Drug use-various effects

An effective drug-free workplace policy is one of the best ways for employers to protect their businesses. An effective program does not end with pre-employment screening, since any drug user can count up to three days before the test and then begin to use again after being hired.

Drug-free workplace policies reduce the amount of sick time, absenteeism, workman’s comp claims, insurance premiums, and protects against civil lawsuits because of an employee who inflicts damage on others because of impairment.

Communities that emphasize and encourage drug-free workplace practices can have an impact on overall drug use in the community. When combined with effective education and prevention, and by increasing the incentive of users to seek treatment, we can promote a drug-free culture and a thriving business environment that protects individuals, families and the community.

While some might think they don’t need a drug-free workplace policy, as we discussed last week, that’s really not true. Small businesses, not just large companies, need firm drug testing policies.

One new form of marijuana that’s growing in popularity nationwide underscores the need for workplace drug testing programs. This dangerous drug, wax marijuana, can easily be used in the workplace because it doesn’t look like regular marijuana — and frighteningly, it’s the most powerful form of the drug.

Here’s what employers need to know about wax marijuana, and why it shows the need to participate in Drug Free Work Week.

The 411 on Wax Marijuana – and What it Means for Drug Free Workplace Programs

With aliases like butter and honeycomb because of its waxy texture, wax is the most powerful form of marijuana.

According to wax marijuana users, a single hit can leave a high lasting all day. One dosage is equal to 20 marijuana cigarettes and can produce powerful hallucinations and psychotic effects. This potency is because wax marijuana is more than 80% pure THC.

Manufacturers produce wax by extracting the main psychoactive compound, Tetrahydrocannabinol (THC), from marijuana. They use flammable substances like butane in the process, which makes it quite dangerous, but renders the wax marijuana very strong.

While wax marijuana is legal in states like Colorado and Washington, it’s illegal under federal law and in most states.

Employers should take note – due to its appearance, wax marijuana can be passed off as lip balm.

This means that your employees could bring the most powerful form of marijuana into the workplace and use it right under your nose.

Remember, any on-the-clock substance abuse has lasting effects on your workplace, particularly when it comes to the safety of your employees. Just one hit of wax marijuana can result in an extremely powerful, daylong high — rendering your worker a serious danger to everyone around them.

Your workplace needs a drug testing policy to combat new trends in substance use, like wax marijuana.

Drug Free Work Week is a great opportunity for you to take stock of your existing drug testing policy or create a new workplace drug testing program. If you don’t take the time now to create or revise a policy, you may pay for it down the line as your employees try new drugs, such as wax marijuana, and end up causing injuries or financial damage to your workplace.

Partner With ARCpoint Labs for Workplace Drug Testing Policies.

Located nationwide, ARCpoint Labs provides workplace drug testing assistance. We can work with you to create and implement a drug testing policy that fits your unique needs, considering desired detection windows, new and emerging drugs, and your community’s particular substance abuse issues. Let us work with you to carry out a custom drug testing program.

Source: http://sober-work-place.com/drug-testing-2/with-wax-marijuana-use-on-the-rise-make-sure-you-celebrate-drug-free-work-week/  Introduction from Monte Stiles from DWI

A teenage rugby player cut off his own penis and stabbed his mother while high on skunk, his father has revealed, as he called for the drug to be reclassified.

The father, named only as Nick because he wants to remain anonymous as his son is rebuilding his life, is backing Lord Nicholas Monson’s campaign to have skunk reclassified from a class B to a class A drug and for the traditional weaker form of cannabis to be decriminalised.

Lord Monson launched his call following the suicide of his 21-year-old son Rupert, who was addicted to skunk.

Nick, speaking for the first time in an interview with Radio Five Live, said his son, a county rugby player, started smoking “weed” when he was around sixteen and a half before switching to skunk because of “boredom”.

That was the beginning of what Nick said his son would describe as “two and a half years of hell” which culminated in a psychotic episode.

His son went from a “very bright, bubbly lad” to a “waste of space”. The teenager became delusional and paranoid, including sleeping “with a tennis racket in his bed because he thought people were living in the walls”.

Describing the horrific incident when his son attacked his mother and inflicted “incredibly deep self harm”, Nick said it had been a “perfectly normal day” before his son woke in the middle of the night ranting and raving.

“It was absolutely devastating, you can’t imagine anything of that nature happening…the whole episode was just surreal, I remember looking back its almost as if I’m peering in through a window and it’s happening to someone else.”

Nick’s son was in a mental institute for around 6 months, and in total spent almost two years in prison following the incident.

He has undergone surgery, and will have more operations to repair the damage, though Nick said he couldn’t say whether his son would be able to have children. He is clean of drink and drugs, but Nick cautioned that even being around other people smoking skunk could trigger another psychotic episode. His ex-wife has recovered, and has fully reconciled with her son who, Nick said, is “actually in really good form.”

“We recognise that this was an illness… he was totally oblivious, actually has no real memory of anything that happened, even now,” Nick said. “Maybe that’s for the best.”

Source:

https://www.telegraph.co.uk/news/2017/06/02/teenage-rugby-player-cut-penis-high-onskunk-says-father-wants/

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

A growing number of drug overdose deaths are due to cocaine laced with fentanyl, NPR reports. Fentanyl is 50 to 100 times more potent than heroin. The image above shows two potentially fatal dosages of fentanyl and heroin

According to the Drug Enforcement Administration (DEA), 7 percent of cocaine seized in New England in 2017 included fentanyl, up from 4 percent the previous year. In Connecticut, the number of deaths involving fentanyl-laced cocaine has increased 420 percent in the last three years. Massachusetts officials say an increasing amount of fentanyl-laced cocaine is changing hands on the streets. The DEA, in its National Drug Threat Assessment, says people typically add fentanyl to cocaine for the purpose of “speedballing,” which combines the rush of cocaine with a drug that depresses the nervous system, such as heroin. Some experts told NPR fentanyl may be mixed with cocaine accidentally during packaging. Others say drug cartels are adding fentanyl to cocaine to expand the market of people who are addicted to opioids.

How Can I Protect My Child from Fentanyl? 5 Things Parents Need to Know

Deaths from fentanyl and other synthetic opioids (not including methadone), rose a staggering 72 percent in just one year, from 2014 to 2015. Government agencies and officials of all types are rightly concerned by what some are describing as the third wave of our ongoing opioid epidemic.

As a concerned parent, whose top priority is keeping your child safe — and alive — the following are the most important things to understand about fentanyl.

1. Fentanyl is 50 to 100 times more potent than heroin or morphine. It is a schedule II prescription drug typically used to treat patients with severe pain or to manage pain after surgery. It is also sometimes used to treat patients with chronic pain who are physically tolerant to other opioids. In its prescription form, fentanyl is known by such names as Actiq®, Duragesic® and Sublimaze®.

2. It is relatively cheap to produce, increasing its presence in illicit street drugs. Dealers use it to improve their bottom line. According to a report from the Office of National Drug Control Policy, evidence suggests that fentanyl is being pressed into pills that resemble OxyContin, Xanax, hydrocodone and other sought-after drugs, as well as being cut into heroin and other street drugs. A loved one buying illicit drugs may think they know what they’re getting, but there’s a real risk of it containing fentanyl, which can prove deadly.

3. Naloxone (Narcan) will work in case of overdose, but extra doses may be needed. Because fentanyl is far more powerful than other opioids, the standard 1-2 doses of naloxone may not be enough. Calling 911 is the first step in responding to any overdose, but in the case of a fentanyl-related overdose the help of emergency responders, who will have more naloxone, is critical. Learn more about naloxone and responding to opioid overdose >>

4. Even if someone could tell a product had been laced with fentanyl, it may not prevent their use. Some individuals claim they can tell the difference between product that has been laced with fentanyl and that which hasn’t, but overdose statistics would say otherwise. Some harm reduction programs are offering test strips to determine whether heroin has been cut with fentanyl, but that knowledge may not be much of a deterrent to a loved one who just spent their last dollar to get high.

5. Getting a loved one into treatment is more critical than ever. If you need help in determining a course of action, please reach out to one of our parent counselors on our free Parent Helpline. Learn more about all the ways you can connect with our free and confidential services and begin getting one-on-one help.

Source: https://drugfree.org/parent-blog April 2017

Abstract

Background

Marijuana is a widely used recreational substance. Few cases have been reported of acute myocardial infarction following marijuana use. To our knowledge, this is the first ever study analyzing the lifetime odds of acute myocardial infarction (AMI) with marijuana use and the outcomes in AMI patients with versus without marijuana use.

Methods

We queried the 2010-2014 National Inpatient Sample (NIS) database for 11-70-year-old AMI patients.

Pearson Chi-square test for categorical variables and Student T-test for continuous variables were used to compare the baseline demographic and hospital characteristics between two groups (without vs. with marijuana) of AMI patients. The univariate and multivariate analyses were used to assess and compare the clinical outcomes between two groups. We used Cochran–Armitage test to measure the trends. All statistical analyses were executed by IBM SPSS Statistics 22.0 (IBM Corp., Armonk, NY). We used
weighted data to produce national estimates in our study.

Results

Out of 2,451,933 weighted hospitalized AMI patients, 35,771 patients with a history of marijuana and 2,416,162 patients without a history of marijuana use were identified. The AMI-marijuana group consisted more of younger, male, African American patients. The length of stay and mortality rate were lower in the AMI-marijuana group with more patients being discharged against medical advice.

Multivariable analysis showed that marijuana use was a significant risk factor for AMI development when adjusted for age, sex, race (adjusted OR 1.079, 95% CI 1.065-1.093, p<0.001); adjusted for age, female, race, smoking, cocaine abuse (adjusted OR 1.041, 95% CI 1.027-1.054, p<0.001); and also when adjusted for age, female, race, payer status, smoking, cocaine abuse, amphetamine abuse and alcohol abuse (adjusted OR: 1.031, 95% CI: 1.018-1.045, p<0.001). Complications such as respiratory failure (OR 18.9, CI 15.6-23.0, p<0.001), cerebrovascular disease (OR 9.0, CI 7.0-11.7, p<0.001), cardiogenic shock (OR 6.0, CI 4.9-7.4, p<0.001), septicemia (OR 1.8, CI 1.5–2.2, p<0.001), and dysrhythmia (OR 1.8, CI 1.5-2.1, p<0.001) were independent predictors of mortality in AMI-marijuana group.

Conclusion

The lifetime AMI odds were increased in recreational marijuana users. Overall odds of mortality were not increased significantly in AMI-marijuana group. However, marijuana users showed higher trends of AMI prevalence and related mortality from 2010-2014. It is crucial to assess cardiovascular effects related to marijuana overuse and educate patients for the same.

Source: Desai R, Patel U, Sharma S, et al. (November 03, 2017) Recreational Marijuana Use and Acute Myocardial Infarction: Insights from Nationwide Inpatient Sample in the United States . Cureus 9(11): e1816. DOI 10.7759/cureus.1816

AS THE LEGAL AND MEDICAL USE OF MARIJUANA BECOMES MORE COMMONPLACE, OFFICIALS ARE STRUGGLING TO DETERMINE AND ENFORCE SAFE LEVELS OF IMPAIRMENT.

Determining how intoxicated someone is can be quite a difficult task. For alcohol consumption, a substance that the body excretes in a quick, linear fashion, we can measure the amount of metabolic by-products present in the blood using a breathalyzer, or directly measure ethanol levels with a blood test.

Although the issue is somewhat complicated by differing tolerances, research conducted throughout the 20th century showed that nearly everyone loses their ability to drive safely above certain blood alcohol levels.

In the US, medical marijuana is legal in 29 states and adult recreational use is legalized in eight. Widespread popularity of this psychoactive drug seems to necessitate a similar method for measuring whether or not someone is too high to drive.

Actually creating a “weed breathalyzer” or other marijuana field sobriety test, however, is fraught with scientific complications. According to a commentary published in Trends in Molecular Medicine, the main psychoactive compound in marijuana, THC, not only lingers in the body inconsistently, it also has unpredictable cognitive effects between users.

Early medical studies implied that THC could be detected in the blood for approximately six hours after smoking. Yet subsequent work by the article’s co-author, Marilyn Huestis, found that behavioral changes and motor impairments may last 6-8 hours after smoking despite near zero blood levels after just 2.5 hours.

Even if THC blood levels could accurately judge impairment, taking blood samples after a suspicious accident is likely to be fruitless for law enforcement.

“[Blood levels decline by] 74 percent in the first 30 minutes, and 90 percent by 1.4 hours,” said Huestis to Wired. “And the reason that’s important is because in the US, the average time to get blood drawn [after arrest] is between 1.4 and 4 hours.”

So why do people continue to feel stoned long after the drug is gone from the blood? Unlike ethanol, a hydrophilic molecule, THC doesn’t like hanging out in the water-based blood plasma and rapidly distributes into the cells of lipophilic fatty tissues, organs, and the brain.

“In fact, individual experiences reflect two different levels of drug ‘high,’” the article states. “..Namely a low ‘high’ effect in the absorption phase during cannabis inhalation, and a much higher effect later during the distribution phase owing to the lag time for full distribution of the active THC to the site of action – in this case, the brain.”

Furthermore, the body does not metabolize all the THC absorbed by body tissues at the time of smoking, vaping, or eating; the excess is slowly broken down over days to weeks. Heavy cannabis users will develop a THC tolerance due to this chronic, low-level exposure.

Consequently, occasional users and heavy users may feel wildly different effects from consuming the same dose of THC, preventing determination of a universal, safe dosage cut-off for drivers. A national poll from 2017 suggests that half of Americans are unconcerned by the prospect of stoned drivers on the roads, but law enforcement officials in many US states have drug-impaired driving laws that they intend to enforce. So, what tools should they use?

Huestis, who is also a senior investigator at the National Institute on Drug Abuse, does not support a legal driving limit for marijuana. She believes that, currently, well-trained police officers are best-suited for recognizing signs of impairment. Meanwhile, researchers such as herself are working to identify biomarkers that are more representative of the drug’s cognitive effects than blood THC. Ideally, these can then be measured using rapid non-invasive tests.

Another interesting prospect: Researchers at University of California San Diego are recruiting participants for a trial to develop an iPad-based cannabis-specialized field sobriety test. Volunteers will randomly receive marijuana joints at various THC concentrations, then complete driving simulations and undergo experimental impairment assessments.

Source: http://www.iflscience.com/health-and-medicine/why-is-it-so-hard-to-test-for-marijuana-intoxication/ January 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

“No One Has Died of an Overdose”

This remains the most outrageous claim of the pro-legalization movement. It is not only dangerously misleading, it is a slap in the face to the families who have lost children, spouses and parents. Everyone admits that people are dying in traffic crashes because of stoned drivers, and that some people have died in butane hash oil explosions, but too many people are turning a blind eye to the other deaths caused by what can only be called an overdose. Tachycardia – a racing heart – is a common, well-known side effect of using marijuana. So is increased blood pressure. A growing body of evidence, here and in other countries, is revealing that marijuana has caused previously overlooked deaths through heart attack and stroke. In Colorado last fall, an 11-month-old infant brought to the ER after being exposed to marijuana died from an inflamed heart muscle (myocarditis) caused by the exposure.

Marijuana can also overwhelm the emotional centers of the brain causing paranoia, delusions, and acute psychosis. The National Academy of Sciences (NAS) report released last January states, “There is substantial evidence of a statistical association between cannabis use and the development of schizophrenia or other psychoses, with the highest risk among the most frequent users.” (The Health Effects of Cannabis and Cannabinoids, Chapter Highlights NAS 2017)

Emergency rooms in Colorado reported a 44 percent increase in marijuana-related visits between 2012 and 2014. Many of these were cases of acute psychosis, particularly in young men, who had to be restrained to keep from harming themselves or others.

Other evidence of marijuana overdose

A growing body of evidence indicates that marijuana is not just associated with suicide but can be a causative factor. The NAS report cited above found an “Increased incidence of suicidal ideation and suicide attempts with a higher incidence among heavier users” and an “Increased incidence of suicide completion.” One of the studies they listed found a seven-fold increase in risk for suicide even after controlling for a prior history of mood disorders.

In 2014, a young man in Colorado either jumped or unwittingly tumbled to his death from a fourth-floor balcony during a psychotic outburst. In July this year, a Vermont father clutching his son to his chest jumped out of a fourth-floor window shortly after smoking marijuana. He said it was God who made him jump.

When a drug drives all sense of reality from your brain, it’s an overdose. In marijuana’s case, these overdoses can and do lead to death.

Dean Whitlock is a freelance writer whose book, Finn’s Clock, a historical fantasy will be coming this fall in paperback. www.deanwhitlock.com.Read the full article in Vermont Digger. Also read why Vermont physicians propose caution with legalization.

Source: http://www.poppot.org/2017/10/18/truth-deaths-by-marijuana-overdose/

Washington’s pot is a bit more potent than the national average. And the state’s teens are more likely to smoke marijuana than young people nationwide.

Although we have the same problems with marijuana as we do with liquor abuse, no blockbuster conclusions came from a recent report on Washington’s marijuana universe.

But a couple of somewhat unexpected environmental wrinkles from Washington’s marijuana industry — both legal and illegal — also emerge in the second annual look at the state’s experience since passage of a 2012 initiative allowing recreational pot sales.

Marijuana growers and processors use 1.63 percent of the state’s electricity, which is a lot, according to the report by the Northwest High Intensity Drug Trafficking Area — a combined effort by several federal, state and local government agencies. By way of comparison, all forms of lighting — in homes, commercial buildings and manufacturing — account for just 7 to 11 percent of electrical consumption nationally. Or, as the report puts it, the power is enough for 2 million homes.

The high power consumption stems from the heat lamps and the accompanying air conditioning for indoor marijuana growing operations. “They are exceedingly energy-consumptive,” said Steven Freng, manager for prevention and treatment for the High Intensity Drug Trafficking Area.

The carbon footprint, according to the report, equals that of about 3 million cars.

And illegal pot growers siphoned off 43.2 million gallons of water from streams and aquifers during the 2016 growing season — water that tribes, farmers and cities would otherwise use as carefully as possible, in part to protect salmon.

Sixty percent of Washington’s illegal pot was grown on state-owned land in 2016. That’s because black-market growers tend to worry about gun-toting owners on private lands, according to Freng and Luci McKean, the organization’s deputy director. The black-market operations use the water during a roughly 120-day growing season.

Marijuana purchases have boomed in Washington. Legal marijuana sales were almost $1 billion in fiscal year 2016 and were on track to be about $1.5 billion in fiscal 2017, which ended June 30. As of February, the state had 1,121 licensed producers, 1,106 licensed processors and 470 licensed retailers.

What Washington’s marijuana users are getting is above average in potency. According to the report, nationwide marijuana products average a THC percentage of 13.2 percent, while Washington state’s THC average percentage was 21.6 percent.

Teen use of marijuana has grown slightly. Depending on how the numbers are crunched, marijuana use among Washington’s young adults and teens ranges from 2 to 5 percent above the national average. Five percent of Washingtonians age 18-to-25 use pot daily, slightly above the national average, the report said.

According to a survey cited in the report, 17 percent of high school seniors and 9 percent of high school sophomores have driven within three hours after smoking pot.

Adult use before driving is still a fuzzy picture. A third of Washingtonians arrested for driving under the influence had THC, the active ingredient in marijuana, in their bloodstreams. One study found an increase in dead drivers with THC above the legal limit in their blood from 7.8 percent in 2013 to 12.8 percent in 2014.

“Adults still don’t understand the effects of impairment behind the wheel of a car,” Freng said.

McKean said that one major unknown is marijuana-laced edibles, which authorities believe have become a significant factor in THC-impaired drivers, but has not been studied enough to provide solid numbers.

Another major unknown, McKean and Freng said, is how marijuana consumption contributes to emergency room and hospital cases because the state hospitals have not agreed to release that data to government officials.

Source: http://crosscut.com/2017/10/washingtons-pot-industry-not-environmentally-friendly-marijuana/

Executive Summary

Purpose

Rocky Mountain High Intensity Drug Trafficking Area (RMHIDTA) is tracking the impact of marijuana legalization in the state of Colorado. This report will utilize, whenever possible, a comparison of three different eras in Colorado’s legalization history:

· 2006 – 2008: Medical marijuana pre-commercialization era

· 2009 – Present: Medical marijuana commercialization and expansion era

· 2013 – Present: Recreational marijuana era

Rocky Mountain HIDTA will collect and report comparative data in a variety of areas, including but not limited to:

· Impaired driving and fatalities

· Youth marijuana use

· Adult marijuana use

· Emergency room admissions

· Marijuana-related exposure cases

· Diversion of Colorado marijuana

This is the fifth annual report on the impact of legalized marijuana in Colorado. It is divided into ten sections, each providing information on the impact of marijuana legalization. The sections are as follows:

Section 1 – Impaired Driving and Fatalities:

· Marijuana-related traffic deaths when a driver was positive for marijuana more than doubled from 55 deaths in 2013 to 123 deaths in 2016.

· Marijuana-related traffic deaths increased 66 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

o During the same time period, all traffic deaths increased 16 percent.

· In 2009, Colorado marijuana-related traffic deaths involving drivers testing positive for marijuana represented 9 percent of all traffic deaths. By 2016, that number has more than doubled to 20 percent.

Section 2 – Youth Marijuana Use:

· Youth past month marijuana use increased 12 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado youth ranked #1 in the nation for past month marijuana use, up from #4 in 2011/2012 and #14 in 2005/2006.

· Colorado youth past month marijuana use for 2014/2015 was 55 percent higher than the national average compared to 39 percent higher in 2011/2012.

Section 3 – Adult Marijuana Use:

· College age past month marijuana use increased 16 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado college-age adults ranked #2 in the nation for past-month marijuana use, up from #3 in 2011/2012 and #8 in 2005/2006.

· Colorado college age past month marijuana use for 2014/2015 was 61 percent higher than the national average compared to 42 percent higher in 2011/2012.

· Adult past-month marijuana use increased 71 percent in the three-year average (2013-2015) since Colorado legalized recreational marijuana compared to the three-year average prior to legalization (2010-2012).

· The latest 2014/2015 results show Colorado adults ranked #1 in the nation for past month marijuana use, up from #7 in 2011/2012 and #8 in 2005/2006.

· Colorado adult past month marijuana use for 2014/2015 was 124 percent higher than the national average compared to 51 percent higher in 2011/2012.

Section 4 – Emergency Department and Hospital Marijuana-Related Admissions:

· The yearly rate of emergency department visits related to marijuana increased 35 percent after the legalization of recreational marijuana (2011-2012 vs. 2013-2015).

· Number of hospitalizations related to marijuana:

o 2011 – 6,305

o 2012 – 6,715

o 2013 – 8,272

o 2014 – 11,439

o Jan-Sept 2015 – 10,901

· The yearly number of marijuana-related hospitalizations increased 72 percent after the legalization of recreational marijuana (2009-2012 vs. 2013-2015).

Section 5 – Marijuana-Related Exposure:

· Marijuana-related exposures increased 139 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

· Marijuana-Only exposures more than doubled (increased 210 percent) in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

Section 6 – Treatment:

· Marijuana treatment data from Colorado in years 2006 – 2016 does not appear to demonstrate a definitive trend. Colorado averages 6,683 treatment admissions annually for marijuana abuse.

· Over the last ten years, the top four drugs involved in treatment admissions were alcohol (average 13,551), marijuana (average 6,712), methamphetamine (average 5,578), and heroin (average 3,024).

Section 7 – Diversion of Colorado Marijuana:

· In 2016, RMHIDTA Colorado drug task forces completed 163 investigations of individuals or organizations involved in illegally selling Colorado marijuana both in and out of state.

o These cases led to:

§ 252 felony arrests

§ 7,116 (3.5 tons) pounds of marijuana seized

§ 47,108 marijuana plants seized

§ 2,111 marijuana edibles seized

§ 232 pounds of concentrate seized

§ 29 different states to which marijuana was destined

· Highway interdiction seizures of Colorado marijuana increased 43 percent in the four-year average (2013-2016) since Colorado legalized recreational marijuana compared to the four-year average (2009-2012) prior to legalization.

· Of the 346 highway interdiction seizures in 2016, there were 36 different states destined to receive marijuana from Colorado.

o The most common destinations identified were Illinois, Missouri, Texas, Kansas and Florida.

Section 8 – Diversion by Parcel:

· Seizures of Colorado marijuana in the U.S. mail has increased 844 percent from an average of 52 parcels (2009-2012) to 491 parcels (2013-2016) in the four-year average that recreational marijuana has been legal.

· Seizures of Colorado marijuana in the U.S. mail has increased 914 percent from an average of 97 pounds (2009-2012) to 984 pounds (2013-2016) in the four-year average that recreational marijuana has been legal.

Section 9 – Related Data:

· Crime in Denver increased 17 percent and crime in Colorado increased 11 percent from 2013 to 2016.

· Colorado annual tax revenue from the sale of recreational and medical marijuana was 0.8 percent of Colorado’s total statewide budget (FY 2016).

· As of June 2017, there were 491 retail marijuana stores in the state of Colorado compared to 392 Starbucks and 208 McDonald’s.

· 66 percent of local jurisdictions have banned medical and recreational marijuana businesses.

Section 10 – Reference Materials:

This section lists various studies and reports regarding marijuana.

THERE IS MUCH MORE DATA IN EACH OF THE TEN SECTIONS. THIS PUBLICATION MAY BE FOUND ON THE ROCKY MOUNTAIN HIDTA WEBSITE; GO TO WWW.RMHIDTA.ORG AND SELECT REPORTS.

Source: WWW.RMHIDTA.ORG October 2017

Abstract

IMPORTANCE:

Over the last 25 years, illicit cannabis use and cannabis use disorders have increased among US adults, and 28 states have passed medical marijuana laws (MML). Little is known about MML and adult illicit cannabis use or cannabis use disorders considered over time.

OBJECTIVE:

To present national data on state MML and degree of change in the prevalence of cannabis use and disorders.

DESIGN, PARTICIPANTS, AND SETTING:

Differences in the degree of change between those living in MML states and other states were examined using 3 cross-sectional US adult surveys: the National Longitudinal Alcohol Epidemiologic Survey (NLAES; 1991-1992), the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC; 2001-2002), and the National Epidemiologic Survey on Alcohol and Related Conditions-III (NESARC-III; 2012-2013). Early-MML states passed MML between NLAES and NESARC (“earlier period”). Late-MML states passed MML between NESARC and NESARC-III (“later period”).

MAIN OUTCOMES AND MEASURES:

Past-year illicit cannabis use and DSM-IV cannabis use disorder.

RESULTS:

Overall, from 1991-1992 to 2012-2013, illicit cannabis use increased significantly more in states that passed MML than in other states (1.4-percentage point more; SE, 0.5; P = .004), as did cannabis use disorders (0.7-percentage point more; SE, 0.3; P = .03).

In the earlier period, illicit cannabis use and disorders decreased similarly in non-MML states and in California (where prevalence was much higher to start with). In contrast, in remaining early-MML states, the prevalence of use and disorders increased.

Remaining early-MML and non-MML states differed significantly for use (by 2.5 percentage points; SE, 0.9; P = .004) and disorder (1.1 percentage points; SE, 0.5; P = .02). In the later period, illicit use increased by the following percentage points: never-MML states, 3.5 (SE, 0.5); California, 5.3 (SE, 1.0); Colorado, 7.0 (SE, 1.6); other early-MML states, 2.6 (SE, 0.9); and late-MML states, 5.1 (SE, 0.8). Compared with never-MML states, increases in use were significantly greater in late-MML states (1.6-percentage point more; SE, 0.6; P = .01), California (1.8-percentage point more; SE, 0.9; P = .04), and Colorado (3.5-percentage point more; SE, 1.5; P = .03).

Increases in cannabis use disorder, which was less prevalent, were smaller but followed similar patterns descriptively, with change greater than never-MML states in California (1.0-percentage point more; SE, 0.5; P = .06) and Colorado (1.6-percentage point more; SE, 0.8; P = .04).

CONCLUSIONS AND RELEVANCE:

Medical marijuana laws appear to have contributed to increased prevalence of illicit cannabis use and cannabis use disorders. State-specific policy changes may also have played a role. While medical marijuana may help some, cannabis-related health consequences associated with changes in state marijuana laws should receive consideration by health care professionals and the public.

Source: JAMA Psychiatry. 2017 Jun 1;74(6):579-588. doi: 10.1001/jamapsychiatry.2017.0724.

For a long time, those in medicine and the law have been concerned about a link between cannabis and violence.

This has been largely dismissed by the pro-drugs lobby as an association, not proof of a cause. The difference is important to scientific enquiry, as revealed by a telling example given recently by Professor Robert Pickard, a former government advisor.

He says the rise in deaths of hedgehogs on the roads since the end of World War II mirrors the rise in television sales, but it would be daft to suggest that TVs are killing hedgehogs: it’s an association, not a cause.

The evidence linking cannabis and violent crime is compelling: regular use of the drug doubles the risk of a psychotic episode or schizophrenia. And time and again, courts hear how people have become psychotic after smoking cannabis and, in the grips of paranoia and delusions, have murdered someone. The gallery of victims should shame those in the liberal elite who insist there’s no definitive evidence of cause and effect.

But a new study has now provided just this. Researchers followed 1,100 patients for a year after discharge from a psychiatric hospital and those who used cannabis were two-and-a-half times more likely to be violent.

So now there’s clear proof of a causative link, have we witnessed a volte-face from the pro-cannabis lobby? Of course we haven’t, because it was never really about the science.

They want to smoke cannabis, and as soon as science brings doing this into question, they simply brush it aside. Particularly frustrating are the smug, ageing hippies who claim that because they’re still here, it must be fine. They look back on a youth spent smoking spliffs with pathetic, misplaced nostalgia, and fail to realise that, not only did plenty of people not make it through the Sixties and Seventies unscathed, but the super-strong cannabis of today is almost an entirely different product.

How many more lives must be ruined before the pro-drugs lobby admit they got it wrong?

Source: http://www.dailymail.co.uk/health/article-4957554/An-uncomfortable-truth-not-life-worth-living.html#ixzz4uppapuW9

· Trials on mice found THC – which causes the ‘high’ in weed, can induce seizures

· The same was shown for JWH-018 – the main part of the synthetic cannabis spice

· Japanese researchers have described their findings are being ‘quite important’

· Skunk, made mostly of THC, dominates the illegal British market of marijuana

Smoking super-strength cannabis or spice may trigger life-threatening seizures, researchers have warned.

Trials on mice showed seizures can be induced by both THC – which causes the ‘high’ in marijuana, and JWH-018 – the main component of spice. The rodents also suffered from a shortness of breath and impaired walking after being given both compounds, the scientists discovered.

Japanese researchers warned the results should act as a wake-up call, given how widely high-potency and synthetic weed is used.

The findings contradicts pro-cannabis campaigners who have long argued that cannabis can help to tackle seizures and highlighted research which shows weed can prevent and control seizures in epileptic patients.

However, lead researcher Dr Olga Malyshevskaya, based at the University of Tsukuba, said the latest findings show cannabis is not a soft drug and warned of its dangers.

She said: ‘Our study is quite important. Unaware of the particularly severe effect by those cannabinoids, people see marijuana as a soft drug, without dangerous health effects.’

She added: ‘It is critically important for health-care professionals and policy makers to be aware of the serious adverse effects, as shown in this report. Clinicians in the emergency departments should always suspect seizure activity in patients who have a history of cannabinoid intoxication.

WHAT IS THC?

THC is found in all forms of cannabis, but is abundant in skunk – a super-strength form of the drug that dominates Britain’s illegal market.

Some 80 per cent of what is available on the streets is believed to be skunk, which is created by growers aiming to make the most potent strain of the drug possible in order to maximise their profits.

They remove high amounts of CBD from the plant, allowing the modified herb to contain only THC. It is unsure how much THC was in the strain of cannabis used in the new study.

Over the years, a host of previous research has pointed to a link between the popular recreational drug and mental health conditions. Last October, University College London researchers found that skunk may be twice as addictive as normal strains of cannabis.

Similar health concerns have been raised about synthetic cannabis spice, which can slump users and turn them into ‘zombies’.

It was previously known as a legal high before it was banned last year following a surge in its use. Now it has reached epidemic levels in prison.

‘The number of clinical cases involving marijuana intoxication has been steadily increasing due to increase in cannabis potency over the last two decades.’

What do other experts think?

Ian Hamilton, a cannabis researcher at York University, cautioned the results, which are published in Scientific Reports.

He told MailOnline: ‘We don’t know if people who use cannabis are using something as potent as this.’ For the study, researchers measured the brain activity of the mice after giving them both compounds and recorded them.

Research that claims to show cannabis can control seizures

The findings contradict a body of research which shows weed can prevent and control seizures in epileptic patients. Campaigners have long argued that cannabis has the opposite effect to the new findings and can help to tackle seizures.

Researchers have previously suggested that CBD – the other compound in cannabis which produces no ‘high’, binds to a receptor in the brain that calms down the electrical activity in the brain which causes a seizure.

First Briton to be prescribed liquid cannabis oil on the NHS

Their case was strengthened when an 11-year-old on the brink of death from a severe form of epilepsy made an ‘incredible’ recovery from taking marijuana.

Billy Caldwell, from Castlederg, Northern Ireland, made headlines in April when he became the first Briton to be prescribed such a drug on the NHS.

And 10 months since he was first given the liquid cannabis oil, he hasn’t had any seizures. He used to suffer up to 100 a day.

THE MAN WHO SUFFERS SEIZURES FROM SYNTHETIC CANNABIS

The news comes just a week after DailyMail.com reported on a disturbing video which shows a man from Des Moines, Iowa, having a seizure as an effect of years smoking synthetic marijuana.

Coby O’Brien-Emerick, 27, has experienced chronic seizures every three months for the past five years, putting him in the hospital for weeks on end.

In the video uploaded in December, Coby is seen on the floor convulsing for about nine minutes while paramedics are being called.

The father-of-two told Dailymail.com he asked for his seizure to be recorded in order to understand the severity of it.

The video was posted to YouTube by his mother-in-law to warn others about the dangerous effects of smoking synthetic marijuana .

Source: http://www.dailymail.co.uk/health/article-4917100/Smoking-super-strength-cannabis-trigger-seizures.html 26 Sept. 2017

A recent review published in the scientific journal Addiction has shed much needed light on an important but rarely discussed condition associated with Substance Use Disorders. Advanced dental disease, including tooth decay and periodontal conditions, are common comorbid conditions among persons with Substance Use Disorders.

To determine the prevalence, investigators conducted an exhaustive systematic search for studies from the past 35 years germane to oral health among substance abusers. Medline, PsycInfo, Ovid, Google Scholar, Embase and article bibliographies were reviewed and analyzed. The results were compared with the general population of non-substance using controls. Parameters of oral health were defined in terms of tooth decay and periodontal disease by comparing the percent of decayed, missing and filled teeth (DMFT) or surfaces (DMFS) and probing gum pocket depth. In total, this review culled the results of 28 studies yielding comparative data on 4,086 dental patients with substance use disorder and 28,031 controls.

Drugs and Dental Disease

Drug abuse affects oral health via direct physiological routes including dry mouth, craving and consumption of sugary sweets and processed carbohydrate snacks (munchies), and most recently processed cannabis sweets, such as gummy bears, candy, cookies and of course…brownies. Cocaine, methamphetamine and other drugs of abuse may interfere with the blood supply to teeth and gums. Teeth clenching and grinding (bruxism), is associated with the chronic use of stimulants and Ecstasy as well as anxiety and depression, which are common comorbidities of Substance Use Disorders. Chemical erosion resulting from excessive use of alcohol, coffee or from applying highly acid drugs such as cocaine to one’s teeth and gums are causative of oral disease. Lastly, given the choice between drug self-administration and flossing or brushing regularly, abusers and addicts pick drugs of abuse.

Why Does This Matter?

As we age, oral health has increasingly significant consequences on our quality of life and overall health. At its best, persons with serious dental and periodontal disease suffer difficulty masticating and observable aesthetic problems that negatively impact self-esteem. At its worse, dental and oral disease cause chronic inflammation and bacteremia, which are risk factors for heart disease, stroke, diabetes and compromised respiratory function. The findings from this study are similar to the outcomes associated with severe mental illness and eating disorders.

The addition of 2.8 million new drug users each year is unsustainable for our current healthcare system. It is difficult to get many users primary medical or addiction care. It is almost impossible to get Substance Use Disorders patients to the dentist. Health disparities and access to care are ongoing public health crises. We will either need a lot more doctors and dentists or a lot fewer drug addicts.

In the clinical setting, we can make a difference. Clinicians who evaluate and treat people with substance use disorders should make certain to include a mouth, gum, and dental history and oral exam. We should routinely screen for oral diseases, arrange for dental care as needed, and educate patients of the oral health risks associated with Substance Use Disorders, dry mouth and cravings for foods with high sugar content.

Source: https://www.rivermendhealth.com/resources/dental-disease-common-serious-seldom-discussed-comorbidity-sud/ September 2017

by  Elizabeth Stuyt, MD

For the past 27 years, working as an addiction psychiatrist, I have struggled with big industries that push their products more for their financial gain rather than the best interests of the clients they serve. The most disconcerting piece occurs when physicians or other treatment providers or governmental entities appear to be influenced by big industry, touting the party line and minimizing any downsides to the product. I have experienced this with the tobacco industry, the pharmaceutical industry and now with the marijuana industry.

It is clear to me that wherever it happens, the push to legalize medical marijuana is simply a back-door effort, by industry, to legalize retail marijuana. However, the lack of any regulations on the potency of THC in marijuana or marijuana products in Colorado has allowed the cannabis industry to increase the potency of THC to astronomical proportions, resulting in a burgeoning public health crisis.

The potency of THC in currently available marijuana has quadrupled since the mid-1990s. The marijuana of the 1980s had <2% THC, 4.5% in 1997, 8.5% in 2006 and by 2015 the average potency of THC in the flower was 17%, with concentrated products averaging 62% THC.

Sadly, the cannabidiol (CBD) concentrations in currently available marijuana have remained the same or decreased. CBD is the component of marijuana that appears to block or ameliorate the effects of THC. Plants that are bred to produce high concentrations of THC cannot simultaneously produce high CBD. Higher-potency THC has been achieved by genetically engineering plants to product more THC and then preventing pollination so that the plant puts more energy into producing cannabinoids rather than seeds. This type of cannabis is referred to as sinsemilla (Spanish for without seed). (It has also been referred to as “skunk” due to its strong smell.)

In my view, this is no different than when the tobacco industry increased the potency of nicotine by genetically engineering tobacco plants to produce more nicotine and then used additives like ammonia to increase the absorption of nicotine. Industry’s efforts to increase the potency of an addictive substance seem to be done purely with the idea of addicting as many people as possible to guarantee continued customers. This certainly worked for the tobacco industry. And we have increasing evidence that high potency THC cannabis use is associated with an increased severity of cannabis dependence, especially in young people.12

Although marijuana has been used for thousands of years for various medical conditions, we have no idea if the benefit comes from the THC or CBD or one of the other multiple cannabinoids present in marijuana, or a combination. And we have no idea how much is needed or how often. Most of the research indicates that it is likely the CBD that is more helpful but we obviously need research on this. There is no evidence that increasing the potency of THC has any medical benefits. In fact, a study on the benefits of smoked cannabis on pain actually demonstrated that too high a dose of THC can cause hyperalgesia – similar to what is seen with high dose opiates – meaning that the person becomes more sensitive to pain with continued use. They found that 2% THC had no effect on pain, 4% THC had some beneficial effects on chronic pain and 8% resulted in hyperalgesia.3

The discovery of the “active component” in marijuana that makes it so desirable is a fairly recent phenomenon. THC and CBD were first discovered in 1963 in Israel.4

Because cannabis was made a DEA schedule I drug in 1970, very little research has been done on cannabis in the United States and most of the indications for medical marijuana have very little good research backing up the use. The chemical that is made by the body and fits the receptor which accommodates THC was discovered in 1992.5

The researcher named the chemical anandamide which means “supreme joy” in Sanskrit.  However, it turns out that the endocannabinoid system plays a very significant role in brain development that occurs during childhood and adolescence. It controls glutamate and GABA homeostasis and plays a role in strengthening and pruning synaptic connections in the prefrontal motor cortex. The consequences of using the high potency THC products during this period, especially without the protective benefits of CBD, are multifaceted and include disturbance of the endocannabinoid system, which can result in impaired cognitive development, lower IQ and increased risk of psychosis.

There is also evidence that marijuana use contributes to anxiety and depression. A very large prospective study out of Australia tracked 1600 girls for 7 years and found that those who used marijuana every day were 5 times more likely to suffer from depression and anxiety than non-users.6

Teenage girls who used the drug a least once a week were twice as likely to develop depression as those who did not use. In this study, cannabis use prior to age 15 also increased the risk of developing schizophrenia symptoms.

While there definitely are people who can use marijuana responsibly without any untoward effects, similar to how some people can drink alcohol responsibly and not have any problems, there are people who are very sensitive to the effects of THC, and its use can precipitate psychosis. The higher the potency of THC the more likely this may happen and we have no idea how to predict who will be affected. In one of the first double blind randomized placebo controlled trials on smoked cannabis (maximum of 8% THC) for the treatment of pain, a cannabis naïve participant had a psychotic reaction to the marijuana in the study and this then required that all future study participants have some experience with smoking marijuana.7

This kind of makes it difficult to have “blind” unbiased participants.

A 2015 study out of London analyzed 780 people ages 18-65, 410 with first episode psychosis and 370 healthy controls, and found that users of high potency (“skunk-like”) cannabis (THC > 15%) are three times as likely to have a psychotic episode as people who never use cannabis, and the risk is fivefold in people who smoke this form of the drug every day.89 There was no association of psychosis with THC levels < 5%. Most of the marijuana in the U.S. is of the high-THC variety. Many retailers in Colorado sell strains of weed that contain 25 percent THC or more.

Sadly, Colorado has now joined several other states in approving PTSD as an indication for the use of medical marijuana. Marijuana does not “treat” PTSD any more than benzodiazepines or opiates “treat” PTSD. All these addictive drugs do is mask the symptoms, allowing the person to continue life unaffected by the memory of the trauma. However, the psychological trauma is never resolved and the individual has to continue to use the substance in order to cope. This sets the individual up for the development of addiction to the substance or the use of other addictive substances. There is absolutely no good research to support the use of marijuana for PTSD, and there is observational data that this would be a bad idea unless this use was supported by a lot more (and better-designed) longitudinal research.

In an excellent longitudinal, observational study from 1992 to 2011, 2,276 Veterans admitted to specialized VA treatment programs for PTSD had their symptoms evaluated at intake and four months after discharge.10

They found that those who never used marijuana or quit using while in treatment had the lowest levels of PTSD symptoms, while those who continued to use or started using marijuana after treatment had worse symptoms of PTSD. Those who started using the drug during treatment had higher levels of violent behavior too.

Those of us working in the trenches in Colorado are seeing the downsides of what our governor has called “one of the great social experiments of the 21st century.” Emergency room physicians are seeing a significant increase in people experiencing consequences from marijuana use since it was legalized. One such physician wrote a very poignant piece about his experience returning to his home town of Pueblo, Colorado where he is now practicing.11

His experiences are totally supported by the Rocky Mountain High Intensity Drug Trafficking Report, volume 4 from September 2016 which documents significant increases in marijuana related emergency department visits (49%) and hospitalizations related to marijuana (32%) compared to rates prior to retail legalization. This report also documents significant increases in the use of marijuana by youth, with Colorado youth “past month marijuana use” for 2013/2014 being 74% higher than the national average, compared with 39% higher in 2011/2012.

 

In Pueblo, Colorado, where I practice, it has developed into a perfect storm. According to the Healthy Kids Colorado Survey in 2015, we have the highest incidence of youth marijuana use in the state, with 30.1% reporting using marijuana in the last 30 days. The legalization of retail marijuana seems to be reflected in the increased abuse of opiates and heroin too. In addition to the highest rates of marijuana use by youth, Pueblo has the highest rates of heroin-related deaths in the state.

 

This is a very disturbing correlation that needs attention. I have definitely seen in my practice that marijuana acts as a gateway drug to opiates, and to relapse to opiates after treatment if the person goes back to using marijuana. The Smart Approaches to Marijuana status report, which assesses state compliance with federal marijuana enforcement policy, following what is known as the Cole memo, documents that Colorado, four years after legalization, has failed to meet the specific DOJ requirements on controlling recreational marijuana production, distribution and use. This report documents a significant increase in drugged driving crashes, youth marijuana use, a thriving illegal black market and unabated sales of alcohol, which supports the idea that people are not using marijuana instead of alcohol but rather in addition to alcohol.

In spite of all this information, powerful people in the government of Colorado have publicly minimized the consequences. Larry Wolk, MD, the Chief Medical Officer for the Colorado Department of Public Health and Environment, has reported that he has “not seen any significant problems” with the legalization of marijuana.

Governor Hickenlooper’s response to Attorney General Sessions recent questions about compliance with the Cole Memo minimized the adolescent use of marijuana by saying that youth marijuana use in Colorado has “remained stable since legalization.” This is not true for Pueblo, but in any event, any use of marijuana by youth in Colorado should not be minimized and should be a major concern for future generations.

While there are people who believe we need to enforce federal law and go back to making marijuana illegal, I am afraid the horse is already out of the barn and cannot be put back in as we already have several states with “legal” retail marijuana and multiple more with “medical marijuana.” I cannot conceive of any way this could be reversed at this point, when the majority of society supports the legalization of marijuana.

Solutions to our marijuana problems have to be realistic to our current situation/environment. The number one solution is more education. Many people seem to lack a true understanding of the drug and all the potential negative consequences of the higher-potency THC. This is why education is so important. Adults should have the right to make their own decisions but they need informed consent, just like with any drug.

The biggest concern is with adolescent use and the developing brain. This requires a lot more education and increased efforts at prevention, early intervention and treatment. I believe society would be truly served by a federal ban on all advertising of addicting drugs including alcohol, tobacco and marijuana, as well as all pharmaceutical drugs. The decision to use a pharmaceutical medication should be between the patient and the medical professional, not influenced by big industry. We clearly have the big industries— alcohol, tobacco and marijuana—doing everything they can to influence the public and convince them to use their product.

Since we only have anecdotal evidence at this point that marijuana can aid any medical condition, I recommend eliminating “medical marijuana” and just have retail marijuana with limits on THC and regulations similar to alcohol and tobacco. This could help take away the perception, which adolescents and others have, that because is it “medical” it must be “safe.” In order to be able to say it is medical, it should go through the same standards for testing the safety and efficacy of any prescription drug.

In this vein, I believe we do need more research and that marijuana should be reclassified as a schedule II drug so this can occur. Since marijuana has been used medicinally for thousands of years, I believe that the plant deserves some true research to determine if and what parts of the plant are helpful medicinally. The reports that marijuana use resulted in less than 10% becoming addicted to it were done back in the 1990s when THC levels were <5%. Since we are seeing significant increases in people developing marijuana use disorder with the higher doses of THC, perhaps the limits on THC should be <5%. Editor’s note: for more information, see the pdf of the author’s talk on this topic.     Show 11 footnotes

Source:  https://www.madinamerica.com/2017/09/unintended-consequences-colorado-social-experiment/  11th September 2017

A Staffordshire bull terrier that mauled its owner to death while taking part in a BBC documentary had eaten a stash of crack cocaine, an inquest was told.

The dog, named Major, repeatedly bit the throat and face of its owner Mario Perivoitos, an IT expert, in front of a two-man crew from the BBC show Drugs Map Britain shortly after filming.

The crew managed to lock the dog in another room and call an ambulance but Mr Perivoitos died at the scene. The animal was found to have taken enough drugs to put a human eight times over the drug-drive limit.

North London coroner’s court was told that Mr Perivoitos, 41, was a heroin user and had suffered an epileptic fit before the dog set upon him at his flat in Wood Green, north London.

Jessica Winteringham, the assistant producer, said that after the crew had finished filming, Mr Perivoitos had appeared angry, before becoming unresponsive and lying on the bed next to the dog. “Then the dog got up and got his right cheek and then his left and then clamped on to his neck,” she said. “We were shouting ‘no Major’ to try and stop him. Mario did not make any attempt to move or do anything.”

Joshua Haddow, the show’s producer, said he struggled to pull Major off its owner: “I just started hitting the dog, I just did not know what else to do and as I did that it started to loosen its grip.

“I picked it up by the scruff of its neck and I threw it into a room . . . the idea being that I shut the door and I went back to Mario to try and see if we could do anything. The dog was very peaceful, it was friendly with us, it would lick our hands and say hello, there was no way we could have pre-empted it.

“When Mario disturbed the dog on the bed he was behaving quite strangely, the dog was relaxing, he essentially clambered and disturbed the dog, he started to nip his face at first a little bit and then it quickly escalated.”

Nicholas Carmichael, an expert in veterinary toxicology, said cocaine and morphine were found. “It is very likely that this dog had consumed drugs, probably eaten them. It is almost impossible to say whether that will make the dog attack. The dog was eight times the drug-drive limit.”

Andrew Walker, senior coroner, recorded a conclusion of death as a consequence of injuries received from a dog.

Source: https://www.thetimes.co.uk/edition/news/staffordshire-bull-terrier-had-eaten-crack-cocaine-before-fatal-attack-on-owner-mario-perivoitos-during-filming-of-bbc-documentary-drugs-map-britain-in-wood-green-bbxfmd6p2    12th Sept.2017

And Addiction-Connected Carcinogenicity, Congenital Toxicity And Heritable Genotoxicity

Albert Stuart Reece, Gary Kenneth Hulse

Extracts from the above research.  Recommend readers go to source for complete study.

A B S T R A C T

The recent demonstration that massive scale chromosomal shattering or pulverization can occur abruptly due to errors induced by interference with the microtubule machinery of the mitotic spindle followed by haphazard chromosomal annealing, together with sophisticated insights from epigenetics, provide profound mechanistic insights into some of the most perplexing classical observations of addiction medicine, including cancerogenesis, the younger and aggressive onset of addiction-related carcinogenesis, the heritability of addictive neurocircuitry and cancers, and foetal malformations.

Tetrahydrocannabinol (THC) and other addictive agents have been shown to inhibit tubulin polymerization which perturbs the formation and function of the microtubules of the mitotic spindle. This disruption of the mitotic machinery perturbs proper chromosomal segregation during anaphase and causes micronucleus formation which is the primary locus and cause of the chromosomal pulverization of chromothripsis and downstream genotoxic events including oncogene induction and tumour suppressor silencing.

Moreover the complementation of multiple positive cannabis-cancer epidemiological studies, and replicated dose-response relationships with established mechanisms fulfils causal criteria. This information is also consistent with data showing acceleration of the aging process by drugs of addiction including alcohol, tobacco, cannabis, stimulants and opioids. THC shows a non-linear sigmoidal dose-response relationship in multiple pertinent in vitro and preclinical genotoxicity assays, and in this respect is similar to the serious major human mutagen thalidomide. Rising community exposure, tissue storage of cannabinoids, and increasingly potent phytocannabinoid sources, suggests that the threshold mutagenic dose for cancerogenesis will increasingly be crossed beyond the developing world, and raise transgenerational transmission of teratogenicity as an increasing concern.

CONCLUSION

As mentioned above high dose cannabis and THC test positive in many genotoxicity assays, albeit often with a highly non-linear threshold like effects above low doses. As long ago as 2004 it was said that 3–41% of all neonates born in various North American communities had been exposed to cannabis [172]. Since cannabis is addictive [187], is becoming more potent [77,83,86], quickly builds up in adipose tissues [62,82] and seems generally to becoming more widely available under fluid regulatory regimes [187,188], real concern must be expressed that the rising population level of cannabinoid exposure will increasingly intersect the toxic thresholds for major genotoxicity including chromosomal clastogenicity secondary to interference and premature aging of the mitotic apparatus.

Under such a conceptualization, it would appear that the real boon of restrictive cannabis regimes [189] is not their supposed success in any drug war, but their confinement in the populations they protect, to a low dose exposure paradigm which limits incident and transgenerational teratogenicity, ageing, mental retardation and cancerogenicity.

Source:   Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis Journal Homepage: www.elsevier.com/locate/molmut    January 2016

Women who inject drugs are about 39% more likely to become infected with hepatitis C virus than men who inject drugs, research suggests.

A range of factors could account for the disparity, the researchers wrote in Clinical Infectious Diseases.

“Our findings provide important evidence that sex disparities in  exist independent of selected behavioral risk and demographic factors,” researcher Kimberly Page, PhD, MPH, division chief of the department of internal medicine at the University of New Mexico Health Sciences Center, and colleagues wrote. “When considering HCV risk differential among women, multiple factors including biological, social and network factors — as well as differential access to prevention services — need to be considered.”

The researchers assessed data from seven of the 10 InC3 Collaborative studies of HIV and HCV among PWID ((people who inject drugs ), which included locations in the United States, Europe and Australia.

Page and colleagues included data from 1,868 PWID, 590 (31.58%) of whom were women. No data from participants who reported being transgender were assessed. In all, the researchers found 511 PWID with incident HCV during follow-up. Of those, 182 (31.5%) were female.

The unadjusted female-to-male HR for HCV infection was 1.38 (95% CI, 1.15-1.65). The disparity remained significant after adjustment for behavioral and demographic risk factors, the researchers said, slightly rising to 1.39 (95% CI, 1.12-1.72).

Page and colleagues cited previous studies suggesting biological and social factors that may help to explain the difference.

“All of these factors should be studied further to better understand sex-related differences in risk and to maximize prevention effects of drug treatment programs and their potential to reduce acquisition of blood-borne viruses, including HCV and HIV,” they wrote.

Disclosure: Esmaeili reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.

Source: https://www.healio.com/infectious-disease/hepatitis-c/news/in-the-journals/%7Be0c3d409-03c9-4d3b-a277-13edeb16b8e6%7D/women-injecting-drugs-at-higher-risk-for-hcv-than-men 2nd Sept.2017

Background

On August 29, 2013, the U.S. Department of Justice (DOJ) issued guidelines to Federal prosecutors and law enforcement officials regarding where to focus their drug enforcement efforts in states that have passed laws legalizing the retail sales of marijuana. The so-called “Cole Memo” directs enforcement officials to focus resources, including prosecutions, “on persons and organizations whose conduct interferes with any one or more of [eight] priorities, regardless of state law.”

Per the memorandum, the eight DOJ priorities are:

● Preventing distribution of marijuana to minors

● Preventing marijuana revenue from funding criminal enterprises, gangs or cartels

● Preventing marijuana from moving out of states where it is legal

● Preventing use of state-legal marijuana sales as a cover for illegal activity

● Preventing violence and use of firearms in growing or distributing marijuana

● Preventing drugged driving or exacerbation of other adverse public health consequences associated with marijuana use

● Preventing growing marijuana on public lands

● Preventing marijuana possession or use on federal property

According to the Department of Justice, the Federal “hands-off” approach to marijuana enforcement enumerated in the Cole Memo is contingent on its expectation that “states and local governments that have enacted laws authorizing marijuana-related conduct will implement strong and effective regulatory and enforcement systems that will address the threat those state laws could pose to public safety, public health, and other law enforcement interests.

A system adequate to that task must not only contain robust controls and procedures on paper, it must also be effective in practice.”

Unfortunately, since Colorado and Washington became the first states to legalize the recreational sale of marijuana in 2012, evidence has emerged that regulations intended to control the sale and use of marijuana have failed to meet the promises made by advocates for legalization.

For example, states with legal marijuana are seeing an increase in drugged driving crashes and youth marijuana use. States that have legalized marijuana are also failing to shore up state budget shortfalls with marijuana taxes, continuing to see a thriving illegal black market, and are experiencing an unabated sales of alcohol, despite campaign promises from advocates promising that marijuana would be used as a “safer” alternative instead.

Moreover, state regulatory frameworks established post-legalization have failed to meet each of the specific DOJ requirements on controlling recreational marijuana production, distribution, and use.

While long-term studies and research on the public health and safety impacts of marijuana legalization are ongoing, this report provides a partial census of readily available information that demonstrates how Colorado, Oregon, and Washington State –

the jurisdictions with the most mature regulatory markets and schemes – have not fulfilled the requirements of the Cole Memo.

DOJ Guideline 1: “Preventing distribution of marijuana to minors”

● According to the nation’s largest and most comprehensive survey of drug use trends in the nation, past-month use of marijuana among 12 to 17-year-olds in Colorado increased significantly – from 9.82% to 12.56% after marijuana retail sales began (Colorado legalized marijuana in 2012 and implemented legal marijuana stores in 2014).

The same study notes that teens and adults in Colorado now use marijuana at a higher rate than the rest of the country. No other representative sample of drug users in Colorado has contradicted this sample.

● A 2017 study from the University of Colorado found that marijuana-related emergency room visits and visits to its satellite urgent care centers by teens in Colorado more than quadrupled after the state legalized marijuana.

● In Colorado, a new report from the state’s public safety agency reveals that after the state legalized the drug, marijuana-related arrests for black and Hispanic youth rose by 58% and 29% respectively, while arrest rates for white kids dropped by eight percent. School Resource Officers in Colorado have reported a substantial increase in marijuana-related offenses in Colorado schools after the state commercialized the drug.

● According to data from the State of Washington, there have been over 240 violations of legal marijuana sales to minors and of minors frequenting restricted marijuana sales areas as of July 2017. ● Youth use – among 8th and 10th graders at least – is increasing in Washington State. According to a special analysis of teenage drug use published in the peer-reviewed, highly regarded Journal of American Medical Association Pediatrics, the perceived  harmfulness of marijuana in Washington declined 14.2% and 16.1% among eighth and 10th graders, respectively, while marijuana use increased 2.0% and 4.1% from 2010-2012 to 2013-2015.

● According to the Washington State Office of the Superintendent of Public Instruction during 2013-2014, 48 percent of statewide student expulsions were for marijuana in comparison to alcohol, tobacco, and other illicit drugs. During the 2014-2015 school year, statewide student expulsions for marijuana increased to 60 percent. Marijuana related suspensions for the 2013-2014 school year reported 42 percent and for the 2014-2015 school year, suspensions increased to 49 percent.

● In Washington State, youth (12-17) accounted for 64.9% of all state marijuana seizures in 2015 as compared to 29.9% in 2010, according to data from the National Incident Based Reporting System (NIBRS).

● From 2012 to 2016, reported exposure calls for marijuana increased 105 percent in Washington. According to the 2016 Annual Cannabis Toxic Trends Report, of exposures related to children under the age of five, 73 percent occurred in those one to three years of age. The counties with the highest reported exposures for both 2015 and 2016 were: King, Spokane, Snohomish, and Pierce.

DOJ Guideline 2: “Preventing revenue of the sale of marijuana from going to criminal enterprises, gangs, and cartels”

● In June 2017, Colorado Attorney General Cynthia Coffman announced a takedown of a massive illegal marijuana trafficking ring in Colorado. The bust is the largest since legalization and indicted 62 individuals and 12 businesses in Colorado. The operation stretched into other states including Kansas, Texas, Nebraska, Ohio and Oklahoma.

● In March 2017, a leaked report from the Oregon State Police uncovered evidence from state officials that the black market for marijuana continues to thrive in the state. The 39-page report noted that, “The illicit exportation of cannabis must be stemmed as it undermines the spirit of the law and the integrity of the legal market…it steals economic power from the market, the government, and the citizens of Oregon, and furnishes it to criminals, thereby tarnishing state compliance efforts.”

Washington State Office of the Superintendent of Instruction. (2016, Jan. 26). Behavior Report. http://www.k12.wa.us/SafetyCenter/Behavior/default.aspx

Washington State Poison Center – Toxic Trends Report: 2016 Annual Cannabis Report

● In 2016, Seattle Police spokesman Sean Whitcomb noted that “large-scale illegal grow operations… are still prevalent in Seattle, and we do come across those with a degree of frequency.” DOJ Guideline 3: “Preventing the diversion of marijuana from states where it is legal under state law in some form to other states”

● In 2014, two states – Nebraska and Oklahoma – sued their neighbor state of Colorado by citing evidence of increased marijuana flowing into those states. Law enforcement officials have reported a substantial increase in marijuana flow across state borders into neighboring states.

● In 2016, there were multiple raids conducted by state law enforcement in Colorado, leading authorities to seize more than 22,0000 pounds of marijuana intended for sales outside of Colorado.

● According to the Oregon State Police, the state has an “expansive geographic footprint” on marijuana exports across the U.S. Several counties in Oregon including Jackson, Multnomah, Josephine, Lane, Deschutes and Washington “lead the way” in supplying marijuana to states where it is not legal.

● According to the Rocky Mountain High Intensity Drug Trafficking Area task force, “there were 360 seizures of marijuana in Colorado destined for other states. This is nearly a 600% increase in the number of individual stops in a decade, seizing about 3,671 pounds in 2014. Of the 360 seizures reported in 2014, 36 different states were identified as destinations, the most common being Kansas, Missouri, Illinois, Oklahoma and Florida.”

● Law enforcement officials report that since legalization in 2012, Washington State marijuana has been found to be destined for 38 different states throughout the United States. Between 2012 and 2017, 8,242.39 kilograms (18,171.35 pounds) have been seized in 733 individual seizure events across 38 states. From 2012 to 2016, 470 pounds of marijuana have been seized on Washington State highways and interstates. Since 2012, 320 pounds of Washington State-origin marijuana have been seized during attempted parcel diversions. DOJ Guideline 4: “Preventing state-authorized marijuana activity from being used as a cover or pretext for the trafficking of other illegal drugs or other illegal activity”

● According to Jorge Duque from the Colorado Department of Law, cartels operating in Colorado are now “trading drugs like heroin for marijuana,” and the trade has since opened the door to drug and human trafficking. Duque also explains that money 5 laundering is a growing problem as “cartels are often disguising their money through legally purchasing marijuana or buying houses and growing marijuana in it.”

● In June 2017, a former Colorado marijuana enforcement officer and a Denver-based marijuana entrepreneur were indicted for running a statewide marijuana trafficking ring that illegally produced and sold “millions of dollars worth of marijuana across state lines.” This trafficking organization obtained 14 marijuana licenses in order to present their activities as protected business endeavors, despite “never ma[king] a single legal sale of cannabis in their two years of operation.”

● In Oregon, State Police officials report that criminals are exploiting Oregon’s legal marijuana industry for financial crimes and fraud. In one example, according to the Oregon State Police report, “Tisha Silver of Cannacea Medical Marijuana Dispensary falsified licensing to solicit investors and worked with Green Rush Consulting to locate unwitting investors. Silver exploited the burgeoning cannabis industry in the state to entice investors to back an illegitimate company, securing a quarter of a million dollars in fraudulent gains. According to some analysts, cannabis investors fell prey to ‘pump and dump’ schemes and lost up to $23.3 billion in 2014 alone.”

● Officials in Oregon note that the U.S. Postal Service is being exploited to ship marijuana products and revenue. According to former Attorney General Eric Holder, “The Postal Service is being used to facilitate drug dealing,” a clear violation of federal law and a violation of the sanctity of the U.S. mailing system.

DOJ Guideline 5: “Preventing violence and the use of firearms in the cultivation and distribution of marijuana”

● While crime rates dropped or remained stable in many of the nation’s largest cities, Colorado’s crime rate increased. There has been an increase in rape, murder, robbery and auto thefts. While it is not possible to link legalization to a direct change in crime rates, officials in Colorado cited marijuana legalization as one of the reasons behind the rise.

● In Colorado, prosecutors are reporting an increase in marijuana-related homicides since the state legalized the drug.  This situation is detailed here: http://www.oregonlive.com/marijuana/index.ssf/2016/07/state_slaps_portland_dispensar.h tml.

Other instances of fraud have been discussed here: Sapient Investigations Newsletters (2015, Feb. 10) “High Times for Fraud,” available online at https://sapientinvestigations.com/spi-news/high-times-for-fraud/

● In Oregon, state police report that, “Cannabis is a lucrative target for robbery. As recently as December 2016, a state-licensed cannabis producer was targeted for a violent armed robbery. In the aforementioned case, a well-known cannabis grower in Jackson County was assaulted, bound, and his harvest was taken by armed assailants.”

● In Prince George’s County Maryland, Police Chief Henry Stawinski noted a significant rise in marijuana-related homicides since neighboring D.C. legalized the drug. Stawinski said 19 homicides in 2016 were related to marijuana.

DOJ Guideline 6:  “Preventing drugged driving and the exacerbation of other public health consequences associated with marijuana use”

● Drugged driving has increased in states with legal marijuana sales. According to a study published by the American Automobile Association, fatal drugged driving crashes doubled in Washington State after the state legalized marijuana. The Governors Highway Safety Association also notes a disturbing rise in drugged driving crashes even as alcohol-related crashes are declining.

● A Denver Post analysis found the number of marijuana-impaired drivers involved in fatal crashes in Colorado more than doubled since 2013, the year after the state voted to legalize recreational marijuana use. Colorado saw a 145 percent increase in the number of marijuana-impaired drivers involved in fatal crashes between 2013 and 2016. Marijuana is also figuring into more of Colorado’s fatal crashes overall: in 2013, marijuana-impaired drivers accounted for 10 percent of all fatal crashes, but by 2016 it reached 20 percent.

● According to a study published in the Annals of Emergency Medicine, poison control calls for children more than tripled after marijuana legalization. Much of this is linked to a boom in the sale of marijuana “edibles.” THC concentrate is mixed into almost any type of food or drink, including gummy candy, soda, and lollipops. Today, these edibles comprise at least half of Colorado’s marijuana market.

● In Washington State, the number of marijuana-involved DUIs are increasing with 38 percent of total cases submitted in 2016 testing above the five nanogram per milliliter of blood legal limit for those over the age of twenty-one. In addition, 10 percent of drivers involved in a fatal accident from 2010 to 2014 were THC-positive.

● A study by the Highway Loss Data Institute reveals that Colorado, Oregon, and Washington have experienced three percent more collision claims overall than would ( NWHIDTA Drug Threat Assessment For Program Year 2018)  have been expected without legalization.

Colorado witnessed the largest jump in claims. The state experienced a rate 14 percent higher than neighboring states.

● In Washington State, from 2012 to 2016, calls to poison control centers increased by 79.48%. Exposures increased 19.65% from the time of marijuana commercialization in 2014 to 2016. Of the marijuana calls answered by the Poison Center in 2016, youth under the age of 20 accounted for almost 40% of all calls.

According to the 2016 Annual Cannabis Toxic Trends Report, 42% of the calls reported were for persons aged 13 to 29. Additionally, among exposures related to children under the age of five, 73% involved children one to three years of age. The counties with the highest reported number of exposures for 2015 remained in the top four for 2016: King, Spokane, Snohomish, and Pierce.

DOJ Guideline 7: “Preventing the growing of marijuana on public lands and the attendant public safety and environmental dangers posed by marijuana on public lands”

● In Washington State, 373,778 marijuana plants were found growing illegally on public and private lands between 2012 and 2016. Of the illegal marijuana plants eradicated in 2016, 60% were being cultivated on state land, and the 58,604 illegal marijuana plants eradicated in 2016 consumed an estimated 43.2 million gallons of water over a full growing season (120-day cycle).

More than 400 pounds of fertilizers, chemicals, and pesticides were removed from illegal marijuana growing operations in 2016, and Furadan, a neurotoxin that is extremely dangerous to humans, was found in an illegal marijuana growing operation the same year.

● In June 2017, Colorado officials found more than 7,000 illegal plants on federal land in the state’s San Isabel National Forest. This was the fifth illegal grow found in that area alone since the year marijuana legalization passed, demonstrating legalization has not curbed the problem of grows exploiting public lands.

● In Oregon, the legalization of marijuana in the state has failed to eliminate illegal growing operations and public lands continue to be exploited despite a legal market. According to a report from state officials, “To date in Oregon, cannabis legalization has not had a noticeable influence on Mexican National [Drug Trafficking Organizations] illicit cannabis cultivation operations on public lands… leaving a lasting scar on Oregon’s unique ecosystems.

Illicit cannabis grows employ excessive amounts of pesticides, rodenticides, and herbicides, thereby threatening local wildlife habitats. Additionally, many illicit grow sites clear-cut timber, furthering soil erosion and water contamination. Research on the environmental impact of illicit cannabis grows indicates that grows tend to be bunched near water sources, resulting in disproportionate impacts on ecologically important areas…

Oregon is robbed of roughly 122 Olympic swimming pools 8 worth of water annually, or roughly 442,200 gallons of water daily during the growth season.”

DOJ Guideline 8: “Preventing marijuana possession or use on federal property”

● Advocates for legal marijuana frequently flout federal laws by possessing and using marijuana on federal properties purportedly in acts of civil disobedience. In January 2017, one group gave away free marijuana in Washington, D.C. to smoke on the National Mall during the inauguration of President Trump. On April 24, 2017, four activists were arrested after purposely flouting federal law and publicly using marijuana on U.S. Capitol grounds.

Conclusion and Key Recommendations

Federal resources should target the big players in the marijuana industry. Individual marijuana users should not be targeted or arrested, but large-scale marijuana businesses, several of which now boast of having raised over $100 million in capital, and their financial backers, should be a priority. These large businesses are pocketing millions by flouting federal law, deceiving Americans about the risks of their products, and targeting the most vulnerable.

They should not have access to banks, where their financial prowess would be expanded significantly, nor should they be able to advertise or commercialize marijuana.

These businesses target many of the marijuana products they sell toward kids, such as pot candies, cookies, and ice cream. And despite state regulations, these products continue to have problems with contamination. Recently, one of the largest, most sophisticated manufacturers of these pot “edibles” was forced to recall a number of products because they contained non-food-grade ingredients.

Additionally, the black market continues unabated in legalized states. A leaked report from Oregon police showed that at least 70 percent of that state’s marijuana market is illegal, despite legalization. In June 2017, Colorado Attorney General Cynthia Coffman said, “The black market for marijuana has not gone away since recreational marijuana was legalized in our state, and in fact continues to flourish.”

Further, state-legal businesses have acted as top cover for these illegal operations, as recent large-scale arrests in Colorado have shown. These large marijuana operations, which combine the tactics of Big Tobacco with black marketeering, should form the focus of federal law enforcement, not individual users.  Recalls are becoming more commonplace because of pesticides, moulds, and other issues.

See The Denver Post for news stories related to these recalls in legalized states: http://www.thecannabist.co/tag/marijuana-recall/

At the same time, the federal government along with non-government partners should implement a strong, evidence-based marijuana information campaign, similar to the truth ® campaign for tobacco, which alerts all Americans about the harms of marijuana and the deceitful practices of the marijuana industry.

