracts and synthetic formulations have been licensed for medicinal use in some countries, including Canada, the USA, Great Britain and Germany, for the treatment of severe spasticity in multiple sclerosis, nausea and vomiting due to cytotoxics, and loss of appetite and cachexia associated with AIDS. The synthetic cannabis product Nabiximols (Sativex), which is delivered as a buccal spray and so avoids the harms of cannabis smoke inhalation, is effective in the management of spasticity and pain associated with multiple sclerosis. The psycho-active effects of Nabiximols can also be managed through controlling dosage.

In Australia, the synthetic cannabinoids nabilone and dronabinol are scheduled by authorities for medicinal use. Sativex is also being trialed in Australia for cancer and cannabis withdrawal. Canada has allowed the medical use of smoked cannabis if this is authorised and monitored by a doctor.
There is a growing body of evidence that certain cannabinoids are effective in the treatment of chronic pain, particularly as an alternative or adjunct to the use of opiates, when the development of opiate tolerance and withdrawal can be avoided. Controlled trials have also shown positive effects of cannabis preparations on bladder dysfunction in multiple sclerosis, tics in Tourette syndrome, and involuntary movements associated with Parkinson’s disease. Based on existing data, the adverse events associated with the short-term medicinal use of cannabis are minor.
However, the risks associated with long-term medicinal use are less well understood, particularly the risk of dependence, and any heightened risk of cardiovascular disease. Though there is a growing body of evidence regarding the therapeutic use of cannabinoids, it is still experimental.

Synthetic Cannabis
Synthetic cannabis products have been developed, usually in herbal form for smoking. These products have been marketed in Australia as ‘legal highs’ with product names such as ‘Spice’, ‘K2’, and ‘Kronic’. The psychoactive components are usually THC analogues that bind to cannabinoid receptors in the brain. These analogues are not easily detectable by routine testing, and until recently have not been captured by legislation. These synthetic cannabis products are attractive to their users because they are perceived as safe, are not easily detectable in drug tests, and until recently have not been illegal.
The synthetic cannabis products can not be considered safe given that the synthesized psychoactive substances in them have not been rigorously tested, and little is known about their long or short-term health effects, dependence potential or adverse reactions. Psychotic
symptoms have been associated with use of some synthetic cannabinoids, as well as signs of addiction and withdrawal symptoms similar to those of cannabis. Adverse outcomes have been reported from the use of Kronic in Australia.

The Control of Cannabis Use and Supply

Australian legislation
The possession, cultivation, use, and supply of cannabis is prohibited in all Australian States and Territories. In some Australian jurisdictions there are criminal penalties for the possession, cultivation and use of cannabis, and in others there are less severe civil penalties. Legislation in Australia often distinguishes between possession of small amounts of cannabis (for personal use) possession of larger amounts (trafficable quantities), and possession of even larger “commercially trafficable” quantities. The supplying of cannabis and the possession of large quantities attract criminal penalties in all Australian jurisdictions. All Australian States and Territories have diversionary schemes for minor and early cannabis offenders which require them to undertake educative and treatment programs as an alternative to receiving a criminal penalty.

Criminalisation and health
It is often thought that criminal penalties are a deterrent to cannabis use and, therefore, an effective way to prevent the health impacts and other harms associated with cannabis use. These beliefs have little foundation. A system of criminal prohibition for cannabis use applied in Australia for many years, but the incidence of cannabis use was still significant. The introduction of less serious civil penalties and diversionary alternatives to criminal sanctions did not significantly increase the rates of uptake and use among Australians.

For those who are not deterred from use by criminal penalties, criminalisation can add to the potential health and other risks to which cannabis users are exposed. These include:

 exposure of cannabis users, including teenage and occasional users, to ‘harder drugs’. Those who acquire cannabis from large scale illicit drug distribution networks will also become exposed to more harmful drugs, including the direct marketing of those drugs to them;
 exposure of cannabis users to criminal networks and activity, including exposure to the threat of violence and the risk of taking part in criminal distribution;
 the personal and health-related costs of a criminal conviction. A criminal conviction can negatively impact on a person’s employment prospects and their accommodation and travel opportunities. Limited employment and accommodation prospects can lead to poor health,
including mental health. Individuals with a criminal record are also at a disadvantage in any subsequent criminal proceedings;
 a deterrent to individuals seeking health advice, treatment and support regarding their cannabis use;
 the inability to collect high quality, reliable data regarding patterns of use and harms.

Harm reduction
A harm-reduction approach is defined as policies and initiatives that aim to reduce the adverse health, social and economic consequences of substance use to individual drug users, their families and the community. Harm reduction considers both the potential harms to individuals using substances like cannabis and the potential harms and negative impacts of the different approaches for controlling the use and supply of these substances. When harm reduction is the primary goal, the key policy focus will be on measures to reduce individuals’ harmful levels of cannabis use, or cannabis use among individuals who are most vulnerable to adverse health impacts, or cannabis use in contexts which involve serious risks to users.

Harm-reduction measures include targeted efforts to reduce the supply of cannabis and to reduce demand for it among vulnerable groups. In certain contexts, and with certain groups, measures emphasizing abstinence may also contribute, in a preventive way, to reducing harms. Policy and legislative approaches that do not effectively address cannabis-related harms or create
significant risks and adverse impacts are not consistent with harm-reduction. Prohibition of cannabis use with criminal penalties has the potential to produce harms and risks. The effectiveness of criminal prohibition of cannabis use in reducing the health-related harms
associated with cannabis use is questionable.

Treatment Options
The number of people seeking treatment for cannabis use is increasing, but most of those who experience cannabis dependence do not seek help. Many regular cannabis users do not believe they need treatment, and there is also a low awareness of the treatment options available and how to access them.
There are fewer treatment options for cannabis dependence than for alcohol or opiate dependence, and limited research on the effectiveness of different cannabis treatment options. Treatments for problematic cannabis use include psychological interventions such as cognitive
behavioural therapy and motivational enhancement, and pharmacological interventions with medications to ease the symptoms of withdrawal or block the effects of cannabis. The research on pharmacological interventions for cannabis is in its infancy, with medications still in the experimental stages of development.

Cognitive behavioural therapy helps the cannabis user develop knowledge and skills to identify risk situations when using cannabis and to modify behaviour accordingly. Motivational enhancement techniques build the cannabis user’s desire to address their problematic use. These counseling interventions are increasingly available online as web-based programs, as well as face-to-face with a counselor. Online programs have the advantage of convenience and anonymity, for those who are concerned about possible stigma. Difficulties in maintaining motivation, and limitations in personalising the programs to individual needs, are drawbacks. According to current research, web-based treatment programs may not be as effective as in-person treatment. Some problematic cannabis users have particular treatment needs, including those with cannabis dependence and mental health issues. These individuals require integrated treatment and coordinated care. General practitioners can play an important role in developing a coordinated care plan to suit the needs of these patients.

The Australian Medical Association Position
The AMA acknowledges that cannabis use is harmful and can lead to adverse chronic health outcomes, including dependence, withdrawal symptoms, early onset psychosis and the exacerbation of pre-existing psychotic symptoms. While the absolute risk of these outcomes is low and those who use cannabis occasionally are unlikely to be affected, those who use cannabis frequently and for sustained periods, or who initiate cannabis use at an early age, or who are susceptible to psychosis, are most at risk.
The AMA also recognises that cannabis use has short-term effects on cognitive and perceptual functioning which can present risks to the safety of users and others. The AMA believes that cannabis use should be seen primarily as a health issue and not primarily as a matter for law enforcement. The most appropriate response to cannabis use should give priority to policies, programs and regulatory approaches that reduce the harms potentially associated with cannabis use, and particularly the health-related harms. The positions outlined below should be read in the light of this harm-reduction principle. The AMA believes the following are the important considerations and central elements in an appropriate harm-reduction response to cannabis use.

Prevention and Early Intervention
 As younger people and those who use cannabis frequently are most at risk of harm, prevention and early intervention initiatives to avoid, delay and reduce the frequency of cannabis use in these populations are essential.
 All children should have access to developmentally appropriate school-based life-skills programs to assist in preventing or reducing potential substance use problems.
 Evidence-based information on the potential risks of cannabis use and where to seek further assistance should be widely available, particularly to young people.
 Medical professionals can play an important role in the early identification of patients they believe to be at risk of adverse health outcomes from cannabis use.
 When a cannabis user comes into contact with law enforcement or justice administration agencies this should be used as an opportunity to direct them to education, counseling or treatment. This is particularly important with young and first time or early offenders.

Diagnosis and Treatment
 Medical professionals have the knowledge and opportunity to screen for and diagnose cannabis-related disorders, including dependence, withdrawal symptoms, and cannabis induced psychosis. Referral networks and linkages should be established within regions between primary care and specialist mental health and drug and alcohol services, to ensure integrated and coordinated treatment support for cannabis use problems.
 Medical professionals, particularly general practitioners, have the opportunity to counsel patients who are at risk of cannabis-related harms, and they should be supported to provide education and advice about those potential harms.
 Targeted treatment regimens should be developed and resourced for groups with particular needs, including those with dual diagnoses, multiple drug use, young teenage users and culturally appropriate services for Aboriginal peoples and Torres Strait Islanders. Of particular importance are suitable treatment services for cannabis users with mental health needs.
 Every effort should be made to address the personal and systemic barriers that cannabis users face in seeking treatment and support when they need it. These include barriers associated with perceptions of stigmatisation, users’ and professionals’ awareness of treatment options, and users’ beliefs that they do not have a health problem.
 Doctors should consider accidental cannabis ingestion in the differential diagnosis of children with impaired consciousness.
 Cannabis users should have access to the rehabilitative services and support they require to manage associated disorders and particularly the risk of relapse.

Medical Uses of Cannabis
The Australian Medical Association acknowledges that cannabis has constituents that have potential therapeutic uses.
 Appropriate clinical trials of potentially therapeutic cannabinoid formulations should be conducted to determine their safety and efficacy compared to existing medicines, and whether their long-term use for medical purposes has adverse effects.
 Therapeutic cannabinoids that are deemed safe and effective should be made available to patients for whom existing medications are not as effective.
 Smoking or ingesting a crude plant product is a risky way to deliver cannabinoids for medical purposes. Other appropriate ways of delivering cannabinoids for medical purposes should be developed.
 Any promotion of the medical use of cannabinoids will require extensive education of the public and the profession on the risks of the non-medical use of cannabis.

Law Enforcement, Cannabis Regulation and Health
 In assessing different legislative and policy approaches to the regulation of cannabis use and supply, primary consideration should be given to the impact of such approaches on the health and well-being of cannabis users.
 The AMA does not condone the trafficking or recreational use of cannabis. The AMA believes that there should be vigorous law enforcement and strong criminal penalties for the trafficking of cannabis. The personal recreational use of cannabis should also be
prohibited. However, criminal penalties for personal cannabis use can add to the potential health and other risks to which cannabis users are exposed. The AMA believes that it is consistent with a principle of harm reduction for the possession of cannabis for personal
use to attract civil penalties such as court orders requiring counselling and education (particularly for young and first time offenders), or attendance at ‘drug courts’ which divert users from the criminal justice system into treatment.
 When cannabis users come into contact with the police or courts, the opportunity should be taken to divert those users to preventive, educational and therapeutic options that they would not otherwise access.
 In allocating resources, priority should be given to policies, programs and initiatives that reduce the health-related risks of cannabis use. Law enforcement should be directed primarily at cannabis supply networks.
 The AMA believes that the availability and use of synthetic cannabis products (including herbal forms) poses significant health risks, given that the psychoactive chemical constituents of these products are unknown and unpredictable in their effect. There are
particular challenges in regulating these products, and Australian governments must make a concerted effort to develop consistent and effective legislation which captures current and emerging forms of synthetic cannabis.

Research
 Further research is needed into the relationship between cannabis use and psychosis and other mental health problems, including the identification of those at greatest risk of cannabis-induced psychosis.
 There should be continuing research to identify the risk factors that contribute to individuals developing problematic or early onset cannabis use, and the factors and interventions that can protect against these.
 Australian governments should fund research into best practice treatment methods, including suitable pharmacotherapies, for those who are cannabis-dependent or who wish to reduce or cease their use.
 There should be systematic ongoing monitoring of the different legislative and policy approaches on cannabis operating in overseas jurisdictions to assess their health and harm-related impacts. The evidence obtained should inform critical reviews of the
approaches that operate in Australia.

Source: 1 (ama.com.au) 2014

Abstract

Background: Little is known about the relative harms of edible and inhalable cannabis products.

Objective: To describe and compare adult emergency department (ED) visits related to edible and inhaled cannabis exposure.

Design: Chart review of ED visits between 1 January 2012 and 31 December 2016.

Setting: A large urban academic hospital in Colorado.

Participants: Adults with ED visits with a cannabis-related International Classification of Diseases, Ninth or 10th Revision, Clinical Modification (ICD-9-CM or ICD-10-CM), code.

Measurements: Patient demographic characteristics, route of exposure, dose, symptoms, length of stay, disposition, discharge diagnoses, and attribution of visit to cannabis.

Results: There were 9973 visits with an ICD-9-CM or ICD-10-CM code for cannabis use. Of these, 2567 (25.7%) visits were at least partially attributable to cannabis, and 238 of those (9.3%) were related to edible cannabis. Visits attributable to inhaled cannabis were more likely to be for cannabinoid hyperemesis syndrome (18.0% vs. 8.4%), and visits attributable to edible cannabis were more likely to be due to acute psychiatric symptoms (18.0% vs. 10.9%), intoxication (48% vs. 28%), and cardiovascular symptoms (8.0% vs. 3.1%). Edible products accounted for 10.7% of cannabis-attributable visits between 2014 and 2016 but represented only 0.32% of total cannabis sales in Colorado (in kilograms of tetrahydrocannabinol) during that period.

Limitation: Retrospective study design, single academic center, self-reported exposure data, and limited availability of dose data.

Conclusion: Visits attributable to inhaled cannabis are more frequent than those attributable to edible cannabis, although the latter is associated with more acute psychiatric visits and more ED visits than expected.

Primary funding source: Colorado Department of Public Health and Environment.

Figures

Flow chart of visit selection and review. 

ED = emergency department; ICD = International Classification of Diseases.

Figure 2.. Exposure to edible and inhalable cannabis products in cannabis-attributable visits at UCHED from 2012 to 2016. 

Error bars indicate 95% CIs. UCHED = UCHealth University of Colorado Hospital Emergency Department.

It’s no secret that substance use disorders (SUDs) can negatively impact the individual struggling, even putting their life in jeopardy.

“For persons with SUDs, their brain is telling them this lie that, ‘You’ve got to use to stay alive,'” said Sterling Shumway, chair of the Texas Tech University Department of Community, Family & Addiction Sciences and director of the Institute for the Study of Addiction, Recovery & Families.

Likewise, groundbreaking new research now indicates that the same thing is happening in the brains of the people caring for those with addiction.

“To further understand the etiology of SUDs and their associations with family systems, research must expand beyond examining the individual struggling with an SUD,” said Shumway, co-principal investigator (P.I.) for the ongoing project. “This includes research that helps us understand the neurological impact of stress, fear and the impairment found in the family system.”

The original hypothesis was that if the person struggling with an SUD’s brain is compelling them to use as a survival mechanism, perhaps the family member’s brain is doing the same thing as it relates to their loved one’s survival, thus leading to the mostly ineffective and compulsive attempts to rescue their loved one.

“It’s really first-of-a-kind research,” Shumway said, “looking to see if the person and their family member have become similarly, what we call, ‘co-impaired.'”

Looking inside the brain

Over the last four years, Shumway and co-P.I. Spencer Bradshaw, director of the Center for Addiction Recovery Research and an assistant professor in the department, have been using functional near-infrared spectroscopy (fNIR) to monitor reactions in the frontal cortex of both those in recovery from an SUD and family members as they participate in a research protocol presenting certain audio and visual cues meant to stimulate the prefrontal cortex (PFC).

“For the person who struggles with alcoholism, this protocol involves sounds and a variety of images that evoke strong emotional responses, including images associated with alcohol. We look at how their brain lights up differently in response to these various images,” Shumway said. “When family members come in, they aren’t presented a picture of a glass of alcohol, they see instead a current image of their loved one seeking recovery. That’s what makes this research groundbreaking, in that a family member’s PFC lights up in a similar way when looking at their addicted loved one as the PFC of someone with an SUD when looking at their substance of choice.”

When the fNIR results showed that family members often exhibited similar impairment and decision-making difficulties as those with an SUD, Shumway and Bradshaw realized they needed to look deeper inside the brain to explain this phenomenon.

“This is the next step in our research: to look at the family member brain at the level of the midbrain – a much deeper, more primitive part of the brain – and compare it with the brains of those struggling with an SUD,” Shumway said. “We want to know if a similar process is also occurring there with respect to these deeper brain structures and their interaction with the PFC.”

Now, with the help of the Texas Tech Neuroimaging Institute, the two are using functional magnetic resonance imaging (fMRI) to do just that.

“What comes from the midbrain is what causes addicts to use – it’s this intense pain associated with craving. Craving is the means by which the brain compels a person to do something they wouldn’t normally do as part of a survival response – that is, to use despite harmful consequences,” Shumway said. “In relation to a person struggling with an SUD, their brain is telling them, ‘You must use drugs and alcohol, or you’re going to die.'”

This message becomes so intrusive that it overrides the more rational frontal cortex, which is attempting to get them to consider the negative consequences. Unfortunately, when the disease of addiction is present, the midbrain wins the battle.

“With family members, particularly those who’ve been fighting the longest to keep their loved one alive, we believe similarly that their midbrain begins to compel them toward behaviors that may enable rather than resolve SUD behavior,” Shumway said. “In other words, they’re reacting to keep their loved one alive. They may know it’s not helping, but they’re going to do it anyway just like the person with an SUD is going to find and use their substance. This, because the midbrain is requiring it of them out of a perceived need for survival.”

Testing the hypothesis

Shumway and Bradshaw will use the fMRI to examine different parts of the brain, how they are connected to one another and which parts are being activated by different activities or presentations.

“Brain structures, their connectivity and their functioning are key to what we now understand about the brain of the person with an SUD and are what we are similarly interested in examining with respect to the family member brain,” Bradshaw said.

As before, Shumway and Bradshaw intend to include a control group.

“With a control group, we’ll be able to compare those who have never been around addiction, never been impacted by addiction, and never have had to make the difficult decisions like those in families where addiction is present,” Bradshaw said.

Shumway emphasized the research is likely one-of-a-kind.

“We’re probably the only ones, perhaps in the world, who have looked at the frontal cortex of family members related to the way it is responding,” he said. “And we probably will be one of the first to look at family members and functioning of the midbrain when given certain stimuli.”

‘They need help, too.’

One of the biggest reasons for this research is to try to help the family members of those with an SUD find their own recovery, which also gives their loved one a better chance

.

“You’ve got two brains – the family member’s and the loved one’s brain –that are trying to keep one person alive. The problem is the family members also suffer

,” Shumway said. “They don’t take care of themselves, and they struggle as well. We’re not very good at taking care of those who struggle with substance use disorders; we’re even worse at taking care of the family members.”

Because dynamics differ between families, the person who is the primary caregiver differs as well – and sometimes that role switches between people within a family.

“It’s often those who have cared for these people the longest who have the most personal investment in their lives and their success,” Bradshaw said. “This person could, at times, be a grandparent, a parent or even a sibling. While we usually find this person to be a close family member, it may include a wide umbrella of people who care about this person.”

This so-called “systems approach” to addiction recovery values everybody in the system. The idea is that if the parents, siblings, etc., are doing well, the person with the disorder has a better chance of doing well. And, reciprocally, if the person with the disorder is doing well, that helps the others in the system do well.

“With SUDs and recovery, it’s a team sport,” Shumway said. “The more people on the team who are healthy makes a big difference in terms of the trajectory of success.”

While the researcher say society if often most concerned about the identified patient with the SUD, and that’s important, it’s not the whole story.

“The health of every family member is important,” Bradshaw said. “Research shows that when family members are impacted by the stress of addiction, they go to the doctor more often, they have higher medical claims and services and they get diagnosed with higher rates of depression.”

Therefore, resources are needed for both the loved one with the SUD and the family member.

“Both deserve happiness and quality of life,” Bradshaw said.

Brain Research: In the Same Way Addiction Sufferers Crave Substances, Their Family Members Crave Them | Texas Tech Today | TTU

 

 

Abstract

Background

Epigenetic modifications of a gene have been shown to play a role in maintaining a long‐lasting change in gene expression. We hypothesize that alcohol’s modulating effect on DNA methylation on certain genes in blood is evident in binge and heavy alcohol drinkers and is associated with alcohol motivation.

Methods

Methylation‐specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and proopiomelanocortin (POMC) genes in peripheral blood samples collected from non-smoking moderate, non-binging, binge, and heavy social drinkers who participated in a 3‐day behavioral alcohol motivation experiment of imagery exposure to either stress, neutral, or alcohol‐related cues, 1 per day, presented on consecutive days in counterbalanced order. Following imagery exposure on each day, subjects were exposed to discrete alcoholic beer cues followed by an alcohol taste test (ATT) to assess behavioral motivation. Quantitative real‐time PCR was used to measure gene expression of PER2 and POMC gene levels in blood samples across samples.

Results

In the sample of moderate, binge, and heavy drinkers, we found increased methylation of the PER2 and POMC DNA, reduced expression of these genes in the blood samples of the binge and heavy drinkers relative to the moderate, non-binge drinkers. Increased PER2 and POMC DNA methylation was also significantly predictive of both increased levels of subjective alcohol craving immediately following imagery (< 0.0001), and with presentation of the alcohol (2 beers) (< 0.0001) prior to the ATT, as well as with alcohol amount consumed during the ATT (< 0.003).

Conclusions

These data establish significant association between binge or heavy levels of alcohol drinking and elevated levels of methylation and reduced levels of expression of POMC and PER2 genes. Furthermore, elevated methylation of POMC and PER2 genes is associated with greater subjective and behavioral motivation for alcohol.

Source:  https://doi.org/10.1111/acer.13932  31st December 2018

 

We are pleased to announce that a new online course at Auburn University Outreach will feature The Marijuana Report website and e-newsletter. Titled “The Harmfulness of Marijuana Use and Public Policy Approaches to Address the Challenges,” the three-week course will be taught by Paula Gordon, PhD, who has worked as a staff member and/or consultant to several federal agencies concerned about addiction treatment and prevention. Course topics will address:

  • The need to defend the brain while nurturing mental and physical well-being: fostering a mental and public health approach to addressing the challenges of drug use and addiction.
  • An extraordinary look at the addiction cycle: the lessons and insights from an October 30, 2013, videotaped exchange between Dr. Nora Volkow and the Dalai Lama in Dharamshala, the morning of Day 3 of the workshop series (See the link here).
  • Comprehensive coordinated strategies aimed at stopping the use of marijuana and other psychoactive and addictive substances in the US: proposed comprehensive and coordinated public health oriented strategies involving all sectors of society, including government, the justice system, and educational institutions.

Register here

Source: Email from National Families In Action The Marijuana Report The Marijuana Report.Org August 2017

The authors compare the clinical features of idiopathic psychosis (eg, schizophrenia) with cannabis-induced psychosis.

As cannabis consumption rises, there has been significant emerging evidence for cannabis-related risks. Here: a comparison of the clinical features of idiopathic psychosis (eg, schizophrenia) versus cannabis-induced psychosis (CIP). Scroll through the slides for 8 distinguishing features

Source: https://www.psychiatrictimes.com/view/8-distinguishing-features-primary-psychosis-versus-cannabis-induced-psychosis August 2017

In a pre-clinical study, researchers from Western University in Ontario, Canada, studied the effects of long-term exposure to THC in both adolescent and adult rats.

They found changes in behavior as well as in brain cells in the adolescent rats that were identical to those found in schizophrenia. These changes lasted into early adulthood long after the initial THC exposure.

The young rats were “socially withdrawn and demonstrated increased anxiety, cognitive disorganization, and abnormal levels of dopamine, all of which are features of schizophrenia,” according to the article. The same effects were not seen in the adult rats.

“With the current rise in cannabis use and the increase in THC content, it is critically important to highlight the risk factors associated with exposure to marijuana, particularly during adolescence,” the researchers warn.

Read Medical News Today story here. Read study abstract in the journal Cerebral Cortex here.

Email from Monte Stiles, National Families in Action January 2016

A University of Pittsburgh Medical Center study published in the journal Psychology of Addictive Behaviors last September found that chronic marijuana use during adolescence did not lead to depression, anxiety, psychosis, or asthma by mid-life.

The U.K.’s Independent was one of many newspapers that celebrated the news, scoffing at the National Health Service help page that warns: “Your risk of developing a psychotic illness is higher if you start using cannabis in your teens.”
 
Now, however, the journal has run a correction. It turns out that the researchers misinterpreted their data. They checked it again after criticism of their study and found that there was a two-and-one-half-fold increase in psychotic disorders in midlife after chronic marijuana use that began in adolescence.
 
The director of the Maryland chapter of SAM (Smart Approaches to Marijuana) caught the error and notified the journal which lead to the correction. SAM is calling on all media who reported the original incorrect story to correct their account of it now.
 
Read Independent story here.  Read SAM account of the correction here.

Source: Email from Monte Stiles, National Families in Action, January 2016

Two recent studies, one in Great Britain and this one from the University of Southern California, contradict the findings of a rigorous 25-year-long study done with a birth cohort in Dunedin, New Zealand a few years ago. That study found that persistent marijuana use that continued into adulthood resulted in an 8-point drop in IQ. The two new studies find the opposite.

The UCLA study looked at 789 pairs of adolescent twins from two ongoing studies—one in Los Angeles and one in Minnesota—who enrolled between ages 9 and 11. Over 10 years, five IQ tests were administered along with confidential surveys of marijuana use. Marijuana-using twins lost 4 IQ points, but so did their non-using twins, leading researchers to conclude that something other than marijuana was lowering IQ.

The other study compared teens who reported daily marijuana use for six months or longer with teens who used the drug less than 30 times and found no difference in IQ.
 
But critics say both studies are flawed in that they did not measure heavy marijuana use over a long 25-year period like the Dunedin study did.
 
Dr. Madeline Meier, lead researcher of the Dunedin study, writes, “Our 2012 study (Meier et al. PNAS 2012) reported cognitive decline among individuals with a far more serious and far more long-term level of cannabis use. That is, we found cognitive decline in individuals followed up to age 38 who started cannabis use as a teen and who thereafter remained dependent on cannabis for many years as an adult. This new study is different; the two papers report about completely different doses of cannabis, and about participants 2 decades apart in age.  The new study reports cognitive test scores for individuals followed up to only age 17-20, fewer than half of whom had used cannabis more than 30 times, and only a fifth of whom used cannabis daily for > 6 months. This new study and our prior study agree and both report the same finding: no cognitive decline in short-term low-level cannabis users. The message from both studies is that short-term, low-level cannabis use is probably safer than very long-term heavy cannabis use. The big problem remains that for some teens, short-term low-level teenaged cannabis use leads onward to long-term dependence on cannabis when they become adults. That is what is cause for concern.”
 
Read Science story here. Read Dr. Meier’s rebuttal here.

Source: Email from Monte Stiles, National Families in Action January 2016

Almost all cannabis sold on British streets can cause psychosis after weaker forms were driven from the market.

The most potent “skunk” accounts for 94 per cent of all cannabis seized by police, up from half in 2005, according to the first study for almost a decade.

Dealers are thought to be pushing higher-strength products to get recreational users hooked, with the milder hashish form barely available, researchers say.

Teenager cannabis smokers have been told that skunk is more dangerous and that they must watch out for paranoia and other symptoms of psychosis.

Skunk, also known as sinsemilla, is made from unpollinated cannabis and contains higher levels of THC, a psychoactive compound, than herbal marijuana or resin, also known as hashish.

A Home Office study of police seizures in 2005 found that 51 per cent were skunk and 43 per cent resin. Three years later skunk seemed to be becoming stronger and more common, but the study has not been repeated since 2008.

Now researchers at King’s College London have analysed almost 1,000 samples seized by police in London, Merseyside, Derbyshire, Kent and Sussex. Resin accounted for just 6 per cent of samples, falling to 3 per cent in London, and even that had become stronger since 2008, according to results published in Drug Testing and Analysis.