Background:

Cannabis is increasingly available for the treatment of chronic pain, yet its efficacy remains uncertain.

Purpose: 

To review the benefits of plant-based cannabis preparations for treating chronic pain in adults and the harms of cannabis use in chronic pain and general adult populations.

Data Sources:

MEDLINE, Cochrane Database of Systematic Reviews, and several other sources from database inception to March 2017.

Study Selection: 

Intervention trials and observational studies, published in English, involving adults using plant-based cannabis preparations that reported pain, quality of life, or adverse effect outcomes.

Data Extraction: Two investigators independently abstracted study characteristics and assessed study quality, and the investigator group graded the overall strength of evidence using standard criteria.

Data Synthesis: From 27 chronic pain trials, there is low-strength evidence that cannabis alleviates neuropathic pain but insufficient evidence in other pain populations. According to 11 systematic reviews and 32 primary studies, harms in general population studies include increased risk for motor vehicle accidents, psychotic symptoms, and short-term cognitive impairment. Although adverse pulmonary effects were not seen in younger populations, evidence on most other long-term physical harms, in heavy or long-term cannabis users, or in older populations is insufficient.

Limitation: Few methodologically rigorous trials; the cannabis formulations studied may not reflect commercially available products; and limited applicability to older, chronically ill populations and patients who use cannabis heavily.

Conclusion: 

Limited evidence suggests that cannabis may alleviate neuropathic pain in some patients, but insufficient evidence exists for other types of chronic pain. Among general populations, limited evidence suggests that cannabis is associated with an increased risk for adverse mental health effects.

Source:  http://annals.org/aim/article/2648595/effects-cannabis-among-adults-chronic-pain-overview-general-harms-systematic#.WZXJbYbta0I.email

Arrests are up. We still have a black market. And people are in danger.

Last week, Senator Cory Booker introduced the Marijuana Justice Act in an effort to legalize marijuana across the nation and penalize local communities that want nothing to do with this dangerous drug. This is the furthest reaching marijuana legalization effort to date and marks another sad moment in our nation’s embrace of a drug that will have generational consequences.

Our country is facing a drug epidemic. Legalizing recreational marijuana will do nothing that Senator Booker expects. We heard many of these same promises in 2012 when Colorado legalized recreational marijuana.

In the years since, Colorado has seen an increase in marijuana related traffic deaths, poison control calls, and emergency room visits. The marijuana black market has increased in Colorado, not decreased. And, numerous Colorado marijuana regulators have been indicted for corruption.

In 2012, we were promised funds from marijuana taxes would benefit our communities, particularly schools. Dr. Harry Bull, the Superintendent of Cherry Creek Schools, one of the largest school districts in the state, said, “So far, the only thing that the legalization of marijuana has brought to our schools has been marijuana.”

In fiscal year 2016, marijuana tax revenue resulted in $156,701,018. The total tax revenue for Colorado was $13,327,123,798, making marijuana only 1.18% of the state’s total tax revenue. The cost of marijuana legalization in public awareness campaigns, law enforcement, healthcare treatment, addiction recovery, and preventative work is an unknown cost to date.

Senator Booker stated his reasons for legalizing marijuana is to reduce “marijuana arrests happening so much in our country, targeting certain communities – poor communities, minority communities.” It’s a noble cause to seek to reduce incarceration rates among these communities but legalizing marijuana has had the opposite effect.

According to the Colorado Department of Public Safety, arrests in Colorado of black and Latino youth for marijuana possession have increased 58% and 29% respectively after legalization. This means that Black and Latino youth are being arrested more for marijuana possession after it became legal.

Furthermore, a vast majority of Colorado’s marijuana businesses are concentrated in neighborhoods of color. Leaders from these communities, many of whom initially voted to legalize recreational marijuana, often speak out about the negative impacts of these businesses.

Senator Booker released his bill just a few days after the Washington Post reported on a study by the Review of Economic Studies that found “college students with access to recreational cannabis on average earn worse grades and fail classes at a higher rate.” Getting off marijuana especially helped lower performing students who were at risk of dropping out.

Since legalizing marijuana, Colorado’s youth marijuana use rate is the highest in the nation, 74% higher than the national average, according to the Rocky Mountain High Intensity Drug Trafficking Area Report. This is having terribly negative effects on the education of our youth.

If Senator Booker is interested in serving poor and minority communities, legalizing marijuana is one of the worst decisions. There is much work to be done to reduce incarceration and recidivism, but flooding communities with drugs will do nothing but exacerbate the problems.

The true impact of marijuana on our communities is just starting to be learned. The negative consequences of legalizing recreational marijuana will be felt for generations. I encourage Senator Booker to spend time with parents, educators, law enforcement, counsellors, community leaders, pastors, and legislators before rushing to legalize marijuana nationally. We’ve seen the effects in our neighborhoods in Colorado, and this is nothing we wish upon the nation.

Jeff Hunt is the Vice President of Public Policy at Colorado Christian University. Follow him on Twitter: @jeffhunt.

Source:  https://www.usatoday.com/story/opinion/2017/08/07/marijuana 

LONDON (Reuters) – People who smoke marijuana have a three times greater risk of dying from hypertension, or high blood pressure, than those who have never used the drug, scientists said on Wednesday. The risk grows with every year of use, they said.

The findings, from a study of some 1,200 people, could have implications in the United States among other countries. Several states have legalized marijuana and others are moving toward it. It is decriminalized in a number of other countries.

“Support for liberal marijuana use is partly due to claims that it is beneficial and possibly not harmful to health,” said Barbara Yankey, who co-led the research at the school of public health at Georgia State University in the United States.

“It is important to establish whether any health benefits outweigh the potential health, social and economic risks. If marijuana use is implicated in cardiovascular diseases and deaths, then it rests on the health community and policy makers to protect the public.”

Marijuana is also sometimes used for medicinal purposes, such as for glaucoma.

The study, published in the European Journal of Preventive Cardiology, was a retrospective follow-up study of 1,213 people aged 20 or above who had been involved in a large and ongoing National Health and Nutrition Examination Survey. In 2005–2006, they were asked if they had ever used marijuana.

For Yankey’s study, information on marijuana use was merged with mortality data in 2011 from the U.S. National Center for Health Statistics, and adjusted for confounding factors such as tobacco smoking and variables including sex, age and ethnicity.

The average duration of use among users of marijuana, or cannabis, was 11.5 years.

The results showed marijuana users had a 3.42-times higher risk of death from hypertension than non-users, and a 1.04 greater risk for each year of use.

There was no link between marijuana use and dying from heart or cerebrovascular diseases such as strokes.

Yankey said were limitations in the way marijuana use was assessed — including that researchers could not be sure whether people had used the drug continuously since they first tried it.

But she said the results chimed with plausible risks, since marijuana is known to affect the cardiovascular system.

“Marijuana stimulates the sympathetic nervous system, leading to increases in heart rate, blood pressure and oxygen demand,” she said.

Experts not directly involved in the study said its findings would need to be replicated, but already raised concerns.

“Despite the widely held view that cannabis is benign, this research adds to previous work suggesting otherwise,” said Ian Hamilton, a lecturer in mental health at Britain’s York University. Source:  https://www.reuters.com/article/us-health-marijuana-hypertension-idUSKBN1AP0JS   9th Aug.201

Cannabis is the most widely used illicit drug in the United States, and trends show increasing use in the general population. As cannabis consumption rises, there has been significant emerging evidence for cannabis-related risks to health.1

Numerous lines of evidence suggest a correlation between cannabis consumption and a variety of psychiatric conditions, including cannabis-induced psychosis (CIP). While it can be difficult to differentiate CIP from other psychoses, CIP holds distinguishing characteristics, which may aid in its diagnosis. Given the increasing push toward cannabis legalization, assessing CIP and employing timely treatments is critical.

Specifically in youth, there is a direct relationship between cannabis use and its risks. The lack of knowledge surrounding its detrimental effects, combined with misunderstandings related to its therapeutic effects, has potential for catastrophic results.

CASE VIGNETTE

Ms. J, a 19-year-old college sophomore, was admitted to the Early Psychosis Unit at the Centre for Addiction and Mental Health (CAMH) displaying signs of agitation and acute psychosis. Her roommates had noted that her behavior had become increasingly bizarre, and she had isolated herself over the past month. She began smoking marijuana at the age of 17 and since starting college used it daily.

Ms. J exhibited signs of paranoia, believing other students in her dorm were stealing from her and trying to poison her. She remained adamant that all her problems were rooted in the competitive environment of the university and that smoking marijuana aided in keeping her sanity. In a sense, she was self-medicating. Her clinical presentation was consistent with a diagnosis of CIP.

After the hospitalization, she received outpatient case management services in the Early Psychosis Program at CAMH, which included motivational interviewing to raise her awareness about the importance of abstaining from cannabis use. She has been abstinent from cannabis for more than a year with no evidence of psychosis; she recently returned to school to finish her degree.

Epidemiology of CIP

Reports have shown a staggering increase in cannabis-related emergency department (ED) visits in recent years. In 2011, the Substance Abuse and Mental Health Services Administration (SAMHSA) and Drug Abuse Warning Network (DAWN) estimated a total of 1.25 million illicit-drug–related ED visits across the US, of which 455,668 were marijuana related.2 A similar report published in 2015 by the Washington Poison Center Toxic Trends Report showed a dramatic increase in cannabis-related ED visits.3 In states with recent legalization of recreational cannabis, similar trends were seen.4

States with medicinal marijuana have also shown a dramatic rise in cannabis-related ED visits. Moreover, states where marijuana is still illegal also showed increases.5 This widespread increase is postulated to be in part due to the easy accessibility of the drug, which contributes to over-intoxication and subsequent symptoms. Overall, from 2005 to 2011, there has been a dramatic rise in cannabis-related ED visits among all age groups and genders.

Neurobiology of CIP

Cannabis is considered an environmental risk factor that increases the odds of psychotic episodes, and longer exposure is associated with greater risk of psychosis in a dose-

dependent fashion. The drug acts as a stressor that leads to the emergence and persistence of psychosis. While a number of factors play a role in the mechanism by which consumption produces psychosis, the primary psychoactive ingredient is considered to be delta 9-tetrahydrocannabinol (delta9-THC). Properties of delta9-THC include a long half-life (up to 30 days to eliminate the long-acting THC metabolite carboxy-THC from urine) and high lipophilicity, which may contribute to CIP.

During acute consumption, cannabis causes an increase in the synthesis and release of dopamine as well as increased reuptake inhibition, similar to the process that occurs during stimulant use. Consequently, patients with CIP are found to have elevated peripheral dopamine metabolite products.

Findings from a study that examined presynaptic dopaminergic function in patients who have experienced CIP indicate that dopamine synthesis in the striatum has an inverse relationship with cannabis use. Long-term users had reduced dopamine synthesis, although no association was seen between dopaminergic function and CIP.6 This observation may provide insight into a future treatment hypothesis for CIP because it implies a different mechanism of psychosis compared with schizophrenia. As cannabis may not induce the same dopaminergic alterations seen in schizophrenia, CIP may require alternative approaches—most notably addressing associated cannabis use disorder.

Polymorphisms at several genes linked to dopamine metabolism may moderate the effects of CIP. The catechol-o-methyltransferase (COMT Val 158Met) genotype has been linked to increased hallucinations in cannabis users.7Homozygous and heterozygous genetic compositions (Met/Met, Val/Met, Val/Val) for COMT Val 158Met have been studied in patients with CIP and suggest that the presence of Val/Val and Val/Met genotypes produces a substantial increase in psychosis in relation to cannabis use. This suggests that carriers of the Val allele are most vulnerable to CIP attacks.

There has been much controversy surrounding the validity of a CIP diagnosis and whether it is a distinct clinical entity or an early manifestation of schizophrenia. In patients being treated for schizophrenia, those with a history of CIP had an earlier onset of schizophrenia than patients who never used cannabis.8Evidence suggests an association between patients who have received treatment for CIP and later development of schizophrenia spectrum disorder. However, it has been difficult to distinguish whether CIP is an early manifestation of schizophrenia or a catalyst. Nonetheless, there is a clear association between the 2 disorders.

Assessment of CIP

DSM-5 categorizes cannabis-induced psychotic disorder as a substance-induced psychotic disorder. However, there are distinguishing characteristics of CIP that differentiate it from other psychotic disorders such as schizophrenia. Clear features of CIP are sudden onset of mood lability and paranoid symptoms, within 1 week of use but as early as 24 hours after use. CIP is commonly precipitated by a sudden increase in potency (eg, percent of THC content or quantity of cannabis consumption; typically, heavy users of cannabis consume more than 2 g/d). Criteria for CIP must exclude primary psychosis, and symptoms should be in excess of expected intoxication and withdrawal effects. A comparison of the clinical features of idiopathic psychosis versus CIP is provided in the Table.

When assessing for CIP, careful history taking is critical. Time of last drug ingestion will indicate if a patient’s psychotic symptoms are closely related to cannabis intoxication/withdrawal effects. While acute cannabis intoxication presents with a range of transient positive symptoms (paranoia, grandiosity, perceptual alterations), mood symptoms (anxiety), and cognitive deficits (working memory, verbal recall, attention), symptoms that persist beyond the effects of intoxication and withdrawal are better categorized as CIP, regardless of the route of administration (smoke inhalation, oral, intravenous). CIP has historically been associated with fewer negative symptoms than schizophrenia; however, without a clear timeline of use, distinguishing schizophrenia from CIP may prove difficult.

A diagnosis of primary psychosis (eg, schizophrenia) is warranted in the absence of heavy cannabis use or withdrawal (for at least 4 weeks), or if symptoms preceded onset of heavy use. The age at which psychotic symptoms emerge has not proved to be a helpful indicator; different studies show a conflicting median age of onset.

Clinical features of schizophrenia and CIP share many overlapping characteristics. However, compared with primary psychoses with concurrent cannabis abuse, CIP has been established to show more mood symptoms than primary psychosis. The mood symptom profile includes obsessive ideation, interpersonal sensitivity, depression, and anxiety. Of significance is the presence of social phobia: 20% of patients with CIP demonstrate phobic anxiety compared with only 3.8% of patients with primary psychosis with cannabis abuse.

Hypomania and agitation have also been found to be more pronounced in cases of CIP.9 Visual hallucinations are more common and more distinct in CIP than in other psychoses such as schizophrenia. Perhaps the most discriminating characteristic of CIP is awareness of the clinical condition, greater disease insight, and the ability to identify symptoms as a manifestation of a mental disorder or substance use. The presence of much more rapidly declining positive symptoms is another distinctive factor of CIP.

Finally, family history may help distinguish CIP from primary psychosis. Primary psychosis has a strong association with schizophrenia and other psychotic disorders in first- or second-degree relatives, whereas CIP has a weaker family association with psychosis.

Treatment of CIP

As with all substance-induced psychotic states, abstinence from cannabis may be the definitive measure to prevent recurrence. With limited research surrounding CIP, achieving symptomatic treatment during acute phases of CIP has proved to be difficult. The Figure suggests possible treatment progression for CIP.

Pharmacotherapeutic interventions include the second-generation antipsychotic drug olanzapine and haloperidol. While both are equally effective, their different adverse- effect profiles should be taken into consideration when treating a patient; olanzapine is associated with significantly fewer extrapyramidal adverse effects.

One report indicates that antipsychotics worsened the condition in some patients.10 Conventional antipsychotics failed to abate the symptoms of CIP in one 20-year old man. Trials of olanzapine, lithium, and haloperidol had little to no effect on his psychosis. Risperidone was tried but elicited temporal lobe epilepsy with auditory, somatic, and olfactory hallucinations. However, the use of valproate sodium markedly improved his symptoms and cognition, returning him to baseline.

Carbamazepine has also been shown to have rapid effects when used as an adjunct to antipsychotics.11 Use of anti-seizure medication in CIP treatment has been hypothesized to reduce neuroleptic adverse effects, resulting in better tolerance of antipsychotics.10,11 These results suggest the use of adjunctive anti-epileptics should be considered in CIP treatment strategies, although further studies in a broad range of patients with CIP are needed.

Abstaining from cannabis is the most beneficial and effective measure for preventing future CIP events; however, it is likely to be the most difficult to implement.

Psychosocial intervention has a significant impact on early-phase psychosis, and when the intervention is initiated plays a role in disease outcomes. A delay in providing intensive psychosocial treatment has been associated with more negative symptoms compared with a delay in administrating antipsychotic medication.12 Employing cannabis- focused interventions with dependent patients who present with first-episode psychosis can decrease use in a clinically meaningful way and subjectively improve patient quality of life.

Compared with the standard of care, motivational interviewing significantly increases number of days abstinent from cannabis and aids in decreasing short-term consumption.13 Patients who are treated with motivational interviewing in addition to standard of care (combination of antipsychotic medication, regular office-based psychiatric contact, psychoeducation) are reported to also have more confidence and willingness to reduce cannabis use.

Patients with CIP who are unwilling or unable to decrease cannabis consumption may be protected from psychotic relapse with aripiprazole (10 mg/d). Its use suppresses the re-emergence of psychosis without altering cannabis levels. However, no direct comparison has been made with aripiprazole and other antipsychotics in treating CIP. Clearly, well-controlled large studies of putative treatments for CIP are needed.

Conclusions

As more countries and states approve legalization, and marijuana becomes more accessible, CIP and other cannabis-related disorders are expected to increase. Efforts should be made by physicians to educate patients and discourage cannabis use. Just as there was an era of ignorance concerning the damaging effects of tobacco, today’s conceptions about cannabis may in fact be judged similarly in the future. The onus is on psychiatrists to take an evidence-based approach to this increasing problem.

Source:  http://www.psychiatrictimes.com/substance-use-disorder/cannabis-induced-psychosis-review  14th July

An UdeM study confirms the link between marijuana use and psychotic-like experiences in a Canadian adolescent cohort. Credit: © Syda Productions / Fotolia

Going from an occasional user of marijuana to a weekly or daily user increases an adolescent’s risk of having recurrent psychotic-like experiences by 159%, according to a new Canadian study published in the Journal of Child Psychology and Psychiatry.

The study also reports effects of marijuana use on cognitive development and shows that the link between marijuana use and psychotic-like experiences is best explained by emerging symptoms of depression.

“To clearly understand the impact of these results, it is essential to first define what psychotic-like experiences are: namely, experiences of perceptual aberration, ideas with unusual content and feelings of persecution,” said the study’s lead author, Josiane Bourque, a doctoral student at Université de Montréal’s Department of Psychiatry. “Although they may be infrequent and thus not problematic for the adolescent, when these experiences are reported continuously, year after year, then there’s an increased risk of a first psychotic episode or another psychiatric condition.”

She added: “Our findings confirm that becoming a more regular marijuana user during adolescence is, indeed, associated with a risk of psychotic symptoms. This is a major public-health concern for Canada.”

What are the underlying mechanisms?

One of the study’s objectives was to better understand the mechanisms by which marijuana use is associated with psychotic-like experiences. Bourque and her supervisor, Dr. Patricia Conrod at Sainte Justine University Hospital Research Centre hypothesized that impairments in cognitive development due to marijuana misuse might in turn exacerbate psychotic-like experiences.

This hypothesis was only partially confirmed, however. Among the different cognitive abilities evaluated, the development of inhibitory control was the only cognitive function negatively affected by an increase in marijuana use. Inhibitory control is the capacity to withhold or inhibit automatic behaviours in favor of a more contextually appropriate behaviour. Dr. Conrod’s team has shown that this specific cognitive function is associated with risk for other forms of substance abuse and addiction.

“Our results show that while marijuana use is associated with a number of cognitive and mental health symptoms, only an increase in symptoms of depression — such as negative thoughts and low mood — could explain the relationship between marijuana use and increasing psychotic-like experiences in youth,” Bourque said.

What’s next

These findings have important clinical implications for prevention programs in youth who report having persistent psychotic-like experiences. “While preventing adolescent marijuana use should be the aim of all drug strategies, targeted prevention approaches are particularly needed to delay and prevent marijuana use in young people at risk of psychosis,” said Patricia Conrod, the study’s senior author and a professor at UdeM’s Department of Psychiatry.

Conrod is optimistic about one thing, however: the school-based prevention program that she developed, Preventure, has proven effective in reducing adolescent marijuana use by an overall 33%. “In future programs, it will be important to investigate whether this program and other similar targeted prevention programs can delay or prevent marijuana use in youth who suffer from psychotic-like experiences,” she said. “While the approach seems promising, we have yet to demonstrate that drug prevention can prevent some cases of psychosis.”

A large youth cohort from Montreal

The study’s results are based on the CIHR-funded Co-Venture project, a cohort of approximately 4,000 adolescents aged 13 years old from 31 high schools in the Greater Montreal area. These teens are followed annually from Grade 7 to Grade 11. Every year they fill out computerized questionnaires to assess substance use and psychiatric symptoms. The teens also complete cognitive tasks to allow the researchers to evaluate their IQ, working memory and long-term memory as well as their inhibitory control skills.

To do their study, the research team first confirmed results from both the United Kingdom and Netherlands showing the presence of a small group of individuals (in Montreal, 8%) among the general population of adolescents who report recurrent psychotic-like experiences. Second, the researchers explored how marijuana use between 13 and 16 years of age increases the likelihood of belonging to the 8%. Finally, they examined whether the relationship between increasing use of marijuana and increasing psychotic-like experiences can be explained by emerging symptoms of anxiety or depression, or by the effects of substance use on developing cognitive abilities.

Source:  University of Montreal. “Marijuana and vulnerability to psychosis.” ScienceDaily. ScienceDaily, 5 July 2017. www.sciencedaily.com/releases/2017/07/170705104042.htm.

 

Today’s Reality

Even if you smoked pot 20+ years ago without harm, today’s situation is different.  We want our children to avoid marijuana because they care about the risks in marijuana itself.

Here’s the facts for raising your children today:

* Marijuana has been modified since 1994. The THC, which gives the high, is 3-10x stronger in the plants of today.  If a child begins using today’s pot , it’s like to learning to drink with grain alcohol, instead of beer or wine.  Also, youth today frequently use the potent “dabs” “wax” and “budder.”  These are extractions can have 40-80% THC.

* Marijuana is addictive, contrary to a popular myth, particularly with today’s stronger strains of pot.

* In states with medical marijuana, teen usage is much higher than in other states, and many teens who use pot get it from some marijuana cardholders.

* Those who begin in adolescence or their teens, have an addiction rate of 17 percent, as opposed to 9 percent for those who begin using marijuana as an adult. *Emergency Department hospitalizations from marijuana rose from 281,000 to 455,000 between 2004 and 2011, making it 2nd amongst the illegal drugs causing ER treatment.

* Individuals responses to marijuana can be vary greatly, and the potential for paranoia and psychotic reactions are real side effects, omitted in the pot propaganda.

* Marijuana is fat soluble and stays in the body for weeks, which is why some people have flashbacks.

* The  brain, which is 1/3 fat, isn’t fully developed until age 25 or later, and until it is, marijuana can cause irreversible damage.

* Marijuana is not as widely used as alcohol,  6-7% of the adult population, vs.  66% who drink, one reason the comparison doesn’t work. * Marijuana usage causes traffic deaths and it is not safe to combine with driving.

* More teens seek substance abuse treatment for pot than any other legal or illegal substance. * Marijuana is a gateway drug,  because nearly every young person who develops a drug addiction begins with marijuana.  Early pot users such as Robert Downey, Jr. (age 9), and Cameron Douglas  (age 13), prove that the stranglehold of drug addiction lasts for years.

* A multi-year study out of New Zealand, tracking marijuana users and through their mid-30s showed IQs decrease an 6-8 percentage points over time.  Again, we point to the medical studies summarized on this webpage.

* In a recent study, schizophrenics who have used marijuana had an onset of the disease 2-1/2 years earlier than those who did not use marijuana. * Marijuana can trigger psychotic symptoms and/or mental illness, and cognitive decline in youth, more quickly than alcohol, while tobacco does not.

* Since marijuana usage increases the odds of developing a mental illness, expansion of pot will expand mental health treatment needs.

* Efforts to legalize for age 21+  hide the motivation to attract young users and build big profits.  Legal pot mean more young users.

* Marijuana usage is associated with greater risk for testicular cancer in males.

* With universal health care, all of us will pay for the increase in medical care for those needing help from pot abuse.

* The number of pot-related hospitalizations in Colorado accelerated in 2009 and went out of control in the first half of 2014.

* Existing mental health issues, such as ADHD, anxiety and depression, greatly increase the use of drugs for self-medication.

Mental Health, Physical Health Alike

“We cannot promote a comprehensive system of mental health treatment and marijuana legalization, which increases permissiveness for a drug that directly contributes to mental illness,”  states former Congressman Patrick Kennedy, who fought tirelessly on behalf of parity for mental health treatment. Kennedy and policy expert Kevin Sabet promote  Smart Approaches to Marijuana.

* The National Alliance for Mental Illness lists four illegal drugs which cause psychosis: cannabis, LSD, methamphetamine and heroin and two classes of legal drugs, amphetamines and steroids. Pharmaceutical drugs are sold with warnings, while marijuana isn’t.

Sharon Levy, Chairwoman of the American Academy of Paediatrics committee on substance abuse, said “We’re losing the public health battle” and policy is being made by legalization advocates who might be misinformed about marijuana’s dangers.”

Source:  http://www.poppot.org/2016/08/08/latest-child-dangers-marijuana-edibles/

Smart Approaches to Marijuana’s 2017 publication references academic studies which suggest that marijuana primes the brain for other types of drug usage.  Here’s the summary on that subject from page 4, Marijuana and Other Drugs: A Link We Can’t Ignore :

MORE THAN FOUR in 10 people who ever use marijuana will go on to use other illicit drugs, per a large, nationally representative sample of U.S. adults.(1) The CDC also says that marijuana users are three times more likely to become addicted to heroin.(2)

Although 92% of heroin users first used marijuana before going to heroin, less than half used painkillers before going to heroin.

And according to the seminal 2017 National Academy of Sciences report, “There is moderate evidence of a statistical association between cannabis use and the development of substance dependence and/or a substance abuse disorder for substances including alcohol, tobacco, and other illicit drugs.”(3)

RECENT STUDIES WITH animals also indicate that marijuana use is connected to use and abuse of other drugs. A 2007 Journal of Neuropsychopharmacology study found that rats given THC later self -administered heroin as adults, and increased their heroin usage, while those rats that had not been treated with THC maintained a steady level of heroin intake.(4) Another 2014 study found that adolescent THC exposure in rats seemed to change the rodents’ brains, as they subsequently displayed “heroin-seeking” behaviour. Youth marijuana use could thus lead to “increased vulnerability to drug relapse in adulthood.”(5)

National Institutes of Health Report

The National Institutes of Health says that research in this area is “consistent with animal experiments showing THC’s ability to ‘prime’ the brain for enhanced responses to other drugs. For example, rats previously administered THC show heightened behavioral response not only when further exposed to THC, but also when exposed to other drugs such as morphine—a phenomenon called cross-sensitization.”(6)

Suggestions that one addictive substance replaces another ignores the problem of polysubstance abuse, the common addiction of today.

Additionally, the majority of studies find that marijuana users are often polysubstance users, despite a few studies finding limited evidence that some people substitute marijuana for opiate medication. That is, people generally do not substitute marijuana for other drugs. Indeed, the National Academy of Sciences report found that “with regard to opioids, cannabis use predicted continued opioid prescriptions 1 year after injury.  Finally, cannabis use was associated with reduced odds of achieving abstinence from alcohol, cocaine, or polysubstance use after inpatient hospitalization and treatment for substance use disorders” [emphasis added].(7)

Moreover, a three-year 2016 study of adults also found that marijuana compounds problems with alcohol. Those who reported marijuana use during the first wave of the survey were more likely than adults who did not use marijuana to develop an alcohol use disorder within three years.(8) Similarly, alcohol consumption in Colorado has increased slightly since legalization. (9)

Source:   http://www.poppot.org/2017/07/03/replacing-one-addiction-another-will-not-work/

Investigating the proposition that cannabis is worth bothering with, this hot topic looks at reports that stronger cannabis on the market is increasing harms to users, prospects of recovery from disorders and dependence, and the emerging response to synthetic forms of cannabis like ‘spice’.

CANNABIS IN THE LAW

A controlled ‘Class B’ substance, cannabis carries legal penalties for possession, supply, and production. Between 2004–2009 cannabis was reclassified as a ‘Class C’ substance, meaning for a brief period of time it carried lesser penalties for possession. In 2009, the Association of Chief Police Officers issued new guidance, advising officers to take an escalating approach to the policing of cannabis possession for personal use: • A warning • A penalty notice for disorder (PND) • Arrest

This three-tiered approach was designed to be “ethical and non-discriminatory”, but also reinforce the “national message that cannabis is harmful and remains illegal”.

In 1990s Britain a common reaction to allocating resources to treating cannabis users was, ‘Why bother? We have more than enough patients with problems with serious drugs like heroin.’ The typically calming use of the drug by adults was seen as preferable to the main alternative – alcohol and its associated violence and disorder. Calls for a treatment response were seen as pathologising what in many societies is both normal and in some ways desirable youth development: trying new experiences, challenging conventions, and exposing the hypocrisy of alcohol-drinking adults. In 1997 the Independent on Sunday launched a campaign to decriminalise cannabis, culminating in a mass ‘roll-up’, and 16,000-strong pro-cannabis march from Hyde Park to Trafalgar Square. Its Editor Rosie Boycott wrote in the paper about her own coming-of-age experience smoking cannabis, telling readers:

“I Rolled my first joint on a hot June day in Hyde Park. Summer of ’68. Just 17. Desperate to be grown-up. … My first smoke, a mildly giggly intoxication, was wholly anti-climatic. The soggy joint fell apart. I didn’t feel changed. But that act turned me – literally – into an outlaw. I was on the other side of the fence from the police – or the fuzz, as we used to call them. So were a great many of my generation.”

The campaign was explosive, but short-lived, apparently subsiding when Boycott left to take up her role as Editor of the Daily Express. A decade later, the Independent issued an apology for the campaign. ‘If only they had known then, what they knew now’, was the message of the article, referring to the reportedly damaging impact of the more potent strains of cannabis and its links to “mental health problems and psychosis for thousands of teenagers”.

Are stronger strains creating more problems?

There has been a long-standing, but controversial, association between cannabis strength and harm. Reading newspaper articles on the subject, it wouldn’t be unusual to see a headline drawing a straight line between ‘super-strength skunk’ and addiction, violence, deaths, or psychosis. In 2008, then Prime Minister Gordon Brown spoke in a similar vein, telling a breakfast-television viewing audience:

I have always been worried about cannabis, with this new skunk, this more lethal part of cannabis.

I don’t think that the previous studies took into account that so much of the cannabis on the streets is now of a lethal quality and we really have got to send out a message to young people – this is not acceptable.

Brown was warning of a dangerous new strain of cannabis on the market, that caused very severe harms to users – contrasting starkly with the common perception of cannabis as a ‘low harm’ or ‘no harm’ drug. The strength or potency of cannabis is determined by the amount of ‘THC’ it contains. THC produces the ‘high’ associated with cannabis, and another major component ‘CBD’ produces the sedative and anti-anxiety effects. As well as potency, the relative amounts of THC and CBD are important for understanding the effects of cannabis – something explored in a University College London study during the programme Drugs Live: Cannabis on Trial. The research team compared two different types of cannabis: the first had high levels of THC (approx. 13%) but virtually no CBD; and the second had a lower level of THC (approx. 6.5%) and substantial amounts of CBD (approx. 8%). They found that CBD had a moderating or protective effect on some of the negative effects of THC, and that “many of the effects that people enjoy are still present in low-potency varieties without some of the harms associated with the high-potency varieties”. At least in the US over the last two decades (between 1995–2014), potency has increased from around 4% to 12%, and the protective CBD content of cannabis has decreased, from around 28% to less than 15%, significantly affecting the ratio of THC to CBD, and with it, the nature and strength of the psychoactive effect of cannabis. Until the 1990s, herbal cannabis sold in the UK was predominantly imported from the Caribbean, West Africa, and Asia. After this time, it was increasingly produced in the UK, being grown indoors using intensive means (artificial lighting, heating, and control of day-length). A study funded by the Home Office analysed samples of cannabis confiscated by 23 police forces in England and Wales in 2008, and found that over 97% of herbal cannabis had been grown by intensive methods; its average potency of 16% compared with just 8% for traditional imported herbal cannabis. This matched other reports of home-grown cannabis being consistently (around 2–3 times) stronger than imported herbal cannabis and cannabis resin.

In 2015, observing a decrease in the use of cannabis in England and Wales, but parallel increase in demand for treatment, a UK study examined whether the trend could be explained by an increase in the availability of higher-potency cannabis. Over 2500 adults were surveyed about their use of different types of cannabis, severity of dependence, and cannabis-related concerns. The researchers found that higher potency cannabis was associated with a greater severity of dependence, especially in young people, and was rated by participants as causing more memory impairment and paranoia than lower potency types. However at the same time, it was reported to produce the best ‘high’, and to be the preferred type.

By definition cannabis is a psychoactive substance, which means it can change people’s perceptions, mood, and behaviour. Higher potency cannabis contains more of the psychoactive component, so it makes sense that higher potency cannabis could increase the risk of temporary or longer-term (adverse) problems with perceptions, mood, and behaviour. However, there is a particular concern that cannabis use could be linked to ‘psychosis’, a term describing a mental illness where a person perceives or interprets reality in a very different way to those around them, which can include hallucinations or delusions.

Whether cannabis causes psychosis, precipitates an existing predisposition, aggravates an existing condition, or has no impact at all on psychotic symptoms, has for decades been hotly contested. With our focus on evaluations of interventions, Drug and Alcohol Findings is in no position to pronounce on this issue, nor on the possibility that the drug might sometimes improve mental health, but some examples of research informing this debate are included below. A 2009 UK study examined whether daily use of high-potency cannabis was linked to an elevated risk of psychosis, comparing 280 patients in London presenting with a first episode of psychosis with a healthy control group. The patients were found to be more likely to smoke cannabis on a daily basis than the control group, and to have smoked for more than five years. Among those who used cannabis, 78% of the patients who had experienced psychosis used higher-potency cannabis, compared with 37% of those in the control group. The findings indicated that the risk of psychosis was indeed greater among the people who were using high potency cannabis on a frequent basis, but couldn’t show that the cannabis use caused the psychosis, or even that the cannabis use made the group more susceptible to psychosis. The wider literature on mental health and substance use would suggest that the association is more complex than this. A recently published paper from the University of York has demonstrated the complications of attributing any association between cannabis use and psychosis to a causal effect of cannabis use rather than other factors or a reverse causal effect. A calculation based on data from England and Wales helped to put this into perspective, indicating that even if cannabis did cause psychosis more than 20,000 people would need to be stopped using cannabis to prevent just one case of psychosis. The apparent steady increase in cannabis potency in the UK since the 1990s is important context for further research. Where higher potency cannabis is increasingly becoming the norm, and is the preference for cannabis users, it would be relevant to generate more evidence of the health-related problems with high potency cannabis, and the treatment and harm reduction solutions based around these health-related problems.

Cannabis accounts for half of all new drug treatment patients

The most widely used illegal drug in Europe, many seemingly enjoy cannabis without it leading to any significant negative social or health effects. However, numbers entering treatment for cannabis use problems have been on the rise (both in the UK, and the rest of Europe), while heroin treatment numbers have fallen  chart. According to Public Health England, this is not because more people are using cannabis, but perhaps because services relieved of some of the recent pressure of opiate user numbers are giving more priority to cannabis, because they are making themselves more amenable to cannabis users, and because of emerging issues with stronger strains of the drug. Whatever the causes, across the UK figures submitted to the European drug misuse monitoring centre show that the proportion of patients starting treatment for drug problems who did so primarily due to their cannabis use rose steadily from 11% in 2003/04 to 22% in 2011/12. With the caveat that data from 2013 onwards is not directly comparabledue to changes in methodology, in 2014 and 2015 the proportion of patients who entered treatment primarily because of a cannabis issue hovered above previous years at 26% (25,278 and 26,295 respectively). Among first ever treatment presentations, the increase from 2003/04 was more pronounced, from 19% to 37%. By 2013, cannabis use had become the main prompt for half the patients who sought treatment for the first time (at 49%), and stayed relatively constant at 47% in 2014, and 48% in 2015.

Showing that more users was not the reason for more starting treatment, over about the same period, in England and Wales the proportion of 16–59-year-olds who in a survey said they had used cannabis in the past year fell from about 11% to 7% in 2013/14, then stayed at that level in 2014/15 and 2015/16. The treatment figures largely reflect trends in England, where in 2013/14 the number of patients starting treatment with cannabis use problems had risen to 30,422, 21% of all treatment starters, up from 23,018 and 19% in 2005/06. Subsequently the number dropped to 27,965 in 2015/16, still around a fifth of all treatment starters. Among the total treatment population – starting or continuing in treatment – cannabis numbers rose from 40,240 in 2005/06 to peak at 64,407 in 2013/14 before falling back to 59,918 in 2015/16; corresponding proportions again hovered around a fifth. As a primary problem substance among under-18s cannabis dominated, accounting for three-quarters of all patients in treatment in 2015/16 and in numbers, 12,863. The dominance of cannabis increased from 2008/09 as numbers primarily in treatment for drinking problems fell.

‘All treatments appear to work’

According to the two main diagnostic manuals used in Europe and the USA, problem cannabis use can develop into a cannabis use disorder or cannabis dependence, identifiable by a cluster of symptoms including: loss of control; inability to cut down or stop; preoccupation with use; neglecting activities unrelated to use; continued use despite experiencing problems; and the development of tolerance and withdrawal. This level of clinical appreciation for cannabis use problems didn’t exist when researcher and writer William L. White entered the addictions field half a century ago:

“When I first entered the rising addiction treatment system in the United States nearly half a century ago, there existed no clinical concept of cannabis dependence and thus no concept of recovery from this condition. In early treatment settings, cannabis was not consider[ed] a “real” drug, the idea of cannabis addiction was scoffed at as remnants of “Reefer Madness,” and casual cannabis use was not uncommon among early staff working in addiction treatment programs of the 1960s. Many in the field remain sceptical of the idea of cannabis dependence, specifically whether problem users at the severe end experience physiological withdrawal. However, reviewing what they believe is mounting evidence, these authors suggest there can be confidence in the existence of a “true withdrawal syndrome” – albeit one that differs qualitatively from the “significant medical or psychiatric problems as observed in some cases of opioid, alcohol, or benzodiazepine withdrawals”. In the case of cannabis, the main symptoms are primarily emotional and behavioural, although appetite change, weight loss, and some physical discomfort are reported. A brief review aimed at practitioners in UK primary care provides guidance on how to manage symptoms of withdrawal among patients trying to stop or reduce their cannabis use.

Research has come a long way, says William L. White, with now “clear data supporting the dependency producing properties of cannabis, a clear conceptualization of cannabis use disorders (CUD) and cannabis dependence (CD)”, but until recently, very little evidence about the prospects of long-term recovery. Yet, key papers – found here and here – indicate that:

• Full remission from cannabis use disorders is not only possible, but probable.

• Stable remission takes time – an average of 33 months.

• Abstinence may not be initially realistic for heavy cannabis users – but those in  remission are usually able to reduce the intensity of their use and its  consequences.

At least in the United States, it seems dependence is more quickly overcome from cannabis than the main legal drugs. A survey of the US general adult population found that within a year of first becoming dependent, 3% each of smokers and drinkers were in remission and remained so until they were surveyed. For cannabis the figure was nearly 5% and for cocaine, nearly 9%. After ten years the proportions in remission had risen to 18% for nicotine, 37% for alcohol, 66% for cannabis and 76% for cocaine. About 26 years after first becoming dependent, half the people at some time dependent on nicotine were in remission, a milestone reached for alcohol after 14 years, for cannabis six years, and for cocaine, five.

Specialised treatment programmes for cannabis users in European countries

Generally for people with cannabis use problems, the European Monitoring Centre for Drugs and Drug Addiction concluded in 2015, and before that in 2008, that “all treatments appear to work”. For adults, effective treatments include motivational interviewing, motivational enhancement therapy and cognitive-behavioural therapy, and for younger people, family-based therapies seem most beneficial. Less important than the type of treatment is the treatment context and the individual’s determination to overcome their problems through treatment. And there is “no firm basis for a conclusion” that cannabis-specific interventions (designed around the risks and harms associated with cannabis) are more effective than general substance use treatment tailored to the individual needs of the cannabis user seeking treatment chart. In some studies brief interventions have been found to work just as well as more intensive treatment, but when the patients are heavily dependent, and the most difficult cases are not filtered out by the research, longer and more individualised therapies can have the advantage. When the World Health Organization trialled its ASSIST substance use screening and brief advice programme in Australia, India, the United States, and Brazil, just over half the identified patients (all had to be at moderate risk of harm but probably not dependent) were primarily problem cannabis users. Among these, risk reduction in relation to this drug was significantly greater among patients allocated to a brief advice session than among those placed on a three-month waiting list for advice. In each country too, risk reduction was greater among intervention patients, except for the USA, where the order was reversed. Suggesting that severity of use was not a barrier to reacting well to brief intervention, only patients at the higher end of the moderate risk spectrum further reduced their cannabis use/risk scores following intervention. The ASSIST study was confined to adults, but young people in secondary schools in the USA whose problem substance use focused mainly on cannabis also reacted well to brief advice.

The relative persistence of opiate use problems versus the transitory nature of those primarily related to cannabis seemed reflected in an analysis of treatment entrants in England from 1 April 2005 to the end of 2013/14, the last time this particular analysis was published. At the end of this period just 7% of primary cannabis users were still in or back in treatment compared to the 30% overall figure and 36% for primary opiate users. The figure peaked at 43% for users of opiates and crack. Over half – 53% – of primary cannabis users had left treatment as planned, apparently having overcome their cannabis problems, compared to 27% of primary opiate users and just 20% with dual opiates and crack use problems. Another 40% of cannabis users had left treatment in an unplanned manner, a slightly higher proportion than among opiate users. The figures tell a tale of relatively high level of success which enables cannabis users to leave treatment, though even in the absence of recorded success, few stay long-term.

However, the forms patients in England complete with their keyworkers while in treatment seem to tell a different story. Compared to how they started treatment, around six months later 45% of primary cannabis users were assessed as using just as often (including a few using more), compared to 30% of opiate users and 42% whose main problem drugs were both opiates and crack, suggesting more rapid and/or more complete remission for opiate users than for cannabis users. One interpretation is that the widespread use of substitute drugs like methadone more reliably reduced the illegal opiate use of opiate users and also helped retain them in treatment, while cannabis users tended quickly to leave treatment, having done well or not. However, these figures relate only to patients who completed the forms at their six-month review, which in practice could have happened anywhere from about one to six months after their assessment for treatment. What proportion of primary cannabis users were still in treatment at that point and available to complete the forms is not clear, but they may have been the patients whose problems were deep seated enough to require extended treatment.

Enjoyable and trouble-free for many, but not without harms Harm reduction – the “set of practical strategies and ideas aimed at reducing negative consequences associated with drug use” – is mostly associated with ‘harder’ drugs like heroin, for which blood-borne viruses and drug-related deaths are clear and severe risks. Yet while “many people experience cannabis as enjoyable and trouble free”, there are also varying degrees of harm with this drug depending on the characteristics of the person using, the type of the cannabis, and the way they consume it. Many formal cannabis harm reduction programmes borrow from the fields of alcohol and tobacco. Advice includes:

• safer modes of administration (eg, on the use of vaporisers, on rolling safer joints, on less risky modes of inhaling) Many people experience cannabis as enjoyable and trouble free … some people require help to reduce or stop

• skills to prevent confrontation with those who disapprove of use

• encouraging users to moderate their use

 

• discouraging mixing cannabis with other drugs

• drug driving prevention and controls

• reducing third-party exposure to second-hand smoke

• education about spotting signs of problematic use

• self-screening for problematic use

In some parts of the UK, National Health Service tobacco smoking cessation services incorporated cannabis into their interventions with adults; and Health Scotland, also addressing the risks of tobacco and cannabis smoking, published a booklet for young people titled Fags ‘n’ Hash: the essential guide to cutting down the risks of using tobacco and cannabis.

Vaporising or swallowing cannabis offers a way to avoid respiratory risks, but only a minority of cannabis do this, most choosing to smoke cannabis joints (or cannabis and tobacco joints). While not all will know about the different health risks, cannabis users may choose against safer consumption methods anyway for a range of reasons (including their own thoughts about safe use):

• Users may find it easier to control the effects (eg, severity, length of effect) of cannabis when inhaling in the form of a joint or spliff

• Preparing and sharing joints can be an enjoyable part of the routine, or part of a person’s social activities

• Alternative methods of smoking (eg, bongs and vaporisers) may be inconvenient to use, or expensive to buy

 

Most harm reduction advice is delivered informally long before users come into contact with drugs professionals – for example through cannabis magazines, websites, and headshops – highlighting the importance of official sources engaging with non-official sources to promote the delivery of accurate, evidence-based harm reduction messages.

A new high

In May 2016 the Psychoactive Substances Act placed a ‘blanket ban’ on new psychoactive substances (previously known as ‘legal highs’), including synthetic cannabinoids (synthetic forms of cannabis). Prior to this, in 2014, there had been 163 reported deaths from new psychoactive substances in the UK, and 204 the year after. The average age was around 28, younger than the average age for other drug misuse deaths of around 38. The fact that these psychoactive substances – which produced similar effects to illicit drugs like cannabis, cocaine, and ecstasy – could be bought so easily online or on the high street, appeared inconsistent; and each fatality prompted “an outcry for something to be done to prevent further tragedies”. This was the context (and arguably the political trigger) for the introduction of the Psychoactive Substances Act. While possession of a psychoactive substance as such wasn’t criminalised;, production, supply, offer to supply, possession with intent to supply, import or export were – with a maximum penalty of seven years’ imprisonment.

Just seven months after the Act came into effect, the Home Office labelled it a success, with a press release stating that nearly 500 people had been arrested, 332 shops around the UK had been stopped from selling the substances, and four people had been sent to prison. But did the Psychoactive Substances Act have the presumably desired effect of limiting access to psychoactive substances (and reducing deaths), or did it just push the drugs the way of dealers? It is perhaps too early to tell, but former chair of the Advisory Council on the Misuse of Drugs Professor Nutt had warned before the Act came into effect that the ‘blanket ban’ would make it harder (not easier) to control drugs. And while Chief executive of DrugWise Harry Shapiro had said the new law would make new psychoactive substances harder to obtain, he also agreed that sale of the drugs would not cease, but merely be diverted to the illicit market: “The same people selling heroin and crack will simply add this to their repertoire.” The paper “From niche to stigma” examined the changing face of the new psychoactive substance user between 2009 and 2016, focusing on people using the synthetic cannabis known as ‘spice’. It looked at the transition of (then) ‘legal highs’ from an “experimental and recreational” scene associated with a “niche middle class demographic”, to “those with degrees of stigma”, especially homeless, prison, and socially vulnerable youth populations (including looked after children, those involved in or at risk of offending, and those excluded or at risk of exclusion from mainstream education). In 2014, the DrugScope Street Drug Survey also observed a problem among these particular groups, recording a “rapid rise in the use of synthetic cannabinoids such as Black Mamba and Exodus Damnation by opiate users, the street homeless, socially excluded teenagers and by people in prison”.

‘SPICE’ AND OTHER SYNTHETICS

Cannabis contains two key components:

• ‘THC’ (tetrahydrocannabinol), which produces the ‘high’

• ‘CBD’ (cannabidiol), which produces the sedative and anti-anxiety effects

Synthetic forms of cannabis contain chemicals that aim to copy the effects of ‘THC’ in cannabis. But the effects of synthetic cannabis can be quite different (and often stronger): firstly, because synthetic production makes it easier to manipulate the amount of the THC-like chemical; and secondly, because of the absence of the moderating equivalent of ‘CBD’. Some synthetics are purposely designed to resemble herbal cannabis, and can be consumed in the same ways (eg, smoked or inhaled). The names also often have deliberate cannabis connotations. The risk of this is that people wishing to take cannabis may be initially unaware that they have been sold the synthetic form, or may believe from the look of it that it will produce similar sought-after effects. The greater intensity of synthetic cannabis at lower dose levels ( box) ensures that it has an appeal in terms of potency and affordability, but may put those with fewer resources at greater harm.

In 2014, the prison inspectorate for England and Wales raised concerns about the rise in the use of psychoactive substances in prisons, in particular synthetic cannabis. A study set in an English adult male prison found that the nature of the market was posing significant challenges to the management of offenders. There, the primary motivation for consumption was being able to take a substance without it being detected. Given this motivation, and the greater likelihood of harms from synthetic versus natural cannabis, the researchers concluded that it was imperative for mandatory drug-testing policies to be revised, and instead rooted in harm reduction – something which would also apply to people on probation subject to mandatory drug-testing.

Cannabis throws up a range of issues rather different from those associated with the drugs treatment in the UK has normally focused on. If current trends continue, understanding the findings will become yet more important to British treatment services.

Source:   http://findings.org.uk/PHP/dl.php?file=cannabis_treat.    Last revised 10 July 2017. 

Cannabis has recently been legalised in many US states

Cannabis itself is harmful to cardiovascular health and increases the chance of early death regardless of related factors such as smoking tobacco, new research reveals.

Data taken from more than 1,000 US hospitals found that people who used the drug had a 26 per cent higher chance of suffering a stroke than those who did not, and a 10 per cent higher chance of having a heart attack.

The findings held true after taking into account unhealthy factors known to affect many cannabis smokers, such as obesity, alcohol misuse and smoking.

‘This leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects’ Dr Aditi Kalla, Einstein Medical Center, Philadelphia

They indicate there is something intrinsic about cannabis which can damage the proper functioning of the human heart.

“Even when we corrected for known risk factors, we still found a higher rate of both stroke and heart failure in these patients, so that leads us to believe that there is something else going on besides just obesity or diet-related cardiovascular side effects,” said Dr Aditi Kalla, Cardiology Fellow at the Einstein Medical Center in Philadelphia and the study’s lead author.

“It’s important for physicians to know these effects so we can better educate patients.”

Previous research in cell cultures has shown that heart muscle cells have cannabis receptors relevant to contractility, or squeezing ability, suggesting that those receptors might be one mechanism through which marijuana use could affect the cardiovascular system.

The research team analysed more than 20 million records of young and middle-aged patients aged between 18 and 55 who were discharged from 1,000 hospitals in 2009 and 2010, when marijuana use was illegal in most states.

It identified 316,000 patients – 1.5 per cent – where marijuana use was diagnosed in the notes.  Their cardiovascular disease rates were compared to those who shunned the drug.

The research was published yesterday at a meeting of the American College of Cardiology in Washington DC.

Source:  http://www.telegraph.co.uk/science/2017/03/09/cannabis-boosts-risk-stroke-heart-attack-independent-tobacco/  

Ketamine Continues to Impress and Confound Researchers

A novel glutamatergic hypothesis of depression, using a 50-year-old anaesthesia medicine, has had a remarkable run as of late. First an anaesthetic, then a popular club drug in the 90s known as “Special K” (and currently still popular in Hong Kong as a “Rave Drug”), and now a novel, fast acting antidepressant, ketamine is a N-Methyl D-Aspartame (NMDA) receptor antagonist. Ketamine was FDA-approved in the U.S. as an anaesthetic nearly 50 years ago. It is used primarily by anaesthesiologists in both hospital and surgical settings. As an N-Methyl D-Aspartame (NMDA) receptor antagonist with dissociative properties, NMDA receptors possess high calcium permeability, which allows ketamine to reach its target quickly. Increasing clinical evidence has shown that a single sub-anaesthetic dose (0.5 mg/kg) of IV-infused ketamine exerts impressive antidepressant effects within hours of administration. These effects have stabilized suicidality in severely depressed, treatment-resistant individuals. The effects of low-dose ketamine infusion therapy can last up to seven days, although the dosing and patient characteristics regarding its optimal effectiveness have not been established.

In my book, “The Good News About Depression: Cures And Treatments In The New Age of Psychiatry”–Revised (1996), I said there was never a better time to be depressed, due in part to recent breakthroughs in understanding of the underlying biology of depression, plus the discovery of novel therapeutics e.g., the SSRIs. Today that book might be called the “Better News About Depression” as a result of the effectiveness of novel treatments such as Transcranial Magnetic Stimulation (TMS) and now ketamine, which has illuminated and broadened our understanding and view of treating depression.

Why Is This Better News?

New clinical and preclinical studies suggest that dysfunction of the glutamatergic system is perhaps more relevant and important than the current catecholamine hypothesis and therapy that targets serotonin, norepinephrine and sometimes dopamine. These medications often take four to six weeks to exert any therapeutic benefit, whereas rapid reductions in depressive symptoms have been observed in response to a single dose of ketamine. This is a vast departure from the SSRIs and SSNRIs that have occupied the mainstream of pharmacological therapy for depression and anxiety disorders for more than 30 years.

Lastly, the mechanism of action of NDMA antagonists are comparatively underexplored but vitally important to our understanding of depression, reversal of suicidality, as well as the debilitating, depressive symptoms induced by abuse of alcohol and other drugs. This review highlights the current evidence supporting the antidepressant effects of ketamine as well as other glutamatergic modulators, such as D-cycloserine, riluzole, CP-101,606, CERC-301 (previously known as MK-0657), basimglurant, JNJ-40411813, dextromethorphan, nitrous oxide, GLYX-13, and esketamine. This all adds up to some very good news for depressed persons and especially those who do not respond to previous SSRI or SSNRI treatments.

Source: http://www.rivermendhealth.com/resources/ketamine-fast-acting-antidepressant/  June2017

 

Cannabis Use, Gender and the Brain

Cannabis is the most widely used illicit drug in the U.S. and, as a result of legalization efforts for both medical remedy and for recreational use, is now the second leading reason (behind alcohol) for admission to addiction treatment in the U.S. The health consequences, cognitive changes, academic performance and numerous neuroadaptations have been debated ad nauseam. Like other drugs and medications, effects are different if exposure occurs in the young vs. the old or in males vs. females. Exposure in utero, early childhood, adolescence-young adult, adult and elderly may have different effects on the brain and outcomes. Yet the best available independent research shows that marijuana use is associated with consistent regionally specific alterations to important brain circuitry in the striatum and pre-frontal and post orbital regions. In this study, Chye and colleagues have investigated the association between marijuana use and the size of specific brain regions that are vitally important in goal-directed behavior, focus and learning within in the orbitol frontal cortex (OFC) and caudate. This investigation suggests that marijuana dependence and recreational use have distinct and region-specific effects.

Why Does This Matter?

This is an important finding, but distinction between cannabis use, abuse and dependence is not always clear, objective, linear or well understood. However, dependence-related medial OFC volume reduction was robust and highly significant. Lateral OFC volume reduction was associated with monthly marijuana use. Greater reductions in brain volume of specific regions were stronger among females who were marijuana dependent. This finding correlates with previous evidence of gender-dependent differences towards the various physiological, behavioral and the reinforcing effect of marijuana for both recreational use and addiction.

The results highlight important neurological distinctions between occasional cannabis use and addiction. Specifically, Chye and colleagues found that smaller medial OFC volume may be driven by marijuana addiction-related mechanisms, while smaller lateral OFC volume may be due to ongoing exposure to cannabinoids. The results highlight a distinction between cannabis use and dependence and warrant future examination of gender-specific effects in studies of marijuana use and dependence.

Source: http://www.rivermendhealth.com/resources/cannabis-use-gender-brain/   June 2017  Author: Mark Gold, MD

Warfarin. A single published case report describes an interaction with a patient taking warfarin who also regularly smoked tobacco and marijuana. The patient had multiple comorbidities and was taking at least 10 other medications. On at least two occasions, the patient’s international normalized ratio (INR) increased to values over 10 with episodes of bleeding. The only change reported for both occasions was an increase in the amount and frequency of marijuana smoking.[24] Patients who take warfarin and use marijuana regularly should receive close INR monitoring for any potential interaction.

Antiepileptic drugs (AEDs). A recent study examined baseline serum AED levels to identify drug-drug interactions between CBD and 19 AEDs during an open-label safety study in 81 patients (39 adults, 42 children) with refractory epilepsy.[25] As doses of CBD were increased, the researchers noted an increase in the serum levels of topiramate (P<.01), rufinamide (P<.01), and desmethylclobazam (P<.01) and a decrease in the levels of clobazam (P<.01) in both adult and pediatric patients. In adult patients, a significant increase in the serum levels of zonisamide (P=.02) and eslicarbazepine (P=.04) was observed with increasing CBD dose. No other drug interactions among the 19 AEDs were noted.   The authors recommended monitoring serum AED levels in patients receiving CBD, as drug-drug interactions may be correlated with adverse events and laboratory abnormalities.

Patients using marijuana should be educated to avoid drugs that affect associated CYP450 enzymes. When these drugs cannot be avoided, and marijuana use is expected to continue, the patient should be monitored closely for potential drug interactions.   Be Aware and Educate Patients

Smoking more than two joints weekly is likely to increase the risk for drug-related interactions.[5,10] No data exist monitoring large-scale marijuana use in the United States. However, in Washington, a state in which marijuana use is legal, the average user is estimated to smoke two to three joints per week.[26]  With growing legalization and use throughout the nation, healthcare professionals must exercise heightened caution in the situation of concomitant use of medications and marijuana.

Source:: Stirring the Pot: Potential Drug Interactions With Marijuana – Medscape – Jun 08, 2017.  http://www.medscape.com/viewarticle/881059#vp

Deputy Attorney General Rod Rosenstein said on Tuesday morning. Rosenstein, along with acting head of the Drug Enforcement Agency, Chuck Rosenberg, and other prominent officials in law enforcement addressed the media at the DEA’s headquarters in Arlington, VA to discuss the ongoing response to the nation’s staggering opioid epidemic.

“We’re not talking about a slight increase. There’s a horrifying surge of drug overdoses in the United States of America. Some people say we should be more permissive, more tolerant, more understanding about drug use. I say we should be more honest and forthcoming with the American people on the clear and present danger that we know face,” opened Rosenstein.

“Fentanyl is especially dangerous. It is 40 to 50 times more deadly than heroin. Just two milligrams, a few grains of salt, an amount you could fit on the tip of your finger, can be lethal. Fentanyl exposure can injure or kill innocent law enforcement officers and first responders. Inhaling a few airborne particles can have dramatic effects,” he continued.

Rosenstein, Rosenberg, and their colleagues used the event to roll out new precautions for first responders in dealing with fentanyl. Such measures predominately featured hazmat suits as a means of avoiding airborne inhalation.

“Fentanyl’s everywhere and it’s killing people,” Rosenberg solemnly remarked.

Despite such a bleak update, Rosenberg claimed reasons for careful optimism in the midst of this epidemic. He has spoken extensively with his Chinese counterparts in law enforcement, given that China is the major source of Fentanyl that enters America. According to Rosenberg, the Chinese government banned 116 synthetic opioids for export and 4 more after his trip to China this March. Additional synthetics are scheduled to be banned as well.

“I do not want to understate such gains, nor do I want to overstate them,” he cautioned. More progress in international cooperation, he said, still has to be made in cutting off fentanyl shipments from China.

Rosenberg and other law enforcement officials such as Jonathan Thompson of the National Sheriffs’ Association assessed the difficulty associated with training first responders in such new duties and admitted that such efforts would strain already stretched resources in fighting what is an overwhelming epidemic.

Rosenberg’s daunting assessment of fentanyl put in perspective the existential danger of the ongoing opioid crisis that, according to Rosenstein, has contributed to the largest yearly increase in overdose deaths on record in America.

Rosenberg pointed out that such statistics tend to “wash over you.” To grasp the enormity of the epidemic he claimed that if three mass-shootings as deadly as the Pulse Nightclub Attack occurred three times every day for 365 days, then the death toll would roughly reach that of drug overdoses in 2015.

Source:   http://www.breitbart.com/big-government/2017/06/07/doj-drug-overdose-now-leading-cause-of-death-for-americans-under-50/

DATE: June 1, 2017

DISTRIBUTION: All First Responders

ANALYST: Ralph Little/904-256-5940

SUBJECT: Grey Death compound in Jacksonville & Florida

NARRATIVE:  The compound opioid known as Grey Death has been detected for the first time in North Florida. Although Purchased in March in St. Augustine, the basic drugs were from Jacksonville and may have been purchased pre-mixed.  Other  samples have occurred from March through May. Delays are due to testing requirements.  Grey Death has been detected in Florida since November 2016 in four counties south of NFHIDTA. Palm Beach reported a related death on May 19th.  Grey Death has been reported in the Southeast, with overdoses and at least  two deaths in Alabama and Georgia. It has  also been found in Ohio, Pennsylvania and Indiana. The compound is  a mixture of U-47700, heroin and fentanyl. Overall, different fentanyls, including carfentanil, have been detected and the amount of each ingredient varies.  The substance’s appearance is similar to concrete mixing powder with a varied texture from fine powder to rock-like. While grey is most common and is the color seen in St. Augustine, pictures indicate tan as well. The potency is much higher than heroin and can be administered via injection, ingestion, insufflation and smoking.

DANGER: Grey Death ingredients and their concentrations are unknown to users, making it particularly lethal. Because these strong drugs can be absorbed through the skin, touching or the accidental inhalation of these drugs  can result in absorption. Adverse effects, such as disorientation, sedation, coughing, respiratory distress or cardiac  arrest can occur very rapidly, potentially within minutes of exposure. Any concoction containing U-47700 may not respond to Narcan, depending on its relative strength in the mix.   Light grey powder in a test tube.

CONCLUSION: Responders are advised to employ protective gear to prevent skin absorption or inhalation. Miniscule (grains) of this substance are dangerous. Treat any particles in the vicinity of scene or potentially adhering to your or victim outer clothing or equipment as hazardous.

Source:  HIDTA Intelligence brief.   1st June 2017

Changes may increase risk of continued drug use and addiction

ANN ARBOR, Mich. — Most people would get a little ‘rush’ out of the idea that they’re about to win some money. In fact, if you could look into their brain at that very moment, you’d see lots of activity in the part of the brain that responds to rewards.

But for people who’ve been using marijuana, that rush just isn’t as big – and gets smaller over time, a new study finds.

And that dampened, blunted response may actually open marijuana users up to more risk of becoming addicted to that drug or others.

The new results come from the first long-term study of young marijuana users that tracked brain responses to rewards over time. It was performed at the University of Michigan Medical School.

Published in JAMA Psychiatry, it shows measurable changes in the brain’s reward system with marijuana use – even when other factors like alcohol use and cigarette smoking were taken into account.

“What we saw was that over time, marijuana use was associated with a lower response to a monetary reward,” says senior author and U-M neuroscientist Mary Heitzeg, Ph.D. “This means that something that would be rewarding to most people was no longer rewarding to them, suggesting but not proving that their reward system has been ‘hijacked’ by the drug, and that they need the drug to feel reward — or that their emotional response has been dampened.”

Watching the reward centers

The study involved 108 people in their early 20s – the prime age for marijuana use. All were taking part in a larger study of substance use, and all had brain scans at three points over four years. Three-quarters were men, and nearly all were white.

While their brain was being scanned in a functional MRI scanner, they played a game that asked them to click a button when they saw a target on a screen in front of them. Before each round, they were told they might win 20 cents, or $5 – or that they might lose that amount, have no reward or loss.

The researchers were most interested at what happened in the reward centers of the volunteers’ brains – the area called the nucleus accumbens. And the moment they cared most about was that moment of anticipation, when the volunteers knew they might win some money, and were anticipating performing the simple task that it would take to win.

In that moment of anticipating a reward, the cells of the nucleus accumbens usually swing into action, pumping out a ‘pleasure chemical’ called dopamine. The bigger the response, the more pleasure or thrill a person feels – and the more likely they’ll be to repeat the behavior later.

But the more marijuana use a volunteer reported, the smaller the response in their nucleus accumbens over time, the researchers found.

While the researchers didn’t also look at the volunteers’ responses to marijuana-related cues, other research has shown that the brains of people who use a high-inducing drug repeatedly often respond more strongly when they’re shown cues related to that drug.

The increased response means the drug has become associated in their brains with positive, rewarding feelings. And that can make it harder to stop seeking out the drug and using it.

If this is true with marijuana users, says first author Meghan Martz, doctoral student in developmental psychology at U-M, “It may be that the brain can drive marijuana use, and that the use of marijuana can also affect the brain. We’re still unable to disentangle the cause and effect in the brain’s reward system, but studies like this can help that understanding.

Change over time

Regardless, the new findings show that there is change in the reward system over time with marijuana use. Heitzeg and her colleagues also showed recently in a paper in Developmental Cognitive Neuroscience that marijuana use impacts emotional functioning.

The new data on response to potentially winning money may also be further evidence that long-term marijuana use dampens a person’s emotional response – something scientists call anhedonia.

“We are all born with an innate drive to engage in behaviors that feel rewarding and give us pleasure,” says co-author Elisa Trucco, Ph.D., psychologist at the Center for Children and Families at Florida International University. “We now have convincing evidence that regular marijuana use impacts the brain’s natural response to these rewards. In the long run, this is likely to put these individuals at risk for addiction.”

Marijuana’s reputation as a “safe” drug, and one that an increasing number of states are legalizing for small-scale recreational use, means that many young people are trying it – as many as a third of college-age people report using it in the past year.

But Heitzeg says that her team’s findings, and work by other addiction researchers, has shown that it can cause effects including problems with emotional functioning, academic problems, and even structural brain changes. And, the earlier in life someone tries marijuana, the faster their transition to becoming dependent on the drug, or other substances.

“Some people may believe that marijuana is not addictive or that it’s ‘better’ than other drugs that can cause dependence,” says Heitzeg, who is an assistant professor of psychiatry at the U-M Medical School and member of the U-M Addiction Research Center. “But this study provides evidence that it’s affecting the brain in a way that may make it more difficult to stop using it. It changes your brain in a way that may change your behavior, and where you get your sense of reward from.”

She is among the neuroscientists and psychologists leading a nationwide study called ABCD, for Adolescent Brain Cognitive Development. That study will track thousands of today’s pre-teens nationwide over 10 years, looking at many aspects of their health and functioning, including brain development via brain scans. Since some of the teens in the study are likely to use marijuana, the study will provide a better chance of seeing what happens over time.

Source: JAMA Psychiatry, doi:10.1001/jamapsychiatry.2016.1161

A new study suggests smoking high-potency marijuana may cause damage to nerve fibers responsible for communication between the brain’s two hemispheres.

The study included MRI scans of 99 people, including some who were diagnosed with psychosis, HealthDay reports.  The researchers found an association between frequent use of high-potency marijuana and damage to the corpus callosum, which is responsible for communication between the brain’s left and right hemispheres.

The corpus callosum is especially rich in cannabinoid receptors. THC, the psychoactive ingredient in marijuana, acts on these receptors.

Today’s high-potency marijuana has been shown to contain higher proportions of THC compared with a decade ago. Scientists have known that the use of marijuana with higher THC content has been associated with greater risk and earlier onset of psychosis, the researchers noted. This study is the first to examine the effect of marijuana potency on brain structure, according to a news release from Kings’s College London.

Frequent use of high-potency marijuana significantly affected the structure of the corpus callosum in patients with or without psychosis, the researchers report in Psychological Medicine.    The more high-potency marijuana a person smoked, the greater the damage.

“There is an urgent need to educate health professionals, the public and policymakers about the risks involved with cannabis use,” said senior researcher Dr. Paola Dazzan of the Institute of Psychiatry, Psychology & Neuroscience at King’s College London. “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 on the type of damage these substances can do to the brain.’

Source:  https://www.ncadd.org/about-addiction   Dec. 2015

As Cpl. Kevin Phillips pulled up to investigate a suspected opioid overdose, paramedics were already at the Maryland home giving a man a life-saving dose of the overdose reversal drug Narcan.

Drugs were easy to find:  a package of heroin on the railing leading to a basement; another batch on a shelf above a nightstand.

The deputy already had put on gloves and grabbed evidence baggies, his usual routine for canvassing a house.  He swept the first package from the railing into a bag and sealed it; then a torn Crayola crayon box went from the nightstand into a bag of its own.  Inside that basement nightstand:  even more bags, but nothing that looked like drugs.

Then—moments after the man being treated by paramedics come to—the overdose hit.

“My face felt like it was burning.  I felt extremely lightheaded.  I felt like I was getting dizzy,” he said.  “I stood there for two seconds and thought, ‘Oh my God, I didn’t just get exposed to something.’ I just kept thinking about the carfentanil.”

Carfentanil came to mind because just hours earlier, Phillips’ boss, Harford County Sheriff Jeffrey Gahler, sent an e-mail to deputies saying the synthetic opioid so powerful that it’s used to tranquilize elephants had, for the first time ever, showed up in a toxicology report from a fatal overdose in the county.  The sheriff had urged everyone to use extra caution when responding to drug scenes.

Carfentanil and fentanyl are driving forces in the most deadly drug epidemic the United States has ever seen.  Because of their potency, it’s not just addicts who are increasingly at risk—it’s those tasked with saving lives and investigating the illegal trade.  Police departments across the U.S. are arming officers with the opioid antidote Narcan.  Now, some first responders have had to use it on colleagues, or themselves.

The paramedic who administered Phillips’ Narcan on May 19 started feeling sick herself soon after;  she didn’t need Narcan but was treated for exposure to the drugs.

Earlier this month, an Ohio officer overdosed in a police station after bushing off with a bare hand a trace of white powder left from a drug scene.  Like Phillips, he was revived after several doses of Narcan.  Last fall, SWAT officers in Hartford, Connecticut, were sickened after a flash-bang grenade sent particles of heroin and fentanyl airborne.

Phillips’ overdose was eye-opening for his department, Gahler said.  Before then, deputies didn’t have a protocol for overdose scenes; many showed up without any protective gear.

Gahler has since spent $5,000 for 100 kits that include a protective suit, booties, gloves, and face masks.  Carfentanil can be absorbed through the skin and easily inhaled. and a single particle is so powerful that simply touching it can cause an overdose, Gahler said.  Additional gear will be distributed to investigators tasked with cataloguing overdose scenes—heavy-duty gloves and more robust suits.

Gahler said 37 people have died so far this year from overdoses in his county, which is between Baltimore and Philadelphia.  The county has received toxicology reports on 19 of those cases, and each showed signs of synthetic opioids.

“This is all a game-changer for us in law enforcement,” Gahler said.  “We are going to have to re-evaluate daily what we’re doing.  We are feeling our way through this every single day . . . we’re dealing with something that’s out of our realm.  I don’t want to lose a deputy ever, but especially not to something the size of a grain of salt.”

Source:  – Erie Times-News, Erie, Pa. – May 28, 2017 – www.goerie.com  The Associated Press

Ohio had the most overdose fatalities in the United States in 2014 and 2015.

A newspaper’s survey of county coroners has painted a grim picture of fatal overdoses in Ohio: more than 4,000 people died from drug overdoses in 2016 in the state badly hit by a heroin and opioid epidemic.

At least 4,149 died from unintentional overdoses last year, a 36 percent climb from the previous year, or a time when Ohio had the most overdose fatalities in the United States so far.

“They died in restaurants, theaters, libraries, convenience stores, parks, cars, on the streets and at home,” wrote The Columbus Dispatch in its report revealing the findings.

Survey Findings

It’s likely getting worse, too, as coroners warned that overdose deaths this year are fast outpacing these figures brought on by overdoses from heroin, synthetic opioids fentanyl and carfentanil, and other drugs.

The Dispatch obtained the number by getting in touch with coroners’ offices in all 88 Ohio counties. Coroners in six smaller counties, according to the paper, did not provide the requested figures.

Leading the counties in rapid drug overdose rises are counties such as Cuyahoga, where there were 666 deaths in 2016, as well as Franklin, Hamilton, Lucas, Montgomery, and Summit.

The devastation, added the survey, did not discriminate against big or small cities and towns, urban or rural areas, and rich and poor enclaves.

“It’s a growing, breathing animal, this epidemic,” said Medina County coroner and ER physician Dr. Lisa Deranek, who has sometimes revived the same overdose patients a few times each week.

Fentanyl Overdoses

Cuyahoga County, which covers Cleveland, had its death toll largely blamed on fentanyl use. Heroin remains a leading killer, but the autopsy reports reflected the major role of fentanyl, a synthetic opiate 50 times stronger than morphine, and animal tranquilizer carfentanil.

“We’ve done so much, but the numbers are going the other way. I don’t see the improvement,” said William Denihan, outgoing CEO of Cuyahoga County Alcohol, Drug Addiction and Mental Health Services Board.

Cuyahoga County had 400 fentanyl-linked deaths from Nov. 21 in 2015 to Dec. 31 last year, more than double related deaths of all previous years in combination. The opioid crisis, too, no longer just affected mostly white drug users, but also minority communities.

Dr. Thomas Gilson, medical examiner of Cuyahoga County, warned that cocaine is now getting mixed into the fentanyl distribution and fentanyl analogs in order to bring the drugs closer to the African-American groups.

Plans And Prospects

The state’s Department of Mental Health and Addiction Services stated that the overdose death toll back in 2015 would have been higher if not for the role of naloxone, an antidote use for opioid overdose cases. It has been administered by family members, other drug users, and friends to revive dying individuals.

State legislature moved to make naloxone accessible in pharmacies without a prescription. Ohio topped the nation’s drug overdose death numbers in 2014 and 2015. In the latter year, it was followed by New York, according to an analysis by the Kaiser Family Foundation using statistics from the U.S. Centers for Disease Control and Prevention.

Experts are pushing for expanding drug prevention as well as education initiatives from schoolkids to young and middle-aged adults, which also make up the bulk of dying people.

And while the state pioneered in crushing “pill mills” that issue prescription painkillers, health officials warned that this sent addicts to heroin and other stronger substances.

Naloxone, too, is merely an overdose treatment and not a cure for the growing addiction. Last May 22 in Pennsylvania, two drug counselors working to help others battle their drug addiction were found dead from opioid overdose at the addiction facility in West Brandywine, Chester County.

Source:  http://www.techtimes.com/articles/208540/20170529/ohio-leads-in-nations-fatal-drug-overdoses-with-4-000-dead-in-2016-survey.htm  29.05.17

The first to die was the family’s pet duck, killed in an attempt to rid the house of evil.

By then, Raina Thaiday had already been on a cleaning frenzy for a week, scrubbing the ceilings of her Cairns home and tossing possessions out into the yard in a bid to “cleanse” the house.  But it was when she heard a dove’s call, which she interpreted as a sign from God, that she decided she must “kill her children in order to save them”.

The Mental Health Court of Queensland last month ruled, in a decision not made public until Thursday, that Raina Mersane Ina Thaiday was of unsound mind when she stabbed to death seven of her children and a niece in her home on December 19, 2014.

In 2009, Raina Thaiday was interviewed thanking paramedics for safely delivering her child in the back of an ambulance. Photo: Nine News

“To her way of thinking at the time, what she was doing was the best thing she could do for her children. She was trying to save them,” Justice Jean Dalton said, exempting the mother from trial and confining her to mental health treatment.

Along the way the court heard details of the 40-year-old’s descent into “schizophrenia at its very depths”, likely exacerbated by years of heavy cannabis use, and culminating in her being in a psychotic state when she killed eight children under the age of 15.

A week before the killing, her then-20-year-old son, Lewis Warria found Mrs Thaiday stressed and serious, spending large amounts of time lecturing him about God, the court heard.  She went on a mission to “cleanse” her house, which Justice Dalton noted went far beyond a “normal spring clean”.

“All the furniture from the house was taken outside and put in the yard,” she said.”Inside the house was cleaned, in a most unusual way, including scrubbing the ceilings and the walls and a lot of Mrs Thaiday’s possessions were thrown away.  “And a lot of them were quite valuable.”

Things deteriorated still further the night of December 18. Her eldest daughter, niece and godchild had gone out shopping and did not return at 10pm as she had requested. Mrs Thaiday walked up and down the street, “preaching” to neighbours about their use of drugs and alcohol.  Agitated, she slept outside on a mattress dragged out in the cleaning.

Justice Dalton said with the benefit of hindsight, the things neighbours heard as Mrs Thaiday walked up and down the street, talking to herself or on the phone, were “clearly psychotic”.  “She was saying things like ‘I am the chosen one’,” the judge said.

“‘I have the power to kill people and to curse people. You hurt my kids, I hurt them first. You stab my kids, I stab them first. If you kill them, I’ll kill them’.”

At 11.40am on December 19, Mr Warria arrived home to find his mother slumped on the front verandah, covered in approximately 35 self-inflicted stab wounds that included a punctured lung. His siblings and cousin were dead inside.

Nearly two-and-a-half years later Mr Warria was in the courtroom inside Brisbane’s Queen Elizabeth II Courts of Law as a judge heard the opinions of six psychiatrists who had painstakingly analysed his mother’s mental state.

The court heard when police and paramedics arrived Mrs Thaiday immediately admitted she had killed the children inside. “Papa God” had been speaking to her, she told

psychiatrists, describing herself as the “anointed one” at risk from demons, who had to rid her Cairns home of an evil presence.

Psychiatrist Dr Angela Voita treated Mrs Thaiday from the day she came into The Park, one of Australia’s largest mental health facilities, on Christmas Eve 2014, five days after the mass killing.  She assessed her more than 50 times and, along with three other psychiatrists who gave evidence to the hearing, unanimously agreed she was mentally ill at the time of the offences.

After examining reams of evidence and interviews, Dr Voita said her patient was not capable of telling right from wrong or being able to control her actions at the time of the killings.  Assisting psychiatrist Dr Frank Varghese described the “unique” crime as “a horrendous case, the likes of which I have never seen before, and hopefully will never see (again).”   This is not ordinary schizophrenia,” he advised the judge.

“This is schizophrenia at its very depths and at its worst in terms of the terror for the patient as well as for the consequences for the individuals killed as a result of psychotic delusions.”

Mrs Thaiday had no psychiatric history or previous contact with mental health services outside of counselling at a local indigenous health service.  Independent psychiatrist Dr Pamela van de Hoef said there was some evidence that in 2007 she was also very disturbed.

“She had cut all her own hair off and threatened to kill one of the children with an axe.”

In 2011, she had ideas to drown herself and similar thoughts two weeks out from the 2014 killing, the psychiatrist said. The court heard cannabis was commonly linked to the onset of schizophrenia in those already vulnerable to the illness.

Ms Thaiday kicked a 10-20 cone a day habit in the months before the slaughter, leading psychiatrists to question whether her “psychosis” was a form of withdrawal, before mostly rejecting the notion.

Instead, Dr Jane Phillips and Dr Donald Grant agreed it was more likely the illness began to affect her while she was still using cannabis, causing to her to develop “religious delusions” that “forced her to live a clean life”.

“Altogether it amounts to a very convincing body of evidence that Mrs Thaiday was psychotic at the time of the killing,” Justice Dalton said.

She ruled Mrs Thaiday had the defence of unsoundness of mind available to her and issued a forensic order for ongoing mental health treatment.

Source: http://www.brisbanetimes.com.au/queensland/schizophrenia-at-its-very-depths-drove-mother-to-kill-eight-children-20170503-gvyf42.html   4th May 2017

 A New Agenda to  Turn Back the Drug Epidemic

Robert L. DuPont, MD, President , Institute for Behavior and Health, Inc.

A. Thomas McLellan, PhD, Senior Strategy Advisor , Institute for Behavior and Health, Inc.  May 2017

Institute for Behavior and Health, Inc. , 6191 Executive Blvd , Rockville, MD 20852 , www.IBHinc.org 1

Background 

The Institute for Behavior and Health, Inc. (IBH) is a 501(c)3 non-profit substance use policy and research organization that was founded in 1978. Non-partisan and non-political, IBH develops new ideas and serves as a force for change.

Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs and Health was published in November 2016. Four months later, in March 2017, IBH held a meeting of 25 leaders in addiction treatment, health care, insurance, government and research to discuss the scope and implications of this historic document. The US Surgeon General, VADM Vivek H. Murthy, MD, was an active participant in the meeting. The significance of this new Surgeon General’s Report is analogous to the historic 1964 Surgeon General’s report, Smoking and Health, a document that inspired an extraordinarily successful public health response in the United States that has reduced the rates of cigarette smoking by over 64% and continues its impact even today, more than 50 years following its release.

The following is a summary of the discussion at the March 2017 meeting and the conclusions and recommendations that were developed.

Introduction: The 2016 Surgeon General’s Report 

The two primary objectives of the US Surgeon General’s Report of 2016 are first to provide scientific evidence that shows that in addition to nicotine, other substance misuse and addiction issues (e.g., alcohol, opioids, marijuana, etc.) also are best understood and addressed as public health problems; and second to encourage the inclusion of addiction – its prevention, early recognition and intervention, treatment and active long-term recovery management – into the mainstream of American health care. At present these elements are not integrated either as a stand-alone continuum or within the general medical system. As is true for other widespread illnesses, addiction to nicotine, alcohol, marijuana, opioids, cocaine and other substances is a serious chronic illness. This perspective is contrary to the common perception that addiction reflects a moral failing, a personal weakness or poor parenting. Such opinions have stigmatized individuals who are suffering from these often deadly substance use disorders and have led to expensive and ineffective public policies that segregate prevention and treatment outside of mainstream medical care. A better public health approach encourages afflicted individuals and their family members to seek and receive help within the current health care system for these serious health problems.

An informed public health approach to reducing the prevalence and the harms associated with substance use disorders requires more than the brief treatment of serious cases. Particularly important are substance use prevention programs in schools, healthcare and in all other parts of the community to protect adolescents (ages 12 – 21), the group most at risk for the initiation of substance-related harms and substance use disorders.  Importantly, abundant tragic experience and accumulating science show that substance use disorders are not effectively treated with only short-term care. Because substance use disorders produce 2 significant long-lasting changes in the brain circuits responsible for memory, motivation, inhibition, reward sensitivity and stress tolerance, addicted individuals remain vulnerable to relapse years following specialized treatment.1, 2, 3 Thus, as is true for all other chronic illnesses, long periods of personalized treatment and monitoring are necessary to assure compliance with care, continued sobriety, and improved health and social function. In combination, science-based prevention, early intervention, continuing care and monitoring comprise a modern continuum of public health care. The overall goals of this continuum comport well with those of other chronic illnesses:

1 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 2. The Neurobiology of Substance Use, Misuse, and Addiction. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

2 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 5. Recovery: The Many Paths to Wellness. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

3 Betty Ford Institute Consensus Panel. (2007). What is recovery? A working definition from the Betty Ford Institute. Journal of Substance Abuse Treatment, 33(3), 221-228.

4 White, W. L. (2012). Recovery/remission from substance use disorders: An analysis of reported outcomes in 415 scientific reports, 1868-2011. Philadelphia, PA: Philadelphia Department of Behavioral Health and Intellectual Disability Services.

· sustained reduction of the cardinal symptom of the illness, i.e., substance use;

· improved general health and function; and,

· education and training of the patient and the family to self-manage the illness and avoid relapses.

In the addiction field achieving these goals is called “recovery.” This word is used to describe abstention from the use of alcohol, marijuana and other non-prescribed drugs as well as improved personal health and social responsibility.3,4 Over 25 million formerly addicted Americans are in stable, long-term recovery of a year or longer.4 Understanding how to consistently accomplish the life-saving goal of recovery must inform health care decisions.

The 2016 Surgeon General’s Report offers a science-informed vision and path to recovery in response to the nation’s serious addiction problem, including specifically the opioid overdose epidemic. Research shows that it is possible to prevent or delay most cases of substance misuse; and to effectively treat even the most serious substance use disorders with recovery as an expectable result of comprehensive, continuous care and sustained monitoring. To do this, substance use disorders must be recognized as serious, chronic health conditions that are both preventable and treatable. The nation must integrate the short-term siloed episodes of specialty treatment that now are isolated from mainstream healthcare into a fully integrated continuum of care comparable to that currently available to those with other chronic illnesses such as diabetes, hypertension, asthma and chronic pain.

Meeting Discussion and Conclusions 

The Surgeon General’s Report and the meeting convened by the Institute for Behavior and Health, Inc. (IBH) to promote its recommendations are significant responses to the expanding epidemic of opioid 3 and other substance use disorders, an epidemic that struck nearly 21 million Americans aged 12 and older in 2015 alone.5 That year saw more than 52,000 overdose deaths.6 This drug epidemic has devastated countless families and communities throughout the US. Unlike earlier and smaller drug epidemics, the current opioid epidemic is not limited to a few regions or communities or a narrow range of ethnicities or incomes in the United States. Instead it afflicts all communities and all socioeconomic groups; its impacts include smaller communities and rural areas as well as suburban areas and inner cities. Fuelled by the suffering of countless grieving families, the nation is in the early stages of confronting the new epidemic. A growing national determination to turn back this deadly epidemic has opened the door to innovation that is sustained by strong bipartisan political support for new and improved efforts in both prevention and treatment of substance use disorders.

5 Center for Behavioral Health Statistics and Quality. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15-4927, NSDUH Series H-50). Available: http://www.samhsa.gov/data/

6 Rudd, R. A., Seth, P., David, F., & Scholl, L. (2016, December 30). Increases in drug and opioid-involved overdose deaths – United States. Morbidity and Mortality Weekly Report, 65(50-51), 1445-1452. Available: https://www.cdc.gov/mmwr/volumes/65/wr/mm655051e1.htm

7 Levy, S. J., Williams, J. F., & AAP Committee on Substance Use and Prevention. (2016). Substance use screening, brief intervention, and referral to treatment. Pediatrics, 138(1), e20161211. Available: http://pediatrics.aappublications.org/content/138/1/e20161211

8 US Department of Health and Human Services (HHS), Office of the Surgeon General. (2016). Chapter 3. Prevention Programs and Policies. In: Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health. Washington, DC: HHS. Available: https://addiction.surgeongeneral.gov/

Abstinence is an Achievable Goal, both for Prevention and for Treatment 

Embracing and synthesizing the 30 years of science supporting the findings of the 2016 Surgeon General’s Report, the group discussed a single goal for the prevention of addiction: no use of alcohol, nicotine, marijuana or other non-prescribed drugs by youth for reasons of health. This goal should be the core prevention message to all children from a very young age. Health care professionals, educators and parents should understand the importance of this simple, clear health message. They should continue to reinforce this message of no-use for health as children grow to adulthood. Even when prevention fails, it is possible for parents, other family members, friends, primary care clinicians, educators and others to identify and to intervene quickly to stop youth substance use from becoming addiction.7

The science behind this ambitious but attainable prevention goal is clear. Alcohol, nicotine products, marijuana and other non-prescribed drug use is uniquely harmful to the still-developing brains of adolescents. Thus any substance “use” among youth must be considered “misuse” – use that may harm self or others. The goal of no substance use is not just for the purpose of preventing addiction, though that is one clear and important by product of successful prevention. Addiction is a biological process that can take years to develop. In contrast, even a single episode of high-dose use of alcohol or other substance could immediately produce an injury, accident or even death. While it is true that most episodes of substance misuse among adults do not produce serious problems, it is also true that substance misuse is associated with 70% or more of the injuries, disabilities and deaths of young people.8 These figures are even higher for minority youth. Many adolescent deaths are preventable 4 because most are related to substance use – including substance-related motor vehicle crashes and overdose.9

9 Subramaniam, G. A., & Volkow, N. D. (2014). Substance misuse among adolescents. To screen or not to screen? JAMA Pediatrics, 168(9), 798-799. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4827336/

10 Data analyzed by the Center for Behavioral Health Statistics and Quality. CBHS. (2015). Behavioral health trends in the United States: Results from the 2014 National Survey on Drug Use and Health (HHS Publication No. SMA 15- 4927, NSDUH Series H-50).

11 2014 data obtained by IBH from the Monitoring the Future study. For discussion of data through 2013 see DuPont, R. L. (2015, July 1). It’s time to re-think prevention; increasing percentages of adolescents understand they should not use any addicting substances. Rockville, MD: Institute for Behavior and Health, Inc. Available: https://www.ibhinc.org/s/IBH_Commentary_Adolescents_No_Use_of_Substances_7-1-15.pdf

Youth who use any one of the three most common “gateway” substances, i.e., alcohol, nicotine and marijuana, are many times more likely than those who do not use that single drug to use the other two substances as well as other illegal drugs.10 The use of any drug opens the door to an endless series of highly risky decisions about which drugs to use, how much to use, and when to use them. This perspective validates the public health goal for youth of no use of any drug.

Complete abstinence from the use of alcohol or any other drug among adolescents is not simply an idealistic goal – it is a goal that can be achieved. Data were presented at the meeting from the nationally representative Monitoring the Future study showing that 26% of American high school seniors in 2014 reported no use of alcohol, cigarettes, marijuana or other non-prescribed drugs in their lifetimes. 11 This is a remarkable increase from only 3% reported by American high school seniors in 1983. Moreover, in the same survey, 50% of high school seniors had not used any alcohol, cigarettes, marijuana or other non-prescribed substance in the past 30 days, up from 16% in 1982. These largely overlooked and important findings show that youth abstinence from any substance use is already widespread and steadily increasing.

In parallel with the goal of abstinence for prevention, the recommended goal for the treatment of those who are addicted is sustained abstinence from the use of alcohol and other drugs, with the caveat, explicitly acknowledged by the group, that individuals who are taking medications as-prescribed in the treatment of substance use disorders (e.g., buprenorphine, methadone and naltrexone) and who do not use alcohol or other non-prescribed addictive substances – are considered to be abstinent and ”in recovery.” Abstinence from all non-prescribed substance use is the scientifically-informed goal for individuals in addiction treatment. This treatment goal is widely accepted in the large national recovery community. The long-lasting effects of addiction to drugs are easily seen among cigarette smokers: smoking only a single cigarette is a serious threat to the former smoker, even decades after smoking the last cigarette. There is incontrovertible evidence from brain and genetic research showing the long-term effects of substance misuse on critical brain regions.2 It is unknown when or if these brain changes will return to being entirely normal following cessation of substance use; however, it is known that the recovering brain is particularly vulnerable to the effects of return to any substance use, often leading to overdose or rapid re-addiction. 5

Participants in the IBH meeting supported the idea that abstinence is the high-value outcome in addiction treatment; and that while any duration of abstinence is valuable, longer-term, stable abstinence of 5 years is analogous to the widely-used standard in cancer treatment of 5-year survival. The scientific basis for the value of sustained recovery is validated by the experience of the estimated 25 million Americans now in recovery. This increasingly visible recovery community is a remarkable and very positive new force in the country.

Measuring and Attaining these Goals 

The mantra from the IBH meeting was, if you don’t measure it, it won’t happen. The group of leaders recognized the paucity of current models for systematic integration of addiction treatment and general healthcare. The group encouraged the identification of promising models and the promotion of innovation to achieve the goal of sustained recovery. Even programs that include fully integrated care of other diseases, managed care and other comprehensive health programs do not reliably achieve the goal of sustained or even temporary recovery for substance use disorders. The meeting participants noted the absence of long-term outcome studies of the treatment of substance use disorders and encouraged all treatment programs not only to extend the care of discharged patients but also to systematically study the trajectories of discharged patients to improve their long-term treatment outcomes. The increasing range of recovery support services after treatment is an important and promising new trend that is now actively promoting sustained recovery.

Meeting participants noted one particularly promising model of public health goal measurement and attainment – the 90-90-90 goals for the treatment of HIV/AIDS: 90% of people with HIV will be screened to know their infection status; 90% of all people with diagnosed HIV infection will receive sustained antiretroviral therapy; and 90% of all patients receiving antiretroviral therapy will have viral suppression (i.e., zero viral load).12 These measurable goals provide an operational definition of public health success for the country, states and individual healthcare organizations.

12 UNAIDS. (2014). 90-90-90: An Ambitious Treatment Target to Help End the AIDS epidemic. Geneva, Switzerland: Joint United Nations Programme on HIV/AIDS. Available: http://www.unaids.org/sites/default/files/media_asset/90-90-90_en_0.pdf

With this model as background, the IBH group concluded that a similar public health approach and similarly specific numeric goals should be established for preventing and treating substance use disorders. Examples of parallel national prevention goals could include 90% rates of screening for substance misuse among adolescents; 90% provision of interventions and follow-up for those screening positive; and 90% total abstinence rates among youth aged 12-21. While these are admittedly ambitious prevention goals, adoption of them could incentivize families, schools and communities to increase the percentage of youth who do not use any alcohol, nicotine, marijuana or other drugs every year.

A similar approach was adopted by the IBH group to improve the impact of addiction treatment. Again, there would be significant public health value if the US adopted the following goals: 90% of individuals aged 12 or older receive annual screening for substance misuse and substance use disorders; 90% of those who receive a diagnosis of a substance use disorder are referred and meaningfully engaged (at 6 least three sessions) in some form of addiction treatment; and 90% of those engaged in treatment achieve sustained abstinence as measured by drug testing, during and for six months following treatment.

Source:  IBH-Report-A-New-Agenda-to-Turn-Back-the-Drug-Epidemic  May 2017

Carfentanil. If there was ever a drug designed to wreak havoc – this is it!

5 milligrams (about 1/16th the size of a baby aspirin) is strong enough to take down a one-ton Buffalo, actually make that 7 one-ton Buffalos, and it’s readily available through illicit sales on street corners throughout the US. It is also now one of the leading causes of opioid related death, which claimed over 33,000 lives (out of 52,000+ drug related overdose deaths) in 2015, the most recent year for which statistics are available.  Carfentanil first showed up in the Ohio area in mid-2016 and has been advancing it’s destructive power across the nation with a vengeance. If it came in a bottle, it would need to have a warning label that is longer than the Great Wall of China, stating something to the effect of “If you take this drug, you are committing suicide. Avoid it at all costs.” In fact, its only legal use is for the sedation of large animals, like “elephants”. Addicts generally work their way up to Carfentanil. The typical gateway is by medical prescription for something like Oxycontin, with the user then graduating to cheaper heroin once the prescriptions run out. In fact, the majority of heroin users admit they started with prescription opioids. They beckon you like the sirens from Greek mythology, tempting you past your breaking point. It eventually gets to a level that heroin is no longer nearly enough, so you start taking fentanyl, many multiple times stronger than morphine which sucked so many war veterans into addiction during the Vietnam era. Your tolerance builds as your habit expands from a few days a week to every day.  Eventually fentanyl too is not enough. What else is there? Carfentanil. ‘Do I risk it?’ is what an addict should now ask himself, but they rarely listen to their voice of reason. They jump ‘all in’ without any thought or concern of consequences, they just want to get high. Then again, oftentimes they don’t even get to make that choice, it’s made for them. Carfentanil is so cheap that it’s used as an additive on the street.

I read an article the other day where someone bought street Xanax. It was laced with Carfentanil; he was dead within minutes. This same scenario has repeated itself throughout the country, as drug dealers seek to convert a small amount of Carfentanil, into a large amount of sale-able product, mixing it with ‘whatever is available’, solely to line their pockets with addicts’ money. Carfentanil is also a concern for first responders. It is odorless, colorless and can be absorbed via skin contact, inhalation, oral exposure or ingestion. EMS crews typically wear protective gloves and masks because a dose as small as a grain of salt could kill a person even if just absorbed through the skin, much like Anthrax. The increases in opioid-related emergencies are overwhelming the country on a state-by-state and city-by-city basis. Incidents are up 13.3 percent in Minnesota, over 20 percent throughout Ohio and the numbers are even worse in Kentucky, New Hampshire, New Mexico and West Virginia. The growth in Native American communities is by far the worst at 32.7 percent. 50 people recently overdosed in one day alone in Philadelphia, which experienced 35 overdose related deaths over five days. Cincinnati had 174 overdoses in six days, Cleveland 46 in one day and tiny Akron 236 over 20 consecutive days. In Maryland, Gov. Larry Hogan declared a state of emergency after opioids killed nearly 1,500 residents in the first nine months of 2016. The US represents just 4.6 percent of the world’s population, yet we consume 80 percent of its opioids. So, where’s all this Carfentanil coming from?  The usual suspects. China and India were the largest suppliers for the illegal online pharmacies during the early 2000s.

Distributors located in the Caribbean and Central American countries, typically run by American ex-pats, bought knock-offs of everything from Viagra to Xanax to Oxycontin for pennies a pill, sending shipments ‘directly to your door’ without the need of a pesky prescription. Those same large suppliers simply shifted to the next hot product and now sell to Mexican cartels distributing it street-by-street. After recent pressure from the US Drug Enforcement Agency (DEA), China clamped down on bootleg opioid operations to curb the flow of illicit drugs into the US. Yet, the Mexican drug-lords are resourceful. I fear it won’t take too much time for them to find other suppliers to fill the gap. There’s already evidence of them trying to produce substantial quantities on their own, to eliminate the need for an outside source. According to the DEA, 144 people now die each day from a drug overdose. As recently as 10 years ago, gun related deaths outnumbered drug overdose deaths by a factor of 5-to-1. Today more people die from opioids than guns and traffic accidents combined. It is estimated that 600 people try heroin for the first time each and every day. The issue is now mission critical. President Trump has appointed a SWAT Team of business executives to tackle the opioid crisis, led by his son-in-law Jared Kushner, a leading businessman and near billionaire in his own right. They are already working with a ‘Who’s Who’ of Fortune 500 Company leaders including such luminaries as Apple’s Tim Cook and Microsoft’s Bill Gates, just to name a few. Kipu and our sister company, InRecovery Magazine, have reached out to this Team to offer our unique experience, knowledge, perspective and support. We are hopeful that this is a key step toward helping to start to turn the tide in this life-or-death struggle against addiction.

Source: http://campaign.r20.constantcontact.com/render?m=1125801102133&ca=c086bc62-9760-47b5-8dad-385b0609ab8d   May 2017

Background:

Cannabis use (CU) has recently been legalized in several states for medicinal purposes and remains the most commonly used illicit drug. Cardiovascular effects of CU are not well established as studies thus far have been limited by size. We therefore utilized a large national database to examine the incidence of cardiovascular risk factors and events amongst patients with CU.

Methods:

Patients aged 18-55 years with CU were identified in the Nationwide Inpatient Sample 2009-2010 database using the Ninth Revision of International Classification of Disease (ICD) code 304.3. Demographics, risk factors, and cardiovascular event rates were collected on these patients and compared to general population data.

Results:

Incidence of heart failure (HF), cerebrovascular accident (CVA), coronary artery disease (CAD), sudden cardiac death, and hypertension (HTN) were significantly higher in patients with CU. After multivariate regression adjusting for age, gender, diabetes mellitus, HTN, CAD, tobacco use, and alcohol use, CU remained an independent predictor of both HF (OR=1.1 [1.03-1.18], p<0.01) and CVA (OR=1.24 [1.14-1.34], p<0.001).

Conclusions:

CU independently predicted the risks of HF and CVA in individuals 18-55 years old. With continued legalization of cannabis, potential cardiovascular effects and their underlying mechanisms need to be further investigated.

1187-055 – Cannabis Use Predicts Risks of Heart Failure and Cerebrovascular Accidents: Results from the National Inpatient Sample

Background: Cannabis use (CU) has recently been legalized in several states for medicinal purposes and remains the most commonly used illicit drug. Cardiovascular effects of CU are not well established as studies thus far have been limited by size. We therefore utilized a large national database to examine the incidence of cardiovascular risk factors and events amongst patients with CU.

Methods: Patients aged 18-55 years with CU were identified in the Nationwide Inpatient Sample 2009-2010 database using the Ninth Revision of International Classification of Disease (ICD) code 304.3. Demographics, risk factors, and cardiovascular event rates were collected on these patients and compared to general population data.

Results: Incidence of heart failure (HF), cerebrovascular accident (CVA), coronary artery disease (CAD), sudden cardiac death, and hypertension (HTN) were significantly higher in patients with CU. After multivariate regression adjusting for age, gender, diabetes mellitus, HTN, CAD, tobacco use, and alcohol use, CU remained an independent predictor of both HF (OR=1.1 [1.03-1.18], p<0.01) and CVA (OR=1.24 [1.14-1.34], p<0.001).

Conclusions: CU independently predicted the risks of HF and CVA in individuals 18-55 years old. With continued legalization of cannabis, potential cardiovascular effects and their underlying mechanisms need to be further investigated.

Source: http://ativsoftware.com/appinfo.php?page=Inthtml&project=ACC17&server=ep70.eventpilot.us&id=2545   March 2017

The opioid epidemic has led to the deadliest drug crisis in US history – even deadlier than the crack epidemic of the 1980s and 1990s.

Drug overdoses now cause more deaths than gun violence and car crashes. They even caused more deaths in 2015 than HIV/AIDS did at the height of the epidemic in 1995.

A new study suggests that we may be underestimating the death toll of the opioid epidemic and current drug crisis. The study, conducted by researchers at the Centers for Disease Control and Prevention (CDC), looked at 1,676 deaths in Minnesota’s Unexplained Death surveillance system (UNEX) from 2006 – 2015. The system is meant to refer cases with no clear cause of death to further testing and analysis. In total, 59 of the UNEX deaths, or about 3.5 percent, were linked to opioids. But more than half of these opioid-linked deaths didn’t show up in Minnesota’s official total for opioid related deaths.

It is unclear how widespread of a problem this is in other death surveillance systems and other states, but the study’s findings suggest that the numbers we have so far for opioid deaths are at best a minimum. Typically, deaths are marked by local coroners or medical examiners through a system; if the medical examiner marks a death as immediately caused by an opioid overdose, the death is eventually added to the US’s total for opioid overdose deaths. But there is no national standard for what counts as an opioid overdose, so it’s left to local medical officials to decide whether a death was caused by an overdose or not. This can get surprisingly tricky – particularly in cases involving multiple conditions or for cases in which someone’s death seemed to be immediately caused by one condition, but that condition had a separate underlying medical issue behind it.

For example, opioids are believed to increase the risk of pneumonia. But if a medical examiner sees that a person died of pneumonia, they might mark the death as caused by pneumonia, even if the opioids were the underlying cause for the death. “In early spring, the Minnesota Department of Health was notified of an unexplained death: a middle-aged man who died suddenly at home. He was on long-term opioid therapy for some back pain, and his family was a little bit concerned that he was abusing his medication,” said Victoria Hall, one of the study’s authors.

“After the autopsy, the medical examiner was quite concerned about pneumonia in this case, and that’s how the case was referred to the Minnesota Department of Health unexplained deaths program. Further testing diagnosed an influenza pneumonia, but also detected a toxic level of opioids in his system. However, on the death certificate, it only listed the pneumonia and made no mention of opioids.”

Since this is just one study of one surveillance system in one state, it’s unclear just how widespread this kind of underreporting is in the United States. But the data suggests that there is at least some undercounting going on – which is especially worrying, as this is already the deadliest drug overdose crisis in US history. “It does seem like it is almost an iceberg of an epidemic,” said Hall. “We already know that it’s bad. And while my research can’t speak to what percent we’re underestimating, we know we are missing some cases.” In 2015, more Americans died of drug overdoses than any other year on record – more than 52,000 deaths in just one year. That’s higher than the more than

38,000 who died in car crashes, the more than 36,000 who died from gun violence, and the more than 43,000 who died due to HIV/AIDS during that epidemic’s peak in 1995.

See more: • The Changing Face of Heroin Use in the US study • Today’s Heroin Epidemic – CDC

Source:  Prevention Weekly. news@cadca.org  May 2017

Beery points to 50 deaths in 2016, most linked to drugs

Dr. Jeff Beery doesn’t agree with those who think marijuana is a relatively harmless drug that carries medicinal qualities and should even be winked at for recreational purposes.

But Beery doesn’t just think marijuana is a gateway to more dangerous drugs.

“It’s a gateway to hell,” he says flatly.

Beery’s perspective is based on four years serving as Highland County coroner, with more than a decade before that as a deputy coroner. He provided statistics this week from 2016 on 50 fatalities he investigated last year that he deemed suspicious, or at least unusually odd or interesting.

Beery said there has been a steady increase in deaths related one way or another to drugs, raising fatalities connected to illicit drugs to alarming proportions. He said the word “epidemic” is not sufficient to describe the toll being taken on Highland County.  “It’s a craze, not an epidemic,” he said, adding that “epidemic” implies something beyond people’s control.

The 50 cases provided by Beery from 2016 range from deaths by car crashes, burns, gun shots, heart attacks, hyperthermia and suicides to asphyxia and embolisms. But most of them have a common denominator, he said – the presence of drug use, or a history of drug use.

At least eight cases out of the 50 cited by Beery include marijuana as a factor contributing to the fatalities, in his opinion. Six fatalities were connected to heroin, three to cocaine, eight to amphetamines, including methamphetamine, and several to drugs like Xanax, Valium, Clonazepam and, especially, Fentanyl, which has been increasingly found mixed with heroin.

Beery blames a lax attitude by society and particularly by elected officials, including at the state and federal level, for contributing to the rise in drug-related deaths. He said former U.S. Attorney General Eric Holder’s decision not to pursue marijuana charges at the federal level “opened the door to the wild progression of illicit drugs.”

Holder consistently expressed views on marijuana that were opposed to treating the drug as seriously as other narcotics. In a 2016 PBS interview, after he was no longer attorney general, Holder said, “It’s hard for me to imagine ever decriminalizing crack cocaine, drugs like that. But the whole question of should marijuana be decriminalized, I mean, that’s a conversation I think that we should engage in.”

Beery is aware of the fierce pushback among many people and organizations to his stand on marijuana. Groups like the National Organization for the Reform of Marijuana Laws (NORML) – whose mission is “to move public opinion sufficiently to legalize the responsible use of marijuana by adults, and to serve as an advocate for consumers to assure they have access to high quality marijuana that is safe, convenient and affordable,” according to its website – have won referendums and convinced legislatures to at least legalize marijuana for medicinal purposes.

Many patients suffering from certain serious illnesses or chronic pain insist that marijuana is the only effective relief they have found. Beery disagrees, saying marijuana has no medicinal qualities. He blames Ohio’s Republican-led “so-called conservative” legislature for caving in on the medical marijuana issue, even though the consequences of marijuana use and cultivation are obvious, especially in southern Ohio, he said.

“Just look at Pike County,” said Beery, referring to the murders last year of the Rhoden family, where a large marijuana growing operation worth hundreds of thousands of dollars on the street was found.  Beery said a lax attitude about border security and drugs also contributes to the problem.

Beery said that while investigating deaths in recent years, “I would see other things,” ranging from marijuana to heroin to cocaine that, to him, were obvious contributors not just to overdoses but to car wrecks, gun shots, homicides, burns and suicides.

Source: http://timesgazette.com/news/13879/highland-county-coroner-marijuana-is-gateway-to-hell

March 2017

Alzheimer’s and Marijuana ?

An estimated 200,000 people in the United States under age 65 are living with younger-onset Alzheimer’s disease. And hundreds of thousands more are coping with mild cognitive impairment, a precursor to Alzheimer’s and other dementias.

“It’s beyond epidemic proportions. There truly is a tidal wave of Alzheimer’s disease,” said Dr. Vincent Fortanasce, a clinical professor of neurology in Southern California who is also a renowned Catholic bioethicist, author and radio host.

Fortanasce, a member of Legatus’ San Juan Capistrano Chapter, for several years has studied Alzheimer’s disease, its underlying causes and treatments. Through his research, he believes there may be a link between chronic use of marijuana — especially when started at a young age — and Alzheimer’s.

Finding the link

Fortanasce notes that medical research shows chronic users of marijuana, in particular the kind with high quantities of THC, have reduced volume in the hippocampus, the region of the brain responsible for memory and learning. In Alzheimer’s disease, Fortanasce said, medical researchers have also noticed reduced hippocampus volume with increased B-amyloid plaques and neurofibrillary tangles.

Taking into account other factors, such as skyrocketing obesity rates and lack of exercise, Fortanasce argues that chronically smoking marijuana and consuming products laced with cannabis are harming the long-term mental health of millions of young Americans. He is trying to convince the American Academy of Neurology to conduct a major survey to see if people diagnosed with dementia have also smoked marijuana.

Source: :  http://legatus.org/kicking-pot-curb/  April 9th 2017

Misleadingly marketed as a legal and safe alternative to marijuana, synthetic cannabinoids have a variety of adverse health effects. A new review summarizes the clinical cases that have so far been linked to the use of the synthetic substances.

A new review warns that so-called synthetic marijuana is actually very different from cannabis and is potentially unsafe. Synthetic cannabinoids (SCBs) are a type of psychotropic chemical increasingly marketed as a safe and legal alternative to marijuana.

They are either sprayed onto dried plants so that they can be smoked, or they are sold as vaporizable and inhalable liquids.

A new review from the University of Arkansas for Medical Sciences (UAMS) warns against the dangerous side effects of the compounds popularly (and misleadingly) referred to as “synthetic marijuana.”

Referring to the SCBs currently sold as “K2” and “Spice,” Paul L. Prather, a cellular and molecular pharmacologist at UAMS and corresponding author of the review, explains the motivation behind it:

“In the United States, in 2007 or so, we started seeing all kinds of people coming into emergency rooms saying they smoked marijuana, but they had these really bizarre symptoms that did not correspond with the effects you see with marijuana.”

The report, therefore, set out to give an overview of the existing literature on SCBs, and to show that not only are they different from marijuana, but also that they do not constitute an appropriate substitute for cannabis. On the contrary, SCBs are drugs in their own right, with many toxic – and sometimes even fatal – effects. The review has been published in the journal Trends in Pharmacological Sciences.

SCBs are different from marijuana

SBCs are known to create psychotropic effects in much the same way as marijuana – by activating the CB1 cannabinoid receptor, which is found primarily in the brain and the central nervous system. Additionally, in the case of marijuana, its main active ingredient is tetrahydrocannabinol (THC), which also activates the CB2 receptor (found mainly in the immune system).

However, as the authors warn, SCBs activate the CB1 receptor to a much higher intensity than THC does.

William E. Fantegrossi, a behavioral pharmacologist at UAMS and co-author of the review, notes that SCBs “are highly efficacious drugs; they tend to activate the CB1 receptor to a greater degree than we can ever get to with THC from marijuana.”

Additionally, the authors caution that because SCBs are chemically different from THC, they may activate other receptors aside from CB1. These cellular receptors, so far unknown, may be causing the negative health effects noticed in SCB users.

SCBs linked to serious adverse health effects and even death

As reported in the review, some of these effects suggest that SCBs cause much more toxicity than marijuana. Toxicity has been reported across a wide range of systems, including the gastrointestinal, neurological, cardiovascular, and renal systems.

The clinical cases documented in the review include acute and long-term symptoms, such as:

  •  Seizures
  •  Convulsions
  •  Catatonia
  • Kidney injury § Hypertension
  •  Chest pain
  •  Myocardial toxicity
  •  Ischemic stroke

Common adverse effects include prolonged and severe vomiting, anxiety, panic attacks, and irritability. Additionally, SCBs reportedly caused extreme psychosis in susceptible individuals, whereas marijuana only causes mild psychosis in those predisposed.

Furthermore, 20 deaths have been linked to SCBs between 2011 and 2014, whereas no deaths were reported among marijuana users during that time.

Finally, SCBs are likely to result in tolerance, dependence, and withdrawal.

SCBs are not safe, authors warn

Because SCBs cannot be detected by standard drug screening, they are particularly popular among users who want to avoid detection, such as teenagers and army personnel. These users often purchase the drugs online, but as Prather and colleagues warn, customers often do not know what they are purchasing because they get something different each time.

“Not only does the amount of the active pharmacological agent change with different batches of drugs, made by different labs, but the active compound itself can change,” says Fantegrossi. Prather adds that “there are usually a minimum of three, if not five, different synthetic cannabinoids in a single product.”

However, the potential therapeutic benefits of cannabinoids should not be dismissed entirely, write the authors. As with opioids in general, misuse or abuse can have severely adverse or even fatal consequences, but proper use may offer significant benefits.

Overall, though, SCBs should be viewed with suspicion and treated with caution.

“The public sees anything with the marijuana label as potentially safe, but these synthetic compounds are not marijuana […] You never know what they are, and they are not safe.”

Source:  http://www.medicalnewstoday.com/articles/315634.php?mc_cid=4a0d722034&mc_eid=46cee4286 0  Feb 2017

In 2014, recreational cannabis use was legalized in Colorado, and seven other states have since followed suit. With an ever-expanding part of the population using marijuana to cure a number of ailments, researchers at Colorado State University have investigated its effects on mood. The researchers – led by Lucy Troup, assistant professor in the university’s Department of Psychology – publish their findings in the journal PeerJ.

They note that the “relationship between cannabis use and symptomatology of mood and anxiety disorders is complex,” adding that although “a great deal of research exists and continues to grow, the evidence remains contradictory.” Troup and colleagues point to a large international survey published in 2013, in which 5.2 percent of respondents reported that they used cannabis to alleviate depressive symptoms. Meanwhile, a survey of medical marijuana users in California revealed that 26.1 percent of participants reported therapeutic benefits for depression, and 37.8 percent reported benefits for anxiety.

“This trend of self-medication for conditions other than the one prescribed is too large to ignore when investigating the associations between cannabis use and mood disorders,” write the Colorado State University researchers.

They add that this increases “the need to include recreational users for research, especially when the casual user group are most likely recreational users and seem to sustain the greatest deficits in mood.”

Is cannabis used correctly for self-medication? For their study, Troup and colleagues wanted to focus on Colorado, which was the first state to legalize recreational marijuana.

As such, they conducted an in-depth, questionnaire-based study of 178 legal cannabis users who were aged 18-22.

They divided their participants into three groups based on self-reported use: a control group who never used cannabis, a casual user group, and a group of chronic users.

Interestingly, the participants who were categorized with subclinical depression, and who also used cannabis to treat their depressive symptoms, scored lower on anxiety symptoms than on their depressive symptoms. In short, they were more depressed than anxious.

The researchers also say that the self-reported anxiety sufferers were found to be more anxious than depressed.

Study co-author Jacob Braunwalder, a researcher in Troup’s laboratory, says that “if they were using cannabis for self-medication, it wasn’t doing what they thought it was doing.”

The questionnaire used in the study was developed by co-author Jeremy Andrzejewski. Called the Recreational Cannabis Use Evaluation, the questionnaire delved into users’ habits, including whether they smoked cannabis or used stronger products such as hash oils or edibles.

The researchers say that inconsistencies in previous studies are better understood when considering how cannabis use is reported. “Phytocannabinoid type and strength is not consistent between studies,” they say, “and there have been significant changes in the strength of these products post-legalization.”

‘Infrequent users have stronger relationship with negative mood’

Troup and colleagues say that it is important to point out that they looked at the residual effects of cannabis use, not administration of specific doses.

However, they do note that their results “suggested that cannabis use had an effect on measurements of mood disorder symptomatology. In particular, those who used cannabis less frequently, the casual user group, had the strongest correlations with overall score and negative effect on the CES-D [Center for Epidemiological Studies depression scale].”

Interestingly, the researchers did not observe a relationship with pre-anxiety symptoms in the cannabis user groups, compared with controls.

The researchers emphasize that their study does not conclude that cannabis causes depression or anxiety. It also does not show that cannabis cures these conditions. However, they add that their analysis displays a need for further study regarding how cannabis affects the brain.

Andrzejewski adds that “there is a common perception that cannabis relieves anxiety,” but this has not been fully backed by research.

“It is important not to demonize cannabis, but also not to glorify it,” adds Troup. “What we want to do is study it, and understand what it does. That’s what drives us.”

Concluding their study, the researchers write:

“Our data indicate that infrequent users have a stronger relationship with negative mood. Our data suggested that those that use cannabis casually scored higher on the CES-D scale for depression, and consequently could be at greater risk for developing pre-depression symptomology compared to both chronic users and controls.”

It is important to note that the study has limitations, including:

  •  Sample size
  •  Control for phytocannabinoids in terms of strength and type
  •  Confounding variables such as multiple drug use and alcohol consumption
  •  The self-report design
  • A limited interpretation of depression due to lack of clinical evaluation.

Still, the researchers say that their study “provides a starting point from which to design controlled experiments to further investigate the relationship between mood and cannabis use in a unique population.”

Source:  http://www.medicalnewstoday.com/articles/314823.php   Dec. 2014

As Manchester police report a spike in spice related incidents, homeless people say the highly addictive drug is causing deaths.

When Alex first tried spice in 2014, he thought it was cannabis. The 23-year-old had been sleeping on the streets in Manchester after his mum had lost her council house. He was just looking to take his mind off his problems, but at lightning speed he became addicted, buying increasing quantities of the drug to feed his habit.

“I was waking up, buying it, smoking it, going to sleep, waking up, buying it, smoking it, going to sleep again,” he says.

Alex spent about a year addicted to spice, while he was living in tents in the city centre, before kicking the habit near the start of 2016. At the peak of his addiction, he was spending around £200 a week on the drug. “It was horrible,” he says. “Every morning I was waking up being physically sick. I was worn out and tired. I couldn’t eat. I couldn’t drink. My bones kept on aching.”

Spice, one of the names used for a group of substances known as synthetic cannabinoids, has been in the UK for more than a decade and was initially marketed as having effects similar to those of cannabis. The highly addictive psychoactive substance, an illegal class B drug since December, induces an inactive state and in recent years has become commonly used among the UK’s homeless population.

Although charities in other big UK cities report spice addiction as an issue among their homeless communities, Manchester’s problem is particularly visible. Between the city’s main train station and Piccadilly Gardens, a transport and shopping hub, it is common to see figures slumped in doorways apparently passed out after smoking the drug.

Earlier this week, Greater Manchester police released figures showing the burden the drug has placed on the city’s emergency services. The force attended 58 spice-related incidents in the city centre on Friday, Saturday and Sunday last week. There were also 23 incidents to which an ambulance was called, and 18 dispersal orders or directions to leave were issued.

Researchers estimate that 90-95% of homeless people in Manchester smoke the drug. And while there is very little research into the effects of spice on the body, there are scores of reports of people dying after smoking it. “We try and keep our outreach teams away from Piccadilly Gardens,” says Yvonne Hope, operations and resources director at the Manchester-based homelessness charity Barnabus. “It’s so unsafe there now.”

The release of police figures prompted a flurry of media interest in the problem. A series of photographs of homeless spice users in Manchester city centre, some covered in vomit and being helped by emergency services, were published by local and national newspapers. Local charities were critical of the coverage, describing it as dehumanising and sensationalist.

Spice’s main attractions are that it is cheap and strong. It is thought to be imported from China in liquid form, then sprayed on an inert plant such as marshmallow before being sold to be smoked. Only the tiniest amount of the chemical is needed to have an effect.

Alex, who has been helped into supported accommodation by the homelessness charity Depaul UK, is due to start a new job next month. He realised he needed to kick the habit when his former partner refused him access to his daughter. “I went cold turkey,” he says. “I got my cousin to lock me in the back of a van and just leave me there to sweat it out.” The withdrawal symptoms include sweating, vomiting, stomach cramps and headaches, he says.

Standing outside Barnabus’s Beacon drop-in centre – which provides showers, cooked breakfasts and cups of tea to Manchester’s rough sleepers – John and Steve, 52 and 35, agree spice has largely replaced heroin, crack and even alcohol as the drug of choice.

“You can go get a fiver, buy half a gram and it’ll knock you out for a few hours,” says John, who has been homeless since 2014. “It’s better than buying a bottle of White Ace [cider].”

“I have tried heroin and it’s worse than that,” says Steve, adding that friends of his have died after taking spice. The last time he smoked a joint of spice he woke up in a hospital bed, he says. “I don’t touch the stuff any more, it doesn’t agree with me.”

Hope says there has been a rise in crime associated with the drug since it was banned in May last year, with fights breaking out among people who visit the drop-in centre. “Up until about 2015, we had people who were mostly a community and people who respected each other, and spice just seems to have killed that,” she says. The use of spice has also reached crisis point in Britain’s prisons, helped by the fact that it does not show up in routine drugs tests. Dr Robert Ralphs, a senior lecturer in criminology at Manchester Metropolitan University, who has conducted research into the use of spice in the city, says the drug is used partly because of its ability to make hours pass in what feels like a few minutes. “People have told me they’ve used [spice] for the last two or three years, but that it seems like a couple of months,” he says.

Dr Oliver Sutcliffe, a senior lecturer in psychopharmaceutical chemistry at Manchester Metropolitan University, says the strength of the drug can vary wildly, which poses serious health risks. Tests on samples of the drug provided by police show the most recent batch to hit the streets in Manchester was 10 times stronger than is usual.

Sutcliffe says that although the packets look the same, they can contain a range of different cannabinoids at varying strengths. “You’re playing Russian roulette,” he adds. The chemicals found in spice in Manchester have been linked to 10 deaths in Japan.

Peter Morgan, a support worker with Depaul UK who is helping Alex in his transition back to work, says there is a need for rehabilitation programmes like those provided for heroin addicts. “Spice is clearly the strongest drug in the country right now,” he says.

Alex agrees with Morgan and swears he will not touch the drug again. He wants to rebuild his life with his girlfriend and hold down his new job. He says he has seen homeless friends in tears because they want to stop using spice. “But they can’t,” he continues. “Because no one’s going to help them do it.”

Some names in this article have been changed.

What is spice?

Spice, or synthetic cannabis, is not a single drug, but a range of laboratory-made chemicals designed to mimic the effects of the main psychoactive compound in cannabis, tetrahydrocannabinol (THC).

The active substance in spice is mass-produced in underground labs, often in China, and sent to Europe in powder form where suppliers typically spray the chemical on to mixes of herbal leaves that are then sold on. The precise chemical formulation of the drug is constantly shifting, meaning there are potentially hundreds or even thousands of variations available.

The THC in natural cannabis works by travelling through the blood to the brain, where it binds to cannabinoid receptors. The synthetic version does the same thing, but can be 100 times more potent, binding to the receptors more efficiently and in some cases for far longer. This has led to anecdotal reports of people remaining under the “high” of the drug for more than a day.

The precise effects are likely to depend on the chemical formula and, probably more importantly, on the concentration of the substance in the product. Since the drug is sprayed on, even within a single bag of the product there can be highly concentrated “hot spots”. This has made it difficult for scientists to come up with a typical profile of the effects of the drug and associated risks.

The positive short-term effects of spice appear to be approximately similar to that of herbal cannabis: users report feeling warm, happy and relaxed, and sometimes report confusion, paranoia and anxiety. But the adverse effects appear to be more severe and wide-ranging. A characteristic side-effect of smoking cannabis is an increased heart rate and there is some evidence that the cardiovascular effects of synthetic cannabis can be more extreme, with case reports of people having heart attacks and strokes after taking the drug. Cases have also been reported of kidney and liver damage and psychosis.

Little is known about the long-term effects of synthetic cannabis, since these products have only been in widespread recreational use since around 2008.

Source:  https://www.theguardian.com/society/2017/apr/15/its-worse-than-heroin-how-spice-is-ravaging-homeless-communities

I am not a long-time user.  I used casually for about six months, but then suddenly had a terrible experience with marijuana-induced psychosis.   I had moved from a state where is was illegal, to Washington.  A dispensary sold me something incredibly strong just recently, in March.   It was a joint mixed with a marijuana wax- I didn’t even know what that was.  I was SO naive, but there is literally NOTHING out there that lets consumers know that ANYthing even remotely bad can happen.

As long as I didn’t drive under the influence, what could go wrong?   I thought all pot was “safe.”    The irony is that I am nearly 40, a stay-at-home mom with honor roll kids, no history, ZERO history with drug usage, or ANY depression, mental illness etc etc.. NONE.  I never used marijuana before I moved to Washington. I literally just set out to listen to music and unwind while I got the house clean….awaiting the arrival of my husband who was gone on a business trip.   My kids were on Spring break, at a friend’s house.

About halfway through I felt very dizzy and unbalanced… So I thought I just needed to sit down, or maybe eat.. I looked at the glass of wine I had poured… and dumped it in the drain…. Then I had a sudden disturbing image of myself biting THROUGH the wine glass… It came over and over.  Bite the glass….. the words wouldn’t leave my head…. I’m biting glass.  My heart began to race, my hands began to shake. I felt freezing cold, yet was sweating. Then I was feeling a sudden surge of Adrenalin and was panic stricken.  I began having suicidal ideations, in MINUTES…

Shooting Myself and Biting Glass

Over and over and over… shoot yourself… bite through the glass… shoot yourself…and much worse.. it was as if a tape of my worst nightmares were playing over and over and over again in my head…and it was just as physical as it was psychological….. With absolute sincerity, I tell you that I barely made it through that night alive, and even the subsequent days and weeks… I still suffered terrible suicidal ideation……….

NEVER, ever did I have suicidal thoughts or feelings in my life. I am happy, well-adjusted, and a warm, outgoing person with lots of friends and a solid marriage.

Within days I began researching, because I KNEW what I had experienced was from smoking…again, I reiterate, I had nothing else in my system or history to indicate otherwise….and there it was.. All the research indicating that it WAS the pot.. Marijuana-induced psychosis is a proven thing and all too common. There is ZERO safety put in place in these recreational pot stores.  They don’t warn a consumer about strength, concentration or side effects.  It as if you are buying a glass of milk to them!! I later found out that marijuana wax is known as a “dab” and I am still unsure of what they really are…

No Warnings Against Psychosis! The ER in Olympia Washington sees on average TWO cases of marijuana-induced psychosis a DAY!! Yet we don’t hear of this!? Why not? I would have NEVER tried any medicine or drink that could even remotely do this to me, but thought I was using something as harmless as a glass of wine because they say it is.   I can’t even fully describe the horror of that night as it’s very, very hard to revisit. Thank you for warning people.  I am glad I was able to use some of the resources and information you have shared to help recover…….People need to know.  Marijuana can be deadly.   I almost lost everything to very casual use.

I am lucky to have health insurance and lucky that my husband could be with me.  My husband had to take an entire week off to stay home with me! Again how fortunate I am and I’m in the position to have someone that could do that.

I am lucky in that I am NOT an addict or addicted to it. So not using isn’t an issue….. I would never smoke pot again, but the suicidal ideation was so intense and such a terrible and traumatic experience…. It is hard to describe how horrific it is was and I’d rather be tortured than ever experience that again…. I just never thought that was even possible….    From BK, Washington

Source:  http://www.poppot.org/2017/04/14/biting-glass-biting-my-way-delirium/

Please share this post with every concerned parent you know! The Parents Against Pot website has many very useful and interesting articles and testimonies and we would thoroughly recommend anyone interested in the arguments for and against the use of marijuana (pot) to log on to: http://www.poppot.org

Highlights

* Cannabis collisions resulted in 75 deaths and 4407 injuries in 2012.

* There were up to 24,879 victims of property damage only cannabis collisions in 2012.

* Cannabis collisions costs ranged from $1.09 to $1.28 billion CAD in 2012.

* Cannabis collision harms were particularly high amongst those ages 16–34 years old.

Abstract

Introduction

In 2012, 10% of Canadians used cannabis and just under half of those who use cannabis were estimated to have driven under the influence of cannabis. Substantial evidence has accumulated to indicate that driving after cannabis use increases collision risk significantly; however, little is known about the extent and costs associated with cannabis-related traffic collisions. This study quantifies the costs of cannabis-related traffic collisions in the Canadian provinces.

Methods

Province and age specific cannabis-attributable fractions (CAFs) were calculated for traffic collisions of varying severity. The CAFs were applied to traffic collision data in order to estimate the total number of persons involved in cannabis-attributable fatal, injury and property damage only collisions. Social cost values, based on willingness-to-pay and direct costs, were applied to estimate the costs associated with cannabis-related traffic collisions. The 95% confidence intervals were calculated using Monte Carlo methodology.

Results

Cannabis-attributable traffic collisions were estimated to have caused 75 deaths (95% CI: 0–213), 4407 injuries (95% CI: 20–11,549) and 7794 people (95% CI: 3107–13,086) were involved in property damage only collisions in Canada in 2012, totalling $1,094,972,062 (95% CI: 37,069,392–2,934,108,175) with costs being highest among younger people.

Discussion

The cannabis-attributable driving harms and costs are substantial. The harm and cost of cannabis-related collisions is an important factor to consider as Canada looks to legalize and regulate the sale of cannabis. This analysis provides evidence to help inform Canadian policy to reduce the human and economic costs of drug-impaired driving.

Source:  Estimating the harms and costs of cannabis-attributable collisions in the Canadian provinces     Drug & Alcohol Dependence , Volume 173 , 185 – 190

The Centers for Disease Control and Prevention (CDC) stated that 33,091 people died from opioid overdoses in 2015, which accounts for 63 percent of all drug overdose deaths in the same year. A recent report from the CDC found that drug deaths from fentanyl and other synthetic opioids, other than methadone, rose 72 percent in just one year, from 2014 to 2015. Last year, the death of music icon Prince was linked to fentanyl and the prescription drug has become a source of concern for government agencies and law enforcement officials alike, as death rates from fentanyl-related overdoses and seizures have risen across the country.

What exactly is fentanyl?

According to the National Institute on Drug Abuse, fentanyl is a powerful synthetic opioid analgesic that is similar to morphine – but is 50 to 100 times more potent. It is a schedule II prescription drug, and it is typically used to treat patients with severe pain or to manage pain after surgery. It is also sometimes used to treat patients with chronic pain who are physically tolerant to other opioids. In its prescription form, fentanyl is known by such names as Actiq®, Duragesic® and Sublimaze®. Like heroin, morphine and other opioid drugs, fentanyl works by binding to the body’s opioid receptors, which are found in areas of the brain that control pain and emotions.

When opioid drugs bind to these receptors, they can drive up dopamine levels in the brain’s reward areas, producing a state of euphoria and relaxation. But fentanyl’s effects resemble those of heroin and include drowsiness, nausea, confusion, constipation, sedation, tolerance, addiction, respiratory depression and arrest, unconsciousness, coma and death.

So why is abuse and misuse of fentanyl so dangerous?

When prescribed by a physician, fentanyl is often administered via injection, transdermal patch or in lozenges. However, the fentanyl and fentanyl analogs associated with recent overdoses are produced in clandestine laboratories.

This non-pharmaceutical fentanyl is sold in the following forms: as a powder; spiked on blotter paper; mixed with or substituted for heroin; or as tablets that mimic other, less potent opioids. Fentanyl sold on the street can be mixed with heroin or cocaine, which markedly amplifies its potency and potential dangers.

Users of this form of fentanyl can swallow, snort or inject it, or they can put blotter paper in their mouths so that the synthetic opioid is absorbed through the mucous membrane. Street names for fentanyl or for fentanyl-laced heroin include Apache, China Girl, China White, Dance Fever, Friend, Goodfella, Jackpot, Murder 8, TNT, and Tango and Cash.

Can misuse of fentanyl lead to death?

Opioid receptors are also found in the areas of the brain that control breathing rate. High doses of opioids, especially potent opioids such as fentanyl, can cause breathing to stop completely, which can lead to death. The high potency of fentanyl greatly increases risk of overdose, especially if a person who uses drugs is unaware that a powder or pill contains fentanyl.

The United States Drug Enforcement Administration issued a nationwide alert in 2015 about the dangers of fentanyl and fentanyl analogues/compounds. Fentanyl-laced heroin is causing significant problems across the country, particularly as heroin use has increased in recent years.

Source: http://drugfree.org/newsroom/news-item/overdose-deaths-fentanyl-rise-know/   Jan 18th 2017

Once again, the echo chamber nature of press releases serves to promote misleading science and health clickbait.  This time it is with headlines like “Tobacco, but not pot, boosts early stroke risk.”

First, it is an imprecise conclusion based on the newly published study.  Second, the research it refers to downplays the significant flaws and limitations of its own work.

Let’s break down the findings for you to draw accurate (and your own) conclusions.  The goal of the work was to determine whether there is an “association between cannabis use and early-onset stroke, when accounting for the use of tobacco and alcohol.”

Who was studied and how was the data acquired? (1)

* Population-based cohort study comprised of 49,321 Swedish men (born between 1949 and 1951) aged 18-20 years old during 1969/70 when conscripted into military service

* All men— at time of conscription— underwent 2-day screening procedure inclusive of a health examination and completion of 2 questionnaires: 1) substance use, 2) social and behavioral factors

* In 1969/70, the conscripts were asked about cannabis, alcohol and tobacco smoking habits.  Vital signs and a physician assessment were performed then and those with Diabetes Mellitus and Migraines were documented.  The researchers linked their data with parental records to assess parental history of death by cardiovascular disease (CVD) and socioeconomic status in childhood based on the father’s occupation.

* Information on stroke events up to around 60 years of age was obtained from national databases; this includes strokes experienced before 45 years of age

* Participants were followed to assess the initial occurrence of strokes (fatal or nonfatal) from 1971-2009 (between roughly ages 20-59) by collecting information through national public hospital and death record databases.

How was the data analyzed?

* After computation of crude models, the authors estimated a model adjusting for body mass index, systolic and diastolic blood pressure along with the other original (from 1969/70) parameters, additionally adjusting for indicators of socioeconomic status until young adulthood, and additionally adjusting for tobacco smoking and alcohol consumption What does Cannabis, Tobacco, Alcohol Use, and the Risk of Early Stroke:  A Population-Based Cohort Study of 45,000 Swedish Men in the journal STROKE claim?

* We found no evident association between cannabis use in young adulthood and stroke, including strokes before 45 years of age.  Tobacco smoking, however, showed a clear, dose-response shaped association with stroke.  In multivariate-adjusted models, the elevated hazards were attenuated both in relation to heavy cannabis use and high alcohol consumption

CONTRADICTION:  “Cannabis use showed no association with stroke before 45 years of age” “Crude models demonstrated that the hazard of ischemic stroke until 59 years of age was almost 2 times higher among men who were heavy cannabis users in young adulthood than among nonusers.”

* Although an almost doubled risk of ischemic stroke (2) was observed in those with cannabis use >50 times, this risk was attenuated when adjusted for tobacco usage.

*

* Smoking more than or equal to 20 cigarettes per day was clearly associated both with strokes before 45 years of age (more than 6 times higher than nonsmokers) and with strokes throughout the follow-up.

*

* 1037 first-time strokes occurred during the follow-up period until 59 years of age, before age 45 specifically there were 192.  Ischemic strokes were significantly more common than hemorrhagic in all categories.

*

* Most common factors of men with stroke before age 60:  parental history of CVD, overweight, poor cardiorespiratory fitness, low socioeconomic position in childhood, short schooling, heavy smoking, high alcohol consumption (in those before 45 risk 4 times higher than nondrinkers).

*

* High blood pressure and heavy cannabis use seemed to be more prevalent among men having a stroke before 45 years of age but did not differ to the same extent between men with and without stroke when followed until age 60

The many FLAWS in this study…

* The researchers lacked the knowledge of adulthood levels of abuse or use of cannabis, tobacco and alcohol (or other drugs) along with environmental exposures during the military service and after in their respective occupations and lifestyles.

*

* No life long or adult disease diagnoses or medication use were included or known (migraine and diabetes were “estimated”

* )

* Basically, there was no follow-up data to the baseline 1969/70 figures.

*

* Such statistics are vital to understanding contributions to strokes in later life outside of adolescence.

*

* Their early data required substance abuse self-reporting which is traditionally under-reported and demonstrated lower norms than the previous and subsequent year anonymous data they had from other conscript surveys.

*

* This report makes no reference to the varying ingredients and changes in modern day cannabis or tobacco and so on to those of that era or the intervening time period

* Only military young men were studied.  The data may not be able to be generalized to other populations.

*

* MAIN PROBLEM:  The cannabis users were routinely tobacco and alcohol users as well— sometimes tobacco is added to cannabis cigarettes (aka joints).  The authors used “crude modeling” to eliminate those confounding factors which reflects math magic more than actual reality.  Multi-drug use is a challenge to the attainment of sufficient data to interpret.  The ideal study would compare full-on abstainers as a control group to only cannabis users to only tobacco users to only alcohol abusers by quantifying their varying degrees of use.

Take Home Messages…

Epidemiological studies are routinely flawed as associations can be mathematically fit into the desired framework.  Otherwise stated, when we look for something we tend to find it.  The notion that the method used to eliminate for tobacco or alcohol use, for example, in assessing the cannabis issue as an effective strategy is not one to which I subscribe. Even an author of the study, Dr. Anna-Karin Danielsson of Karolinska Institute in Stockholm, revealed to Reuter’s Health:

“The almost doubled risk of ischemic stroke following heavy cannabis use that was observed in our study disappeared when we controlled for tobacco smoking.”  But, she added, the fact that almost all the pot smokers were also tobacco smokers makes it hard “to rule out possible associations between cannabis and stroke.”

There is no doubt —which the authors of this study appreciate— that more research needs to be done on the health effects of cannabis.  There is a growing existing body of literature linking cannabis use to stroke especially in young adults. (3)  Typically, these are in current or heavy users who also are tobacco smokers.  A United States study deemed “cannabis use was associated with a 17% increase in the risk of hospitalization because of acute ischemic stroke, even if both tobacco and amphetamine use constituted bigger risks” while another found its abuse or dependence was linked to ischemic, not hemorrhagic stroke.  (4)  The National Institute on Drug Abuse is a valuable resource, click here.

Once again, exercising, eating and sleeping well, maintaining an optimal weight, pursuing education, and avoiding such substances as marijuana, tobacco smoking along with heavy and binge alcohol consumption will likely best serve all of us and our well-being.  As the laws begin changing with respect to marijuana legality and accessibility, the necessary work needs to be done to determine the genuine risks of its use and abuse so as to most aptly inform the public.

NOTES: (1)  The bullet point answers are direct or paraphrased quotes from the study itself.

(2)  This paper explored ischemic and hemorrhagic strokes, more so the former.  Ischemic ones occur when something blocks the flow of blood to the brain like a clot, for example, so that that region of the brain gets deprived of proper nourishment

and oxygen and is injured as a result.  Hemorrhagic is when too much blood or a massive bleed injures the brain tissue.

Source:  National Families in Action’s The Marijuana Report <srusche=nationalfamilies.org@mail116.atl11.rsgsv.net>; 11th January 2017

Researchers who tested marijuana sold in Northern California found multiple bacterial and fungal pathogens that can cause serious infections. The study was published this month in the journal Clinical Microbiology and Infection.

The mould and bacteria was so widespread and potentially dangerous that the UC Davis academics concluded that they cannot recommend smoking raw or dried weed. “We cannot recommend inhaling it,” says George Thompson III, an associate professor of clinical medicine at the university who helped conduct the cannabis research.

The findings might also apply to indoor, hydroponic marijuana popular at Southern California collectives, according to Thompson. Using pot in baked goods such as brownies might be “theoretically” safer because the products could be heated enough to kill bacteria and fungus, he says.

Asked if concentrates such as wax, honey oil, dabs and shatter would be safe because heat is involved in the production process of “butane extraction,” Thompson says he isn’t sure.

The key finding of the research  is that patients with weak immune systems, such as those with HIV or cancer, should avoid smoking raw and dried pot. Though Thompson told the Sacramento Bee that “for the vast majority of cannabis users, this is not of great concern,” he stresses that there really isn’t a safe way to smoke marijuana buds, even for those who are healthy.

He says it’s possible that filters used with tobacco cigarettes could help with marijuana: Tobacco and all natural plant products have these kinds of bacterial and fungal issues. Irradiated marijuana, though unappealing, also could be an answer, he adds.

Researchers sampled weed samples from Northern California dispensaries and found they tested positive for the fungi Cryptococcus, Mucor and Aspergillus, and for the bacteria E. coli, Klebsiella pneumoniae and Acinetobacter baumannii. The academics said these can lead to serious and lethal illness, noting that smoking the mould and bacteria can embed them directly where they can do the most damage — the lungs.

“Infection with the pathogens we found in medical marijuana could lead to serious illness and even death,” Joseph Tuscano, a professor of internal medicine at UC Davis, said in a statement. “Inhaling marijuana in any form provides a direct portal of entry deep into the lungs, where infection can easily take hold.” The state Department of Public Health is working on guidelines for marijuana testing with the goal that both medical and recreational pot sold next year at permitted dispensaries would be labelled as safe. It’s not clear how this research will affect those guidelines. Thompson says he has reached out to state officials to share his findings.

“We are aware of the study, and while it’s certainly concerning, this is exactly why we need regulation,” Alex Traverso, spokesman for the state Bureau of Medical Cannabis Regulation, said via email. “The Bureau is working with the Department of Public Health to develop strong standards for testing because patient safety is extremely important to us all.”

Source: http://www.laweekly.com/news/marijuana-is-not-safe-to-smoke-researchers-say-7927826 Wednesday, Feb. 14, 2017

Abstract

Background Amphetamine abuse is becoming more widespread internationally. The possibility that its many cardiovascular complications are associated with a prematurely aged cardiovascular system, and indeed biological organism systemically, has not been addressed.

Methods

Radial arterial pulse tonometry was performed using the SphygmoCor system (Sydney). 55 amphetamine exposed patients were compared with 107 tobacco smokers, 483 non-smokers and 68 methadone patients (total=713 patients) from 2006 to 2011. A cardiovascular-biological age (VA) was determined.