“The increase of high-potency cannabis on the streets poses a significant hazard to users’ mental health,” said Marta Di Forti, senior author of the paper. “It’s a big worry. It’s pretty much the only kind of cannabis you can buy out there.”

Her previous work suggests that skunk users are five times more likely to develop psychosis than non-users, while there is no extra risk for hash smokers. Britain is largely self-sufficient in skunk as farms take over from hash grown in Morocco and Dr Di Forti said that the stronger product could be a deliberate policy by gangs.

“If high potency is more likely to induce dependence, that’s an advantage for the drug dealer because he wants people to come back as much as possible, rather than recreational users who only use at the weekend when they’re listening to music or going to a party,” she said.

Skunk has not got stronger since 2005, which she said could be because users could not tolerate higher THC concentrations without side-effects.

About 2.2 million people are estimated to have smoked cannabis in the past year, a million of them aged 16-24.

While there is some evidence that users can partially detect higher strength cannabis and cut back, Ian Hamilton, a lecturer in mental health at the University of York, said: “If the cannabis market is saturated with higher potency cannabis this increases the risk of younger and more naive users developing problems as they are less likely to adjust the amount of cannabis they ingest than more experienced users.”

Source: https://www.thetimes.co.uk/edition/news/mental-illness-risk-as-skunk-drives-out-milder-cannabis-wgd58b56l# February 2018 

Britain could set off a schizophrenia timebomb if it ignores the dangers of super-strength ‘skunk’ cannabis, one of the UK’s most eminent psychiatrists warns today.

Strong evidence now shows that smoking potent forms of the Class B drug increases the chance of psychosis, paranoid delusions and schizophrenia.

But too many people – from teenagers to top officials – have little idea of the terrible toll it can take on the mind, says Professor Sir Robin Murray.

Labour, the Liberal Democrats and the Scottish National Party all back legalisation of cannabis in some form. But Prof Murray said the dangers were not being recognised – and legalising skunk would amount to ‘a major pharmaceutical experiment’ with the brains of young people.

Prof Murray, from the Institute of Psychiatry at King’s College London, said: ‘I don’t think any serious researcher or psychiatrist would now dispute that cannabis consumption is a component cause of psychosis.’

He warned that:

  • MRI scans show long-term use of skunk can shrink a vital part of the brain;
  • The substance – now dominant on Britain’s streets – is four times stronger on average than cannabis smoked in the past;
  • A clear majority of studies show those who regularly smoke cannabis are at ‘significant increased risk’ of developing psychosis or schizophrenia-like illness;
  • Heavy users of skunk are up to four times more likely than non-users to develop psychotic symptoms.

Prof Murray said the cannabis being sold on our streets had changed almost beyond recognition in the past 20 years. Dealers have dropped weaker varieties in favour of skunk, which is made from non-pollinated parts of the plant, and provides a stronger ‘hit’ that may be more addictive.

A recent study revealed that almost all cannabis sold in the UK is now skunk. On average, skunk is 16 per cent tetrahydrocannabinol (THC), the main psychoactive compound – four times more than the THC in marijuana and hash.

Brain scans show skunk has a far stronger impact on the mind, said Prof Murray, due to both its high THC content and its very low content of the protective compound cannabidiol.

Experiments on volunteers at King’s College show THC boosts the brain’s natural fear response – making the merely worrisome seem positively frightening.

And MRI scans reveal that long-term use of skunk shrinks the hippocampus – the part of the brain essential for regulating emotions and long-term memory – by 11 per cent, according to researchers at Monash University in Australia. Only ‘prolonged abstinence’ could reverse the brain atrophy, they concluded.

MRI scans reveal that long-term use of skunk shrinks the hippocampus – the part of the brain essential for regulating emotions and long-term memory – by 11 per cent 

Prof Murray and colleague Dr Marco Colizzi have emphasised their concerns in a hard-hitting article for the British Journal Of Psychiatry, titled Cannabis And Psychosis: What Do We Know And What Should We Do?

They say UK authorities should watch what happens in America, where a number of states have recently legalised cannabis use.

‘The USA has embarked on a major pharmaceutical experiment with the brains of its youth and we should wait and see the outcome of the experiment,’ they write. ‘While we wait, we need education to make the public aware of the risks associated with heavy cannabis use.

‘It would be a shame when we are in sight of ridding the country of the scourge of tobacco use, if it were to be replaced by use of a drug that, although less harmful to the body, is more toxic to the mind.’

To help educate people about the dangers, Prof Murray is giving a series of talks in London, organised by events company Funzing. And he believes that health officials should be playing a far more active role in warning of the perils of skunk.

His intervention comes three years after The Mail on Sunday revealed his groundbreaking research suggesting up to a quarter of all new psychosis cases could be caused by skunk. Among those deeply affected is hereditary peer Nicholas Monson, whose son Rupert, 21, took his own life last year after developing drug-related psychosis.

Lord Monson said: ‘He descended into complete, utter madness.’

Rupert Green (pictured) the son of Lord Monson, was just 21 when he killed himself last year after descending into drug-related pyschosis, having gone in a few short years from ‘the occasional spliff’ to habitually smoking skunk

Rupert first admitted smoking ‘the occasional spliff’ at 19 and, like many parents, his father reacted with relief that it was nothing harder. But his behaviour gradually became ‘more and more peculiar’, said Lord Monson, adding: ‘He was a mixture of self-pity and outright aggression. I found him very difficult to deal with.’

The family managed to get Rupert referred to an NHS mental health team, and after being diagnosed, the youngster stopped smoking skunk and went on medication. However, he later killed himself.

Lord Monson said: ‘He hadn’t touched skunk for four months. But his mind continued to be overwhelmed. What I’ve learnt since his death is once a young man gets into a state of drug-induced psychosis, he doesn’t get out of it.’

Lord Monson has lobbied hard for better public education, including writing to the Prime Minister. He said he wanted cannabis below five per cent THC legalised to take it out of criminals’ hands, but anything stronger to be banned.

Incredibly, Government agencies provide almost no information on the risks of skunk, despite millions smoking it. Three years ago, the Advisory Council on the Misuse of Drugs said there was ‘strong evidence’ that ‘standalone’ information or warning campaigns were ‘ineffective’. But Lord Monson said: ‘The Government is doing an enormous disservice by not educating people about skunk’s dangers.’

Last night Public Health England said its Rise Above programme helped young people cope with a range of ‘diverse challenges’ including drug misuse, while its dedicated drug information website, Talk To Frank, provides ‘easily accessible information for young people about the risks and harms of drug misuse’.

Yet Rise Above, which is aimed at teenagers, does not mention cannabis at all. Talk To Frank, for an older audience, does state that regular cannabis use is ‘associated with an increase in the risk of later developing psychotic illnesses including schizophrenia’. But it contains no information on the greater danger posed by skunk. 

Source: https://www.dailymail.co.uk/health/article-5539941/Top-doctor-warns-psychosis-paranoid-delusions-superskunk-schizophrenia-timebomb.html

As a growing number of U.S. states legalize the medicinal and recreational use of marijuana, an increasing number of American women are using cannabis before becoming pregnant and during early pregnancy often to treat morning sickness, anxiety, and lower back pain. Although emerging evidence indicates that this may have long-term consequences for their babies’ brain development, how this occurs remains unclear.

A University of Maryland School of Medicine study using a preclinical animal model suggests that prenatal exposure to THC, the psychoactive component of cannabis, makes the brain’s dopamine neurons (an integral component of the reward system) hyperactive and increases sensitivity to the behavioral effects of THC during pre-adolescence. This may contribute to the increased risk of psychiatric disorders like schizophrenia and other forms of psychosis later in adolescence that previous research has linked to prenatal cannabis use, according to the study published today in journal Nature Neuroscience.

The team of researchers, from UMSOM, the University of Cagliari (Italy) and the Hungarian Academy of Sciences (Hungary), found that exposure to THC in the womb increased susceptibility to THC in offspring on several behavioral tasks that mirrors the effects observed in many psychiatric diseases. These behavioral effects were caused, at least in part, by hyperactivity of dopamine neurons in a brain region called the ventral tegmental area (VTA), which regulates motivated behaviors.

More importantly, the researchers were able to correct these behavioral problems and brain abnormalities by treating experimental animals with pregnenolone, an FDA-approved drug currently under investigation in clinical trials for cannabis use disorder, schizophrenia, autism, and bipolar disorder.

The researchers concluded that as physicians caution pregnant women against alcohol and cocaine intake because of their detrimental effects to the fetus, they should also, based on these new findings, advise them on the potential negative consequences of using cannabis specifically during pregnancy.

Abstract
Marijuana is currently a growing risk to the public in the United States. Following expanding public opinion that marijuana provides little risk to health, state and federal legislatures have begun changing laws that will significantly increase accessibility of marijuana. Greater marijuana accessibility, resulting in more use, will lead to increased health risks in all demographic categories across the country. Violence is a well-publicized, prominent risk from the more potent, current marijuana available.
We present cases that are highly popularized storylines in which marijuana led to unnecessary violence, health risks, and, in many cases, both. Through the analysis of these cases, we will identify the adverse effects of marijuana use and the role it played in the tragic outcomes in these and other instances. In the analysis of these cases, we found marijuana as the single most common, correlative variable in otherwise diverse populations and circumstances surrounding the association of violence and marijuana.

Conclusion
According to research studies, marijuana use causes aggressive behavior, causes or exacerbates psychosis and produce paranoias. These effects have been illustrated through case studies of highly publicized incidents and heightened political profiles.
These cases contain examples of repeated illustrations of aggression, psychosis and paranoia by marijuana users and intoxication.
Ultimately, without the use and intoxication of marijuana, the poor judgment and misperceptions displayed by these individuals would not have been present, reducing the risk for actions that result in senseless deaths.

Import to these assertions, is that the current marijuana is far more potent in THC concentrations, the psychoactive component. Accordingly, and demonstrated in direct studies, more potent marijuana results in a greater risk for paranoid thinking and psychosis.
In turn, paranoid behavior increases the risk for paranoid behaviors and predictably associated with aggressive and violent behaviors. Marijuana use causes violent behavior through increased aggressiveness, paranoia and personality changes (more suspicious, aggressive and anger).
Recent illicit and “medical marijuana” (especially grown by care givers for medical marijuana) is of much high potency and more likely to cause violent behavior. Marijuana use and its adverse effects should be considered in cases of acts of violence as its role is properly assigned to its high association.
Recognize that high potency marijuana is a predictable and preventable cause of tragic violent consequences.

Source: https://www.omicsonline.org/open-access/marijuana-violence-and-law-2155-6105-S11-014.pdf January 2017

Researchers at the University of Exeter and UCL (University College London) have identified a gene which can be used to predict how susceptible a young person is to the mind-altering effects of smoking cannabis. The finding could help identify otherwise healthy users who are most at risk of developing psychosis.

The research, funded by the Medical Research Council and published in Translational Psychiatry, also show that female cannabis smokers are potentially more susceptible to short-term memory loss than males. Previous studies in this field have looked at people who already have psychosis, but this is the first study to look at healthy people and to examine their acute response — or how the drug affects their minds.

Previous research has found a link between the AKT1 gene and people who have gone on to develop psychosis. In the new study, Celia Morgan, Professor of Psychopharmacology at the University of Exeter and Professor Val Curran and her team from UCL found that young people with variation in the ‘AKT1’ gene experienced visual distortions, paranoia and other psychotic-like symptoms more strongly when they were under the influence of cannabis.

Around one per cent of cannabis users develop psychosis. Although low in number, the impact can be devastating and long lasting. It is known that smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, but it has been difficult to establish who is most vulnerable. Researchers have previously found a high prevalence of one variant of the AKT1 genotype in cannabis users who went on to develop psychosis as a result of their use. This is the first research that shows the link between the same gene and the effects of smoked cannabis in healthy young people.

It is hoped that it will help identify those most at risk of the negative effects of cannabis smoking and may aid the development of genotype targeted medication.

Professor Morgan said: “These findings are the first to demonstrate that people with this AKT1 genotype are far more likely to experience strong effects from smoking cannabis, even if they are otherwise healthy. To find that having this gene variant means that you are more prone to mind-altering affects of cannabis when you don’t have psychosis gives us a clue as to how it increases risk in healthy people. Putting yourself repeatedly in a psychotic or paranoid state might be one reason why these people could go on to develop psychosis when they might not have done otherwise. Although cannabis-induced psychosis is very rare, when it happens it can have a terrible impact on the lives of young people. This research could help pave the way towards the prevention and treatment of cannabis psychosis.”

Professor Curran added: “The current study is the largest ever to be conducted on the acute response to cannabis. Our finding that psychotic-like symptoms when young people are ‘stoned’ are predicted by AKT1 variants is an exciting breakthrough as this acute reaction is thought to be a marker of a person’s risk of developing psychosis from smoking the drug.”

The study involved 442 young cannabis users who were tested while under the influence of the drug, and while sober. The researchers measured the extent of the symptoms of intoxication and effect on memory loss and compared it to results seven days later when the young people were drug free. They found that those who with this variation in the AKT1 geneotpye were more likely to experience a psychotic response.

As part of the study, researchers gained permission from the Home Office to analyse the cannabis samples for their make-up and strength. Samples were dropped off at a police station and analysed by the forensic science service.

The research also found that females were more vulnerable than males to impairment in short term memory after smoking cannabis.

“Animal studies have found that males have more of the receptors that cannabis works on in parts of the brain important in short term memory, such as the prefrontal cortex. We need further research in this area, but our findings indicate that men could be less sensitive to the memory impairing effects of cannabis than females,” added Professor Morgan.

Source: https://www.sciencedaily.com/releases/2016/02/160216111357.htm February 2016

  • Polly Ross, 32, suffered with Hyperemesis Gravidarum during second pregnancy
  • Mother smoked cannabis and magic mushrooms to ease pain, an inquest heard
  • ‘Talented and clever’ translator took her life in 2015 after battling with psychosis

A mother-to-be who took cannabis after developing the same morning sickness condition as the Duchess of Cambridge killed herself after developing a drug-induced psychosis, an inquest heard.  

Talented translator Polly Ross, 32, suffered Hyperemesis Gravidarum (HG), the condition which saw Kate Middleton rushed to hospital in August while visiting the queen in Aberdeen.

Hull Coroner’s Court in East Yorkshire was told today how a desperate Mrs Ross took cannabis and magic mushrooms in a bid to tackle the severe bouts of sickness.

However in July 2015, just a year after the birth of her second daughter, she died after stepping out in front of a train.  

A coroner heard Mrs Ross had developed ‘drug induced psychosis’ after taking cannabis to stop symptoms of HG.

Mrs Ross told her GP, Dr Daniella Malesknasr, she had taken cannabis during her pregnancy after visiting the doctors suffering from post natal depression.

Dr Malesknasr told the hearing: ‘She had told me when she was pregnant with her second child that she was taking cannabis and magic mushrooms to help combat HG during her pregnancy – but she was no longer taking it.’

Talented Polly Ross, 32, suffered the same condition but tried to soothe symptoms herself by taking cannabis and magic mushrooms

Professor Paul Marks, the senior coroner, questioned: ‘And does taking cannabis actual benefit those suffering from HG?.’

The doctor replied: ‘I can’t possibly comment on that.’

Dr Malesknasr said ‘alarm bells were ringing’ after Polly had told her she wanted to commit suicide on February 13, 2015.

Mrs Ross tried to take her life three times with self harm and taking an overdose twice in a three month period

The inquest heard the GP had called in at her home to find her in a psychotic episode and Mrs Ross was sectioned the following month.

By March 18, Dr Malesknasr said Mrs Ross was diagnosed with drug induced psychosis following the amounts of magic mushrooms and cannabis she had been taking.

The GP said she was then given Respiradon to help battle the psychosis.

Mrs Ross tried to take her life three times with self harm and taking an overdose twice in a three month period.

However, the court heard she was remarkably allowed to discharge herself voluntarily following the last attempt to take her own life.

Professor Marks said: ‘So after taking an overdose of paracetamol tablets, Polly was allowed to just leave voluntarily?’

Dr Malesknasr said: ‘I can’t comment on that because it is a hospital matter.’

However, in May 2015 a psychiatrist in the community said that psychosis was no longer a problem and she should come off the anti-psychosis drug Respiradon.

The translator was given help by a crisis team to give her a ‘higher and intense level of support’, but Mrs Ross had refused them entry to her house in Driffield, East Yorkshire.

Mrs Ross died on July 12, 2015, by stepping in front of a train in Hull, East Yorkshire, and ‘death was instant’, Hull Royal Infirmary Consultant Histopathologist Dr Ian Richmond told the hearing.

She had told mental health workers at the women-only care centre at Westlands voluntary care unit in Hull, East Yorkshire, that she was going to the shop.

Mrs Ross died on July 12, 2015, by stepping in front of a train in Hull, East Yorkshire

A statement from Mrs Ross’s aunt Emma May, who cared for her during her final months, read: ‘With the right guidance, medication and support, Mrs Ross could have made a full recovery.

‘There should be systems in place to protect that life especially because there are so many suicides attempts of post natal women.

‘I cannot understand why she was allowed to leave the hospital unit before she died.

‘Polly clearly said many times that she would kill herself, many months before she did.

‘I feel that she posed a significant risk to herself, did not have sufficient capacity to make decision and more should have been done to protect and care for her.’

Mrs Ross, who ran her own ‘very good’ translation business in Paris, was described as ‘an extremely intelligent lady and very driven in her own ambition’, by Mrs May.

She was also described as ‘frighteningly clever’.

She met her English husband Samuel Ross in 2011 in the French capital and the pair quickly married and had two daughters born in June 2012 and June 2014 respectively.

Mrs Ross suffered HG during pregnancy with both children and had post natal depression following the birth of both children.

The inquest, expected to last three days, continues.

WHAT IS HG?

Excessive nausea and vomiting during pregnancy is known as hyperemesis gravidarum (HG), and often needs hospital treatment.
Unlike regular morning sickness, HG may not get better by 14 weeks.
It may not clear up completely until the baby is born, although some symptoms may improve at around 20 weeks.
Some pregnant women be sick many times a day and be unable to keep food or drink down, which can have a negative effect on their daily life.
Exactly how many pregnant women get HG is not known as some cases may go unreported, but it’s thought to be around 1 in every 100.
Signs and symptoms of HG include prolonged and severe nausea and vomiting, dehydration and low blood pressure. Source: NHS Choices  

Source: https://www.dailymail.co.uk/news/article-5063227/Pregnant-mum-killed-developing-drug-habit.html November 2017

As more cases turn up, doctors are concerned about the extent to which memory loss may be undetected.

Just over five years ago, a man suffering from amnesia following a suspected drug overdose appeared at Lahey Hospital and Medical Center in Burlington, Massachusetts, a Boston suburb. He was 22, and had injected what he believed to be heroin. When he woke up the next morning, he was extremely confused, repeatedly asking the same questions and telling the same stories. Doctors at Lahey quickly diagnosed the man with anterograde amnesia—the inability to form new memories.

His brain scan revealed why. “I thought it was an extremely strange scan—it was almost hard to believe,” says Jed Barash, a neurologist working at Lahey at the time. In the scan, the twin, seahorse-shaped structures of the man’s hippocampi were lit up against the dark background of the rest of the brain—a clear sign of severe injury to just that one region.

“It was strange because that was all there was,” Barash says.

Memory researchers have known since the late 1950s that the hippocampi are responsible for turning short-term memories into lasting ones, so the amnesia was not surprising. Just how the damage occurred, however, remained a mystery. Lack of oxygen to the brain that would have occurred during the overdose could not be the only explanation. The number of survivors in the state that year could easily have numbered in the thousands, so why was there only one patient with this seemingly unique brain damage?

Along with his colleagues, Barash—now the medical director at the Soldiers’ Home health-care facility in Chelsea, Massachusetts—figured that the opioids must have played a role, and that hunch became only more acute as three more patients—each fitting the same pattern—appeared at Lahey over the next three years. All had the same unique destruction of the hippocampi, all had amnesia, and all were suspected to have overdosed. By that point, the doctors at Lahey faced two fundamental questions: What was causing the strange new syndrome? And precisely how rare was it?

Both questions remain unanswered, but a case report published Tuesday in the Annals of Internal Medicine adds to a growing body of evidence suggesting that the problem is far from isolated, and that a potent opioid variation could be involved. A total of 14 patients have now been identified in Massachusetts, one of whom was first admitted to a hospital in his home state of New Hampshire. The new case study reveals two more patients—one from Virginia, and one from Maryland. Both turned up at a medical facility in West Virginia.

Although many of the patients had taken a variety of drugs, all but one either have a history of opioid use or tested positive for opioids. The most recent case, a 30-year-old man examined last year in West Virginia, is the first patient proven to have taken fentanyl, an extremely potent and dangerous opioid that is rarely tested for in toxicology screens.

There are many barriers to determining the true scope of the problem, from lack of proper testing to the fact that many patients never come to attention in the first place. And amid a larger opioid crisis that some experts say could claim as many as 500,000 lives over the next decade, pinning down the cause of a dozen or so amnesia cases can seem trifling. “It’s sort of like the Titanic going down and you’re worried about some details,” says Alfred DeMaria, the state epidemiologist for Massachusetts.

At the same time, DeMaria suggests that, at the very least, these patients may offer a different route for understanding a disorder, as was the case with a small cluster of patients in the early 1980s who developed Parkinson’s disease after taking contaminated drugs—a misfortune that turned out to be limited to a few people, but which nonetheless gave Parkinson’s researchers a new tool for studying the disease. More worryingly, he also points to several examples of medical investigations that began with a small number of mysterious cases and turned out to have significant public health-implications, such as the appearance of West Nile Virus, or the AIDS epidemic.

Bertha Madras, a psychobiologist at McLean Hospital in Belmont, Massachusetts, and a member of President Donald Trump’s Commission on Combating Drug Addiction and the Opioid Crisis, agreed that getting to the bottom of these amnesia cases is crucial—particularly given that many cases may be going undetected since the type of cognitive testing needed to diagnose amnesia may not be routinely done in overdose survivors. She also suspects that with overdose-antidote drugs like naloxone becoming more widely available, it is possible that more patients, rather than turning up dead, will show up at hospitals.

And with more survivors, Madras said in an email message, “there conceivably will be more cases of brain damage, especially in the very oxygen-sensitive hippocampus, the ‘epicenter’ of initial learning and memory.”

* * *

After encountering more patients following that first one in 2012, Barash contacted the Massachusetts Department of Public Health in 2015, which put out a request to emergency-room physicians, neurologists, and radiologists statewide for information that might identify additional cases. By the end of 2016, a total of 14 people who matched the pattern had been identified. Then, in May of 2017, the DPH made what they called “an unusual amnestic syndrome” with “acute, bilateral hippocampal” damage a reportable disease syndrome—a status that requires any doctor who sees such a case to forward patients’ medical records for review.

As of today, however, DeMaria believes there is no such mechanism in place in other states, and that’s one of the barriers to getting a handle on the prevalence of the amnestic syndrome. Marc Haut, the neuropsychologist who examined the man from Virginia in 2015, and one of the authors on the new Annals paper, had no way of knowing about the investigation in Massachusetts and initially chalked up the damage to cocaine use. At the time, he saw no reason to consider opioids, in part because of the information the patient shared with him. “Patient reports about substance use [are] not always accurate for a couple of reasons, one being the patients themselves,” he says. “And the other being that patients often don’t know what they’re buying and using.”

So it was not until he received an email from Barash that Haut, the chair of the behavioral medicine and psychiatry department at West Virginia University, reconsidered whether opioids could have played a role. To date, only eight of the 16 patients reported in the cluster had cocaine in their system, making opioids a more consistent link than any other drug. Barash, who is also an author on the Annals paper, wonders if fentanyl—considered to be 50 times more potent than heroin—is a key component, in part because the timing and location of the appearance of these amnestic cases parallels the rise of fentanyl overdoses in two of the hardest hit regions in the country. Teasing this out is complicated with the ever-changing landscape of drugs that people are taking, often in combination. “Cocaine overdose deaths are escalating,” said Madras, “along with evidence of combined use of fentanyl, heroin, and cocaine in some deaths.”

And despite the fact that fentanyl abuse has become so common, routine toxicology screens don’t test for the presence of the drug. It was only because Haut had been tipped off that he requested the advanced toxicology screen for the 2017 patient, which found evidence that he had taken fentanyl in addition to cocaine. His MRI scan also revealed the signature hippocampal damage: “bright, big, and intense,” according to Haut.

Like Barash, Haut is concerned about the possibility that what they’ve seen so far could be just the tip of the iceberg. “We don’t know if this is a rare occurrence, or if this has occurred more, and people have not noticed,” he says, “because some of the folks who have these events are pretty marginalized in society. If they don’t have family to notice, it may not be noticed even though it’s pretty dense amnesia.”Several other doctors who contributed cases to the Massachusetts cluster have also raised the question of whether more patients are going undetected. They point to the fact that many illegal drug users don’t go to a hospital after an overdose. If they do, their confusion is likely to be chalked up to a temporary symptom of the overdose. If they don’t get to a hospital within a narrow window of approximately one week, the telltale signal may have faded from the brain and all evidence of drugs will likely have cleared the system.

Even if all those conditions are met, doctors across the country don’t know where or how to share the information. DeMaria, the state epidemiologist for Massachusetts, believes his is the only state that has notified physicians and is collecting cases. If doctors in other states are seeing cases that fit the pattern, they may assume that it’s a one-off phenomenon, just as Barash and others did when they first saw the cases.

Michael Lev, an emergency-room neuroradiologist at Massachusetts General Hospital who contributed cases to the Massachusetts cluster, thinks it’s possible that the appearance of this amnestic syndrome may date back far earlier than 2012. He recalls seeing similar brain images in a few sporadic cases between 1986 and 1989 when he was working at Boston City Hospital. The patient history was always the same, he says. “The history was ‘heroin found down,’”—emergency-room shorthand for an overdose victim.

* * *

For now, doctors can only go on the well-documented data that they have—the 16 patients identified between October 2012 and May 2017—and one key question is whether they represent just one narrow band along a spectrum of damage, which would have ramifications for the ability of addicts to get the treatment they need. “Getting a sense of the severity and scope of this is important,” Haut says. “If we find that these dense amnesias are really rare, that’s good. But if we find in the interim that they have significant memory problems even though they’re not amnestic as a result of these events, that have gone under the radar, then we have to take that into account when we’re trying to get people into treatment and staying in treatment.”

Barash agrees, pointing out that understanding the amnestic syndrome may give medical professionals insight into some of the larger problems that can accompany overdoses. “These cases are a very particular subset of brain damage that can occur from use of opioids,” he notes. “But I think more likely there are probably cases of patients who may not necessarily have this particular syndrome but suffer cognitive difficulties from longer-term use of opioids and it’s important to know the scope of that.” It’s also plausible that there are more extreme cases on the other end of the spectrum—people who have taken sublethal doses but are too far gone to have their memory tested.

Source: https://www.theatlantic.com/health/archive/2018/01/fentanyl-overdose-amnesia/551846/ January 2018

This collection of articles has been collated to show how the use of cannabis has been involved in many murders and attacks of violence.

Attacker Smoked Cannabis: suicide and psychopathic violence in the UK and Ireland
“Those whose minds are steeped in cannabis are capable of quite extraordinary criminality.”

What do we want?

Our demands are simple:

· acknowledge that cannabis is a dangerous drug and a prime factor in countless acts of suicide and psychopathic violence, and that no amount of ‘regulation’ will eliminate this danger;
· acknowledge that the alleged medicinal benefits of certain aspects of cannabis are a red herring to soften attitudes to the pleasure drug and ensure that certain corporations are well placed if and when the pleasure drug is legalised;
· admit that since around 1973 cannabis has been decriminalised in all but name, and that this has been a grave mistake;
· begin punishing possession: a caution for a first offence, a mandatory six-month prison sentence and £1000 fine thereafter.