Results

The age of the patient groups was 30.03±0.51–40.45±1.15 years. This was controlled for with linear regression. The sex ratio was the same in all groups. 94% of amphetamine exposed patients had used amphetamine in the previous week. When the (log) VA was regressed against the chronological age (CA) and a substance-type group in both cross-sectional and longitudinal models, models quadratic in CA were superior to linear models (both p<0.02). When log VA/CA was regressed in a mixed effects model against time, body mass index, CA and drug type, the cubic model was superior to the linear model (p=0.001). Interactions between CA, (CA)2 and (CA)3 on the one hand and exposure type were significant from p=0.0120. The effects of amphetamine exposure persisted after adjustment for all known cardiovascular risk factors (p<0.0001).

Conclusions

These results show that subacute exposure to amphetamines is associated with an advancement of cardiovascular-organismal age both over age and over time, and is robust to adjustment. That this is associated with power functions of age implies a feed-forward positively reinforcing exacerbation of the underlying ageing process.

To read the whole research study log on to:

Source:    http://dx.doi.org/10.1136/heartasia-2016-010832

UC Davis researcher Dr. George Thompson advises cancer patients and others with weakened immune systems to avoid vaping or smoking marijuana.

In uneasy news for medical marijuana users, UC Davis researchers have identified potentially lethal bacteria and mold on samples from 20 Northern California pot growers and dispensaries, leading the doctors to warn patients with weakened immune systems to avoid smoking, vaping or inhaling aerosolized cannabis.

“For the vast majority of cannabis users, this is not of great concern,” said Dr. George Thompson, professor in the UC Davis Department of Medical Microbiology and Immunology. But those with weakened immune systems – such as from leukemia, lymphoma, AIDS or cancer treatments – could unwittingly be exposing themselves to serious lung infections when they smoke or vape medical marijuana.

“We strongly advise them to avoid it,” Thompson said.

The study’s findings were published online in a research letter in the journal Clinical Microbiology and Infection.  It comes as California and a majority of states have eased laws on medical and recreational marijuana use, and a majority of U.S. doctors support the use of medical marijuana to relieve patients’ symptoms, such as pain, nausea and loss of appetite during chemotherapy and other treatments.

Typically, patients with lower-functioning immune systems are advised to avoid unwashed fruits or vegetables and cut flowers because they may harbor potentially harmful bacteria and mold, or fungi. Marijuana belongs in that same risk category, according to Thompson.

“Cannabis is not on that list and it’s a big oversight, in our opinion,” Thompson said. “It’s basically dead vegetative material and always covered in fungi.”

The study began several years ago after Dr. Joseph Tuscano, a UC Davis blood cancer specialist, began seeing leukemia patients who were developing rare, very severe lung infections. One patient died.

Suspecting there might be a link between the infections and his patients’ use of medical marijuana, Tuscano teamed with Thompson to study whether soil-borne pathogens might be hiding in medical marijuana samples.

The marijuana was gathered from 20 Northern California growers and dispensaries by Steep Hill Labs, a cannabis testing company in Berkeley. It was distilled into DNA samples and sent to UC Davis for analysis, which found multiple kinds of bacteria and fungi, some of which are linked to serious lung infections.

There was a “surprisingly” large number of bacteria and mold, said Donald Land, a UC Davis chemistry professor who is chief scientific consultant for Steep Hill Labs. The analysis found numerous types of bacteria and fungi, including organic pathogens that can lead to a particularly deadly infection known as Mucor.

“There’s a misconception by people who think that because it’s from a dispensary, then it must be safe. That’s not the case,” said UC Davis’ Tuscano. “This is potentially a direct

inoculation into the lungs of these contaminated organisms, especially if you use a bong or vaporization technique.”

Patients with compromised immune systems are especially susceptible to infections, usually acquired in their environment or in the hospital. But given the testing results, Tuscano said, it’s possible that even some of the more common infections, such as aspergillus, could also be attributed to contaminated medical marijuana.   Tuscano emphasized that until more research is done, he can’t be 100 percent assured that contaminated cannabis caused the infections, but “it’s highly suspicious.” Under California’s Proposition 64, the voter-approved initiative that eased restrictions on personal marijuana use, the state is expected to have cannabis testing regulations in place for medical marijuana by Jan. 1.

“Patient safety is one of our chief concerns in this process,” said Alex Traverso, spokesman for the state Bureau of Medical Cannabis Regulation, in an email. He said the state’s new medical-marijuana testing standards will soon be available for public review. “We welcome everyone’s input to ensure that testing standards are as strong as we need them to be.”

Until then, consumers are largely on their own.  The vast majority of cannabis sold in California is not tested, according to Land.

“You can’t tell what’s in (a marijuana product) by looking at it, smelling it, feeling it, or a person in a dispensary telling you it’s safe or clean,” he said. “The only way to ensure you have a safe, clean product is to test it and be sure it’s handled according to good manufacturing practices.”

Some medical marijuana clinics already do voluntary testing of their products. Kimberly Cargile, director of A Therapeutic Alternative, a medical marijuana clinic in Sacramento, said a sample from every incoming pound of pot is sent to a local, independent testing lab.

“It’s for consumer protection. It’s a healthy first step,” Cargile said.

To avoid the risk of exposure to severe lung infections, Thompson and Tuscano advise cancer patients and others with hampered immune systems to avoid smoking, vaping or inhaling aerosolized cannabis altogether. Cannabis edibles, such as baked cookies or brownies, could be a safer alternative.  Theoretically, Thompson said, the consumption of cooked edibles seems safer than smoking or vaping, but it’s not scientifically proven.

“I give that advice with a caveat: We don’t know it’s safer; we think it probably is,” he said.

For patients heeding the UC Davis advice to avoid smoking or vaping medical marijuana, “it’s always better to err on the side of caution,” said medical marijuana advocate Cargile. There are plenty of alternatives, she noted, including cannabis salves, lotions, sprays, tinctures and suppositories.

Source:  http://www.sacbee.com/news/local/health-and-medicine/article131391629.html Feb.2017

Since the state legalized marijuana for recreational use, the Colorado Department of Public Health and Environment has issued a report on marijuana and health every two years. Colorado legalized recreational pot in 2012 to go into effect in 2014. This is the second health report. The report contains a huge amount of data. An executive summary appears on pages 1-6. The most startling data about the consequences of legalization are the number of marijuana-related hospitalizations that have occurred from 2000, the year Colorado legalized marijuana for medical use to September 2015, 21 months after recreational legalization began. A graph showing rates of these hospitalizations by age is pictured below. They are rates per 100,000 and have nearly doubled among adolescents and quintupled among young adults. A graph of the data broken down by race on page 291 of the report are equally stunning. Read report here.

Source:  http://themarijuanareport.org/  Feb.2017

Jamaica’s recent decriminalization of possession of up to two ounces of ganja is contributing to a dangerous practice that officials warn needs urgent attention.

Disturbing findings in the 2016 National Drug Prevalence Survey show that one in six males and 17 females drive under the influence, with most admitting to using ganja since it has been decriminalized.

Executive director of the National Council on Drug Abuse Michael Tucker has raised a red flag about the data, which he said highlights the fact that people behind the wheel as well as non-drivers are in serious danger.

He told the Jamaica Gleaner: “This is very troubling, as potentially these persons are not only a harm to themselves, but to other users of the road. Many times they might be carrying passengers, including children.”

More than 4,500 people across Jamaica participated in the survey conducted in April and July last year which sought to find out the pattern of substance abuse among citizens between 12 and 65, and attitudes towards ganja decriminalization, among other things. Tucker was particularly concerned that some of the frequent road users, including the drivers of public transport, were among the offenders.

“We don’t want to raise any alarm on a particular group of persons, but if you look at the population, I would assume that a reasonable number of them, (respondents) would have come from that group (bus drivers),” he said.

At the same time, vice-chairman of the National Road Safety Council Dr Lucien Jones lamented that the problems associated with drug use were often misunderstood and underestimated.  Pointing to police data, he noted that distracted driving has been identified as one of the main causes of accidents.

“It goes back to the basic problem we have on the road, which is indiscipline. It’s a mindset, which we are definitely trying to change. So it’s one other issue, apart from just driving recklessly on the road. It’s a major concern for us that people don’t understand the problems, which are associated with drug use,” Jones told The Gleaner.

Health Minister Dr Christopher Tufton has suggested that educating citizens about the effects of substance abuse is a key way to tackle the problem.

He noted that while Jamaica is positioning itself to be a major player in the marijuana industry, government would ensure that the drug is not misused or abuse.

Source:  http://www.caribbean360.com/news/jamaica_news/influence-jamaicans-driving-high#ixzz4WEiVvycI   Caribbean360 – January 18, 2017

Once you drop, you can’t stop – sometimes for up to 15 hours. Images revealing how LSD interacts with receptors in the brain could explain why a trip lasts so long, while another study involving a similar receptor unpicks how the drug makes these experiences feel meaningful.

LSD acts on with a number of different receptors in the brain, including ones for the chemicals serotonin and dopamine, but it’s not known exactly which receptors are responsible for its various effects. Daniel Wacker and his colleagues at the University of North Carolina, Chapel Hill, used crystallography to look at the structure of LSD when it binds to a receptor in the brain that normally detects serotonin. They discovered that part of this serotonin 2B receptor acts as a lid, closing around the LSD molecule and trapping it.

This could explain the extended trips the drug produces. “It takes LSD very long to get into the receptor, and once it’s stuck it doesn’t go away,” says Wacker.

However, there is conflicting evidence. Other studies have shown that LSD hangs around in the blood for a long time. “No prolonged action at the receptor is needed to explain the duration of action,” says Matthias Liechti at the University of Basel, Switzerland.

But if Wacker is right, the fact that LSD seems to get stuck inside the receptor might mean it can have effects at very low doses. In recent years, there have been reports of some people taking LSD in amounts too small to cause hallucinations, in an attempt to boost creativity or general well-being.

There’s little hard evidence about whether this microdosing works, but Wacker says psychoactive effects at low doses are plausible. “Our study suggests even very low amounts of LSD may be enough to cause psychoactive effects.” Scientific interest in LSD’s clinical use has revived in recent years – notably to relieve severe psychiatric conditions such as PTSD and anxiety. There are also signs that LSD has helpful non-psychoactive effects on other ailments, such as cluster headaches.

Suppressing bliss

A second study finds evidence that LSD affect the brain by binding to serotonin receptors, and hints at possible ways to harness some of its effects therapeutically. Katrin Preller and her colleagues at the University of Zurich, Switzerland, gave 22 volunteers 100 micrograms of LSD each to determine the role of the serotonin 2A receptor, which is similar to the one studied by Wacker’s team.

In some of the tests, subjects were also given ketanserin, a drug that blocks the serotonin 2A receptor. In those tests, the trippy effects of LSD – including hallucinations, feeling separate from the body, and feelings of bliss – were completely blocked, showing that this receptor must be responsible for them.

The researchers also played songs to the participants. Some of the songs were ones the volunteers had chosen as meaningful beforehand, while others were not. While on LSD, they rated what had been non-meaningful songs as highly meaningful – an effect that, once again, ketanserin blocked.

Preller thinks these findings suggest that the serotonin 2A receptor is important for how we decide which things are relevant to us. “This is something that’s incredibly important for our everyday life,” she says. “We do it constantly, for example if you see a familiar face.”

Some psychiatric conditions, such as schizophrenia and phobias, are associated with paying too much attention to unimportant stimuli. Preller speculates that LSD might help people refocus their attention in a different direction.

“If you have a depressed patient ruminating about negative thoughts, LSD might facilitate a process where you attribute meaning to other things,” says Preller.

Alternatively, people with these conditions might benefit from drugs that reduce the action of the serotonin 2A receptor, like ketanserin.

Source: Journal reference: Current Biology, DOI: 10.1016/j.cub.2016.12.030 Journal reference: Cell, DOI: 10.1016/j.cell.2016.12.033

A medical marijuana patient in Lower Sackville, N.S., said he’s worried after the marijuana he consumed for nearly a year was recalled by Health Canada because it was grown with two pesticides that, if heated, can emit hydrogen cyanide.

John Percy, 67, smokes, vapes and bakes his cannabis to control pain in his hip caused by osteoarthritis. The former Green Party leader had been ordering his medical marijuana from OrganiGram in Moncton, N.B., the only licensed producer in Atlantic Canada.

He said his pain was an “eight out of 10.”

“I was shocked,” said Percy, when he first learned of the voluntary recall in late December. The letter said the marijuana he consumed “tested positive for bifenazate and/or myclobutanil, both unapproved pesticides and not registered for use on marijuana.”

“I assumed like most patients that the product would be organic,” he said.

According to Health Canada hydrogen cyanide interferes with how oxygen is used in the body and may cause headaches, dizziness, nausea, and vomiting. Larger concentrations may cause gasping, irregular heartbeats, seizures, fainting, and even death.

‘I got angry’

He said he was willing to take a wait-and-see approach. But less than two weeks later, there was another, higher-level recall notice from OrganiGram saying all products manufactured since February had been recalled.

“That’s when I got angry and I started to consider what the effects on me have been,” said Percy, who also sits on the board of Maritimers Unite for Medical Marijuana.

He said he plans to talk to his doctor about whether the recalled medical marijuana he’d been consuming, about three grams a day, has adversely affected his health.

‘Patient safety at risk’

Percy said he’s upset that Health Canada did not issue a mandatory recall. Health Canada said no cases of adverse reactions have been reported.

“Putting patient safety at risk is unacceptable, and for a government department that is supposed to take care of people’s safety, I think they’ve fallen down on the job,” said Percy.

He said he’s written to the health minister and to members of Parliament. He believes Health Canada should test marijuana for more than 13 compounds to ensure it’s safe for consumption.

Percy said he and other licensed medical marijuana patients have discussed starting a class-action lawsuit.

Without a licensed producer, he’s going to an illegal dispensary — and paying 30 per cent more for his medication. There’s no compassionate pricing at the illegal spot, so his monthly marijuana budget has shot up to about $850 from $600. “It hurts, it hurts,” he said.

He said getting a prescription filled for another one of the 30-plus licensed producers in Canada would take months, but didn’t want to wait in pain.

Source:  https://ca.news.yahoo.com/medical-marijuana-user-shocked-recall-120500202.html

Abstract

The objective of the present research was to examine the association between lifetime cannabis use disorder (CUD), current suicidal ideation, and lifetime history of suicide attempts in a large and diverse sample of Iraq/Afghanistan-era veterans (N = 3233) using a battery of well-validated instruments.

As expected, CUD was associated with both current suicidal ideation (OR = 1.683, p = 0.008) and lifetime suicide attempts (OR = 2.306, p < 0.0001), even after accounting for the effects of sex, posttraumatic stress disorder, depression, alcohol use disorder, non-cannabis drug use disorder, history of childhood sexual abuse, and combat exposure.

Thus, the findings from the present study suggest that CUD may be a unique predictor of suicide attempts among Iraq/Afghanistan-era veterans; however, a significant limitation of the present study was its cross-sectional design. Prospective research aimed at understanding the complex relationship between CUD, mental health problems, and suicidal behavior among veterans is clearly needed at the present time.

Source:  https://www.ncbi.nlm.nih.gov/pubmed/28129565 J Psychiatr Res. 2017 Jan 5;89:1-5. doi: 10.1016/j.jpsychires.2017.01.002. [Epub ahead of print]

Abstract

Cannabis use is observationally associated with an increased risk of schizophrenia, but whether the relationship is causal is not known.

Using a genetic approach, we took 10 independent genetic variants previously identified to associate with cannabis use in 32,330 individuals to determine the nature of the association between cannabis use and risk of schizophrenia. Genetic variants were employed as instruments to recapitulate a randomized controlled trial involving two groups (cannabis users vs nonusers) to estimate the causal effect of cannabis use on risk of schizophrenia in 34 241 cases and 45 604 controls from predominantly European descent.

Genetically-derived estimates were compared with a meta-analysis of observational studies reporting ever use of cannabis and risk of schizophrenia or related disorders. Based on the genetic approach, use of cannabis was associated with increased risk of schizophrenia (odds ratio (OR) of schizophrenia for users vs nonusers of cannabis: 1.37; 95% confidence interval (CI), 1.09-1.67; P-value=0.007). The corresponding estimate from observational analysis was 1.43 (95% CI, 1.19-1.67; P-value for heterogeneity =0.76).

The genetic markers did not show evidence of pleiotropic effects and accounting for tobacco exposure did not alter the association (OR of schizophrenia for users vs nonusers of cannabis, adjusted for ever vs never smoker: 1.41; 95% CI, 1.09-1.83). This adds to the substantial evidence base that has previously identified cannabis use to associate with increased risk of schizophrenia, by suggesting that the relationship is causal. Such robust evidence may inform public health messages about cannabis use, especially regarding its potential mental health consequences.

Source:Molecular Psychiatry advance online publication, 24 January 2017; doi:10.1038/mp.2016.252.

The letter below speaks of the heroin epidemic in the USA.  The figure of heroin and opioid addiction that has destroyed countless families and killed more than 50,000 Americans in 2015 alone is salutary.

A chronicle of President Barack Obama’s tenure must include the heroin epidemic that he leaves us with. Our nation is plagued with a systemic heroin and opioid addiction that has destroyed countless families and killed more than 50,000 Americans in 2015 alone. This one-year death toll is greater than the total number of Americans killed in action during the Vietnam War.

The opioid casualty count only tells part of the story. More than half a million Americans admit to being addicted to heroin, and each of them has a very difficult, if not impossible, road to recovery. Yet, heroin flows into our nation every day and is readily available for $5 a bag 24/7 on street corners throughout the cities and suburbs of America.

How was this level of accessibility not reason enough for President Obama to make slowing our porous borders a priority?  Obama, in his final days as president is now becoming more vocal about the epidemic he leaves behind. However, this is too little, too late in the extreme. His record-setting pardoning and lessening of drug dealer sentences, which have included heroin dealers, further erodes his record on the heroin epidemic. Classifying a heroin dealer as a nonviolent criminal in the face of the American opioid death toll is nonsense.

Perhaps Obama was one of the lucky ones that didn’t have a close friend or relative addicted or taken by heroin and he just didn’t notice the plague that took root under his watch.

Robert Cochran Stafford

Source:  http://www.app.com/story/opinion/readers/2017/01/14/letter-obama-legacy-includes-drug-addiction-epidemic/96557686/

Regularly smoking cannabis may damage users’ eyesight by triggering an abnormality in the retina, a new study has found.   Researchers in France tested 28 cannabis smokers and 24 people who did not use the drug to see how well their retinal cells responded to electrical signals.

A small but significant delay was found in the time taken for the signals to be processed by the retina of the marijuana users by comparison with the control group.  “This finding provides evidence for a delay of approximately 10 milliseconds in the transmission of action potentials evoked by the retinal ganglion cells,” the researchers wrote in the JAMA Ophthalmology.

“As this signal is transmitted along the visual pathway … to the visual cortex, this anomaly might account for altered vision in regular cannabis users. Our findings may be important from a public health perspective since they could highlight the neurotoxic effects of cannabis use on the central nervous system as a result of how it affects retinal processing.”

A statement issued by the Journal of the American Medical Association described the study as “small” and “preliminary”.  But the researchers, led by Dr Vincent Laprevote, of the Pole Hospitalo-Universitaire de Psychiatrie du Grand Nancy, added: “Independent of debates about its legalisation, it is necessary to gain more knowledge about the different effects of cannabis so that the public can be informed.   “Future studies may shed light on the potential consequences of these retinal dysfunctions for visual cortical processing and whether these dysfunctions are permanent or disappear after cannabis withdrawal.”

In a related article commenting on the research, Dr Christopher Lyons, of the University of British Columbia in Vancouver, and Dr Anthony Robson, of Moorfields Eye Hospital, London, wrote that it dealt with “an important and neglected issue, namely the possible toxic effects of cannabis, with all its implications for the many users of this ubiquitous drug”.

“Addressing this issue through the visual system, as the authors have done, is an elegant concept. Any deleterious effect on the visual system would also have implications for driving, work and other activities and thus warrants further study,” they added.

“Electrophysiology can provide reliable and reproducible measurements of retinal and visual pathway function and is useful in the investigation and localisation of dysfunction, including that caused by toxicity.

“However, the conclusion that cannabis causes retinal ganglion cell dysfunction cannot be made with any degree of certainty based on the evidence provided in the current study.

Source:  http://www.independent.co.uk/news/science/cannabis-eyesight-vision-damage-toxic-effects-study-a7463331.html

Randomised controlled trial 

Battistella G, et al. PLoS One. 2013.

Abstract

Marijuana is the most widely used illicit drug, however its effects on cognitive functions underlying safe driving remain mostly unexplored.

Our goal was to evaluate the impact of cannabis on the driving ability of occasional smokers, by investigating changes in the brain network involved in a tracking task. The subject characteristics, the percentage of Δ(9)-Tetrahydrocannabinol in the joint, and the inhaled dose were in accordance with real-life conditions.

Thirty-one male volunteers were enrolled in this study that includes clinical and toxicological aspects together with functional magnetic resonance imaging of the brain and measurements of psychomotor skills. The fMRI paradigm was based on a visuo-motor tracking task, alternating active tracking blocks with passive tracking viewing and rest condition.

We show that cannabis smoking, even at low Δ(9)-Tetrahydrocannabinol blood concentrations, decreases psychomotor skills and alters the activity of the brain networks involved in cognition. The relative decrease of Blood Oxygen Level Dependent response (BOLD) after cannabis smoking in the anterior insula, dorsomedial thalamus, and striatum compared to placebo smoking suggests an alteration of the network involved in saliency detection.

In addition, the decrease of BOLD response in the right superior parietal cortex and in the dorsolateral prefrontal cortex indicates the involvement of the Control Executive network known to operate once the saliencies are identified. Furthermore, cannabis increases activity in the rostral anterior cingulate cortex and ventromedial prefrontal cortices, suggesting an increase in self-oriented mental activity.

Subjects are more attracted by intrapersonal stimuli (“self”) and fail to attend to task performance, leading to an insufficient allocation of task-oriented resources and to sub-optimal performance. These effects correlate with the subjective feeling of confusion rather than with the blood level of Δ(9)-Tetrahydrocannabinol. These findings bolster the zero-tolerance policy adopted in several countries that prohibits the presence of any amount of drugs in blood while driving.

Source:  PLoS One. 2013;8(1):e52545. doi: 10.1371/journal.pone.0052545. Epub 2013 Jan 

THE level of people being hospitalised after taking cannabis and related ‘legal highs’ has reached a 10-year peak, according to official figures from the Scottish Government.  More than 900 acute stays in general hospitals – as opposed to psychiatric admissions – involved the drug last year.

The Scottish Tories said the data showed cannabis was not the benign drug some claimed.

The latest figures show that in 2015-16 there were 7537 hospital stays in Scotland with a diagnosis of drug misuse, involving 5922 people, some admitted more than once.

Of these stays, 913 or 12 per cent, involved “cannabinoids”, which include synthetic highs such as Spice as well as the plant form of cannabis.   This was the highest percentage involving cannabinoids since 13 per cent in 2005-06.

Cannabinoids were the most common cause of drug stays among children – accounting for 45 per cent of cases involving under-15s.

The health boards with the most stays were NHS Greater Glasgow and Clyde (306), NHS Lothian (165) and NHS Lanarkshire (106).  Although still sometimes called a legal high, synthetic cannabis was criminalised last May, with its production and sale made punishable by up to seven years in prison.

Hospital admissions associated with cannabis were almost double those linked to cocaine.

Acute stays involving cocaine were at their highest since 2008-09 last year, but involved 553 admissions, or 7 per cent of all general drug-related cases.

The drugs most associated with hospital admissions were opioids, such as heroin, morphine, oxycodone and fentanyl.

Last year, opioids were behind 4656 stays, or 62 per cent of the drug-related total.  The number and prevalence of opioid admissions has increased hugely in the last 20 years.  In 1996-97, opioids accounted for just 791 stays, then equal to 34 per cent of drug admissions.

Scottish Tory justice spokesman Douglas Ross criticised campaigns to decriminalise cannabis and Police Scotland taking a soft touch approach to its use.  The force said in 2015 it might give people caught with cannabis on-the-spot recorded warnings as an alternative to prosecution.   Mr Ross said: “It’s quite alarming that quite so many people are being hospitalised through using cannabis, a drug many people feel authorities are going soft on.

“Not only is it dangerous in its own right, as these statistics prove, but it’s a gateway drug to even more harmful substances.

“We have a massive fight on our hands in Scotland both with illegal drugs and so-called legal highs.   “Now is not the time to give in and wave the white flag.  “We need to crack down on those circulating drugs of all kinds on our streets, and reinforce the message about just how damaging taking these substances can be.”

Scottish LibDem health spokesman Alex Cole-Hamilton said it was a concern that the figures were rising, but said the Conservatives’ solution was “completely wrong and regressive”.  He said: “If anything these figures show that the LibDems have been right in calling for this dark market to be brought out of the shadows.  “If the Tories had their way then they would drive the market further underground exposing people to more dangerous drugs and endangering more lives leading to more hospitalisations.

“The answer is to educate and regulate not to punish as the Tories want to do.”

Health Secretary Shona Robison said drug use continued to fall in the general population.  She said: “We have greatly reduced drug and alcohol waiting times with 94 per cent of people now being seen within three weeks of being referred.

“We have also invested over £630m to tackle problem alcohol and drug use since 2008 and over £150m over five years to improve mental health services in Scotland.”

Source: http://www.heraldscotland.com/news/15005884.Hospital_stays_linked_to_cannabis_at_10_year_high/   Jan,2017

Since marijuana is currently illegal in all but physician-approved circumstances, there have been no properly constructed clinical trials of smoking this drug in Canada, writes Lawrie McFarlane of the Victoria Times .

The greatest public-health disaster our species ever brought upon itself began in Europe 400 years ago — the introduction and use of tobacco.

In the 20th century alone, 100 million people died from cigarette smoking worldwide. And while the incidence rate has fallen in western countries, it remains high in Third World nations. Six million tobacco users still die each year. The cause of smoking deaths is not, primarily, the active ingredient in tobacco — nicotine. Rather it is the chemicals that comprise tobacco smoke — among them various tars, ammonia, hydrogen cyanide and formaldehyde.  Collectively, these chemicals cause a host of fatal maladies, including cancer, heart disease and emphysema. In short, a perfect horror show.

Now at this point, you’re probably saying: Tell me something I didn’t know. Well, here it is: Many of those same chemicals form marijuana smoke, and we are about to legalize the consumption of this drug. It’s not clear yet which forms of use might be authorized. If smoking is not among them, we might yet avoid another public-health calamity.

True, there are worrisome effects that come with consuming marijuana by other means, among them elevated pulse rates and memory loss. But these are minor matters, by comparison.

However, if smoking marijuana is blessed for general use, we might have an entirely different situation on our hands. For here is what is currently known with medical certainty about the health impacts of lighting up a joint: Nothing.  Since marijuana is currently illegal in all but physician-approved circumstances, there have been no properly constructed clinical trials of smoking this drug.

For the same reason, there have been no robust after-market research projects, in which users are tracked down years later, and their health status compared with that of non-users. Yet this is an essential process in revealing whether drugs that appear safe at first blush turn out to have serious side-effects downstream.  There have been suggestions that marijuana might act as a gateway drug to such potent narcotics as heroin and fentanyl. But whether these are anecdotal or fact-based, no one really knows.

There is also the matter of what is called the dose effect. Cigarettes have a high dose effect, meaning the risk of illness increases exponentially the more you consume. Hence the toxicology maxim: “The dose is the poison.”  So what is the dose effect of smoking marijuana? Again, we simply do not know and this is no small concern.

Generally speaking, it seems fair to assume that making an addictive substance more readily available will increase consumption rates. So what happens if people begin smoking 20 marijuana joints a day?  What happens if manufacturers find ways to strengthen the active ingredient — THC — while making their product less harsh? That’s what cigarette companies did.

In short, we are on the brink of approving a form of drug use, the medical consequences of which remain uncertain, but which might involve inhaling carcinogens. You would think the history of tobacco might have taught us something about fooling with addictive substances before we know the facts. In particular, you might think we would have learned how difficult, if not impossible, it is to close a Pandora’s box like this after it has been opened.

Once a government-sanctioned infrastructure of production, marketing and distribution is erected around marijuana, and millions of additional users are recruited, there will be no going back, regardless of whatever medical verdict is finally rendered. That’s principally why we continue to license tobacco production, despite its many ills.

I recognize we already turn a blind eye to occasional or “recreational” use of marijuana. But between turning a blind eye and conferring on this drug an official stamp of approval lies a world of unknown harm.

— Lawrie McFarlane is a columnist for the Victoria Times Colonist

Source:   http://theprovince.com/opinion/little-research-on-marijuanas-dangers  2nd Jan 2017

November 28, 2016

This shows a sample case of a visual 3-D rendering of a baseline SPECT scan of a long standing marijuana user compared to a control subject. The marijuana user has multiple perfusion defects with lower perfusion shown as scalloping and gaps …more

As the U.S. races to legalize marijuana for medicinal and recreational use, a new, large scale brain imaging study gives reason for caution. Published in the Journal of Alzheimer’s Disease, researchers using single photon emission computed tomography (SPECT), a sophisticated imaging study that evaluates blood flow and activity patterns, demonstrated abnormally low blood flow in virtually every area of the brain studies in nearly 1,000 marijuana compared to healthy controls, including areas known to be affected by Alzheimer’s pathology such as the hippocampus.

Hippocampus, the brain’s key memory and learning center, has the lowest blood flow in marijuana users suggesting higher vulnerability to Alzheimer’s. As the U.S. races to legalize marijuana for medicinal and recreational use, a new, large scale brain imaging study gives reason for caution. Published in the Journal of Alzheimer’s Disease, researchers using single photon emission computed tomography (SPECT), a sophisticated imaging study that evaluates blood flow and activity patterns, demonstrated abnormally low blood flow in virtually every area of the brain studies in nearly 1,000 marijuana compared to healthy controls, including areas known to be affected by Alzheimer’s pathology such as the hippocampus.

All data were obtained for analysis from a large multisite database, involving 26,268 patients who came for evaluation of complex, treatment resistant issues to one of nine outpatient neuropsychiatric clinics across the United States (Newport Beach, Costa Mesa, Fairfield, and Brisbane, CA, Tacoma and Bellevue, WA, Reston, VA, Atlanta, GA and New York, NY) between 1995-2015. Of these, 982 current or former marijuana users had brain SPECT at rest and during a mental concentration task compared to almost 100 healthy controls. Predictive analytics with discriminant analysis was done to determine if brain SPECT regions can distinguish marijuana user brains from controls brain. Low blood flow in the hippocampus in marijuana users reliably distinguished marijuana users

from controls. The right hippocampus during a concentration task was the single most predictive region in distinguishing marijuana users from their normal counterparts. Marijuana use is thought to interfere with memory formation by inhibiting activity in this part of the brain.

According to one of the co-authors on the study Elisabeth Jorandby, M.D., “As a physician who routinely sees marijuana users, what struck me was not only the global reduction in blood flow in the marijuana users brains , but that the hippocampus was the most affected region due to its role in memory and Alzheimer’s disease. Our research has proven that marijuana users have lower cerebral blood flow than non-users. Second, the most predictive region separating these two groups is low blood flow in the hippocampus on concentration brain SPECT imaging. This work suggests that marijuana use has damaging influences in the brain – particularly regions important in memory and learning and known to be affected by Alzheimer’s.”

Dr. George Perry, editor in chief of the Journal of Alzheimer’s Disease said, “Open use of marijuana, through legalization, will reveal the wide range of marijuana’s benefits and threats to human health. This study indicates troubling effects on the hippocampus that may be the harbingers of brain damage.”

According to Daniel Amen, M.D., Founder of Amen Clinics, “Our research demonstrates that marijuana can have significant negative effects on brain function. The media has given the general impression that marijuana is a safe recreational drug, this research directly challenges that notion. In another new study just released, researchers showed that marijuana use tripled the risk of psychosis. Caution is clearly in order.”

More information: Daniel G. Amen et al. Discriminative Properties of Hippocampal Hypo perfusion in Marijuana Users Compared to Healthy Controls: Implications for Marijuana Administration in Alzheimer’s Dementia, Journal of Alzheimer’s Disease (2016). DOI: 10.3233/JAD-160833

Source:http://medicalxpress.com/news/2016-11-marijuana-users-bloodbrain.html#nRlv

Cannabinoid AMB-FUBINACA in New York

ABSTRACT

BACKGROUND

New psychoactive substances constitute a growing and dynamic class of abused drugs in the United States. On July 12, 2016, a synthetic cannabinoid caused mass intoxication of 33 persons in one New York City neighborhood, in an event described in the popular press as a “zombie” outbreak because of the appearance of the intoxicated persons.

METHODS

We obtained and tested serum, whole blood, and urine samples from 8 patients among the 18 who were transported to local hospitals; we also tested a sample of the herbal “incense” product “AK-47 24 Karat Gold,” which was implicated in the outbreak. Samples were analyzed by means of liquid chromatography–quadrupole time-of-flight mass spectrometry.

RESULTS

The synthetic cannabinoid methyl 2-(1-(4-fluorobenzyl)-1H-indazole-3-carboxamido)-3-methylbutanoate (AMB-FUBINACA, also known as MMB-FUBINACA or FUB-AMB) was identified in AK-47 24 Karat Gold at a mean (±SD) concentration of 16.0±3.9 mg per gram. The de-esterified acid metabolite was found in the serum or whole blood of all eight patients, with concentrations ranging from 77 to 636 ng per milliliter.

CONCLUSIONS

The potency of the synthetic cannabinoid identified in these analyses is consistent with strong depressant effects that account for the “zombielike” behavior reported in this mass intoxication. AMB-FUBINACA is an example of the emerging class of “ultrapotent” synthetic cannabinoids and poses a public health concern. Collaboration among clinical laboratory staff, health professionals, and law enforcement agencies facilitated the timely identification of the compound and allowed health authorities to take appropriate action.

Source: New England Journal of Medicine;  10.1056/NEJMoa1610300

After three tours in Iraq and Afghanistan, C. J. Hardin wound up hiding from the world in a backwoods cabin in North Carolina. Divorced, alcoholic and at times suicidal, he had tried almost all the accepted treatments for post-traumatic stress disorder: psychotherapy, group therapy and nearly a dozen different medications. “Nothing worked for me, so I put aside the idea that I could get better,” said Mr. Hardin, 37. “I just pretty much became a hermit in my cabin and never went out.”

Then, in 2013, he joined a small drug trial testing whether PTSD could be treated with MDMA, the illegal party drug better known as Ecstasy.  “It changed my life,” he said in a recent interview in the bright, airy living room of the suburban ranch house here, where he now lives while going to college and working as an airplane mechanic. “It allowed me to see my trauma without fear or hesitation and finally process things and move forward.”

Based on promising results like Mr. Hardin’s, the Food and Drug Administration gave permission Tuesday for large-scale, Phase 3 clinical trials of the drug — a final step before the possible approval of Ecstasy as a prescription drug.   If successful, the trials could turn an illicit street substance into a potent treatment for PTSD.   Through a spokeswoman, the F.D.A. declined to comment, citing regulations that prohibit disclosing information about drugs that are being developed.

“I’m cautious but hopeful,” said Dr. Charles R. Marmar, the head of psychiatry at New York University’s Langone School of Medicine, a leading PTSD researcher who was not involved in the study. “If they can keep getting good results, it will be of great use. PTSD can be very hard to treat. Our best therapies right now don’t help 30 to 40 percent of people. So we need more options.”  But he expressed concern about the potential for abuse. “It’s a feel-good drug, and we know people are prone to abuse it,” he said. “Prolonged use can lead to serious damage to the brain.”

The Multidisciplinary Association for Psychedelic Studies, a small non-profit created in 1985 to advocate the legal medical use of MDMA, LSD, marijuana and other banned drugs, sponsored six Phase 2 studies treating a total of 130 PTSD patients with the stimulant. It will also fund the Phase 3 research, which will include at least 230 patients.

Two trials here in Charleston focused on treating combat veterans, sexual assault victims, and police and firefighters with PTSD who had not responded to traditional prescription drugs or psychotherapy. Patients had, on average, struggled with symptoms for 17 years.

After three doses of MDMA administered under a psychiatrist’s guidance, the patients reported a 56 percent decrease of severity of symptoms on average, one study found. By the end of the study, two-thirds no longer met the criteria for having PTSD. Follow-up examinations found that improvements lasted more than a year after therapy.

“We can sometimes see this kind of remarkable improvement in traditional psychotherapy, but it can take years, if it happens at all,” said Dr. Michael C. Mithoefer, the psychiatrist who conducted the trials here.   “We think it works as a catalyst that speeds the natural healing process.”  The researchers are so optimistic that they have applied for so-called breakthrough therapy status with the Food and Drug Administration, which would speed the approval process. If approved, the drug could be available by 2021.

Under the researchers’ proposal for approval, the drug would be used a limited number of times in the presence of trained psychotherapists as part of a broader course of therapy. But even in those controlled circumstances, some scientists worry that approval as a therapy could encourage more illegal recreational use.

“It sends the message that this drug will help you solve your problems, when often it just creates problems,” said Andrew Parrott, a psychologist at Swansea University in Wales who has studied the brains of chronic Ecstasy users. “This is a messy drug we know can do damage.”

Allowing doctors to administer the drug to treat a disorder, he warned, could inadvertently lead to a wave of abuse similar to the current opioid crisis.  During initial studies, patients went through 12 weeks of psychotherapy, including three eight-hour sessions in which they took MDMA. During the sessions, they lay on a futon amid candles and fresh flowers, listening to soothing music.

Dr. Mithoefer and his wife, Ann Mithoefer, and often their portly terrier mix, Flynn, sat with each patient, guiding them through traumatic memories.  “The medicine allows them to look at things from a different place and reclassify them,” said Ms. Mithoefer, a psychiatric nurse. “Honestly, we don’t have to do much. Each person has an innate ability to heal. We just create the right conditions.”

Research has shown that the drug causes the brain to release a flood of hormones and neurotransmitters that evoke feelings of trust, love and well-being, while also muting fear and negative emotional memories that can be overpowering in patients with post-traumatic stress disorder. Patients say the drug gave them heightened clarity and ability to address their problems.

For years after his combat deployments, Mr. Hardin said he was sleepless and on edge. His dreams were marked with explosions and death. The Army gave him sleeping pills and antidepressants. When they didn’t work, he turned to alcohol and began withdrawing from the world.

Ed Thompson, a former firefighter, took part in a study of Ecstasy as a treatment for PTSD. Without the drug, “he’d be dead,” his wife said.  “I just felt hopeless and in the dark,” he said. “But the MDMA sessions showed me a light I could move toward. Now I’m out of the darkness and the world is all around me.”  Since the trial, he has gone back to school and remarried.

The chemist Alexander Shulgin first realized the euphoria-inducing traits of MDMA in the 1970s, and introduced it to psychologists he knew. Under the nickname Adam, thousands of psychologists began to use it as an aid for therapy sessions. Some researchers at the time thought the drug could be helpful for anxiety disorders, including PTSD, but before formal clinical trails could start, Adam spread to dance clubs and college campuses under the name Ecstasy, and in 1985, the Drug Enforcement Administration made it a Schedule 1 drug, barring all legal use.

Since then, the number of people seeking treatment for PTSD has exploded and psychiatry has struggled to keep pace. Two drugs approved for treating the disorder worked only mildly better than placebos in trials. Current psychotherapy approaches are often slow and many patients drop out when they don’t see results. Studies have shown combat veterans are particularly hard to treat.

In interviews, study participants said MDMA therapy had not only helped them with painful memories, but also had helped them stop abusing alcohol and other drugs and put their lives back together.

On a recent evening, Edward Thompson, a former firefighter, tucked his twin 4-year-old girls into bed, turned on their night light, then joined his wife at a backyard fire. “If it weren’t for MDMA …” he said   “He’d be dead,” his wife, Laura, finished.   They both nodded.

Years of responding to gory accidents left Mr. Thompson, 30, in a near constant state of panic that he had tried to numb with alcohol and prescription opiates and benzodiazepines.  By 2015, efforts at therapy had failed, and so had several family interventions. His wife had left with their children, and he was considering jumping in front of a bus.

A member of a conservative Anglican church, Mr. Thompson had never used illegal drugs. But he was struggling with addiction from his prescription drugs, so he at first rejected a suggestion by his therapist that he enter the study. “In the end, I was out of choices,” he said.

Three sessions with the drug gave him the clarity, he said, to identify his problems and begin to work through them. He does not wish to take the drug again.  “It gave me my life back, but it wasn’t a party drug,” he said. “It was a lot of work.”

Correction: November 29, 2016

An earlier version of this article misstated the year that the Multidisciplinary Association for Psychedelic Studies was founded. It was 1985, not 1986. A picture caption misspelled the surname of a psychiatrist and his wife, a psychiatric nurse, who studied the use of Ecstasy. They are Dr. Michael C. Mithoefer and Ann Mithoefer, not Mitheofer.

Source:  http://www.nytimes.com/2016/11/29/us/ptsd-mdma-ecstasy.html

Hippocampus, the brain’s key memory and learning center, has the lowest blood flow in marijuana users suggesting higher vulnerability to Alzheimer’s. As the U.S. races to legalize marijuana for medicinal and recreational use, a new, large scale brain imaging study gives reason for caution. Published in the Journal of Alzheimer’s Disease, researchers using single photon emission computed tomography (SPECT), a sophisticated imaging study that evaluates blood flow and activity patterns, demonstrated abnormally low blood flow in virtually every area of the brain studies in nearly 1,000 marijuana compared to healthy controls, including areas known to be affected by Alzheimer’s pathology such as the hippocampus.

All data were obtained for analysis from a large multisite database, involving 26,268 patients who came for evaluation of complex, treatment resistant issues to one of nine outpatient neuropsychiatric clinics across the United States (Newport Beach, Costa Mesa, Fairfield, and Brisbane, CA, Tacoma and Bellevue, WA, Reston, VA, Atlanta, GA and New York, NY) between 1995-2015. Of these, 982 current or former marijuana users had brain SPECT at rest and during a mental concentration task compared to almost 100 healthy controls.

Predictive analytics with discriminant analysis was done to determine if brain SPECT regions can distinguish marijuana user brains from controls brain. Low blood flow in the hippocampus in marijuana users reliably distinguished marijuana users from controls.

The right hippocampus during a concentration task was the single most predictive region in distinguishing marijuana users from their normal counterparts. Marijuana use is thought to interfere with memory formation by inhibiting activity in this part of the brain.

According to one of the co-authors on the study Elisabeth Jorandby, M.D., “As a physician who routinely sees marijuana users,  what struck me was not only the global reduction in blood flow in the marijuana users brains, but that the hippocampus was the most affected region due to its role in memory and Alzheimer’s disease.

Our research has proven that marijuana users have lower cerebral blood flow than non-users. Second, the most predictive region separating these two groups is low blood flow in the hippocampus on concentration brain SPECT imaging.

This work suggests that marijuana use has damaging influences in the brain – particularly regions important in memory and learning and known to be affected by Alzheimer’s.”

Dr. George Perry, Editor in Chief of the Journal of Alzheimer’s Disease said, “Open use of marijuana, through legalization, will reveal the wide range of marijuana’s benefits and threats to human health.  This study indicates troubling effects on the hippocampus that may be the harbingers of brain damage.”

According to Daniel Amen, M.D., Founder of Amen Clinics, “Our research demonstrates that marijuana can have significant negative effects on brain function. The media has given the general impression that marijuana is a safe recreational drug, this research directly challenges that notion.  In another new study just released, researchers showed that marijuana use tripled the risk of psychosis. Caution is clearly in order.”

Source: Press http://content.iospress.com/articles/journal-of-alzheimers-disease/jad160833 – DOI: 10.3233/JAD-160833

 

A man holds a sheet of THC concentrate known as “shatter,” in Denver, Colorado. (Brennan Linsley/Associated Press)

An emergency psychiatrist in Victoria warns that a dramatic increase in severe mental illness cases may be connected to use of a powerful, relatively new drug called “shatter.” Dr, Kiri Simms told On the Island host Gregor Craigie she treated 10 patients needing hospitalization in the past year after using shatter or other highly concentrated marijuana-based products made from butane hash oil.

“They’re coming in with symptoms of depression, anxiety and sometimes psychosis, which for a psychiatrist means a break from reality, hallucinations, delusions,” Simms said.

Marijuana psychosis previously rare

In the past, when most marijuana use involved smoking dried leaves and buds, she said the infrequent cases of marijuana-related psychosis usually were patients with a family history of schizophrenia.  “Most people did not become psychotic from marijuana alone.” Simms said.

Several medical marijuana stores in Victoria openly advertise shatter and related marijuana products which an emergency psychologist links to an increasing number of cases of severe psychosis. (CBC)

That has changed. Now, most of the patients she currently sees are regular users of different marijuana products, often what she calls butane hash oil products. Those include shatter, wax and a gooey substance called honey or butter or oil, she said.

Simms said she has personally seen 10 people in the past year, “very, very ill and with the kind of psychotic experience that requires a stay in our psychiatric intensive care or on one of our in-patient wards.”    She said it’s not like the ‘old days’ when symptoms of psychosis would pass in a few hours or days.  “Now, sometimes it’s taking weeks before there is a clearing and occasionally it’s taking months and the patients are not cleared yet,” Simms said.   “Almost all of our patients, even our young patients tell us they can easily obtain these products in the local dispensaries.”

Shatter is openly advertised online by a number of medical marijuana storefront businesses in Victoria.Dana Larsen, the director of the Vancouver Dispensary Society, acknowledged that products such as shatter are too strong for inexperienced users but he does not support new rules or regulations for selling it.

“I think perhaps there should be better labelling and warnings on how to use cannabis products,” Larsen said. “I don’t think this is inherently more dangerous than other cannabis products.”

Source:  http://www.cbc.ca/news/canada/british-columbia/illicit-drugs-shatter-victoria-mental-illness-1.3862535    22nd  Nov. 2016

Current brain science is suggesting strong plausibility that the opiate and heroin epidemic will continue to worsen with commercializing and industrializing production and sales of marijuana at levels the likes of tobacco, alcohol and prescription drugs. With more 21st century marijuana in our communities, opiate and heroin use rises. The brain science is beginning to explain why this is. We are, with marijuana research, where we were in the 1920s and 30s with tobacco research linking smoking to cancer.

Studies are revealing that the cannabinoid-opioid systems of the brain are intimately connected.

In the areas of the brain where cannabinoids bind, opioids bind as well, and if you modify one system, you automatically change the other. Specifically, there is a functional interaction between the mu and Cb1 receptors of the brain; these receptors commonly exist together on brain cells. The mechanism is not yet well understood; more research is needed. But ultimately cannabinoids and opioids are known to strictly interact in many physiological and pathological functions, including addiction. Overall, evidence confirms a neurobiological convergence of the cannabinoid and opioid systems that is manifest at both receptor and behavioral levels.

What does this mean? We are learning that brain cross-talk between the endocannabinoid and endogenous opioid systems may cause, if there has been early brain exposure to marijuana, changes in the sensitivity to other drugs of abuse such as heroin.

Specifically, the sensitivity may be blunted, which would cause a greater risk for abuse and addiction. This new science supports the plausibility that a person who uses marijuana as a teenager may be increasing his/her risk of opiate addiction later in life. For example, a 20 year old who takes an opiate pain killer for a skiing injury or wisdom tooth removal may become much more at risk of becoming addicted to that pain killer as a result of his or her earlier marijuana use – no matter how insignificant that earlier use may seem. To be clear, this does not mean every teen marijuana user will be challenged with opioid addiction when they take an opiate-based pain killer later in life, as certainly, not every cigarette smoker ends up with lung cancer. Nor does this remove the enormous accountability opioid medications have in the current opiate crisis. It does put some teeth behind that old-school term “gateway drug” as now there is clear scientific evidence of a neuropathway link between opioids and cannabinoids in the brain. Perhaps “pathway drug” is a more accurate term.

The opioid-marijuana brain cross talk is very real and the newest research shows very important experimental evidence on “epigenetics.” A study in rodents showed that somehow, sperm or ova evade genetic cleansing during reproduction and epigenetic modifications triggered by THC are carried forward to the next generation. These changes were produced by THC exposure during adolescence, and yet persisted during reproduction in adulthood long AFTER exposure ended. The research needs to be reproduced in humans but there are others studies on trans-generational effects of other drugs in humans that appear to be consistent with discoveries in rodents.

This research is indicating that with more 21st century marijuana use, we are not only exposing more people to a serious decline in cognitive & mental-health functioning, but we conceivably are also priming populations for more opiate addiction and brain changes. And alarmingly, this priming can take place in utero, even if marijuana use ceases prior to childbearing years.

So frankly, it may not be a coincidence that the states with highest rates of youth marijuana use are also experiencing a soaring heroin epidemic – a trend we are seeing rise across the United States.

This science-based possibility that marijuana exposures in the brain are a foundational feature of the opiate addiction crisis deserves to be weighed heavily in the current decision-making process in how best to change marijuana law – especially given our nation’s tobacco history and tobacco’s impact on health and healthcare costs.  We will learn more about all of this opioid-cannabinoid brain connection, and very soon. with what this science is revealing, if it takes 50 years like it did with tobacco to confirm smoking cigarettes causes lung cancer, our species may be facing a profound and permanent decline in cognitive functioning.

Those in the field of substance abuse and drug use prevention are grateful to our esteemed researchers in Massachusetts and throughout our nation working diligently every day to not only figure out this opioid-cannabinoid neuropathway link, but to explain it to the rest of us so we begin to truly understand what is at stake as the marijuana lobby pushes for full government protection to engineer, produce, market and sell marijuana products in every community for recreational use, like tobacco.

Source:   http://marijuana-policy.org/marijuana-and-opiateheroin-epidemic-brain-science-explains-a-connection/ Feb.2016     By Heidi Heilman, Founder and CEO Massachusetts Prevention Alliance (MAPA); Founder and CEO, Edventi  

The Marijuana Policy Initiative

Don’t Legalize. We Change Minds About Marijuana Legalization/Commercialization

A volunteer non-partisan coalition of people from across the US and Canada who have come to understand the negative local-to-global public health and safety implications of an organized, legal, freely-traded, commercialized and industrialized marijuana market.

With special thanks to Dr. Bertha Madras, Dr. Sion Harris, and Dr. Sharon Levy for their work in translating the complexities of the latest brain science. ___

References (partial list of a lengthy list)

1. Ellgren M, Spano SM, Hurd YL. Adolescent cannabis exposure alters opiate intake and opioid limbic neuronal populations in adult rats. Neuropsychopharmacology. 2007 Mar;32(3):607-15

2. Spano MS, Ellgren M, Wang X, Hurd YL. Prenatal cannabis exposure increases heroin seeking with allostatic changes in limbic enkephalin systems in adulthood. Biol Psychiatry. 2007 Feb 15;61(4):554-63.

3. Ellgren M, Artmann A, Tkalych O, Gupta A, Hansen HS, Hansen SH, Devi LA, Hurd YL. Dynamic changes of the endogenous cannabinoid and opioid mesocorticolimbic systems during adolescence: THC effects. Eur Neuropsychopharmacol. 2008 Nov;18(11):826-34.

4. 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.

5. Spano MS, Ellgren M, Wang X, Hurd YL. Prenatal cannabis exposure increases heroin seeking with allostatic changes in limbic enkephalin systems in adulthood. Biol Psychiatry. 2007 Feb 15;61(4):554-63.

Getting behind the wheel while high or mashed off your face is obviously a terrible idea.

But even though new laws were introduced last year to clamp down on drug driving, tonnes of people still take the risk.

Illegal or medical drugs contributed to 62 fatal road crashes last year and another 259 causing serious injury. On top of that some 8,000 people were arrested for drug driving between March 2015 and April this year.

This is despite how badly having drugs in your system impairs your driving.  All of the most commonly used illegal drugs will make you a terrible driver. Just take a look at Brake’s summary below:

Drug driving

More than 8,000 people were arrested for drug driving in the first year of the new law .

Cannabis (2µg/L): Slows reactions; affects concentration; often gives a sedative-like effect, resulting in fatigue; affects co-ordination. Research using driver simulators has found cannabis makes drivers less able to steer accurately and slower to react to another vehicle pulling out

Cocaine (10µg/L) : Causes over-confidence; can cause erratic behaviour. After a night out using cocaine, people may feel like they have flu, feel sleepy and lack concentration

Ecstasy (10µg/L) : Makes the heart beat faster, which can cause a surge of adrenaline and result in a driver feeling over-confident and taking risks

Ketamine (20µg/L): Can cause muscle paralysis; hallucinations; confusion, agitation, panic attacks; and memory impairment

LSD: Can speed up or slow down time and movement, making the speed of other vehicles difficult to judge; can distort colour, sound and objects; may cause people to see objects which aren’t there; makes people feel panicky and confused

Speed: Makes people feel wide awake and excited, causing erratic behaviour and risk-taking; and can make people panicky. Users have difficulty sleeping, so will be unsafe to drive due to tiredness, sometimes for several days

But it’s not just illegal drugs that will impair your ability to drive, many prescription drugs will do to.  A UK study in 2000 found 5% of drivers and 4% of motorcyclists who died in road crashes had taken medicines that could have affected their driving.  Aside from the dangers you pose to other drivers by getting behind the wheel with drugs on your system, the legal ramifications are bad too.

Drivers convicted of drug driving receive::

* A minimum 12-month driving ban

* A criminal record; and

* A fine of up to £5,000, or up to 6 months in prison, or both Greg Marah, a spokesperson for Brake, told metro.co.uk that It is estimated that 200 deaths a year in the UK may result from drug driving.

He added: ‘Drink-driving is rightly seen as socially unacceptable, yet the dangers of driving under the influence of drugs are not as well-known and the drivers who choose to drug drive need to know that it’s illegal and potentially lethal.

‘With Police now having the power to test for drugs at the roadside, there is no hiding place for those who engage in this behaviour and endanger lives on our roads.  ‘However, with traffic policing being hit hard by budget cuts and resources stretched, more drivers may still be escaping prosecution despite these advances in testing for drug driving.

‘Every day we see the devastating consequences of crashes caused by drug drivers and people need to understand that these substances will seriously affect their ability to drive safely.’

Source:  http://metro.co.uk/2016/11/22/how-taking-drugs-before-you-get-behind-the-wheel-will-make-you-a-terrible-driver-6276207/

(Medical Xpress)—An international team of researchers has found what they believe is the source of memory loss in people who smoke marijuana—disruption to mitochondria. In their paper published in the journal Nature, the group describes their study of receptor activation due to exposure to active ingredients in cannabis and its impact on mitochondria.

A mitochondrion is an organelle located inside of most cells—it is commonly referred to as the part of the cell responsible for energy regulation. In this new effort, the researchers looked into the impact of cannabis on mitochondria in brain cells to find out if it may play a role in immobility, catalepsy (onset of seizures or a trance-like state) or memory loss due to use of the controversial drug.

Prior research has shown that CB1 receptors are located in the plasma membrane that surrounds typical brain cells. Other research has also shown that chronic use of cannabis can cause memory loss and other problems and that substances in it bind to CB1 receptors on nerve terminals, which, in turn, can cause a disruption in the transmissions of messages between cells. The net result is memory loss, catatonic states or blackouts. In this new effort, the researchers found that chemicals in cannabis also caused activation of CB1 receptors in mitochondria in brain cells located in the hippocampus, which is where most memory processing occurs. This, they claim, suggests memory loss due to use of cannabis can be sourced to the impact it has on the organelles.

The team came to this conclusion by removing the CB1 receptors in mitochondria in mice brain cells and testing the mice to see if they continued to experience memory loss due to the introduction of the cannabis chemicals. The team reports they did not, which suggests that interactions between cannabis chemicals and mitochondria plays a major role in memory loss and likely other negative health effects associated with chronic use of marijuana. They suggest their findings indicate that chronic use of the drug could cause permanent damage to mitochondria, leading to long-term or permanent memory loss and other health problems.

The researchers also suggest their findings indicate that there may be a way to modify medical cannabis used to treat diseases such as glaucoma so that it does not cause memory loss or other associated health problems, by removing its impact on mitochondria.

Source:http://medicalxpress.com/news/2016-11-memory-loss-due-cannabis-mitochondria.html

More information: Etienne Hebert-Chatelain et al. A cannabinoid link between mitochondria and memory, Nature (2016). DOI: 10.1038/nature20127

Abstract  Cellular activity in the brain depends on the high energetic support provided by mitochondria, the cell organelles which use energy sources to generate ATP.

Acute cannabinoid intoxication induces amnesia in humans and animals, and the activation of type-1 cannabinoid receptors present at brain mitochondria membranes (mtCB1) can directly alter mitochondrial energetic activity. Although the pathological impact of chronic mitochondrial dysfunctions in the brain is well established, the involvement of acute modulation of mitochondrial activity in high brain functions, including learning and memory, is unknown.

Here, we show that acute cannabinoid-induced memory impairment in mice requires activation of hippocampal mtCB1 receptors. Genetic exclusion of CB1 receptors from hippocampal mitochondria prevents cannabinoid-induced reduction of mitochondrial mobility, synaptic transmission and memory formation. mtCB1 receptors signal through intra-mitochondrial Gαi protein activation and consequent inhibition of soluble-adenylyl cyclase (sAC).

The resulting inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system eventually leads to decreased cellular respiration. Hippocampal inhibition of sAC activity or manipulation of intra-mitochondrial PKA signalling or phosphorylation of the Complex I subunit NDUFS2 inhibit bioenergetic and amnesic effects of cannabinoids. Thus, the G protein-coupled mtCB1 receptors regulate memory processes via modulation of mitochondrial energy metabolism. By directly linking mitochondrial activity to memory formation, these data reveal that bioenergetic processes are primary acute regulators of cognitive functions.

The risk of developing psychosis is more than tripled for those who abuse cannabis, according to results from a new twin study.

Researchers from the Norwegian Institute of Public Health (NIPH), together with colleagues from Virginia Commonwealth University, examined the relationship between cannabis and psychosis using psychiatric interviews of Norwegian twins. The interviews reveal whether the twins had symptoms of psychosis and cannabis abuse.

“Previous research has shown that patients with psychotic disorders use cannabis more often than the general population. However research has been divided over whether cannabis use was the cause of the psychotic disorders,” says Ragnar Nesvåg, senior researcher at NIPH and the main author of the study.

Genetic factors influence both cannabis abuse and psychosis and the same genes may lead to an increased risk for both problems. “The relative importance of genes in the causes of a disease is known as heritability, and we know from previous studies at the NIPH that cannabis abuse is very heritable, explains Eivind Ystrom, senior researcher at NIPH. “In order to determine whether cannabis abuse can lead to psychosis, it is important to account for genetic risk,” he adds.

The researchers therefore tested both the hypotheses that cannabis use causes psychotic symptoms and that psychotic symptoms lead to cannabis abuse.

Abuse increased the risk by 3.5

The hypothesis best suited to the data was that cannabis abuse caused symptoms of psychosis. Within a twin pair, the twin with symptoms of cannabis abuse had a 3.5 times higher risk of developing symptoms of psychosis compared with the twin who did not have symptoms of cannabis abuse.

“Our analyses showed a significant association between cannabis abuse and symptoms of psychosis in the general population. We also tested the hypothesis that symptoms of psychosis caused cannabis abuse, but the hypothesis was less suited to the data. Therefore, it appears that cannabis abuse can be a cause of psychosis,” says Ystrom.

Confirmed high heritability

Previous studies have shown that cannabis abuse is very heritable, which was also confirmed in this study. As much as 88 per cent of the causes of why some people abused cannabis, yet others did not, could be attributed to some people having risk genes.  Despite this, the researchers found that a common genetic risk could not explain the entire association with symptoms of psychosis. Even after genetic risk and risk of childhood environment were taken into account, people with cannabis abuse still had a multiplied risk of developing symptoms of psychosis. Nesvåg says that psychosis is associated with huge costs to society. These findings should be considered when evaluating the cost of policies for increased cannabis availability, such as decriminalisation or legalisation.

About twin studies

Investigating whether a particular risk factor causes disease requires studies where you look at two people who are otherwise identical, where one is exposed to a risk factor and the other is not. The effects on their health can be investigated. For obvious reasons, these experiments are neither practical, ethical or legally feasible.

Studying twins is a viable option because they have genetic similarity, they have grown up in the same family, and they have the same socioeconomic background.

More information: Ragnar Nesvåg et al. Genetic and Environmental Contributions to the Association Between Cannabis Use and Psychotic-Like Experiences in Young Adult Twins,

Source:  Schizophrenia Bulletin (2016). DOI: 10.1093/schbul/sbw101  Provided by: Norwegian Institute of Public Health

If Marijuana is Medicine, How Come it Makes People So Sick?

There’s a great irony that comes from the pot industry’s claims that marijuana is medical and it’s supposed to help with nausea.   It’s called Cannabis Hyperemesis, and it hits with a vengeance.

This past week a parent wrote to PopPot, saying: “Parents should watch for red flags of pot use in their children including frequent, long hot showers; weight loss; unexplained nausea and vomiting.”

“I took my teen to the doctor assuming the stress of a rigorous course load combined with the demands of an after school sport were taking a physical toll on my child, ” the mom wrote.  “In hindsight, these were the signs of escalating pot use as described in this Pub Med article about cannabinoid hyperemesis. Unfortunately many in the medical community are ignorant of the detrimental effects of pot use on our young people —  ranging from psychotic breaks to debilitating gastrointestinal symptoms.”

From another mother in Pueblo, Colorado who also wrote this past week:  “Last week I met a 14-year-old girl suffering from Cannabis Hyperemesis Syndrome.  When I met her, at first I thought she had an addiction to meth because she was so very thin and malnourished.  She was asking me how can she return to live with her parents who are marijuana users when marijuana is so toxic for her.”

Incidences of this severe illness appear to be on the rise since the rollout of legal weed.  The high THC content of today’s weed — 5x the amount in the 1980s — seems to be involved also.  Because of misdiagnosis or denial of drug use by patients, this syndrome is going undetected.  Furthermore, users self-medicate and exacerbate this severe illness, as a medical marijuana patient was doing for more than eight months.

From veterans hospitals to addiction specialists as well as gastroenterologists, there’s suddenly an increased interest in and diagnoses of this condition.  Further research into this mysterious illness turns up numerous medical journal articles on the link between excessive and/or long-term cannabis use and hyperemesis.

Cannabis Hyperemesis: How to Know if You or Someone You Love is Afflicted

This syndrome is still largely unknown throughout the medical profession and even among cannabis users. The most prominent cases are among long-term users that started using the drug at a very early age and have used daily for over 10 years, according to the MedScape article, Emerging Role of Chronic Cannabis Use and Hyperemesis Syndrome. The article goes on to say that it can also effect newer users and even non-daily users.

In Practical Gastroenterology, there’s a case of a 19 year old Hispanic man who contracted the problem within only two years of marijuana use.  Symptoms reported in a Current Psychiatry article include cyclic vomiting, abdominal pain, nausea, gastric pain and compulsive hot bathing or showers to ease pain.  Frequent bathing and vomiting can also lead to dehydration and excessive thirst. Mild fever, weight loss, and a drop in blood pressure upon standing are other symptoms.

Sufferers find they need to take many showers or baths a day just to get relief from the chronic nausea and vomiting. The bouts of illness are so severe and frightening they lead to frequent trips to the emergency room. And finally, this debilitating illness can be very disruptive to life and relationships. The many absences from work lead to job loss and the inability to hold down a job.

Parents may mistake this situation as bulimia, particularly if the teens hide the vomiting.  Another common way this disease is misdiagnosed as cyclic vomiting syndrome. According to the Current Psychiatry article, 50% of those diagnosed with CVS are daily cannabis users.  Another common misreading by doctors of the compulsive habit of frequent hot baths is as Obsessive Compulsive Disorder.

Further complicating matters, doctors find that even when cannabis use is consistent, the bouts of hyperemesis come and go, which further serves to keep the patient in denial about the connection to their drug use.

In Spite of Cannabis Hyperemesis, Addiction is a Stronghold

Complete cessation of marijuana use is the only known cure for Cannabis Hyperemesis Syndrome.

Sadly, even those who have greatly suffered over a long period of time, still want to be able to consume marijuana. The claim by the industry that marijuana is not addictive is easily disproved when you see the comments to a High Times article, What is Cannabinoid Hyperemesis Syndrome?  Not only do many commenters admit they suffer from this detrimental effect of this drug, they confess they still love marijuana. The commenters lament having to give up their stoner lifestyle even after years of disabling illness! A number of them state that once they are well, they plan to return to the habit, albeit to a lesser degree.

Source:  http://www.poppot.org/2016/11/19/cannabis-hyperemesis-toxic-side-effect-of-dangerous-drug/   19th Nov. 2016

The surgeon general’s recent report is a much-needed call to arms around a public health crisis.

On Nov. 17, Dr. Vivek Murthy, a vice admiral of the U.S. Public Health Service Commissioned Corps and U.S. surgeon general, issued a timely and much-needed report on what has become a public health crisis and menace in this country – namely, misuse and addiction to legal and illegal psychoactive drugs.

In the report preface, Murthy remarks that before starting his current job he stopped by the hospital where he had practiced. It was the nurses who said to him, he writes, “please do something about the addiction crisis in America.” He knew they were right, and he took their wise counsel.

Why are they right? Substance use disorders, where a person is functionally impaired and often physically dependent on a drug, affect nearly 21 million Americans annually – the same number of people who have diabetes and 150 percent of those with a cancer diagnosis, of any type.

In 2015, about 67 million people reported binge drinking in the past month, and 48 million were using illegal drugs or misusing prescribed drugs. In the past year, 12.5 million Americans reported misusing prescription pain relievers. In 2014, 47,055 people died from a drug overdose, with more than half of those using an opioid (like OxyContin, Percodan, Vicodin, methadone and heroin).

The numbers chill the mind, and yet with the widespread use, abuse and potentially deadly consequences, only 1 in 10 of those with a substance use disorder obtain any treatment. The nurses to whom Murthy spoke were surely seeing the consequences of drug misuse in their emergency rooms, clinics and inpatient units. They also were likely seeing the consequences among their family, friends and co-workers. (Health professionals are prone to misuse alcohol and drugs.)

What distinguishes the surgeon general’s report is its call for a long overdue shift in alcohol and drug policy – away from a criminal justice approach to a clinical or public health approach. What also distinguishes every cover note and chapter is a spirit of hope, that substance use can be prevented, detected early, effectively treated and its manifold adverse impacts mitigated.

To start, the surgeon general urges that we begin by “improving public awareness of substance misuse and related problems.” Negative attitudes, critical judgments and moral invective towards people with addiction not only interfere with delivering good care they deter people who need services from getting them.

But the report also makes clear that there is no single solution or path, nor should we expect one with problems this broad and deep. The heart of the report then, chapter by chapter, speaks to comprehensive policy action: prevention, early intervention, ongoing treatment, so-called wellness activities, identifying and reaching out to high-risk populations and supporting research efforts.

Central to the report is that we must integrate health care services with substance use treatment: not by referral from one to the other but by embedding screening and basic forms of treatment into primary care and family practice. We screen for hypertension, lipids, diabetes and much more; why aren’t we screening for problem alcohol and drug use where these problems are most likely to appear? Screening, Brief Intervention and Referral for Treatment, or SBIRT, is perhaps the best-known and most effective means of extending substance screening and management into the general health system.

Of course, all these efforts must be financed. A powerful argument can be made that it costs more to not treat these conditions than to treat them. Substance use disorders cost the U.S. more than $400 billion every year on health care expenses, criminal justice costs, social welfare consequences and lost workplace productivity. However, our health, social welfare and criminal justice systems are simply too siloed, (separated) and we pay the human and financial price of not reaching across the ersatz boundaries of government and community agencies.

Still, some laws are making inroads to improve care. The Affordable Care Act requires treatment for substance use disorders to be an “essential benefit,” no different from any other illness. The 2008 Federal Parity Act, now finally with regulations, also requires insurers to not discriminate against people with addictions. The policy and legislative pillars are there, and we need to keep using them.

The surgeon general ends his report with a vision for the future. He is deeply sanguine that we can disrupt the addiction epidemic that has seized our country. The path is a public health one, as I have illustrated above, but the report talks also of what individuals and families can do: reach out to those we see in trouble, withhold judgment, support those in recovery, and, for parents, talk to your child about alcohol and drugs. “Making [these changes] will require a major cultural shift in the way Americans think about, talk about, look at, and act toward people with substance use disorder,” the report reads. “For example, cancer and HIV used to be surrounded by fear and judgment, but they are now regarded by most Americans as medical conditions like many others.”

We owe a great thanks to the surgeon general and the many experts and advocates who put together this call for how we can respond to what is now a public health crisis. We can do that. It will be hard, but the alternative of not taking collective action will be far harder to bear.

Source: http://www.usnews.com/opinion/policy-dose/articles/2016-11-21/surgeon-general-is-right-to-target-the-public-health-crisis-of-addiction

Nora D. Volkow, Aidan J. Hampson, and Ruben Baler

Abstract:

INTRODUCTION

The search for a state of mental relaxation and well-being is one of the factors driving the widespread consumption of cannabis. The most frequently abused illicit substance worldwide, cannabis is consumed regularly by about 2.4% of the world population (approximately 181 million people in 2013) (1).

The principal psychoactive component of cannabis is_9-tetrahydrocannabinol (THC), which acts as an orthosteric agonist for cannabinoid receptors and mediates both the positive and negative effects of cannabis. The cannabinoid receptors are part of the brain’s endocannabinoid system (ECS), which modulates multiple neurobiological processes including reward and stress, a fact that is relevant for understanding not just the recreational use of cannabis but also its therapeutic potential.

This review focuses on the role of the ECS in the modulation of stress responses, its interaction with the reward system in the brain, and the implications of this emerging understanding for cannabis abuse, mental illnesses, and therapeutics.

CONCLUSIONS

Cannabis has been used for centuries across the globe. However, the recent changes in laws regarding legalization of recreational or medicinal cannabis, along with the availability of cannabis with increasingly higher THC levels (94, 163), are generating a sense of urgency for understanding the potential adverse effects of cannabis exposure as well as its purportedly medicinal actions.

Although many studies have been published on deleterious effects of chronic cannabis vis-´a-vis cognition, emotion, and psychiatric symptoms, the findings are inconsistent, which has made it easier for proponents of cannabis legalization to dismiss them and wrongly claim that cannabis use has no harmful effects. At the same time, major advances in our understanding of ECS neurobiology have opened exciting new opportunities for the development of novel, smarter medications for psychiatric and neurological disorders.

Source:     Annu. Rev. Pharmacol. Toxicol. 2017. 57:2.1–2.23

The new data confirms mounting body of scientific evidence highlighting problems with rising marijuana use; SAM Honorary Advisor Patrick Kennedy to speak as part of report’s official release

[ALEXANDRIA, VA] – A new report, released today by the office of the U.S. Surgeon General, adds to the mounting body of scientific evidence highlighting the dangers of marijuana use and emphasizing prevention as essential for protecting youth. It also stands as a further warning of the large impending public health costs of marijuana legalization policies, which permit the marijuana industry to profit from the patterns of heavy marijuana use that pose the greatest threat to public health and safety.

Among the report’s findings:

* Long-term health consequences of marijuana use:  mental health problems, chronic cough, frequent respiratory infections, increased risk for cancer, and suppression of the immune system.

* Other serious health-related issues stemming from marijuana use: breathing problems; increased risk of cancer of the head, neck, lungs, and respiratory tract; possible loss of IQ points when repeated use begins in adolescence; babies born with problems with attention, memory, and problem solving (when used by the mother during pregnancy).

* Increased risk for traffic accidents:  Marijuana use “is linked to a roughly two-fold increase in accident risk.”

* Increased risk of schizophrenia:  “[T]he use of marijuana, particularly marijuana with a high THC content, might contribute to schizophrenia in those who have specific genetic vulnerabilities.

* Increased risk of addiction from high-potency marijuana available in legalized states:  “Concern is growing that increasing use of marijuana extracts with extremely high amounts of THC could lead to higher rates of addiction among marijuana users.”

* Permanent Loss of IQ:  “One study followed people from age 13 to 38 and found that those who began marijuana use in their teens and developed a persistent cannabis use disorder had up to an eight point drop in IQ, even if they stopped using in adulthood.”

“Once again, the scientific community has spoken loud and clear on the numerous, and serious health risks of marijuana,” said Kevin Sabet, President of SAM. “The more we know about marijuana, the worse it appears for public health and safety. Policymakers, especially those in the incoming Presidential administration and Congress, should read this report closely and heed the advice of the scientific community.”

“In particular, the Surgeon General’s report underscores the serious problems with patterns of heavy marijuana use — the same patterns that furnish the pot industry with the vast majority of its revenues,” commented Jeffrey Zinsmeister, SAM’s Executive Vice President. “As we seek to avoid the mistakes we made with Big Tobacco, we should be aware that the pot industry profits off of the very types of marijuana use that most harm public health and safety.”

Source:     http://www.learnaboutsam.org.  Press release  17th Nov.2016   Email: austin.galovski@curastrategies.com

Authors: Daniela Vergara1 *, L. Cinnamon Bidwell2 , Reggie Gaudino3 , Anthony Torres3 , Gary Du3 , Travis C. Ruthenburg3 †, Kymron deCesare3 , Donald P. Land3 , Kent E. Hutchison4 and Nolan C. Kane1 * Affiliations: 1 University of Colorado Boulder, Department of Ecology and Evolutionary Biology. 2 University of Colorado Boulder, Institute of Cognitive Science. 3 Steep Hill Labs Inc. 1005 Parker Street, Berkeley, CA 94710. 4 University of Colorado Boulder, Department of Psychology and Neuroscience. *Correspondence to: daniela.vergara@colorado.edu or nolan.kane@colorado.edu University of Colorado Boulder 1900 Pleasant Street Boulder, CO 80309 †Current address: SC Laboratories Inc. 4000 Airport Way South, Seattle, WA 98108.

Abstract: 

As the most widely used illicit drug, the basis of the fastest growing major industry in the US, and as a source of numerous under-studied psychoactive compounds, understanding the psychological and physiological effects of Cannabis is essential. The National Institute on Drug Abuse (NIDA) is designated as the sole legal producer of Cannabis for use in US research studies. We sought to compare the chemical profiles of Cannabis varieties that are available to consumers in states that have state-legalized use versus what is available to researchers interested in studying the plant and its effects.

Our results demonstrate that the federally produced Cannabis has significantly less variety and lower concentrations of cannabinoids. Current research, which has focused on material that is far less diverse and less potent than that used by the public, limits our understanding of the plant’s chemical, biological, psychological, medical, and pharmacological properties. Investigation is urgently needed on the diverse forms of Cannabis used by the public in state-legal markets.

Introduction:

The United States has witnessed enormous changes concerning public acceptance of marijuana. Use has more than doubled since 2002, across all genders, ethnicities and socioeconomic status

Considering changes on the cultural, political, and legal fronts, research on the effects of Cannabis products that are consumed though legal outlets in states that have legalized is urgently needed. The Cannabis plant is unique in producing a diversity of cannabinoids, a terpenoid chemical compound that interacts with the endocannabinoid system in the brain and nervous system

One of the primary cannabinoids produced, Δ-9-tetrahydrocannabinolic acid (THCA), is converted to the neutral form Δ-9-tetrahydrocannabinol (THC) when heated, e.g. by smoking. THC interacts with the endocannabinoid system producing a wide range of physiological and neurological effects. Studies have found that marijuana’s effects on mood, reward, and cognitive dysfunction appear to follow a dose dependent function based on the THC content

Due to this and other purported psychotropic effects, THCA has been actively selected for by the Cannabis industry and varieties containing more than 30% THCA by weight have been cultivated  In addition to THC, marijuana’s effects are likely related to a number of other compounds including nearly 74 different cannabinoids present at varying ratios across strains. For example, another cannabinoid produced by the plant, is converted to cannabidiol (CBD) when heated. CBD may mitigate the effects of THC and may have other beneficial effects

Demand for high CBDA plants has increased, due to potential therapeutic uses for cancer 19 and  epilepsy.    Other important cannabinoids produced by the plant include cannabigerol (CBG cannabichrome (CBC)  and Δ-9-tetrahydocannabivarin (THCV)

Because research universities across the nation have national grants and must verify compliance with federal law, scientists at these institutions are restricted to research with the only federally legal source of Cannabis. Our current understanding of the effects of marijuana in humans (e.g. on mood, cognition, or pain) has therefore relied exclusively on government-grown marijuana, often administered in a laboratory setting,

Thus, nearly all published US laboratory studies have used Cannabis material obtained from the National Institutes of Health/National Institute on Drug Abuse (NIDA) supply, the only federally legal source for Cannabis plant material. At the same time, dispensary-grade Cannabis available to consumers in state-regulated markets is becoming increasingly potent and diverse. Strains differ substantially in potency and cannabinoid content, and hence, are likely to differ in terms of their effects .

Strains bred for high THCA content are thought to result in greater levels of intoxication as well as differing psychological and physiological effects compared to strains bred for high CBDA content. Accordingly, NIDA has recently developed plant material with varying levels of cannabinoids for research purposes, but the extent to which government cannabis is consistent with cannabis produced in the private market is not clear. To address the critical question of whether the potency and variety of NIDA-provided cannabis reflects products available to consumers through state-regulated markets, we compared the cannabinoid variation and potency from plants from four different cities in the US where peer-reviewed cannabis is legal for medical or recreational reasons (Denver, Oakland, Sacramento, and Seattle; cannabinoid data provided by Steep Hill Labs Inc.) to the cannabinoid content of plants supplied for research purposes by NIDA, using the data publicly available on their website 28.

Results 

NIDA differs from all other locations except Seattle in production of CBD (fig. 1A), and differs significantly from all other locations in production of THC. NIDA has the lowest CBD and THC percent with a mean and s.d. of 6.16 ± 2.43%, and 5.15 ± 2.60% respectively.

Sacramento has the highest percent CBD with 12.83 ± 4.73% and Seattle has the highest percent THC with 19.04 ± 4.43%. There are significant differences between the percent of both CBD and THC between US city locations, in addition to differences with NIDA (fig. 1A). CBG production does not differ in any location.

Cannabis plants grown in all locations produce very little CBG, particularly NIDA with only a single sample producing more than 1% CBG (fig. 1B). THC-V is also produced in low quantities in all locations. The only statistically significant difference is between Denver, whose mean and s.d is 1.12 ± 0.13%, and Oakland 2.35 ± 0.68%

Source:  http://biorxiv.org/content/biorxiv/early/2016/10/26/083444.full.pdf

Ben Cort, an addiction treatment specialist from Colorado, speaks in opposition to Proposition 64 during a panel about the legalization of marijuana at the Anaheim Convention Center.

An addiction expert from Colorado, where marijuana is legal, Cort is drowning in a sea of concern over Proposition 64, California’s ballot initiative that would allow recreational weed.

Once an addict himself, Cort can’t believe the Golden State appears on the verge of legalizing something that terrifies him. Though he’s no fan of pot, it’s not so much the plant that scares Cort. What worries him is that science allows THC – the active ingredient in marijuana that gets you high – to become nuclear-charged.

A little THC wax or oil, he cautions, can go a very long way, especially when it’s ingested.

“We’re the canary in the coal mine,” says Cort, a manager with the University of Colorado Hospital’s rehab program. “We’re treating more addicts for cannabis than we are for opiates.”

Cort says he’s seen THC levels in so-called gummy bears 20 times higher than levels that are legal in Oregon, another state where recreational marijuana is law but where THC percentages are controlled.

Prop. 64, Cort says, will legalize dangerously high THC. That’s not Snoop Dogg cool. That’s emergency room serious.

The federal National Institute on Drug Abuse reports, “These extracts can deliver extremely large amounts of THC to users, and their use has sent some people to the emergency room.” Such high THC levels, institute officials warn, also can turn what many consider a relatively benign drug into something addictive.

UNICORN PROMISES

While writing about marijuana, I’ve interviewed doctors, lawyers, pot growers, medical marijuana dispensary owners, officials with the National Organization for the Reform of Marijuana Laws and patients in pain.

Until I attended a two-hour informational panel discussion Tuesday sponsored by the Anaheim Police Department, I figured I knew all about pot. Speakers included Cort; Police Chief John Jackson of the Greenwood Village, Colo., Police Department; Chief Justin Nordhorn of the Washington State Liquor and Cannabis Board; Attorney Robert Bovett of Oregon Counties Legal Counsel; Lauren Michaels, legislative affairs manager

for the California Police Chiefs’ Association; and Nate Bradley, executive director of the California Cannabis Industry Association.

When a speaker asked who had read Prop. 64, only one hand went up and it wasn’t mine. So to prepare for this column I also read – OK, I skimmed some chunks – all 62 pages. A lot of Prop. 64 is wonky and details who can do what and where. But some reads more like dreams of fairies and unicorns than reality.

“Incapacitate the black market,” the proposal promises “and move marijuana purchases into a legal structure with strict safeguards against children accessing it.”

Untrue, said Jackson, who stressed that illegal sales continue in Colorado.

“Revenues will,” Prop. 64 predicts, “provide funds to invest in public health programs that educate youth to prevent and treat serious substance abuse.”

Wrong, Jackson said. More teens in Colorado are being sent to emergency rooms because of THC-laced edibles.

Revenues will pay to “train local law enforcement to enforce the new law with a focus on DUI enforcement.”

Incorrect again. Jackson said his department is busier than ever dealing with more drivers high on weed and handling more THC-related traffic fatalities.

Other parts of Prop. 64 are just dumb and dumberer.   Like allowing radio and television advertising.

“Make no mistake,” Jackson said of Prop. 64. “This whole thing is about money.

“A drug dealer in a suit is still a drug dealer.”

‘NECESSARY REFORM’

Once marijuana became legal in Washington in 2012, Nordhorn said, children and teens considered it less harmful, and that had ripple effects.

With the advent of vaping, for example, young people inhale THC without anyone knowing if they are taking in an innocent type of e-juice or marijuana.

“Legal marijuana,” Nordhorn said, “is not a silver bullet to get rid of marijuana problems.”

Bovett echoed other panelists, saying that Oregon also has seen an increase in impaired driving, although he added that has been going up since the state approved medical marijuana.

The Oregon Poison Center also reports increases in marijuana-related calls.

Even Bradley, the lone pro-Prop. 64 voice on the panel, admitted he’s concerned about edibles.

Instead of THC levels, Bradley focused on dollars. He said the initiative will take $100 million out of the hands of criminals and the measure will generate $300 million for law enforcement to focus on such things as protecting children.

Bradley has plenty of backers. Among the most visible are Gavin Newsom, lieutenant governor, and Rep. Dana Rohrabacher, R-Costa Mesa. Our local representative has said, “Current marijuana laws have undermined many of the things conservatives hold dear – individual freedom, limited government and the right to privacy.”

Rohrabacher went on to say, “This measure is a necessary reform which will end the failed system of marijuana prohibition in our state, provide California law enforcement the resources it needs to redouble its focus on serious crimes while providing a policy blueprint for other states to follow.”

‘SEED TO SALE’

The most sobering speaker was Michaels of the chiefs’ association. She simply defended California’s newly revamped medical marijuana policies.

Called “seed to sale,” three new laws inked last year shoot down the need for Prop. 64, Michaels said. She stated California now has an enhanced working system to distribute medicinal marijuana legally.

California, Michaels said, already allows local control, protects current producers and includes checkpoints at distribution.

In contrast, she said, Prop. 64 is vertically integrated, favors big business and independent distribution, appoints the state as sole actor for operating licenses and ensures regulatory confusion. Research, learn, vote. Contact the writer: dwhiting@scng.com

Source:   http://www.ocregister.com/articles/marijuana-731244-thc-prop.html   5th October 2016

correspondence should be addressed; Norwegian Institute of Public Health, Department of Mental Disorders, PO Box 4404, Nydalen, N-0403 Oslo, Norway; tel: +47-21078373, fax: +47-22118470, e-mail: ragnar.nesvag@fhi.no

Abstract

To investigate contributions of genetic and environmental risk factors and possible direction of causation for the relationship between symptoms of cannabis use disorders (CUD) and psychotic-like experiences (PLEs), a population-based sample of 2793 young adult twins (63.5% female, mean [range] age 28.2 [19–36] y) were assessed for symptoms of CUD and PLEs using the Composite International Diagnostic Interview.

Latent risk of having symptoms of CUD or PLEs was modelled using Item Response Theory. Co-twin control analysis was performed to investigate effect of familiar confounding for the association between symptoms of CUD and PLEs.

Biometric twin models were fitted to estimate the heritability, genetic and environmental correlations, and direction for the association.

Lifetime use of cannabis was reported by 10.4 % of the twins, and prevalence of PLEs ranged from 0.1% to 2.2%. The incidence rate ratio of PLEs due to symptoms of CUD was 6.3 (95% CI, 3.9, 10.2) in the total sample and 3.5 (95% CI, 1.5, 8.2) within twin pairs.

Heritability estimates for symptoms of CUD were 88% in men and women, and for PLEs 77% in men and 43% in women. The genetic and environmental correlations between symptoms of CUD and PLEs were 0.55 and 0.52, respectively. The model allowing symptoms of CUD to cause PLEs had a better fit than models specifying opposite or reciprocal directions of causation. The association between symptoms of CUD and PLEs is explained by shared genetic and environmental factors and direct effects from CUD to risk for PLEs.

Source:  http://schizophreniabulletin.oxfordjournals.org/content/early/2016/07/18/schbul.sbw101

In  2014, an estimated 22.2 million Americans aged 12 years or older had used marijuana in the past month.1

Under federal law, marijuana is considered an illegal Schedule I drug. However, over the last 2 decades, more than half of the states have allowed limited access to marijuana or its components, Δ9-tetrahydrocannabinol (THC) and cannabidiol, for medical reasons.2 More recently, 4 states and the District of Columbia have legalized marijuana for recreational purposes.

Currently, evidence for the therapeutic benefits of marijuana are limited to treatment and improvements to certain health conditions (eg, chronic pain, spasticity, nausea).3 Recreational use of marijuana is established by patterns of individual behaviors and lifestyle choices. In either case, use of marijuana or any of its components, especially in younger populations, is associated with an increased risk of certain adverse health effects, such as problems with memory, attention, and learning, that can lead to poor school performance and reduced educational and career attainment, early-onset psychotic symptoms in those at elevated risk, addiction in some users, and altered brain development.4- 7

In September 2016, the Substance Abuse and Mental Health Services Administration and the Centers for Disease and Control and Prevention (CDC) released an issue of the CDC’s Morbidity and Mortality Weekly Report—Surveillance Summary describing historical trends in marijuana use and related indicators among the non-institutionalized civilian population aged 12 years or older using 2002-2014 data from the National Survey on Drug Use and Health (NSDUH).8

During the last 13 years, marijuana access (ie, perceived availability) and use (ie, past-month marijuana use) have steadily increased in the United States, particularly among people aged 26 years or older, increasing from 54.9% in 2002 to 59.2% in 2014 and from 4.0% in 2002 to 6.6% in 2014, respectively. The factors associated with the national behavior patterns of marijuana use cannot be attributed solely to the heterogeneous body of state laws and policies that vary considerably with respect to year of enactment, implementation lag time, and access stipulations.

However, as state laws and policies continue to evolve, these data will be useful as a baseline to monitor changes in patterns of use and associated variables. Monitoring behavioral patterns is important given the possible increased risk of adverse health consequences due to potency changes—higher concentrations of THC (the psychoactive compound)—of the cannabis plant in the United States in the last 2 decades.9

Estimates from NSDUH data suggest that in 2014, 2.5 million persons aged 12 years or older had used marijuana for the first time within the past 12 months; this projected estimate suggests that there is an average of about 7000 new users each day (approximately 1000 more new users each day in 2014 compared with in 2002). In 2014, mean age at first use of marijuana was 19 years among persons aged 12 years or older and was 15 years among persons aged 12 to 17 years.8

During 2002-2014, the estimated prevalence of marijuana use in the past month, in the past year, and daily or almost daily increased among persons aged 18 years or older but

not among those aged 12 to 17 years, while the perceived risk from smoking marijuana decreased across all age groups. Conversely, the estimated prevalence of past-year marijuana dependence decreased from 1.8% in 2002 to 1.6% in 2014 among all persons aged 12 years or older and from 16.7% in 2002 to 11.9% in 2014 among past-year marijuana users.

Overall, the perceived availability to obtain marijuana among persons aged 12 years or older increased, and acquiring marijuana by buying the drug and growing it increased vs obtaining marijuana for free and sharing the drug. The percentage of persons aged 12 years or older perceiving that the maximum legal penalty for the possession of 1 oz or less of marijuana in their state of residence is a fine and no penalty increased vs perceptions that penalties included probation, community service, possible prison sentence, and mandatory prison sentence.8

These findings on perceived availability to obtain marijuana and fewer punitive legal penalties (eg, no penalty) for the possession of marijuana for personal use may play a role in the observed increased prevalence in use among adults in the United States. However, surveillance data do not reveal causal relationships; therefore, more granular research is needed.

As states adopt policies that increase legal access to marijuana, new indicators will be needed to understand trends in marijuana use and the risk of health effects. Questions regarding mode of use (eg, smoked, vaped, dabbed, eaten, drunk), frequency of use, potency of marijuana consumed, and reasons for use (ie, medical use, recreational use, or both) could be added to existing surveillance systems or launched in new systems.

Traditionally, understanding factors underlying the trends in marijuana use have been assessed by looking at 1 or 2 indicators (eg, perception of harm risk or dependence or abuse). A multivariable approach that includes environmental (eg, law enforcement, laws/policies) and cultural (eg, religion, individual choice) factors might be required to understand the relationship between the perceptions and attitudes toward marijuana and use behavior.

The health effects associated with marijuana use are still widely debated. Nonetheless, marijuana use during early stages of life, when the brain is developing, poses potential public health concerns, including reduced educational attainment, addiction in some users, poor education outcomes, altered brain structure and function, and cognitive impairment.4- 7

Given these potential health and social consequences of marijuana use, additional data sources at the federal and state levels may be required to assess the public health effects of marijuana use. These sources may include data from sectors such as health care (eg, emergency department data), criminal justice (eg, law enforcement data), education (eg, school attendance and performance data), and transportation (eg, motor vehicle injury data).

Assessing the prevalence and public health effects of marijuana use in the United States remains important given the evolving policies for marijuana for medical or recreational use at the state level. Therefore, it is vital to continue to monitor key traditional marijuana indicators but also to enhance public health surveillance to include monitoring of indicators that assess emerging issues so that public health actions could prevent adverse health consequences.

Given that legislation, types of products, use patterns, and evidence for potential harms and benefits of marijuana and its compounds are all evolving, clinicians need to understand the magnitude of marijuana use and associated behaviors so they can provide informed answers to patient questions, screen, counsel, treat, and refer patients to community treatment or counseling centers if abuse or adverse effects are identified.

Source: JAMA. 2016;316(17):1765-1766. doi:10.1001/jama.2016.13696

* Cannabis impairs cognitive and psychomotor performances.

* An 8-h delay after maximal effects is recommended for cannabis self-treatment.

* Blood THCCOOH level >40 μg/l suggests regular cannabis use and long-term impairment.

* No correlation was found between psychomotor task performance and THC blood levels.

* Acute cannabis consumption nearly doubles the risk of a collision.

Abstract

Traffic policies show growing concerns about driving under the influence of cannabis, since cannabinoids are one of the most frequently encountered psychoactive substances in the blood of drivers who are drug-impaired and/or involved in accidents, and in the context of a legalization of medical marijuana and of recreational use.

The neurobiological mechanisms underlying the effects of cannabis on safe driving remain poorly understood. In order to better understand its acute and long-term effects on psychomotor functions involved in the short term ability and long-term fitness to drive, experimental research has been conducted based on laboratory, simulator or on-road studies, as well as on structural and functional brain imaging.

Results presented in this review show a cannabis-induced impairment of actual driving performance by increasing lane weaving and mean distance headway to the preceding vehicle. Acute and long-term dose-dependent impairments of specific cognitive functions and psychomotor abilities were also noted, extending beyond a few weeks after the cessation of use.

Some discrepancies found between these studies could be explained by factors such as history of cannabis use, routes of administration, dose ranges, or study designs (e.g. treatment blinding). Moreover, use of both alcohol and cannabis has been shown to lead to greater odds of making an error than use of either alcohol or cannabis alone. Although the correlation between blood or oral fluid concentrations and psychoactive effects of THC needs a better understanding, blood sampling has been shown to be the most effective way to evaluate the level of impairment of drivers under the influence of cannabis. The blood tests have also shown to be useful to highlight a chronic use of cannabis that suggests an addiction and therefore a long-term unfitness to drive. Besides blood, hair and repeated urine analyses are useful to confirm abstinence

Source:  Elsevier Journal Alerts Volume 268, Pages 92–102  November 2016

A research team from the University of Edinburgh examined data from 284 adults who attended primary care centers in the United Kingdom between 2011 and 2013.  Some 170 were marijuana users, 114 smoked cigarettes but did not use marijuana. Heavy users had smoked marijuana 47,000 times in their lifetime; occasional users averaged about 1,000 times. Using a special x-ray process, researchers examined study participants’ bone density and found the heavy marijuana users had a 5 percent lower bone density than nonusers.  “We have known for a while that the components of cannabis can affect bone cell function, but we had no idea up until now of what this might mean to people who use cannabis on a regular basis. Our research has shown that heavy users of cannabis have quite a large reduction in bone density compared with nonusers, and there is a real concern that this may put them at increased risk of developing osteoporosis and fractures later in life,” said the team’s leader, Professor Stuart Ralston. The team says more research is needed to confirm this association.

Source:  National Families in Action’s The Marijuana Report srusche=nationalfamilies.org@mail145.atl121.mcsv.net   19th Oct 2016

This November, several states will vote on whether to legalize marijuana for recreational use, and the proponents of legalization have seized on a seemingly clever argument: marijuana is safer than alcohol.  The Campaign to Regulate Marijuana Like Alcohol, an effort of the Marijuana Policy Project (or MPP), has taken this argument across the country.  Their latest strategy is labelled Marijuana vs. Alcohol.  It is a very misleading, even dangerous, message, based on bad social science and sophistic public deception. Citing out-of-date studies that go back ten years and more, even using that well-known scientific journal, Wikipedia, the MPP never references current research on the harms of today’s high potency and edible marijuana, studies that come out monthly if not more frequently.  Indeed, their Marijuana vs. Alcohol page concludes with a 1988 statement about the negligible harms of marijuana—but that is a marijuana that simply does not exist anymore, neither in mode nor potency.  Today’s marijuana is at least five times more potent, and sold in much different form.  And the science of marijuana and its effects on the brain have come some distance since 1988 as well.

So out-of-date is the science and knowledge of marijuana from thirty years ago, it would be malpractice in any other field to suggest that kind of information about a drug having any contemporary relevance at all.  One almost wonders if the MPP thinks public health professors still instruct their students on how to use microfiche to perform their research as they prepare to write their papers on 5k memory typewriters.

It is simply misleading in a public health campaign to cite dated research while at the same time ignore a larger body of current evidence that points in the opposite direction of a desired outcome.  At great potential peril to our public health, political science (in the hands of the marijuana industry) is far outrunning medical science.  But the danger is clear: with the further promotion, marketing, and use of an increasingly known dangerous substance, public health and safety will pay the price.

Consider three basic problems with the industry’s latest campaign:

I.  Comparisons of relative dangers of various drugs are simply impossible and can often lead to paradoxical conclusions.  It is impossible to compare a glass of chardonnay and its effects on various adults of various weights and tolerance levels with the inhalation or consumption of a high-potency marijuana joint or edible.  Is the joint from the 5 percent THC level or the 25 percent level?  How about a 30 mg—or stronger—gummy bear?  A glass of wine with dinner processes through the body in about an hour and has little remaining effect.  A marijuana brownie or candy can take up to 90 minutes to even begin to take effect.

Consider a consumer of a glass of wine who ate a full meal and waited an hour or more before driving and a consumer of a marijuana edible taking the wheel of a plane, train, automobile, or anything else.  The wine drinker would likely be sober, the marijuana consumer would just be getting high, and, given the dose, possibly very high at that.

True, marijuana consumption rarely causes death, but its use is not benign.  Last year, an ASU professor took a standard dose of edible marijuana, just two marijuana coffee beans. The effect?  “Episodes of convulsive twitching and jerking and passing out” before the paramedics were called.  Such episodes are rare for alcohol, but they are increasingly happening with marijuana.

Beyond acute effects, the chronic impact of marijuana is also damaging.  Approximately twice the percentage of regular marijuana users will experience Marijuana Use Disorder than will alcohol users experience Alcohol Use Disorder—both disorders categorized by the Diagnostic Statistics Manual (DSM).[1]   Marijuana is also the number one substance of abuse for teens admitted to treatment, far higher than the percentage who present with alcohol problems.  In fact, the most recent data out of Colorado shows 20 percent of teens admitted for treatment have marijuana listed as their primary substance of abuse compared to less than one percent for alcohol.

Still, the Campaign persists in its deceptions—as if they have not even read their own literature.  One online marketing tool it recently deployed was the “Consume Responsibly” campaign.  Delve into that site and you will find this warning: “[Smoked marijuana] varies from person to person, you should wait at least three to four hours before driving a vehicle.”  And: “Edible marijuana products and some other infused products remain in your system several hours longer, so you should not operate a vehicle for the rest of the day after consuming them.”  Who has ever been told that they should not operate a vehicle for four hours, much less for the rest of the day, if they had a glass of wine or beer?  Safer than alcohol?  This is not even true according to the MPP’s own advice.

Beyond unscientific dose and effect comparisons, there is a growing list of problems where marijuana use does, indeed, appear to be more harmful than alcohol.  According to Carnegie Mellon’s Jonathan Caulkins: “Marijuana is significantly more likely to interfere with life functioning” than alcohol and “it is moderately more likely to create challenges of self-control and to be associated with social and mental health problems.” Additionally, a recent study out of UC Davis revealed that marijuana dependence was more strongly linked to financial difficulties than alcohol dependence and had the same impacts on downward mobility, antisocial behavior in the workplace, and relationship conflict as alcohol.

II.  The marijuana industry pushes and promotes the use of a smoked or vaped substance, but never compares marijuana to tobacco.  Indeed, the two substances have much more in common than marijuana and alcohol, especially with regard to the products themselves and the method of consumption (though we are also seeing increasing sales of child-attractive marijuana candies).  But why is the comparison never made?  The answer lies in the clear impossibility.

Consider: Almost every claim about marijuana’s harms in relation to alcohol has to do with the deaths associated with alcohol.  But, hundreds of thousands more people die from tobacco than alcohol.  Based on their measures of mortality, which is safer: alcohol or tobacco?  Can one safely drink and drive?  No.  Can one smoke as many cigarettes as one wants while driving?  Of course. So, what’s the more dangerous substance?  Mortality does not answer that question.

Alcohol consumption can create acute problems, while tobacco consumption can create chronic problems.  And those chronic problems particularly affect organs like the lungs, throat, and heart.  But what of the chronic impact on the brain?  That’s the marijuana risk, and, seemingly, society is being told that brains are less important than lungs.  Nobody can seriously believe that, which is why these comparisons simply fail scrutiny.

This illustrates but one of the problems in comparing dangerous substances. As Professor Caulkins recently wrote:

The real trouble is not that marijuana is more or less dangerous than alcohol; the problem is that they are altogether different….The country is not considering whether to switch the legal statuses of alcohol and marijuana. Unfortunately, our society does not get to choose either to have alcohol’s dangers or to have marijuana’s dangers. Rather, it gets to have alcohol’s dangers…and also marijuana’s dangers. Further, marijuana problems are associated with alcohol problems.  New research out of Columbia University reveals that marijuana users are five times more likely to have an alcohol abuse disorder.  Society doesn’t just switch alcohol for marijuana—too often, one ends up with use of both, compounding both problems.

The larger point for voters to understand:  The marijuana legalization movement is not trying to ban or end alcohol sales or consumption; rather, it wants to add marijuana to the dangerous substances already available, including alcohol.  This is not about marijuana or alcohol, after all.  It’s about marijuana and alcohol. We can see this effect in states like Colorado, with headlines such as “Alcohol sales get higher after weed legalization.”  And, according to the most recent federal data [2], alcohol use by teens, as well as adults, has increased in Colorado since 2012 (the year of legalization). If alcohol is the problem for the MPP, in their model state–Colorado–alcohol consumption has increased with marijuana legalization.  Legalizing marijuana will, in the end, only make alcohol problems worse. III.  The legalization movement regularly cites to one study in the Journal of Scientific Reports to “prove” that marijuana is safer than alcohol.  But this study leads to odd conclusions in what the authors, themselves, call a “novel risk assessment methodology.”  For instance, the researchers find that every drug, from cocaine to meth to MDMA to LSD, is found to be safer than alcohol. (See this graph).  By the MPP standard, we should thereby make these substances legal as well.  But, seeing such data in its full light, we all know this would be nonsensical.

Further, the authors specifically write that they only looked at acute effects and did not analyze “chronic toxicity,” and cannot judge marijuana and “long term effects.”  Indeed, they specifically write in their study the toxicity of marijuana“may therefore be underestimated” given the limitations of their examination.  Yet legalizers ignore these statements.  Always.  It simply does not fit their narrative. What long-term effects are we talking about?  To cite the New England Journal of Medicine: “addiction, altered brain development, poor educational outcomes, cognitive impairment,” and “increased risk of chronic psychosis disorders.”  Now think about what it will mean to make a drug with those adverse effects more available, and for recreational use.

Finally, the very authors of the much-cited Journal of Scientific Reports study specifically warn their research should be “treated carefully particularly in regard to dissemination to lay people….especially considering the differences of risks between individuals and the whole population.”  But this is precisely what commercialization is about—not individual adult use but making a dangerous drug more available to “the whole population.”

Given what we know in states like Colorado, we clearly see that legalization creates more availability which translates into more use, affecting whole populations—Colorado college-age use, for example, is now 62 percent higher than the national average. [See FN2, below]. And the science is coming in, regularly.  Indeed, the same journal the MPP points to in its two-year old “novel” study, just this year published another study and found:

Neurocognitive function of daily or near daily cannabis users can be substantially impaired from repeated cannabis use, during and beyond the initial phase of intoxication. As a consequence, frequent cannabis use and intoxication can be expected to interfere with neurocognitive performance in many daily environments such as school, work or traffic.

That is why these comparisons of safety and harm are—in the end—absurd and dangerous.  In asking what is safer, the true answer is “neither.”  And for a variety of reasons.  But where one option is impossible to eliminate (as in alcohol), society should not add to the threat that exists:  One doesn’t say because a playground is near train tracks you should also put a highway there.  You fence off the playground.

That, however, is not the choice the MPP has given us.  They are not sponsoring legislation to reduce the harms of alcohol, they are, instead, saying that with all the harms of alcohol, we should now add marijuana.  But looking at all the problems society now has with substance abuse, the task of the serious is to reduce the problems with what already exists, not advance additional dangers.

If the MPP and its Campaigns to Regulate Marijuana Like Alcohol are serious about working on substance abuse problems, we invite them to join those of us who have labored in these fields for years.  One thing we do know: adding to the problems with faulty arguments, sloppy reasoning, and questionable science, will not reduce the problems they point to.  It will increase them.  And that, beyond faulty argument and sloppy reasoning, is public policy malfeasance. [1] See http://archpsyc.jamanetwork.com/article.aspx?articleid=2464591 compared to http://archpsyc.jamanetwork.com/article.aspx?articleid=2300494

Source:  http://amgreatness.com/2016/09/25/lie-travels-comparing-alcohol-marijuana/  Sept 25th 2016

If you smoke weed for five years or more, on a daily basis, prepare to lose your eloquence. A study by a team of researchers from the University of Lausanne in Switzerland, published earlier this year, found that people who smoked marijuana on a daily basis for a long period of time had poorer verbal memory in their middle age, than others.

This occurred when controlling for a number of other factors, such as age, education, other substance use and mental health issues.  The team found that the relationship between marijuana use and memory problems was fairly direct – that the more pot people smoked, the worse they performed in memory tests.

Although the difference wasn’t stark over five years – the more years for which you smoke daily the more you compound the issue.  However, few people reach these levels of exposure – of the 3,385 study subjects, only 311 had more than five marijuana years’ (if you smoke pot every day for a year) worth of exposure.

The upshot? Other cognitive abilities didn’t seem to be significantly affected by heavy cannabis use, such as ability to focus and problem solving speed.  Testimony from people who have decided to quit the drug has previously supported these findings. Stuart Angel told news.com.au:

Even when I smoked, I always had a great long term memory.

But my short term memory has really suffered. When I was smoking, I would say something, and then get distracted. I couldn’t focus when I smoked, not even for 10 minutes. Now I can focus for much longer periods of time. A reddit user also posted on the r/trees subreddit a lengthy post explaining his motives for quitting:

I’ve missed a lot of things because of it. Chief among these is my memory: often, when discussing a film with people, I’ve had to admit that I couldn’t really remember it because I was stoned when I watched it the first time. Often, when watching television with my girlfriend, I would ask, ‘Who the hell is this character?’ and she would reply, ‘That’s the protagonist. It’s the main character.’ Oops. I guess I was in my own world.

You are your memories, your past experiences, and an enormously high percentage of my memories were stoned. Thus, even when I wasn’t high, weed was affecting who I was, and who I could become.

Source: https://www.indy100.com/article/what-happens-when-you-smoke-weed-every-day-for-5-years-7347796     Oct.2010

1.  Marijuana use creates neurocognitive impairments and cannabis intoxication in both frequent and infrequent users. –Journal of Scientific Reports, May 2016. (Cannabis and Tolerance: Acute Drug Impairment as a Function of Cannabis Use History).

2. Prevalence of cannabis use is expected to increase if cannabis is legal to use and legally available. –International Journal of Drug Policy, May 2016 (Correlates of Intentions to Use Cannabis among US High School Seniors in the Case of Cannabis Legalization).

3. Regular exposure to cannabis is associated with neuroanatomic alterations in several brain regions. –Journal of Biological Psychiatry, April 2016  (The Role of Cannabinoids in Neuroanatomic Alterations in Cannabis Users).

4. Marijuana is addicting, has adverse effects upon the adolescent brain, is a risk for both cardio-respiratory disease and testicular cancer, and is associated with both psychiatric illness and negative social outcomes. –Statement of the American College of Pediatricians, April 2016 (Marijuana Use: Detrimental to Youth).

5. Marijuana use has significant neuropharmacologic, cognitive, behavioral, and somatic   consequences. –Statement of the American Academy of Pediatrics, March 2015 (The Impact of Marijuana Policies on Youth: Clinical, Research, and Legal Update).

6. Marijuana use is associated with increased incidence and worsened course of psychotic, mood, anxiety, and substance use disorders across the lifespan….and marijuana’s deleterious effects on adolescent brain development, cognition, and social functioning may have immediate and long-term implications. –Statement of the American Academy of Child & Adolescent Psychiatry, 2014 (AACAP Marijuana Legalization Policy Statement).

7. Marijuana use may cause impairment in memory, concentration, and executive  functioning…and may lead to permanent nervous system toxicity. –Statement of the American Academy of Neurology (Position Statement: Use of Medical Marijuana for Neurologic Disorders).

8. There is a strong association of cannabis use with the onset of psychiatric disorders. Adolescents are particularly vulnerable to harm, given the effects of cannabis on neurological development. –Statement of the American Psychiatric Association (Position Statement on Marijuana as Medicine).

9. Both marijuana-related hospitalizations and ED visits have increased substantially in recent years. –Newsletter of the American College of Physicians, January 2016 (Public Health Researchers Look at Rise in Marijuana-related Hospitalizations).

10. Cannabis dependence is not associated with fewer harmful economic and social

problems than alcohol dependence. –Journal of Clinical Psychological Science, June 2016 (Persistent Cannabis Dependence and Alcohol Dependence Represent Risks for Midlife Economic and Social Problems:  A Longitudinal Cohort Study.)

11. Repeated exposure to cannabis during adolescence may have detrimental effects on brain resting functional connectivity, intelligence, and cognitive function. –Journal of the Cerebral Cortex, February 2016 (Adverse Effects of Cannabis on Adolescent Brain Development: A Longitudinal Study).

12. Negative health effects of marijuana use can include addiction, abnormal brain development, psychosis, and other negative outcomes. –New England Journal of Medicine, June 2014 (Adverse Health Effects of Marijuana Use).

13. One in six infants and toddlers admitted to a Colorado hospital with coughing, wheezing and other symptoms of bronchiolitis tested positive for marijuana exposure. –American Academy of Pediatrics, April 2016 (One in Six Children Hospitalized for Lung Inflammation Positive for Marijuana Exposure).

14. Study respondents who were high had higher odds driving while intoxicated (on either marijuana or alcohol). –Journal of Health Education Research, April 2016 (Association Between Self-reports of Being High and Perceptions About the Safety of Drugged and Drunk Driving).

15. Cannabis use during adolescence increases the risk of developing a psychiatric disorder in adulthood, including anxiety, depression, and schizophrenia. –Frontiers in Neuroscience, November 2014.  (Long-term Consequences of Adolescent Cannabinoid Exposure in Adult Psychopathology).

16. Childhood exposure to marijuana increases in marijuana friendly states and can lead to coma, decreased breathing, or seizures. –Journal of Clinical Pediatrics, June 2015, (Marijuana Exposure Among Children Younger Than Six Years in the United States).

17. Use of marijuana in adolescence found to increase developing psychosis, schizophrenia, anxiety, and depression in adulthood. –Boston Children’s Hospital/Harvard Medical School, 2014 (Marijuana 101, Dr. Sharon Levy).

18. Cannabis use may cause enduring neuropsychological impairment that persists beyond the period of acute intoxication. –Proceedings of the National Academy of Sciences, July 2012. (Persistent Cannabis Users Show Neuropsychological Decline from Childhood to Midlife).

19. Cannabis use disorder is prevalent, associated with comorbidity and disability, and largely untreated. –The American Journal of Psychiatry, March 2016. (Prevalence and Correlates of DSM-5 Cannabis Use Disorder, 2012-2013: Findings from the National Epidemiologic Survey on Alcohol and Related Conditions–III).

20. We recorded clear and consistent associations and dose-response relations between the frequency of adolescent cannabis use and all adverse young adult outcomes. –The Lancet-Psychiatry, September 2014.  (Young Adult Sequelae of Adolescent Cannabis Use: An Integrative Analysis).

21. While marijuana may be safer than alcohol in some respects, there are important dimensions along which marijuana appears to be the riskier substance. –Carnegie Mellon Research/Jonathan P. Caulkins, October 2014. (Is Marijuana Safer than Alcohol? Insights from Users’ Self-Reports).

22. Potential impacts of recreational marijuana include not only increased availability, resulting in ED visits for acute intoxicating effects of marijuana use, but also effects on mental health disorders and psychiatric-related illnesses. –American College of Emergency Physicians/ACEP NOW, October 2014. (How Legalizing Marijuana Has Impacted Colorado).

23. Marijuana changes the structure and function of the adolescent brain. –Bertha Madras, Professor of Psychobiology, Harvard University, May 2014.  (Marijuana and Opioids Risks for the Unborn, the Born).

24. Dramatic increase in newborns testing positive for marijuana in Colorado hospitals.

–Parkview Medical Center, St. Mary-Corwin Medical Center, Pueblo Community Health Center, April 2016. (Recreational Retail Marijuana Endangers Health of Community & Drains Precious Health Resources).

25. Casual use of marijuana is related to major brain changes. –Journal of Neuroscience, April 2014.  (Cannabis Use Is Quantitatively Associated with Nucleus Accumbens and Amygdala Abnormalities in Young Adult Recreational Users).

26. It needs to be emphasized that regular cannabis use, defined here as once a week, is not safe and may result in addiction and neurocognitive damage, especially in youth. –Journal of Current Addiction Reports, April 2014. (Considering Cannabis: The Effects of Regular Cannabis Useon Neurocognition in Adolescents and Young Adults).

27. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood. –Journal of Current Addiction Reports, June 2014.  (Impact of Cannabis Use on the Development of Psychotic Disorders).

28. Marijuana is not benign and there’s a mountain of scientific evidence, compiled over nearly 30 years, to prove it poses serious risks, particularly for developing brains.

–Diane McIntosh, Professor of Psychiatry-University of British Columbia, April 2016.  (You Can’t Deny Marijuana Is Dangerous For Developing Minds).

28. Marijuana may actually worsen PTSD symptoms or nullify the benefits of specialized, intensive treatment. Cessation or prevention of use may be an important goal of treatment. –Journal of Clinical Psychiatry, September 2015.  (Marijuana Use is Associated With Worse Outcomes in Symptom Severity and Violent Behavior in Patients With Posttraumatic Stress Disorder).

29. Converging epidemiological data indicate that adolescent cannabis abusers are more likely to develop psychosis and PFC-related cognitive impairments later in life. –Journal of Molecular Psychiatry, March 2014. (CB1 Cannabinoid Receptor Stimulation During Adolescence Impairs the Maturation of GABA Function in the Adult Rat Prefrontal Cortex).

30. Regular cannabis use in adolescence approximately doubles the risk of being diagnosed with schizophrenia or reporting psychotic symptoms in adulthood. –Journal of Addiction, January 2015. (What Has Research Over the Past Two Decades Revealed About the Adverse Health Effects of Recreational Cannabis Use).

**This is a sample of 30 studies and statements, of over 20,000, on the harms of marijuana.  More found here.

Source:  https://noprop205.com/research/    2016

Since many drug dependent individuals are known to be depressed and sometimes suicidal this research is encouraging. NDPA

Suicide is the cause of more than 42,000 deaths in the United States every year, making it the 10th leading cause of death in the country. Now, a new study paves the way for a drug to avert suicidal behavior, after identifying an enzyme related to brain inflammation that has the potential to predict and prevent suicide.

Researchers say their findings may bring us closer to a drug that can prevent suicidal behavior.

In the journal Translational Psychiatry, researchers reveal how a certain variant of the enzyme ACMSD leads to abnormal levels of two acids in the brain, which may encourage suicidal behavior.

The research team – including senior author Dr. Lena Brundin of the Center for Neurodegenerative Science at Van Andel Research Institute in Grand Rapids, MI – say their findings could bring us closer to a blood test that can identify patients at high risk of suicide.

What is more, the study suggests ACMSD could be a promising drug target for suicide prevention.

According to Dr. Brundin and colleagues, previous research has suggested the immune system plays a role in depression and suicidal behavior, primarily by responding to stress with inflammation.

However, the underlying mechanisms of this association have been unclear, which has hampered the discovery of clinical strategies to prevent suicide. The new study aimed to shed some light.

Past studies have shown patients with suicidal behavior experience persistent inflammation in their blood and cerebrospinal fluid (CSF).

With this in mind, the researchers assessed the blood and CSF samples of more than 300 individuals from Sweden, some of whom had attempted suicide.

ACMSD enzyme variant more prevalent in people with suicidal behavior

On comparing samples, the team found that individuals who had attempted suicide had abnormal levels of both picolinic acid and quinolinic acid. These irregular acid levels were identifiable in samples taken straight after a suicidal attempt and at various points over the subsequent 2 years.

Among subjects with suicidal behavior, levels of picolinic acid – known to have neuroprotective effects – were too low, while their levels of quinolinic acid – a known neurotoxin – were too high.

These abnormal levels were most prominent in CSF, the team reports, though they could still be identified in blood samples.

Since previous research had shown that both picolinic and quinolinic acid are regulated by the enzyme ACMSD – known to regulate brain inflammation – the researchers conducted a genetic analysis of individuals with suicidal behavior, as well as healthy controls.

From this, they found that individuals who had attempted suicide were more likely to possess a specific variant of ACMSD, and this variant was associated with increased levels of quinolinic acid.

While the study is unable to demonstrate that ACMSD activity is directly linked to suicide risk, the researchers say their findings suggest the enzyme could be a potential drug target for suicide prevention. “We now want to find out if these changes are only seen in individuals with suicidal thoughts or if patients with severe depression also exhibit this. We also want to develop drugs that might activate the enzyme ACMSD and thus restore balance between quinolinic and picolinic acid.”

Co-study leader Dr. Sophie Erhardt, Karolinska Institutet, Sweden

Additionally, since the results show that abnormal levels of picolinic and quinolinic acid can be identified in the blood, the team says they may bring us closer to a blood test that can identify patients at high risk of suicidal behavior.

Source:  http://www.medicalnewstoday.com/articles/313287.php  4th Oct.2016

Like the viral dance move of the same name, using marijuana by “dabbing” is having a moment.

The latest marijuana-consumption craze has users chasing bigger highs through a process called “flash vaporization.” But unlike the dance, marijuana dabbing poses some major health and safety risks, according to both anecdotal evidence and experts, and is illegal in some states. Dabbing is when you take a marijuana concentrate, a waxy or butter-like substance that contains highly concentrated amounts of tetrahydrocannabinol (THC) — the psychoactive ingredient in weed — apply it to a hot surface to create smoke, and inhale to get high. There are countless ways to heat the material, from burning in it an electronic vaporizer to lighting it on fire with a blowtorch over a glass bong piece called a nail, and it’s up to user preference.

When the internet tells you dabbing gets you high, it means really, really high. The potency of dabs can cause users to pass out, become uncomfortably stoned, or even experience psychedelic effects that border on hallucinations, with one too many rips from a bong. Marijuana concentrates pack a punch no matter how you ingest them. They’re made from blasting a solvent, like butane or carbon dioxide, through marijuana plant matter to extract the THC, then letting the solvent evaporate. The yellow, gooey substance that remains has a THC concentration that’s four times stronger than the plant itself, The New York Times reports.

“Marijuana is the beer of THC, as dabbing is to vodka,” as one New York City teenager seen dabbing down Fifth Avenue put it to The Times.

In pot-friendly Colorado, where weed is sold legally for recreational purposes, concentrates make up about one-third of overall marijuana sales, the Marijuana Business Daily reports. Some industry insiders are calling concentrates “the future of the industry.”

Not everyone is on board with the dabbing craze.

For starters, dousing marijuana in butane, a highly flammable gas, can cause explosions when it meets an ignition source. As dabbing becomes popular, more amateurs turn to the internet for DIY tutorials on how to extract concentrates. But these at-home operations have led to explosions and deaths in recent years, especially when run indoors without proper ventilation.

Dabbing itself appears to be less dangerous than making the supplies, though the risks are still known. Research on how marijuana concentrates affect the body is slim.

“There is some evidence to suggest that the outcomes, like the effects, may be supercharged,” Emily Feinstein, director of health law and policy for the National Center on Addiction and Substance Abuse, tells The Times. “Side effects can include: a rapid heartbeat, blackouts, psychosis, paranoia, and hallucinations that cause people to end up in psychiatric facilities.”

The negative side effects often last longer than the high.

Dr. Michael Miller, the ex-president of the American Society of Addiction Medicine, tells L.A. Weekly that if you have a predisposition for addiction, the intensity and swift kick of the high that dabbing produces may trigger cravings and cues to use again.

More research around the health risks of dabbing is required, along with better regulation to squash the at-home operations that threaten to undermine the industry’s legitimacy.

Even the name, dabbing, has caused confusion among some.

When a news reporter asked two Seattle Seahawks football players, “Do either of you guys dab?” at a press conference in January, they tripped and fumbled over their answers.

“That’s illegal in, in … no, actually it’s legal in Washington!” Michael Bennett exclaimed.

Of course, the reporter was referring to the viral dance move, made popular by Carolina Panthers quarterback Cam Newton. It looks like you’re sneezing in your arm.

Source:  http://uk.businessinsider.com/what-is-marijuana-dabbing-2016-9?r=US&IR=T  2nd Oct. 2016

To watch the video  ‘This is how long drugs actually stay in your system’ click on thesource link above and then scroll down to the bottom of the page to find the video.

Chelsea Clinton recently suggested that marijuana might be deadly when taken with other drugs. But is this really true?

Although marijuana can interact with other drugs, there do not appear to be any reports of deaths that directly resulted from taking marijuana in combination with other drugs.

While speaking in Ohio on Sept. 24, Clinton was asked whether her mother, Hillary Clinton, supports changing the way marijuana is categorized by the Drug Enforcement Administration so that it would be easier for researchers to conduct studies on the drug. Chelsea Clinton replied that her mother does support research on marijuana. Then, she added, “But we also have anecdotal evidence now from Colorado, where some of the people who were taking marijuana for those purposes, the coroner believes, after they died, there was drug interactions with other things they were taking.”

A spokesperson for Clinton later said Clinton “misspoke about marijuana’s interaction with other drugs contributing to specific deaths,” according to The Huffington Post.

By itself, marijuana is not known to have direct lethal effects. According to the U.S. Drug Enforcement Administration, no overdose deaths from marijuana have been reported in the United States.

In addition, the evidence that marijuana may interact with other drugs is limited, according to a 2007 review paper in the American Journal of Health-System Pharmacy.

Still, marijuana does appear to interact with a number of drugs, the review said. If marijuana is taken with alcohol, benzodiazepines (drugs that treat anxiety) or muscle relaxants, the combination can result in “central nervous system depression,” the review said, which means that people can experience decreased breathing and heart rate, and loss of consciousness. [How 8 Common Medications Interact with Alcohol]

There also have been reports of people experiencing a rapid heart rate and delirium after using marijuana while taking older forms of antidepressants (known as tricyclic antidepressants), the review said.

Marijuana may also interact with drugs that are broken down by enzymes in the liver known as cytochrome P450 enzymes, according to the Mayo Clinic. That’s because a compound in marijuana called cannabidiol can inhibit these enzymes. Therefore, marijuana may prevent other drugs from being broken down properly, and as a result,

levels of these other drugs may be increased in the blood, which “may cause increased effects or potentially serious adverse reactions,” the Mayo Clinic says.

One example is the drug sildenafil, commonly known by the brand name Viagra, which is broken down by cytochrome P450 enzymes. In 2002, researchers in the United Kingdom reported that a 41-year-old man had a heart attack after taking marijuana and Viagra together. This report could not prove that the marijuana-Viagra combination was definitely the cause of the man’s heart attack. However, the researchers said that doctors “should be aware” of the effects of inhibiting cytochrome P450 enzymes when prescribing Viagra.

Still, Live Science could not find any scientific or news reports of people who have died as a result of marijuana interacting with another drug.

But that doesn’t mean marijuana is harmless — the drug can impair coordination and slow down reaction time, and it has been linked with fatal car crashes, according to the National Institute on Drug Abuse (NIDA). A 2011 study found that people who reported driving within 3 hours of using marijuana, or drivers who tested positive for the drug, were more than twice as likely to be involved in a car crash compared with other drivers.

The Mayo Clinic says marijuana can increase the drowsiness caused by some drugs, including diazepam (Valium), codeine, antidepressants and alcohol, and so people need to be cautious if they drive or operate machinery after using these drugs with marijuana.

People who take high doses of marijuana may experience anxiety attacks or hallucinations, according to the NIDA. In some rare cases, intoxication with marijuana has been linked with suicide. In 2014, researchers from Germany reported that two men died from heart problems that were brought on by smoking cannabis. But marijuana may have a benefit in terms of reducing deaths from opioid painkillers. A 2014 study found that rates of overdose death from opioids were lower in states where medical marijuana is legal. Another study, published earlier this month, found that rates of opioid use decreased among younger adults in states that had legalized medical marijuana. It’s possible that people are substituting medical marijuana for opioids to treat chronic pain, the researchers said.

Source:http://www.livescience.com/56356-marijuana-drug-interactions.html

3rd Oct.2016

Drug misuse causes 10 times as many deaths as collisions on the roads in parts of England and Wales.

Analysis by BBC News has found drug misuse deaths outnumbered road fatalities in three quarters of local authority areas between 2013 and 2015.  The number of people dying of drug misuse has recently reached a record high.

Public Health England (PHE) said it needed to ensure the most vulnerable drug users could access treatment. Analysing data from the Office for National Statistics BBC News has found that that 75% of all local authorities in England and Wales have seen more people die because of drug misuse than on the roads. Get the data here

There were 6,648 drug misuse deaths recorded compared with 4,683 road deaths between 2013 and 2015.

A drug misuse death is recorded when someone dies after abusing a substance or when they are poisoned by an illegal drug.   Portsmouth saw the highest drug to road death rate, where 18 people died because of drug misuse for every one recorded road fatality.

Other parts of the country such as Blackpool, South Tyneside and Brighton and Hove recorded more than 10 times as many drug deaths in comparison to road deaths.   The rise in drug misuse deaths is being attributed to the greater availability and strength of drugs like heroin.

Ian Hamilton, from the University of York, said it was “horrifying” the number of people dying has continued to rise.   “What this shows is that the issue of drug deaths is not just confined to certain areas but is in fact affecting nearly every part of the country”.  The lecturer in mental health and addiction studies says a decision in 2010 to end a treatment process that saw addicts often prescribed replacement substances like methadone has had unintended consequences.

“Since a policy of total abstinence was introduced we’ve seen the number of people dying of drugs increase every year, I don’t think that’s a coincidence”.  Public Health England says there is no evidence to suggest that changes in drug policy have contributed to an increase in drug deaths.

“Reassuringly, overall drug use has declined” said Rosanna O’Connor, from PHE.

“There is though a need to ensure the most vulnerable can access treatment. We know that the majority of those dying from opiates like heroin have never been involved with treatment services”.

Source:  http://www.bbc.co.uk/news/uk-england-37374513   27th September 2016

Heavy marijuana use alters adolescent brain structure and impairs brain function for people of all ages. On March 10, Colorado launched its Drive High, Get a DUI campaign. Colorado was the first state to legalize recreational marijuana use and is the first state to roll out public service announcements warning marijuana users about driving when you’re high.

The latest marijuana statistics are noteworthy. Marijuana consumption has increased over 30 percent since 2006. From 2006 through 2012, about half of drivers involved in fatal car accidents were tested for drugs and about 11 percent of those drivers tested positive for marijuana. In a September 2014 Colorado survey, 21 percent of respondents reported consuming marijuana and then driving at some point in the past month.

The Colorado Department of Transportation is now airing three television ads as part of its Drive High, Get a DUI campaign. The public service announcements target men ages 21-34, the demographic that tends to have the highest number of DUIs.

In another PSA, a man finishes installing a new flat screen TV on the wall, gives his partner a high five, and a moment later the TV falls off the wall and shatters on the floor. “Installing your TV while high is now legal,” reads the text in the ad … “Driving to get a new one isn’t.” The campaign also includes tourist outreach to rental car companies and dispensaries about marijuana driving laws in Colorado.

One Trillion Dollars of Illegal Drugs A March 2014 study on national drug use found the amount of marijuana consumed by Americans increased by more than 30 percent from 2006 to 2010. The report was compiled for the White House Office of National Drug Control Policy and was conducted by researchers affiliated with the RAND Drug Policy Research Center.

“Having credible estimates of the number of heavy drug users and how much they spend is critical for evaluating policies, making decisions about treatment funding and understanding the drug revenues going to criminal organizations,” said Beau Kilmer, the study’s lead author and co-director of the RAND Drug Policy Research Center. “This work synthesizes information from many sources to present the best estimates to date for illicit drug consumption and spending in the United States.”

The researchers say that because the study only includes data through 2010 the report doesn’t address the recent reported spike in heroin use or the consequences of marijuana legalization in Colorado and Washington. The report also does not try to explain the causes behind changes in drug use or evaluate the effectiveness of drug control strategies.

Researchers say that drug users in the United States spent around $100 billion annually on cocaine, heroin, marijuana and methamphetamine throughout the decade. While the amount remained stable from 2000 to 2010, the spending shifted. While much more was spent on cocaine than on marijuana in 2000, the opposite was true by 2010.

“Our analysis shows that Americans likely spent more than one trillion dollars on cocaine, heroin, marijuana and methamphetamine between 2000 and 2010,” Kilmer said. The surge in marijuana use is related to an increase in the number of people who reported using the drug on a daily or near-daily basis.

Source: https://www.psychologytoday.com/blog/the-athletes-way  March 2016

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September 25th, 2013

The club drug “Molly” is often laced with other synthetic drugs such as bath salts, making it more dangerous, according to law enforcement officials.

Molly, a club drug blamed for several recent deaths among young people attending music festivals, is sold as a pure form of Ecstasy, or MDMA. Drug dealers are now selling a variety of potentially more dangerous drugs under the name Molly, according to The Wall Street Journal.

Jeff Lapoint, an attending physician at Kaiser Permanente in San Diego, says while Molly generally leads to feelings of empathy, bath salts “are potent stimulants and tend to induce paranoia and hallucinations. It’s like the worst combination: While they’re agitated, now they’re seeing things, too.”

“Molly is just a marketing tool,” said Rusty Payne, a spokesman for the Drug Enforcement Administration, told the newspaper. “It could be a whole variety of things.”

MDMA is difficult to manufacture, so some drug makers get bath salts ingredients and repackage them as Molly, explained James Hall, an epidemiologist at the Center for Applied Research on Substance Use and Health Disparities in Miami. Payne noted bath salts ingredients, such as methylone, are much less expensive than MDMA. Molly is suspected of causing two deaths at a recent New York City music festival. A19-year-old girl in Boston died of a suspected overdose of Molly following a concert, and a man in Washington state died after taking the drug, with dozens more treated for Molly overdoses.

Source:  http://www.drugfree.org/news-service/bath-salts-often-added-to-molly-making-the-drug-more-dangerous-officials/  25th Sept. 2013

 September 12, 2016
Gaining scientific proof of adverse effects of cannabis, a world first
Suppression of thalamocortical projection by chronic administration of Δ9-THC (cannabinoid, active ingredient of marijuana). Photomicrograph of cerebral cortex from transgenic mice expressing GFP in thalamocortical axons at postnatal day 7 (P7). (left) : Normal thalamocortical projections. In the middle layer (layer 4), blobs of GFP showing dense termination of thalamocortical axons can be seen (under number 1~5). (right): Thalamocortical projection at P7 from a mouse received chronic administration of Δ9-THC (P2~7). Massive retraction of thalamocortical projections including middle layer (layer 4) can be observed. Credit: Osaka University

Researchers have clarified important mechanisms involved in the formation of neural circuits in the brain. This group also discovered that delta-9-tetrahydrocannabinol (THC), a psychoactive substance also found in cannabis, causes disruption of neural circuits within the cortex. These results explain why cannabis may be harmful and have potential to find application in the functional recovery of brain injury and in cases of dementia.

Neural activity is known to play an important role in the formation of neural circuits. However, we still do not know much about what kind of neural activities are involved in this formation process. This process is especially complex in projections from the thalamus to the cortex, of which so far we only knew that as these projections develop, unnecessary projections are eliminated, thereby leaving only correct projections.

A group of researchers led by Fumitaka Kimura, associate professor at the Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, has now clarified the involvement of several mechanisms in the formation of this neural circuit. The researchers also put forth scientific evidence that cannabis intake causes the unnecessary trimming of neural connections, leading to a breakdown of neural circuits (Figure 1).

In their study, this group of researchers discovered that in a different section of the cortex, the rule (Spike Timing-Dependent Plasticity: STDP) by which synaptic strength (a functional measure of connections) between neurons was determined suddenly changed at a certain point in development. Building on this finding, the group examined whether a similar STDP change occurred in the projection from the thalamus and the cortex as well. They found that initially, the synapses were strengthened due to the synchronized activities of the pre- (thalamic) and post- (cortical) synaptic neurons. But after the projections had spread widely, the synchronized activities weakened all but some synapses, thereby eliminating unnecessary projections to enable more systematic ones. As the synapses are weakened, endogenous cannabinoid is released from neural cells via these synchronized activities, leading to a regression of unnecessary neuron projections (Figure 2). The researchers also confirmed such regression when cannabinoid was taken in externally.

The researchers also confirmed such regression when cannabinoid was taken in externally.

Gaining scientific proof of adverse effects of cannabis, a world first
Endogenous cannabinoid regulates the termination area of thalamocortical axons.(left): Normal thalamocortical projection terminates within a square area in layer 4 (barrel, indicated in red), revealed by visualization of individual thalamocortical axons at P12.(left): Disorganized projections of thalamocortical axons at P12 in animals in which gene of cannabinoid receptor was knocked out. Thalamocortical axons overshoot layer 4 and invade upper layers (layer 2/3); the axons seem to ignore barrels boundaries. Credit: Osaka University

These findings may have an impact on further research focused on advancing our understanding of the mechanisms involved in the formation of neural circuits and have the potential to lead to the development of new therapies to improve recovery from brain damage and dementia. In addition, the findings provide for the adverse effects of cannabis consumption on brain development and therefore may help to decrease abuse of marijuana.

This research was featured in the electronic version of Journal of Neuroscience on June 29, 2016.

More information: C. Itami et al, Developmental Switch in Spike Timing-Dependent Plasticity and Cannabinoid-Dependent Reorganization of the Thalamocortical Projection in the Barrel Cortex,Journal of Neuroscience (2016). DOI: 10.1523/JNEUROS

Source:  http://medicalxpress.com/news/2016-09-adverse-effects-cannabis-scientifically.html 12 Sept 2016

New research from the Icahn School of Medicine at Mount Sinai using electroencephalography, or EEG, indicates that adults addicted to cocaine may be increasingly vulnerable to relapse from day two to one month of abstinence and most vulnerable between one and six months. The findings, published online today in JAMA Psychiatry, suggest that the most intense periods of craving for illicit substances often coincide with patients’ release from addiction treatment programs and facilities.

It is not known why individuals with substance use disorders relapse even after remaining abstinent from illicit substances for long periods of time. However, it is clear that cue-induced craving—craving elicited by the exposure to cues previously associated with drug use—plays a major role in relapse. Until now, studies have used self-reported measures to assess cue-induced craving. This is the first study that uses EEG to quantify cue-induced craving in humans with cocaine use disorder, showing a similar trajectory of craving demonstrated in previous studies using animal models. In this study and in contrast to the EEG measures, self-reported craving showed a gradual decline with increasing abstinence duration, underscoring a potential disconnect between the physiological response to drug-related cues in addicted individuals and their perception of this response.

“Our results are important because they identify an objectively ascertained period of high vulnerability to relapse,” says Muhammad Parvaz, PhD, Assistant Professor of Psychiatry and Neuroscience, Icahn School of Medicine at Mount Sinai, and the study’s lead author. “Unfortunately, this period of vulnerability coincides with the window of discharge from most treatment programs, perhaps increasing a person’s propensity to relapse.”

Over five and a half years, the research team collected data from EEG recordings in 76 adults addicted to cocaine with varying durations of abstinence (two days, one week, one month, six months, and one year). EEG was recorded while participants looked at different types of pictures, including pictures that depicted cocaine and individuals preparing, using, and simulating use of cocaine. After EEG, participants also self-rated their level of craving for each cocaine-related picture.

“Results of this study are alarming in that they suggest that many people struggling with drug addiction are being released from treatment programs at the time they need the most support,” said Rita Goldstein, PhD, Professor of Psychiatry and Neuroscience at the Icahn School of Medicine and Principal Investigator of the study. “Our results could help guide the implementation of alternative, individually tailored and optimally timed intervention, prevention, and treatment strategies.”

Source:  http://img.medicalxpress.com/newman/gfx/news/hires/2015/cocaine.jpg  7th Sept.2016

50-year study finds causal link between cannabis and subsequent violent behavior  New research published on-line in advance of print in the journal Psychological Medicine, concludes that continued use of cannabis causes violent behavior as a direct result of changes in brain function that are caused by smoking weed over many years.

Researchers have long debated a possible link between use of marijuana and violent crime.  In contrast to alcohol, meth, and many other illegal drugs, the mellowing effects of cannabis seem unsuited to promoting violent behavior.  However, ample previous research has linked marijuana use to increased violent behavior.  The sticky problem in such studies are the many confounding factors involved in interpreting this correlation.

It is very difficult to determine whether any statistical correlation between marijuana use and violent behavior are causally linked, or instead the two are associated through some other factor, such as socioeconomic status, personality traits, or many other variables that are related to the propensity to use marijuana.  Moreover, the causal relation between smoking pot and violent behavior could be in exactly the opposite direction.  That is, individuals who are involved in violence or who commit criminal offenses may also be people who are more open to using marijuana.

After all, marijuana is an illegal substance in most places, so people with antisocial personality traits and those with tendencies toward lawlessness may be the type of individuals inclined to be more open to obtaining and using the illegal substance.  Not so, conclude neuroscientist Tabea Schoeler at Kings College London, and her colleagues, “Together, the results of the present study provide support for a causal relationship between exposure to cannabis and subsequent violent outcomes across a major part of the lifespan.”  Let’s examine the evidence provided by this new study. What makes this new study more compelling than previous studies is that the researchers followed the same individuals for over 50 years from a young age to adulthood.  This is precisely what one needs to solve the chicken or egg riddle with respect to cannabis and violence:  just look and see which one happens first.

These subjects were in the Cambridge Study in Delinquent Development, comprised of 411 boys who were born around 1953 and living in working-class urban neighborhoods of London.  97% of them were Caucasian and all of them were raised in two parent households.  The researchers took into consideration other factors, including antisocial traits as assessed by the Antisocial Personality Scale, alcohol use, other drug use, cigarette smoking, mental illnesses, and family history.

Heres’s what they found:  Most of the participants never used cannabis and they were never reported to have violent behavior.  38% of the participants did try cannabis at least once in their life.  Most of them experimented with cannabis in their teens, but then stopped using it. However, 20% of the boys who started using pot by age 18 continued to use it through middle age (32-48 years).  One fifth of those who were pot smokers (22%) reported violent behavior that began after beginning to use cannabis, whereas only 0.3% reported violence before using weed.  Continued use of cannabis over the life-time of the study was the strongest predictor of violent convictions, even when the other factors that contribute to violent behavior were considered in the statistical analysis.

In conclusion, the results show that continued cannabis use is associated with a 7-fold greater odds for subsequent commission of violent crimes.  This level of risk is similar to the increased risk of lung cancer from smoking cigarettes over a similar duration (40 years).  The authors suggest that impairments in neurological circuits controlling behavior may underlie impulsive, violent behavior, as a result of cannabis altering the normal neural functioning in the ventrolateral prefrontal cortex.

Source:  https://www.psychologytoday.com/blog/the-new-brain/201603/marijuana-use-increases-violent-behavior     March 2016

6-suprising-ways-alcohol-affects-your-health

Some of the ways alcohol affects our health are well known, but others may surpriseyou. Here are six less-known effects that alcohol has on your body, according to gastroenterologist Ibrahim Hanouneh, MD:

  1. Drinking gives your body work to do that keeps it from other processes. Once you take a drink, your body makes metabolizing it a priority — above processing anything else. Unlike proteins, carbohydrates and fats, your body doesn’t have a way to store alcohol, so it has to move to the front of the metabolizing line. This is why it affects your liver, as it’s your liver’s job to detoxify and remove alcohol from your blood.

  2. Abusing alcohol causes bacteria to grow in your gut, which can eventually migrate through the intestinal wall and into the liver, leading to liver damage.

  3. Too much is bad for your heart. It can cause the heart to become weak (cardiomyopathy) and have an irregular beat pattern (arrhythmias). It also puts people at higher risk for developing high blood pressure.

  4. People can develop pancreatitis, or inflammation of the pancreas, from alcohol abuse.

  5. Drinking too much puts you at risk for some cancers, such as cancer of the mouth, esophagus, throat, liver and breast.

  6. It can affect your immune system. If you drink every day, or almost every day, you might notice that you catch colds, flu or other illnesses more frequently than people who don’t drink. This is because alcohol can weaken the immune system and make the body more susceptible to infections.

Your liver heads up alcohol breakdown process. When you drink, here’s what happens in your liver, where alcohol metabolism takes place.

Your liver detoxifies and removes alcohol from the blood through a process known as oxidation. Once the liver finishes the process, alcohol becomes water and carbon dioxide. If alcohol accumulates in the system, it can destroy cells and, eventually, organs. Oxidative metabolism prevents this.

But when you’ve ingested too much alcohol for your liver to process in a timely manner, the toxic substance begins to take its toll on your body, starting with your liver. “The oxidative metabolism of alcohol generates molecules that inhibit fat oxidation in the liver and, subsequently, can lead to a condition known as fatty liver,” says Dr. Hanouneh.

Fatty liver, early stage alcoholic liver disease, develops in about 90 percent of people who drink more than one and a half to two ounces of alcohol per day. So, if you drink that much or more on most days of the week, you probably have fatty liver. Continued alcohol use leads to liver fibrosis and, finally, cirrhosis.

The good news is that fatty liver is usually completely reversible in about four to six weeks if you completely abstain from drinking alcohol. Cirrhosis, on the other hand, is irreversible and likely to lead to liver failure despite abstinence from alcohol, according to Dr. Hanouneh. If you drink heavily, see your doctor immediately if you notice a yellow tinge to your skin, feel pain in the upper right portion of your abdomen or experience unexplained weight loss.