Woman killed by taxi driver ‘might be alive if he had been properly managed’
Shropshire Star | 19 Mar 2018 |

“From the limited evidence which was available to the independent investigation team, it appears possible that, if MB had been fully compliant with anti-psychotic medication and had refrained from misuse of cannabis, then he may not have suffered from a relapse of his psychotic illness.”
Martin Bell had been sectioned for about nine months in August 1999 and was released around six weeks before he killed Gemma Simpson.
The family of a woman who was killed and partially dismembered by a taxi driver who was suffering from a psychotic illness have said she “might still be alive today” if he had been managed properly.
Gemma Simpson’s family were responding to the publication of a report into the treatment of Martin Bell, who killed 23-year-old Miss Simpson in 2000 with a hammer and a knife before sawing her legs off and burying her at a beauty spot near Harrogate, in North Yorkshire.
Bell admitted manslaughter on the grounds of diminished responsibility after leading police to her body 14 years later, and was told he must serve a minimum of 12 years in prison.
Bell had been sectioned in a hospital for about nine months in August 1999 and was released around six weeks before he killed Miss Simpson.
On Monday, NHS England published an independent report into his care and treatment.
The report, which said its authors were severely hampered by a lack of medical records, concluded: “From the limited evidence which was available to the independent investigation team, it appears possible that, if MB had been fully compliant with anti-psychotic medication and had refrained from misuse of cannabis, then he may not have suffered from a relapse of his psychotic illness.
“In these circumstances, the death of Gemma Simpson might have been prevented.”
The new report confirmed that doctors had considered Bell’s cannabis use may have contributed to or exacerbated Bell’s illness and he had smoked the drug on the day he killed Miss Simpson in his Harrogate flat.
But it said that “notwithstanding the failures in service provision outlined in this report, there were no actions that clinicians could have specifically taken to enforce the continuation of medication given MB’s presentation in May 2000, nor to enforce his abstinence from cannabis.”
In a statement issued by the campaign group Hundred Families, Miss Simpson’s family said they broadly welcomed the findings of the report but added: “In 2000 Martin Bell was known to carry a knife, was delusional, and recognised as a real risk to others, yet he was able to be released without any effective package of care, monitoring, or even a proper assessment of how the risks he posed to others would be managed.
“There appear to have been lots of red flags, just weeks and days before Gemma’s death, that should have raised professional concerns.
“We believe that if he had been managed properly, Gemma might still be alive today.”
The family said they understood the pressures on mental health services but said: “We keep hearing that lessons have been learned, but we want to make sure they are truly learned in this case.”
In court in 2013, prosecutors said Bell struck Miss Simpson, who was from Leeds, an “uncountable” number of times with the knife and hammer in a “frenzied” attack before leaving her body for four days in a bath.
He then sawed off the bottom of her legs so she would fit in the boot of a hire car before burying her at Brimham Rocks, near Harrogate.
Bell, who was 30 at the time of the attack, handed himself in at Scarborough police station in 2013 and later took police to where she was buried.

Source: https://www.shropshirestar.com/news/uk-news/2018/03/19/woman-killed-by-taxi-driver-might-be-alive-if-he-had-been-properly-managed/ NHS England report: https://www.england.nhs.uk/north/wp-content/uploads/sites/5/2018/03/independent-investigation-mb-march-18.pdf

On 14 May 2017, Akshar Ali, acting with his friend Yasmin Ahmed, murdered his wife and mother-of-four Sinead Wooding, stabbing her with a knife six times and bludgeoning her with a hammer before dumping her body in a woodland and setting it alight. On 17 January 2018, he and his accomplice were sentenced to 22 years in prison.
One might think the fact that the guilty pair smoked and grew cannabis together would be of interest to reporters, and worthy of at least a fleeting sentence or two, but I have found it mentioned in only two news reports, one in the Yorkshire Evening Post, the other in South African news site IOL.
Of far more interest to some British media, sadly, is the fact that Ali was an ostensible Muslim and Ms Wooding a Muslim convert who had, in the weeks before she was murdered, defied her husband by wearing western clothing and seeing a friend he did not approve of. Some media, including the BBC, the Guardian and, curiously, British media abnormally incurious about the role of cannabis in a gruesome act of uxoricide the Sun managed to avoid mentioning either the matter of Islam or the smoking of cannabis.
Is it, I wonder, an abnormal lack of curiosity that prevents reporters from mentioning the smoking of a powerful psychoactive drug that is a prime factor in countless thousands of similar cases? Or is it a deliberate omission?

An extraordinary murder in Ireland

The following story from Ireland, which occurred ten years ago, is extraordinary for two reasons. First, the 143 injuries the attacker inflicted is, as far as I’m aware, a record. As I have noted many times, a frenzy of violence involving multiple stab wounds is nearly always a sign of a mind unhinged by drugs. 143, though, points to a frightening level of madness, and, as such, the verdict of not guilty by reason of insanity is unsurprising.
But then there is this:
The jury had deliberated for under one hour and had returned during that hour to ask if the fact that Mr Connors had smoked cannabis before the killing was relevant to his culpability.
Mr Justice Birmingham told the jury that consultant psychiatrist, Dr Damien Mohan, had considered whether Mr Connors’ behaviour was attributable to drugs or mental illness and was of the “firm and clear” view that the accused’s mental disorder was the causative factor.
In other words, the fact that the defendant had smoked cannabis before the killing, which occurred around six o’clock in the morning, was not deemed relevant, and the link between his mental disorder and his consumption of cannabis appears to have gone unexplored.

Man found not guilty of murder by reason of insanity
Irish Examiner 4 Feb 2009

A jury has found a Dublin man who killed a stranger with garden shears not guilty of murder by reason of insanity at the Central Criminal Court.
Thomas Connors (aged 25) thought Michael Hughes (aged 30), from Banagher in Offaly, was the embodiment of the devil when he found him sleeping in the stairwell of an apartment block.
Mr Justice George Birmingham told the jury that it had reached “absolutely the right verdict in accordance with the expert evidence”. He thanked it for its careful attention to the case and exempted its members from jury service for seven years.
Mr Connors, of Manor Court, Mount Argos, Harold’s Cross, killed Mr Hughes in a savage attack in the stairwell of an adjacent apartment block, Manor Villa, on the morning of December 15, 2007.
Mr Justice Birmingham said this was a case of “mind boggling sadness” and, were it not for the issue of insanity, would have been a perfectly clear and appalling case of murder.
He said: “Consequent on the special verdict of not guilty by reason of insanity I direct that Mr Connors be committed to a specially designated centre, the Central Mental Hospital, until further order.”
Prosecuting counsel, Paul O’Higgins SC, said Mr Hughes’ family were aware that victim impact evidence would not be heard because the case did not involve the imposition of a sentence.
Mr Justice Birmingham said to the family: “You truly have been through the most appalling experience. Words can’t and don’t describe it and all I can do is express my sympathy.”
The jury had deliberated for under one hour and had returned during that hour to ask if the fact that Mr Connors had smoked cannabis before the killing was relevant to his culpability.
Mr Justice Birmingham told the jury that consultant psychiatrist, Dr Damien Mohan, had considered whether Mr Connors’ behaviour was attributable to drugs or mental illness and was of the “firm and clear” view that the accused’s mental disorder was the causative factor.
Yesterday, the jury heard that Mr Hughes had gone out for a night in Dublin with his cousin and friends. He was to stay at his cousin’s flat in Harold’s Cross but the cousin had gone home early and Mr Hughes was unable to get into the flat when he returned after 4am.
Mr Hughes decided to sleep in the stairwell and sometime after 6am Mr Connors came crashing through the glass doors of the apartment block with garden shears and savagely attacked him, inflicting 143 injuries.
Residents heard screaming and rang gardaí who found Mr Connors walking away from the scene with the shears. He told gardaí that he had fought with the devil and the devil was gone now.
In the days leading up to the killing Mr Connors, a married man with one child, had gone to hospital three times seeking help. He was hearing voices and suffering delusions that his wife was the daughter of the devil. On the second visit he was given tablets. His wife was so frightened by his behaviour that she took their child to a women’s shelter.
On the third occasion, the day before the killing, doctors at Saint Vincent’s Hospital decided Mr Connors should be admitted to Saint James’ but he absconded during the four-hour wait for an ambulance.
In the hours before he killed Mr Hughes, Mr Connors thought the devil was in his apartment and had taken a duvet outside and stabbed it, believing the devil had been hiding in it.
Dr Mohan told the jury that Mr Connors suffered from schizophrenia, as did his father. He had been hospitalised with psychosis in 2004 and 2005 and believed that his father-in-law was the devil.
The victim’s father, Liam Hughes, made a statement outside the Four Courts on behalf of the Hughes family. He said that the family’s thoughts, as always but especially today, were on the 30 years of “love, kindness and generosity of spirit they enjoyed with the deceased”.
Mr Hughes said his son would be remembered by his friends as “a respectful and decent person”. He said a former teacher had contacted the family to pay tribute to Michael as “an honest, kind, sincere, popular and respected person who was a credit to his family and school”.
Mr Hughes said Michael had been a hard-working young man who commuted from Offaly to Dublin each day to work and had recently entered into further education. Mr Hughes said his son had coped admirably with the demands of full-time work and part-time study.
On October 27, 2007, he had become engaged to Deborah Lynch, who was with the family in court. Mr Hughes said his family had shared in their joy at setting up a home together and planning for their future.
He said: “Only seven short weeks later Deborah’s hopes and dreams were shattered.”
He said the Hughes family earnestly hoped that she would find happiness in the future.
Mr Hughes thanked UCD, which had honoured Michael recently on what would have been his conferring day, and his employer, Dublin Bus. He also thanked the team who investigated his son’s death, the Garda family liaison officer and the many friends who had offered comforting words.
He said it had been 13 months since the killing but the pain and horror of it had “scarcely lessened”. He said the natural “role reversal” in the cycle of life could not now happen as he had lost his son.
He said the family was disturbed and saddened by the evidence given in court, but there relieved that the process was over. He asked that the family’s privacy be respected at this time.

Source: https://www.irishexaminer.com/breakingnews/ireland/man-found-not-guilty-of-murder-by-reason-of-insanity-397642.html Posted on May 6, 2019 Leave a comment on An extraordinary murder in Ireland

Jail for man who shot girlfriend 13 times with airgun – before trying to strangle and suffocate her
Leicester Mercury | 27 July 2017 |

Kristian Pole had been smoking cannabis when he ‘flipped out’ and attacked his partner at his home in Leicester
A man who failed to take a chance given by a judge, following an airgun attack on a girlfriend, has been jailed for two years.
Kristian Pole repeatedly fired pellets at close range into his then girlfriend’s face, limbs and body. Then he tried to strangle her and suffocate her with a pillow, Leicester Crown Court was told.
The frightened woman managed to run from Pole’s home in Leicester and alert the police, having suffered bruising and red marks from 13 plastic pellets and being gripped around her neck, in August last year.
Judge Robert Brown gave Pole a chance, in June, by imposing a two-year community order, with rehabilitation requirements, because he had already served several months on remand in custody.
Pole later failed to inform the probation service he had moved address – a condition of the order. He also refused to tell them where he was living with a new partner. This resulted in him being brought back to court, where Judge Brown re-sentenced him on Tuesday.
The judge told 24-year-old Pole, of no known address: “I’ve no choice but to revoke the order and impose custody. You’ve thrown away the chance of a community order by your own actions. When I sentenced you in June, for possessing a BB gun with intent to cause fear of violence and causing actual bodily harm, you’d already served eight or nine months in custody.”
He told Pole, who admitted the offences: “You’d done well on remand and changed your attitude. I was invited to take a chance on you and put you on a community order.
“You’ve failed to engage with the probation service and moved out of your mother’s address, without notifying those concerned about where you were living. This was a serious example of an assault.”
Lynsey Knott, prosecuting, said the assault with the BB gun happened when Pole’s then girlfriend visited his home, where he was smoking cannabis with a male friend.
When the cannabis ran out he erupted in violence, attacking her and shooting “at close range” her face and limbs.
James Varley, mitigating, said: “He’d smoked too much cannabis and flipped out.
“Your Honour will have told many defendants it’s not the harmless drug that many young people think it is.
“It has deleterious effects … what else could explain his conduct other than he was completely out of it when his cannabis supply was cut off.”

Source:https://www.leicestermercury.co.uk/news/leicester-news/jail-man-who-shot-girlfriend-243489

Couple killed friend, set him on fire and then had sex to celebrate, court told
ITV News | 16 Feb 2019 |

Cold-hearted killers who brutally murdered a vulnerable friend before setting him on fire and then having sex will spend at least 28 years in jail.

Evil William Vaill and Deborah Andrews were handed life sentences for killing Skelmersdale dad Eamon Brady in a “brutal and sustained” attack.
Mr Brady was hit in the head with a hammer at least 17 times and repeatedly stabbed and slashed in the neck and body in the early hours of July 21.
Vaill, 37, and Andrews, 44, then wrapped his body in bedding and set it on fire before stealing a PlayStation 4, sound bar, DVD player and bank card belonging to their victim.
Andrews later described the couple as “the new Bonnie and Clyde”.
After the callous killing, the pair went to Beacon Country Park where they burned clothing and hid the weapons. They are also believed to have had sex in a nearby park hours after the attack, the court heard.
They also went on to attempt to sell his PlayStation 4 and use the stolen bank card in a local shop.
The evil couple, who had been friends with Mr Brady for several years, bumped into him by chance after Vaill had attended a funeral. They went back to his flat in Elmridge, Skelmersdale, where they drank and smoked cannabis.
By the time of the murder, Vaill, whose previous convictions include arson and criminal damage, had been drinking for 40 straight hours.
The pair left the flat at around around 4:50am and later told police that Mr Brady was alive and well when they left. But recordings in the police van heard that Andrews was ‘buzzing’ about the murder and describing the pair as the new Bonnie and Clyde.
Vaill, of Evington, Skelmersdale, pleaded guilty to murder and arson last month and was today given a life sentence with a minimum of 28-and-a-half years in prison.
Andrews, of Elmstead, Skelmersdale, was found guilty after a trial and given a life sentence with a minimum of 28 years in prison.
Both appeared emotionless throughout the sentencing at Preston Crown Court while Andrews sat with her hands in her pockets throughout.
Prosecuting, Francis McEntree said Mr Brady was a vulnerable man who was regularly taken advantage of by those around him. He had earlier told family that he wanted to move out of Skelmersdale to escape from people who were ‘leeching off him’.
He knew both of the victims well, having been friends for several years and they had all spent the together socially in a “happy, if noisy” manner.
Mr Brady had been friends with Vaill since their teenage years and an earlier incident in which Vaill stabbed him in the foot with a penknife was considered no more than horseplay after Mr Brady had laughed at him getting hurt when he kicked a lamppost.
An emotional victim statement read on behalf of Mr Brady’s daughter Amy Brady told of the devastating effects she has suffered since the murder of her best friend.
Her father’s death came 17 days short of the second anniversary of her brother Ryan’s death and that after seeing his battered and burnt body, Ms Brady now regularly suffers nightmare and is left “angry with the world”.
“There was a hole in my heart when my brother died that has been made bigger and will never be filled,” it stated.
“My dad was not only my dad, he was my entire being.”
Defending Vaill, Stuart Denney said he had begun cannabis and alcohol use since before he was a teenager and that Skelmersdale was “the worst place in the world for him”.
Michael Lavery, defending Andrews, said she had “limited capabilities and intelligence” and was previously of good character.
Sentencing the pair, Judge Mark Brown said: “Having killed him you set fire to his body to destroy evidence of what had happened and in doing so you committed arson with reckless disregard for the lives of the other residents in the building who were asleep at the time.
“It’s another matter of this case that having just murdered this a man in extremely violent and brutal circumstances that you had sex with each other soon after.”

Source: https://www.itv.com/news/granada/2019-02-16/couple-killed-friend-set-him-on-fire-and-then-had-sex-to-celebrate-court-told/

Teenager found guilty of fatal stabbing of Luke Howard
Liverpool Echo | 22 Jan 2009 |

A LIVERPOOL teenager has been found guilty of killing a friend he stabbed 12 times in a drunk and drug-fuelled rage.

A jury at Liverpool Crown Court found Charlijo Calvert, 15, not guilty of the murder of 16-year-old Luke Howard but unanimously convicted him of manslaughter.
Calvert, of Ronald Street, Old Swan, stabbed Luke, from Dovecot, in the early hours of August 30 at the house of a friend in Ashcombe Road, Knotty Ash.
During the week-long trial, the court heard a group of teenage boys, including the victim and defendant, had gone to the house and drank alcohol, smoked cannabis and snorted cocaine.
Throughout the night, and into the early hours, witnesses said they saw Luke prodding Calvert with a screwdriver and the pair “winding each other up”. At one point, the court heard, they threatened to stab each other but the fatal attack at around 7am.

Source: https://www.liverpoolecho.co.uk/news/liverpool-news/teenager-found-guilty-fatal-stabbing-3462600

Four ‘racist’ killings, two years apart, with one important commonality
1. Skunk addicted schizophrenic fulfils sick fantasy by killing a black woman: ‘Psychiatric reports stated that Maxwell was suffering from paranoid schizophrenia, and his abnormality was so great that it affected his judgment [sic].The reports also said his condition was exacerbated by the heavy use of skunk.’ (3 Apr 2007)
2. Drive caught in gang’s ‘revenge’: ‘The 41-year-old minibus taxi driver was dragged screaming from his cab and beaten to death in July by several white teenagers in Huddersfield… Some of the teenagers had been drinking and smoking cannabis with some girls, who they then persuaded to call up and order the minibus – with fatal consequences.’ (26 Jan 2007)
3. Racist thugs face 30 years in prison for axe murder: ‘The two men who murdered black teenager Anthony Walker were last night each facing up to 30 years in jail after the trial judge ruled the killing was racially motivated, effectively doubling the time they will serve… Anthony Walker wanted to be a lawyer, maybe a judge. He loved God, worked hard at his studies, practised his basketball skills whenever he could, though not on a Sunday if it clashed with church.
Paul Taylor and Michael Barton revelled in the nicknames Chomper and Ozzy. One wanted to be a burglar, the other wanted to join the army, but was too stupid to pass the exams. They spent their time hanging around, smoking cannabis and, in the words of one, “going out robbing”.’ (1 Dec 2005)
4. Asian gang kicked man to death: ‘Three Asian men who kicked a white computer expert to death and bragged: “That will teach an Englishman to interfere in Paki business” were found guilty of murder at the Old Bailey yesterday… The court heard that the three had been drinking all evening in the West End before returning to east London to drink vodka and smoke cannabis.’ (23 Nov 2005)
You know, of course, what the important commonality is, a much more important factor than apparent ‘racism’. I will note here only, as the article does not, that the ‘skunk addicted schizophrenic’ who deliberately targeted a black woman is himself black.

In defence of Peter Hitchens (@ClarkeMicah) and the theory of mental illness

Mail on Sunday columnist Peter Hitchens, author of The War We Never Fought, has received a lot of abuse recently for pointing out in his MoS column of 7 April that the killer of Jo Cox, Thomas Mair, was mentally ill, not a ‘political actor’, and that his mental state was not discussed at his trial (at which Mair himself did not speak).
This matters a great deal, because those who cannot accept that, far from being part of a ‘far-right terrorist plot’, Mair was simply mentally unhinged, and that this mental illness was likely the result of or exacerbated by psychoactive medication, often equally refuse to believe that the prime factor in a particular act of suicide or psychopathic violence isn’t terrorism, Islam, immigration, austerity, video games, gangs, gun laws, ‘depression’, or racism, but cannabis.
Many have cited the following sentencing remarks of the judge in the Mair case, Mr Justice Wilkie, as evidence that Mr Hitchens is barking up the wrong tree:
There is no doubt that this murder was done for the purpose of advancing a political, racial and ideological cause namely that of violent white supremacism and exclusive nationalism most associated with Nazism and its modern forms.
Those who believe that Mair was a ‘terrorist’ are not open to the possibility that the judge is mistaken, nor aware that his remarks are, as Mr Hitchens points out, unusually political in tone. I wonder, then, what such people would make of these sentencing remarks of Judge Findlay Baker, QC, to a man who stabbed his friend’s father to death with a pair of garden shears: “This was an attack of extreme and persistent violence. And I have no doubt it would not have happened if you had not consumed cannabis.”
Or these, of Judge Anthony Niblett, to a man who punched his girlfriend and burnt down her house: “Those whose minds are steeped in cannabis are capable of quite extraordinary criminality. Your mind has been steeped in cannabis for much of your adult life.”
Or these, of Judge Rosalind Coe, QC, to a young man who attempted to murder his infant son: “If any case demonstrates the dangers and potentially tragic consequences of cannabis abuse, such as you had taken part in for many years, this is such a case.”
I could go on.
By contrast, some judges all but shrug and hold up their hands when trying to make sense of a heinous crime. The judge who sentenced 16-year-old Aaron Campbell, for example, said he had “no idea” why Campbell abducted, raped and murdered six-year-old Alesha MacPhail, even though it was noted during the trial that he was high on cannabis when he committed the crime, and knew the MacPhail family from having bought the drug from Alesha’s father. Some judges, like some people, can see the wood amid the trees. Some cannot.

Violence and legalised cannabis in Uruguay: a clarification

I would like to clarify the meaning of a tweet I sent yesterday of a link to an article on violence and homicide in Uruguay, ‘Uruguay gets tough on crime after posting record homicide rate’.
The article reports that in 2018, a year after cannabis went on sale, following legalisation in 2013, there were a record 414 homicides in Uruguay, a small nation of 3.5 million people once famed for its peace and tranquillity. So alarming was this figure (up from 284 in 2017) that 400,000 voters signed a petition calling for exceptional measures against violent crime.
I must stress first that, while it is likely that at least some of these acts of homicide were committed by people whose minds have been damaged by cannabis, I do not say that cannabis legalisation was the cause. I tweeted the article whilst arguing about correlation and causation with a dim-witted young drugs enthusiast who had claimed that an apparent decrease in rates of cannabis consumption amongst teenagers in Washington state was caused by cannabis being legalised there. I have written before that dope heads parrot the phrase ‘correlation does not equal causation’ only when the correlation upsets them. When they find a correlation they like they immediately claim cannabis legalisation as the cause.
Again, I do not say that homicide rate in Uruguay is exceptionally high because cannabis has been legalised. As Peter Hitchens points out in an article on Portugal, ‘The Alleged Portuguese Drug Paradise Examined’, legalisation or decriminalisation nearly always follows years of lax enforcement, making any before-and-after comparison meaningless. By contrast, in his largely excellent book Tell Your Children, Alex Berenson spends too much time, as I write in my review, trying to prove that violent crime has risen in those American states that have legalised cannabis, when he would have done better to expand his section on the alleged ‘war’ on drugs in America and the fact that, contrary to popular opinion, rates of incarceration solely for drugs possession in the USA have been quite low for many years.
I would further add that suggestions that ‘gang warfare’ is involved in Uruguay’s high homicide rate seem similarly erroneous. Drug rivals killing each other makes a good subject for a film or TV series,
but the reality is often a much blander case of a paranoid young man in possession of a weapon killing somebody (often not his ostensible target) out of fear or delusion.

Xixi Bi Llandaff murder: Jordan Matthews jailed for life

He accepted he was smoking “quite a lot” of cannabis at the time and the court heard he felt “insecure” when his girlfriend visited her family in China.

Source: https://www.bbc.co.uk/news/uk-wales-south-east-wales-39026270

‘Cannabis made my boy a killer’

THE mother of a violent schizophrenic who stabbed his best friend to death last night described how her son’s long-term cannabis habit turned him into a monster.
Julie Morgan, formerly from Cardiff, claimed her 20-year-old son Richard Harris’ ‘kind and gentle’ side disappeared not long after he started smoking cannabis from the age of 14.
“Cannabis took my son from me, I have no problem saying that,” said the 45-year-old.

Carl Madigan knifed Sam Cook in heart two weeks after friend slashed man’s stomach open

Facebook accounts show Carl Madigan, 23, and Shaun Bethell, 19, hanging around together and smoking cannabis before the shocking offences which will now define their young lives.
In a dreadful two week period last October, Madigan killed tragic Sam Cook while Bethell, a teenager with a record to rival any career criminal’s, left a man’s bowel hanging out of his body.

Man found guilty of murdering girlfriend’s toddler before claiming he slipped underwater in bath in 999 call

Smith was also found to have a high reading of cannabis in his bloodstream almost six hours after the 999 call – while a makeshift Ribena bottle ‘bong’ and the remains of six cannabis joints were found in a rear annex.
Despite Willett claiming she “always put the kids first,” text messages showed a woman desperate to buy cannabis, even on the night before Teddy’s death.

Cork man, 26, who shattered skull of girlfriend’s infant daughter jailed for eight years
Brendan Kelly, defence barrister, said[…] that the accused appeared to be detached from what was going on and that the defendant had been a long-time cannabis user.

Dad shook baby daughter to death as he was agitated at running out of cannabis
Daily Mirror

A dad who shook his baby daughter to death because he was agitated at running out of cannabis was today jailed for six years.
William Stephens, aged 25, shook daughter Paris so violently she suffered catastrophic head injuries and was bleeding in the eyes.
The thug attacked 16-week-old Paris for crying after he was left to look after her while mum Danah Vince, 19, went to see a doctor.
The little girl died two days later in hospital and one shocked expert said he had never before seen such a severe case of bleeding in the eyes.
Stephens had a history of violence and social services were called in because of his volatile relationship with mum Vince.
A serious case review is being carried out into the way public bodies handled the case.
Stephens – who had serious learning difficulties – was convicted of manslaughter after a seven-week trial.
Vince was cleared of causing or allowing the baby’s death in January.
Passing sentence, the judge Mr Justice Teare told Stephens: “This is a case where a loss of temper and control has resulted in fatal violence to a defenceless baby.
“You will have to live with the fact that you killed your daughter.”
Defence lawyer Ignatious Hughes QC, told the jury: “There is plenty of evidence that he and Danah Vince are likely to have been in a state of agitation due to lack of cannabis.”
Bristol crown court heard Stephens and Vince often fought and argued and social services stepped in to get the pair to sign agreements against domestic violence.
Stephens, from Southmead, Bristol, was given a restraining order to stay away from Vince but defied the ban and continued living with her and their daughter.
He appeared in juvenile court in 2006 for three assaults on a previous girlfriend and received a community order.
Five months later he appeared in front of magistrates for battery and was given the same punishment.
A year later he was given a caution for repeatedly punching a pregnant woman and in November 2008 got another caution for common assault.
In April 2010, he was hauled before magistrates for assaulting a police officer.
The local council is conducting a serious case review which will be published next year.
A spokesman said: “This is an extremely sad case where there has been the tragic loss of a young life.
“If nothing else I hope that today’s verdict offers some small measure of closure.
“An independent Serious Case Review by the Bristol Safeguarding Children Board is being completed, carefully examining the role of public bodies involved in the case to see if there are any lessons to be learnt.
“The complexity of this case will become apparent once that review is published early next year following the conclusion of all relevant legal processes.”
A year later, Danah Vince, the mother of the baby, committed suicide.

Source: https://www.mirror.co.uk/news/uk-news/william-stephens-shook-baby-paris-2923262

Teen faces one year for vicious attack on man outside takeaway

A 17-year-old boy has been warned he faces a one-year sentence for leading a vicious gang attack on a young man who was repeatedly punched and kicked outside a takeaway in Dublin.
The boy, who cannot be named because he is a minor, has pleaded guilty at the Dublin Children’s Court to assault causing harm and violent disorder in connection with the incident on the night of November 14, 2015.
Judge John O’Connor adjourned sentencing to see if the boy’s solicitor can organise a psychological assessment of the teenager whose behaviour, he said, has become more violent and aggressive.
The judge also noted the boy had tragic personal circumstances.
He said it was unacceptable that the boy had started smoking cannabis at the age of 12, and anyone who says it is not addictive “is not living in the real world”.
Garda Dave Jennings had told Judge O’Connor that the victim, a foreign national who is also aged in his late teens, had been at a Chinese takeaway at Kiltalown Way, Tallaght. A group of youths shouted in to him that they were going to rob him when he came out.
When he walked out one of them grabbed the handlebars of his bicycle and the youth then punched him in the side of his face.
The rest of the youths then joined in, grabbing the man, who was repeatedly punched and kicked before his bike was stolen.
The defendant struck the first blow but was not involved in the rest of the attack.
The victim fled back into the takeaway but was followed and had to run into the kitchen area for his safety. Garda Jennings agreed with Damian McKeone, defending, that the attack was not racially motivated.
CCTV footage was shown to Judge O’Connor, who described it as a “vicious assault”.