Healthy people can drink — a little

If you’re healthy, Dr. Hanouneh says you don’t have to avoid alcohol altogether, but you should not drink every day, or even most days of the week. And, when you drink, men should not drink more than two or three ounces and women should not consume over one or two ounces. If you have liver disease, or some other health issue, you should not drink alcohol at all.

This article was written by Digestive Health Team from Cleveland Clinic and was legally licensed through the NewsCred publisher network.

Source: http://www.msn.com/en-us/health 17th March 2015

A study by doctors from the National Institute of Drug Abuse found that people who smoked marijuana had changes in the blood flow in their brains even after a month of not smoking. The marijuana users had PI (pulsatility index) values somewhat higher than people with chronic high blood pressure and diabetes, which suggests that marijuana use leads to abnormalities in the small blood vessels in the brain. These findings could explain in part the problems with thinking and remembering found in other studies of marijuana users.

According to two studies, marijuana use narrows arteries in the brain, similar to patients with high blood pressure and dementia, and may explain why memory tests are difficult for marijuana users. In addition, chronic consumers of cannabis lose molecules called CB1 receptors in the brain‘s arteries, leading to blood flow problems in the brain which can cause memory loss, attention deficits, and impaired learning ability.

Source: drugabuse.gov

A study that followed children from birth to midlife found that heavy marijuana users who smoked for years often fared worse as adults than their parents: Many ended up in jobs that paid less, required fewer skills and were less prestigious.

That wasn’t so much the case for other people.

“The rest of the people in the study who were not regular and persistent cannabis users ended up in a higher social class than their parents,” said Magdalena Cerda, lead investigator and associate professor at the University of California, Davis.

The study, published Wednesday in the journal Clinical Psychological Science, also found that marijuana users who smoked at least four times a week experienced more financial difficulties, such as problems with debt and food insecurity, than their parents. Their lives were fraught with more social problems, too.

“They experienced more antisocial behaviour at work such as lying to get a job or stealing money and more relationship problems such as intimate partner violence or controlling behaviour towards their partner,” Cerda said.

Other studies have associated heavy and persistent marijuana use with problems in adulthood but haven’t always ruled out other factors. This research tried to do that by tracking and comparing variables such as intelligence, family structure, gender, ethnicity, parental substance abuse, criminal convictions and antisocial behaviour and depression in childhood.

In accounting for so many variables, researchers made the study’s conclusions stronger, Cerda said, acknowledging that there may be unknown factors that they didn’t track.

Dr. Colin Roberts, a paediatric neurologist at Oregon Health & Science University and a member of Oregon’s Cannabis Research Task Force created to study medical marijuana, said the findings are worth considering.

“It’s a good study,” Roberts said. “They established an association that’s pretty compelling.”

The study’s sample size, almost 950 people, also gives it heft, he said.

The study is based on four decades of data collected in New Zealand, where marijuana is illegal. Investigators have been following people born between 1972 and 1973 in Dunedin, the second largest city on the South Island. The participants in the study come from a range of socio-economic classes, from professionals to unskilled labourers, who had physical, psychological, social and financial assessments at birth and ages 3, 5, 9, 11, 13, 15, 18, 21, 26, 32 and 38.

“There was a large number of people that were looked at which is really important,” Roberts said. “We can’t do studies like this in the U.S. because it’s really hard to collect information on people over that period of time. We don’t have a central source for people’s medical records.”

The study analyzed the data from the childhood evaluations to determine pre-existing conditions that might cause financial or social problems later in life. Then it evaluated the marijuana use of people starting at age 18 through 38 and financial and social problems at age 38. It found that 15 percent were frequent users, which they defined as smoking marijuana four or more times a week.

The longer those people smoked, the worse their problems in midlife.

That’s consistent with what professionals like Dr. Kevin Hill see in their practices. He’s the author of “Marijuana: The Unbiased Truth about the World’s Most Popular Weed” and an addiction psychiatrist at McLean Hospital, an affiliate of Harvard Medical School in Massachusetts.

“This paper supports what we see clinically,” Hill said. “If you’re using at a level that’s consistent with cannabis addiction, you will have problems in multiple spheres – work, school and relationships.”

Not everyone who smoked marijuana four times or more a week for years experienced downward mobility and not everyone who abstained fared better than their parents. But a higher proportion of the former group – nearly 52 percent – had a worse outcome compared with 14 percent of the latter.

The study also looked at alcohol use. Those with an alcohol dependency experienced more social problems than their parents and landed lower-paying jobs. But the marijuana users who were dependent on the drug had even more financial worries than those addicted to alcohol.

“Those of us in the field know that cannabis is potentially dangerous but the same argument should be made with alcohol,” Hill said. “We have 22 million Americans who used cannabis last year and yet we rarely talk about cannabis being dangerous and we should.”

Yet he cautioned that people who are dependent on marijuana remain in the minority, just as those who abuse alcohol are.

Alcohol remains the bigger problem because it’s more widespread, Cerda said, but she added that the increasing acceptance of marijuana could increase the cost to society. Oregon is one of 23 states where marijuana is legal for medical use and four states that have approved recreational marijuana use.

The study points to a need for investment in prevention and treatment, she said.

“If we do that, it may have long-term consequences for the potential burden that this may place on communities, families and on the broader social welfare system,” Cerda said.

Source:  http://www.oregonlive.com/marijuana   23rd March 2016

leonard-nimoy-5774458356-1-bynimoy

Photo:Gage Skidmore/Wikimedia Commons*

 “Live long and prosper.” The Vulcan salute is immediately identifiable with the actor Leonard Nimoy  and his most famous character, Mr. Spock. The  beloved cultural icon was admired for his sterling character on Star Trek and off-screen as well. In  recent years and up until his last few months, while  suffering the debilitating effects of a respiratory illness, he took steps to ensure that others would indeed “live long and prosper” by speaking clearly about the role that smoking played in the illness that caused his death.

Nimoy started smoking, like many, when he was young. He managed to quit more than 30 years before his death, but not early enough to prevent the respiratory disease that took his life late February. Nimoy took great pains to show us that cigarettes are a deadly addiction – encouraging followers on Twitter to quit or never start. While he was just one of the 480,000 people in the U.S. who will die prematurely from tobacco-related diseases in 2015, he will surely be among the most well-known and widely missed by an admiring public. That makes the steps took to tell his story so vital.

Tobacco is one of the toughest addictions to overcome and by far the most deadly product available. About 14 million major medical conditions in the U.S. can be blamed on smoking. Yet, despite that inescapable fact, more than 42 million Americans still smoke.

And it isn’t just smoking. Smokeless tobacco products, like those used by sports legend,Tony Gwynn, and other professional baseball players, are linked to oral cancer and other illnesses. Like Nimoy, Gwynn was outspoken before his death last year in naming chewing tobacco as the cause of his cancer. His efforts to speak the truth give meaning to the efforts of a coalition working to eliminate tobacco consumption on and around American baseball fields. Knock Tobacco Out of the Park will succeed, in part, because icons like Gwynn and Nimoy shared their stories and demonstrated the painful cost of tobacco-related illness.

The glamour and appeal of smoking and the power of nicotine addiction are forces that we work to counter every day at Legacy. Even that first cigarette does damage to your body and can spur a life-long addiction and struggle. Nimoy could not imagine what would happen to him five decades after he smoked his first cigarette. By sharing his story, he may help other smokers comprehend the illness and death that lie in wait for them.

As fans remember Leonard Nimoy and Tony Gwynn for cherished memories and contributions to our shared culture, we celebrate them as ambassadors of truth and of knowledge in the fight to build a future where illness and death, caused by the use of tobacco, are things of the past.

Source: www.drugfree.org 18th March 2015

Highlights

* •People arrested multiple times for drug-related offences have shorter life expectancy.

* •Accidental overdosing with drugs was a common manner of death in repeat offenders.

* •In 44% of poisoning deaths four or more drugs were identified in autopsy blood samples.

* •Illicit recreational drugs, such as heroin, cannabis and amphetamine were common findings.

* •The major prescription drugs identified in blood were opioid analgesics and sedative-hypnotics.

Abstract

Background

Multiple arrests for use of illicit drugs and/or impaired driving strongly suggests the existence of a personality disorder and/or a substance abuse problem.

Methods

This retrospective study (1993–2010) used a national forensic toxicology database (TOXBASE), and we identified 3943 individuals with two or more arrests for use of illicit drugs and/or impaired driving. These individuals had subsequently died from a fatal drug poisoning or some other cause of death, such as trauma.

Results

Of the 3943 repeat offenders 1807 (46%) died from a fatal drug overdose and 2136 (54%) died from other causes (p < 0.001). The repeat offenders were predominantly male (90% vs 10%) and mean age of drug poisoning deaths was 5 y younger (mean 35 y) than other causes of death (mean 40 y). Significantly more repeat offenders (46%) died from drug overdose compared with all other forensic autopsies (14%) (p < 0.001). Four or more drugs were identified in femoral blood in 44% of deaths from poisoning (drug overdose) compared with 18% of deaths by other causes (p < 0.001). The manner of death was considered accidental in 54% of deaths among repeat offenders compared with 28% for other suspicious deaths (p < 0.001). The psychoactive substances most commonly identified in autopsy blood from repeat offenders were ethanol, morphine (from heroin), diazepam, amphetamines, cannabis, and various opioids.

Conclusions

This study shows that people arrested multiple times for use of illicit drugs and/or impaired driving are more likely to die by accidentally overdosing with drugs. Lives might be saved if repeat offenders were sentenced to treatment and rehabilitation for their drug abuse problem instead of conventional penalties for drug-related crimes.

Source:  www.fsijournal.org. August 2016  Volume 265, Pages 138–143  DOI: http://dx.doi.org/10.1016/j.forsciint.2016.01.036

Abstract

It has been shown that cosmetic treatment like bleaching and perming may lead to an important decrease of drugs of abuse content in hair. Currently, hair straightening has become a regular hair treatment especially for women. The aim of this preliminary study was to investigate the effect of in vitro treatment of hair with heat straightener on cannabis and cocaine concentrations in hair.

17 positive cannabis and 7 positive cocaine hair samples were treated in vitro with a hair straightener. During this treatment hair was put sequentially 30 times in contact with heated iron plates at 200 °C during 2 s corresponding to a total time of contact of 1 min. THC and Cannabinol (CBN) were analysed in cannabis positive hair and cocaine, benzoylecgonin (BZE) and cocaethylene were analysed in cocaine positive hair. Analyses were performed with routine methods using GC/MS in electron impact mode.

Regarding cannabis results a decrease of THC concentrations was found in 11 of 17 hair samples after thermal treatment, whereas in 6 cases an increase was shown. In all the hair samples CBN concentrations was explicitly higher after the in vitro treatment. Regarding cocaine results cocaine and cocaethylene concentrations decreased after treatment in all seven hair samples; in contrast, higher concentrations of BZE were determined.

The strong increase of CBN and BZE content in hair after thermal treatments may be due to the fact that THC is converted by heat into CBN and cocaine into BZE, thus changing the respective ratios of the analysed substances. In conclusion, thermal straightening should be considered as other cosmetic hair treatments for a correct interpretation of hair results.

Source:  http://www.fsijournal.org/    August 2016   Volume 265, Pages 13–16 DOI: http://dx.doi.org/10.1016/j.forsciint.2016.01.002

Dr. Raj Waghmare says Cannabinoid Hyperemesis syndrome is stomach pain and nausea that can be helped by hot baths or stopping cannabis use.

Marijuana is having a moment. The once recreational-use-only drug is now considered by many as a medicine, an anti-nauseant and pain reliever, even an epilepsy medication.

But some long-term “pot heads” are finding the drug they once loved can suddenly turn on them and become almost toxic.   These users are developing a little-understood condition called cannabinoid hyperemesis syndrome that brings on unrelenting vomiting, nausea and stomach pain.

Standard medications do not relieve it, smoking more marijuana only seems to worsen it, and some doctors say they are seeing a lot more cases of it.

It was intense stomach pains that brought Dave to his doctors four months ago. The 45-year-old from southern Ontario (who’d prefer not to use his full name) knew he needed help when intense cramping left him balled up on the sofa, unable to work.  “I really wasn’t able to function much at all. I was constantly having to lie down with a constant pain,” he told CTVNews.ca by phone.

Even after Dave’s doctor ordered reams of ultrasounds, CT scans, and colonoscopies, no one could find anything wrong with him, leaving Dave frustrated.  “It was starting to take a toll on me after a few months. I was doing all these tests and not knowing what was wrong with me or who to turn to,” he says.  Dave finally turned to the internet, where he stumbled on discussions about cannabinoid hyperemisis, a condition he had never heard of.

History of hyperemesis

The first mention of the syndrome appeared in 2004, when a doctor in Australia published an article in the journal Gut describing several patients with a “cyclical vomiting illness” (or hyperemesis). All the patients had a history of “chronic cannabis abuse” and all seemed to find relief from their symptoms by taking multiple hot showers or baths a day.

“Everything I read about this CHS fit the picture,” Dave says.

“The only thing I didn’t have was the vomiting. But I had nausea and constant stomach pain and I was getting relief with hot baths and showers,” he said.

Dave also had a 25-year history of daily pot smoking. He had recently switched to smoking “shatter,” a marijuana concentrate high in THC, that he believes made things worse. Though Dave had told his doctor about his drug use, he connect his symptoms to

CHS. In fact, the physician may have never seen another patient with CHS. Emergency room doctors such as Dr. Raj Waghmare are seeing them, however. Waghmare recently wrote a blog post about the first time hediagnosed a patient with CHS, just under two years ago.

The well-dressed man had come into his ER with non-stop vomiting and abdominal pain. Like Dave, this man’s blood and urine test came out normal, yet no matter what drug Waghmare offered him, nothing seemed to quell his nausea.

Then the man mentioned that hot baths helped to dull the pain. That’s when Waghmare recognized CHS from an article he had read about in a Canadian medical journal.

It’s a condition that can’t be easily diagnosed, since there is no one test that can spot it. It’s only after everything else has been ruled out and a history of pot use has been established that doctors are left with CHS.

Waghmare says he’s since seen dozens more patients with CHS come through the doors of Southlake Regional Health Centre where he works.

“I probably see this every week in the ER,” he says. “if we were to go through all the charts from a full week, I’m sure we’d see at least a case of day among all the doctors.”

Most of the patients Waghmare sees had no idea that the drug they used every day could suddenly become toxic to them.  “People don’t know that this exists,” he says.

What actually causes CHS remains a mystery. The THC (tetrahydrocannabinol) in marijuana causes the drug’s high by stimulating the brain’s cannabinoid receptors, but one theory is that in some patients, those receptors eventually become overloaded.

“So it will work for nausea in the beginning, but then it will totally desensitize the receptors so that people will just feel nauseated all the time,” says Waghmare.

Why some patients develop the syndrome and others don’t remains a mystery; the condition hasn’t been the subject of rigorous scientific study. It appears to develop in those who smoke weed several times a day for a decade or so. But there is some evidence that people who begin daily pot use at a young age are more at risk.

The majority of CHS patients coming to see Waghmare are young men who have been smoking marijuana since high school. By the time they reach their mid-20s, they have a decade of use under their belts.

And yet many refuse to believe the pot is the problem.

When Waghmare tells young pot users the only thing that will end their vomiting and pain is to quit smoking weed for good, they often stop listening.  “A lot of these patients who come in are ‘frequent flyers,’ They’ve heard it before and they refuse to believe it. They refuse to give it up,” he says.

But older patients often take his advice and quit cold turkey, as the patient who Waghmare wrote about promised he would do. As an ER doc, however, he has no way of following up. At least one Facebook group has also been formed in which users discuss their symptoms and experiences.

As for Dave, he says has stopped smoking both marijuana and shatter. In fact, he wishes he never tried shatter at all, since he suspects that is what triggered his symptoms. Now, after three months of pain, he’s finally beginning to feel better. He’s also found a new doctor and has begun a new drug regimen for his Type 2 diabetes, which is also helping him feel better.

But doctors like Waghmare says there needs to be more awareness that this syndrome can develop in some pot users.

With all the recent discussions about the medicinal uses for marijuana, and the ongoing discussion about legalization, Waghmare says many pot users assumes the drug is benign, that it relieves pain and nausea, that there’s no way it could cause it.

“There’s this belief that (marijuana) is totally safe, a miracle drug, Not true,” he says.

Source:  http://www.ctvnews.ca/health/pot-pains-why-marijuana-can-become-toxic-for-some-1.2984756     13th July 2016

A backlash is growing in a state where marijuana has quickly become a $1 billion legal business. For months, Paula McPheeters and a handful of like-minded volunteers have spent their weekends in grocery-store parking lots, even in 95° F heat. Sitting around a folding table draped with an American flag, they asked passing shoppers to sign a petition. Inevitably a few sign-wielding young protesters would show up to argue that McPheeters’s group was dead wrong. With the two sides often just yards away from each other, shouting matches erupted. “We’re peaceful people,” one woman yelled. “You’re drugged out,” countered an angry man. Threats and phone calls to police became the norm.  The wedge dividing the people of this small blue-collar city of Pueblo, Colo.?   Legal marijuana.

Colorado gave the green light to recreational marijuana back in 2012, when it passed a law to make nonmedical pot sales legal starting Jan. 1, 2014. But now opposition is rising in communities across the state. Colorado has become a great social experiment, the results of which are still not clear. “The jury is still out as to whether this was a good idea,” says Colorado attorney general Cynthia Coffman.

What’s undeniable is this: Legal marijuana is in high demand in Colorado. Only three other states—Alaska, Washington, and Oregon—plus the District of Columbia currently permit recreational adult use of cannabis. (It’s legal for medical use in another 19 states.) Of that group, Colorado led the way in 2015 with $996.5 million in licensed pot sales—a 41.7% jump over 2014 and nearly three times the figure in Washington State. Recreational sales made up nearly two-thirds of the total.

Now, as citizen groups attempt to put the brakes on the growing industry, a heated debate has emerged about the drug’s societal impact. Doctors report a spike in pot-related emergency room visits—mostly due to people accidentally consuming too much of potent edible pot products. Police face new cartel-related drug operations. Parents worry about marijuana being sold near their homes and schools. And less affluent communities like Pueblo struggle with the unintended consequences of becoming home to this emerging and controversial industry.

Amendment 64 decriminalized marijuana statewide, but Colorado’s cities and counties still decide if the drug can be grown and sold locally. At least 70% of the municipalities in the state have banned commercial operations, either by popular vote or board decisions.

Many other communities have begun pushing back. Last fall, controversy arose in the small western Colorado town of Parachute when an antipot group attempted to recall members of the town council who had welcomed pot shops. (Voters defeated the recall 3 to 1.) Debate has since emerged in Aspen, Carbondale, Glenwood Springs, Grand Junction, Littleton, and Rifle over the number, location, smell, and mere existence of retail and cultivation facilities. Citizens in the San Luis Valley, in the southern part of the state, say their schools and social services have been overwhelmed by a flood of newcomers coming to grow cannabis on cheap land, despite limited water. And just this spring officials in Colorado Springs and Englewood opted to ban pot social clubs, which are akin to lounges in which people can legally smoke weed in public.

“I’m getting calls now from people who voted for legalization thinking it wouldn’t affect them,” says Kevin Sabet, co-founder of national antimarijuana legalization group Smart Approaches to Marijuana. “They’re surprised to see these are sophisticated businesses opening up next to their schools selling things like marijuana gummy bears. And they’re angry.”

Officials in Denver, which is home to one-third of the state’s cannabis market, moved this spring to rein in pot capitalism. The city passed an ordinance capping the number of dispensaries and grow facilities at the present level. But discontent continues to fester in poorer communities, where many of these operations inevitably land. “We were told that legalization would take drugs out of our community,” says Candi CdeBaca, a community activist who grew up in the mostly Latino and poor Denver neighborhood of Elyria-Swansea. “The drugs stayed—and the drug dealers changed.”

CdeBaca points to, for example, an increase in school suspensions related to marijuana. And unlike the meatpacking plants and refineries that once dotted the area, CdeBaca says, this new industry hasn’t brought her neighbors jobs. Instead, the money is flowing to outsiders.

“It’s the Wild West, and the well-funded marijuana industry has dominated the regulatory process, and people are finally speaking up,” says Frank McNulty, a lawyer for Healthy Colorado, which plans to put a measure on the November state ballot—an easier task in Colorado than in many other states—that would limit the active drug ingredient THC in cannabis candy and concentrates and require health warnings on packaging. The marijuana industry has objected to the proposal, and the issue is now before the Colorado Supreme Court.

Cannabis backers bristle at the pushback, calling it a back-door effort by prohibitionists who simply disagree with the legalization of the drug. Mason Tvert, director of the Marijuana Policy Project, which leads legalization efforts nationwide, cites studies showing minimal impact on society and no harm to Colorado’s growing economy. Says Tvert: “Anyone who says it’s caused an increase in this or that [problem] is full of shit.”

What plays out in Colorado may influence what happens across the nation. Pot remains illegal under federal law. But legalization of recreational marijuana for adult use will be on the November ballot in California, Massachusetts, and Nevada, and likely in Arizona and Maine too. Voters in Arkansas, Florida, and Missouri will be voting on whether to approve it for medical use. The growth of the cannabis industry has begun to attract the interest of big companies. Microsoft announced in mid-June that it has developed a software product to help states track marijuana growth and sales.

In a recent appearance on CNBC, Colorado Gov. John Hickenlooper offered this advice to other states considering legalization: “I would suggest wait a year or two and see how it goes.”

Nowhere has the impact of legalization in Colorado been felt more powerfully than in the small community of Pueblo, located 114 miles south of Denver. At least 20 dispensaries and 100 growing facilities with 4 million square feet of cultivation now dot the highways near this town of 160,000, which has aggressively embraced the budding industry, making it the top cultivation spot in the state. “We’re sort of like the Napa Valley of cannabis,” says Pueblo County commissioner Sal Pace.

Pueblo has struggled for decades, ever since the 1983 recession, when most of the jobs at the local CF&I steel mill disappeared. Today the community is dealing with failingschools, rising gang activity, and increased crime. With a total of 26 homicides in 2014 and 2015, Pueblo earned the highest per capita murder rate in the state.

When the county’s three commissioners approved licenses for marijuana operations in 2014, Pueblo’s problems got worse, argues McPheeters, a Pueblo mom and community-college budget manager who is the driving force behind a group called Citizens for a Healthy Pueblo. “The promises of marijuana have not come true,” she argues. After weeks of contentious petition drives, McPheeters’s group believes it has gathered enough signatures to put a measure on the November ballot to revoke all the recreational marijuana licenses in the county. Marijuana industry groups, however, have sued, arguing that the number of signatures falls short under a new state law. A judge is set to decide in July.

Groups serving the poor in Pueblo report a flood of homeless people arriving from other states. Local homeless shelter Posada, for instance, has witnessed a 47% jump in demand since 2014, including 1,200 people who reported to shelter workers that they came to smoke pot or get jobs in the industry, says Posada’s director, Anne Stattelman. She says her funding is tapped out. “It’s changed the culture of our community,” she says.

The city’s three hospitals officially threw their support behind the antipot ballot measure after reporting a 50% spike in marijuana-related ER visits among youth under age 18 and more newborns with marijuana in their system. A number of local businesses are also backing the ban after struggling to find sober employees.

Commissioner Pace, in particular, has emerged as a target of criticism for citizens hoping to rid Pueblo of legal marijuana.  As a state legislator he drafted early pot regulations and then as commissioner led local efforts to launch the industry in Pueblo County after 56% of voters in the city approved Amendment 64. “It will take time to change some people’s opinions that pot is bad,” he says.

The pro-marijuana contingent in Pueblo say critics are misplacing blame for the area’s problems. They argue that the pot business has generated jobs and taxes as well as a college scholarship and a local playground. Revoking the licenses of cannabis shops, they say, will only fuel the black market. Says Chris Jones, an employee at a local dispensary clad in a Bob Marley T-shirt: “We already voted on this one time. Let it stand.”

Both antipot groups and marijuana advocates tend to cherry-pick data to support their claims. However, Larry Wolk, chief medical officer for the state department of health, says it’s too early to draw conclusions about the true social and health impacts on Colorado.

Marijuana-related hospitalizations have tripled in Colorado since legalization, and emergency room visits have climbed 30%, according to a state report released this spring. And pot-related calls to poison control have jumped from 20 to 100 a year, says Wolk. Drug-related school suspensions have also climbed. Yet teen usage hasn’t shot up dramatically, and crime has remained fairly stable. Marijuana-related DUIs increased 3%, and traffic fatalities involving THC increased 44%—but the absolute numbers were small in comparison to those that involved alcohol, according to the report.

The data is tricky, Wolk says, because Colorado didn’t track these numbers the same way prior to legalization. Are there more suspensions, he asks, because teachers are more aware? Are doctors now asking about marijuana at hospitals when they didn’t previously? “It may be a year or two before we’ll really have good answers,” says Wolk.

Marijuana legalization has delivered some surprises statewide to regulators, police, and citizens alike. For instance, many people thought legalization would quash the black market for the drug. “That’s been a fallacy,” says Coffman, Colorado’s attorney general. Legalization of cannabis stores and grow operations has drawn more drug-related crime, she says, including cartels that grow the plant in Colorado and then illegally move it and sell it out of state. “They use the law,” she says, “to break the law.”

Since 2013, law officials say, they have busted 88 drug cartel operations across the state, and just last year law-enforcement made a bust that recovered $12 million in illegal marijuana. Adds Coffman: “That’s crime we hadn’t previously had in Colorado.”

The state legislature is trying to play catch-up. Last year it passed 81 bills enacting changes to drug laws, prompting state law-enforcement groups to request a two-year moratorium on new laws so that they could have time to adjust. Lawsuits are also flying—including one from Colorado’s neighbors. Nebraska and Oklahoma have sued Colorado, claiming that it is violating federal drug statutes and contributing to the illegal drug trade in their states.

Another surprise to many Coloradans is that a promised huge tax windfall to benefit schools hasn’t materialized. Of the $135 million generated in 2015, for example, $20 million goes to regulatory and public-safety efforts related to cannabis, $40 million funds small rural school construction projects, and the rest goes to youth drug prevention and abuse programs. That’s a drop in the bucket for a $6.2 billion education budget.

A third revelation to parents in particular is the potency of today’s pot, says Diane Carlson, a mother of five who started Smart Colorado to protect teens from the drug. The weed, edibles, and concentrates sold in stores have THC levels that average 62% and sometimes as high as 95%, according to a 2015 state report. That compares with levels of 2% to 8% in the 1990s. “We passed this thinking it was benign, that it was the stuff from college,” says Carlson. “The industry is just moving too fast, and we’re playing catch-up while the industry is innovating.”

Sitting in a Denver café, Carlson compares marketing by the marijuana industry to that of Big Tobacco in the 1950s, portraying the product as a harmless cure-all for everything from ADHD to anxiety. Yet research shows that marijuana is harmful to the developing brain. She supports Healthy Colorado’s ballot initiative to limit the active drug ingredient in THC in marijuana edibles, candy, and concentrates to 17%.

The backlash worries Mike Stettler, the founder of Marisol, one of Pueblo County’s largest dispensaries, which has been endorsed by comedian and weed smokers’ icon Tommy Chong. The onetime construction worker fears that Pueblo’s pushback against pot will shut down his entire recreational dispensary and its 10-acre grow operation,

which generated $4.5 million in revenue last year. “I’m hoping and praying this thing doesn’t go through, but you don’t know,” he says.

He says he has invested millions in his business and has more plans for growth. In May he flew to Las Vegas to discuss a partnership with famed guitarist Carlos Santana to create a Santana brand of weed called Smooth, named after the artist’s hit song.

Inside, Marisol is a veritable wonderland for cannabis enthusiasts. Customers can consult a “budtender” for advice on the right weed for energy, sleep, or relaxation. They can also choose from a seemingly boundless variety of marijuana merchandise—from vegan “dabbing” concentrates for water pipes to pot-infused bottled beverages to peanut-butter-and-jelly-flavored THC candies. There are even liquid products designed to alleviate marijuana overdoses.

Giving a tour of the store, employee Santana O’Dell, clad in green tights with tiny marijuana leaves on them, sighs as a beatific smile appears on her face. “This is freedom,” she says.

For a growing number of her neighbors, however, legalized marijuana is starting to feel like a really bad high.

Source:  a version of this article appears in the July 1, 2016 issue of Fortune.

A new study, published in Archives of Sexual Behavior by researchers affiliated with New York University’s Center for Drug Use and HIV Research (CDUHR), compared self-reported sexual experiences related to use of alcohol and marijuana. Since marijuana has increased in popularity in the U.S., the researchers examined if and how marijuana use may influence risk for unsafe sexual behavior.

“With marijuana becoming more accepted in the U.S. along with more liberal state-level policies,” notes Joseph J. Palamar, PhD, MPH, an affiliate of CDUHR and an assistant professor of Population Health at NYU Langone Medical Center (NYULMC), “it is important to examine users’ sexual experiences and sexual risk behavior associated with use to inform prevention and harm reduction.”

In this study, the researchers interviewed 24 adults (12 males and 12 females, all self-identified as heterosexual and HIV-negative) who recently used marijuana before sex. Compared to marijuana, alcohol use was more commonly associated with social outgoingness and use often facilitated connections with potential sexual partners; however, alcohol was more likely than marijuana to lead to atypical partner choice or post-sex regret.

Alcohol was commonly used as a social lubricant to meet sexual partners, and this was related, in part, to alcohol being readily available in social gatherings.

“Interestingly, some users reported that the illegality of marijuana actually facilitated sexual interactions,” notes Dr. Palamar. “Since smoking marijuana recreationally is illegal in most states and smoking it tends to produce a strong odor, it usually has to be used in a private setting. Some individuals utilize such private or intimate situations to facilitate sexual encounters.”

While users often described favorable sexual effects of each drug, both alcohol and marijuana were reportedly associated with a variety of negative sexual effects including sexual dysfunction. For example, marijuana use was linked to vaginal dryness and alcohol was commonly described as increasing the likelihood of impotence among males.

The researchers noted that the sexual effects tended to be similar across males and females, and both alcohol and marijuana were generally associated with loss of inhibitions. Both drugs appear to be potentially associated with increased feelings of self-attractiveness, but possibly more so for alcohol, and participants reported feelings of increased sociability and boldness while consuming alcohol.

While some participants reported that marijuana use made them more selective in choosing a partner, many participants— both male and female—felt that their “standards” for choosing a partner were lowered while under the influence of alcohol.

“It wasn’t surprising that alcohol use reportedly led to less post-sex satisfaction than marijuana,” said Dr. Palamar. “Participants reported feelings of regret more frequently after sex on alcohol, but compared to alcohol they generally didn’t report poor judgment after using marijuana.”

When smoking marijuana, participants tended to reported increased feelings of anxiety or a sense of wariness in unfamiliar situations that they did not generally seem to experience after using alcohol. Therefore, these drugs appear to have different effects with regard to socialization that may precede a sexual encounter.

“Sexual encounters on marijuana tended to be with someone the individual knew,” comments Dr. Palamar. “Sex on alcohol was often with a stranger so the situation before sex may be much more important than the drug used.” Marijuana and alcohol are associated with unique sexual effects, with alcohol use reportedly leading to riskier sexual behavior. Both drugs appear to potentially increase risk for unsafe sex.

“Research is needed continue to study sexual effects of recreational drugs to inform prevention to ensure that users and potential users of these drugs are aware of sexual effects associated with use,” emphasizes Dr. Palamar. “Our results can inform prevention and harm reduction education especially with regard to marijuana, since people who smoke marijuana generally don’t receive any harm reduction information at all. They’re pretty much just told not to use it.”

More information: Joseph J. Palamar et al. A Qualitative Investigation Comparing Psychosocial and Physical Sexual Experiences Related to Alcohol and Marijuana Use among Adults, Archives of Sexual Behavior (2016). DOI: 10.1007/s10508-016-0782-

Source:  http://medicalxpress.com/news/2016-08-drunk-stonedcomparing-sexual-alcohol-marijuana.html   4th Aug.2016

Newswise — New research from the University of British Columbia suggests there may be some truth to the belief that marijuana use causes laziness– at least in rats.

The study, published today in the Journal of Psychiatry and Neuroscience, found that tetrahydrocannabinol (THC), the main psychoactive ingredient in marijuana, makes rats less willing to try a cognitively demanding task.

“Perhaps unsurprisingly, we found that when we gave THC to these rats, they basically became cognitively lazy,” said Mason Silveira, the study’s lead author and a PhD candidate in UBC’s department of psychology. “What’s interesting, however, is that their ability to do the difficult challenge was unaffected by THC. The rats could still do the task– they just didn’t want to.”

For the study, researchers looked at the effects of both THC and cannabidiol (CBD) on rats’ willingness to exert cognitive effort.  They trained 29 rats to perform a behavioural experiment in which the animals had to choose whether they wanted an easy or difficult challenge to earn sugary treats.  Under normal circumstances, most rats preferred the harder challenge to earn a bigger reward. But when the rats were given THC, the animals switched to the easier option, despite earning a smaller reward.

When they looked at the effect of CBD, an ingredient in marijuana that does not result in a high, researchers found the chemical did not have any effect on rats’ decision-making or attention. CBD, which is believed to be beneficial in treating pain, epilepsy and even cancer, also didn’t block the negative effects of THC.

“This was surprising, as it had been suggested that high concentrations of CBD could modulate or reduce the negative effects of THC,” said Catharine Winstanley, senior author of the study and an associate professor in UBC’s department of psychology. “Unfortunately, that did not appear to be the case.”  Given how essential willingness to exert cognitive effort is for people to achieve success, Winstanley said the findings underscore the importance of realizing the possible effect of cannabis use on impairing willingness to engage in harder tasks.

While some people view marijuana as a panacea that can cure all ailments, the findings also highlight a need for more research to determine what THC does to the human brain to alter decision-making. That could eventually allow scientists to block these effects of THC, allowing those who use medical marijuana to enjoy the possible benefits of cannabis without the less desirable cognitive effects.

Method

At the beginning of each behavioural experiment, rats chose between two levers to signal whether they wanted an easy or hard challenge.

Choosing the easy challenge resulted in a light turning on for one second, which the rats could easily detect and respond to by poking it with their nose, receiving one sugar pellet as a reward. In the more difficult challenge, the light turned on for only 0.2 seconds, rewarding the rat with two sugar pellets if they responded with a nose poke.

Source:  http://www.newswise.com/articles/view/659725/?sc=dwtn  24th Aug.2016

New psychoactive substances (NPS) are synthesized compounds that are not usually covered by European and/or international laws. With a slight alteration in the chemical structure of existing illegal substances registered in the European Union (EU), these NPS circumvent existing controls and are thus referred to as “legal highs”. They are becoming increasingly available and can easily be purchased through both the internet and other means (smart shops). Thus, it is essential that the identification of NPS keeps up with this rapidly evolving market.

In this case study, the Belgian Customs authorities apprehended a parcel, originating from China, containing two samples, declared as being “white pigments”. For routine identification, the Belgian Customs Laboratory first analysed both samples by gas-chromatography mass-spectrometry and Fourier-Transform Infrared spectroscopy. The information obtained by these techniques is essential and can give an indication of the chemical structure of an unknown substance but not the complete identification of its structure. To bridge this gap, scientific and technical support is ensured by the Joint Research Centre (JRC) to the European Commission Directorate General for Taxation and Customs Unions (DG TAXUD) and the Customs Laboratory European Network (CLEN) through an Administrative Arrangement for fast recognition of NPS and identification of unknown chemicals. The samples were sent to the JRC for a complete characterization using advanced techniques and chemoinformatic tools.

The aim of this study was also to encourage the development of a science-based policy driven approach on NPS.

These samples were fully characterized and identified as 5F-AMB and PX-3 using1H and 13C nuclear magnetic resonance (NMR), high-resolution tandem mass-spectrometry (HR-MS/MS) and Raman spectroscopy. A chemo-informatic platform was used to manage, unify analytical data from multiple techniques and instruments, and combine it with chemical and structural information.

Source:    http://www.fsijournal.org/   August 2016   Volume 265, Pages 107–115

DOI: http://dx.doi.org/10.1016/j.forsciint.2016.01.024

Objective: Adolescent marijuana use continues to increase in prevalence as harm perception declines. Better understanding of marijuana’s impact on neurodevelopment is crucial. This prospective study aimed to investigate cortical thickness and neurocognitive performance before and after 28 days of monitored abstinence in adolescent marijuana and alcohol users. 

Method: Subjects (N = 54; >70% male) were adolescent marijuana users (ages 15–18 years) with regular alcohol use (MJ + ALC; n = 24) and non-using controls (CON; n = 30) who were compared before and after 4 weeks of sequential urine toxicology to confirm abstinence. Participants underwent magnetic resonance imaging, neuropsychological assessment, and substance use assessment at both time points. Repeated-measures analysis of covariance was used to look at the main effects of group, time, and Group × Time interactions on cortical thickness and neurocognitive functioning. Bivariate correlations estimated associations between cortical thickness, substance use severity, and cognitive performance.

Results: Marijuana users showed thicker cortices than controls in the left entorhinal cortex (ps < .03) before and after monitored abstinence, after adjusting for lifetime alcohol use. More lifetime marijuana use was linked to thinner cortices in temporal and frontal regions, whereas more lifetime alcohol use and heavy episodic drinking episodes was linked to thicker cortices in all four lobes (ps < .05). Age of onset of regular marijuana use was positively related to cortical thickness (ps < .03).

Conclusions: Adolescent alcohol and marijuana use may be linked to altered longer-term neurodevelopmental trajectories and compromised neural health. Cortical thickness alterations and dose-dependent associations with thickness estimates were observed both before and after monitored abstinence and suggest neural differences continue to persist 28 days after cessation of marijuana use. Neural recovery may be identified with longer follow-up periods; however, observed changes related to use severity could have implications for future psychosocial outcomes.  

Joanna Jacobus, Lindsay M. Squeglia, Scott F. Sorg, Tam T. Nguyen-Louie, Susan F. Tapert

Source:  www.jsad.com  (J. Stud. Alcohol Drugs, 75, 729–743, 2014) 

Those using strong strains of illegal drugs such as cannabis skunk, or the illegal use of prescription drugs are risking their mental health and the lives of others. Suicidal thoughts are not unknown and this letter from a doctor discusses the problems of confidentiality versus life saving – of the patient or others.

To the Clinicians of the Co-Pilot of Germanwings Flight 9525

Dear German Medical Colleagues,

Please bear with me through this rather long letter. There is so much that I have been wondering and worrying about—including you.

I may never know who you are, but if you provided medical or psychiatric care for Andreas Lubitz, co-pilot of Germanwings Flight 9525, we are colleagues. Whether you saw Mr Lubitz years ago or more recently, or whether you saw him privately or as an airline-appointed medical examiner, you had some responsibility for his care.

And you too are his victims, of sorts. I hope your reputation does not suffer unduly. I hope PTSD does not develop as a result of his apparent suicide. If you provided ethical care (ie, competent care), I hope you are not scapegoated. “Monday morning quarterbacking”—an American football saying about reviewing a game the day after it is played—is always so much easier than preventing problems in real time.

After all, if reports of Mr Lubitz taking an injectable antipsychotic during training in 2009 are true, that doesn’t for sure mean that he had an ongoing or intermittent psychosis. Maybe, just maybe, it could have been a short-acting injection for acute agitation due to extreme stress and/or drug abuse. Similarly, treatment back then for an “episode” of “severe” depression could have seemed to be a one-time episode.

On the other hand, there are reports that Lubitz saw psychotherapists “over a long period of time.” Those psychotherapists probably knew the patient best, especially if he had a particular personality disorder or significant traits of concern (eg, undue narcissism, paranoia).

We have not yet heard anything about whether Lubitz had PTSD, but people with this disorder can appear normal. Perhaps the co-pilot dissociated as he crashed the airplane, which would have allowed him to ignore for minutes the passengers’ screams and the banging on the door of the cockpit. That could account for the fact that voice recording picked up no triumphal shouts, only his steady breathing.

This analysis is all speculation, of course. Maybe it’s the kind of “wild analysis” that Freud so deplored.

I do not know how prominent so-called “anti-psychiatrists” are in Germany, but if they are anything like they are here in the US, they are likely to blame psychiatric medication for the co-pilot’s bizarre and tragic behavior. Of course, they could well have a point. Some antidepressants, which can cause visual side effects, were prescribed for Mr Lubitz, agents perhaps, that we don’t in the US.

We know he was concerned about his vision, but speculation so far is that this complaint was psychosomatic. In addition, sudden withdrawal from some antidepressants can lead to increased agitation. Moreover, antidepressants can trigger a (hypo)manic episode, although of course a manic episode can occur that leads to grandiosity and agitation. On the other hand, no one seems to have described such changes in Mr Lubitz before the crash.

Therefore, I hope your medical documentation was good—better than mine usually was. I hope you documented your risk assessment adequately. If you were unsure of what to do, I hope you obtained consultation and/or supervision. If you worked in a system of care, I hope they adequately monitored the quality of care you provided.

I understand that your medical privacy laws are much more stringent than our patchwork of state and national privacy laws are here in the US, both in life and in death. I heard that you can be imprisoned for up to 5 years for not following strict standards of patient confidentiality. Perhaps that prevented you from contacting Lufthansa instead of just giving the patient an unfit-for-work note, which he subsequently tore up. That, and other reasons, may be causing you to bite your tongue to offer further explanation.

I wonder if your stringent privacy laws are a reaction to the breaches of physicians when the Nazis ruled, as well as the subsequent invasion of privacy in East Germany. Are they an overreaction that needs some degree of correction? After all, airline safety is good, and this may have been a perfect confluence of various factors. Further, to exacerbate our existential anxiety, we have the unexplained disappearance of the Malaysian airliner from just about 2 years ago. Was there a copycat aspect to the Germanwings crash?

All medical colleagues must weigh risk to others against the need for patient confidentiality. This can include whether to divulge patient information such as highly contagious diseases like AIDS or Ebola; abuse of a minor or domestic violence; driving while impaired; carrying a gun; running a nuclear power plant; and being responsible for all kinds of public transportation and safety.

Maybe you wish you could talk and give condolences to those who lost family and friends on the doomed airliner. That would be the human thing to do, but perhaps you can’t?

As psychiatrists, suicide and homicide are essentially our only life and death challenges. So when a patient commits suicide and kills 149 others at the same time, what could feel professionally worse?

Yet we all know that we are not particularly successful at predicting actual suicide or homicide. Complicating that, someone troubled who decides that his or her solution is suicide and/or homicide often seems surprisingly well right before the act. He or she is relieved, having decided on the solution to his problems. We must appreciate our limitations.

Everyone wants to know the co-pilot’s motivation. So do I. But nothing is convincing yet about why he would make sure to kill everyone on board. Way back when, I was taught that in general, suicide was motivated by a desire to die, to kill, and/or be killed. This is a rare example of all—a triple play.

We may need system and cultural changes to how we approach some aspects of mental illness, such as the Air Force Suicide Prevention Program in the US. This program has significantly reduced suicide attempts as well as violence to others.

We and our psychiatric patients are stigmatized in many countries. If such stigma can cause inadequate attention to mental health in routine annual check-ups, no wonder mental health examinations are inadequate for airline pilots.

Complicating our work is the denial, lack of insight, and/or loss of memory among some of our patients. The people that we (clinicians and the public) need to fear most (ie, sociopaths) can be the best at hiding the risk they pose. Periodic research about faking psychiatric symptoms in the emergency department indicates how easily we, in our quest to be helpful, can be fooled. We don’t have corroborating lab tests to fall back on, unlike in other areas of medicine.

During my career, I evaluated and treated a fair number of pilots. Almost always, we grappled with the implications of getting treatment and taking medication. What might help their mental problems might, at the same time, cost them their job, and thereby worsen their mental health. No wonder so many pilots hide psychiatric treatment from their employers.

Who knows? Maybe some of you who treated him didn’t even know that Andreas Lubitz was a pilot. We often know little about the real day to day lives of our patients. Maybe we need to know more.

About a century ago, Freud concluded that his was “an impossible profession.” This may well still be so. The burnout rate of physicians and psychiatrists in the US is over 50%. Know that.

I appreciate why we may never hear your side of the story. That may be a shame, for you probably have much to teach us and can transform some of our fantasies into reality.

In terms of our ethical responsibilities to each other, we are indeed our brothers’—and sisters’—keepers. In that regard, let me know if there is anything more I should know or do.

Your colleague,
H. Steven Moffic, MD (Steve)

Source: Psychiatric Times psychiatrictimes@email.cmpmedica-usa.com 16th April 2015

PSA Warning Issued in 2005 was Ignored

Eleven years ago the ONDCP and SAMHSA held a press conference to inform of research that confirms what many families already knew–that marijuana use was a trigger for psychosis and mental illness.

The ONDCP is the White House Office of National Drug Control Policy; SAMHSA is the Substance Abuse and Mental Health Services Administration.  Each agency has a crucial role in trying to ascertain usage and reduce demand for drugs. Specifically, Dr. Neil McKehaney from the University of Glasgow came to the US and spoke at the national Press Club on May 5, 2005. The agencies went to great effort to share important information.  A video was recently found online.

Cover up of the Marijuana – Mental Illness  Risk

At this same Press Conference, a couple who had lost their 15-year-old son to suicide due to the mental health problems arising from marijuana use, spoke.  The Press covered the story, but did not use their considerable investigative skills to probe into what those parents and Dr. McKenagey were describing.  It is true that about one quarter of American high school students are depressed, which points to multiple problems of American culture, not just drugs. However, knowing how vulnerable teens are, and then not exposing the factors that could make their outcomes worse, is lamentable.

In addition to depression, anxiety and suicide, there are the risks of psychosis, bipolar disorder and schizophrenia that arise from marijuana use.  Pot proponents love to state that anyone who has a psychotic reaction to pot already had the problem before they used it.  They tend to blame family members for not  wanting to admit  mental health problems, and argue that pot is used as a scapegoat.

Several studies have shown a link between marijuana and schizophrenia.  Explains pharmacologist Christine Miller, Ph.D:  “No one is destined to develop schizophrenia. With identical twins, one can develop the disease and the other one will do so only 50% of the time, illustrating the importance of environmental factors in the expression of the disease.  Marijuana is one of those environmental factors and it is one we can do something about.”

A Missed Opportunity

One person who worked in the office of ONDCP Director John Walters told Parents Opposed to Pot, “They accused us of being pot-crazy during a time when there was a methamphetamine crisis going on.  Marijuana is almost always the first drug introduced to young people and the evidence for the mental health risks were very strong by 2005.  Although pot was getting stronger as it is today, the warning was falling on deaf ears.  Members of Congress wanted us to focus on the meth crisis, but marijuana was a growing issue and we had a myriad of issues.”

This Public Service Announcement reached audiences in the Press, and some newspapers and magazines reported about it.  Since the Internet and search engines were not as they are  today,  few parents, children,  schools and mental health professionals took notice.   (Did the marijuana lobbying groups bully and try squelch the information?)

Lori Robinson, whose son suffered the mental health consequences of marijuana said:  “I will always deeply regret Shane not hearing this PSA .  Shane was a smart, gregarious and fun-loving young man who naively began using pot never knowing he was playing Russian roulette with his brain in ’05-’06 at the age of 19.   Dr McKeganey so clearly stated that the public views marijuana as harmless, not realizing the potency of THC was rising while the “antipsychotic” property of CBD was being bred out.  Sadly, despite both parents never used an illegal drug in our lives, our son assumed that since a few of his friend had smoked in high school, it was just a “harmless herb.”   Shane’s story is on the Moms Strong website.

Robinson added, “This video is absolutely current TODAY.  Let’s keep this video circulating & it WILL save young brains & families the destruction that lies ahead when marijuana hijacks your kid’s brain.

The research has expanded since that time and scientific evidence on each of the following outcomes from marijuana use is voluminous: marijuana & psychosis, marijuana & violence and marijuana & psychiatric disorders.

Lessons to be Learned

Lives could have been saved, and so many cases of depression, psychotic breakdowns and crimes could have been prevented – if the public had become more aware back in 2005.   Congress, the Press and most of all, the American psychiatric community was wrong to ignore the warnings that were issued with this PSA. Let’s not continue to ignore  the evidence. Today in the US, mental health is worse than it’s ever been, and the promotion of drug usage may be a huge factor in this problem.  Harm reduction in preference to primary prevention strategies is practiced in many jurisdictions.  Drug overdose deaths have overtaken gun violence deaths and traffic fatalities in the USA — by far — under this strategy. Today Dr. McKeganey is the Director of the Center for Substance Use Research in Glasgow.

Parents Opposed to Pot is totally funded by private donations, rather than industry or government. If you have an article to submit, or want to support us, please go to Contact or Donate page.

Source:  http://www.poppot.org/2016/07/06/warning-pot-causes-mental-illness

For most people, the idea of winning some money will ignite a rush of emotions – joy, anticipation, excitement.

If you were to scan their brains at that very moment, you would see a surge of activity in the part of the brain that responds to rewards.

But, for people who’ve been smoking cannabis, that rush is not as big – and gets smaller and smaller over time, new research suggests.

And that dampened, blunted response may actually increase the risk that marijuana users are more likely to become addicted to pot and other drugs.

Dr Mary Heitzeg, senior author of the new study, a neuroscientist from the University of Michigan Medical School, said: ‘What we saw was that over time, marijuana use was associated with a lower response to a monetary reward.

‘This means that something that would be rewarding to most people was no longer rewarding to them, suggesting but not proving that their reward system has been “hijacked” by the drug, and that they need the drug to feel reward – or that their emotional response has been dampened.’

The findings come from the first long-term study of young marijuana users, that tracked brain responses to rewards over time, and is published in the JAMA Psychiatry.

They reveal measurable changes in the brain’s reward system with cannabis use – even when other factors like alcohol use and cigarette smoking were taken into account.

The study involved 108 people in their early 20s – the prime age for cannabis use.

All were taking part in a larger study of substance abuse, and all had brain scans at three points over a four-year period.

Three-quarters were men, and nearly all were white.

While MRI scans were performed, participants were invited to play a game.

People who smoke cannabis regularly show less activity in the area of the brain that releases the ‘pleasure’ hormone, dopamine

They were required to click a button when they saw a target on a screen in front of them.

Before each round, they were told they could win 20 cents, or $5 – or that they might lose that amount, have no reward or loss.

The researchers were most interested in assessing what happened to the volunteers’ brains – specifically activity in the reward center – the area called the nucleus accumbens.

And the moment that was deemed most important, was the moment of anticipation – when the volunteers knew they might win some money, and were anticipating what it would take to win the simple task.

In that moment of anticipating reward, that area of the brain should spark into action, pumping out the ‘pleasure’ hormone, dopamine.

The greater a person’s response, the more pleasure or thrill a person feels – and the more likely they will be to repeat the behavior later.

The researchers found that the more marijuana use a volunteer reported, the smaller the response in this part of the brain over time.

Past research has shown the brains of people who use a high-inducing drug repeatedly respond more prominently when they are shown cues related to that drug.

That increased response means the drug has been associated in their brains with positive, rewarding feelings.

And, that can make it harder for users to stop seeking out the drug and using it.

First author, Meghan Martz, doctoral student in developmental psychology, said: ‘It may be that the brain can drive marijuana use, and that the use of marijuana can also affect the brain.

‘We’re still unable to disentangle the cause and effect in the brain’s reward system, but studies like this can help that understanding.’

Regardless of that fact, the new findings show there is a change in the reward system over time, when a person regularly uses cannabis, the researchers noted.

Dr Heitzeg and her colleagues also showed recently in a paper in Developmental Cognitive Neuroscience that marijuana use impacts emotional functioning.

The new data on response to potentially winning money may also be further evidence that long-term marijuana use dampens a person’s emotional response – something scientists call anhedonia.

‘We are all born with an innate drive to engage in behaviors that feel rewarding and give us pleasure,’ said co-author Dr Elisa Trucco, a psychologist at the Center for Children and Families at Florida International University.

‘We now have convincing evidence that regular marijuana use impacts the brain’s natural response to these rewards.

‘In the long run, this is likely to put these individuals at risk for addiction.’

Marijuana’s reputation as a ‘safe’ drug, and one that an increasing number of states are legalizing for small-scale recreational use, means that many young people are trying it – as many as a third of college-age people report using it in the past year.

But Dr Heitzeg said that her team’s findings, and work by other addiction researchers, has shown that it can cause effects including problems with emotional functioning, academic problems, and even structural brain changes.

And, the earlier in life someone tries marijuana, the faster their transition to becoming dependent on the drug, or other substances.

‘Some people may believe that marijuana is not addictive or that it’s ‘better’ than other drugs that can cause dependence,’ said Dr Heitzeg.

‘But this study provides evidence that it’s affecting the brain in a way that may make it more difficult to stop using it.

‘It changes your brain in a way that may change your behavior, and where you get your sense of reward from.’

Source: http://www.dailymail.co.uk/health/article    6th July  2016

VANCOUVER, BRITISH COLUMBIA–(Marketwired – May 31, 2016)

Researchers at the University of Western Australia have identified the causal links between marijuana use and the development of serious diseases, cancers, birth defects, and the inheritance of traits that can cause such problems in children and grandchildren including the development of Down’s Syndrome. Parental use of marijuana is a children’s rights issue.

Associate Professor Stuart Reece and Professor Gary Hulse from UWA’s School of Psychiatry and Clinical Sciences found illnesses are likely caused by cell mutations resulting from cannabis properties having a chemical interaction with a person’s DNA. Even if a mother has never used cannabis, the mutations passed on by a father’s sperm can cause serious and fatal illnesses in offspring. The parents DNA carrying these mutations can lie dormant and may only affect generations down the road. The study was published in the Mutation Research — Fundamental and Molecular Mechanisms of Mutagenesis.

Source: http://www.sciencedirect.com/science/article/pii/S0027510716300574

Introduction

This essay is about the drug problem in society, particularly in the United States. By “drug” I mean alcohol, tobacco, and illegal drugs such as marijuana, hallucinogens, stimulants, depressants, and opiates. In regard to youth, inhalants (household chemicals inhaled to get a “high”) are also included.

This is not about the struggles faced by individuals who are addicted, or who struggle with any of the many life problems that can arise from drug use. Others are well addressing those issues in the treatment programs they offer and the publications they write. That society should be more diligent in ensuring availability of treatment for all who need it has been well stated by others. This essay is not about people’s drug problems so much as society’s drug problem.

The problem is that drugs are significantly decreasing our collective quality of life: decreasing our capacity to solve the problems that we collectively face in living. Whether you turn to issues of economics, health, social justice, family life, or the strength of the work force, the magnitude of the damage done by drugs is striking:

  • The number of deaths due to drugs in the United States alone each year exceeds 400,000 from tobacco, 100,000 from alcohol, and 35,000 from other drugs.
  • The most recent estimate of cost to U.S. society (not to users) of alcohol and other drug abuse was 246 billion dollars: 148 billion from alcohol abuse and 98 billion from other drug abuse.
  • A large percentage of health problems and health care costs are due to alcohol or other drugs.
  • Substance abuse in a single year costs American businesses 37 billion dollars due to premature deaths and another 44.6 billion dollars due to employee illness. Drug dependence and alcohol together cost businesses 200 billion dollars. A majority of the alcohol problems are caused by light and moderate drinkers, rather than alcoholics.
  • A high percentage of child abuse and neglect is associated with parental AOD (alcohol or other drug) abuse.
  • A recent study of teen marijuana users found they were 4 times more likely than non-users to attack someone, 3 times more likely to destroy others’ property, and 5 times more likely to have stolen things.
  • The combination of alcohol-related accidents, assaults, and suicides makes alcohol the leading risk factor for adolescent death and injury.

Whether or not you have directly experienced a drug problem in your life, society’s drug problem is shared by all of us. Most of the people who are aware of the impact of drugs on families and other relationships would argue forcefully one person’s drug use hurts more than just that person. The issue may be debatable in the case of any single individual, but collectively there can be no doubt: the drug problem is a problem for all of us.

In the twelve years I have worked in drug prevention, I have learned a lot about how drug use develops, and how it can be prevented. I have discovered that there is tremendous energy and potential in drug prevention, but progress has sometimes been slow, for good reason. The reason is that the general public, and in some cases even prevention professionals, hold some core assumptions about the drug problem that are actually incorrect. As a result, much of the effort put into prevention strays slightly, but significantly, from what is needed.

This essay is an attempt to identify, describe, and correct those faulty assumptions. This is not a “how to” book on prevention. I have written such a book (Best Practices in ATOD Prevention, 1997), with much help. But having the right tools are not enough to become a builder. To be successful with “how to,” you have to start with, “what’s that?” This essay is about understanding the drug problem: what causes it and what is needed to stop it. The application of this knowledge is up to each reader. I hope you find some valuable insights here, or perhaps find support for some of your own observations.

I am convinced that if we stop going down dead-end streets, we can really get places in prevention. Thanks for letting me share the results of my explorations in drug prevention.

Fallacy #1: The primary target of drug prevention should be hard-core drug abuse.

This fallacy has three main parts: (a.) which drugs are the problem, (b.) which drug users are the problem, and (c.) the relation of addiction to drug abuse.

a. “Shouldn’t crack, speed, and heroin be our number one concern?”

No. Ounce for ounce these drugs are certainly among the most potent, but they are (or should be) of secondary concern to drug prevention because of the developmental nature of drug abuse, the limitations of prevention, and the greater amount of societal problems associated with other drugs.

Development of Drug Abuse

It is exceedingly rare for an adult who has never used any drug to use drugs like cocaine or heroin. Nearly as rare is a youth or adult who uses one of these drugs without a history of use of at least one, and often all three, “gateway” drugs: alcohol, tobacco, and marijuana.

Don’t misunderstand the gateway drug phenomenon: obviously not all people who use alcohol, tobacco, or marijuana progress to other drug use. But, the odds of other drug use depend on gateway use because those who don’t use gateway drugs are so extremely unlikely to use other drugs.

The gateway phenomenon includes two other notable features in addition to the issue of whether or not gateway drugs are used. One is that the younger a person is when they begin gateway use, the greater their likelihood of drug problems (with gateway and other drugs) later in life. The other is that people who use two or three gateway drugs are more likely to progress to other drugs than people who use one (use of all three is most significant).

So alcohol, tobacco, and marijuana are truly “gateways” to other drug use. Although most of the people who go through the gate don’t do on to other drug use, nearly everyone who goes on to other drugs passes first through the threshold of gateway use. This alone doesn’t conclude the case for where to direct drug prevention, but sets the stage for two other two facts.

Limitations of Prevention

Prevention is just one of the major strands of anti-drug efforts. The other two are treatment and legal restrictions (regarding use, possession, and sale of drugs). To a great extent the target population for prevention and the target for treatment are opposite. By the time people go through gateway use and begin using other drugs, they have become (due to some combination of self-selection and the results of earlier gateway use) fairly habituated to drugs. In many cases they are already addicted. The habit formed from regular drug use is hard to break. When addiction is also present, the strong forces involved are not only psychological but also bio-chemical. We like to think our minds are in control, but addiction can rule behavior at a level so deep and powerful that rational thought pales in comparison.

As a result, prevention efforts that may be appropriate for youth who are non-users or experimenters with drugs are simply not effective with more committed users, and certainly not with addicts. Addiction calls for drug treatment: prevention is inadequate for those trying to back away from heavy drug use.

On the other hand, treatment is not appropriate for first-time experimenters. The treatment process is not designed for that population, and the cost of providing such intensive services is neither justified for the individual drug experimenter nor remotely available for the whole population of experimenters. For them and for those who are yet to experiment, prevention is the key.

Of those who use gateway drugs, some require treatment (or cessation aid, in the case of tobacco), but most do not. Of those who use other drugs, a large proportion requires treatment, and few would benefit from prevention. This strengthens the case for targeting gateway drugs in prevention, and leads to the third point.

Societal Cost of Gateway Drug Problems

Recall that ounce per ounce, gateway drugs are not as destructive as crack, crank, and heroin. But the scope of any one drug’s impact on society depends on the amount of use (including number of users and degree of use by each) as well as the drug’s dangers. Unlike crack and heroin, gateway drugs are used by a large portion of the population. And, though gateway drugs seem less dangerous than so called “hard” drugs, research and bitter experience have shown that the gateway drugs are dangerous enough:

  • Tobacco kills four times as many Americans as does alcohol, and alcohol kills three times as many as all illegal drugs combined.
  • Alcohol seems to be the leading cause of teen deaths, based on the high percent of instances in which alcohol is a major factor in car crashes, suicides, homicides, drownings, and other unintended injuries.
  • Marijuana combines the cancer potential of tobacco with the cognitive impairment of alcohol, except that impaired thought lasts longer after each marijuana use than after each alcohol use.

As a result, the benefit to society of cutting gateway drug use in half would be much greater than cutting other drug use in half. Combine this point with the point about prevention’s limits and the point about the development of drug abuse, and you get a strong case for making gateway drug use (particularly by youth) the prime target of prevention.

b. Shouldn’t prevention always target “high risk” youth?

No. Although it may be appropriate to devote extra preventive effort to some groups of youth, conceiving ATOD prevention in only those terms is problematic for reasons that include the breadth of risk, the importance of environmental risk, and the need for different approaches according to the nature of different risk conditions.

Breadth of Risk

While some characteristics act as “risk factors” for youth ATOD use, the absence of those risk factors doesn’t guarantee a drug-free youth. To some extent, everyone is at risk. The older a persons gets without using, the lower the risk that they will use. Furthermore, while the primary aim of ATOD prevention is to prevent use, an important secondary function is to help prepare all youth for addressing the drug problem in society: as family members, co-workers, or citizens. We are currently a society at risk.

This is not to say that community risk conditions shouldn’t be considered, nor that “selective” ATOD prevention efforts can’t be done for groups of medium risk youth or families. I use the term “medium risk” to refer to youth who haven’t begun ATOD use, but whose family or personal characteristics include some risk factors (e.g., poverty, low academic achievement, parental drug use or addiction, etc.) for youth ATOD use. But these efforts are a supplement to prevention efforts for all youth, rather than a replacement.

Environmental Risk

Preoccupation with risk profiles of individual youths, or even groups of youths, diverts attention away from the strongest influences of whether most youth will try drugs or avoid drugs. The combination of youths’ peer social environment, family environment, school environment, media environment, and their community’s adult social environment account for the vast majority of variation in youth drug behavior. A “low risk” youth who enters a “high risk” environment (e.g., a “no-use” youth who moves to a school where drinking is the norm) is no longer low risk.

Prevention planners who only look at what’s “inside” youth can miss the environmental factors (including media influences) that shape youths’ attitudes. If not directly addressed, these environmental factors can misdirect youths’ attitudes and behaviors as fast or faster than youth-focused programs can positively affect them.

Different Risks – Different Approaches

The risk factor that is most important to the largest number of youth in regard to initiation of gateway drug use is their perception of peer attitudes about drugs, as will be discussed in regard to “Fallacy #3.” However, for a smaller number of youth other factors play a major role. For example, children raised in households with parental violence, neglect, or addiction are more likely than average to develop their own problems with alcohol or other drugs. The number of children in this kind of situation, though much larger than it should be, is small compared to the overall number of children and families.

For a child in a household with parental violence (domestic violence and/or child abuse), what happens to that violence may be the most important “risk factor” for their future mental health, including their relation to drugs. Their greatest need may have little to do with drug prevention, and everything to do with appropriate resolution of the violence.

For a youth failing school, the greatest need may be assistance with whatever is interfering with school achievement.

In each case, the most effective form of drug prevention may be to resolve the problem(s) that increase risk for drug use, rather than to directly address the issue of drugs. On the other hand, a youth who has started to experiment with drugs may need intervention services, sometimes called “indicated prevention”, but actually more closely akin to some forms of substance abuse treatment counseling. In all these instances, the kinds of programs that constitute “universal” drug prevention programs may be less relevant. So, these kinds of “high risk” youth need more focused and intensive assistance than is available through what I am calling drug prevention, i.e. programs designed to impact the gateway drug attitudes and behaviors of large groups of youth. They may be helped somewhat by such programs, and so should not be excluded, but to limit participation in prevention programs only to such “high risk” youths is probably not appropriate, particularly given the risk of a norm of gateway drug use arising among program participants if all are “high risk.”

c. Isn’t addiction prevention the main goal of substance abuse prevention?

No. Addiction is one major outcome of drug use, but the impairment of rational thought, the plethora of anti-social and injurious behaviors caused or heightened by that impairment, and the direct toxic effects of drugs are all substantial societal problems worthy of prevention. Addiction increases these other problems, but a person need not be addicted in order to seriously injure of kill themselves or others while impaired, typically due to negligence (as in DUI crashes) rather than violent intent.

Further, since the number of alcohol or other drug users at any given point in time far exceeds the number of addicts (including alcoholics), the societal damage done by non-addicted persons can cumulatively exceed the damage done by addicts. Even though individual addicted persons are more problematic to society than individual non-addicted AOD (alcohol and other drug) users, the much larger number of non-addicted users makes them a major part of societal AOD problems.

Efforts to make the public more aware of realities of addiction should continue, but preventing addiction is one main goal of drug prevention: not the main goal.

Fallacy # 2: Alcohol and other drug problems are mainly a result of other problems, and drug prevention can best be accomplished by addressing those other problems.

Drug abuse has multiple causative factors: this has become an oft stated truism. Unfortunately, people tend to notice and magnify the causative strand that is most evident in their personal or professional experience. Their observations are strengthened by studies which demonstrate the connection between each of a variety of “risk factors” and drug abuse, but which fail to consider the larger context of the societal drug problem, including which of the many risk factors play the most important roles within the largest numbers of people. Rather than starting with convergence on the most prevalent and powerful risks, people therefore tend to diverge into various less central issues:

  • Persons who focus on poverty see poverty as the main root of drug problems.
  • Persons concerned with stimulating positive youth development see their work as the best form of drug prevention.
  • Persons familiar with dysfunctional family systems see family dysfunction as the main root of drug problems.

Attention to this whole range of negative factors may be appropriate, but mistaking any one of these for the “main” cause of drug problems is not. One person or subgroup may be profoundly influenced by one of these factors, but the prevalence of each factor in the population is far less than the prevalence of drug problems.

Family Dysfunction: Major dysfunction (such as family violence) greatly heightens the chance of youth drug problems, but the majority of youth AOD users (and hence, most of the future AOD abusers) do not come from dysfunctional families. Dysfunctional family life is a potent risk factor but not a prevalent one, in comparison to the scope of youth AOD problems.

Poverty: Poverty makes drug problems more likely, but only slightly more likely: a large number of well-to-do people are among those who children use and abuse alcohol and other drugs.

Positive Youth Development: Policies that empower youth development are a good idea, but aren’t sufficient to prevent youth drug use. The notion that positive youth development can substitute for specific attention to drug prevention is similar to the 1970’s notion that good self-esteem is the key to drug prevention. Unfortunately, ignoring drug prevention in favor of self-esteem tends to produce drug users with high self-esteem. Self-esteem doesn’t protect from the destructive effects of drugs. Youth development programs can be an important aid for youths who lack key developmental assets, but will only impact drug use if:

  1. anti-drug norms are already present in the lives of those youth, or
  2. the youth development program includes building anti-drug norms as part of its mission.

Two kinds of problems arise from the mis-attribution of heightened importance of these factors as causes of substance abuse:

  1. More global causes of ATOD problems, such as youths’ and parents’ attitudes about drug use, may be glossed over in the design of prevention strategies. In other words, potentially efficacious approaches to prevention may be ignored in favor of less broadly effective approaches.
  2. Parents may believe that avoiding family dysfunction is sufficient to prevent youth drug problems.

The worst instances of this fallacy in action have parents or other adults allowing and enabling youth alcohol or other drug use under the misguided notion that only troubled individuals abuse substances. Statements like, “It’s no big deal,” or “They’re just going through a phase,” or “It’s part of growing up” tend to be evidence of this. While it’s true that troubled youth are more likely to develop a drug problem, also true is that alcohol or other drug use can cause a person to become troubled – especially if addiction is involved.

Youth alcohol and other drug use is a bad idea no matter how positive an individual’s circumstances. Youth with substantial personal or family problems are more likely to experience significant problems with drugs, but the initial absence of personal disturbance is no insurance policy against addiction or other ATOD problems. And, although family problems constitute a risk factor for youth ATOD use, family wellness is not a sufficient protective factor to counter other negative influences on youth ATOD decisions. Parents who don’t have general problems with family management can take steps (particularly in regard to monitoring youth activities) to decrease their children’s likelihood of ATOD use, but just being a “good” parent isn’t a cure-all. Drug prevention needs to go beyond the foundation of healthy families and positive youth development, to build attitudes and behaviors that especially counter ATOD influences in society.

Fallacy #3: The main essence of successful drug prevention is communication about the dangers of drugs.

This very common misperception probably sidetracks more prevention efforts than any other single error. Actually the essence of success in preventing youth use of gateway drugs is making drug use unpopular: destroying the myth that peers approve of drug use. This can be supplemented by fact-based approaches and parent programs, but the most basic reason youth as a whole start gateway drug use is because they believe their peers approve of it. No matter how dangerous they are told drug use may be, if they think many others are doing it they will tend to do the same, unless they consistently see very negative effects on those believed to be using.

There are two reasons I see for the continuing strength of Fallacy #3 in spite of evidence to the contrary. The first is our nature as human beings. We like to think we are logical, sensible beings. To some extent we are, but most of us, and especially children and youth, base our actions first on what we observe from those around us, and only secondly on what we believe.

Remember that we are talking about society as a whole here: there are certainly some people who are less prone to be influenced by others (psychology calls them “field independent” as opposed to field dependent), and all of us vary in our susceptibility. But as a whole, we’re just not as logical as we like to think. To be human is to be influenced by our observations of others.

The second reason for the fallacy is a more complex one having to do with the nature of scientific studies of youth alcohol and other drug use. Common scientific method in the social sciences involves looking for things that go together in large populations. The question is what “factors” tend to go with, and particularly to predict, youth ATOD use. A basic premise is that correlation does not necessarily equate to causation, especially in cross-sectional one-time studies. However, when a factor such as “perception of harm” is closely matched with drug use over a period of years, as has been the case in the national “Monitoring the Future” study, observers are hard pressed to ignore the likely conclusion that changing perception of harm is the key to prevention.

The problem is, how does one change perception of harm? The common assumption is that you do this by communicating drug dangers. Often overlooked is that there is an equally strong association with perceived peer approval or disapproval for use of drugs: what youth believe their peers think of drugs. I think that, contrary to common assumptions, the perception of peer attitude drives youths’ own attitudes about drugs (both perceived harmfulness and intent to use). Perception of harm then ends up being a strong indicator of whether a youth will use a drug, especially because it is probably also affected by other risk factors. But the route to turning around perception of harm usually has to go through perceptions of peer approval/ disapproval. When we present logical facts about drug dangers to youth, if they think most of their peers approve of drug use, and indeed use drugs, then the warnings seem ungrounded and are easily ignored.

I base this point on a variety of research, but some of the most striking and easiest to communicate is research about what works in prevention. Of all the things that have been tried in prevention curricula for young teens, the most powerful is simply to correct their typically exaggerated assumptions about how many peers use drugs. When they are shown that far fewer than thought peers use, their attitudes change to a degree not seen with mere truth about drugs.

This is not to say that education about drug dangers is not important for youth: it is! These facts back up the facts about peer attitudes, and may be especially important for some youth who are able to base their behavior on rational truth about drug dangers. Even if this weren’t the case, it would simply not be right to let youth grow up in this society without exposing them to the truth about drugs. But to assume that exposure is the key element of prevention is to severely limit the effectiveness of one’s prevention efforts.

One of the important implications of this is that the images presented by mass media, especially in regard to images of youth attitudes and behaviors, should be a vital concern of prevention. We all like to think that we are too sophisticated to be influenced by the images of television and other media, but it’s just not so. We are influenced. That’s why advertising works. While any one youth may be more influenced by their parents than by the media, youth as a whole are dramatically influenced (as has been demonstrated by studies showing that youth smoke those cigarette brands that are most heavily advertised to youth). Media plays the role of a “super-peer,” playing directly into the heart of youth decisions by telling them what is cool and what isn’t. Prevention cannot afford to ignore this. Luckily, the same principles currently used by alcohol and tobacco advertisers to snare youth users can also be used in prevention. But, first we have to get past this fallacy that drug facts are the key.

Fallacy # 4: Making and enforcing laws against the use of drugs, and against underage use of alcohol and tobacco, is contrary to prevention and treatment of drug use.

This premise has been advanced by legalization groups, claiming all would be well if we did away with laws against drug use and relied solely on prevention and treatment. But the truth is that prevention, treatment, and legal barriers to use all depend on each other for effectiveness. The kind of “prevention” touted by legalization groups is not prevention of use but facilitation of “safe” use, called “harm reduction.” The role of prevention in this scenario is to teach people how to use drugs safely. The problem with this is that the laws against each particular drug are enacted because its use is inherently unsafe. An analogy would be explosives manufacturers lobbying to take the funds used to enforce laws against possessing bombs and instead just teaching youth how to use them “safely,” and of course not until they were 18 or 21. Would the public stand for that? Would even the most avid libertarians be crazy enough to support it? Legalizers suggest that drugs hurt only the user, but impacts of our society’s drug problem go far beyond the circle of users, as was discussed earlier.

Even if, after legalization, the current drug-free message of prevention were maintained, a country that tolerates drug use would be giving a strange message that would undercut any such “no-use” message. “Drugs are dangerous and hurt society, but you can go ahead and do them if you want.” Use would soon rise, not so much from drug-free adults starting use but from every new generation of teens becoming more and more enmeshed in drug use, in spite of any legal age restrictions. This is what has happened when legalization has been tried. Similarly, the number of people entering treatment, cooperating with treatment, and avoiding relapse would be far less without the force of law to compel users to quit.

High quality drug prevention and treatment are currently vital to our society, but their success would be lessened, not increased, if legal sanctions against use were eliminated. The specific workings of the legal and criminal justice system in regard to drug use can always be examined for improvement, but most groups who currently call for drug law “reform” are using the term as a euphemism for legalization.

Fallacy # 5: Marijuana is not dangerous.

We tend to think of drugs as poisons to the body, and measure the potency of a drug by how fast and how completely it can interfere with physical health. We are less quick to recognize that the most crucial characteristics of drugs are their “psychoactive” effect: their alteration of thought, feelings, and behavior. Measured by physical effects only, marijuana is not as dangerous as many other drugs (though it has the potential to kill as many people as tobacco does, if it were as popular as tobacco). But, examined for its behavioral effect, marijuana is quite potent. The subtlety with which it alters behavior, typically over a period of weeks or months, makes it all the more effective as a behavioral change agent. The data that has begun to emerge as younger teens and pre-teens smoke more potent marijuana shows a devastating effect on the social functioning of many users. Some users may have been self-centered when they began use, but marijuana heightens that characteristic, killing the empathy and capacity for altruism that embody the best qualities of society. What is left is a person addicted to marijuana and concerned about marijuana, but not so much about relationships, achievement, or even obeying the law. People sometimes discount the effects of marijuana because many users do not seem to be greatly impaired, but the luck of some in warding off clear impairment is a poor balance to the studies and accumulated life experiences of those who have been severely changed by marijuana use.

Fallacy # 6: Anti-drug laws and anti-drug law enforcement is driven by national bureaucracy and the zealousness of federal officials.

People who travel in a sub-culture of drug tolerance tend to perceive the government’s anti-drug actions as being out of touch with the populace, but polls show that a large majority of the American (and other) public opposes drug legalization. The greatest passion in favor of enforcing drug laws comes not from any government but from families that have seen the worst that drugs do. The proper balance between society’s interest in stopping drugs and the freedom of individuals becomes clear when one has witnessed a family or community ravaged by drug use and addiction. The social value of drugs is far below zero. Any loosening of restrictions on drug use has tended to lead to a cycle of increased use, increased damage to society, and a resulting determination to toughen enforcement of laws against drug use. Ultimately, the source of calls for strict enforcement of laws against drugs come not from any one group but from the power of drugs to damage people, and damage society.

Alan Markwood is the Prevention Projects Coordinator at Chestnut Health Systems, Inc. in Bloomington, Illinois. Responsibilities include:

  • Participating in prevention research, development, and training projects as a contractor to the Illinois Department of Human Services.
  • Directing prevention coalitions in three counties, funded by the federal Center for Substance Abuse Prevention and the Illinois Department of Human Services under grants he wrote.

Mr. Markwood is the principal author of the Best Practices in ATOD Prevention Handbook (1997), and has managed a series of statewide studies on youth substance use in Illinois. He served as InTouch Area 14 Prevention Coordinator at Chestnut Health Systems from 1987 until promoted to his current position in 1995. Prior to his work in prevention, he worked as a School Psychologist for seven years in Illinois and Massachusetts. He has a Master of Arts degree in Psychology from Alfred University and a Certificate of Advanced Graduate Study in Education from Boston University.

Source: www.drugwatch.org Sept.1999

Summary

The 2012/13 New Zealand Health Survey (NZHS) provides valuable information about cannabis use by adults aged 15 years and over. It builds upon and adds value to the findings of the 2007/08 New Zealand Alcohol and Drug Use Survey report on cannabis.

This report presents information on cannabis use in New Zealand, including patterns of use, drug-driving, harms from use (productivity and learning, and mental health), legal problems, and cutting down and seeking help. Information on the medicinal use of cannabis is also presented.

Patterns of cannabis use

Eleven percent of adults aged 15 years and over reported using cannabis in the last 12 months (defined here as cannabis users). Cannabis was used by 15% of men and 8.0% of women. Māori adults and adults living in the most deprived areas were more likely to report using cannabis in the last 12 months. Thirty-four percent of cannabis users reported using cannabis at least weekly in the last 12 months. Male cannabis users were more likely to report using cannabis at least weekly in the last 12 months.

Cannabis and driving

Thirty-six percent of cannabis users who drove in the past year reported driving under the influence of cannabis in the last 12 months. Men were more likely to have done so.

Cannabis-related learning and productivity harms

Six percent of cannabis users reported harmful effects on work, studies or employment opportunities, 4.9% reported difficulty learning, and 1.7% reported absence from work or school in the last 12 months due to cannabis use.

Cannabis and mental health harms

Eight percent of cannabis users reported a time in the last 12 months that cannabis use had a harmful effect on their mental health. Younger cannabis users (aged 25–34 years) were most affected, with reported harm to mental health decreasing markedly by age 55+ years.

Cannabis and legal problems

Two percent (2.1%) of cannabis users reported experiencing legal problems because of their use in the last 12 months.

Cutting down and help to reduce cannabis use

Most cannabis users (87%) did not report any concerns from others about their use. Seven percent of cannabis users reported that others had expressed concern about their drug use or had suggested cutting down drug use within the last 12 months. Of cannabis users, 1.2% had received help to reduce their level of drug use in the last 12 months. Few cannabis users who wanted help did not get it (3.6%).

Cannabis use for medicinal purposes

Forty-two percent of cannabis users reported medicinal use (ie, to treat pain or another medical condition) in the last 12 months. Rates were similar for men and women. Older cannabis users (aged 55+ years) reported higher rates of medicinal use.

An  infographic (PDF, 174 KB)  provides a short overview of these findings.

The methodology report for the 2012/13 New Zealand Health Survey is also available on this website.

If you have any queries please email hdi@moh.govt.nz

Downloads

Source:  Ministry of Health. 2015. Cannabis Use 2012/13: New Zealand Health Survey. Wellington: Ministry of Health. Published online:  28 May 2015

http://www.health.govt.nz/publication/cannabis-use-2012-13-new-zealand-health-survey

SUSAN SCHENK AND DAVID HARPER

REUTERS

Ecstasy deserves to remain an illegal drug, as there is substantial evidence of it causing harm.

A dangerous case is being made in New Zealand for the legalisation of MDMA, the primary active ingredient of the street drug, Ecstasy.

Ecstasy rose in popularity among the rave party scene in the early 1980s. Use has since spread to more mainstream groups. New Zealanders are some of the heaviest users of ecstasy worldwide, with an estimated 13 per cent of Kiwi respondents to the Global Drug Survey having used ecstasy in the past year.  Supporters of the move to legalise claim the drug is safe, and recent comments made by Wellington Hospital emergency department specialist, Dr Paul Quigley, would seem to support this position.  Quigley has reported few emergency admissions related to ecstasy use, and from this he has incorrectly assumed this means that MDMA use poses minimal harm.

Emergency room admissions are a flawed benchmark for determining the safety of a drug, such as MDMA, as the major harm associated with MDMA is the death of brain cells, and associated behaviour changes.   These effects are generally not life-threatening and would therefore not lead users to seek emergency care.

This does not, however, indicate that MDMA is safe.

Rather, considerable published evidence has demonstrated that memory loss and attention issues are common in MDMA users and there is compelling evidence for the loss of the brain chemical, serotonin, which leads to further problems associated with sleep patterns and emotional wellbeing.

These effects can seriously impact the individual’s ability to lead a productive life, and it is common for users to experience negative emotional after-effects of ecstasy. Importantly, there are no quick fixes for the many detrimental effects of ecstasy and these effects may persist for years.

It has also been suggested that MDMA dependence is not a likely consequence of use, providing proponents of legalisation another indication that MDMA use poses minimal harm.   This too is unsupported in the scientific literature.

* John Key unconvinced by emergency doctor’s call to legalise MDMA

* Don’t freak out over changing drug laws

For most drugs of abuse, including cocaine and methamphetamine (P), about 10-15 per cent of users become dependent on the drug. The same is true of ecstasy users.

Studies have suggested that a subset of ecstasy users progress to misuse and consume the drug frequently and in high dosages.  In New Zealand, the Illicit Drug Monitoring System provides a snapshot of heavy drug users over time.

According to this authoritative survey, ecstasy use among heavy drug users is substantial, and 15 per cent use ecstasy weekly.  An online survey in Britain suggests MDMA users were more likely to report dependence symptoms than users of cocaine.

Another assumption is that by regulating the supply of MDMA, both producers and users will engage in safe drug production and use.  While it is true that most users don’t know what else they are actually taking when taking an ecstasy pill – it is frequently mixed with any range of other substances, some harmful, some not – that doesn’t mean that pure MDMA is actually safe.

Perhaps ‘safer’, but not ‘safe’.

New Zealand has toyed with legalisation of psychoactive substances for many years. First there were the BZP-TFMPP “legal highs” that were subsequently banned as they were shown to be dangerous after all.  The same was true of synthetic cannabis products that have also recently been banned because they were shown to pose more than an acceptable risk of harm.

Despite what has recently been suggested in the media, there is substantial evidence of harm and risk arising from the use of MDMA.  We have been studying the effects of MDMA on brain and behaviour for about 10 years, and the negative effects of ecstasy have been well-documented by us and many other researchers.

Knowing what we know about ecstasy use, and the well-documented negative consequences of its use, the potential for misuse and the persistent and prolific adverse consequences of MDMA use, it is clear that unrestricted use of MDMA poses a great risk of harm, and that it would be irresponsible to provide MDMA for legal sale in New Zealand.

Professor Susan Schenk is from Victoria University’s school of psychology, and Professor David Harper is the dean of science.

Source:  stuff.co.nz  29th June 2015

Freisthler B1Gruenewald PJ2Wolf JP2.

Abstract

The current study extends previous research by examining whether and how current marijuana use and the physical availability of marijuana are related to child physical abuse, supervisory neglect, or physical neglect by parents while controlling for child, caregiver, and family characteristics in a general population survey in California.

Individual level data on marijuana use and abusive and neglectful parenting were collected during a telephone survey of 3,023 respondents living in 50 mid-size cities in California.

Medical marijuana dispensaries and delivery services data were obtained via six websites and official city lists. Data were analyzed using negative binomial and linear mixed effects multilevel models with individuals nested within cities.

Current marijuana use was positively related to frequency of child physical abuse and negatively related to physical neglect.

There was no relationship between supervisory neglect and marijuana use. Density of medical marijuana dispensaries and delivery services was positively related to frequency of physical abuse.

As marijuana use becomes more prevalent, those who work with families, including child welfare workers must screen for how marijuana use may affect a parent’s ability to provide for care for their children, particularly related to physical abuse.

Copyright © 2015 Elsevier Ltd. All rights reserved.

Source:  Child Abuse Negl. 2015 Jul 18. pii: S0145-2134(15)00237-9. doi: 10.1016/j.chiabu.2015.07.008.  [Epub ahead of print]

Neuroscientist Woody Hopf opens a cabinet in his alcohol research laboratory at the University of California, San Francisco. Inside is a cage containing a rat that is being taught addictive behaviours. The rat has been conditioned to press a lever to release a squirt of alcohol when it hears a beep. Hopf closes the cabinet so that the rat will not be distracted by the sights and sounds of human visitors. Just as it takes time for people to undergo the characteristic brain changes that enforce addiction, he says, it will take time for his rat to become dependent on alcohol.

Researchers such as Hopf view addiction as a disease of the brain circuits responsible for pleasure, stress and decision-making. “Addictive substances come at the brain in different ways,” says George Koob, director of the US National Institute on Alcohol Abuse and Alcoholism (NIAAA) in Bethesda, Maryland. “But in the end, they’re activating some of the same circuitry and patterns of behaviour.”

For decades, researchers have been mapping the electrical and chemical circuits that underlie addiction. Now they are working on strategies for healing these neural pathways. Imaging studies show how the brain rewires during recovery from addiction. When combined with studies of how the brain develops during adolescence, the work could help researchers to understand how the brain changes that are characteristic of addiction occur, as well as who is most vulnerable and why. This work is rapidly being translated into treatments. By using electrodes and fibre-optic cables, researchers can intervene in neural circuits with great precision, causing animals to lose their taste for alcohol or their interest in cocaine, not just for days but for weeks or months. This work is now being tested in people. Researchers hope that therapies to heal damaged brain circuits will improve the odds of people overcoming addictions.

Crossed wires

Koob divides addiction into three stages, each with its own brain circuit — groups of neurons or larger structures that interact in a characteristic way (see page S46). Addiction starts with the feel-good binge stage, which is fuelled by the brain’s reward circuit, particularly at the nucleus accumbens. Withdrawal brings stress, centred in the emotional amygdala. Finally, craving and compulsion circuits extending from the prefrontal cortex keep someone using a drug, regardless of negative consequences. Impulsive bingeing leads to habits as the user needs the drug to feel normal.

The changes to the brain’s circuitry are long-lasting, so people trying to give up will often relapse. Even years after recovery, people often start using again when some cue, such as the smell of alcohol or the site of an old hangout, retriggers old patterns. But the changes are not permanent. “The brain can enjoy some recovery, probably through remodelling to override the broken parts,” says Edith Sullivan, an experimental psychologist at Stanford University in California.

Some of the physical damage caused by alcohol misuse can be undone. For example, says Sullivan, the brains of people who have misused alcohol for a long period shrink, but some of that brain volume can be regained by sustained sobriety. There is also some functional recovery — even if the pathways are not fully restored, the recovering brain starts to find workarounds.

Sullivan’s group has been using functional magnetic resonance imaging (fMRI) to study cognition in those recovering from alcoholism. A cognitive skill the researchers focused on is spatial working memory — the thinking that helps you to remember where you parked your car, for example. Poor spatial working memory is characteristic of alcohol misuse.

Sullivan’s research suggests that people recovering from alcohol addiction manage to work around brain damage; in other words, their brains find ways of accomplishing tasks by avoiding using damaged areas and they start to regain their working memory1. The group found that alcohol-dependent people who had been sober for at least a month performed as well as non-alcohol-dependent controls on spatial working-memory tasks, but used a different part of the brain to do it. Sullivan gave them a more abstract task than looking for a lost object or a parked car, but like those tasks it required visual processing, which can take one of two broad neural paths. Patients without brain damage typically rely on a ‘where’ pathway to do the task, whereas those in recovery from alcohol dependence activate a ‘what’ pathway, which tends to be used for recognizing and identifying what we see.

“The next step is to find out how to train a person with brain damage to use these new pathways,” says Sullivan. Encouraging the natural recovery process could help people who are dependent on alcohol to make faster progress. Sullivan compares the brain damage from alcohol addiction to that caused by stroke. “Recovery won’t take three days, it may take three or six months, or a year,” she says. It takes time for changes to occur in the brain when someone develops a dependence on alcohol, and it takes time to undo that.

Sullivan is currently investigating whether there is a cost to this rewiring. She suspects that people in recovery are performing the cognitive steps needed for these tasks sequentially, so they take longer than people without addictions who do the steps rapidly in parallel. The damaged brain has fewer circuits to use, so the brain finds it harder to multitask.

Early start

“There is a lot of debate about how harmful substance abuse is for brain development.”

Our understanding of the addicted brain comes from animal studies and from research on people who are already addicted or are in recovery, such as Sullivan’s participants. Researchers can only guess at how these changes develop in people. Henning Tiemeier, a psychiatric epidemiologist at Erasmus Medical Center in Rotterdam, the Netherlands, says that the only way to see these changes is to follow people over time. “There is a lot of debate about how harmful substance abuse is for brain development, and you cannot prove it with one brain image,” he says.

Two studies, one planned in the United States and one already underway in the Netherlands, could provide some answers. Both will follow adolescents. The adult brain is already formed, although it is still plastic, which is why alcoholism and drug addiction become so engrained, and why the resulting damage cannot be fully repaired. The worry, says Koob, is that the developing brain may not form properly under the influence of drugs and alcohol. Children do not have the cognitive skills to make good choices, making them particularly vulnerable. “Young people have a well-developed reward system but they don’t have a good executive control centre,” says Koob. The key part of that centre, in the brain’s prefrontal cortex, does not finish developing until about the age of 25.

The US National Institutes of Health (NIH), a federal agency that includes the NIAAA and the National Institute on Drug Abuse (NIDA), is currently accepting proposals for the Adolescent Brain Cognitive Development study, which will enrol 10,000 children aged 10 and follow them into adulthood, using neuropsychological tests, brain imaging and surveys, focused specifically on addiction.

Tiemeier is working on the Generation R study in the Netherlands, which has a broader focus on fetal and childhood development and has been following 10,000 children from before birth. The youngest are now aged 9, and the oldest are 12, a stage when some will begin experimenting with cigarettes and alcohol.

Generation R is collecting the first set of brain MRI scans from children in the study, and has about 3,300 so far. By continuing to collect them as the children grow, changes over time will become clear. This is by far the largest brain-imaging study on adolescents in the world, says Tiemeier, so it should provide evidence about how substance use affects the developing organ. He does not expect to see major developmental changes associated with the occasional substance use likely to be found in Generation R because it is a general population study, rather than being focused on people who are addicted to a substance. For this reason, such studies need to be as large as possible if they are to find out what damage drug use does, and how it interacts with puberty, when surges of hormones affect behaviour and brain development.

More information will be available when the Generation R data are combined with results from the NIH study, says Nora Volkow, director of NIDA. These studies will provide a better understanding of the brain changes that reflect what she calls “the skeleton of addictive behaviours”. Addiction to cigarettes is different from addiction to heroin, for example, but all addictions have a common neurological framework. These studies will show how it grows. They should also yield insight into who is vulnerable and why, and how they might be helped sooner.

But as further research deepens our understanding of addiction as a disease characterized by changes in the brain, researchers and policymakers need to think about better ways to evaluate medications and therapies, says Volkow. Currently, any pharmaceutical treatment for addiction needs to show that the patient is now completely free of their addiction, which is difficult to prove and takes a long time (see page S53). “Rather than ask for an outcome of complete abstinence, shouldn’t we evaluate these treatments on their ability to counteract these brain changes?” she asks.

Painful realities

This focus on reversing changes to the addicted brain is leading to therapy ideas that are showing promising early results in animals. Hopf’s rat studies, for example, have led to a potential therapy for alcoholism that is focused on countering the compulsion to use despite negative consequences such as the loss of relationships with family and friends, employment or health. Because rats do not fear these outcomes, Hopf uses simpler analogues. In some experiments, alcohol-dependent rats are given extremely bitter alcohol instead of the expected normal flavour, or in the lever-pressing test they occasionally receive a painful electric shock to their paw. “The rats want the alcohol but they are not happy about it,” Hopf says.

After years of painstaking research and some luck, Hopf found that a particular group of neurons in the reward-centred nucleus accumbens has a key role in promoting compulsive drinking. This year, he found that an approved drug called D-serine binds to receptors on these neurons, causing them to fire less often, leading the alcohol-dependent rats to drink less2. It seems to work by disabling the compulsive behaviour — by turning off the power to deny painful realities. Rats that experience bitter or painful consequences drink less when given the drug. Rats have no such negative consequences to fear and are not affected by the drug and drink as normal.

The nucleus accumbens and a denial of the reality of the situation are involved in multiple stages of addiction, according to Koob, and have a role in both intoxication and the withdrawal process. Hopf is now writing up a plan for a clinical trial of D-serine.

Other techniques target addiction circuits by using physical interventions, rather than drugs. Researchers at the University of Geneva in Switzerland led by neurologist Christian Lüscher have used a method called optogenetics to target a particular group of cells and receptors involved in cocaine addiction in mice. Optogenetics allows researchers to turn off gene expression precisely by shining light into the brain through implanted optical fibres. When Lüscher’s group used the method to calm a group of overactive dopamine-receptor neurons in the nucleus accumbens, the mice stopped seeking cocaine3.

However, optogenetics cannot be used to treat people. The method first requires genetic engineering to render the target cells sensitive to light, and it is not yet possible to safely implant optical fibres in the human brain.

Stimulating recovery

Instead, Lüscher’s team is attempting to emulate the effects of optogenetics by using methods that translate better to the clinic. They are developing a variation on deep-brain stimulation (DBS), a technique that uses an electric current to silence overactive neurons, which is commonly used to treat movement disorders such as Parkinson’s disease. By careful placement of the electrodes, clinicians can target DBS to a particular region in the brain. Researchers have tried using it to treat addiction in people, but results have been mixed.

Lüscher is combining DBS with drugs to block particular receptors in the rat brain, making it possible to silence specific cell types. First they implant an electrode in the nucleus accumbens. Then they use a drug that blocks the neurons’ dopamine receptors. Finally, they switch on the electrode for ten minutes. The effects of DBS for treating Parkinson’s are transient: when the electric field is turned off, the tremor returns. But Lüscher’s combined therapy had a longer-lasting effect4. After 10 minutes of stimulation, the rats exhibited normal behaviour for the following 21 days. Lüscher thinks this means that the treatment may be repairing part of the circuit that was damaged by addiction. He says that the group’s next step will be to test this approach in primates, or possibly take it to clinical trials.

This demonstration of an apparently long-term reversal of drug-related behaviour is “a miracle”, says Jessica Wilden, a neurosurgeon at the Louisiana State University Health Center in Shreveport. Could this lead to a therapy in which you give a patient a pill and a day of brain stimulation and then they are drug free? “In a small way that’s what they’re showing,” she says. But doing it in people will be harder, she warns.

Wilden is investigating whether DBS can be used to treat methamphetamine (meth) addiction. Meth affects dopamine receptors (see ‘Methamphetamine misuse’) and is a growing problem, particularly in Iran and in the southern United States, often for military veterans. Unlike other drugs, which tend to be misused mostly by men, meth use is equally common in women, and has a burden on children because women tend to be the primary caretakers, says Wilden.

“I’m trying to set up a stable model of meth abuse, abstinence and relapse in rats, and then try DBS treatment,” says Wilden. It is a huge challenge. The drug is a potent stimulant, with effects lasting for 16–20 hours in the rats; the animals become agitated and stressed, and get tangled up in the equipment used to administer the drug and the cables that connect them to the DBS system.

Although DBS is a helpful research tool, Wilden and Lüscher both doubt whether it can be widely used to treat addiction — and Wilden’s work with meth illustrates the difficulties. The therapy is expensive, invasive and requires patients to care for the implants and to return to the clinic for regular follow-ups. Those motivated to overcome alcoholism might be able to do it. But people with more destructive addictions, particularly to meth, are less cooperative and have high rates of homelessness, making the treatment even less suitable. “The deep-brain stimulator is a pacemaker, with wires going under the skin into the chest where they connect to a battery,” says Wilden. “That’s a lot of metal, especially in people who are fragile. There’s no way I can implant this in someone living on the streets.”

Lüscher and Wilden plan to validate their interventions with optogenetics and DBS in animals, and then adapt the results to clinically realistic techniques. The most likely candidate is transcranial magnetic stimulation (TMS), which uses a magnetic field to stimulate electrical activity in neurons deep in the brain. One advantage is that TMS is non-invasive: treatment simply involves wearing a magnetic helmet for a few minutes. It is currently used to treat depression and migraines.

So TMS is more patient friendly, but it is also more mysterious — researchers do not know why it works. Furthermore, it has poor spatial precision, which frustrates neuroscientists who want to target specific brain locations. But this might not matter, says Antonello Bonci, a clinical neurologist and scientific director at NIDA.

In 2013, Bonci published a paper describing how his team had used optogenetics to reactivate an area of the prefrontal cortex that was abnormally quiet in cocaine-addicted rats5. The treated rats lost interest in pressing a lever to get cocaine. A few months later, Luigi Gallimberti and Alberto Terraneo at the University of Padova in Italy started using TMS to target the equivalent area in the brains of people addicted to cocaine. They have since been successfully using the technique to treat such people.

“It’s up to us to figure out who’s getting better and why, and how many sessions it takes.”

Bonci says that the results are anecdotal, but exciting: most people who stuck with the treatment for a few weeks have now been clean for several months, and testify that they do not even think about cocaine any more, he says. With this black cloud lifted, they are able to enjoy food, sex, reading, family time and all the other good things in life. Bonci is now working with the Italian group to design a double-blind clinical trial, and is collaborating with another group to work out how the TMS works. “It’s up to us now to figure out who’s getting better and why, and how many sessions it takes,” he says.

In addition to TMS, the Italian patients also received supportive medical care and psychological therapy. Even with brain stimulation or medication, people still need emotional support, as well as therapy “to identify triggering cues and memories, and practise making new grooves of thought”, says Hopf. But with tools such as DBS and TMS, neuroscientists’ deepening understanding of the circuitry of addiction is now being translated to the clinic much more rapidly than ever before.

“For the first time in the history of neuroscience, we can think about translating basic science to the clinic in months, as opposed to the 15 years it can take for drug development,” says Bonci. Thanks to the new technologies, he says, “we’re close to a treatment”.

Source:   Nature 522, S50–S52(25 June 2015) doi:10.1038/522S50a

A woman who was admitted to rehab three times because of her severe drug addiction has turned her life around by becoming an addiction therapist helping others going through what she did.

Vicky, from Hale, Manchester, reveals that her drug addiction started at a young age; she was smoking weed when she was 11 and took acid and mushrooms by the age of 16.

The 49-year-old, who attended Altrincham Grammar School, comes from a wealthy background and was expected to go into medicine or dentistry.

However, her parents split when she was young and she hasn’t seen her biological father since she was seven years old. The breakdown of the family unit, she explains, led her to feel as though there was a deficit in her life.

As a result, she began to use food, substances and sex to fill the void to help her feel better about herself.

Vicky explains that she’s had obsessive behaviours towards food – often bingeing on a whole box of crisps at once – since a young age.

At the age of 11 she moved to Canada for six months to live with relatives where she started smoking cannabis. By 16 she was aware her drinking habits weren’t ‘normal’. Vicky felt she had no cut off point and regularly had memory loss. She also started taking what she considered to be recreational drugs: cannabis, acid and mushrooms.

When she was 17, she was introduced to amphetamine. Looking back, Vicky says she considers that her recreational drug use was about helping her to feel better about herself.

After college, Vicky flitted between working for her mother’s business and restaurants jobs in Hale, during which time the Cheshire-set friendships and free-flowing champagne encouraged her drinking and drug taking habits.

She admits that she was living for the moment, seeking fun and excitement but her lifestyle choices were slowly ruining the opportunities she had been given. When she was 20, Vicky returned to Canada and dated a cocaine dealer – a time that she describes as her ‘Nirvana’ with cocaine on tap.

When her visa expired, she moved back to the UK and began dating someone who had a similar background of drug misuse. She started using heroin and crack for two years and whilst she was able to hold down a job, she admits she started to function less and less.

She started to steal to pay for drugs, received a drink driving conviction at aged 22 and received multiple cautions for drug possession and related incidents. Vicky believes she was merely given a slap on the wrist due to her background.

Aged 23, Vicky felt very isolated and ended up living back at home at which point her parents became aware there was a problem. They called a psychiatrist for help and Vicky was admitted to rehab for eight weeks in 1988, she returned on two more occasions.

Following Vicky’s third admittance to rehab, the alcohol and drug induced death of a close friend and former boyfriend on her 25th birthday hit Vicky very hard. She reached her lowest point and attempted suicide more than once. However, she began to turn her life around.

She had to sign a contract to agree to secondary care treatment at a female-only facility where she was taught to take personal responsibility for her own happiness.

Vicky, who now lives with the father of her two youngest children that she met in recovery 18 years ago, studied for a Diploma in Counselling at the University of the West of England and a Masters at Bristol University; she has been qualified as a counsellor for 18 years.

She met her partner and father of her two youngest children in recovery 18 years ago. Vicky is dedicated to helping others affected by addiction, and has a particular passion for helping and working with families and the ‘forgotten others’. Helping others through her own business, Victoria Abadi Therapies, has helped Vicky’s own recovery.

She said: ‘I had always thought I was fascinated by substances and drugs, but over the years I’ve come to realise that what really interests me is addiction itself. I knew from as young as 21 that I wanted to be an addiction therapist. A lot has changed since my days in detox and rehab, we know so much more about addiction but there’s still more to learn.

‘My main advice to anyone affected by addiction, whether it’s yourself or someone you care about, is to talk. It might seem obvious but it’s not always easy to reach that stage.

‘Once you reach the point of realisation that addiction is a medical issue not simply a moral choice the path to recovery will come easier. Likewise, for families shedding the shame and stigma by talking about your experience will open up the possibility of helping your loved one through it.

‘There are some great impartial services, such as Port of Call, who can help with pointing you in the right direction and getting you or a loved the help they need. ‘The best thing that comes out recovery is the ability to have close meaningful relationships.’

For help and advice on addiction recovery visit Port of Call, Victoria Abadi Therapies or call 0800 0029010.

Source: http://www.dailymail.co.uk

* Marijuana Use Impairs Verbal Memory

Researchers at the National Institute on Drug Abuse (NIDA) are sounding the alarm over a possible increase in unknown cognitive and behavioral harms that widespread cannabis use may unmask.

A clinical review conducted by NIDA director Nora Volkow, MD, points out that as legalization of the drug for recreational and medical use spreads, vulnerable populations, especially adolescents, are exposed to toxic effects of the drug.

“This is not a problem that is specific to marijuana,” Dr Volkow told Medscape Medical News. “Young brains and drugs shouldn’t mix. Period.” The study was published in the March issue of JAMA Psychiatry.

Powerful Disruptors

Dr Volkow explained that young brains are engaged in a protracted period of “brain programming,” in which everything an adolescent does or is exposed to can affect the final architecture and network connectivity of the brain.

“Drugs are powerful disruptors of brain programming because they can directly interfere with the process of neural pruning and interregional brain connectivity,” she added.

In the short term, she said, this kind of interference can negatively affect academic performance. However, long-term use can impair behavioral adaptability, mental health, and life trajectories.

Currently, four states ― Colorado, Washington, Oregon, and Alaska ― as well as the District of Columbia have legalized cannabis for recreational use among adults. Twenty-three other states, plus the District of Columbia, also regulate cannabis use for medical purposes.

As a result of this rising tide of legalized marijuana, Dr Volkow and colleagues believed a more focused and in-depth study of its use and consequences was urgently needed.

Neuropsychological Decline

“Emerging evidence suggests that adolescents may be particularly vulnerable to the adverse effects of cannabis use,” the investigators write.

Several studies, for example, have shown that individuals who use cannabis at an earlier age have greater neuropsychological impairment and that persistent use of cannabis from adolescence was associated with neuropsychological decline from the age of 13 to 38 years. This was not found to be the case when cannabis was first used in adulthood.

There is also “fairly clear evidence” of structural alterations in a number of areas in the brain associated with exposure to cannabis, although some evidence suggests that concomitant drinking may explain some of the structural alterations attributed solely to cannabis use.

fMRI studies have also pointed to changes in neural activity among cannabis users, including inefficient processing during a working memory task.

Differences in neuropsychological test performance as well as in brain structures and function in cannabis users vs nonusers may well have been there before users took up the drug, the investigators note.

Evidence suggesting alterations in brain structure and function in cannabis users is inconsistent, and both areas evidently require further research.

“There is both preclinical and clinical evidence supporting the view that cannabis use is associated with an ‘amotivational’ state,” said Dr Volkow. The term “cannabis amotivational syndrome” is distinguished by apathy and difficulty with concentration.

She also notes that long-term, heavy cannabis use has been associated with underachievement in terms of educational pursuits.

On the other hand, it is also likely that diminished motivation could impair learning as well, she adds, inasmuch as tetrahydrocannabinol (THC), the active ingredient in cannabis, has been shown to disrupt reward-based learning.

“Amotivation in chronic heavy users may also reflect the fact that cannabis itself has become a major motivator,” Dr Volkow writes, “so other activities (eg, schoolwork) become demoted in the individual’s reward hierarchy.”

What now needs to be established is whether higher concentrations of THC might make the risk of developing amotivation or even addiction more likely, investigators add.

Cannabis and Psychosis

There is also a lingering controversy over whether cannabis can trigger psychiatric disorders, notably, psychotic disorders and schizophrenia.

“It is recognized that cannabis with a high THC can trigger an acute psychotic episode,” Dr Volkow writes.

However, she cautions that the extent to which cannabis can result in schizophrenia is still being debated, although the consensus is that cannabis use in those at risk for schizophrenia can trigger the disease and exacerbate its course.

Particularly at high doses, THC has been known to trigger schizophrenialike positive and negative symptoms.

Studies have also consistently shown an association between the use of cannabis and schizophrenia in cases in which cannabis use precedes psychosis.

“The association between cannabis use and chronic psychosis (including a schizophrenia diagnosis) is stronger in those individuals who have had heavy or frequent cannabis use

during adolescence, earlier use, or use of cannabis with high THC potency,” Dr Volkow and colleagues observe.

“From these studies, ever use of cannabis is estimated to increase the risk of schizophrenia by approximately 2-fold, accounting for 8% to 14% of cases, with frequent use or use of cannabis with high THC potency increasing the risk of schizophrenia 6-fold.”

Dr Volkow cautions that legitimate controversy remains as to how much cannabis use contributes to psychosis and the degree to which cannabis can precipitate psychosis in patients who have no genetic predisposition for the illness.

Key Questions

A number of key questions need to be adequately researched before a clearer picture emerges about the potential harms of cannabis use.

The first is, how much cannabis use is too much? Dr Volkow noted that it is not clear whether the effects of cannabis among heavy users apply equally to those who use cannabis much more casually.

The second is, at what age is cannabis use most harmful?

It is fairly clear that cannabis does have negative effects among adolescent users, the researchers note, but it may also have negative effects in older adults who undergo changes in brain plasticity and age-related cognitive decline, both of which could make them more susceptible to toxic effects of the drug.

“Physicians are in a key position to help prevent cannabis use disorder,” said Dr Volkow. “This will require that they screen adolescents and young adults for cannabis consumption and that they intervene to prevent further use,” she added.

In cases in which the adolescent or young person already suffers from the disorder, physicians need to tailor their intervention on the basis of the severity of the disorder and the presence of comorbidities, such as anxiety or depression.

“Science has shown us that marijuana is not a benign drug. The morbidity and mortality from legal drugs is much greater than that for illegal drugs, not because the drugs are more dangerous but because their legal status makes them more accessible and a larger percentage of the population is exposed to them on a regular basis,” she said.

“The current ‘normalization’ movement presses on with complete disregard for the evidence of marijuana’s negative health consequences, and this bias is likely to erode our prevention efforts by decreasing the perception of harm and increasing use among young people, which is the population most vulnerable to the deleterious effects of regular marijuana use.”

Contributor to Mental Illness

Commenting on the article for Medscape Medical News, Oliver Howes, MD, PhD, Institute of Psychiatry, King’s College London, United Kingdom, said he endorses the NIDA’s position on cannabis use.

“I agree that there are potential issues around the use of cannabis, especially if you start it early, in adolescence,” Dr Howes said.

“Early use seems to be what increases your risk of psychosis in particular, but it also seems to be associated with more marked effects generally, and we’ve certainly seen the effects of long- term, early cannabis use on the brain’s dopamine systems that are linked to effects on motivation, or rather the lack of motivation, that you commonly see in heavy cannabis users,” he added.

Dr Howes also shared the NIDA’s viewpoint that there is much that is not known about the long-term effects of cannabis use, especially heavy cannabis use.

He also noted that “as a physician, I quite commonly see young adults who started using cannabis at the age of 12, 13, and 14 and who have come to see me in early adulthood with mental health problems.

“And yes, I do think early cannabis use contributes to the mental health problems that we see later

Source:   Medscape Medical News  17th March 2016

Most of us who drink alcohol won’t die from liver disease – but it still kills more of us than diabetes and road deaths combined The recent report into life on the liver ward makes sobering reading. John has alcohol-induced dementia (Korsakoff’s syndrome) and doesn’t know where he is. Rita has cirrhosis of the liver and is homeless. Her life has spiralled downwards as a wine habit segued into damaging dependence. It’s easy to feel sorry for the Johns and Ritas, though most of us think it’ll never happen to us. But will it? Are we becoming a nation of drinkers and drunks? The UK death rate from liver disease has increased fourfold in the past 30 years as cheap alcohol has flooded our shores and our gullets. Alcohol-related emergencies resulted in over a quarter of a million admissions in 2013/14, most of whom were 45-64-year-olds, who see themselves as regular rather than binge drinkers. Jackie Ballard, the chief executive of Alcohol Concern, says “Alcohol is linked to over 60 medical conditions including cancer, diabetes and high blood pressure.” And the chief medical officer, Sally Davies is so concerned that she has published new and controversial guidelines on safe drinking. The good news is that the tide seems to be turning against alcohol use in the UK. The percentage of men drinking alcohol in a typical week fell from 72% in 2005 to 64% in 2012 (in women the fall was from 57% to 52%). Frequent drinking has also been reported to be in decline.  Most of us who drink alcohol won’t die of liver disease, just as many smokers don’t die of lung cancer. It’s a question of weighing the risks against the benefit that alcohol gives us. It’s my drug of choice but I wouldn’t pretend that it’s harmless.   The great British booze problem: how a few glasses a day has led to an epidemic for the NHS

How much alcohol is too much? Some can probably safely drink more than others; your size, genetics, lifestyle and state of your liver make a difference. But in general, less than 14 units, spread over at least three days a week should be OK. That’s just under a bottle-and-a-half of wine (ABV 13.5%), or an average of one 175ml glass per day. For beer drinkers, that’s less than five pints of higher strength beer (ABV 5.2%) a week.

The liver is a resilient and vital organ. With the kidneys, it acts as a waste-disposal system, filtering our blood of toxins. The liver plays a key role in digestion and also produces hormones, bile to digest fats and proteins for blood clotting. We have two kidneys, which is handy if one fails, but only one liver. Luckily, it can withstand a tremendous battering and still recover. We can survive on a liver that is only 30% operational; after that it gets critical.

Viruses, drugs, chemicals, toxins and some genetic conditions can take their toll on even the youngest and meatiest of livers. At first, these irritants cause inflammation, which is reversible. But long-standing damage causes cirrhosis, which is irreversible thickening (fibrosis) that stops the liver from functioning. We can’t live without a liver, so a transplant becomes the only option. Liver disease kills more of us than diabetes and road deaths combined and is the fifth-biggest killer now after heart attacks, cancer, strokes and lung diseases. It is the only major cause of death in the UK that is still increasing year on year. The hope is that as awareness rises and alcohol intake falls, the crowded NHS liver wards will become a thing of the past.

Source:  http://www.theguardian.com/society/shortcuts/2016/jan/25

Abstract

Smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, yet indicators of specific vulnerability have proved largely elusive. Genetic variation is one potential risk modifier. Single-nucleotide polymorphisms in the AKT1 and catechol-O-methyltransferase (COMT) genes have been implicated in the interaction between cannabis, psychosis and cognition, but no studies have examined their impact on an individual’s acute response to smoked cannabis. A total 442 healthy young cannabis users were tested while intoxicated with their own cannabis—which was analysed for delta-9-tetrahydrocannbinol (THC) and cannabidiol content—and also ±7 days apart when drug-free. Psychotomimetic symptoms and working memory were assessed on both the sessions. Variation at the rs2494732 locus of the AKT1 gene predicted acute psychotic response to cannabis along with dependence on the drug and baseline schizotypal symptoms. Working memory following cannabis acutely was worse in females, with some suggestion of an impact of COMT polymorphism on working memory when drug-free. These findings are the first to demonstrate that AKT1 mediates the acute response to cannabis in otherwise healthy individuals and implicate the AKT1 pathway as a possible target for prevention and treatment of cannabis psychosis.

Discussion

To our knowledge, this study provides the first evidence that the acute psychotic effects of cannabis are predicted by variation at the rs2494732 locus of the AKT1 genotype. No evidence was found for an interaction of the COMT Val158Met genotypes with cannabis use, in producing psychotomimetic symptoms in this group of healthy cannabis users. Cannabis dependence predicted non-intoxicated schizotypal symptoms, but neither genotype had any impact on these. COMT Val158Met genotype had a marginal impact on performance on a working memory task when non-intoxicated and when memory load was low; however, at higher load, schizotypy was the only emerging predictor of performance. When intoxicated with cannabis, gender was the only predictor of working memory performance, with poorer performance in females at a high working memory load.

In the current study, which is the largest ever to be conducted on the acute response to cannabis, psychotomimetic symptoms while intoxicated were found to be predicted by variation at the rs2494732 locus of the AKT1 genotype in healthy young cannabis smokers, increasing with C allele dosage. These data are very important as acute psychotic response to cannabis is thought to be a marker of the risk of developing psychosis from smoking the drug.1 Two previous studies have implicated this polymorphism in the interaction with cannabis and psychosis,9, 18 but this work concentrated on individuals who were at familial risk of schizophrenia. This study is the first to demonstrate that the acute response to cannabis is modulated by AKT1 in otherwise healthy cannabis smokers. The mechanism for this modulation of acute effects may be through the interaction of AKT1 with dopamine.2, 9Our sensitivity analyses suggested that these effects may be confined to dependent cannabis smokers but further investigation of these data with larger samples is required.

AKT1 codes for a protein that is a serine/threonine kinase, which has a variety of functions, one of which is as a signalling molecule downstream of the dopamine D2 (DRD2) receptor. Decreased AKT1 functionality may result in enhanced responses to DRD2 receptor stimulation.19 THC has been found to acutely induce dopamine release in

rats20, 21 and in humans,22, 23 although not in all studies.24 Dopamine release is thought to occur via the blockade of cannabinoid 1 (CB1) receptors on GABAergic neurons that target pyramidal cells. These neurons normally exert an inhibitory effect on the firing of dopamine neurons that project back to the nucleus accumbens, so agonism of CB1 receptors by THC may produce increased dopamine release. This THC-mediated increase in dopamine release may be further exacerbated by decreased AKT1 functionality. Elevated levels of mesolimbic dopamine are known to have a role in the development of psychotic symptoms, potentially through disrupted salience attribution.25

In contrast to the role of variation at the rs2494732 locus of AKT1, this study found no support for the direct involvement of the functional polymorphism of the COMT gene in mediating acute psychotic response to cannabis. This is in contrast to one previous small-scale acute laboratory study giving acute THC to patients with schizophrenia,26 and other work that suggested that COMT may mediate the psychotomimetic risk of cannabis3 but in agreement with subsequent larger studies that failed to replicate these findings.4, 27 There was a marginal effect of COMT on working memory performance at a low load when not intoxicated. This polymorphism of COMT initially caused some excitement as several studies emerged demonstrating its association with working memory,28, 29 but this finding was not confirmed by meta-analyses,30 which suggested that this may be a case of publication bias.

Greater schizotypal symptoms predicted in poorer working memory performance on the more difficult section of the task among drug-free cannabis users. This echoes recent findings of poorer working memory in individuals high in schizotypy31 and indeed of the relationship between working memory performance and transition to psychosis.32 Working memory impairment is considered a central cognitive impairment in schizophrenia, and there is some evidence that such impairments are related to symptoms, particularly to negative symptoms.33, 34

Only gender predicted acute working memory impairment from cannabis, with greater impairment in females. Very few studies have examined gender differences in neurocognitive acute response to THC, with those that have using very small samples and in finding little evidence of gender differences.35 However, this study examined the acute effects of cannabis in over 400 cannabis smokers. There is an emerging preclinical literature that might explain this effect. CB1 density has been found to vary by gender, with animal studies reporting greater CB1 receptor density among males across several brain regions.36, 37 However, across their lifetime, adult female brains show increases in CB1 receptor density, with levels eventually surpassing those observed in males.38 Furthermore, greater CB1 de-sensitization after exposure to THC in the prefrontal cortex, hippocampus, striatum, amygdala and midbrain is seen in female adolescent rats.36, 37 Preclinical studies have also demonstrated that female rats preferentially metabolize THC to its most highly active metabolite, while male rats metabolize THC to multiple compounds.39 In combination, these findings may in part explain the finding of greater acute working memory impairment from cannabis in females. This also may partly be driven by gender differences in frequency of cannabis use. Users who smoked cannabis less frequently experienced stronger effects, and as there was a higher proportion of low frequency female cannabis users compared to males this may have contributed to the observed gender differences in working memory following the drug.

Strengths of this study include the large sample size for assessing acute cannabis effects. We also used independent verification of the cannabinoid content of the cannabis consumed and drug history. Further, the hypothesis-driven approach we took to genetic analysis was a strength, examining only loci implicated in previous studies and, therefore, circumventing some of the problems of type I error that have dogged earlier research. However, inevitably there are several limitations of the study. For the cannabis use data, while verifying past 3 months use with hair analysis, we inevitably relied on retrospective self-reports of drug use, which are particularly complicated as cannabis is known to acutely impair episodic memory. However, we opted to use years of cannabis use in this model as this was considered the most reliable to estimate. As we purposely recruited a young group of cannabis users, there was restricted variation in years used and future studies may investigate this further. We used a predominantly white Caucasian sample. However, it is unlikely that ethnic differences in allele frequency at rs2494732 biased the outcome of the study, as there was no difference between the frequency of rs2494732 alleles across the dichotomized ethnic groups. In addition, analyses with only Caucasian participants gave the same results to the analysis containing all ethnicities.

In summary, we found that the AKT1 rs2494732 C allele was associated with increased psychotomimetic symptoms after smoking cannabis. The other factor impacting on acute psychotomimetic response to cannabis was baseline schizotypy. Gender was the only factor to predict acute working memory impairment, with poorer performance in females. When drug free, cannabis dependence weakly predicted schizotypal symptoms and COMT genotype had a marginal impact on working memory, along with ethnicity. The findings of this study contribute to a recent and growing body of evidence suggesting that variation at the AKT1 locus confers details of the risk of cannabis smoking for schizophrenia. This is likely to be in the context of numerous other genetic variants, so the clinical utility at the moment is unclear. It is nonetheless encouraging that there is concordance between genetic influences on acute effects of cannabis and those mediating risk of psychosis. However, the fact that AKT1 is relevant to the biology of psychotic symptoms suggests that this might be a promising direction for novel therapeutics for cannabis-induced psychosis.

Source:  Citation: Translational Psychiatry (2016) 6, e738; doi:10.1038/tp.2015.219 Published online 16 February 2016 

For complete paper log on to: http://www.nature.com/tp/journal/v6/n2/full/tp2015219a.html

Nora D. Volkowa,b,1, Gene-Jack Wanga, Frank Telanga, Joanna S. Fowlerc,1, David Alexoffc, Jean Logand, Millard Jaynea, Christopher Wonga, and Dardo Tomasia

Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857; National Institute on Drug Abuse, Rockville, MD  20857; Biosciences Department, Brookhaven National Laboratory, Upton, NY 11973; and Department of Radiology, New York University Langone Medical Center, New York, NY 10016

Contributed by Joanna S. Fowler, June 20, 2014 (sent for review April 9, 2014; reviewed by Bertha Madras, Harvard University Medical School, and Karen Berman, National Institute of Mental Health)

Moves to legalize marijuana highlight the urgency to investigate effects of chronic marijuana in the human brain. Here, we challenged  48 participants (24 controls and 24 marijuana abusers) with methylphenidate (MP), a drug that elevates extracellular dopamine (DA) as a surrogate for probing the reactivity of the brain to DA stimulation. We compared the subjective, cardiovascular, and brain  DA responses (measured with PET and [11Craclopride) to MP between controls and marijuana abusers.

Although baseline (placebo) measures of striatal DA D2 receptor availability did not differ between groups, the marijuana abusers showed markedly blunted responses when challenged with MP. Specifically, compared with controls, marijuana abusers had significantly attenuated behavioural (“self-reports” for high, drug effects, anxiety, and restlessness), cardiovascular (pulse rate and diastolic blood pressure), and brain DA [reduced decreases in distribution volumes (DVs) of [11Craclopride, although normal reductions in striatal nondis placeable binding potential  (BPND)] responses to MP. In ventral striatum (key brain reward region),M P-induced reductions in DVs and BPND (reflecting DA increases) were inversely correlated with scores of negative emotionality, which were significantly higher for marijuana abusers than controls. In marijuana abusers, DA responses in ventral striatum were also inversely correlated with addiction severity and craving.

The attenuated responses to MP, including reduced decreases in striatal DVs, are consistent with decreased brain reactivity to the DA stimulation in marijuana abusers that might contribute to their negative emotionality (increased stress reactivity and irritability) and addictive behaviors.

Despite the high prevalence of marijuana consumption, the effects of marijuana abuse in the human brain are not well understood. Marijuana, like other drugs of abuse, stimulates brain dopamine (DA) signalling in the nucleus accumbens (1, 2), which is a mechanism believed to underlie the rewarding effects of drugs (3–5) and to trigger the neuroadaptations that result in addiction (reviewed in ref. 6). Indeed, in humans, imaging studies have shown that drugs of abuse increase DA release in striatum (including the nucleus accumbens), and these increases have been associated with the subjective experience of reward (7–9).

However, for marijuana, the results have been inconsistent: One study reported striatal DA increases during intoxication (10); two studies showed no effects (11, 12); and one study reported DA increases in individuals with a psychotic disorder and in their relatives, but not in controls (13). Imaging studies of the brain DA system in marijuana abusers have also shown different findings from those reported for other types of substance abusers. Specifically, substance abusers (cocaine, methamphetamine, alcohol, heroin, and nicotine), but not marijuana abusers (14–16), show reduced baseline availability of DA D2 receptors in striatum (reviewed ref. 6). Similarly, cocaine abusers (17, 18) and alcoholics (19, 20),but not marijuana abusers (16), show attenuated DA increases instriatum when challenged with a stimulant drug, although marijuana abusers with comorbid schizophrenia or risk for schizophrenia showed blunted DA increases to stimulants (21) and to stress (22). However, prior studies are limited by their small sample sizes (ranging from six to 16 subjects). Also, prior studies did not control for the potential confounds that the changes in cerebral vascular resistance associated with marijuana abuse (23– 25) could have on the delivery of the radiotracer to the brain when using a stimulant drug as pharmacological challenge, because stimulants decrease cerebral blood flow (26). Thus, the extent to which there are changes in brain DA signalling in marijuana abusers is still unclear. Here, we compared brain DA reactivity in healthy controls and marijuana abusers on a larger sample than that in prior studies and measured arterial concentration of non metabolized radiotracer to control for differences in radiotracer delivery to brain. We used PET and [11Craclopride (radioligand that binds to D2/D3 receptors not occupied by DA) to assess the effects of methylphenidate (MP) on the nondisplaceable binding potential [BPND; ratio of the distribution volume (DV) in striatum to that in cerebellum], which is the most frequent model parameter used to estimate DA changes (27), in 24 healthy controls and 24 marijuana abusers.We also quantified the DV,  which corresponds to the equilibrium measurement of the ratio of the concentration of the radiotracer in tissue to that in  arterial plasma, to control for potential changes in radiotracer delivery that could confound group comparisons of stimulant-induced changes in BPND. We used MP, which is a stimulant drug that blocks DA transporters, because it induces robust and reproducible DA increases in the human brain (28, 29). We predicted that MP’s behavioral effects in marijuana abusers would be attenuated, consistent with preclinical findings (30), and that decreased DA reactivity in ventral striatum would be associated with higher scores in negative emotionality (neuroticism), which mediates genetic risk for marijuana dependence (31), and with addiction severity.

Results

Participant Characteristics.

Tobacco smoking was more prevalent in marijuana abusers than controls; otherwise, there were no differences in demographics between groups (Table 1). However, the groups differed significantly in personality measures; marijuana abusers had significantly lower scores in positive emotionality (P = 0.05) and higher scores in negative emotionality (P = 0.002) than controls (Table 1).

Correlation analysis between scores in negative emotionality and history of marijuana abuse showed a negative correlation between age of I  the scores. The correlations with reported daily doses of marijuana and negative emotionality were not correlations with positive emotionality and history of marijuana abuse were not significant.

Plasma Concentrations of MP and Behavioral and Cardiovascular Effects. 

MP concentrations in plasma (nanograms per milliliter) did not differ between groups at 10 min (controls, 195 ± 51; abusers, 194 ± 45), 25 min (controls, 125 ± 24; abusers, 121 ± 19), or 40 min (controls, 102 ± 25; abusers, 94 ± 15). MP had significant behavioral effects, and these effects were attenuated in marijuana abusers compared with controls (Fig. 1A). Specifically, MP significantly increased scores on self-reports (averaged measures), and the effects differed between groups, with controls reporting a more robust “high” (drug effect: F = 92, P = 0.0001; interaction: F = 6.2, P = 0.02), “restlessness” (F = 35, P = 0.0001; interaction: F = 5.8, P = 0.02), “anxiety” (F = 7, P = 0.01; interaction: F = 5.8, P = 0.02), and “drug effects” (F = 100, P = 0.0001; interaction F = 4, P = 0.05) than marijuana abusers.

Also, comparisons of “peak” behavioral effects to MP were significantly stronger for controls for high (P = 0.01), restlessness (P = 0.003), anxiety (P=0.03),and drug effects

(P=0.02), than for the marijuana abusers. The potency of MP was also reported to be stronger by the controls than by the marijuana abusers (8.3 ± 2 vs. 5.8 ± 3; t = 3.4, P = 0.002). In marijuana abusers, MP increased self-reports of marijuana craving (Placebo: 4.0 ± 3–MP: 6.3 ± 3; P = 0.006) and tobacco craving (Placebo: 2.4 ± 2–MP: 3.8 ± 4; P = 0.05).

PLUS

MP increased heart rate

(F = 98, P = 0.0001) and systolic (F = 153, P = 0.0001) and diastolic (F = 65, P = 0.0001) blood pressure in both groups, and MP’s effects differed between groups for heart rate (interaction effect; F = 4.6, P = 0.04) and diastolic blood pressure (interaction effect: F = 4.0, P = 0.05), but not for systolic blood pressure (Fig. 1B). Post hoc t tests revealed that MP-induced increases in heart rate and diastolic pressure were significantly stronger (P < 0.05) in controls than in marijuana abusers.

Effects of MP on the DVs of [11Craclopride.

The SPM analysis showed no group differences in baseline measures of DV. It also showed that MP significantly decreased DV in brain and that the effects were significantly larger in controls than in marijuana abusers (Fig. 2). Individual plotting of MP-induced changes in DV showed that MP-induced changes in cerebellum were decreased in controls but not in marijuana abusers and that there were larger decreases of MP-induced changes in striatum in controls than in marijuana abusers (Fig. 2). The ROI analysis corroborated that MP decreased the DV in cerebellum and striatum and that the effects were larger for controls than abusers.

For cerebellum, the drug (F = 15, P = 0.0004) and drug × group interaction (F = 8.2, P = 0.007) were significant; post hoc t tests showed larger decreases in controls (13 ± 11%) than abusers (1.4 ± 16%) (P = 0.01). For caudate, the drug (F = 41, P = 0.0001) and interaction (F = 4.8, P = 0.04) were significant; post hoc t tests revealed larger decreases in controls (22 ± 18%) than abusers (9 ± 22%) (P = 0.05).

For putamen, drug (F = 93, P = 0.0001) and interaction (F = 6.9, P = 0.02) were significant; post hoc t tests showed larger decreases in controls (30 ± 16) than abusers (16 ± 21%) (P = 0.02). For ventral striatum, drug (F = 56, P = 0.0001) and interaction (F = 7.3, P = 0.01) were significant; post hoc t tests showed greater decreases in controls (25 ± 18%) than abusers (11 ± 25%) (P = 0.02). A group (controls vs. abusers) by region (delta DV in caudate, putamen, ventral striatum, and cerebellum) comparison revealed that group differences differed between regions (F = 3.5, P = 0.02); post hoc analysis showed that group differences in cerebellum were larger than in putamen (P = 0.02) and ventral striatum (P = 0.02), and showed a trend in caudate (P = 0.07).

This finding is significant; it confounds group comparisons of BPND because the latter measure is normalized to the DV in cerebellum. Note that attenuated decreases in cerebellar DV with MP in the marijuana abusers could result in an overestimation of their DA increases, reflecting an apparent lower striatal-DV/cerebellar-DV ratio (BPND) with MP (see below).

Correlations Between MP-Induced Changes in DV and Clinical Measures.

Correlation analysis revealed that MP-induced decreases in DV in ventral striatum were negatively associated with scores in negative emotionality (r = 0.51, P = 0004), and weaker correlations were observed in putamen (r = 0.37, P = 0.02) and caudate

(r = 0.35, P = 0.02) such that the larger the DV decreases, the lower were the scores of negative emotionality. Correlation with positive emotionality and constraint were not significant. MP-induced craving for marijuana in the marijuana abusers was negatively associated with DV decreases in putamen (r = 0.46, P = 0.03) and ventral striatum (r = 0.51, P = 0.01) such that participants with the smallest decreases had the most intense craving.

Baseline Measures of D2/D3 Receptor Availability (BPND).

For the baseline (placebo) measures, the SPM analysis revealed no group differences in BPND (D2/D3 receptor availability). When we decreased the threshold of significance to uncorrected P < 0.05, SPM showed lower values in marijuana abusers than in controls in ventral striatum (0, −2, −8; statistical t values = 2.59, P uncorrected = 0.007). The ROI analysis also showed a nonsignificant trend toward lower baseline BPND in marijuana abusers than in controls in ventral striatum (controls, 3.20 ± 0.3; abusers, 2.97 ± 0.59; P = 0.11) and no differences in caudate (controls, 2.80 ± 0.36; abusers 2.76 ± 0.57) or putamen (controls, 3.42 ± 0.41; abusers, 3.35 ± 0.57).

Effects of MP on BPND. 

The SPM analysis revealed significant decreases in BPND with MP compared with placebo (interpreted as reflecting DA increases) in striatum in both controls and marijuana abusers (Fig. 3 and Table 2). The SPM analysis revealed no group differences in MP-induced decreases in BPND in striatum but unexpectedly revealed larger BPND decreases in marijuana abusers than in controls in midbrain (region centered in susbtantia nigra that also encompassed sub thalamic nucleus; center of cluster left: 12, −14, −10, and 132 voxels, t = 3.1; center of cluster right: 14, −18, −8, and 27 voxels; t = 2.9; PFWE < 0.05; SVC = 10 voxels) (Fig. 3 and Table 2). The ROI analysis corroborated a significant group × drug interaction in midbrain (F = 14, P = 0.0006), and post hoc t test analyses showed that whereas in marijuana abusers, MP decreased BPND in midbrain (−3.5 ± 8%; F = 5.4, P = 0.03), MP increased BPND in controls (4 ± 6%; F = 9.2, P = 0.006).

Correlations Between MP-Induced Changes on BPND and Clinical Measures.

Voxel-wise correlation analysis revealed that MP-induced decreases in BPND in ventral striatum were inversely associated with scores in negative emotionality (Fig. 3 B and C) such that the larger the BPND decreases, the lower the scores. The striatal correlations with positive emotionality and constraint were not significant. Because the SPM revealed a significant group difference in MP-induced changes in midbrain BPND, we also performed correlations with this brain region and showed a significant correlation with positive emotionality (r = 0.42, P = 0.003) such that the greater the BPND decreases, the lower the scores. In the marijuana abusers, MP-induced decreases in BPND in midbrain were correlated with increases in marijuana (r = 0.40, P = 0.05) and tobacco (r = 0.45, P = 0.03) craving, as well as with the dependency scores (r = 0.43, P = 0.04), such that the greater the decreases in BPND, the higher was the craving triggered by MP and the higher were the dependency scores.

Discussion

Here, we show that marijuana abusers had attenuated behavioural and cardiovascular responses and blunted reductions in striatal DV (although normal reductions in BPND) when challenged with MP compared with controls, which is consistent with decreased brain reactivity to DA stimulation. We also corroborate prior findings (14–16) of no significant differences in baseline striatal D2/D3 receptor availability between controls and marijuana abusers and provide preliminary evidence of abnormal midbrain

DA reactivity in marijuana abusers. DA D2/D3 Receptor Availability in Striatum.

Only four brain imaging studies (totalling 42 marijuana abusers) have measured DA D2/ D3 receptors (14–16, 42). These studies showed no differences in striatal D2/D3 receptors between marijuana abusers and controls, but their generalizability is limited by the small sample sizes (samples ranged from n = 6 to n = 16). Thus, our results showing no differences in D2/D3 receptor availability (except for a trend in ventral striatum), using a larger sample (24 marijuana abusers) than that used for studies that identified reductions in striatal D2/D3 receptors in alcoholics and cocaine abusers, indicate that marijuana abusers, different from other drug abusers, do not show significant striatal D2/D3 receptor reductions. This difference could reflect marijuana’s agonist properties at cannabinoid 1 (CB1) receptors, which heteromerize with D2 receptors, antagonizing their effects (43). Both CB1 and D2 receptors couple to Gi-o proteins and inhibit adenylyl-cyclase, whereas their co-stimulation results in Gs protein-dependent activation of adenylylcyclase (44, 45).

Moreover, CB1 receptor agonists and antagonists counteract and potentiate, respectively, D2 receptor agonist effects (46–49), although D2 and CB1 receptor interactions might differ between rodents and primates (50, 51). It is therefore possible that in marijuana abusers, chronic CB1 receptor stimulation prevented the striatal D2/D3 receptor down-regulation observed < 0.005) and group comparisons for the effects of MP (ΔBPND) (P < 0.01, cluster size of 10 voxels). The contrast MA > HC indicates that MP induced with repeated drug use (reviewed in ref. 6). However, it should be noted that the marijuana abusers studied in the present and prior studies have been at least 10 y younger than the cocaine abusers and alcoholics studied by prior PET studies, which is relevant because striatal D2/D3 receptors decrease with age (52), and it is hypothesized that drugs accelerate the effects of brain aging (53). Thus, studies in older marijuana abusers are needed to clarify this.

MP-Induced Changes in DV.

In controls but not in marijuana abusers, MP reduced cerebellar DV. To ensure that the DV responses in the controls were consistent with prior findings, we performed a secondary analysis on the effects of MP on the cerebellar DV in an independent cohort of controls, which showed a 12% reduction, and in a sample of adults with attention deficit hyperactivity disorder (ADHD), which also showed an 11% reduction (for controls of the current cohort, the cerebellar DV decrease was 13 ± 11%). The mechanism underlying the lack of an effect of MP in cerebellar DV in abusers is unclear but could reflect the effects of chronic marijuana on cerebrovascular reactivity (increased cerebral vascular resistance) (23–25), which might have prevented MP-induced vasoconstriction and associated reductions in radiotracer delivery to the brain.

The attenuated decreases in DV with MP in the marijuana abusers were observed throughout the brain but were most accentuated in cerebellum. The higher sensitivity of the cerebellum to what we interpret to reflect changes in vascular reactivity with marijuana abuse is consistent with clinical findings that report strokes associated with marijuana abuse are more frequently localized in the posterior circulation and ischemia is most frequently observed in cerebellum (25, 54–56). Cerebellar arteries express CB1 receptors in the smooth muscle layer (57), but because comparisons with arteries in other brain regions have not been done, it is not possible to determine if higher levels of CB1 receptors in cerebellar arteries underlie their higher sensitivity to vascular effects from marijuana.

However, CB1 receptors in cerebellum are also expressed in neurons and glia (58), and the cerebellum is a region that is affected in marijuana abusers (59–61); thus, we cannot rule out the possibility that other factors contribute to the lack of an effect of MP on the cerebellar DV in the marijuana abusers. MP also decreased the DV in striatum to a greater extent in controls than in abusers (Fig. 2). In ventral striatum, these decreases were associated with negative emotionality and with marijuana craving such that the lower the response, the higher the negative emotionality and the craving. This would suggest that these attenuated responses might reflect reduced striatal DA reactivity in marijuana abusers compared with controls even though there were no group differences in MP-induced decreases in BPND (see below). This is consistent with findings from an imaging study with [18F]-dopa that reported lower than normal DA synthesis capacity in the striatum of marijuana abusers (62).

MP-Induced Changes in BPND.

We showed no group differences in MP-induced changes in BPND in striatum, which is the standard measure for assessing DA changes. Similarly, a prior study reported no differences in amphetamine-induced decreases in BPND between marijuana abusers and controls (16). However, the significant group differences in MP’s effects on the DV in cerebellum confound the findings because BPND uses the cerebellum as a reference region to normalize for nonspecific binding. Because the DV in cerebellum was not decreased by MP in marijuana abusers but was decreased in controls, this would result in an overestimation of the decrease in BPND with MP (cerebellar denominator would have a relatively larger value) and an overestimation of DA increases in marijuana abusers compared with controls.

Interestingly, an imaging study comparing DA increases using BPND and 4-propyl-9-hydroxynaphthoxazine ([11C]PHNO)

(radiotracer with >20-fold higher affinity for D3 over D2 receptors, and presumably more sensitive to competition with endogenous DA) (63, 64) in response to a stressor in individuals at high risk for schizophrenia showed that those who abused marijuana had a blunted response, consistent with decreased DA signalling (22). Because the study used cognitive stress as a challenge, it was not confounded by potential group differences in stimulant-induced changes in cerebellar radiotracer delivery.  Unexpectedly, SPM revealed that MP decreased BPND in midbrain (centered in substantia nigra) in marijuana abusers but not in controls. Although the mechanism(s) underlying this group difference is unclear, we speculate that because the midbrain has a high concentration of D3 receptors (65), which are more sensitive to endogenous DA than D2 receptors (66), it could reflect up-regulation of D3 receptors in marijuana abusers.

Indeed, in rodents, chronic Δ (9)-tetrahydrocannabinol (THC; the main psychoactive ingredient of marijuana) increased D3 receptors in midbrain (30). In the marijuana abusers, an MP-induced decrease in midbrain BPND correlated with craving and with dependency scores. A similar finding was reported in methamphetamine abusers, in whom up-regulation of D3 receptors in midbrain (assessed with [11C]PHNO) correlated with amphetamine-induced craving (30, 67). This, along with preclinical studies showing that D3 receptor antagonists interfere with drug seeking and cue- and receptor signalling in midbrain might contribute to drug craving and to decreased sensitivity to reward in marijuana abusers (see below).

However, because the midbrain finding was unexpected, we report it as a preliminary finding in need of replication.

Blunted Behavioral and Cardiovascular Responses to MP in Marijuana Abusers.

Behavioral and cardiovascular effects of MP have been associated with MP-induced DA increases in striatum (9, 69), so the blunted responses in the marijuana abusers are also consistent with decreased striatal reactivity to DA signaling. Although, to our  knowledge, this is the first clinical report of an attenuation of the effects of MP in marijuana abusers, a preclinical study had reported that rats treated chronically with THC exhibited attenuated locomotor responses to amphetamine (2.5 mg/kg

administered i.p.) (30). Such blunted responses to MP could reflect neuroadaptations from repeated marijuana abuse, such as downregulation of DA transporters (70). The attenuation of MP’s effects could also reflect abnormal D2 receptor function, as was previously suggested to explain findings in marijuana-abusing schizophrenic patients, who, despite displaying low DA release, showed increases in psychotic symptoms when challenged with amphetamine (21). Finally, it is also possible that the attenuated responses reflect blunting of MP’s noradrenergic effects because MP blocks both DA and norepinephrine transporters. Our findings of blunted responses to MP in marijuana abusers have clinical implications because they suggest that individuals with ADHD who abuse marijuana might be less responsive to the therapeutic benefits derived from stimulant medications.

Reduced Positive Emotionality and Increased Negative Emotionality in Marijuana Abusers.