Source: https://www.irishexaminer.com/ireland/teen-faces-one-year-for-vicious-attack-on-man-outside-takeaway-399847.html

Robbers who held knife to man’s neck before stealing his phone and laptop jailed

Two males who robbed a man at knifepoint at his home in north Belfast have been jailed.
Bennet Donaghy and his accomplice, who at the time of the offence was 16, targeted their victim in the early hours of September 13, 2015.
He managed to escape and ran down the Shore Road in the middle of the night shouting for help.
Donaghy (20), a father-of-one from Cheston Close in Carrickfergus, was handed a 30-month sentence at Belfast Crown Court yesterday. His accomplice, who cannot be named, was given 15 months’ jail.
Both men were informed they would spend half their sentences in custody, with the remainder on licence.
The pair admitted a charge of assault with intent to rob, while the youth also admitted stealing the man’s laptop and mobile phone.
Prior to sentencing, Judge Gordon Kerr QC was informed that the victim was asleep on his sofa at around 4am when he heard persistent knocking at his front door.
He recognised the youth, who he knew from the area, with another young man.
The younger man asked the victim to lend him money, but when he handed them £5 the pair told him: “That’s not enough.”
Crown prosecutor Robin Steer said Donaghy then produced a knife and held it against the occupant’s neck.
The youth, who the man said looked like he was under the influence of drugs, punched the victim a number of times while Donaghy told him he was from the UDA and ordered him to hand over drugs and money.
The man’s home was ransacked, but he escaped and ran down the Shore Road barefoot and with a bruised face, only to be stopped by police.
Officers subsequently called at a house in the area, where they arrested Donaghy and the youth. Also located was a four-inch knife, along with the man’s laptop and mobile phone.
During police interviews, the youth admitted he knew the occupant, but claimed he was unable to remember what had happened because he had smoked a cannabis cigarette.
Like his accomplice, Donaghy claimed to have no recollection of the incident because he too had been smoking drugs.
Mr Steer told Belfast Crown Court there were a number of aggravating factors.
These included the use of violence and threats during the robbery, the presence of a weapon and the fact the victim was targeted in his home in the middle of the night.
Defence barrister Jon Paul Shields, representing the youth, confirmed that his client was under the influence of drugs on the night in question.
He also added that he had since “recognised the seriousness of the offences.”
Telling the court his client knew his behaviour had been unacceptable, Mr Shields said: “At the time, he simply did not give any thought to what he was doing.”
The barrister also told how the young man, who has been working with the Youth Justice Agency, had expressed shame over the incident.
The lawyer said that at the time of the offence, his client had just lost a child, which led to him self-medicating.
Barrister Chris Holmes, acting on behalf of Donaghy, said that his client “apologises profusely to the victim”.
He added that on the night of the robbery, Donaghy was “very, very much under the influence” of drugs.
Mr Holmes also spoke of the defendant’s troubled background, telling the judge his client “didn’t have his sorrows to seek when he was being brought up”, which in turn contributed to poor mental health.

Source: https://www.belfasttelegraph.co.uk/news/northern-ireland/robbers-who-held-knife-to-mans-neck-before-stealing-his-phone-and-laptop-jailed-35560290.html

Sally Hodkin murder: Killer ‘had miscarriage’ prior to fatal stabbing

A patient who murdered a grandmother believed she had suffered a miscarriage and was smoking cannabis in the lead up to the killing, an inquest has heard.
Nicola Edgington virtually decapitated Sally Hodkin with a stolen butcher’s knife in Bexleyheath, in 2011, six years after killing her own mother.
Edgington told hospital staff she needed to be sectioned and felt like killing someone.
A recent report found NHS and police failings led to Mrs Hodkin’s murder.
Edgington, a diagnosed schizophrenic, was discharged from the Bracton Centre mental health facility in 2009 despite an order she be detained indefinitely following the killing of her mother Marion in Forest Row, Sussex, in 2005.
Around two weeks before the killing on 10 October, 2011, Edgington made a number of emergency calls to police about “crackheads” stealing from her flat in early October. She had also been using skunk cannabis, the inquest heard.
On 29 September, she sent a message to her brother telling him about the miscarriage, saying she wanted to reconnect.
The message also mentioned their mother, with Edgington saying: “No-one’s taking care of me like she would.”
Her brother replied on the same day: “You stabbed her to death and left me to find the body. Good news about your miscarriage … do us a favour and slit your wrists.”
On the day of Mrs Hodkin’s murder, Edgington was taken to Oxleas House mental health unit, but was later allowed to walk out of the building.
She got a bus to Bexleyheath, bought a large knife from Asda and stole a steak knife from a butcher’s shop.
Edgington then stabbed Mrs Hodkin and another woman in the street.
Elizabeth Lloyd-Folkard, a forensic social worker who was looking after Edgington, told the inquest that around a week before the killing, she had “no cause of concern about her state of mind”.
Contact with family members, substance misuse, and any issues around pregnancy were noted in reports as high-risk factors that could affect Edgington’s mental health, the inquest heard.
Mrs Hodkin’s son Len Hodkin told the inquest: “All of those risk factors were present in the two to three weeks leading up to October 10.
“It’s not coming with the benefit of hindsight, this information was available to you and other members of the multi-disciplinary team at the time.”
The inquest continues.

Source: https://www.bbc.co.uk/news/uk-england-london-46022330

January 2019 • Volume 48, Number 1 • Alex Berenson
Alex Berenson Author, Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence

The following is adapted from a speech delivered on January 15, 2019, at Hillsdale College’s Allan P. Kirby, Jr. Center for Constitutional Studies and Citizenship in Washington, D.C.

Seventy miles northwest of New York City is a hospital that looks like a prison, its drab brick buildings wrapped in layers of fencing and barbed wire. This grim facility is called the Mid-Hudson Forensic Psychiatric Institute. It’s one of three places the state of New York sends the criminally mentally ill—defendants judged not guilty by reason of insanity.
Until recently, my wife Jackie—Dr. Jacqueline Berenson—was a senior psychiatrist there. Many of Mid-Hudson’s 300 patients are killers and arsonists. At least one is a cannibal. Most have been diagnosed with psychotic disorders like schizophrenia that provoked them to violence against family members or strangers.
A couple of years ago, Jackie was telling me about a patient. In passing, she said something like, Of course he’d been smoking pot his whole life.
Of course? I said.
Yes, they all smoke.

So marijuana causes schizophrenia?
I was surprised, to say the least. I tended to be a libertarian on drugs. Years before, I’d covered the pharmaceutical industry for The New York Times. I was aware of the claims about marijuana as medicine, and I’d watched the slow spread of legalized cannabis without much interest.
Jackie would have been within her rights to say, I know what I’m talking about, unlike you. Instead she offered something neutral like, I think that’s what the big studies say. You should read them.
So I did. The big studies, the little ones, and all the rest. I read everything I could find. I talked to every psychiatrist and brain scientist who would talk to me. And I soon realized that in all my years as a journalist I had never seen a story where the gap between insider and outsider knowledge was so great, or the stakes so high.

I began to wonder why—with the stocks of cannabis companies soaring and politicians promoting legalization as a low-risk way to raise tax revenue and reduce crime—I had never heard the truth about marijuana, mental illness, and violence.
***
Over the last 30 years, psychiatrists and epidemiologists have turned speculation about marijuana’s dangers into science. Yet over the same period, a shrewd and expensive lobbying campaign has pushed public attitudes about marijuana the other way. And the effects are now becoming apparent.
Almost everything you think you know about the health effects of cannabis, almost everything advocates and the media have told you for a generation, is wrong.
They’ve told you marijuana has many different medical uses. In reality marijuana and THC, its active ingredient, have been shown to work only in a few narrow conditions. They are most commonly prescribed for pain relief. But they are rarely tested against other pain relief drugs like ibuprofen—and in July, a large four-year study of patients with chronic pain in Australia showed cannabis use was associated with greater pain over time.
They’ve told you cannabis can stem opioid use—“Two new studies show how marijuana can help fight the opioid epidemic,” according to Wonkblog, a Washington Post website, in April 2018— and that marijuana’s effects as a painkiller make it a potential substitute for opiates. In reality, like alcohol, marijuana is too weak as a painkiller to work for most people who truly need opiates, such as terminal cancer patients. Even cannabis advocates, like Rob Kampia, the co-founder of the Marijuana Policy Project, acknowledge that they have always viewed medical marijuana laws primarily as a way to protect recreational users.

As for the marijuana-reduces-opiate-use theory, it is based largely on a single paper comparing overdose deaths by state before 2010 to the spread of medical marijuana laws— and the paper’s finding is probably a result of simple geographic coincidence. The opiate epidemic began in Appalachia, while the first states to legalize medical marijuana were in the West. Since 2010, as both the epidemic and medical marijuana laws have spread nationally, the finding has vanished. And the United States, the Western country with the most cannabis use, also has by far the worst problem with opioids.
Research on individual users—a better way to trace cause and effect than looking at aggregate state-level data—consistently shows that marijuana use leads to other drug use. For example, a January 2018 paper in the American Journal of Psychiatry showed that people who used cannabis in 2001 were almost three times as likely to use opiates three years later, even after adjusting for other potential risks.
Most of all, advocates have told you that marijuana is not just safe for people with psychiatric problems like depression, but that it is a potential treatment for those patients. On its website, the cannabis delivery service Eaze offers the “Best Marijuana Strains and Products for Treating Anxiety.” “How Does Cannabis Help Depression?” is the topic of an article on Leafly, the largest cannabis website. But a mountain of peer-reviewed research in top medical journals shows that marijuana can cause or worsen severe mental illness, especially psychosis, the medical term for a break from reality. Teenagers who smoke marijuana regularly are about three times as likely to develop schizophrenia, the most devastating psychotic disorder.

After an exhaustive review, the National Academy of Medicine found in 2017 that “cannabis use is likely to increase the risk of developing schizophrenia and other psychoses; the higher the use, the greater the risk.” Also that “regular cannabis use is likely to increase the risk for developing social anxiety disorder.”
***
Over the past decade, as legalization has spread, patterns of marijuana use—and the drug itself—have changed in dangerous ways.
Legalization has not led to a huge increase in people using the drug casually. About 15 percent of Americans used cannabis at least once in 2017, up from ten percent in 2006, according to a large federal study called the National Survey on Drug Use and Health. (By contrast, about 65 percent of Americans had a drink in the last year.) But the number of Americans who use cannabis heavily is soaring. In 2006, about three million Americans reported using cannabis at least 300 times a year, the standard for daily use. By 2017, that number had nearly tripled, to eight million, approaching the twelve million Americans who drank alcohol every day. Put another way, one in 15 drinkers consumed alcohol daily; about one in five marijuana users used cannabis that often.
Cannabis users today are also consuming a drug that is far more potent than ever before, as measured by the amount of THC—delta-9-tetrahydrocannabinol, the chemical in cannabis responsible for its psychoactive effects—it contains. In the 1970s, the last time this many Americans used cannabis, most marijuana contained less than two percent THC. Today, marijuana routinely contains 20 to 25 percent THC, thanks to sophisticated farming and cloning techniques—as well as to a demand by users for cannabis that produces a stronger high more quickly. In states where cannabis is legal, many users prefer extracts that are nearly pure THC. Think of the difference between near-beer and a martini, or even grain alcohol, to understand the difference.

These new patterns of use have caused problems with the drug to soar. In 2014, people who had diagnosable cannabis use disorder, the medical term for marijuana abuse or addiction, made up about 1.5 percent of Americans. But they accounted for eleven percent of all the psychosis cases in emergency rooms—90,000 cases, 250 a day, triple the number in 2006. In states like Colorado, emergency room physicians have become experts on dealing with cannabis-induced psychosis.
Cannabis advocates often argue that the drug can’t be as neurotoxic as studies suggest, because otherwise Western countries would have seen population-wide increases in psychosis alongside rising use. In reality, accurately tracking psychosis cases is impossible in the United States. The government carefully tracks diseases like cancer with central registries, but no such registry exists for schizophrenia or other severe mental illnesses.

On the other hand, research from Finland and Denmark, two countries that track mental illness more comprehensively, shows a significant increase in psychosis since 2000, following an increase in cannabis use. And in September of last year, a large federal survey found a rise in serious mental illness in the United States as well, especially among young adults, the heaviest users of cannabis.
According to this latter study, 7.5 percent of adults age 18-25 met the criteria for serious mental illness in 2017, double the rate in 2008. What’s especially striking is that adolescents age 12-17 don’t show these increases in cannabis use and severe mental illness.

A caveat: this federal survey doesn’t count individual cases, and it lumps psychosis with other severe mental illness. So it isn’t as accurate as the Finnish or Danish studies. Nor do any of these studies prove that rising cannabis use has caused population-wide increases in psychosis or other mental illness. The most that can be said is that they offer intriguing evidence of a link.
Advocates for people with mental illness do not like discussing the link between schizophrenia and crime. They fear it will stigmatize people with the disease. “Most people with mental illness are not violent,” the National Alliance on Mental Illness (NAMI) explains on its website. But wishing away the link can’t make it disappear. In truth, psychosis is a shockingly high risk factor for violence. The best analysis came in a 2009 paper in PLOS Medicine by Dr.Seena Fazel, an Oxford University psychiatrist and epidemiologist. Drawing on earlier studies, the paper found that people with schizophrenia are five times as likely to commit violent crimes as healthy people, and almost 20 times as likely to commit homicide.

NAMI’s statement that most people with mental illness are not violent is of course accurate, given that “most” simply means “more than half”; but it is deeply misleading. Schizophrenia is rare. But people with the disorder commit an appreciable fraction of all murders, in the range of six to nine percent.
“The best way to deal with the stigma is to reduce the violence,” says Dr. Sheilagh Hodgins, a professor at the University of Montreal who has studied mental illness and violence for more than 30 years.

The marijuana-psychosis-violence connection is even stronger than those figures suggest. People with schizophrenia are only moderately more likely to become violent than healthy people when they are taking antipsychotic medicine and avoiding recreational drugs. But when they use drugs, their risk of violence skyrockets. “You don’t just have an increased risk of one thing—these things occur in clusters,” Dr. Fazel told me.

Along with alcohol, the drug that psychotic patients use more than any other is cannabis: a 2010 review of earlier studies in Schizophrenia Bulletin found that 27 percent of people with schizophrenia had been diagnosed with cannabis use disorder in their lives. And unfortunately—despite its reputation for making users relaxed and calm—cannabis appears to provoke many of them to violence.
A Swiss study of 265 psychotic patients published in Frontiers of Forensic Psychiatry last June found that over a three-year period, young men with psychosis who used cannabis had a 50 percent chance of becoming violent. That risk was four times higher than for those with psychosis who didn’t use, even after adjusting for factors such as alcohol use. Other researchers have produced similar findings. A 2013 paper in an Italian psychiatric journal examined almost 1,600 psychiatric patients in southern Italy and found that cannabis use was associated with a ten-fold increase in violence.

The most obvious way that cannabis fuels violence in psychotic people is through its tendency to cause paranoia—something even cannabis advocates acknowledge the drug can cause. The risk is so obvious that users joke about it and dispensaries advertise certain strains as less likely to induce paranoia. And for people with psychotic disorders, paranoia can fuel extreme violence. A 2007 paper in the Medical Journal of Australia on 88 defendants who had committed homicide during psychotic episodes found that most believed they were in danger from the victim, and almost two-thirds reported misusing cannabis—more than alcohol and amphetamines combined.

Yet the link between marijuana and violence doesn’t appear limited to people with pre-existing psychosis. Researchers have studied alcohol and violence for generations, proving that alcohol is a risk factor for domestic abuse, assault, and even murder. Far less work has been done on marijuana, in part because advocates have stigmatized anyone who raises the issue. But studies showing that marijuana use is a significant risk factor for violence have quietly piled up. Many of them weren’t even designed to catch the link, but they did. Dozens of such studies exist, covering everything from bullying by high school students to fighting among vacationers in Spain.

In most cases, studies find that the risk is at least as significant as with alcohol. A 2012 paper in the Journal of Interpersonal Violence examined a federal survey of more than 9,000 adolescents and found that marijuana use was associated with a doubling of domestic violence; a 2017 paper in Social Psychiatry and Psychiatric Epidemiology examined drivers of violence among 6,000 British and Chinese men and found that drug use—the drug nearly always being cannabis—translated into a five-fold increase in violence.

Today that risk is translating into real-world impacts. Before states legalized recreational cannabis, advocates said that legalization would let police focus on hardened criminals rather than marijuana smokers and thus reduce violent crime. Some advocates go so far as to claim that legalization has reduced violent crime. In a 2017 speech calling for federal legalization, U.S. Senator Cory Booker said that “states [that have legalized marijuana] are seeing decreases in violent crime.” He was wrong.

The first four states to legalize marijuana for recreational use were Colorado and Washington in 2014 and Alaska and Oregon in 2015. Combined, those four states had about 450 murders and 30,300 aggravated assaults in 2013. Last year, they had almost 620 murders and 38,000 aggravated assaults—an increase of 37 percent for murders and 25 percent for aggravated assaults, far greater than the national increase, even after accounting for differences in population growth.

Knowing exactly how much of the increase is related to cannabis is impossible without researching every crime. But police reports, news stories, and arrest warrants suggest a close link in many cases. For example, last September, police in Longmont, Colorado, arrested Daniel Lopez for stabbing his brother Thomas to death as a neighbour watched. Daniel Lopez had been diagnosed with schizophrenia and was “self-medicating” with marijuana, according to an arrest affidavit.

In every state, not just those where marijuana is legal, cases like Lopez’s are far more common than either cannabis or mental illness advocates acknowledge. Cannabis is also associated with a disturbing number of child deaths from abuse and neglect—many more than alcohol, and more than cocaine, methamphetamines, and opioids combined—according to reports from Texas, one of the few states to provide detailed information on drug use by perpetrators.

These crimes rarely receive more than local attention. Psychosis-induced violence takes particularly ugly forms and is frequently directed at helpless family members. The elite national media prefers to ignore the crimes as tabloid fodder. Even police departments, which see this violence up close, have been slow to recognize the trend, in part because the epidemic of opioid overdose deaths has overwhelmed them.
So the black tide of psychosis and the red tide of violence are rising steadily, almost unnoticed, on a slow green wave.
***
For centuries, people worldwide have understood that cannabis causes mental illness and violence—just as they’ve known that opiates cause addiction and overdose. Hard data on the relationship between marijuana and madness dates back 150 years, to British asylum registers in India. Yet 20 years ago, the United States moved to encourage wider use of cannabis and opiates.
In both cases, we decided we could outsmart these drugs—that we could have their benefits without their costs. And in both cases we were wrong. Opiates are riskier, and the overdose deaths they cause a more imminent crisis, so we have focused on those. But soon enough the mental illness and violence that follow cannabis use will also be too widespread to ignore.

Whether to use cannabis, or any drug, is a personal decision. Whether cannabis should be legal is a political issue. But its precise legal status is far less important than making sure that anyone who uses it is aware of its risks. Most cigarette smokers don’t die of lung cancer. But we have made it widely known that cigarettes cause cancer, full stop. Most people who drink and drive don’t have fatal accidents. But we have highlighted the cases of those who do.
We need equally unambiguous and well-funded advertising campaigns on the risks of cannabis. Instead, we are now in the worst of all worlds. Marijuana is legal in some states, illegal in others, dangerously potent, and sold without warnings everywhere.

But before we can do anything, we—especially cannabis advocates and those in the elite media who have for too long credulously accepted their claims—need to come to terms with the truth about the science on marijuana. That adjustment may be painful. But the alternative is far worse, as the patients at Mid-Hudson Forensic Psychiatric Institute—and their victims—know.

Source: Imprimis January 2019 • Volume 48, Number 1

People who are mentally ill or addicted can’t work effectively, if at all, so they have to turn to crime and/or public support for survival.  Marijuana escalates the risk of mental illness 5 times.[i] On average, 17% of adolescents and 9% of adults  will become addicted.[ii]Based on federal research  7,000 people use marijuana for the first time each day.[iii] Taking an average of 13%, nationally over 332,000 new marijuana addicts will be created.  California’s share at 13% of the population will be over 33,000 new addicts annually, adding another 1.3 billion in cost at $40,000 each.  Instead of preventing these problems, we can expect more academic failure, lost productivity, mental illness, addiction and crime. In Sacramento, 59% of all arrestees for any crime tested positive just for marijuana; 83% for any drug[iv]. Jail overcrowding is also a factor as those deemed mentally ill languish there for weeks and months, waiting for space in a mental health facility.

Marijuana causes permanent brain damage and loss of IQ for anyone under 25.[v]  It causes psychotic breaks leading to gruesome acts, including decapitations, stabbings, mass murders and suicides. Other harms include DNA damage causing birth abnormalities[vi] not just in the next generation, but the next four (100 years).  Because marijuana is fat soluble, it stays in the body and brain for one month, compounding with each additional use.  The impairment adversely affects cognition, judgement and memory all of which contribute to traffic deaths. [vii]

MARIJUANA – THE ECONOMIC COSTS 
Aside from the devastating environmental cost, the social costs are huge.  For alcohol and tobacco, the social costs exceed tax revenues by 9 to 1. The black market won’t disappear. In Colorado the black market is still about 50% of the total.  In California only about 16% of cultivators have signed up to be licensed and taxed. The rest will avoid taxes and sell to the black market throughout the US. In 2009, a study called Shoveling Up: The Impact of Substance Abuse on Federal, State and Local Governments[viii] was done which showed in 2005, California spent 19.5% of its budget ($19.9 billion) on substance abuse, of which only $38 million (1/3rd of 1%) on prevention, and the rest shoveling up the damage. This is horrible economic policy, and its much worse today.  Instead of preventing this preventable disease, we cultivate it.

Voters bought the Gavin Newsom lie that Prop 64 would be a good thing. The orchestrated legislative analysis, approved by our Attorney General, Secretary of State, et al., suggested the state would save $100 million in prison costs, get rid of the black market and earn up to $1 billion in tax revenues. No mention of the environmental devastation and reclamation costs.  It outrageously suggested marijuana had no serious health impacts.  To cap it off, the illicit drug trade and out-of-state billionaires spent $35 million to back the campaign. If we care about our kids, and our future, its time to fight back.

[i] https////health.harvard.edu/Teens who smoke pot at risk for later schizophrenia

[ii] www.drugabuse.gov

[iii] www.theatlantic.com/Everyday 7,000 Americans try weed for the first time

[iv] www.ncjrs.gov/pdfiles1/ondcp/ADAMII Arrestee Drug Abuse Monitoring Program

[v] www.healthline.com.  The Effects of Marijuana on your body.

[vi] www.sciencedaily.com.  Marijuana Damages DNA and may cause cancer

[vii] www.nbcnews.com/health/healt-news/Pot Fuels Surge In Driving Deaths

[viii] www.casacolumbia.org/Shoveling Up:  The Impact of Substance Abuse on Federal, State and Local Budgets

Source: http://tbac.us/2018/09/15/marijuana-causes-mental-illness-and-addiction-in-turn-more-homelessness-poverty-and-crime/ September 2018

Abstract

Major self-mutilation (amputation, castration, self-inflicted eye injuries) is frequently associated with psychiatric disorders and/or substance abuse. A 35-year-old man presented with behavioral disturbances of sudden onset after oral cannabis consumption and major self-mutilation (attempted amputation of the right arm, self-enucleation of both eyes and impalement) which resulted in death. During the enquiry, four fragments of a substance resembling cannabis resin were seized at the victim’s home. Autopsy confirmed that death was related to hemorrhage following the mutilations. Toxicological findings showed cannabinoids in femoral blood (tetrahydrocannabinol (THC) 13.5 ng/mL, 11-hydroxy-tetrahydrocannabinol (11-OH-THC) 4.1 ng/mL, 11-nor-9-carboxy-THC (THC-COOH) 14.7 ng/mL, cannabidiol (CBD) 1.3 ng/mL, cannabinol (CBN) 0.7 ng/mL). Cannabinoid concentrations in hair (1.5 cm brown hair strand/1 segment) were consistent with concentrations measured in chronic users (THC 137 pg/mg, 11-OH-THC 1 pg/mg, CBD 9 pg/mg, CBN 94 pg/mg). Analysis of the fragments seized confirmed that this was cannabis resin with high levels of THC (31-35%). We discuss the implications of oral consumption of cannabis with a very high THC content.

Source: https://www.ncbi.nlm.nih.gov/pubmed/29125965 January 2018

Researchers have long known that there is a link between nicotine and alcohol consumption. But the nature of the connection—how long it lasts, which begets which—remains a mystery.

A new Tel Aviv University study finds that nicotine exposure during adolescence can predict increased alcohol intake in adulthood. This suggests that memories of smoking tobacco as a teenager alter the brain’s reaction to alcohol even after a prolonged nicotine withdrawal. The research indicates that these nicotine “memories” may even lead to a tendency toward heavier drinking later in life.

The research was led by Dr. Segev Barak and his research team at TAU’s School of Psychological Sciences and Sagol School of Neuroscience. It was published in Scientific Reports.

The influence of memory

“Previously, it was believed that the mere consumption of nicotine during adolescence could trigger the use of other drugs—cocaine, heroin and alcohol,” Dr. Barak said. “Our study shows that nicotine ‘memories’ from adolescence are the culprit, not the nicotine itself.”

The researchers found that nicotine “memories” caused long-lasting changes in the brain, long after the cessation of nicotine consumption. A brief exposure to the nicotine environment triggered a robust decrease in the expression of the growth factor GDNF in the brain’s pleasure center. “We have previously shown that GDNF serves as a brain regulator of alcohol consumption,” Dr. Barak said. “We assume that this drop in GDNF following the retrieval of nicotine memories leads to loss of control, thus boosting drinking.”

The researchers used rat models to test the link between nicotine and alcohol consumption. To study the effects on alcohol consumption, the researchers installed an experimental self-serve alcohol dispenser, operated by a lever press. When placed in this “bar,” rats were free to consume unlimited amounts of alcohol.

Group 1 received nicotine during adolescence in Chamber B, and then drank alcohol in adulthood in Chamber A—in other words, drinking alcohol in an environment different to that in which they used nicotine. Conversely, Group 2 received nicotine during adolescence in Chamber A, and then in adulthood drank alcohol in the same chamber (that is, in the nicotine-associated environment), triggering a reminder of the nicotine experience.

“The rats eagerly drink alcohol,” said Yossi Sadot-Sogrin, who contributed to the research. “During the daily one-hour sessions, most of them consumed the amount of alcohol equivalent to a glass or two of wine.”

But when the self-serve alcohol dispenser was installed in the same chamber in which rats received nicotine during their adolescence, the amount of alcohol consumed rose sharply.

“In the nicotine-associated environment, rats drank the amount of alcohol that corresponded to four glasses of wine, and even more,” said Koral Goltseker, who collaborated on the study.

The team is currently researching the specific changes to the brain caused by nicotine memories. “If we can prevent these brain changes, we hope we can prevent the long-term increase in alcoholconsumption,” said Dr. Barak. “It will also teach us a lot about the brain mechanisms that lead to alcoholism.”

Source: https://medicalxpress.com/news/2017-11-consumption-nicotine-adolescence-alcohol-intake.html November 2017

With no age restrictions on its use, some people – even children – are likely consuming CBD on a very frequent basis.

While a growing chorus of voices recommend CBD oil for all manner of ailments with glowing reviews and assurances of its safety, consumers would be wise to think very carefully before jumping on the bandwagon.

This article seeks to pull back the curtain on the CBD story and reveal the very real potential dangers of use by otherwise healthy people so that you can make a truly informed decision for your family.

Please note that I am not disputing the benefits of cannabis in this article. I know it helps a lot of very sick people manage their illness in a comfortable way without the need for pharmaceuticals. What I am presenting is the other side of the story that is usually not discussed – even glossed over in favor of aggressive marketing to otherwise healthy people.

What is CBD Oil?

CBD oil is an alternative remedy for inflammation, pain, seizures and many other conditions. It is gaining widespread popularity over pharmaceutical drugs to treat the same ailments.

Manufacturers make CBD oil by diluting the active ingredient cannabidiol with a carrier fat such as coconut oil. Depending on what carrier oil is used (i.e., saturated fats or vegetable oils), the remedy then appeals to a wider variety of people. In other words, CBD fans can find an oil that fits their particular food philosophy on fats.

Cannabidiol

You might be surprised to learn that cannabidiol is one of over a hundred compounds known as cannabinoids. The buds, flowers, leaves and stalks (not seeds) of the hemp plant contain them. Other common names for this plant are marijuana or cannabis.

Tetrahydrocannabinol, better known as THC, is another well known cannabinoid in hemp plant matter. It is best known for its mind altering effects, which pot smokers experience firsthand. (1)

Fans of CBD oil claim that cannabidiol is safe because it has zero inherent psychoactive properties like THC. However, this is disputable, if not downright false, in light of research on both animals and humans. More on this later.

Hash (Cannabis) Oil vs CBD Oil vs Hemp Seed Oil

It is important to understand the key differences between the three primary oils derived from the hemp or marijuana plant. These characteristics determine whether the oil is used as food or medicine and, in turn, whether it is even legal or not.

CBD oil falls in the gray area, which is why it is so confusing and potentially dangerous for anyone except those who are gravely ill with few other treatment options. Hopefully, the discussion below will help clear things up for you!

Cannabidiol (CBD) Oil

As described above, manufacturers create medicinal CBD oil by blending cannabidiol with a carrier oil. This active ingredient is either isolated or alcohol extracted from whole cannabis plant matter.

CBD was legalized in all 50 states by the 2014 Farm Bill, which served as the springboard for its explosive growth. However, this approval came with an important caveat. The legislation required extraction of CBD for academic research or under a state pilot program. Since then, a number of states broadened this narrow definition, which legalized other CBD manufacturing processes. (2)

Hemp Seed Oil

CBD oil is vastly different from hemp seed oil, which is a food and not medicine. It is made by cold pressing the seeds on the cannabis plant. The resulting oil is high in inflammatory omega-6 fats. Hemp seeds contain no THC and hence the oil should technically not contain any either.

Some countries require testing for THC in hemp seed oil to verify purity. Typical requirements are that there are no more than 5-10 or even zero parts per million (ppm) detected in the final product.

Hemp Oil (Hash or Cannabis Oil)

In comparison, hash or cannabis oil does contain high inducing THC. It is also misleadingly known as honey oil.

It comes from aerial parts of the marijuana plant except the seeds. This medicinal or recreational oil can be made from any of the three sub-species of the cannabis plant – Cannabis sativa, Cannabis indica, and more rarely Cannabis ruderalis.

Hash oil is illegal for recreational use in most states but is approved for medicinal use by a growing list of others. It is usually consumed by eating or smoking. It is also sold in cartridges for use in vaping pens.

In summary, while hemp seed oil is widely recognized as safe and available on healthfood store shelves all across the country, hemp oil is still regulated as as a medicinal only drug in some states and completely outlawed in others. CBD oil falls in the gray area somewhere between the two.

The question that remains to be answered is its safety. Does the narrow legalization of CBD in the 2014 Farm Bill guarantee its safety? Or is it actually more risky than consumers have been led to believe?

CBD Oil Risks

The side effects of consuming cannabidiol are very real though commonly glossed over by those selling it.

Drug Contraindications

CBD oil may potentially interact in a negative way with anti-epilepsy drugs. As of now, only in vitro (test tube) observations exist with no living organism testing proving safety. Drugs that may interact include: (3)
•carbamazepine (Tegretol)
•phenytoin (Dilantin)
•phenobarbital (Luminal, Solfoton, Tedral)
•primidone (anti-seizure)

Side Effects

According to a review of existing research by the journal Cannabis and Cannabinoid Research, the most common side effects of consuming CBD or CBD oil include:
•fatigue
•nausea or vomiting
•diarrhea
•dizziness
•anxiety or depression
•changes in appetite/weight
•Psychosis

While there is a well known link between psychotic disorders and pot, CBD is generally regarded as anti-psychotic. (4)

How can this be if a CBD side effect is psychosis? (5)

Perhaps this common belief is simply not true!

Psychoactive Effects of Cannabinoids

Perhaps cannabinoid oil purveyors tend to ignore the well established reactions because the side effect profile of CBD is better than pharmaceutical drugs used to treat similar conditions.

In addition, proponents of CBD oil use insist on its safety because cannabidiol is not mind altering like its cousin cannabinoid THC.

Research from the 1970s seems to confirm that CBD is well tolerated up to 600 mg without psychotic episodes. (6)

However, more recent research disputes this assumption.

Conversion of CBD to THC

Researcher Kazuhito Watanabe, PhD and his team at Daiichi College of Pharmaceuticals, Japan discovered a disturbing problem with cannabidiol. (7)

They found that CBD converts into THC, the same psychosis inducing substance found in weed. In addition, CBD converted into two other THC-like cannabinoids known as HHCs (hexahydroxycannabinols). All three produced high inducing symptoms in mice.

This research indicates that THC is not the only mind altering cannabinoid in hemp. It also suggests the possibility that a person can be exposed to brain altering, high inducing substances by simply consuming CBD.

Getting High on CBD?

Acidity is necessary for the conversion of CBD to THC and the two psychoactive HHCs. Researchers performed this conversion using artificial digestive juices. The change accelerated in the presence of some kind of sugar (or alcohol).

In people consuming CBD oil, this would parallel as acidity in the stomach. Since people commonly consume CBD oil in sugary lattes, candy, goodies, smoothies or alcoholic beverages, this situation mimics the reality of many people who use it.

Effects of THC Derived from CBD

To test the effects of these components, the researchers then injected mice with small quantities of the THC and HHCs converted from CBD. The researchers tested for the four most common symptoms of THC exposure including:
•Catalepsy – loss of sensation or consciousness
•Hypothermia – drop in body temperature
•Prolonged sleep
•Reduced pain perception

Mice injected with small amounts of THC and HHCs converted in artificial gastric juices from CBD tested positively for all 4 pot exposure symptoms.

Human Studies

Follow-up research in 2016 published in the journal Cannabis and Cannabinoid Research gives additional pause.

More than 40% of epileptic children orally administered CBD exhibited adverse events, with THC like symptoms the most common. In their conclusion, researchers challenged the accepted premise that CBD is not high-inducing.

Gastric fluid without enzymes converts CBD into the psychoactive components Δ9-THC and Δ8-THC, which suggests that the oral route of administration may increase the potential for psychomimetic adverse effects from CBD. (8)

Is CBD Oil Safe for Children?

The takeaway of existing research as of this writing seems to indicate extreme caution when it comes to ingestion of CBD oil especially by children.

Research definitively shows that THC exposure affects their developing brains in a negative way – perhaps permanently. The important point here is that consuming CBD or CBD infused oil can initiate this THC exposure – not just smoking or vaping pot. The Journal of Current Pharmaceutical Design warns:

The literature not only suggests neurocognitive disadvantages to using marijuana in the domains of attention and memory that persist beyond abstinence, but suggest possible macrostructural brain alterations (e.g., morphometry changes in gray matter tissue), changes in white matter tract integrity (e.g., poorer coherence in white matter fibers), and abnormalities of neural functioning (e.g., increased brain activation, changes in neurovascular functioning). (9)

CBD During Pregnancy

The Journal Future Neurology warns that cannabis exposure crosses the placenta. “Human epidemiological and animal studies have found that prenatal cannabis exposure influences brain development and can have long-lasting impacts on cognitive functions.” (10)

Since CBD partially converts to THC under acidic conditions, women who consume CBD oil for morning sickness or other discomforts of pregnancy should understand that use may mimic using pot directly. Just because CBD oil is natural and works effectively to alleviate symptoms does not mean it is safe for your baby.

Always discuss any supplemental foods with a practitioner before use!

CBD from Hops and Other Non-Cannabis Plants

Some CBD products and oil come from plants other than cannabis. Hops is one that is popular currently. (11)

People that use non-cannabis CBD mistakenly believe that they are safe from THC. False marketing of these products encourages this line of thinking.

Be warned that no matter where CBD comes from, the potential for conversion of CBD to THC in the digestive tract exists. CBD is ultimately a cannabinoid no matter what plant it comes from. Thus, unless the CBD is applied transdermally or intravenously to avoid the acidic conditions within the digestive tract, the risk for THC exposure and brain-altering effects still exists.

To give you a example of how this works, consider how beta carotene converts to Vitamin A in the digestive tract. It doesn’t matter if the beta carotene comes from carrots, peppers or squash. This nutrient will still potentially convert to Vitamin A. The same principle applies to CBD that is consumed orally. The digestive process can result in conversion to THC no matter what plant is the source of the CBD.

Is CBD Safe for Anyone?

Consumers desperately need more research about the high-inducing effects of CBD-to-THC that could manifest as a result of the digestive process.

The half life of oral CBD in the body is about 2 days. Thus, depending on how much a person consumes and how often, the potential risk of psychosis could increase over time depending on individual metabolism.

It seems that, as of this writing, the prudent course of action for the cautious consumer is to adopt a wait and see attitude toward CBD and CBD oil products pending further research on the very real potential for mind altering, pot-like effects.

Some companies are already working to develop synthetic transdermal CBD. Such a drug would bypass the gastrointestinal tract and avoid bioconversion to psychoactive THC and/or HHCs. Of course, this treatment likely has its own set of yet unknown dangers!

While the risks of THC exposure from CBD oil and other products are likely of little concern for gravely ill people who desperately need it, for otherwise healthy people and children, beware! It seems wise until further research is concluded to treat CBD oil, candy, and other products just like any other high inducing drug. Just. Say. No.

Sarah Pope MGA

Since 2002, Sarah has been a Health and Nutrition Educator dedicated to helping families effectively incorporate the principles of ancestral diets within the modern household.

Sarah was awarded Activist of the Year at the International Wise Traditions Conference in 2010.

Sarah received a Bachelor of Arts (summa cum laude, Phi Beta Kappa) in Economics from Furman University and a Master’s degree in Government (Financial Management) from the University of Pennsylvania.

Mother to three healthy children, blogger, and best-selling author, her work has been covered by USA Today, The New York Times, National Review, ABC, NBC, and many others.

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Comments (115)

Anna

Well, by now Healthline has corrected the article you reference as evidence for CBD causing psychosis, after I (and maybe others, who knows) pointed out to them that they had mistakenly put the side effects of THC for those of CBD. Now it lists only diarrhoea, changes in appetite and fatigue. Time for you to follow suit? You both reference the same scientific article, and now that this is the only remaining reference to back up your claim, I think it is time you actually looked at it and realised that it does not support your claim either. Could you then still go on and claim to have truth on your side, knowing that your claim is based on nothing at all? And keep on calling people who disagree with you biased? It’s pretty clear to me who is the biased one here, and probably to most others as well.
Sarah, you may have good intentions but you are not making the world a better place by publishing misinformation. Maybe a few people will be kept from trying CBD due to reading it, but most people will realise right away how ridiculous it is. It will just contribute to their mistrust of official information and authority figures on the subject of drugs. Because fact is that a lot of fairly harmless drugs have been needlessly demonised along with the genuinely dangerous ones since Nixon started his war on drugs. You might believe otherwise, but people who try them know better. And the more misinformation they see around them, the more they will be inclined to disbelieve also the genuine warnings about those drugs which can actually be really harmful. Especially now in this age of ‘fake news’ where people are more and more unsure of what information they can trust. People actually end up harming themselves much more due to ignorance than they would if they had full knowledge of the whole subject in advance! Proper education is the way to reduce the harm from drugs the most, not waging a war against them with misinformation – isn’t it obvious by now that this war has totally failed, because it is unwinnable?

April 20th, 2019 2:14 pm Reply

Sarah Pope MGA

I actually cited a scientific study about CBD converting to THC in the gut! You are welcome to believe anything you like, but the fact is that some people do experience psychosis from CBD. Read through the comments and read the referenced research study.

April 22nd, 2019 7:39 am Reply

rooislangwtf

The effort the Japanese study went to, to convert cbd to thc makes me wonder what the likelihood is of it actually happening in the human body (ph of 1.2 that’s lower than normal gastric acid and then a heck of a lot of purification). The epilepsy study didn’t go past observation to indicate thc effects (urine tests would’ve helped).

So the real conclusion to draw is until more tests are done:
Dont take cbd with alcohol or a lot of sugars or get a way to take cbd non orally (a patch or a suppository maybe).

April 10th, 2019 7:34 pm Reply

PATRICIA DONOVAN

I believe you picked and chose your so-called info from a multitude of sources without validating ANY of it. You are doing an extreme dis-service to those who use CBD effectively. People have to do their own research and find what works for them. Not all brands are created equal. I could write a book, with VALID sources, disputing virtually every point you made.

February 13th, 2019 1:06 pm Reply

Sarah Pope MGA

I find it amusing that people who disagree with an article frequently get in a huff and claim that “all” the sources/references are invalid and that they could “write a book” disputing every point. LOL Go read a site then that confirms all your biases. You don’t want the truth .. you want an article validating your belief system.

February 13th, 2019 1:37 pm Reply

Tim Wolford

I believe failed to include that the types of CBD oils in question are the Full Spectrum which has THC properties. The two other types will NOT produce THC and they are Broad Spectrum and Isolate Spectrum. The majority of CBD oils on the market today are Full Spectrum with THC compounds, however when the THC is extracted from the CBD Oils you have a Broad Spectrum product which may cost more, but will NOT have THC period! Do your homework and don’t always believe everything you read, especially when the Spectrums were never discussed

February 12th, 2019 11:23 am Reply

Sarah Pope MGA

Please read the article. You have apparently missed the point completely as have several other commenters. There is NO BRAND of CBD oil that is safe. ANY cannabidiol even if from another plant (like hops) will potentially trigger a conversion to THC in the gut. When NYC just banned CBD from edibles sold at restaurants, healthfood stores etc, there was NO distinction between “full spectrum” and isolate spectrum.

February 13th, 2019 8:56 am Reply

Dela Baldwin

Not all CBDs are created equal. Not all CBD has THC. A lot have trace amounts however not all. My company is 100% 0.00000 % THC free.

February 5th, 2019 9:52 am Reply

Sarah Pope MGA

I don’t think you understood the article! I am not suggesting that any CBD oil has THC in it … it DOESN’T MATTER how your CBD oil is produced … some CAN AND DOES CONVERT to small amounts of THC in the acidity of the digestive tract when consumed. Some people have a HUGE negative reaction to this.

Beta carotene partially converts to Vitamin A in the digestive tract too as do many other substances.

February 5th, 2019 10:26 am Reply

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Randi Melissa Schuster, PhD; Jodi Gilman, PhD; David Schoenfeld, PhD; John Evenden, PhD; Maya Hareli, BA; Christine Ulysse, MS; Emily Nip, BA; Ailish Hanly, BA; Haiyue Zhang, MS; and A. Eden Evins, MD, MPH

J Clin Psychiatry 2018;79(6):17m11977

10.4088/JCP.17m11977

Objective: Associations between adolescent cannabis use and poor neurocognitive functioning have been reported from cross-sectional studies that cannot determine causality. Prospective designs can assess whether extended cannabis abstinence has a beneficial effect on cognition.

Methods: Eighty-eight adolescents and young adults (aged 16–25 years) who used cannabis regularly were recruited from the community and a local high school between July 2015 and December 2016. Participants were randomly assigned to 4 weeks of cannabis abstinence, verified by decreasing 11-nor-9-carboxy-∆9-tetrahydrocannabinol urine concentration (MJ-Abst; n = 62), or a monitoring control condition with no abstinence requirement (MJ-Mon; n = 26). Attention and memory were assessed at baseline and weekly for 4 weeks with the Cambridge Neuropsychological Test Automated Battery.

Results: Among MJ-Abst participants, 55 (88.7%) met a priori criteria for biochemically confirmed 30-day continuous abstinence. There was an effect of abstinence on verbal memory (P = .002) that was consistent across 4 weeks of abstinence, with no time-by-abstinence interaction, and was driven by improved verbal learning in the first week of abstinence. MJ-Abst participants had better memory overall and at weeks 1, 2, 3 than MJ-Mon participants, and only MJ-Abst participants improved in memory from baseline to week 1. There was no effect of abstinence on attention: both groups improved similarly, consistent with a practice effect.

Conclusions: This study suggests that cannabis abstinence is associated with improvements in verbal learning that appear to occur largely in the first week following last use. Future studies are needed to determine whether the improvement in cognition with abstinence is associated with improvement in academic and other functional outcomes.

Trial Registration: ClinicalTrials.gov identifier: NCT03276221

Christina Brezing, MD, Frances Levin, MD

It is vital that physicians—particularly psychiatrists who are on the frontlines with patients who struggle with cannabis use—are able to identify and characterize cannabis use disorders; provide education; and offer effective, evidence-based treatments. This article provides a brief overview of each of these topics by walking through clinical decision-making with a case vignette that touches on common experiences in treating a patient with cannabis use disorder.

A separate and important issue is screening for emerging drugs of abuse, including synthetic “marijuana” products such as K2 and spice. Although these products are chemically distinct from the psychoactive compounds in the traditional cannabis plant, some cannabis users have tried synthetic “marijuana” products because of their gross physical similarity to cannabis plant matter.

CASE VIGNETTE

Mr. M is a 43-year-old legal clerk who has been working in the same office for 20 years. He presents as a referral from his primary care physician to your outpatient psychiatry office for an initial evaluation regarding “managing some mid-life issues.” He states that while he likes his job, it is the only job he has had since graduating college and he finds the work boring, noting that most of his co-workers have gone on to law school or more senior positions in the firm. When asked what factors have prevented him from seeking different career opportunities, he states that he would “fail a drug test.” Upon further inquiry, Mr. M says he has been smoking 2 or 3 “joints” or taking a few hits off of his “vaping pen” of cannabis daily for many years, for which he spends approximately $70 to $100 a week.

He first used cannabis in college and initially only smoked “a couple hits” in social settings. Over time, he has needed more cannabis to “take the edge off” and has strong cravings to use daily. He reports liking how cannabis decreases his anxiety and helps him fall asleep, although he thinks the cannabis sometimes makes him “paranoid,” which results in his avoidance of family and friends.

More recently, he identifies conflict and regular arguments with his wife over his cannabis use—she feels it prevents him from being present with his family and is a financial burden. He admits missing an important awards ceremony for her work and sporting events for his children, for which he had to “come up with excuses,” but the truth is that he ended up smoking more than he had intended and lost track of the time.

Mr. M reports multiple previous unsuccessful attempts to reduce his use and 2 days when he stopped completely, which resulted in “terrible dreams,” poor sleep, sweating, no appetite, anxiety, irritability, and strong cravings for cannabis. Resumption of his cannabis use relieved these symptoms. He denies tobacco or other drug use, including use of synthetic marijuana products such as K2 or spice, and reports having a glass of wine or champagne once or twice a year for special occasions.

The diagnosis

In the transition from DSM IV-TR to DSM-5, cannabis use disorders, along with all substance use disorders, have been redefined in line with characterizing a spectrum of pathology and impairment. The criteria to qualify for a cannabis use disorder remain the same except for the following:

1. The criterion for recurrent legal problems has been removed.

2. A new criterion for craving or a strong desire or urge to use cannabis has been added, and the terms abuse and dependence were eliminated.

To qualify as having a cannabis use disorder, a threshold of 2 criteria must be met. Severity of the disorder is characterized as “mild” if 2 or 3 criteria are met, “moderate” if 4 or 5 criteria are met, and “severe” if 6 or more criteria are met. Mr. M demonstrates 3 symptoms of impaired control: using longer than intended, unsuccessful efforts to cut back, and craving; 3 symptoms of social impairment: failure to fulfill home obligations, persistent problems with his wife, and reduced pursuit of occupational opportunities; 1 symptom of risky use: continued use despite paranoia; and 2 symptoms of pharmacological properties: tolerance and withdrawal. As such, he meets 9 criteria, which qualify him for a diagnosis of severe cannabis use disorder.

You summarize Mr. M’s 9 symptoms and counsel him about severe cannabis use disorder. He becomes upset and states that he was not aware one could develop an “addiction” to cannabis. He expresses an interest in treatment and asks what options are available.

Treatment options

Psychotherapeutic treatments, including motivational enhancement treatment (MET), cognitive behavioral therapy (CBT), and contingency management (CM), have demonstrated effectiveness in reducing frequency and quantity of cannabis use, but abstinence rates remain modest and decline after treatment. Generally, MET is effective at engaging individuals who are ambivalent about treatment; CM can lead to longer periods of abstinence during treatment by incentivizing abstinence; and CBT can work to enhance abstinence following treatment (preventing relapse). Longer duration of psychotherapy is associated with better outcomes. However, access to evidence-based psychotherapy is frequently limited, and poor adherence to evidence-based psychotherapy is common.

In conjunction with psychotherapy, medication strategies should be considered. Because there are no FDA-approved pharmacological agents for cannabis use disorder, patients should understand during the informed consent process that all pharmacotherapies used to treat this disorder are off-label. A number of clinical trials provide evidence for the off-label use of medications in the treatment of cannabis use disorder. The current strategies for the off-label treatment of cannabis use disorder target withdrawal symptoms, aim to initiate abstinence and prevent relapse or reduce use depending on the patient’s goals, and treat psychiatric comorbidity and symptoms that may be driving cannabis use. Here we focus on the evidence supporting these key strategies.

Targeting withdrawal and craving

Cannabis withdrawal is defined by DSM-5 as having 3 or more of the following signs and symptoms that develop after the cessation of prolonged cannabis use:

• Irritability, anger, or aggression

• Nervousness or anxiety

• Sleep difficulty

• Decreased appetite or weight loss

• Restlessness

• Depressed mood

• At least one of the following physical symptoms that causes discomfort: abdominal pain, shakiness/tremors, sweating, fever, chills, or headache

Withdrawal symptoms may be present within the first 24 hours. Overall, they peak within the first week and persist up to 1 month following the last use of cannabis. In the case of Mr. M, insomnia, poor appetite, and irritability as well as sweating are identified, which meet DSM-5 criteria for cannabis withdrawal during the 2 days he abstained from use. He also identifies strong craving and vivid dreams, which are additional withdrawal symptoms included on marijuana withdrawal checklists in research studies, although not included in DSM-5 criteria. These and other symptoms should be considered in clinical treatment.

Medication treatment studies for cannabis withdrawal have hypothesized that if withdrawal symptoms can be reduced or alleviated during cessation from regular cannabis use, people will be less likely to resume cannabis use and will have better treatment outcomes. Studies have shown that dronabinol and nabilone improved multiple withdrawal symptoms, including craving; and quetiapine, zolpidem, and mirtazapine help with withdrawal-induced sleep disturbances.

Combining dronabinol and lofexidine (an alpha-2 agonist) was superior to placebo in reducing craving, withdrawal, and self-administration during abstinence in a laboratory model. However, in a subsequent treatment trial, the combined medication treatment was not superior to placebo in reducing cannabis use or promoting abstinence.

Six double-blind placebo-controlled pharmacotherapy trials in adults with cannabis use disorder have looked at withdrawal as an outcome. Of these studies, only dronabinol, bupropion, and gabapentin reduced withdrawal symptoms. In addition to reducing withdrawal symptoms, nabiximols/Sativex (a combination tetrahydrocannabinol [THC] and cannabidiol nasal spray not available in the US) increased retention (while actively on the medication in an inpatient setting) but did not reduce outpatient cannabis use at follow-up.

All of the medications available for prescription in the US can be monitored reliably with urine drug screening to assess for illicit cannabis use except dronabinol, which will result in a positive screen for cannabis. When using urine drug screening, remember that for heavy cannabis users the qualitative urine drug screen can be positive for cannabis up to a month following cessation. When selecting a medication, take into account the cost of the medication, particularly since insurance will likely not cover THC agonists such as dronabinol for this indication, and possible misuse or diversion of scheduled substances (eg, dronabinol, nabilone). In addition, monitoring for reductions in substance use and withdrawal symptoms is key.

Abstinence initiation and relapse prevention

Other clinical trials have looked at medications to promote abstinence by reducing stress-induced relapse, craving (not as a component of withdrawal), and the reinforcing aspects of cannabis. Of these trials, the following results show potential promise with positive findings: gabapentin reduced quantitative THC urine levels and improved cognitive functioning (in addition to decreasing withdrawal), and buspirone led to more negative urine drug screens for cannabis (although the difference was not significant compared with placebo). However, in a follow-up larger study, no differences were seen compared with placebo and women had worse cannabis use outcomes on buspirone.

N-acetylcysteine resulted in twice the odds of a negative urine drug screen in young adults and adolescents (although there was no difference between adolescent groups in self-report of cannabis use).Gray and colleagues reported that no differences were seen between N-acetylcysteine and placebo (results of the trial are soon to be published). Topiramate resulted in significantly decreased grams of cannabis used but no difference in percent days used or proportion of positive urine drug screens.16 In a recent small clinical trial, reductions in cannabis use were seen with oxytocin in combination with MET.17Studies with nabilone and long-term naltrexone administration reduced relapse and cannabis self-administration and subjective effects, respectively, which suggests promising avenues yet to be explored by clinical trials.

Treatment of psychiatric comorbidity

Other studies have looked at the effects of treating common comorbid psychiatric disorders in adults with cannabis use disorder, postulating that if the psychiatric disorder is treated, the individual may be more likely to abstain or reduce his or her cannabis use. For example, if a person is less depressed, he may better engage in CBT for relapse prevention.

Fluoxetine for depression and cannabis use disorder in adolescents decreased cannabis use and depression, although there was no difference compared with placebo. A trial of venlafaxine for adults with depression and cannabis use disorder demonstrated less abstinence with greater withdrawal-like symptoms compared with placebo. These findings suggest that this antidepressant might not be beneficial for treatment-seeking individuals with cannabis use disorder and may actually negatively affect outcomes.

 

CASE VIGNETTE CONT’D

After discussing and presenting the different psychotherapy and medication treatment options to Mr. M, you and he decide to start CBT to help with abstinence initiation. In addition, you prescribe 20 mg of dronabinol up to 2 times daily in combination with 50 mg of naltrexone daily, to help globally target Mr. M’s withdrawal symptoms and prevent relapse once abstinence is achieved. However, a few days later, Mr. M calls to say that his insurance will not cover the prescription for dronabinol and he cannot afford the high cost. Given his main concerns of cannabis withdrawal symptoms, you select gabapentin up to 400 mg 3 times daily and continue weekly individual CBT.

Mr. M calls back several days later and reports that he has made some improvements in reducing the frequency of his cannabis use, which he attributes to the medication, but he thinks he needs additional assistance. After reviewing the treatment options again, he gives informed consent to start 1200 mg of N-acetylcysteine twice daily. After 10 weeks of this medication, his urine screens are negative.

You continue to provide relapse prevention CBT. He reports to you that his anxiety and insomnia are almost resolved, and you suspect that withdrawal was the cause of these symptoms. He reports significant improvement in his relationship with his family and recently received a promotion at work for “going above and beyond” on a project he was given the lead.

Over the next 6 months, he has 2 relapses that in functional analysis with you are determined to be triggered by unsolicited contact from his former drug dealer. Together, you develop a plan to block any further contact from the drug dealer. After several months, both the gabapentin and N-acetylcysteine are tapered and discontinued. Mr. M continues to see you for biweekly therapy sessions with random drug screens every 4 to 6 weeks.

 

Conclusion

Based on the available evidence, gabapentin, THC agonists, naltrexone, and possibly N-acetylcysteine show the greatest promise in the off-label treatment of cannabis use disorders. System considerations, such as medication cost, need to be factored into the decision-making as well as combination medication and psychotherapy approaches, which—as demonstrated in the case of Mr. M—may ultimately work best. Until further research elucidates the standard of medication practices for cannabis use disorder, the best off-label medication strategy should target any co-occurring disorders as well as any identified problematic symptoms related to cannabis use and cessation of use. When available, referral for evidence-based psychotherapy should be made.

Source: https://www.psychiatrictimes.com/special-reports/treatment-cannabis-use-disorders-case-report/ August 2017

 

Abstract

BACKGROUND:

Violence is a major concern and is prevalent across several mental disorders. The use of substances has been associated with an exacerbation of psychiatric symptoms as well as with violence. Compared to other substances such as alcohol and cocaine, existing literature on the cannabis-violence relationship has been more limited, with most studies being conducted in the general population, and has shown controversial results. Evidence has suggested a stronger relationship when examining the effects of the persistency of cannabis use on future violent behaviors. Though, while cannabis use is highly prevalent amid psychiatric patients, far less literature on the subject has been conducted in this population. Hence, the present prospective study aims to investigate the persistency of cannabis use in psychiatric patients.

METHOD:

The sample comprised of 1,136 recently discharged psychiatric patients provided by the MacArthur Risk Assessment Study. A multi-wave (five-assessment) follow-up design was employed to allow temporal sequencing between substance use and violent behaviors. Generalized estimating equations (GEE) were used to examine the effect of persistency of cannabis use on violence, while controlling for potential confounding factors. Potential bidirectional association was also investigated using the same statistical approach.

RESULTS:

Our results suggest a unidirectional association between cannabis use and violence. GEE model revealed that the continuity of cannabis use across more than one time wave was associated with increased risks of future violent behavior. Patients who reported having used cannabis at each follow-up periods were 2.44 times more likely to display violent behaviors (OR = 2.44, 95% CI: 1.06-5.63, p < 0.05).

Odds ratios for violent behaviors associated with substance use across each time points. x-Axis represent the number of follow-up periods with substance-use, y-axis represent the Odds Ratios; Reference is no use of substance across time points; Odds Ratios are controlled for the effects of time, other substances used at each time point, age, age at first hospitalization, sex, ethnicity, Schizophrenia-Spectrum disorders (presence/absence), affective disorders (presence/absence), psychopathic traits (PCL), impulsivity (BIS-11) (*p < 0.05; **p < 0.01; ***p < 0.001; N.S., Not statistically significant).

CONCLUSION:

These findings are particularly relevant as they suggest that the longer individuals report having used cannabis after a psychiatric discharge, the more likely they are of being violent in the following time waves. These results add to our understanding of the negative consequences of chronic cannabis use amid psychiatric patients.

Source: https://www.ncbi.nlm.nih.gov/pubmed/28983261 September 2017

  • The rapper is suing insurance company, claiming it is refusing to pay him after he was forced to cancel shows in November last year
  • In legal documents Lloyd’s suggest marijuana may have led to Kanye’s mental health issues in a bid to invalidate the performer’s insurance claim
  • Psychosis affects the mind and causes the sufferer to lose touch with reality
  • Dr Lucy Troup, from Colorado State University, explained it cannabis use could cause a psychotic breakdown
  • She said there are a variety of factors that influence it, but research shows it is linked to psychosis and other mental health issues 

By Abigail Miller

Kanye West is suing his tour’s insurer after the company allegedly refused to pay for his canceled shows in November – and blamed his cannabis use.

The rapper was forced to cancel the last 21 shows of his North American tour after he had a mental breakdown and had to be checked into a hospital.

While his insurer Lloyd’s of London would normally cover the costs, the company said they don’t have to pay because his marijuana use caused the breakdown.

The 40-year-old is asking for $10 million in damages from Lloyd’s, claiming the company has yet to pay him out for his cancelled shows, and has no intent to do so.

His company said in a legal document filed on Tuesday that insurers have yet to pay and is ‘implying that Kanye’s use of marijuana may provide them with the basis to deny the claim’.

Here, Daily Mail Online takes a closer look at how marijuana use could cause psychosis and potentially cause a mental breakdown, as Lloyd’s claims.

Marijuana legalization began in the United States in 1996, when California legalized the drug for medical use.

That sparked a wave.

In the next decade, 14 states followed suit: Oregon, Alaska, Washington, Maine, Hawaii, Nevada, Colorado, Montana, Vermont, New Mexico, Michigan, New Jersey, Arizona and Massachusetts.

Then in 2012, Colorado and Washington state legalized the drug for recreational use.

Now, just five years later, marijuana is legal for medical and recreational use in eight states: Massachusetts, Colorado, Washington, Alaska, Oregon, Nevada, California and Maine.

It is also legal for strictly medical use in the District of Columbia and 21 states: Montana, North Dakota, Arizona, New Mexico, Arkansas, Louisiana, Florida, Illinois, Minnesota, Michigan, Ohio, New York, Pennsylvania, Maryland, Vermont, New Hampshire, New Jersey, Rhode Island, Connecticut, Delaware and Hawaii.

The wave has given rise to a booming industry of edibles, dispensaries, cannabis healthcare professionals, and paraphernalia.

Marijuana is the national favorite according to a report published by Addictions.com, making up more than 70 percent of all drug use in the United States.

But experts warn researchers are struggling to keep up with the pace of legalization, and there are still many gaps in our knowledge.

However, some experts warn people are using the drug to self medicate for things like depression and anxiety despite research showing it does more harm than good.

In fact, there research shows that increased risk of depression as a result of frequent marijuana use is thought to be behind psychosis’ onset. The two mental health conditions have previously been linked.

‘A number of people choose to self medicate, but it could actually make things like anxiety and depression worse,’ Dr Lucy Troup, a professor of cognitive neuroscience at Colorado State University told Daily Mail Online.

‘We can’t fully understand yet the brain mechanisms that cause mental illness, but we’ve seen a clear link between marijuana use and users who report psychotic breaks. But again, it’s different for every person.’

In California medical marijuana can be used as a treatment for anxiety. In the other states and DC, someone suffering from anxiety or depression can apply for a medical marijuana license if their conditions are considered to be severe and debilitating.

COULD CANNABIS TREAT MIGRAINES?

Chemicals in cannabis could be effective at treating painful migraines, research revealed last month.

Cannabinoids, the compounds in marijuana that make you feel high, may be better at treating pain than recommended migraine medication, a study found.

Researchers from the Interuniversity Center in Florence found that pills containing the chemicals reduce the pain felt by migraine sufferers by 43.5 per cent.

The drug also had a number of additional effects, including stopping stomach aches and muscle pain, according to the researchers.

Previous research has found cannabis reduces migraines by targeting cells in the body that control pain relief and inflammation.

CAN MARIJUANA USE CAUSE A PSYCHOTIC BREAK?

Psychosis is defined as a condition that affects the mind and causes the sufferer to lose touch with reality.

Symptoms include:

  • delusions and hallucinations
  • feelings of paranoia and suspiciousness
  • disorganized thinking and speaking
  • loss of or decreased motivation
  • loss of or decreased ability to initiate or come up with new ideas
  • difficulties expressing emotion

Studies have found that marijuana is thought to cause psychosis-like experiences by increasing a user’s risk of depression. The two mental health conditions have been linked.

Frequently abusing the substance also significantly reduces a user’s ability to resist socially unacceptable behavior when provoked, research suggests.

‘We don’t understand the precise mechanisms for psychosis, but there is clear research that supports that cannabis use can lead to it,’ Dr Lucy Troup, a professor of cognitive neuroscience at Colorado State University told Daily Mail Online.

‘I can’t comment particularly on Kanye West’s case, because I don’t know a lot about him other than what the media says. But there are different variables that could have made it more likely such as how long it’s been used, when someone first started, how concentrated or potent the drug is that they are using, how they are taking it, and their specific genotype.’

Drug-induced psychosis is most commonly associated with LSD or amphetamines, but can also be caused by marijuana, cocaine and alcohol.

Results of a study by the University of Montreal revealed that going from being an occasional marijuana user to abusing the substance once a week or as often as every day, increases the risk of psychosis-like experiences by 159 percent.

The results also demonstrated that marijuana use reduces a person’s ability to resist socially unacceptable behavior in response to a particular stimulus.

KANYE WEST’S PAST MARIJUANA USE: COULD THE DRUG HAVE CAUSED THE RAPPER’S MENTAL BREAK?

In the past Kanye has been candid about his weed habit. He’s made multiple references in his songs. He also admitted to smoking before the 2015 Video Music Awards where he infamously announced his 2020 presidential candidacy.

Dr Troup explained that while she doesn’t know much about the rapper’s circumstance in particular, she was surprised to hear that Lloyd’s of London isn’t paying out.

She said that if a bank makes that claim about anyone, be it Kanye or someone less well known, the process to support that claim is long and complicated.

‘There isn’t enough knowledge about his [Kanye’s] medical history for anyone but his doctor to say for sure what caused his mental break,’ Dr Troup explained. ‘It would be a long and complicated process because they would have to look at his blood work, a hospital report, and a number of other things.’

‘I’m guessing when you insure a rock star you have to expect these kinds of things,’ she added.

A source has also told InTouch that Kim and Kanye are now worried footage taken by the rapper’s team in days prior to the tour’s cancellation could be used against him in court.

The video allegedly shows his mental state deteriorating before he broke down in the days leading up to his hospitalization.

Source: https://www.dailymail.co.uk/health/article-4758542/Could-marijuana-caused-Kanye-s-mental-breakdown.html
August 2017

Psychology of Addictive Behaviors journal makes corrections, SAM calls on media to correct stories

A prominent journal article about marijuana and health which resulted in media outlets reporting on marijuana’s harmlessness has now been corrected. A recheck of the statistics has now found that the incidence of psychotic disorders trended toward a 2.5-fold increase in marijuana users, a difference that went beyond a trend to reach significance in a one-tailed statistical test. This degree of impact matches very well the results of many prior studies involving marijuana use and psychosis though falls short of the five-fold increase in psychosis risk for marijuana users seen with the high strength strains that are more recently available.

Dr. Christine Miller, a former schizophrenia researcher from Johns Hopkins University and now Director of SAM Maryland, first alerted the journal, Psychology of Addictive Behaviors, last December. Some media outlets have already corrected their original story. 

“We commend the Washington Post’s Ariana Cha for now updating her story, and hope many more will follow her lead,” remarked Dr. Miller. “The flaw in the original University of Pittsburgh report were certain correction factors applied to the raw data, factors which are strongly affected by psychosis rather than being causes of such a disorder. These inappropriate corrections overpowered the marijuana effect. We’re glad the corrections have been made.”

SAM urges other media outlets to correct their headlines and stories.

The new data comes on the heels of a major report released by the State of Vermont’s Health Department which found that marijuana worsened conditions ranging from mental illness to motor vehicle accidents to negative pregnancy effects – and almost all of them are found to be worsened by marijuana:

Source: Email from SAM (Smart Approaches to Marijuana) <info@learnaboutsam.org>, January 2016

Link to clarification:

https://psycnet.apa.org/record/2015-58335-001

  • Cannabis interferes with a user’s ability to recognize, process and empathize with human emotions including happiness, sadness and anger
  • Pot smokers were shown faces depicting different emotions in tests
  • They were hooked up to brain monitoring device, looking at activity levels 
  • Cannabis users showed greater response to negative emotions 
  • And those smoking marijuana showed lower response to happy emotions 

Smoking cannabis alters a person’s ability to perceive and judge emotions, a study has found.

The drug interferes with user’s capacity to recognize, process and empathize with human emotions, including happiness, sadness and anger.

But the results also suggest that the brain may be able to counteract these effects depending on whether the emotions are directly, or indirectly detected.

The complex biochemistry of marijuana and how it affects the brain is only beginning to be understood.

Dr Lucy Troup, assistant professor of psychology at Colorado State University, has set out to answer specifically how, if at all, cannabis use affects a person’s ability to process emotions.

She has long been fascinated by the psychology of drugs and addiction.

‘We’re not taking a pro or anti stance, but we just want to know, what does it do? It’s really about making sense of it,’ she said. 

For almost 20 years Dr Troup and her graduate students have been conducting experiments to measure the brain activity of about 70 volunteers.

They all identified themselves as chronic, moderate or non-users of cannabis.

They were all vetted as legal users of cannabis, and were either medical marijuana users aged 18 or older, or recreational users aged 21 or older.

The experiments involved the participants looking at faces depicting four separate expressions: neutral, happy, fearful and angry, while they were hooked up to an electroencephalogram (EEG), which shows the electrical activity of the brain.

Cannabis users showed a greater response to faces showing negative expressions, especially angry faces, when compared with a control group of non-cannabis users. In contrast, those who used the drug showed a smaller response to positive expressions – happy faces – compared with the control group

Cannabis users showed a greater response to faces showing negative expressions, especially angry faces, when compared with a control group of non-cannabis users.

In contrast, those who used the drug showed a smaller response to positive expressions – happy faces – compared with the control group.

Those taking part in the study were also asked to pay attention to the emotion and identify it.

Researchers noted in those cases, users and non-users of cannabis could not be told apart.

But, when they were asked to focus on the sex of the face, and then identify the emotion, cannabis users scored much lower than non-users.

This signified a depressed ability to ‘implicitly’ identify emotions.

Cannabis users were also less able to empathize with the emotions, the scientists found.

They said their findings seem to suggest the brain’s ability to process emotion is affected by cannabis, but there may be some compensation that counteracts those differences.

The study is published in the journal PLOS ONE.

Source: https://www.dailymail.co.uk/health/article-3472039/Cannabis-DOES-alter-brain-s-ability-process-emotions-experts-warn.html  March 2016

Anybody wondering what happens to the 8 per cent of the skunk-smoking population who develop mental illness should visit any psychiatric hospital in Britain or speak to somebody who has done so What is really needed in dealing with cannabis is a “tobacco moment”, as with cigarettes 50 years ago, when a majority of people became convinced that smoking might give them cancer and kill them. Since then the number of cigarette smokers in Britain has fallen by two-thirds.

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

Anybody wondering what happens to this 8 per cent of the skunk-smoking population should visit any mental hospital in Britain or speak to somebody who has done so. Dr Humphrey Needham-Bennett, medical director and consultant psychiatrist of Cygnet Hospital, Godden Green in Sevenoaks, explained to me that among his patients “cannabis use is so common that I assume that people use or used it. It’s quite surprising when people say ‘no, I don’t use drugs’.”

The connection between schizophrenia and cannabis was long suspected by specialists but it retained its reputation as a relatively benign drug, its image softened by the afterglow of its association with cultural and sexual liberation in the 1960s and 1970s.

This ill-deserved reputation was so widespread that even 20 years ago, the possible toxic side effects of cannabis were barely considered. Zerrin Atakan, formerly head of the National Psychosis Unit at the Maudsley Psychiatric Hospital and later a researcher at the Institute of Psychiatry,

said: “I got interested in cannabis because I was working in the 1980s in an intensive care unit where my patients would be fine after we got them well. We would give them leave and they would celebrate their new found freedom with a joint and come back psychotic a few hours later.”

She did not find it easy to pursue her professional interest in the drug. She recalls: “I was astonished to discover that cannabis, which is the most widely used illicit substance, was hardly researched in the 1990s and there was no research on how it affected the brain.” She and fellow researchers made eight different applications for research grants and had them all turned down, so they were reduced to taking the almost unheard of course of pursuing their research without the support of a grant.

Studies by Dr Atakan and other psychiatrists all showed the connection between cannabis and schizophrenia, yet this is only slowly becoming conventional wisdom. Perhaps this should not be too surprising because in 1960, long after the link between cigarettes and lung cancer had been scientifically established, only a third of US doctors were persuaded that this was the case.

A difficulty is that people are frightened of mental illness and ignorant of its causes in a way that is no longer true of physical illnesses, such as cancer or even HIV. I have always found that three quarters of those I speak to at random about mental health know nothing about psychosis and its causes, and the other quarter know all too much about it because they have a relative or friend who has been affected.

Even those who do have experience of schizophrenia do not talk about it very much because they are frightened of a loved one being stigmatised. They may also be wary of mentioning the role of cannabis because they fear that somebody they love will be dismissed as a junkie who has brought their fate upon themselves.

This fear of being stigmatised affects institutions as well as individuals. Schools and universities are often happy to have a policy about everything from sex to climate change, but steer away from informing their students about the dangers of drugs. A social scientist specialising in drugs policy explained to me that the reason for this is because “they’re frightened that, if they do, everybody will think they have a drugs problem which, of course, they all do”.

The current debate about cannabis – sparked by the confiscation of the cannabis oil needed by Billy Caldwell to treat his epilepsy and by William Hague’s call for the legalisation of the drug – is missing the main point. It is all about the merits and failings of different degrees of prohibition of cannabis when it is obvious that legal restrictions alone will not stop the 2.1 million people who take cannabis from going on doing so. But the legalisation of cannabis legitimises it and sends a message that the government views it as relatively harmless. The very fact of illegality is a powerful disincentive for many potential consumers, regardless of the chances of being punished.

The legalisation of cannabis might take its production and sale out of the hands of criminal gangs, but it would put it into the hands of commercial companies who would want to make a profit, advertise their product and increase the number of their customers. Commercialisation of cannabis has as many dangers as criminalisation.

A new legal market in cannabis might be regulated and the toxicity of super-strength skunk reduced. But the argument of those who want to legalise cannabis is that the authorities are unable to enforce regulations when the drug is illegal, so why should they be more successful in regulating it when its production and sale is no longer against the law?

The problem with these rancorous but sterile arguments for and against legalisation and decriminalisation is that they divert attention from what should and can be done: a sustained campaign to persuade people of all ages that cannabis can send them insane. To a degree people are learning this already from bitter experience. As Professor Murray told me five years ago, the average 19- to 23-year-old probably knows more about the dangers of cannabis than the average doctor “because they have a friend who has gone paranoid. People know a lot more about bad trips than they used to.”

Patrick Cockburn is the co-author of Henry’s Demons: Living With Schizophrenia, A Father and Son’s Story

A depressing aspect of the present debate about cannabis is that so many proponents of legalisation or decriminalisation have clearly not taken on board that the causal link between cannabis and psychosis has been scientifically proven over the past ten years, just as the connection between cancer and cigarettes was proved in the late 1940s and 1950s.

The proofs have emerged in a series of scientific studies that reach the same grim conclusion: taking cannabis significantly increases the risk of schizophrenia. One study in The Lancet Psychiatry concludes that “the risk of individuals having a psychotic disorder showed a roughly three times increase in users of skunk-like cannabis, compared with those who never used cannabis”. As 94 per cent of cannabis seized by the police today is super-strength skunk, compared to 51 per cent in 2005, almost all those who take the drug today will be vulnerable to this three-fold increase in the likelihood that they will develop psychosis.

Home Secretary Sajid Javid: The government will carry out a review of the scheduling of cannabis for medicinal use

Mental health professionals have long had no doubts about the danger. Five years ago, I asked Sir Robin Murray, professor of psychiatric research at the Institute of Psychiatry in London, about them. He said that studies showed that “if the risk of schizophrenia for the general population is about one per cent, the evidence is that, if you take ordinary cannabis, it is two per cent; if you smoke regularly you might push it up to four per cent; and if you smoke ‘skunk’ every day you push it up to eight per cent”.

 

Source:

http://www.pnas.org/content/109/40/E2657

July 2012

  • Cannabis is responsible for 91% of drug addiction cases involving teenagers
  • Skunk – high-potency herbal cannabis – causing more people to seek treatment 
  • Backs up research that skunk is having detrimental impact on mental health

Supporters of the drug claim it is harmless, but an official report now warns the ‘increased dominance of high-potency herbal cannabis’ – known as skunk – is causing more young people to seek treatment.

The revelation comes amid growing concerns that universities – and even some public schools – are awash with high-strength cannabis and other drugs.

The findings also back up academic research, revealed in The Mail on Sunday over the past three years, that skunk is having a serious detrimental impact on the mental health of the young. At least two studies have shown repeated use triples the risk of psychosis, with sufferers repeatedly experiencing delusional thoughts. Some victims end up taking their own lives.

The latest UK Focal Point on Drugs report, drawn up by bodies including Public Health England, the Scottish Government and the Home Office, found that:

Cannabis is responsible for 91 per cent of cases where teenagers end up being treated for drug addiction, shocking new figures reveal (file photo)
Cannabis is responsible for 91 per cent of cases where teenagers end up being treated for drug addiction, shocking new figures reveal 
  • Over the past decade, the number of under-18s treated for cannabis abuse in England has jumped 40 per cent – from 9,043 in 2006 to 12,712 in 2017;
  • Treatment for all narcotics has increased by 20 per cent – up from 11,618 to 13,961;
  • The proportion of juvenile drug treatment for cannabis use is up from four in five cases (78 per cent) to nine in ten (91 per cent);
  • There has been a ‘sharp increase’ in cocaine use among 15-year-olds, up 56 per cent from 16,700 in 2014 to 26,200 in 2016.

Last night, Lord Nicholas Monson, whose 21-year-old son Rupert Green killed himself last year after becoming hooked on high-strength cannabis, said: ‘These figures show the extent of the damage that high-potency cannabis wreaks on the young.

‘The big danger for young people – particularly teens – is that their brains can be really messed up by this stuff because they are still developing biologically. If they develop drug-induced psychosis – as Rupert did – the illness can stick for life.’

The large rise in the number of youngsters treated for cannabis abuse comes despite the fact that total usage is falling slightly.

The report concludes: ‘While fewer people are using cannabis, those who are using it are experiencing greater harm.’

Almost all cannabis on Britain’s streets is skunk, which is four times more powerful than types that dominated the market until the early 2000s. It can even trigger hallucinations.

Lord Monson said: ‘We really need Ministers to get a grip and launch a major publicity campaign about the dangers.’ 

Source: https://www.dailymail.co.uk/news/article-5642917/Nine-ten-teens-drug-clinics-treated-marijuana-use.html  April 2018

By William Ross Perlman, Ph.D., CMPP, NIDA Notes Contributing Writer

This research:

  • Identified a gene variant that promotes impulsive behavior and enhanced responses to heroin in rats.
  • Linked the corresponding human gene variant to increased risk for impulsivity and drug use.

People who are highly impulsive and those diagnosed with ADHD are at increased risk for substance use disorders (SUD). Recent research implicates a variant of the gene for a protein called cAMP-response element modulator (CREM) in these associations. Drs. Michael L. Miller and Yasmin L. Hurd from the Icahn School of Medicine at Mount Sinai in New York, with colleagues from several other institutions, showed that the gene variant promotes impulsive and hyperactive behavior in both animals and humans, and can contribute to a person’s risk for developing SUD.

Of Rats…

The Icahn researchers began their investigations with a strain of rats that exhibit impulsive behaviors resembling human attention-deficit/hyperactivity disorder (ADHD). Initial experiments confirmed that, compared with a strain (Western Kyoto) of rats that are not known for impulsivity, these “spontaneously hypertensive” (SH) rats:

  • Were more impatient to receive rewards, fidgeted more while waiting to receive rewards, ran around more, and were more attracted to novel experiences.
  • Self-administered more heroin and, when it was made unavailable, gave up seeking it less readily.  
  • Had enhanced elevation of dopamine levels in response to heroin.

The researchers screened the rats’ DNA for genetic differences that might contribute to these behavioral differences. The results revealed that the two strains carried different variants of the gene for CREM. As a result, the SH rats had lower concentrations of CREM in the core of the nucleus accumbens—a key brain region governing reward and movement.

…And People

 

Figure 1. A CREM Gene Variant Increases HyperactivityHyperactivity scores were higher in ADHD subjects than in control subjects. In addition, ADHD subjects who carried at least one copy of the less highly expressed A variant (i.e., with the G/A or A/A CREM genotype) reported significantly higher hyperactivity than did those carrying only the more highly expressed G variant (i.e., with the G/G genotype). Genotype had no effect on hyperactivity in non-ADHD control subjects

The researchers used genetic and behavioral evidence from previous studies conducted by other researchers to demonstrate that the corresponding variant in the human CREM gene similarly predisposes people to impulsivity. This variant occupies approximately the same position on the human gene that the rodent variant occupies on the rodent gene. At this site, known as rs12765063, the CREM gene exists in two versions—called A and G—and the A variant dials down CREM production. In one study, preschool children with the A variant were found to be more distractible and to engage in more dangerous activities than peers with only the G variant (Figure 1). In another, among adolescents with ADHD, those who carried the A variant reported more symptomatic hyperactivity than those who did not.

The researchers further found that by promoting impulsivity, the variant raises the risk of drug use. Thus, in two studies of adolescents, neither the A variant alone nor ADHD alone increased the risk for drug use, but the two together did. The first analysis looked at adolescents with ADHD, and found higher rates of drug use among those with the A variant than among those with only the G variant. The second analysis looked at adolescents who had the A variant of rs12765063 and histories of childhood ADHD. It found that those whose childhood ADHD still persisted reported more use of alcohol, tobacco, marijuana, and prescription stimulants than those who had outgrown their ADHD (Figure 2). Moreover, those who no longer had ADHD reported no more drug use than a comparison group who did not carry the A variant.

 

Figure 2. The A Variant of the CREM Gene Is Associated With Increased Drug Use in People With Persistent ADHD Among a cohort whose childhood ADHD persisted through adolescence, those with the CREM A variant reported more drug use than those with only the G variant. Genotype was not linked to risk for drug use in people without ADHD (i.e., those who never had ADHD or those with remitted ADHD).

A Key to Prevention and Treatment?

Dr. Hurd suggests that CREM may be a key link between impulsivity and vulnerability to addiction. Understanding these relationships may help identify new ways of treating or preventing SUD. The protein is known to regulate multiple gene networks and their biological functions, and to influence the growth of structures that neurons use to communicate with each other.

Dr. Hurd says, “These results highlight that CREM is a mediating factor between impulsivity and substance abuse vulnerability. It brings attention to CREM in the nucleus accumbens as a regulator of impulsive action and structural plasticity.”

The study was supported by NIH grants DA015446, DA030359, DA006470, DA038954, DA031559, and DA007135.

Source: https://www.drugabuse.gov/news-events/nida-notes/2018/06/gene-links-impulsivity-drug-use-vulnerability June 2018

Sydney Parliament House, 09.07.2018

Cannabis has been greatly oversold by a left leaning press controlled by globalist and centralist forces while its real and known dangers have not been given appropriate weight in the popular press. In particular its genotoxic and teratogenic potential on an unborn generation for the next hundred years has not been aired or properly weighed in popular forums.

These weighty considerations clearly take cannabis out of the realm of personal choice or individual freedoms and place it squarely in the realm of the public good and a matter with which the whole community is rightly concerned and properly involved.

Cannabinoids are a group of 400 substances which occur only in the leaves of the Cannabis sativa plant where they are used by the plants as toxins and poisons in natural defence against other plants and against herbivores.

Major leading world experts such as Dr Nora Volkow, Director of the National Institute of Drug Abuse at NIH 1, Professor Wayne Hall, Previous Director of the Sydney Based National Drug and Alcohol Research Centre at UNSW 2, and Health Canada 3 – amongst many others – are agreed that cannabis is linked with the following impressive lists of toxicities:

1) Cannabis is addictive, particularly when used by teenagers

2) Cannabis affects brain development

3) Cannabis is a gateway to other harder drug use

4) Cannabis is linked with many mental health disorders including anxiety, depression,

psychosis, schizophrenia and bipolar disorder

5) Cannabis alters and greatly impairs the normal developmental trajectory – getting a

job, finishing a course and forming a long term stable relationship 4-11

6) Cannabis impairs driving ability 12

7) Cannabis damages the lungs

8) Cannabis is immunosuppressive

9) Cannabis is linked with heart attack, stroke and cardiovascular disease

10) Cannabis is commonly more potent in recent years, with forms up to 30% being widely available in many parts of USA, and oils up to 100% THC also widely available.

Serious questions have also been raised about its involvement in 12 different cancers, increased Emergency Room presentations and exposures of developing babies during pregnancy. It is with this latter group that the present address is mainly concerned.

Basic Physiology and Embryology Cells make energy in dedicated organelles called mitochondria. Mitochondrial energy, in the form of ATP, is known to be involved in both DNA protection and control of the immune system. This means that when the cell’s ATP is high DNA maintenance is good and the genome is intact. When cellular ATP drops DNA maintenance is impaired, DNA breaks remain unsealed, and cancers can form. Also immunity is triggered by low ATP.

As organisms age ATP falls by half each 20 years after the age of 20. Mitochondria signal and shuttle to the cell nucleus via several pathways. Not only do cells carry cannabinoid receptors on their surface, but they also exist, along with their signalling machinery, at high density on mitochondria themselves 13-19. Cannabis, and indeed all addictive drugs, are known to impair this cellular energy generation and thus promote the biochemical aging process 14-16,19,20. Most addictions are associated with increased cancers, increased infections and increased clinical signs of ageing 21-34.

The foetal heart forms very early inside the mother with a heartbeat present from day 21 of human gestation. The heart forms by complicated pathways, and arises from more than six groups of cells inside the embryo 35,36. First two arteries come together, they fold, then flex and twist to give the final shape of the adult heart. Structures in the centre of the heart mass called endocardial cushions grow out to form the heart valves between the atria and ventricles and parts of the septum which grows between the two atria and ventricles. These cardiac cushions, and their associated conoventricular ridges which grow into and divide the cardiac outflow tract into left and right halves, all carry high density cannabinoid type 1 receptors (CB1R’s) and cannabis is known to be able to interfere with their growth and development.CB1R’s appear on foetal arteries from week nine of human gestation 37.

The developing brain grows out in a complex way in the head section 35,36. Newborn brain cells are born centrally in the area adjacent to the central ventricles of the brain and then migrate along pathways into the remainder of the brain, and grow to populate the cortex, parietal lobes, olfactory lobes, limbic system, hypothalamus and hippocampus which is an important area deep in the centre of the temporal lobes where memories first form.

Developing bipolar neuroblasts migrate along pathways and then climb out along 200 million guide cells, called radial glia cells, to the cortex of the brain where they sprout dendrites and a major central axon which are then wired in to the electrical network in a “use it or lose it”, “cells that fire together wire together” manner.

The brain continues to grow and mature into the 20’s as new neurons are born and surplus dendrites are pruned by the immune system. Cannabinoids interfere with cellular migration, cellular division, the generation of newborn neurons and all the classes of glia, axonal pathfinding, dendrite sprouting, myelin formation around axons and axon tracts and the firing of both inhibitory and stimulatory synapses 14-16,19,20,38-40. Cannabinoids interfere with gene expression directly, via numerous epigenetic means, and via immune perturbation.

Cannabinoids also disrupt the mechanics of cell division by disrupting the mitotic spindle on which chromosomal separation occurs, causing severe genetic damage and frank chromosomal mis-segregation, disruption, rupture and pulverization 41-43.

Cannabis was found to be a human carcinogen by the California Environmental Protection agency in 2009 44. This makes it a likely human teratogen (deforms babies). Importantly, while discussion continues over some cancers, it bears repeating that a positive association between cannabis and testicular cancer was found in all four studies which investigated this question 45-49.

Cannabis Teratogenesis

The best animal models for human malformations are hamsters and rabbits. In rabbits cannabis exhibits a severe spectrum of foetal abnormalities when applied at high dose including shortened limbs, bowels hanging out, spina bifida and exencephaly (brain hanging out). There is also impaired foetal growth and increased foetal loss and resorption 50,51.

Many of these features have been noted in human studies 52. In 2014 Centres for Disease Control Atlanta Georgia reported increased rates of anencephaly (no brain, usually rapid death) gastroschisis (bowels hanging out), diaphragmatic hernia, and oesophageal narrowing 53,54. The American Heart Association and the American Academy of Pediatrics reported in 2007 an increased rate of ventricular septal defect and an abnormality of the tricuspid valve (Ebstein’s anomaly) 55. Strikingly, a number of studies have shown that cannabis exposure of the father is worse than that of the mother 56. In Colorado atrial septal defect is noted to have risen by over 260% from 2000-2013 (see Figure 1; note close correlation (correlation coefficient R = 0.95, P value = 0.000066) between teenage cannabis use and rising rate of major congenital anomalies in Colorado to 12.7%, or 1 in 8 live births, a rate four times higher than the USA national average !) 57.

And three longitudinal studies following children exposed to cannabis in utero have consistently noted abnormalities of brain growth with smaller brains and heads – persisting into adult life – and deficits of cortical and executive functioning persistent throughout primary, middle and high schools and into young adult life in the early 20’s 58-63. An Australian MRI neuroimaging study noted 88% disconnection of cortical wiring from the splenium to precuneus which are key integrating and computing centres in the cerebral cortex 38,39,64. Chromosomal defects were also found to be elevated in Colorado (rose 30%) 57, in Hawaii 52 in our recent analysis of cannabis use and congenital anomalies across USA, and in infants presenting from Northern New South Wales to Queensland hospitals 65. And gastroschisis shows a uniform pattern of elevation in all recent studies which have examined it (our univariate meta-analysis) 52,54,66-71.

Interestingly the gastroschisis rate doubled in North Carolina in just three years 1997-2001 72, but rose 24 times in Mexico 73 which for a long time formed a principal supply source for Southern USA 74. Within North Carolina gastroschisis and congenital heart defects closely followed cannabis distribution routes 74-76. In Canada a remarkable geographical analysis by the Canadian Government has shown repeatedly that the highest incidence of all anomalies – including chromosomal anomalies – occurs in those northern parts where most cannabis is smoked 77,78.

Congenital anomalies forms the largest cause of death of babies in the first year of life. The biggest group of them is cardiovascular defects. Since cannabis affects several major classes
of congenital defects it is obviously a major human teratogen. Its heavy epigenetic footprint,
by which it controls gene expression by controlling DNA methylation and histone modifications 79-81, imply that its effects will be felt for the next three to four generations – that is the next 100 years 82,83. Equally obviously it is presently being marketed globally as a major commodity apparently for commercial – or ideological – reasons. Since cannabis is clearly contraindicated in several groups of people including:

1) Babies

2) Children

3) Adolescents

4) Car drivers

5) Commercial Drivers – Taxis, Buses, Trains,

6) Pilots of Aeroplanes

7) Workers – Manual Tools, Construction, Concentration Jobs

8) Children

9) Adolescents

10) Males of Reproductive age

11) Females of Reproductive age

12) Pregnancy

13) Lactation

14) Workers

15) Older People – Mental Illness

16) Immunosuppressed

17) Asthmatics – 80% Population after severe chest infection

18) People with Personal History of Cancer

19) People with Family History of Cancer

20) People with Personal History of Mental Illness

21) People with Family History of Mental Illness

22) Anyone or any population concerned about ageing effects 34

… cannabis legalization is not likely to be in the best interests of public health.

Concluding Remarks

In 1854 Dr John Snow achieved lasting public health fame by taking the handle off the Broad Street pump and saving east London from its cholera epidemic, based upon the maps he drew of where the cholera cases were occurring – in the local vicinity of the Broad Street pump.

Looking across the broad spectrum of the above evidence one notices a trulyremarkable concordance of the evidence between:

1) Preclinical studies in

i) Rabbits and

ii) Hamsters

2) Cellular and biological mechanisms, particularly relating to:

i) Brain development

ii) Heart development

iii) Blood vessel development

iv) Genetic development

v) Abnormalities of chromosomal segregation

i. Downs syndrome

ii. Turners syndrome

iii. Trisomy 18

iv. Trisomy 13

vi) Cell division / mitotic poison / micronucleus formation

vii) Epigenetic change

viii) Growth inhibition

3) 84Cross-sectional Epidemiological studies, especially from:

i) Canada 77,85

ii) USA 86,87

iii) Northern New South Wales 65,88 4) Longitudinal studies from 58:

i) Ottawa 59-63

ii) Pittsburgh

iii) Netherlands

Our studies of congenital defects in USA have also shown a close concordance of congenital anomaly rates for 23 defects with the cannabis use rate indexed for the rising cannabis concentration in USA, and mostly in the three major classes of brain defects, cardiovascular defects and chromosomal defects, just as found by previous investigators in Hawaii 52.

Of no other toxin to our knowledge can it be said that it interferes with brain growth and development to the point where the brain is permanently shrunken in size or does not form at all. The demonstration by CDC twice that the incidence of anencephaly (no brain) is doubled by cannabis 53,54 implies that anencephaly is the most severe end of the neurobehavioural teratogenicity of cannabis and forms one end of a continuum with all the other impairments which are implied by the above commentary.

(Actually when blighted ova, foetal resorptions and spontaneous abortion are included in the teratological profile anencephaly is not the most severe end of the teratological spectrum – that is foetal death). It is our view that with the recent advent of high dose potent forms of cannabis reaching the foetus through both maternal and paternal lines major and clinically significant neurobehavioural teratological presentations will become commonplace, and might well become all but universal in infants experiencing significant gestational exposure.

One can only wonder if the community has been prepared for such a holocaust and tsunami amongst its children?

It is the view of myself and my collaborators that these matters are significant and salient and should be achieving greater airplay in the public discussion proceeding around the world at this time on this subject.

Whilst cannabis legalization may line the pockets of the few it will clearly not be in the public interest in any sense; and indeed the public will be picking up the bill for this unpremeditated move for generations to come. Oddly – financial gain seems to be one of the primary drivers of the present transnational push. When the above described public health message gets out amongst ambitious legal fraternities, financial gain and the threat of major medico-legal settlements for congenital defects – will quickly become be the worst reason for cannabis legalization.

Indeed it can be argued that the legalization lobby is well aware of all of the above concerns – and their controlled media pretend debate does not allow such issues to air in the public forum. The awareness of these concerns is then the likely direct reason that cannabis requires its own legislation. As noted in the patient information leaflet for the recently approved Epidiolex (cannabidiol oil for paediatric fits) the US Food and Drug Administration (FDA) is well aware of the genotoxicity of cannabinoids.

The only possible conclusion therefore is that the public is deliberately being duped. To which our only defence will be to publicize the truth.

Source: Summary of Address to Sydney Parliament House, 09.07.2018 by Professor Dr. Stuart Reece, Clinical Associate Professor, UWA Medical School. University of Western Australia

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  • Trials on mice showed those exposed to cannabinoids had memory impairments
  • Brain scans by British and Portuguese researchers then confirmed the finding
  • The new experiment shines a light on the little-known dangers of cannabinoids

Smoking cannabis or taking medication based on the drug can harm the brain and damage memory, research has found. Trials on mice showed those exposed long-term to cannabinoids – compounds found in the marijuana plant – suffered ‘significant’ memory impairments.

Brain scans confirmed the finding, and showed cannabis can stop vital memory-controlling regions of the organ communicating with each other. Experts fear both recreational users and those who rely on it to combat their health conditions may be at risk of memory problems.

The study comes after Government advisers yesterday declared doctors should be able to prescribe medicinal cannabis, which contains the potentially harmful cannabinoids.

The Advisory Council on the Misuse of Drugs (ACMD) agreed cannabis does possess a medicinal benefit, in a review sent to to Home Secretary Sajid Javid.

He commissioned the review after two high profile cases, including that of epileptic 12-year-old Billy Caldwell, whose mother had seven bottles of cannabis oil that helped combat his seizures confiscated at Heathrow Airport.

For years scientists have warned smoking cannabis can lead to mental health problems, such as schizophrenia. Studies have shown cannabis can also shrink memory-related structures in the brain, most notably the hippocampus. But there is little understanding of the potential negative side effects of cannabinoids, such as CBD.

The new experiment, led by scientists at the universities of Lancaster and Lisbon, shines a light on the dangers.

They studied the effects of cannabinoid drug WIN 55,212-2 in mice. It is similar to THC, the compound that causes a high in cannabis.

Researchers discovered long-term exposure to the cannabinoid impaired the learning ability and memory of mice. Rodents who had been exposed to the drug could not even distinguish between a familiar and novel object.

Brain scans backed up the initial finding – and showed the drug affected the healthy function of brain regions involved in learning and memory.

It was discovered that the cannabinoid stopped the hippocampus and prefrontal cortex from communicating with each other.

Researchers led by Lancaster’s Dr Neil Dawson suggested this was to blame for the negative effects of cannabinoids on memory.

The findings were published in the Journal of Neurochemistry.

Dr Dawson said: ‘This work offers valuable new insight into the way in which long-term cannabinoid exposure negatively impacts on the brain.’ He called for further trials to confirm their finding, in order to establish exactly how cannabinoids can damage memory.

Ian Hamilton, a drug researcher at York University, told Mail Online: ‘We know that heavy use of cannabis impairs memory, although the good news is this can be reversed if the person abstains.

‘But studies like this add to the need for young people to avoid daily use of cannabis as this will hinder their ability to learn and recall information for exams.’ 

The use of medicinal cannabis has been increasing worldwide over the past decade. It is currently not legal medicinally in the UK.

Evidence published in respected journals shows the drug can help to combat epilepsy, multiple sclerosis and chronic pain.

And in recent years, Spain, South Africa, Uruguay and several states in the US have even made cannabis legal for recreational use.

Lisbon’s Professor Ana Sebastiao said: ‘As for all medicines, cannabinoid-based therapies have not only beneficial disease-related actions, but also negative side effects.

‘It is for the medical doctor to weight the advantages of the therapy… against the potential side effects.’   

THE DIFFERENCES BETWEEN THC AND CBD

Tetrahydrocannabinol (THC) and cannabidiol (CBD) are both derived from the cannabis plant. 

Together, they are part of the cannabinoid group of compounds found in hashish, hash oil, and most strains of marijuana. 

THC is the psychoactive compound responsible for the euphoric, ‘high’ feeling often associated with marijuana.

THC interacts with CB1 receptors in the central nervous system and brain and creates the sensations of euphoria and anxiety. 

CBD does not fit these receptors well, and actually decreases the effects of THC, and is not psychoactive. 

CBD is thought to help reduce anxiety and inflammation. 

Source:

https://www.dailymail.co.uk/health/article-5975265/Long-term-use-cannabis-impairs-memory-conclude-researchers.html July 2018

Childhood adversity permanently alters the peripheral and central immune systems, increasing the sensitivity of the body’s immune response to cocaine, reports a study by researchers at the IRCCS Santa Lucia Foundation and University of Rome “La Sapienza,” Italy.

The study, published in Biological Psychiatry, showed that exposure to psychosocial stress early in life altered the structure of immune cells and inflammatory signals in mice and led to increased drug-seeking behavior. Exposure to early psychosocial stress in mice, or a difficult childhood in humans, increased the immune response to cocaine in adulthood, revealing a shared mechanism in the role of immune response in the effects of early life stress on cocaine sensitivity in mice and humans.

The findings help explain why as many as 50 percent of people who experience childhood maltreatment develop addiction problems. The results in mice and humans suggest that exposure to adversity during childhood triggers activation of the immune system, leading to permanent changes that sensitize the immune system and increase susceptibility to the effects of cocaine in adulthood.

“This paper suggests the existence of an extraordinary degree of interplay between the neural and immune systems related to the impact of early life stress on later risk for cocaine misuse. It both highlights the complex impact of early life stress and suggests an immune-related mechanism for reducing later addiction risk,” said John Krystal, MD, Editor of Biological Psychiatry.

After inducing psychosocial stress in 2-week-old mice by exposing them to a threatening male, first author Luisa Lo Iacono, PhD, and colleagues examined brain immune cells, called microglia, in adulthood. Early social stress altered the structure of microglia in the ventral tegmental area, a brain region important for the reward system and drug-seeking, and increased the response of microglia to cocaine. In the peripheral immune system, early social stress increased the release of inflammatory molecules from white blood cells, which was further amplified by exposure to cocaine, compared with control mice.

“Remarkably, pharmacologically blocking this immune activation during early life stress prevents the development of the susceptibility to cocaine in adulthood,” said senior author Valeria Carola, PhD. Mice who received an antibiotic to prevent activation of immune cells during social stress did not have cellular changes or drug-seeking behavior.

The study also compared immune system function of 38 cocaine addicts and 20 healthy volunteers. Those who experienced childhood maltreatment had increased expression levels of genes important for immune system function. And the highest levels were found in cocaine addicts who had experienced a difficult childhood.

The findings add to the growing collection of evidence from the research group for the negative effects of early life trauma on brain development. “Our work emphasizes once again the importance of the emotional environment where our children are raised and how much a serene and stimulating environment can provide them with an extra ‘weapon’ against the development of psychopathologies,” said Dr. Carola.

Source:  https://medkit.info/2018/07/17/childhood-adversity-increases-susceptibility-to-addiction-via-immune-response/

Abstract
Core deficits in social functioning are associated with various neuropsychiatric and neurodevelopmental disorders, yet biomarker identification and the development of effective pharmacological interventions has been limited. Recent data suggest the intriguing possibility that endogenous cannabinoids, a class of lipid neuromodulators generally implicated in the regulation of neurotransmitter release, may contribute to species-typical social functioning. Systematic study of the endogenous cannabinoid signaling could, therefore, yield novel approaches to understand the neurobiological underpinnings of atypical social functioning.

This article provides a critical review of the major components of the endogenous cannabinoid system (for example, primary receptors and effectors—Δ9-tetrahydrocannabinol, cannabidiol, anandamide and 2-arachidonoylglycerol) and the contributions of cannabinoid signaling to social functioning. Data are evaluated in the context of Research Domain Criteria constructs (for example, anxiety, chronic stress, reward learning, motivation, declarative and working memory, affiliation and attachment, and social communication) to enable interrogation of endogenous cannabinoid signaling in social functioning across diagnostic categories. The empirical evidence reviewed strongly supports the role for dysregulated cannabinoid signaling in the pathophysiology of social functioning deficits observed in brain disorders, such as autism spectrum disorder, schizophrenia, major depressive disorder, posttraumatic stress disorder and bipolar disorder. Moreover, these findings indicate that the endogenous cannabinoid system holds exceptional promise as a biological marker of, and potential treatment target for, neuropsychiatric and neurodevelopmental disorders characterized by impairments in social functioning.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5048207/

Researchers map out a cellular mechanism that offers a biological explanation for alcoholism, and could lead to treatments

Credit: Getty Images

You can lead a lab rat to sugar water, but you can’t make him drink—especially if there’s booze around.

New research published Thursday in Science may offer insights into why some humans who drink alcohol develop an addiction whereas most do not. After caffeine, alcohol is the most commonly consumed psychoactive substance in the world. For the majority of people the occasional happy hour beer or Bloody Mary brunch is where it stops. Yet we all know that others will drink compulsively, despite whatever consequence or darkness it brings.

The new research confirms earlier work showing this is true for rats; but it takes things a step further and supports a study design that could help scientists better understand addiction biology, and possibly develop more effective therapies for human addictive behaviors. Led by a team at Linköping University in Sweden, the researchers found that when given a choice between alcohol and a tastier, more biologically desirable sugar substitute, a subgroup of rats consistently preferred the alcohol. The authors further identified a specific brain region and molecular dysfunction most likely responsible for these addictive tendencies. They believe their findings and study design could be steps toward developing an effective pharmaceutical therapy for alcohol addiction, a kind of treatment that has eluded researchers for years.

A taste for sweetness is evolutionarily embedded in the mammalian brain; in the wild, sugar translates into fast calories and improved survival odds. For the new study, 32 rats were trained to sip a 20 percent alcohol solution for 10 weeks until it became habit. They were then presented with a daily choice between more alcohol or a solution of the noncaloric sweetener saccharine. (The artificial sweetener provides sugary-tasting enticement without the potential confounding variable of actual calories.) The majority of rats vastly preferred the faux sugar over the alcohol option.

But the fact that four rats—or 12.5 percent of the total—stuck with the alcohol was telling to senior author Markus Heilig, director of the Center for Social and Affective Neuroscience at Linköping, given the rate of alcohol misuse in humans is around 15 percent. So Heilig expanded the study. “There were four rats who went for alcohol despite the more natural reward of sweetness,” he says. “We built on that, and 600 animals later we found that a very stable proportion of the population chose alcohol.” What’s more, the “addicted” rats still chose alcohol even when it meant receiving an unpleasant foot shock.

To get a better sense of what was going on at a molecular level, Heilig and his colleagues analyzed which genes were expressed in the rodent subjects’ brains. The expression of one gene in particular—called GAT-3—was found to be greatly reduced in the brains of those who opted for alcohol rather than saccharine. GAT-3 codes for a protein that normally controls levels of a neurotransmitter called GABA, a common chemical in our brains and one known to be involved in alcohol dependence.

In collaboration with co-author and University of Texas at Austin research scientist Dayne Mayfield, Heilig’s team found that in brain samples from deceased humans who had suffered from alcohol addiction, GAT-3 levels were markedly lower in the amygdala—generally considered the brain’s emotional center. One might assume that any altered gene expression contributing to addictive behaviors would instead manifest in the brain’s reward circuitry—a network of centers involved in pleasurable responses to enticements like food, sex and gambling.

Yet the decrease in GAT-3 expression in both rats and humans was by far strongest in the amygdala. “Figuring out the reward circuitry has been a fantastic success story, but it’s probably of limited relevance to clinical addiction,” Heilig says. “The rewarding effect of drugs happens in everybody. It’s a completely different story in the minority of people who continue to take drugs despite adverse consequences.” He believes altered activity in the amygdala makes perfect sense, given that addiction—in both rats and humans—often brings with it negative emotions and anxiety.

Much previous addiction research has relied on models in which rodents learn to self-administer addictive substances, but without other options that could compete with drug use. It was French neuroscientist Serge Ahmed who recognized this as a major limitation to understanding addition biology given that, in reality, only a minority of humans develops addiction to a particular substance. By offering an alternative reward (that is, sweet water), his team showed only a minority of rats develop a harmful preference for drug use—a finding that has now been confirmed with several other commonly abused drugs.

Building on Ahmed’s concept, Heilig added the element of choice to his research. “You can’t determine the true reward of an addictive drug in isolation; it’s dependent on what other options are available—in our case a sugar substitute.” He says most models that have been used to study addiction, and to seek ways to treat it, were probably too limited in their design. “The availability of choice,” he adds, “is going to be fundamental to studying addiction and developing effective treatments for it.”

Paul Kenny, chair of neuroscience at Icahn School of Medicine at Mount Sinai, agrees. “In order to develop novel therapeutics for alcoholism it is critical to understand not just the actions of alcohol in the brain, but how those actions may differ between individuals who are vulnerable or resilient to the addictive properties of the drug,” he says. “This Herculean effort to impressively map out a cellular mechanism that likely contributes to alcohol dependence susceptibility will likely provide important new leads in the search for more effective therapeutics.” Kenny was not involved in the new research.

Heilig and his team believe they have already identified a promising addiction treatment based on their latest work,  and have teamed up with a pharmaceutical company in hopes of soon testing the compound in humans. The drug suppresses the release of GABA and thus could restore levels of the neurotransmitter to normal in people with a dangerous taste for alcohol. With any luck, one of civilization’s oldest  vices might soon loosen its grip.. Illumination.

Source:  www.scientificamerican.com/article/scientists-pinpoint-brain-region-that-may-be-center-of-alcohol-addiction/   June 21st 2018

Watch Here and Share!

As the legal status of marijuana changes its perceived dangers are lessening while the potency of the drug is increasing.

This video covers marijuana as a psychoactive substance that induces its effects by manipulation of natural brain chemicals known as  the endocannabinoids.The toxic and addictive impact that results from the drug’s disruption of natural endocannibinoids is characterized in this video by the testimony of those impacted by the drug and by the scientists who are studying its effects.

This video is 26 minutes and will help to clarify the many myths and misconceptions regarding the effects of marijuana.

Source: Email from SAM (Smart Approaches to Marijuana) <info@learnaboutsam.org>

March 2018

Psychology of Addictive Behaviors journal makes corrections, SAM calls on media to correct stories

FOR IMMEDIATE RELEASE

January 19, 2015

Contact: Jeffrey Zinsmeister

jeff@learnaboutsam.org

+1 (415) 680-3993

[WASHINGTON, DC] – A prominent journal article about marijuana and health which resulted in media outlets reporting on marijuana’s harmlessness has now been corrected. A recheck of the statistics has now found that the incidence of psychotic disorders trended toward a 2.5-fold increase in marijuana users, a difference that went beyond a trend to reach significance in a one-tailed statistical test. This degree of impact matches very well the results of many prior studies involving marijuana use and psychosis though falls short of the five-fold increase in psychosis risk for marijuana users seen with the high strength strains that are more recently available.

Dr. Christine Miller, a former schizophrenia researcher from Johns Hopkins University and now Director of SAM Maryland, first alerted the journal, Psychology of Addictive Behaviors, last December. Some media outlets have already corrected their original story.

“We commend the Washington Post’s Ariana Cha for now updating her story, and hope many more will follow her lead,” remarked Dr. Miller. “The flaw in the original University of Pittsburgh report were certain correction factors applied to the raw data, factors which are strongly affected by psychosis rather than being causes of such a disorder. These inappropriate corrections overpowered the marijuana effect. We’re glad the corrections have been made.”

SAM urges other media outlets to correct their headlines and stories.

The new data comes on the heels of a major report released by the State of Vermont’s Health Department which found that marijuana worsened conditions ranging from mental illness to motor vehicle accidents to negative pregnancy effects – and almost all of them are found to be worsened by marijuana:

For more information about marijuana use and its effects, see http://www.learnaboutsam.org.

###

About SAM

Smart Approaches to Marijuana (SAM) is a nonpartisan, non-profit alliance of physicians, policy makers, prevention workers, treatment and recovery professionals, scientists, and other concerned citizens opposed to marijuana legalization who want health and scientific evidence to guide marijuana policies. SAM has affiliates in 31 states.

www.learnaboutsam.org

Source:

http://psycnet.apa.org/record/2015-58335-001

Submitted by Livia Edegger

A study conducted by the US Substance Abuse and Mental Health Services Administration (SAMHSA) found that individuals who had started taking drugs early on in life were more likely to develop mental disorders and become polydrug users. At the time of clinical admission, three quarters of drug users between 18 and 30 years of age had started taking drugs at age 17 or younger. A tenth of drug users had started at an even earlier age. 78.1% of drug users that had started taking drugs at age 11 or younger were taking more than one drug compared to 30.4% of individuals that had initiated drug use after the age of 25. 38.6% of drug users that had begun taking drugs at age 11 or under had developed some form of mental disorder. These results underline the importance of prevention programmes in childhood and early adolescence, phases that are critical for young people’s development.

Links:

Source:

http://preventionhub.org/en/prevention-update/early-onset-drug-use-linked-mental-disorders-and-multi-drug-use

Submitted by Livia Edegger on – 15:38

A group of researchers has developed a test to predict fourteen year old teenagers’ future drinking behaviour. The test takes a wide variety of factors that might influence young adults’ susceptibility to binge drinking into consideration such as family background, personality traits, availability of alcohol as well as brain-related variables. “There is no one really big thing. It’s a bunch of little things adding up to give you this prediction,” says Dr Robert Whelan from the University College Dublin. As of today, the test is far from practical as it lacks accuracy and relies on expensive brain scans. A more simplified and cost-effective version of the test could help identify at-risk adolescents for interventions in the future. Hugh Perry, chairman of the Medical Research Council Neurosciences and Mental Health Board, said further research could “lead to breakthroughs in this field and provide compelling evidence to inform public health policy and lay the groundwork for the design of interventions”.

Links:

Source:

http://preventionhub.org/en/prevention-update/researchers-create-tool-predict-teens%E2%80%99-drinking-behaviour

9th July 2014

Henrietta Szutorisza, Yasmin L. Hurda,

A B S T R A C T

Extensive debates continue regarding marijuana (Cannabis spp), the most commonly used illicit substance in many countries worldwide. There has been an exponential increase of cannabis studies over the past two decades but the drug’s long-term effects still lack in-depth scientific data. The epigenome is a critical molecular machinery with the capacity to maintain persistent alterations of gene expression and behaviors induced by cannabinoids that have been observed across the individual’s lifespan and even into the subsequent generation.

Though mechanistic investigations regarding the consequences of developmental cannabis exposure remain sparse, human and animal studies have begun to reveal specific epigenetic disruptions in the brain and the periphery. In this article, we focus attention on long-term disturbances in epigenetic regulation in relation to prenatal, adolescent and parental germline cannabinoid exposure. Expanding knowledge about the protracted molecular memory could help to identify novel targets to develop preventive strategies and treatments for behaviors relevant to neuropsychiatric risks associated with developmental cannabis exposure.

Source: Neuroscience and Biobehavioral Reviews 85 (2018) 93–101

While writing, I wondered what kind of details I should publish about the previous lives of people in the marijuana industry. Virgil Grant, one of the article’s subjects, told me stories about how he would sell marijuana from his family grocery store in Compton in the 1980s and 1990s by putting the weed in empty boxes of Lucky Charms. He mentioned, without much elaboration, that would-be competitors in Compton regretted going up against him.

It’s an awkward and confusing transition period in the marijuana industry. What was illegal yesterday in California may be legal today, but that’s of course not the way the federal government sees it. Mr. Grant has spent time in both federal and state prisons.

Since legalization of recreational sales came into effect in California in January, there have been stories about cities and counties that banned marijuana. But I had never seen reporting on the bigger picture. So I reached out to a company called Weedmaps, a website that hosts online reviews of cannabis businesses. When they added it up, the data surprised me: Only 14 percent of California’s cities and towns authorize the sale of recreational marijuana. By contrast, Proposition 64, the ballot measure that allowed marijuana legalization, passed with 57 percent voter approval in 2016, a seemingly solid majority.

The low acceptance of marijuana businesses strikes me as part of the liberal, not-in-my-backyard paradox in California. Yes, Californians want shelters for the homeless, but just not across the street. Yes, Californians want more housing built, but not if it changes the character of the neighborhood. A marijuana dispensary? Sure, preferably in the next town.

A New York Times reporter wanted to find out why California cities are taking such different approaches to legal pot. Previously, he covered a story about why California growers are so reluctant to leave the black market and seek a state license to become legitimate. He found that only about 10 percent have done so. The other 90 percent remain in black market. California is the nation’s biggest producer and consumer of marijuana. One estimate projects the state produces seven times the amount of pot it consumes and exports the surplus to non-legal states. Pursuing this story took the reporter to Compton, in Los Angeles County, where residents voted in January to ban marijuana businesses by a 3-to-1 margin. He compared this to Oakland, near San Francisco, which has embraced the marijuana industry. It’s as if the two cities had been asked the same question and come up with completely different answers, he opined. To get a bigger picture, he consulted Weedmaps to find out how common industry bans are. He was surprised to find that only 14 percent of California’s cities and towns authorize marijuana sales, even though legalization passed in 2016 with 57 percent voter approval.

It’s still early days — it’s been less than three months since legal sales started — but for now the trend is that larger cities like Oakland, San Francisco, Los Angeles, Sacramento and San Diego are the hubs of the marijuana industry, while smaller cities and towns are ambivalent or outright hostile to the idea of opening marijuana dispensaries. Orange County, in Southern California, is a recreational marijuana desert, with only a handful of dispensaries allowed.

California has a reputation for very tolerant attitudes toward pot, and it’s the biggest consumer and producer of the drug in the United States by a wide margin. It is also the nation’s premier exporter to other states: By one estimate, the state produces seven times more than it consumes.

But the visit to Compton helped peel back another, more conservative set of attitudes toward marijuana.

At the Compton airport, Shawn Wildgoose, a former enlisted Marine who lives in Compton and works in the construction industry, told me he wanted to see the city focusing on its homeless problem and reducing crime, which is sharply down from previous decades.

Legal marijuana?

“Compton has other issues,” Mr. Wildgoose said. “We don’t need that distraction.”

Source: National Families in Action’s The Marijuana Report nfia@nationalfamilies.org 21st March 2018

The mechanism by which dopamine cells in the brain signal the passage of time has received some new light via a recent study from researchers at University of Texas at San Antonio. To make decisions about the salience of a potential reward is mediated by small group of neurons in the midbrain that release dopamine.

The amount of dopamine released can influence our decisions by telling us how good a reward will be in the future. For example, more dopamine is released in response to the smell of turkey baking relative to the smell of leftovers.

But does the length of time between the anticipatory release of dopamine and the actual reward mediate the release and volume of dopamine? To answer this question, investigators used voltammetry to record dopamine release in rodents trained by Pavlovian conditioning.

This novel experiment utilized different audible tones that predicted the delivery of food. One tone was presented only after a short wait time— while the other tone was presented only after a long wait time.

The data showed that more dopamine was released during the short wait tone compared to the long wait tone. These results show that imminent reward is associated with dopamine release in the midbrain.

This is not unlike telling a 6-year-old child that her next birthday party is tomorrow versus telling her it won’t occur for two months. The time differentiation will predict the amount of excitement the child experiences.

Why Does This Matter?

We established many years ago the power of simply showing a recovering cocaine addict a piece of their drug paraphernalia. The release of dopamine is triggered by this visual cue and is also related to the amount of abstinence and how soon a drug reward could be attained. Monitoring via drug testing is one way that addicts are able to think through their behavioral choices when craving is induced.

For persons in early recovery from substance use disorder, anticipatory cues trigger the release of dopamine, cause craving and increase the risk of relapse. Continuing care planning for recovering addicts must address the power of anticipatory reward and help each recovery person set up obstacles that deter and delay access to a mood altering substance and avoid environmental drug cues.

Source: Fonzi KM, Lefner MJ, Phillips PEM, Wanat MJ. Dopamine Encodes Retrospective Temporal Information in a Context-Independent Manner. Cell Rep. 2017 Aug 22;20(8):1765-1774. doi: 10.1016/j.celrep.2017.07.076.

Filed under: Brain and Behaviour :

One in five Canadians between 15 and 24 years of age reports daily or almost daily use of cannabis prior to legalization. They see it as “much safer than alcohol and tobacco” and “not as dangerous as drunk driving.”

Author 1. Paul W Bennett

Research Associate in Education, Saint Mary’s University

Disclosure statement

Paul W Bennett does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Partners

The Conversation UK receives funding from Hefce, Hefcw, SAGE, SFC, RCUK, The Nuffield Foundation, The Ogden Trust, The Royal Society, The Wellcome Trust, Esmée Fairbairn Foundation and The Alliance for Useful Evidence, as well as sixty five university members.

One of the enduring myths about marijuana is that it is “harmless” and can be safely used by teens.

Many high school teachers would beg to disagree, and consider the legalization of marijuana to be the biggest upcoming challenge in and around schools. And the evidence is on their side.

As an education researcher, I have visited hundreds of schools over four decades, conducting research into both education policy and teen mental health. I’ve come to recognize when policy changes are going awry and bound to have unintended effects. As Canadian provinces scramble to establish their implementation policies before the promised marijuana legalization date of July 2018, I believe three major education policy concerns remain unaddressed.

These are that marijuana use by children and youth is harmful to brain development, that it impacts negatively upon academic success and that legalization is likely to increase the number of teen users.

‘Much safer than alcohol’

Across Canada, province after province has been announcing its marijuana implementation policy, focusing almost exclusively on the control and regulation of the previously illegal substance. This has provoked fierce debates over who will reap most of the excise tax windfall and whether cannabis will be sold in government stores or delegated to heavily regulated private vendors.

All of the provincial pronouncements claim that their policy will be designed to protect “public health and safety” and safeguard “children and youth” from “harmful effects.”

Still, one in five young people between 15 and 24 years of age, according to a recent national study, report daily or almost daily use of cannabis.

They also see marijuana as “much safer than alcohol and tobacco” and “not as dangerous as drunk driving.”

Few either know about or seem concerned over the clear linkage between heavy use and early-onset psychosis.

Early-onset paranoid psychosis

So what does the evidence say? First, heavy marijuana use can, and does, damage brain development in youth aged 13 to 18. A 2015 Canadian Centre on Substance Abuse study confirmed the direct link between cannabis use and loss of concentration and memory, jumbled thinking and early onset paranoid psychosis.

One of the leaders in the medical field, Dr. Phil Tibbo, initiator of Nova Scotia’s Weed Myths campaign targeting teens, has seen the evidence, first hand, of what heavy use can do as director of Nova Scotia’s Early Psychosis Program. His brain research shows that regular marijuana use leads to an increased risk of developing psychosis and schizophrenia and effectively explodes popular and rather blasé notions that marijuana is “harmless” to teens and “recreational use” is simply “fun” and “healthy.”

Damaging to academic performance Second, marijuana negatively impacts neurocognitive performance in teens and users perform more poorly in quantitative subjects requiring precision — like mathematics and senior science.

In 2017, Dutch researchers Olivier Marie and Ulf Zolitz found that the academic performance of Maastricht University students increased substantially when they were no longer legally permitted to buy cannabis. The effects were stronger for women and low performers and academic gains were larger for courses needing numerical or mathematical skills.

Third, legalization of marijuana is likely to increase the number of teen users. Research from Oregon Research Institute conducted in 2017 showed that teenagers who were already using marijuana prior to legalization increased their frequency of use significantly afterwards. Research from New York University, published in 2014, indicated that many high school students normally at low risk for marijuana use (e.g., non-cigarette-smokers, religious students, those with friends who disapprove of use) reported an intention to use marijuana if it were legal. Medical researchers and practitioners have warned us that legalization carries great dangers, particularly for vulnerable and at-risk youth between 15 and 24 years of age.

Age of restriction

Marijuana legalization policy across Canada is a top-down federal initiative driven largely by changing public attitudes and conditioned by the current realities of the widespread use of marijuana, purchased though illicit means.

Setting the age of restriction, guided by the proposed federal policy framework, has turned out to be an exercise in “compromise” rather than one focused on heeding the advice of leading medical experts and the Canadian Medical Association (CMA). In a 2016 submission to the government, the CMA argued that 25 would be the ideal age for legal access to marijuana, as the brain is still developing until then, but that a lower minimum age of 21 should be considered — to discourage children from purchasing marijuana from organized crime groups.

The report argued that: “Marijuana use is linked to several adverse health outcomes, including addiction, cardiovascular and pulmonary effects (e.g., chronic bronchitis), mental illness, and other problems, including cognitive impairment and reduced educational attainment. There seems to be an increased risk of chronic psychosis disorders, including schizophrenia, in persons with a predisposition to such disorders.” In fact, the minimum age for purchasing and possessing marijuana is going to be age 18 in Alberta and Quebec, and 19 in most other provinces. Getting it “out of high schools” was a critical factor in bumping it up to age 19 in most provinces.

Every Canadian province is complying with the federal legislation, but — in our federal system – it’s “customized” for each jurisdiction.

The Canadian Western provinces — Alberta, British Columbia and Saskatchewan —have opted for regulating private retail stores, while Ontario and the Maritime provinces (Nova Scotia, New Brunswick and P.E.I.) are expanding their liquor control commissions to accommodate retail sales of cannabis. High school teachers, as of September 2018, may be battling a spike in marijuana use and greater peer pressure to smoke pot on the mistaken assumption that it is “harmless” at any age.

Clamping down in schools

For high school principals and staff, this will be a real test.

By September 2018, the old line of defence that using marijuana is illegal will have disappeared. Recreational marijuana will be more socially acceptable. The cannabis industry will be openly marketing its products. High school students who drive to school will likely get caught under new laws prohibiting motor vehicle use while impaired by drugs or alcohol. Fewer students are likely to abstain when it is perfectly legal to smoke pot when you reach university, college or the workplace. We have utterly failed, so far, in getting through to the current generation of teens, so a much more robust approach is in order.

“Be firm at the beginning” is the most common sage advice given to beginner teachers. Clamping down on teen marijuana use during and after school hours will require clarity and firm resolve in the year ahead — and the support of engaged and responsible parents.

Legalization of recreational marijuana is bound to complicate matters for Canadian high schools everywhere. Busting the “Weed Myths” should not be left to doctors and health practitioners. Pursuing research-based, evidence-informed policy and practice means getting behind those on the front lines of high school education.

Source: https://theconversation.com/marijuana-at-school-loss-of-concentration-risk-of-psychosis-90374 January 25th 2018

Comments below from David Evans Esq., a lawyer and special adviser to the Drug Free America Foundation, re the suggestion that marijuana could assist in treating opiate addiction.

WHAT ARE THE PHYSICAL AND BEHAVIORAL ADVERSE EFFECTS OF USING “MEDICAL” MARIJUANA WHILE IN OPIATE TREATMENT?

Memory defect (short and long term) – how are they to remember compliance issues and new problem solving? Masks other mental health issues – anxiety, PTSD, Bipolar

Marijuana use impacts the brain, creates a delay in learning skills to NOT have substance use in life.

In order for change to occur, person must acknowledge loss of control – how can someone do this when control is still lost with marijuana?

Changes in coordination, mood swings, memory/learning problems

Marijuana use deters the return to normal brain functioning and the continued drive for more substances and stimuli in the pleasure seeking area of the brain.

Marijuana use is A-motivational – knocks out drive and ambition

Continued use maintains Arrested Development – low emotional maturity – the maturity level is stumped when start using substances

Recovery – means not using drugs

THC suppresses neurons in information processing system of the hippocampus, the part of the brain that is crucial for learning memory and integration of sensory experiences with emotions and motivations. Learned behaviors, which depend on the hippocampus, deteriorate after chronic exposure

· Because marijuana use impacts learning a person falls behind in accumulating intellectual, job, or social skills. This can directly translate to need for more treatment both with intensity and length

Users have trouble sustaining and shifting their attention in and registering, organizing and using information.

Increase risk of motor vehicle/work accidents

For more detailed information log on to a paper in Support of the UN Drug Conventions: The Arguments Against Illicit Drug Legalisation and Harm Reduction also by David Evans.

Source: https://nationalallianceformarijuanaprevention.files.wordpress.com/2011/12/2009-un-drug-conventions-the-argument-against-legaliztion.pdf

Summary:

Several studies have demonstrated that the primary active constituent of cannabis, delta-9-tetrahydrocannabinol, induces transient psychosis-like effects in healthy subjects similar to those observed in schizophrenia. However, the mechanisms underlying these effects are not clear. A new study shows that this active ingredient increases random neural activity, termed neural noise, in the brains of healthy human subjects. The findings suggest that increased neural noise may play a role in the psychosis-like effects of cannabis.

Cannabis. Credit: © olyas8 / Fotolia

Several studies have demonstrated that the primary active constituent of cannabis, delta-9-tetrahydrocannabinol (∆9-THC), induces transient psychosis-like effects in healthy subjects similar to those observed in schizophrenia. However, the mechanisms underlying these effects are not clear.

A new study, published in the journal Biological Psychiatry, reports that ∆9-THC increases random neural activity, termed neural noise, in the brains of healthy human subjects. The findings suggest that increased neural noise may play a role in the psychosis-like effects of cannabis.

“At doses roughly equivalent to half or a single joint, ∆9-THC produced psychosis-like effects and increased neural noise in humans,” explained senior author Dr. Deepak Cyril D’Souza, a Professor of Psychiatry at Yale School of Medicine.

“The dose-dependent and strong positive relationship between these two findings suggest that the psychosis-like effects of cannabis may be related to neural noise which disrupts the brain’s normal information processing,” added first author Dr. Jose Cortes-Briones, a Postdoctoral Associate in Psychiatry at Yale School of Medicine.

The investigators studied the effects of ∆9-THC on electrical brain activity in 24 human subjects who participated in a three-day study during which they received two doses of intravenous ∆9-THC or placebo in a double-blind, randomized, cross-over, and counterbalanced design.

If confirmed, the link between neural noise and psychosis could shed light on the biology of some of the symptoms associated with schizophrenia.

“This interesting study suggests a commonality between the effects on the brain of the major active ingredient in marijuana and symptoms of schizophrenia,” stated Dr. John Krystal, Editor of Biological Psychiatry. “The impairment of cortical function by ∆9-THC could underlie some of the cognitive effects of marijuana. Not only does this finding aid our understanding of the processes underlying psychosis, it underscores an important concern in the debate surrounding medical and legalized access to marijuana.”

Source:   http://www.sciencedaily.com/releases/2015  3 Dec.2015

During the late 1970s, my colleague, Dr. Herb Kleber, and I introduced a novel neuroanatomical model to explain the pathophysiology of opioid withdrawal and put forth our contention that addiction was not simply a matter of avoiding withdrawal. Using what was then a novel new drug, clonidine, we were able to effectively detox heroin and methadone addicts in half the time, and without the surge of norepinephrine release from the locus coeruleus. This minimized the agitation and somatic anxiety that can be unbearable for some patients.

This helped prove our conviction that addictive disease was the result of numerous and largely unknown factors, and not simply to avoid withdrawal. In spite of effectively and humanely withdrawing addicts from opioids, we also discovered that something was clearly different and unique about their brain and behavior. After being clean and sober for 6-8 months in a safe and secure rehab environment, most addicts returned to using heroin as soon as the door was unlocked. This looked like Pavlovian principles on steroids. Although it was not due to avoidance of withdrawal symptoms, the answer remained unclear.

In some ways, we have travelled light years in furthering our understanding of the brain and addictive disease. Yet, relapse remains the norm and not the exception for opioid addicts. The development and use of naltrexone in the 1990s followed by buprenorphine has helped many addicts achieve a better quality of life. Yet, relapse remains the norm.

In a recent placebo-controlled clinical trial by Kowalczyk, et al, participants were given (0.3 mg/d) of clonidine or placebo during 18 weeks of Medication-Assisted Treatment (MAT) with buprenorphine, and documented their mood and activities via a pre-programmed smart phone.

Study participants receiving clonidine in addition to buprenorphine had increased abstinence from opioids and were able to decouple their stress from drug craving. Additionally, participants in the buprenorphine-plus-clonidine group, not only experienced longer periods of abstinence, but were also better in managing, or coping with their “unstructured” time. In other words, clonidine helped persons deal with their boredom and inability to create or engage in healthy activities, which is a strong predictor of relapse.

Why Does This Matter?

The study replicates previous research demonstrating that 1.) unstructured time, especially during early recovery is a trigger and predictor of relapse, 2.) engaging in responsible or helpful activities is associated with better outcomes among patients receiving Medication-Assisted Treatment, and 3.) clonidine helped participants engage in unstructured-time activities with less risk of craving or use than they might otherwise have experienced.

From a personalized-medicine perspective, these data are a good reminder that addiction is a multifaceted disease requiring a multimodal approach. It is not treatable with any singular intervention. At best, psychopharmacology is adjunctive. And remember before any MAT, many addicted persons enjoyed sustained recovery via 12-step programs.

Source: https://www.rivermendhealth.com/resources/clonidine-plus-mat-improves-treatment-outcomes/ November 2017

Pain and pleasure rank among nature’s strongest motivators, but when mixed, the two can become irresistible. This is how opioids brew a potent and deadly addiction in the brain. Societies have coveted the euphoria and pain relief provided by opioids since Ancient Sumerians referred to opium poppies as the “joy plant” circa 3400 B.C. But the repercussions of using the drugs were ever present, too. For centuries, Chinese patients swallowed opium cocktails before major surgeries, but by 1500, they described the recreational use of opium pipes as subversive. The Chinese emperor Yung Cheng eventually restricted the use of opium for medical purposes in 1729. Less than 100 years later, a German chemist purified morphine from poppies, creating the go-to pain reliever for anxiety and respiratory conditions. But the Civil War and its many wounds spawned mass addiction to the drugs, a syndrome dubbed Soldier’s Disease. A cough syrup was concocted in the late 1800s — called heroin — to remedy these morphine addictions. Doctors thought the syrup would be “non-addictive.” Instead, it turned into a low-cost habit that spread internationally. More than 70 percent of the world’s opium — 3,410 tons — goes to heroin production, a number that has more than doubled since 1985. Approximately 17 million people around the globe used heroin, opium or morphine in 2016.

Today, prescription and synthetic opioids crowd America’s medicine cabinets and streets, driving a modern crisis that may kill half a million people over the next decade. Opioids claimed 53,000 lives in the U.S. last year, according to preliminary estimates from the Centers for Disease Control and Prevention — more than those killed in motor vehicle accidents.

How did we arrive here? Here’s a look at why our brains get hooked on opioids.

The pain divide

Let’s start with the two types of pain. They go by different names depending on which scientist you ask. Peripheral versus central pain. Nociceptive versus neuropathic pain.

The distinction is the sensation of actual damage to your body versus your mind’s perception of this injury.

Your body quiets your pain nerves through the production of natural opioids called endorphins.

Stuff that damages your skin and muscles — pin pricks and stove burns — is considered peripheral/nociceptive pain.

Pain fibers sense these injuries and pass the signal onto nerve cells — or neurons — in your spine and brain, the duo that makes up your central nervous system.

In a normal situation, your pain fibers work in concert with your central nervous system. Someone punches you, and your brain thinks “ow” and tells your body how to react.

Stress-relieving hormones get released. Your immune system counteracts the inflammation in your wounded arm.

Your body quiets your pain nerves through the production of natural opioids called endorphins. The trouble is when these pain pathways become overloaded or uncoupled.

One receptor to rule them all

Say you have chronic back pain. Your muscles are inflamed, constantly beaming pain signals to your brain. Your natural endorphins aren’t enough and your back won’t let up, so your doctor prescribes an opioid painkiller like oxycodone.

Prescription opioids and natural endorphins both land on tiny docking stations — called receptors — at the ends of your nerves. Most receptors catch chemical messengers — called neurotransmitters — to activate your nerve cells, triggering electric pulses that carry the signal forward.

But opioid receptors do the opposite. They stop electric pulses from traveling through your nerve cells in the first place. To do this, opioids bind to three major receptors, called Mu, Kappa and Delta. But the Mu receptor is the one that really sets everything in motion.

The Mu-opiate receptor is responsible for the major effects of all opiates, whether it’s heroin, prescription pills like oxycodone or synthetic opioids like fentanyl, said Chris Evans, director of Brain Research Institute at UCLA. “The depression, the analgesia [pain numbing], the constipation and the euphoria — if you take away the Mu-opioid receptor, and you give morphine, then you don’t have any of those effects,” Evans said.

Opioids receptors trigger such widespread effects because they govern more than just pain pathways. When opioid drugs infiltrate a part of the brain stem called the locus ceruleus, their receptors slow respiration, cause constipation, lower blood pressure and decrease alertness. Addiction begins in the midbrain, where opioids receptors switch off a batch of nerve cells called GABAergic neurons.

GABAergic neurons are themselves an off-switch for the brain’s euphoria and pleasure networks.

When it comes to addiction, opioids are an off-switch for an off-switch. Opioids hold back GABAergic neurons in the midbrain, which in turn keep another neurotransmitter called dopamine from flooding a brain’s pleasure circuits. Image by Adam Sarraf

Once opioids shut off GABAergic neurons, the pleasure circuits fill with another neurotransmitter called dopamine. At one stop on this pleasure highway — the nucleus accumbens — dopamine triggers a surge of happiness. When the dopamine rolls into amygdala, the brain’s fear center, it relieves anxiety and stress. Both of these events reinforce the idea that opioids are rewarding.

These areas of the brain are constantly communicating with decision-making hubs in the prefrontal cortex, which make value judgments about good and bad. When it hears “This pill feels good. Let’s do more,” the mind begins to develop habits and cravings.

Taking the drug soon becomes second nature or habitual, Evans said, much like when your mind zones out while driving home from work. The decision to seek out the drugs, rather than participate in other life activities, becomes automatic.

The opioid pendulum: When feeling good starts to feel bad

Opioid addiction becomes entrenched after a person’s neurons adapt to the drugs. The GABAergic neurons and other nerves in the brain still want to send messages, so they begin to adjust. They produce three to four times more cyclic AMP, a compound that primes the neuron to fire electric pulses, said Thomas Kosten, director of the division of alcohol and addiction psychiatry at the Baylor College of Medicine.

That means even when you take away the opioids, Kosten says, “the neurons fire extensively.”

The pendulum swings back. Now, rather than causing constipation and slowing respiration, the brain stem triggers diarrhoea and elevates blood pressure. Instead of triggering happiness, the nucleus accumbens and amygdala reinforce feelings of dysphoria and anxiety. All of this negativity feeds into the prefrontal cortex, further pushing a desire for opioids.

While other drugs like cocaine and alcohol can also feed addiction through the brain’s pleasure circuits, it is the surge of withdrawal from opioids that makes the drugs so inescapable.

Could opioid addiction be driven in part by people’s moods?

Cathy Cahill, a pain and addiction researcher at UCLA, said these big swings in emotions likely factor into the learned behaviors of opioid addiction, especially with those with chronic pain. A person with opioid use disorder becomes preoccupied with the search for the drugs. Certain contexts become triggers for their cravings, and those triggers start overlapping in their minds.

“The basic view is some people start with the pain trigger [the chronic back problem], but it gets partially substituted with the negative reinforcement of the opioid withdrawal,” Cahill said.

That’s why Cahill, Evans and other scientists think the opioid addiction epidemic might be driven, in part, by our moods.

Chronic pain patients have a very high risk of becoming addicted to opioids if they are also coping with a mood disorder. A 2017 study found most patients — 81 percent — whose addiction started with a chronic pain problem also had a mental health disorder. Another study found patients on morphine experience 40 percent less pain relief from the drug if they have mood disorder. They need more drugs to get the same benefits.

People with mood disorders alone are also more likely to abuse opioids. A 2012 survey found patients with depression were twice as likely to misuse their opioid medications.

“So, not only does a mood disorder affect a person’s addiction potential, but it also influences if the opioids will successfully treat their pain,” Cahill said.

Meanwhile, the country is living through sad times. Some research suggests social isolation is on the rise. While the opioid epidemic started long before the recession, job loss has been linked to a higher likelihood of addiction, with every 1 percent increase in unemployment linked to a 3.6 percent rise in the opioid-death rate.

Can the brain swing back?

As an opioid disorder progresses, a person needs a higher quantity of the drugs to keep withdrawal at bay. A person typically overdoses when they take so much of the drug that the brain stem slows breathing until it stops, Kosten said.

Many physicians have turned to opioid replacement therapy, a technique that swaps highly potent and addictive drugs like heroin with compounds like methadone or buprenorphine (an ingredient in Suboxone).

These substitutes outcompete heroin when they reach the opioid receptors, but do not activate the receptors to the same degree. By doing so, they reduce a person’s chances for overdosing. These replacement medications also stick to the receptors for a longer period of time, which curtails withdrawal symptoms. Buprenorphine, for instance, binds to a receptor for 80 minutes while morphine only hangs on for a few milliseconds.

For some, this solution is not perfect. The patients need to remain on the replacements for the foreseeable future, and some recovery communities are divided over whether treating opioids with more opioids can solve the crisis. Plus, opioid replacement therapy does not work for fentanyl, the synthetic opioid that now kills more Americans than heroin. Kosten’s lab is one of many working on a opioid vaccine that would direct a person’s immune system to clear drugs like fentanyl before they can enter the brain. But those are years away from use in humans.

And Evans and Cahill said many clinics in Southern California are combining psychological therapy with opioid replacement prescriptions to combat the mood aspects of the epidemic.

“I don’t think there’s going to be a magic bullet on this one,” Evans said. “It’s really an issue of looking after society and looking after of people’s psyches rather than just treatment.

Source: http://www.pbs.org/newshour/updates/brain-gets-hooked-opioids/

Researchers from the McGill Group for Suicide Studies, based at the Douglas Mental Health University Institute and McGill University’s Department of Psychiatry, have just published research in the American Journal of Psychiatry that suggests that the long-lasting effects of traumatic childhood experiences, like severe abuse, may be due to an impaired structure and functioning of cells in the anterior cingulate cortex. This is a part of the brain which plays an important role in the regulation of emotions and mood.

The researchers believe that these changes may contribute to the emergence of depressive disorders and suicidal behaviour.

Crucial insulation for nerve fibres builds up during first two decades of life

For the optimal function and organization of the brain, electrical signals used by neurons may need to travel over long distances to communicate with cells in other regions. The longer axons of this kind are generally covered by a fatty coating called myelin. Myelin sheaths protect the axons and help them to conduct electrical signals more efficiently. Myelin builds up progressively (in a process known as myelination) mainly during childhood, and then continue to mature until early adulthood.

Earlier studies had shown significant abnormalities in the white matter in the brains of people who had experienced child abuse. (White matter is mostly made up of thousands of myelinated nerve fibres stacked together.) But, because these observations were made by looking at the brains of living people using MRI, it was impossible to gain a clear picture of the white matter cells and molecules that were affected.

To gain a clearer picture of the microscopic changes which occur in the brains of adults who have experienced child abuse, and thanks to the availability of brain samples from the Douglas-Bell Canada Brain Bank (where, as well as the brain matter itself there is a lot of information about the lives of their donors) the researchers were able to compare post-mortem brain samples from three different groups of adults: people who had committed suicide who suffered from depression and had a history of severe childhood abuse (27 individuals); people with depression who had committed suicide but who had no history of being abused as children (25 individuals); and brain tissue from a third group of people who had neither psychiatric illnesses nor a history of child abuse (26 people).

Impaired neural connectivity may affect the regulation of emotions

The researchers discovered that the thickness of the myelin coating of a significant proportion of the nerve fibres was reduced ONLY in the brains of those who had suffered from child abuse. They also found underlying molecular alterations that selectively affect the cells that are responsible for myelin generation and maintenance. Finally, they found increases in the diameters of some of the largest axons among only this group and they speculate that together, these changes may alter functional coupling between the cingulate cortex and subcortical structures such as the amygdala and nucleus accumbens (areas of the brain linked respectively to emotional regulation and to reward and satisfaction) and contribute to altered emotional processing in people who have been abused during childhood.

The researchers conclude that adversity in early life may lastingly disrupt a range of neural functions in the anterior cingulate cortex. And while they don’t yet know where in

the brain and when during development, and how, at a molecular level these effects are sufficient to have an impact on the regulation of emotions and attachment, they are now planning to explore this in further research.

Source: http://www.mcgill.ca/newsroom/channels/news/child-abuse-affects-brain-wiring-270024

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