Marijuana abusers showed lower scores on positive emotionality and higher scores on negative emotionality than controls, consistent, on the one hand, with lower reward sensitivity and motivation and, on the other hand, with increased stress reactivity and irritability. These characteristics overlap with the amotivational syndrome (71) and with the enhanced sensitivity to stress associated with marijuana abuse and other addictions (72, 73). Positive emotionality was inversely associated with MP induced increases in midbrain DA, which could reflect the fact that in midbrain, D2 and D3 are autoreceptors; therefore, their stimulation would result in decreased DA release in striatum (including accumbens) (74), leading to decreased sensitivity to reward and amotivation (75). In contrast, MP-induced DA increases in ventral striatum were negatively associated with scores on negative emotionality, which is consistent with the protective role of DA signalling in negative emotions (76). The association between negative emotionality and age of initiation of marijuana abuse is consistent with prior findings of worse outcomes with earlier initiation of marijuana abuse (77).

Study Limitations.

The main limitation of this study was the inadequacy of BPND for comparing the DA increases between controls and marijuana abusers due to the group differences on  the effects of MP on cerebellar DV. Also, [11Craclopride cannot distinguish between D2 and D3 receptors, so studies with D3 receptor ligands are needed to determine if the increased midbrain DA response in marijuana abusers reflects D3 receptor upregulation. The relatively poor spatial resolution of PET limits accuracy in the quantification of small brain regions, such as midbrain. Our study cannot ascertain if group differences reflect chronic use of marijuana rather than premorbid differences, and whether marijuana abusers will recover with detoxification. Although attenuation of the effects of MP could reflect interference from CB1 receptor stimulation by marijuana, this is unlikely because marijuana abusers reported that their last use of marijuana was 1–7 d before the study when cannabinoids in plasma are still detectable but at concentrations unlikely to have pharmacological effects (78). However, future studies done after longer periods of withdrawal are needed to control for potential confounds from THC and its metabolites in plasma and to determine if the blunted responses recover.

We did not obtain MRI scans on the participants. However, this is unlikely to have affected the results because measures of [11Craclopride binding are equivalent when using a region extracted from an MRI scan or from the [11Craclopride scan

(79), and there is no evidence that marijuana abusers have striatal or cerebellar atrophy (reviewed in ref. 80). Finally, the groups differed in smoking status, but this is unlikely to account for the group differences because CO levels were used as a covariate in the analysis and there were no differences in the effects of MP between marijuana abusers who smoked cigarettes and those who did not.

Conclusions

The significantly attenuated behavioral and striatal DV response to MP in marijuana abusers compared with controls, indicates reduced brain reactivity to DA stimulation that in the ventral striatum might contribute to negative emotionality and drug craving.

Source:  http://www.pnas.org/content/111/30/E3149

Study Highlights:

* Secondhand marijuana smoke may have similar cardiovascular effects as tobacco smoke.

* Lab rats exposed to secondhand marijuana smoke had a 70 percent drop in blood vessel function.

*  Breathing secondhand marijuana smoke could damage your heart and blood vessels as much as secondhand cigarette smoke, according to preliminary research presented at the American Heart Association’s Scientific Sessions 2014.  In the study, blood vessel function in lab rats dropped 70 percent after 30 minutes of exposure to secondhand marijuana smoke. Even when the marijuana contained no tetrahydrocannabinol (THC) — a compound in marijuana that produces intoxication — blood vessel function was still impaired.  Reduced blood vessel function may raise the chances of developing atherosclerosis and could lead to a heart attack. Atherosclerosis is the disease process that causes plaque build-up in the arteries which narrows them and restricts blood flow.  “Most people know secondhand cigarette smoke is bad for you, but many don’t realize that secondhand marijuana smoke may also be harmful,” said Matthew Springer, Ph.D., senior author of the study and cardiovascular researcher and associate professor of Medicine at the University of California, San Francisco’s Cardiology Division.  Marijuana and tobacco smoke are chemically and physically alike, aside from their active ingredients.  The drop in blood vessel function from THC-free marijuana suggests that the compound isn’t responsible for the effect. Similarly, this study confirms that nicotine is not required for smoke to interfere with blood vessel function.  In the study, researchers used a modified cigarette smoking machine to expose rats to marijuana smoke. A high-resolution ultrasound machine measured how well the main leg artery functioned. Researchers recorded blood vessel dilation before smoke exposure and 10 minutes and 40 minutes after smoke exposure.  They also conducted separate tests with THC-free marijuana and plain air. There was no difference in blood vessel function when the rats were exposed to plain air.  In previous tobacco studies, blood vessel function tended to go back to normal within 30 minutes of exposure. However, in the marijuana study, blood vessel function didn’t return to normal when measured 40 minutes after exposure.  Now that marijuana is becoming increasingly legalized in the United States, its effect on others is a growing public health concern, Springer said.  “If you’re hanging out in a room where people are smoking a lot of marijuana, you may be harming your blood vessels,” he said. “There’s no reason to think marijuana smoke is better than tobacco smoke. Avoid them both.”  Secondhand tobacco smoke causes about 34,000 premature deaths from heart disease each year in the United States among non-smokers according to the U.S. Surgeon General’s 2014 report on the consequences of smoking.  More research is needed to determine if secondhand marijuana smoke has other

similar effects to secondhand cigarette smoke in humans.  The National Institute on Drug Abuse and the Elfenworks Foundation funded the study.  Here is the abstract:

* Brief Exposure to Marijuana Secondhand Smoke Impairs Vascular Endothelial Function

Xiaoyin Wang, Ronak Derakhshandeh, Shilpa Narayan, Emmy Luu, Stephenie Le, Olivia M. Danforth, Hilda J. Rodriguez, Richard E. Sievers, Suzaynn F. Schick, Stanton A. Glantz, Matthew L. Springer, Univ of California, San Francisco, San Francisco, CA Objectives: Despite general public awareness that tobacco secondhand smoke (SHS) is harmful, much of the public still regards marijuana SHS as benign. Because marijuana smoke and tobacco smoke are chemically and physically similar (other than nicotine and tetrahydrocannabinol (THC)), we tested this assumption by asking whether short exposure to marijuana SHS causes acute vascular endothelial dysfunction similar to that caused by tobacco SHS. Exposure to tobacco SHS impairs arterial flow-mediated dilation (FMD) in humans and rats.

Methods: We used a rat model to test the effects of secondhand marijuana smoke on FMD. We exposed anesthetized rats to marijuana SHS using a modified cigarette smoking machine, and measured FMD three times: before 30-min exposure (“pre”), 10 min after end of exposure (“post10”), and 40 min after end of exposure (“post40”). FMD was measured by micro-ultrasound measurements of femoral artery diameter before and after transient (5 min) surgical ligation of the common iliac artery. Concentrations of respirable suspended particles <2.5 μm (RSP) fell during exposure; exposure conditions are denoted by starting concentrations.

Results: Marijuana SHS starting at 667±62 μg/m3 RSP (n=8) caused FMD to fall from 7.5±0.94% (SEM) pre to 2.3±0.50% at post10 and 2.2±0.80 at post40 (P<0.01 for both post10 and post40 vs. pre, adjusted for multiple comparisons). SHS from placebo marijuana lacking THC starting at 671±49 μg/m3 RSP (n=7) similarly impaired FMD (9.9±1.4% pre, 4.3±0.64% post10 (p<0.01), 5.5±1.3% post40 (P<0.05)), confirming that impairment did not depend on the THC. In contrast, air in the exposure chamber (1.8±0.7 μg/m3RSP; n=8) did not alter FMD (11.0±0.64% pre, 11.4±0.72% post10, 11.7±0.86% post40, P>0.70).

Conclusions: Marijuana and tobacco SHS impair endothelial function similarly under comparable exposure conditions. Public exposure to SHS should be avoided whether the source is tobacco or marijuana.

Source:  https://tobacco.ucsf.edu/secondhand-marijuana-smoke-may-damage-blood-vessels-much-tobacco-smoke  2014-11-16

In the winter issue of National Affairs, Jon Caulkins seeks to answer the question, “is marijuana dangerous?” While acknowledging some of the known harms of the drug, he ultimately undersells marijuana’s health risks, calling them “minor.” He characterizes the drug as a “performance degrader” and “more dangerously, a temptation commodity with habituating tendencies.”

Caulkins’ evidence regarding respective drug dangers, such as comparison to alcohol, turns on damage to organs (excluding, notably, the brain) and lethality. One wishes that he was more familiar with the 1974 testimony before a Senate Committee that also examined alcohol and marijuana in comparative fashion:

Brain activities in relationship to [alcohol and marijuana] are drastically different. Alcohol does not … directly and profoundly affect brain function as the cannabis preparations do…. You can use alcohol for a long period of time without producing any sort of persistent damage. But with marihuana … it seems as though you have to use it only for a relatively short time … before (it) produces distinctive and irreversible changes in the brain.

Since the time of that over-forty-year-old testimony, the evidence for marijuana’s brain-altering damage has only grown, as has the average potency, dramatically, something Caulkins’ analysis critically leaves out. There are also changes to the “habituating tendency” of the developmentally-adolescent to use the drug on a daily basis.

The drug is increasingly ingested in additional forms beyond smoked leaves (Caulkins notices the pulmonary consequences of smoking). Today, youth are consuming edibles with high doses of THC (the intoxicating and damaging component), and drinks, and “vaped” combustible concentrates, while at the same time often combining the drug with continued use of alcohol.

The impact of increased potency is still unknown, but will not be inconsequential. Forms of the drug now contain 70-80 percent THC, in contrast to the more familiar THC potencies found in smoked leaves of earlier years, which only rarely exceeded 5-10 percent.

Two things immediately follow from these chemical facts. First, most longitudinal studies of the risks of marijuana for producing cognitive effects and chemical dependency tracked youth using low-potency marijuana. The future for today’s adolescents is simply an unknown, but all signs indicate that the damage will escalate.

Second, the realization of potency renders somewhat irrelevant one of Caulkins’ key policy points, which follows his careful calculation of the volumes of the drug being consumed by users with different use profiles. Because Caulkins analyzes only the amount of (largely) self-reported leaf consumption by either slight or heavy users, he misses the critical variable, which is the amount of THC actually being consumed. As potency has escalated and is not factored in to his equations, his calculations are not as meaningful as he supposes.

A single candy bar purchased today in Colorado, for instance, can contain ten times the amount of THC as a single, premium quality marijuana “joint” of recent years. Psychotic episodes related to the consumption of these edibles are escalating in both emergency room episode reports as well as mortality toxicology reports. Caulkins needs to re-do his analysis with this factor considered.

There is also the matter of his reliance on the National Household Survey on Drug Use and Health (NSDUH) as input for his analysis. The survey, consisting of self-reports of use, also depends upon self-reports of problems in relation to DSM-established criteria for dependency. But these self-reports depend upon (no matter whether they are understated or not) a person’s sense of their behavior as it is affected by the drug.

The problem lies here: a drug that can be shown to alter brain structure and function (albeit in subtle ways, in some instances, and the permanency of such changes is today largely unknown) does not necessarily produce an impact that rises to the level of self-apprehension. That is, the user likely has a blind-spot about the actual impact, which can occur without noticeable manifestations for the person or his friends, until the impact becomes pronounced.

Rather than behavior alone, we should attend to, in addition to clinical judgments, the results of brain analysis, such as MRI analyses, of brain changes. Such a literature exists, and it is not comforting. Even casual use, a profile that Caulkins is inclined to treat as non-threatening in his policy recommendations, has been linked to “neural noise” as well as structural brain changes, even at relatively low exposure – that is, “youthful recreational use” or even “half-a-joint.”

Caulkins also appeals to relatively standard policy postures adopted by libertarians who count on market forces to shape drug behavior futures. It remains an open question whether such market forces are appropriate regulators for adolescents who are, says the medical literature, doing major but unwitting damage to themselves. And under legalization youth exposure increases considerably.

But more importantly, it’s hard to reconcile the pure public health impact of expanding drug use by adults (or semi-adults) with the recent literature showing detrimental effects of maternal use on offspring, including (in animal studies) permanent impairment of the brains of embryos exposed through maternal use. Recent findings are troubling, and call into question the conventional wisdom that drug use “harms only the user him/her self.” Should not drug policy concern itself with these effects?

There is also the question of Caulkins’ use of the literature regarding the ratios of users to those who become dependent users for various forms of drug use, including alcohol, as a means of evaluating respective dangers. The research has been interpreted to rank-order relative dangers from drugs and alcohol by calculating the respective number of users who become dependent users, seeing the outcomes as a reflection of the drug’s impact. Somewhat carelessly, this literature is cited to argue that marijuana is actually “less dangerous” than other drugs, particularly alcohol and tobacco. The most common citation is to research (Antony, 1994) that found roughly one in nine marijuana users become dependent. Caulkins wisely notes that the ratio is likely higher than that (in fact, NIDA has indicated that for daily users, the ratio is about one-in-two). Very likely the potency issue will render those early ratio assumptions to be even farther off than we today experience.

But more importantly, Caulkins misses the clear policy caveats contained in the original research, which, when grasped, weaken his main theme—that we can accommodate by a new legal “architecture” some “permissible” level of non-dependent use and only suffer public health consequences consistent with what the past literature suggests.

What the Antony research actually demonstrates is that we have fixed on the wrong interpretation of the study’s findings. One cannot conclude from Antony’s ratios anything reliable about the respective “dangers” of the substances themselves, taken in isolation, as potentially dependency-producing drugs. Nor does the original research make that claim. In fact, the researchers are well aware of the potential limitations of these results, and explicitly discuss the complexities they present.

As they write:

The array of interrelated factors includes relative drug availability, and opportunities for use of different drugs as well as their costs; patterns and frequencies of drug use that differ across drugs; different profiles of vulnerabilities of individuals … as well as both formal and informal social controls and sanctions against drug use or in its favor…. Considered all together … the transition from drug use to drug dependence runs a span from the microscopic (e.g. the dopamine receptor) through the macroscopic (e.g. social norms for or against drug use; international drug control policies).

When this position is understood, we see that, if anything, it is an argument cutting against the policy of marijuana legalization under any liberalized architecture. Both tobacco and alcohol are legal substances, and have use rates multiple times in excess of (illicit) marijuana. Moreover, they are used in patterns that make exposure to them considerably in excess of exposure to marijuana. Those who smoke tobacco do so multiple times a day, commonly every day; in relative fashion the same holds true for alcohol use.

And this research specifically notes that it is just such patterns of access, frequency, and persistence of use that contribute to the overall dependency-producing potential, in conjunction with the biology of the substance itself in relation to the brain. Simply put, were marijuana to be legal, and subject to access and use patterns comparable to alcohol or tobacco on a daily basis, the impact on subjects as found in dependency and addiction rates, while unknown, would likely be staggering.

And then, to make the final observation, Caulkins envisions possible legal architectures for dispensing the drug, without any consideration of this overwhelming fact: wherever we today find commercial, legal marijuana, there we also find, robust and thriving, the very criminal and violent and corrupting black market. The danger is great and it is getting worse rapidly.

Source:  David Murray replies to article in National Affairs.  Quoted in email from Drugwatch International  January 2016

A study of mice found that the drug can trigger out-of-control “autophagy”, a process by which cells digest themselves.

When it is properly regulated, autophagy provides a valuable clean-up service – getting rid of unwanted debris that is dissolved away by enzymes within cell “pockets”.

Dr Prasun Guha, from Johns Hopkins University School of Medicine in the US, who led the research published in the journal Proceedings of the National Academy of Sciences, said: “A cell is like a household that is constantly generating trash. Autophagy is the housekeeper that takes out the trash – it’s usually a good thing. But cocaine makes the housekeeper throw away really important things, like mitochondria, which produce energy for the cell.”

The scientists carried out post mortems that showed clear signs of autophagy-induced cell death in the brains of mice given high doses of cocaine. They also found evidence of autophagy in the brain cells of mice whose mothers received the drug while pregnant.

The scientists showed that an experimental drug called CGP3466B was able to protect mouse nerve cells from cocaine death due to autophagy. Since the drug has already been tested in clinical trials to treat Parkinson’s and motor neurone disease, it is known to be safe in humans. But much more research is needed to find out whether the drug can prevent the harmful effects of cocaine in people, said the team.

Co-author Dr Maged Harraz said: “Since cocaine works exclusively to modulate autophagy versus other cell death programs, there’s a better chance that we can develop new targeted therapeutics to suppress its toxicity.”

Source:     http://www.theguardian.com/science/2016/jan/18/high-cocaine-doses-can-cause-brain-to-eat-itself 

Examining Linkages with Criminal Behavior and Psychopathic Features into the Mid-30s

Abstract

Objectives: Examine whether young men who chronically use marijuana are at risk for engaging in drug-related and non-drug-related criminal offending and exhibiting psychopathic personality features in their mid-30s.

Methods: Patterns of marijuana use were delineated in a sample of predominately Black and White young men from adolescence to the mid-20s using latent class growth curve analysis. Self-report and official records of criminal offending and psychopathic personality features were assessed in the mid-30s. Analyses controlled for multiple factors indicative of a pre-existing antisocial lifestyle and co-occurring use of other substances and tested for moderation by race.

Results: Four latent marijuana trajectory groups were identified: chronic high, adolescence-limited, late increasing, and low/nonusers. Relative to low/nonusers, chronic high and late increasing marijuana users exhibited more adult psychopathic features and were more likely to engage in drug-related offending during their mid-30s. Adolescence-limited users were similar to low/nonusers in terms of psychopathic features but were more likely to be arrested for drug-related crimes. No trajectory group differences were found for violence or theft, and the group differences were not moderated by race.

Conclusions: Young men who engage in chronic marijuana use from adolescence into their 20s are at increased risk for exhibiting psychopathic features, dealing drugs, and enduring drug-related legal problems in their mid-30s relative to men who remain abstinent or use infrequently.

1. Source:  http://jrc.sagepub.com/content/52/6/797  Published online before print June 29, 2015, doi:10.1177/0022427815589816Journal of Research in Crime and DelinquencyNovember 2015 vol. 52 no. 6 797-828  Email: dap38@pitt.edu

Driving after smoking even a small amount of marijuana almost doubles the risk of a fatal highway accident, according to an extensive study of 10,748 drivers involved in fatal crashes between 2001 and 2003.

A study by the French National Institute for Transport and Safety Research published in the British Medical Journal found that seven percent of drivers involved in a fatal highway crash used marijuana.

The researchers estimated that at least 2.5 percent of the 10,748 fatal crashes studied were directly caused by the use of marijuana.

Small Amounts Can Cause Impairment

The researchers concluded that the risk of being responsible for a fatal crash increased as the blood concentration of THC, the active ingredient in marijuana, increased. Even small amounts of marijuana could double the chance of a driver suffering an accident, researchers said, and larger doses could more than triple the risk.

The number of highway deaths contributed the smoking weed were significant, even though they were dwarfed by the number caused by drinking alcohol. Of the drivers involved in fatal accidents, 21.4 percent tested positive for alcohol consumption. Alcohol was estimated to be responsible for 28.6 percent of all fatal highway accidents.

The French research found that 2.9 percent of drivers involved in fatal crashes tested positive for both marijuana and alcohol. Men were more often involved in fatal crashes than women and were more often tested positive for both marijuana and alcohol.

Totally Irresponsible

Young drivers and drivers of motorcycles and mopeds were also more likely to test positive for both substances.

“Research like this proves just how dangerous it is to take drugs, and then get behind the wheel of a car,” Roger Vincent, of the Royal Society for the Prevention of Accidents, told the BBC. “It is totally irresponsible, as taking drugs such as cannabis does affect your reactions.”

Source: The study was published in the Dec. 3, 2005 issue of the British Medical Journal.  Updated June 04, 2014.

The Washington Traffic Safety Commission released new data showing that legalizing marijuana increases marijuana-impaired traffic fatalities. From 2010 to 2014, some 60 percent of drivers involved in fatal crashes were tested for drugs. About 20 percent (349 drivers) tested positive for marijuana. The new data can distinguish between drivers who were high at the time of the crash as opposed to those who had residual traces of marijuana in their systems from use days earlier. The number of drivers involved in fatalities who tested positive for active THC increased from 65 percent (38 of 60 drivers) in 2013 to 85 percent (75 of 89 drivers) in 2014, the year Washington implemented legal pot. About half of these drivers exceeded the 5 ng/ml THC designation denoting impairment in Washington’s legalization law. The driver with the highest THC level tested at 70 mg/ml. Half of the THC positive drivers were also impaired by alcohol, the majority exceeding 0.08 BAC. The largest increase in active THC positive drivers involved in fatal crashes were young males ages 21 to 25, from 6 in 2013 to 19 in 2014.   From 2008 to 2014, more than 1,100 people died in impaired collisions in Washington State, accounting for nearly half of all traffic deaths and more than one-fifth of serious injury collisions.

Source: marijuanareport.org.  Sept.23rd 2015

Heavy users suffer from severe nausea and pain that can only be relieved by bathing in hot water several times a day

PUBLISHED: 14:00, 31 August 2015 |

A bizarre syndrome that makes heavy cannabis users violently ill and leads them to take frequent hot baths to ease the pain has been reported by doctors.

Symptoms of the illness include severe stomach pain, nausea and vomiting – and bathing in very hot water up to five times a day for relief.

At least two cases of the syndrome which involve multiple visits to accident and emergency have been reported in the UK and worldwide the conditions is ‘increasing acutely’.

* Cannabinoid hypermesis syndrome was first recorded in Australia

* Symptoms include severe stomach pain, nausea and vomiting

* Sufferers often report having a hot bath up to 5 times a day to relieve pain

* Expert warns condition is responsible for a rise in ‘unecessary’ hospital admissions for heavy cannabis users – and is ‘increasing acutely’

But doctors in the UK warn that the failure to recognise CHS is likely to be draining hospital resources as it is being wrongly diagnosed.

Dr Sauid Ishaq, professor of gastroenterology at Birmingham City University, who was one of the first to observe the syndrome in the UK said: ‘This is a highly unrecognised condition, resulting in numerous unnecessary admissions. ‘There is an urgent need to highlight this.’

In the US, doctors in Colorado report an ‘acute’ rise in cases of the syndrome there since marijuana laws became relaxed.

CHS, which stands for cannabinoid hyperemesis syndrome, was first reported in medical literature in 10 patients in Adelaide, Australia in 2004.

Recognition of the condition is increasing and doctors are now recognising the condition in patients regularly visiting hospital with severe nausea.

Dr Ishaq, of Russells Hall Hospital, Dudley, reported a 42-year-old man presented on eight occasions with vomiting, abdominal pain, fever and dehydration last year in the east Midlands. Dr Ishaq and colleagues found the man had been a chronic cannabis smoker since the age of 14.

After a series of investigations, they found the symptoms ceased when the patient stopped smoking the drug.

In the medical journal GHFBB the authors write better awareness of the condition ‘would result in fewer hospital admissions and needless investigations, and may provide patients with real motivation to abstain from cannabis’.

At Macclesfield General Hospital, a 21-year-old chef had been admitted on seven occasions over a two year period with profuse vomiting – but his symptoms ended after he stopped smoking the drug.

Cannabinoid hypermesis syndrome is characterised by heavy use of the drug, triggering nausea and vomiting as well as frequent hot baths or showers.

Despite studies promoting the use of marijuana’s anti-emetic (anti-sickness) qualities, there is increasing evidence of its negative affect on the gastrointestinal tract, triggering CHS.

Sufferers have reported frequent hot bathing helps to provide temporary relief from the nausea, vomiting and abdominal pain typical of the illness.

Lead author Dr Enrico Roche wrote in the journal Gut: ‘The observation that the patient wanted to take regular baths because he had found that bathing eased the sickness was documented in the nursing notes but its significance was not appreciated.’

In one case reported in the Journal of American Family Medicine a man ‘spent three days in a hot shower while awake’ to alleviate his symptoms.

His case was not the most extreme however, as researchers reported that one sufferer reported spending ‘300 out of 365 days’ in the bath.

The findings that cannabis can cause severe nausea runs counter to a widespread view that the drug has a powerful anti-nausea effect.

Doctors in Colorado – where cannabis has been legalised – suspected that some of the cases of extreme nausea they had been seeing may have been caused by chronic cannabis use. They reviewed admission data to hospitals and found an acute rise in the condition since marijuana became legalised and widely available for medical use.

The research, in Academic Emergency Medicine, compared the numbers of people suffering from the condition from November 1, 2008 to October 31, 2009, after which cannabis use became liberalised in the state and between June 1, 2010 to May 31, 2011.

They found 41 cases of suspected CHS – where patients had been admitted three or more times for nausea – before legalisation,  rose to 87 cases after legalisation at two hospitals, Denver Health and the University of Colorado.  The sufferers were predominantly female (71 per cent) and white (72 per cent) with an average age of 31, the authors note.

The authors, led by Dr Kim Howard, wrote they think that the most likely explanation for the marijuana use contributed to an increased rate of cyclic vomiting presentations.

Marijuana is the most commonly used illicit substance in the United States, the authors note, with 18.9 million users in 2012.

But they add: ‘Unfortunately, there is little information on the deleterious effects of chronic use and its implications for public health. ‘As the number of new and chronic marijuana users grows annually, it is important to measure its effect on public health…the rate of cyclic vomiting seems to have increased acutely.’

By COLIN FERNANDEZ, SCIENCE CORRESPONDENT FOR THE DAILY MAIL

Source: http://www.dailymail.co.uk/health/   UPDATED:  31/08/15 

Colorado, March 2014. Hancock-Allen JB, Barker L, VanDyke M, Holmes DB.

Abstract

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.

Abstract

BACKGROUND:

In Brazil, crack cocaine use remains a healthcare challenge due to the rapid onset of its pleasurable effects, its ability to induce craving and addiction, and the fact that it is easily accessible. Delayed action on the part of the Brazilian Government in addressing the drug problem has led users to develop their own strategies for surviving the effects of crack cocaine use, particularly the drug craving and psychosis. In this context, users have sought the benefits of combining crack cocaine with marijuana. Our aim was to identify the reasons why users combine crack cocaine with marijuana and the health implications of doing so.

METHODS:

The present study is a qualitative study, using in-depth interviews and criteria-based sampling, following 27 crack cocaine users who combined its use with marijuana. Participants were recruited using the snowball sampling technique, and the point of theoretical saturation was used to define the sample size. Data were analyzed using the content analysis technique.

RESULTS:

The interviewees reported that the combination of crack cocaine use with marijuana provided “protection” (reduced undesirable effects, improved sleep and appetite, reduced craving for crack cocaine, and allowed the patients to recover some quality of life).

CONCLUSIONS:

Combined use of cannabis as a strategy to reduce the effects of crack exhibited several significant advantages, particularly an improved quality of life, which “protected” users from the violence typical of the crack culture. Crack use is considered a serious public health problem in Brazil, and there are few solution strategies. Within that limited context, the combination of cannabis and crack deserves more thorough clinical investigation to assess its potential use as a strategy to reduce the damage associated with crack use.

Source:  http://www.ncbi.nlm.nih.gov/pubmed/26209238  BMC Public Health. 2015 Jul 25;15(1):706. doi: 10.1186/s12889-015-2063-0.

NDPA would thoroughly recommend you to read this excellent article – backed up with references.  Adolescent users of cannabis need to know that research 

has shown:

‘…….structural changes within the brain of adolescent patients using marijuana….’

‘….The cannabis users were noted to have striatal, globus pallidus, and thalamus changes showing these brain regions appearing to shrink and collapse inward.’

Thus using marijuana to get high can actually result in real brain damage.

 

Abstract 

With the recent legalization of recreational marijuana in Colorado, Washington, Alaska, the District of Columbia and legislation pending for both medical and recreational marijuana in several other states, it is important for the facts regarding its potential for serious mental health consequences to be known. Little has been said about the psychiatric risks of this substance, particularly in youth. Several studies have shown increased rates of depression, anxiety and schizophrenia among those who use marijuana on a regular basis. In addition, permanent loss of IQ and structural changes in the brain have been demonstrated with habitual use. Legalization of marijuana for recreational use can influence an adolescent’s perception of this substance as “safe.” In states that have legalized marijuana for medical purposes, there is the very real problem of “diversion.” As many as 34 percent of 12th-graders who use marijuana in states with legalized marijuana had obtained it from a person who had received it through a prescription.

Introduction

With the recent legalization of recreational marijuana in Colorado and Washington and the legal use of medical marijuana in 23 states, South Dakota will likely face another concerted effort to legalize marijuana for both medical and recreational purposes. Proponents of marijuana legalization state that marijuana is no different than alcohol and would increase tax revenues and lower the expense of prosecuting users. However, there are significant deleterious effects to the use of this substance that weigh heavily in favor of keeping the laws in South Dakota as they are. Background While known by a variety of different names (cannabis, pot, Mary Jane, weed, etc.) marijuana is a drug that is familiar to most people.

Research into the use of this drug is bringing to light a number of very serious concerns, especially within the adolescent population, that many familiar with the drug have failed to recognize in the past. The legalization of marijuana, compounded with the continued illegal use of cannabis, continues to have a major impact on the lives of the youth that we treat in our medical practices and interact with in our communities. Many users of the drug consider it to be a “safe” alternative to “hard core” drugs or alcohol; however, this belief is in stark contrast to the reputable research findings being published on this topic.

Review 

According to data published by the Centers for Disease Control and Prevention’s (CDC) Youth Risk Behaviour Surveillance (YRBS) survey in 2013 which surveyed ninth through 12th grade students in public and private schools throughout the U.S., 40.7 percent of ninth through 12th grade students reported that they had used marijuana one or more times during their lifetime – 8.6 percent of which indicated that they had tried marijuana for the first time prior to age 13. These percentages were noted to be slightly lower in South Dakota’s adolescent population with 29.6 percent of ninth through 12th grade students reporting having used cannabis one or more times in their life, and 7.2 percent of those indicating that they had first used marijuana prior to age 13. 1

One of the leading arguments of proponents for legalized marijuana is that the regulated, legal use of cannabis obtained through legal channels will result in a decrease in the overall amount of marijuana being used due to the disruption of the underground market by which people currently obtain the drug. One study, published between 2002 and 2008, which looked at adolescent marijuana use, showed that the use was lower and the perception of its riskiness was higher in states where medical marijuana was not legal. On the other hand, adolescent marijuana use was noted to be “higher and perception of its riskiness lower” in states where medical marijuana was legal. 2

Gil Kerlikowske, director of the White House Office of National Drug Control Policy stated, “Today…there is evidence suggesting that regulation schemes that have been promoted by the marijuana legalization lobby are not succeeding in preventing the diversion of marijuana into the hands of young people, as was promised to the voters.” Of interest, it should be noted that “34 percent of the 12th-graders who used marijuana and lived in states with medical marijuana laws reported that they obtained the drug through someone else’s prescription – and 6 percent said they had their own prescription”. 3

Not only are there a growing number of adolescents reporting cannabis use, but the perceived dangers of this drug are shifting as well. According to a Feb. 6, 2013 article in JAMA, adolescent attitudes toward marijuana use seem to be changing. When looking at adolescent attitudes towards marijuana use, this article indicated that only 41.7 percent of eighth-graders felt that occasional marijuana use was dangerous. 4

One of the greatest misconceptions surrounding marijuana safety is a false belief that the marijuana of the boomer generation is the same marijuana that is being used by our youth today. According to a report by the National Institute on Drug Abuse, “The amount of tetrahydrocannabinol (THC) in marijuana samples confiscated by police has been increasing steadily over the past few decades. In 2012, THC concentrations in marijuana averaged close to 15 percent, compared to around 4 percent in the 1980s.”5

Marijuana, or cannabis, is a derivative of the plant cannabis sativa. 6

Cannabis exists in many forms and levels of potency with herbal cannabis being the most commonly used form. 7   The active ingredient in cannabis is tetrahydrocannabinol. 7

Research has demonstrated that the effects of cannabis on the human body are related to the agonistic effects at the cannabinoid receptors (CB1 and CB2). 8 The CB1 receptor is a pre-synaptic receptor that is found in large quantities in the striatum, hippocampus and cerebellum and also in lesser amounts in peripheral tissues, liver adipocytes, the pancreas, the gastrointestinal tract, skeletal muscle and in immune cells. 8   In contrast, CB2 receptors are located mainly in the immune cells in tissues such as the spleen and liver. 8   Cannabinoid receptors found in neurons are activated by the neurotransmitter anandamide. 7

It is the endocannabinoid system that has been identified as one of the key components “for cortical development, neuronal migration, connectivity and synaptogenesis. During adolescence, many brain regions undergo dramatic levels of growth and synaptic remodeling,” particularly in the prefrontal cortex. 9

THC, the active ingredient in cannabis, acts like anandamide and leads to activation of the neuron. It is activation of the CB1 receptor that leads to the psychoactive effects of cannabis. 7   One theory that explains how this occurs is that by stimulating the cannabinoid receptors, the glutamate and gammaaminobutryic acid functioning is altered. This in turn leads to structural changes within the brain of adolescent patients using marijuana. 10

It is these changes in neuronal structure that may account for many of the very serious neurological effects that can accompany adolescent marijuana use. It is also the large number of CB receptors in the striatum, amygdale, hippocampus, cerebellum, and prefrontal cortex that give rise to the brain’s pleasure and reward centers, contributing to the addictive potential of the drug. 7

It is worth noting that there exists an abundance of cannabinoid receptors in the prefrontal cortex, a region of the brain that has been identified in the development of schizophrenia. 9 Research looking at the effects of marijuana use on the developing brain support the theory noted above. In a recent study at Northwestern University, it was reported that teens who smoked marijuana daily for a three year period had abnormal changes in the structure of their brain compared to teens in the control group. Brain abnormalities and memory problems were observed in these individuals in their early twenties, two years after they had stopped using marijuana. The cannabis users were noted to have striatal, globus pallidus, and thalamus changes showing these brain regions appearing to shrink and collapse inward. These individuals also had poorer working memory. The earlier the age of cannabis use, the more dramatic the brain changes and memory deficits were noted to be. 11

Although many proponents of cannabis legalization have refuted the claim that cannabis is a “gateway drug” to using even more dangerous and addictive substances of abuse, studies that have looked at substance use trends among cannabis users seem to support the “gateway drug” theory. Not only does it appear that cannabis use itself is a potential precursor to future drug use, but the age of first use of cannabis and the frequency of cannabis use seem to also be predictors of future substance abuse issues. Studies have shown that over two-thirds of those under the age of 18 who have been admitted to a drug treatment program identify cannabis as their substance of choice. It is estimated that the “risk for illicit drug initiation appeared 21 times higher among cannabis experimenters and 124 times higher among daily cannabis users than among non-users.”7

Data from the Treatment Episode Data Set (TEDS), which is a national data base of annual admissions to substance abuse treatment facilities in the U.S., shows that among adults who first used marijuana at the age of 14 or younger, 13.2 percent went on to develop drug dependence or abuse. This rate was noted to be six times higher than that of adults who first used marijuana starting after the age of 18. A 2011 review of demographic data looking at age showed that 74 percent of those surveyed in drug treatment facilities across the U.S. reported that they had first started to use substances of abuse at the age of 17 or younger, with 34.1 percent reporting they had first used substances of abuse between that ages of 15-17 and 29.7 percent reporting their first use between the ages of 12-14. Another 10.2 percent reported that they had first begun using substances of abuse before they were 11 years of age.

Of those surveyed, only 26 percent reported that they began using substances of abuse at the age of 18 or older. 12   Another claim that is often made by those in favour of marijuana legalization is that cannabis is not an addictive drug. Popular belief is that cannabis use is safe and does not carry any long term addictive potential. Credible research contradicts this belief. According to The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), the current criteria for a substance use disorder is a “cluster of cognitive, behavioural, and physiological symptoms indicating that the individual continues using the substance despite significant substance related problems.” One important characteristic that defines a substance use disorder is “an underlying change in brain circuits that may persist beyond detoxification, particularly in individuals with severe disorder.” These brain changes may be demonstrated by “the repeated relapses and intense drug craving when the individuals are exposed to drug-related stimuli.” As indicated earlier in this article, the activation by THC of the CB receptors in the striatum, amygdale, hippocamupus, cerebellum and prefrontal cortex areas, which are known to give rise to the brain’s pleasure and reward center, contribute to the addictive potential of the drug. 13   DSM-5 has defined cannabis-related disorders by the following diagnostic criteria:

A problematic pattern of cannabis use leading to clinically significant impairment or distress, as manifested by at least two of the following, occurring within a 12-month period:

1. Cannabis is often taken in larger amounts or over a longer period than was intended

2. There is a persistent desire or unsuccessful efforts to cut down or control cannabis use.

3. A great deal of time is spent in activities necessary to obtain cannabis, use cannabis, or recover from its effects.

4. Craving, or a strong desire or urge to use cannabis.

5. Recurrent cannabis use resulting in a failure to fulfill major role obligations at work, school or home.

6. Continued cannabis use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of cannabis.

7. Important social, occupational, or recreational activities are given up or reduced because of cannabis use

8. Recurrent cannabis use in situations in which it is physically hazardous.

9. Cannabis use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by cannabis.

10. Tolerance, as defined by either of the following: a. A need for markedly increased amounts of cannabis to achieve intoxication or desired effect. b. Markedly diminished effect with continued use of the same amount of cannabis.

11. Withdrawal, as manifested by either of the following: a. The characteristic withdrawal syndrome from cannabis. b. Cannabis is taken to relieve or avoid withdrawal.

12 . While many of the acute effects of cannabis tend to be reversible (increased heart rate, blood shot eyes, euphoria and relaxation) proponents and opponents of marijuana legalization tend to disagree on cannabis’s ability to cause withdrawal symptoms once the drug has been discontinued. Research has identified a number of symptoms related to cannabis withdrawal such as irritability, anger, aggression, anxiety, depressed mood, restlessness, sleep difficulty and decreased appetite or weight loss. These withdrawal symptoms typically begin within 24-48 hours after discontinuation of the drug and typically last between one and three weeks. These symptoms may cause the user of the drug significant distress and contribute to relapse among those trying to abstain. 7

13.  For those who do choose to use cannabis, the use of this drug does not come without the potential for serious health risks. Research has shown that there is nearly a five time increased risk of myocardial infarction in the hour after one uses marijuana. Cannabis smokers are also exposed to many of the same harmful chemicals that cigarette smokers are exposed to. This exposure to chemicals puts one at a greater risk for developing cancer, bronchitis and recurrent lung infections. 7  Marijuana has also been shown to affect one’s level of cognition and motivation. Consider for a moment the image that comes to mind when you think of the term “pot head,” a slang term often used to describe someone that frequently smokes marijuana. This phrase, often used as a comedic portrayal of a marijuana user, depicts these frequent users of the drug as being extremely laid back, unmotivated, lazy, excessively hungry and as having poor memory.

14   Research shows that there is a connection between marijuana use and one’s motivation. Many experts agree that excessive use of marijuana, as well as a number of other “psychoactive” drugs, can lead to amotivational syndrome, a term used to describe the “variety of changes in personality, emotions and cognitive functions such as lack of activity, inward-turning, avolition, apathy, incoherence, blunted affect, inability to concentrate and memory disturbance” that is noted in chronic users of these drugs.

15.   Not only does marijuana affect one’s motivation, but also one’s cognitive ability. Marijuana use has been shown to affect adolescent academic performance. Results from the U.S. National Survey on Drug Use and Health showed that “youth with poor academic results were more than four times likely to have used cannabis in the past year than youth with average or higher grades.”

Cannabis use has also been shown to lead to decreased attention span, slower reaction times and motor/coordination deficits. Studies have also demonstrated that the use of cannabis may result in a decrease in adolescent IQ. It has also been shown that adolescents who are heavy users of marijuana have “poorer complex attention functioning, as well as poor sequencing ability, slower psychomotor speed, and difficulties in verbal story memory.”7   The motivation and cognitive affects of cannabis are also seen in adults who use marijuana. Studies indicate that a strong correlation exists between chronic cannabis use and unemployment, increased dependency on social welfare programs, and a decrease in life satisfaction rates. 7

The National Institute on Drug Abuse has also released studies showing that employees who used cannabis were more likely to have increased absences, accidents, worker’s compensation claims and job turnover when compared to non-cannabis users. 7   In recent years there has been more research into the role that marijuana plays in the development of mood disorders, anxiety disorders and psychosis. In one study of over 50,000 Swedish patients published by Zammit et al., a link was identified between marijuana use and the development of schizophrenia, a risk that was notably greater with increased marijuana use.

16.   In fact, in one published article, it was noted that of the research subjects who used cannabis over 50 times, there was a sevenfold increase in the risk for developing schizophrenia. 16   In another study, performed by Arseneault et al., it was demonstrated that in those subjects who used marijuana prior to the age of 15, there was a four times increased risk of developing schizophrenia by age 26. 16 .

Not only has marijuana been linked to increased rates of psychosis and schizophrenia, but more evidence is being reported on the link between cannabis and other mental health conditions. A study in Australia demonstrated that there was a relationship that existed in adolescent males and females with regard to the daily use of marijuana and the development of depression. 8.   This relationship was found to be the most profound in adolescent girls. In fact, in girls under the age of 15, it was found that there was a significant increase in suicidal ideation or attempts over the course of the next 15 years of their life. 8   Another research study performed in Australia found that in teens ages 13-17 who had used marijuana, there was a three times increased risk of developing depression when compared to those teenagers who had never used the drug. 8.   Increased levels of anxiety have also been linked to marijuana use. For those adolescents who used cannabis on a weekly basis and who continued to use until the age of 29, there was a significantly increased likelihood of developing an anxiety disorder. 7.

From a cognition standpoint, cannabis is known to slow a person’s ability to react, decrease their motor coordination, and decrease one’s ability to concentrate and focus. This increased level of distractibility, along with slower reaction times, has been shown to be a contributing factor in motor vehicle accidents when users of the drug attempted to drive while under the influence of cannabis. In a laboratory setting, cannabis and THC where noted to “produce dose-related deficits in reaction time, attention, motor performance and coordination, and information processing that can last up to 28 days after abstinence from the drugs.”7.

There are over 60 pharmacologically active cannabinoids in marijuana. One such chemical, cannabidiol (CBD), is a compound that may have anti-anxiety, anti-inflammatory and antispasmodic actions. It has been reported that CBD does not cause cognitive deficits or the perception of feeling “stoned.” The level of THC in medically dispensed marijuana is extremely high while CBD is low. THC is the chemical responsible for euphoria, or the “high” in marijuana. Indications for legally available marijuana for medicinal use vary from State to State and include cancer, glaucoma, AIDS, hepatitis, ALS, seizure disorders, Crohn’s disease, Parkinson’s disease and multiple sclerosis. Data collected in states where marijuana is legal for medicinal purposes suggests that the majority of those who possess medical marijuana user cards do not have one of these conditions.

Conclusion

There is a significant amount of evidence to support that the long-term use of marijuana is harmful to individuals and society, especially to adolescents. Research has shown that marijuana use can lead to an increased risk of chronic mental illnesses such as schizophrenia, depression, and anxiety by causing structural changes in a young, maturing brain. Adolescent use of marijuana can also lead to decreased intelligence levels and poor working memory which can interfere with educational attainment and create psychosocial and financial problems that no amount of increased tax revenue can offset. Although there are many in society who will lobby for legalization of this drug due to its “safety” profile, the evidence on this topic refutes this claim and we in South Dakota would be wise to continue to defeat any attempt at legalization of this harmful substance.

REFERENCES

1. Centers for Disease Control and Prevention. Youth risk behavior surveillance – United States, 2013. Morbidity and Mortality Weekly Report. 2014;63(4): 1- 170.

2. Wall MM, Poh E, Cerda A, Keyes KM, Galea S, Hasin DS. Adolescent Marijuana Use from 2002 to 2008: Higher in States with Medical Marijuana Laws, Cause Still Unclear. AEP. 2011; 21(9): 714-716.

3. Brauser D. Regular marijuana use in teens on the rise.Medscape. December 18, 2013; 1-3

4. Kuehn B M. Teen perceptions of marijuana risks shift: Use of alcohol, illicit drugs, and tobacco declines. JAMA. 2013;309(5): 429-430.

5. National Institute on Drug Abuse. Drug facts: Marijuana. January 2014;1-6.

6. Cohen M, Rasser PE, Peck G, Carr VJ, Ward PB, Thomson PM, Johnston P, Baker A, Schall U. Cerebellar grey-matter deficits, cannabis use and firstepisode schizophrenia in adolescents and young adults. International Journal of Neuropsychopharmacology. 2012;15: 297-307.

7. Douaihy A. Cannabis revisited. UPMC Synergies. 2013;1-11.

8. Rubino T, Zamberletti E, Parolaro D. Adolescent exposure to cannabis as a risk factor for psychiatric disorders. Journal of Psychopharmacology. 2012;26(1): 177-188.

9. Hill MN. Clearing the smoke: What do we know about adolescent cannabis use and schizophrenia? Journal of Psychiatry Neuroscience. 2014;133: 75-76.

10. Hilt RJ. Cannabis and the adolescent brain. Pediatric Annals. 2014;43(3): 89-90.

11. Smith MJ, Cobia DJ, Wang L, et al. Cannabis-related working memory deficits and associated subcortical morphological differences in healthy individuals and schizophrenia subjects. Schizophrenia Bulletin. 2013;40(2): 287-299.

12. SAMHSA. The TEDS report: Age of substance use initiation among treatment admissions aged 18 to 30. 2014;1-8.

13. Diagnostic and statistical manual of mental disorders. American Psychiatric Publishing; 5th edition. 2013.

14. Merriam-Webster online dictionary. http://www.merriam-webster.com. 2014.

15. Ozaki S, Wada K. Amotivational syndrome in organic solvent abusers. Nihon Yakurigaku Zasshi. 2001;117 (1): 42-48.

16. Shapiro GK, Buckley-Hunter L. What every adolescent needs to know: Cannabis can cause psychosis. Journal of Psychosomatic Research. 2010;69: 533-539.

About the Authors: Shawn Van Gerpen, MD, Assistant Professor and Residency Director, Department of Psychiatry, University of South Dakota Sanford School of Medicine. Tamara Vik, MD, Assistant Professor and Child and Adolescent Residency Director, Department of Psychiatry, University of South Dakota Sanford School of Medicine. Timothy Soundy, MD, Professor and Chair, Department of Psychiatry, University of South Dakota Sanford School of Medicine.

Source:  https://www.sdsma.org  2015

BACKGROUND: The Gateway Drug Theory suggests that licit drugs, such as tobacco and alcohol, serve as a “gateway” toward the use of other, illicit drugs. However, there remains some discrepancy regarding which drug—alcohol, tobacco, or even marijuana—serves as the initial “gateway” drug subsequently leading to the use of illicit drugs such as cocaine and heroin. The purpose of this investigation was to determine which drug (alcohol, tobacco, or marijuana) was the actual “gateway” drug leading to additional substance use among a nationally representative sample of high school seniors.

METHODS: This investigation conducted a secondary analysis of the 2008 Monitoring the Future 12th-grade data. Initiation into alcohol, tobacco, and other drug use was analyzed using a Guttman scale. Coefficients of reliability and scalability were calculated to evaluate scale fit. Subsequent cross tabulations and chi-square test for independence were conducted to better understand the relationship between the identified gateway drug and other substances’ use.

RESULTS: Results from the Guttman scale indicated that alcohol represented the “gateway” drug, leading to the use of tobacco, marijuana, and other illicit substances. Moreover, students who used alcohol exhibited a significantly greater likelihood of using both licit and illicit drugs.

CONCLUSION: The findings from this investigation support that alcohol should receive primary attention in school-based substance abuse prevention programming, as the use of other substances could be impacted by delaying or preventing alcohol use. Therefore, it seems prudent for school and public health officials to focus prevention efforts, policies, and monies, on addressing adolescent alcohol use.

Source:  “Alcohol as a Gateway Drug: A Study of US 12th Graders” that was published in the Journal of School Health in August 2012 

Cannabis causes chaos in the brain as nerve activity becomes uncoordinated and inaccurate, a study has found. The results may help explain links between cannabis and schizophrenia, scientists believe.

Researchers at the University of Bristol measured the brain responses of rats given a drug that mimics the psychoactive ingredient in cannabis. They found that the drug completely disrupted coordinated brain waves across the hippocampus and prefrontal cortex. The first brain region plays a key role in the formation of memories. The second is essential to planning, decision making and social behaviour. Both are heavily implicated in schizophrenia.

Rats exposed to the cannabis like drug became unable to make accurate decisions when navigating through a maze. The research is reported in the Journal of Neuroscience. Study leader Dr Matt Jones said: “Marijuana abuse is common among sufferers of schizophrenia and recent studies have shown that the psychoactive ingredient of marijuana can induce some symptoms of schizophrenia in healthy volunteers. “These findings are therefore important for our understanding of psychiatric diseases, which may arise as a consequence of ‘dis-orchestrated brains’ and could be treated by retuning brain activity.” Co-author Michal Kucewicz, also from the University of Bristol, said: “These results are an important step forward in our understanding of how rhythmic activity in the brain underlies thought processes in health and disease.”

Source: ‘Cannabis causes chaos in the brain’ http://www.independent.co.uk/life-style/healthandfamilies/healthnews/cannabiscauseschaosinthebrain. 8/05/2015 The research was part of a Medical Research Council funded collaboration between the university and drug company Eli Lilly & Co.

Some cannabis users think they are better drivers after taking the drug, according to a poll by the National Cannabis Prevention and Information Centre (NCPIC).

The NCPIC, based at the University of New South Wales, survey targeted 4,600 Australians over the age of 18 using social media.

It found nearly 70 per cent of recent cannabis users had driven while under the influence of the drug.  Sixteen per cent of users said they had driven on a daily basis less five hours after using.

“We hear a number of myths from cannabis users like that they may be more aware of their driving when they’re stoned or that they’re driving slower”.

said Dr Peter Gates, Senior researcher at the NCPIC.  Dr Gates said many users were oblivious to the impact cannabis had on driving skills.

He said users’ attitudes conflicted with established scientific evidence, showing cannabis increased the risk of motor vehicle crashes by up to 300 per cent.

“We know from research that any cannabis use will affect your tracking ability, your reaction time, your attention span, your awareness of distance, your co-ordination, concentration,” Dr Gates said.

Dr Gates said users were also unaware of the risk of being drug tested, despite a rise in the number of random roadside drug tests being conducted.

“It is time for a wake-up call,” he said.

Source:  http://www.abc.net.au/news/2015-06-10

* A National Institute on Drug Abuse study tasked stoned participants with driving a highly sophisticated driving simulator

* Researchers found that after their blood levels of THC reached a certain point, the drivers weaved similarly to a driver with a BAC of .08

* The study also found that combining cannabis and alcohol decreased motor skills even more than just one or the other

A first-of-its-kind study by the National Institute on Drug Abuse has determined that smoking marijuana can, in fact, adversely affect driving ability.  The comprehensive government study put 18 marijuana users behind the wheel of a sophisticated driving simulator after they were given different combinations of marijuana, alcohol or a placebo.

The data revealed that, at certain blood concentrations, marijuana’s active chemical THC affects weaving within a road lane in a similar way to a blood alcohol level of .08, the legal limit in many states. The study was the first to make a sophisticated, scientific examination of the differences in effects of marijuana versus alcohol while driving.

+’One of the things we know happens with cannabis is that it reduces your field of vision and you get tunnel vision, so you’re unable to react as quickly,’ Marilyn Huestis of the NIDA told KABC.

Despite this, drugged driving penalties vary state-to-state as compared to those for drunk driving. In Colorado, where recreational marijuana is legal, a first offense high driver can expect a mandatory minimum sentence of two days in jail. A first offense DUI can get you up to a year.

The study also found that pot and alcohol have more of an impact on driving when used together, TIME notes.  They found that when people drank alcohol before inhaling marijuana, the level of THC in their blood was ‘significantly higher than without alcohol’.

The combination of cannabis and alcohol raises the chance of crashing more than either substance by itself, they added, pointing to previous research which came to this conclusion.

‘We know cannabis is primarily found with a low dose of alcohol,’ Huestis said. ‘Many young people have a couple beers and then cannabis.’ And this worries researchers in a country where the drug has become legal in some states, a trend that is likely to grow.

‘The significantly higher blood THC values with alcohol possibly explain increased performance impairment observed from cannabis-alcohol combinations,’ said Huestis.

She added she hopes the findings will inform discussions around legislation on driving on drugs.

Previously, experts have warned that the increased concentration of THC in today’s cannabis compared to previous years means smokers are more likely to experience negative effects. These include anxiety, confusion, panic attacks, hallucinations or extreme paranoia, with women more at risk than men.

Source: http://www.dailymail.co.uk/news/article-3137943/Marijuana-DOES-impair-driving-kind-comprehensive-government-study-reveals-cannabis-use-affect-motor-skills-three-drinks.html#ixzz3e5YLNFMo 

CHICAGO (AP) — Medical marijuana has not been proven to work for many illnesses that state  laws have approved it for, according to the first comprehensive analysis of research on its potential benefits.

The strongest evidence is for chronic pain and for muscle stiffness in multiple sclerosis, according to the review, which evaluated 79 studies involving more than 6,000 patients. Evidence was weak for many other conditions, including anxiety, sleep disorders, and Tourette’s syndrome and the authors recommend more research.

The analysis is among several medical marijuana articles published Tuesday in the Journal of the American Medical Association. They include a small study suggesting that many brand labels for edible marijuana products list inaccurate amounts of active ingredients. More than half of brands tested had much lower amounts than labeled, meaning users might get no effect.

Highlights from the journal:

THE ANALYSIS

The researchers pooled results from studies that tested marijuana against placebos, usual care or no treatment. That’s the most rigorous kind of research but many studies found no conclusive evidence of any benefit. Side effects were common and included dizziness, dry mouth and sleepiness. A less extensive research review in the journal found similar results.

It’s possible medical marijuana could have widespread benefits, but strong evidence from high-quality studies is lacking, authors of both articles say.

“It’s not a wonder drug but it certainly has some potential,” said Dr. Robert Wolff, a co-author and researcher with Kleijnen Systematic Reviews Ltd., a research company in York, England.

EDIBLE PRODUCTS

Researchers evaluated 47 brands of medical marijuana products, including candy, baked goods and drinks, bought at dispensaries in Los Angeles, San Francisco and Seattle. Independent laboratory testing for THC, marijuana’s leading active ingredient, found accurate amounts listed on labels for just 13 of 75 products. Almost 1 in 4 had higher amounts than labeled, which could cause ill effects. Most had lower-than-listed amounts. There were similar findings for another active ingredient. Products were not identified by name. Johns Hopkins University researcher Ryan Vandrey, the lead author, said he was surprised so many labels were inaccurate. The researchers note, however, that the results may not be the same in other locations. MARIJUANA LAWS Twenty-three states and Washington, D.C. have laws permitting medical marijuana use. Approved conditions vary but include Alzheimer’s disease, epilepsy, glaucoma, kidney disease, lupus and Parkinson’s disease. An editorial in the journal says approval in many states has been based on poor quality studies, patients’ testimonials or other  non-scientific evidence. Marijuana is illegal under federal law and some scientists say research has been stymied by government hurdles including a declaration that marijuana is a controlled substance with no accepted medical use. But in a notice published Tuesday in the Federal Register, the Department of Health and Human Services made it a little easier for privately funded medical marijuana research to get approved. The department said that a federal Public Health Service review of research proposals is no longer necessary because it duplicates a required review by the Food and Drug Administration. THE FUTURE Colorado, one of a few states where recreational marijuana use is legal, has pledged more than $8 million in state funds for several studies on the drug’s potential medical benefits, including whether it can reduce veterans’ symptoms of post-traumatic stress disorder. That study may begin recruiting participants later this year, said Vandrey, one of that study’s leaders. Vandrey said there’s a feeling of optimism in the research community that “we’ll start to get a good science base” for the potential medical uses of marijuana. THE RECOMMENDATIONS The editorial by two Yale University psychiatrists suggests enthusiasm for medical marijuana has outpaced rigorous research and says widespread use should wait for better evidence. Federal and state governments should support and encourage such research, the editorial says. “Perhaps it is time to place the horse back in front of the cart,” Drs. Deepak Cyril D’Souza and Mohini Ranganathan wrote in the editorial. They note that repeated recreational marijuana use can be addictive and say unanswered questions include what are the long-term health effects of medical marijuana use and whether its use is justified in children whose developing brains may be more vulnerable to its effects.

Source:  JAMA: http://jama.ama-assn.org   National Institute on Drug Abuse: http://tinyurl.com/axxzhrj   Jun 23, 2015

Prof Philip Murphy

Prof Murphy, who is head of psychology at Edge Hill University, has worked professionally in drug misuse since 1984 and has carried out extensive research into how the misuse of cannabis and ecstasy impairs cognitive performance such as memory and its effect on mood disturbances.

However, although he against the legalisation of cannabis and its use recreationally, he believes there is political confusion which has hampered it being used to produce beneficial medication.

He explains: “I am opposed to the legalisation of cannabis. But I am perfectly happy to see cannabinoids prescribed as medication. I think there is confusion surrounding this at a political level.  There is a fear among politicians that they will be seen to have legalised cannabis.”

Prof Murphy says cannabis is comprised of more than 400 compounds and around 60 of these are regarded as active cannabinoids.

He explains that pharmaceutical preparations of cannabinoid medications will have carefully selected the clinically beneficial cannabinoids for a given condition requiring treatment.  As a result, he says clinically prescribed cannabinoid medications bear very little similarity to black market cannabis.

Prof Murphy says: “Such preparations have been designed for administration by routes other than smoking such as tablets and sprays.  When you extract the therapeutic compounds of cannabis – notably one known as CBD which has a number of very powerful medicinal applications – you are talking about something very different from the black market supplies of cannabis bought in pubs or on street corners.

“It is the difference between a properly produced pharmaceutical product and something in its raw form.  I cannot see any logical argument against the use of a pharmaceutical preparation involving cannabinoids.”

Prof Murphy has done a lot of work looking at the negative effects of cannabis when used recreationally and has found it impairs memory performance, makes the brain work harder to maintain the level of performance of non-users and is linked to episodes of psychotic behaviour, especially where a predisposition to psychotic episodes exists.

Prof Murphy says: “There is evidence cannabis can impair memory functioning, can change the levels of activity in the brain which suggest the brain has to work harder to match the performance of a non-user on some laboratory tasks and that some black market preparations very high in concentrations of a cannabinoid known as THC can lead to psychotic episodes in people with a predisposition to such episodes.

“With recreational cannabis users, I have found cannabis to be a very dependance producing drug. The main psycho active compound of cannabis is THC. THC levels in the days of the hippies were one to two per cent.

“However, today, particularly in skunk cannabis, THC levels can be 20 per cent or even more.  People say cannabis is not addictive, but that is now an outdated view as cannabis has changed so much from what it used to be.”

Despite knowing the negative implications of cannabis, Prof Murphy says it is perfectly possible to have a drug made using cannabinoids and available by prescription only.

He explains: “Carefully manufactured pharmaceutical preparations need to be prescribed by qualified clinicians in a context of professional clinical management.

“Cannabis should not be legalised for recreational use and open sale.

“This does not logically contradict its appropriate use in treating illness and curbing suffering.  Sadly, it is likely that political considerations around a fear of having been seen to have legalised cannabis may have retarded the development of cannabinoid based medications.

“This is very unfortunate and likely to have perpetuated suffering for some people unnecessarily. All the work I have done on illegal cannabis affecting memory still holds true.  But as with any other medication, we have to hold potential problems in consideration against the potential benefits.

“That is for the clinician treating the patient to do as they would with any other medication.  There are negative effects to every medication. It is about balancing the benefits against the potential risk.”

Source:  http://www.lep.co.uk/news    17th April 2015

A major challenge in neuroscience is to determine the nanoscale position and quantity of signalling molecules in a cell type– and subcellular compartment–specific manner.

We developed a new approach to this problem by combining cell-specific physiological and anatomical characterization with super-resolution imaging and studied the molecular and structural parameters shaping the physiological properties of synaptic endocannabinoid signalling in the mouse hippocampus. We found that axon terminals of perisomatically projecting GABAergic interneurons possessed increased CB1 receptor number, active-zone complexity and receptor/effector ratio compared with dendritically projecting interneurons, consistent with higher efficiency of cannabinoid signalling at somatic versus dendritic synapses.

Furthermore, chronic Δ9-tetrahydrocannabinol administration, which reduces cannabinoid efficacy on GABA release, evoked marked CB1 down regulation in a dose-dependent manner. Full receptor recovery required several weeks after the cessation of Δ9-tetrahydrocannabinol treatment.

These findings indicate that cell type–specific nanoscale analysis of endogenous protein distribution is possible in brain circuits and identify previously unknown molecular properties controlling endocannabinoid signalling and cannabis-induced cognitive dysfunction.

Source:Nature Neuroscience18,75–86(2015) doi:10.1038/nn.3892 Pub. online 08/12/14 

Abstract

Background and Purpose

An increasing number of case reports link cannabis consumption to cerebrovascular events. Yet these case reports have not been scrutinized using criteria for causal inference.

Methods

All case reports on cannabis and cerebrovascular events were retrieved. Four causality criteria were addressed: temporality, adequacy of stroke work-up, effects of re-challenge, and concomitant risk factors that could account for the cerebrovascular event.

Results

There were 34 case reports on 64 patients. Most cases (81%) exhibited a temporal relationship between cannabis exposure and the index event. In 70%, the evaluation was sufficiently comprehensive to exclude other sources for stroke. About a quarter (22%) of patients had another stroke after subsequent re-exposure to cannabis. Finally, half of patients (50%) had concomitant stroke risk factors, most commonly tobacco (34%) and alcohol (11%) consumption.

Conclusion

Many case reports support a causal link between cannabis and cerebrovascular events. This accords well with epidemiological and mechanistic research on the cerebrovascular effects of cannabis.

  1. Daniel G. Hackam, MD, PhD, FRCPC

+Author Affiliations

  1. From the Division of Clinical Pharmacology, Department of Medicine, Western University, London, Ontario, Canada.

  1. Correspondence to Daniel G. Hackam, MD, PhD, FRCPC, 1400 Western Rd, London, Ontario, Canada N6G 2V2. E-mail dhackam@uwo.ca

Source: http://stroke.ahajournals.org/content/early/2015/02/19

These remarkable scans clearly reveal how smoking during pregnancy harms an unborn baby’s development.

New ultrasound images show how babies of mothers who smoke during pregnancy touch their mouths and faces much more than babies of non-smoking mothers.

Foetuses normally touch their mouths and faces much less the older and more developed they are. Experts said the scans show how smoking during pregnancy can mean the development of the baby’s central nervous system is delayed. Doctors have long urged pregnant women to give up cigarettes because they heighten the risk of premature birth, respiratory problems and even cot death.

Now researchers believe they can show the effects of smoking on babies in the womb – and use the images to encourage mothers who are struggling to give up.

Image shows the 4-D ultrasound scan of two foetuses at 32 weeks gestation, one whose mother was a smoker (top) and the other carried by a non-smoker (bottom). The foetus carried by the smoker touches its face and mouth much more, indicating its development is delayed

As part of the study, Dr Nadja Reissland, of Durham University, used 4-D ultrasound scan images to record thousands of tiny movements in the womb.

She monitored 20 mothers attending the James Cook University Hospital in Middlesbrough, four of whom smoked an average of 14 cigarettes a day.

After studying their scans at 24, 28, 32 and 36 weeks, she detected that foetuses whose mothers smoked continued to show significantly higher rates of mouth movement and self-touching than those carried by non-smokers. Foetuses usually move their mouths and touch themselves less as they gain more control the closer they get to birth, she explained.

The pilot study, which Dr Reissland hopes to expand with a bigger sample, found babies carried by smoking mothers may have delayed development of the central nervous system. Dr Reissland said: ‘A larger study is needed to confirm these results and to investigate specific effects, including the interaction of maternal stress and smoking.’

She believed that videos of the difference in pre-birth development could help mothers give up smoking.

But she was against demonising mothers and called for more support for them to give up. Currently, 12 per cent of pregnant women in the UK smoke but the rate is over 20 per cent in certain areas in the North East. All the babies in her study were born healthy, and were of normal size and weight.

Dr Reissland, who has an expertise in studying foetal development, thanked the mothers who took part in her study, especially those who smoked. ‘I’m really grateful, they did a good thing,’ she said. ‘These are special people and they overcame the stigma to help others.’

Co-author Professor Brian Francis, of Lancaster University, added: ‘Technology means we can now see what was previously hidden, revealing how smoking affects the development of the foetus in ways we did not realise.

‘This is yet further evidence of the negative effects of smoking in pregnancy.’ The research was published in the journal Acta Paediatrica. 


Read more: http://www.dailymail.co.uk  23 March 2015

“Even at normal doses, taking psychiatric drugs can produce suicidal thinking, violent behavior,  aggressiveness, extreme anger,  hostility, irritability, loss of ability to control impulses, rage reactions, hallucinations, mania, acute psychotic episodes, akathisia, and bizarre, grandiose, highly elaborated destructive plans, including mass murder.

“Withdrawal from psychiatric drugs can cause agitation, severe depression, hallucinations, aggressiveness, hypomania, akathisia, fear, terror, panic, fear of insanity, failing self-confidence, restlessness, irritability, aggression, an urge to destroy and, in the worst cases, an urge to kill.” -  From “Drug Studies Connecting Psychotropic Drugs with Acts of Violence” – unpublished.

My previous article on Global Research discussed the frustration of large numbers of aware observers around the world that were certain that Andreas Lubitz, the suicidal mass murderer of 149 passengers and crewmembers of the of the Lufthansa airliner crash, was under the intoxicating influence of brain-disabling, brain-altering, psychotropic medicines that had been prescribed for him by his German psychiatrists and/or neurologists who were known to have been prescribing for him.

These inquiring folks wanted and needed to know precisely what drugs he had been taking or withdrawing from so that the event could become a teachable moment that would help explain what had really happened and then possibly prevent other “irrational” acts from happening in the future. For the first week after the crash, the “authorities” were closed mouthed about the specifics, but most folks were willing to wait a bit to find out the truth.

However, another week has gone by, and there has still been no revelations from the “authorities” as to the exact medications, exact doses, exact combinations of drugs, who were the prescribing clinics and physicians and what was the rationale for the drugs having been  prescribed. Inquiring minds want to know and they deserve to be informed.

There are probably plenty of reasons why the information is not being revealed. There are big toes that could be stepped on, especially the giant pharmaceutical industries. There are medico-legal implications for the physicians and clinics that did the prescribing and there are serious implications for the airline corporations because their industry is at high risk of losing consumer confidence in their products if the truth isn’t adequately covered up. And the loss of consumer confidence is a great concern for both the pharmaceutical industry and its indoctrinated medical providers.

It looks like heavily drugged German society is dealing with the situation the same way the heavily drugged United States has dealt with psychiatric drug-induced suicidality and drug-induced mass murders (such as have been known to be in a cause and effect relationship in the American epidemic of school shootings – see www.ssristories.net).

The Traffickers of Illicit Drugs That Cause Dangerous and Irrational Behaviors Such as Murders and Suicides are Punished. Why not Legal Drug Traffickers as Well?

But there is a myth out there that illegal brain-altering drugs are dangerous but prescribed brain-altering drugs are safe. But anyone who knows the molecular structure and understands the molecular biology of these drugs and has seen the horrific adverse effects of usage or withdrawal of legal psychotropic drugs knows that the myth is false, and that there is a double standard being applied, thanks to the cunning advertising campaigns from Big Pharma.

But there is an epidemic of legal drug-related deaths in America, so I submit a few questions that people – as well as journalists and lawyers who are representing drug-injured plaintiffs – need to have answered, if only for educational and preventive practice purposes:

1) What cocktail of 9 different VA-prescribed psych drugs was “American Sniper” Chris Kyle’s Marine Corps killer taking after he was discharged from his psychiatric hospital the week before the infamous murder?

2) What were the psych drugs that Robin Williams got from Hazelden just before he hung himself?

3) What were the myriad of psych drugs, tranquilizers, opioids, etc that caused the overdose deaths of Philip Seymour Hoffman, Michael Jackson, Whitney Houston, Heath Ledger, Anna Nicole Smith, etc, etc, etc (not to mention Jimi Hendrix, Bruce Lee, Elvis Presley and Marilyn Monroe) – and who were the “pushers” of those drugs?

4) What was the cocktail of psychiatric and neurologic brain-altering drugs that Andreas Lubitz was taking before he intentionally crashed the passenger jet in the French Alps – and who were the prescribers?

5) What are the correctly prescribed drugs that annually kill over 100,000 hospitalized Americans per year and are estimated to kill twice that number of out-patients?

(See http://www.collective-evolution.com/2013/05/07/death-by-prescription-drugs-is-a-growing-problem/)

Because the giant pharmaceutical companies want these serious matters hushed up until the news cycle blows over (so that they can get on with business as usual), and because many prescribing physicians seem to be innocently unaware that any combination of two or more brain-altering psychiatric drugs have never been tested for safety (either short or long-term), even in the rat labs, future celebrities and millions of other patient-victims will continue dying – or just be sickened from a deadly but highly preventable reality.

But what about “patient confidentiality”, a common excuse for withholding specific information about patients (even if crimes such as mass murder are involved)? It turns out that what is actually being protected by that assertion are the drug providers and manufacturers. Common sense demands that such information should not be withheld in a criminal situation.

America’s corporate controlled media makes a lot of money from its relationships with its wealthy and influential corporate sponsors, contributors, advertisers, political action committees and politicians, but, tragically, the media has been clearly abandoning its historically-important investigative journalistic responsibilities (that are guaranteed and protected by the Constitution). It is obvious that the media has allied itself with the corporate “authorities” that withhold, any way they can, the important information that forensic psychiatrists (and everybody else) needs to know.

We should be calling out and condemning the authorities that are withholding the information about the reported “plethora of drugs” that is known to have been prescribed for Lubitz by his treating “neurologists and psychiatrists”, drugs that were found in his apartment on the day of the crash and identified by those same authorities who have not revealed the information to the people who need to know. Two weeks into the story and there still has been no further information given, or as far as I can ascertain, or asked for by journalists.

So, since the facts are being withheld by the authorities, I submit some useful lists of common adverse effects of commonly prescribed crazy-making psych drugs that Lubitz may have been taking. Also included are a number of withdrawal symptoms that are routinely  and conveniently mis-diagnosed as symptoms of a mental illness of unknown cause.

And at the end of the column are some excerpts from the FAA on psych drug use for American pilots. I do not know how different are the rules in Germany, but certainly both nations have to rely on voluntary information from the pilots.

1) Common Adverse Symptoms of Antidepressant Drug Use

Agitation, akathisia (severe restlessness, often resulting in suicidality), anxiety, bizarre dreams, confusion, delusions, emotional numbing, hallucinations, headache, heart attacks  hostility, hypomania (abnormal excitement), impotence, indifference (an “I don’t give a damn attitude”), insomnia, loss of appetite, mania, memory lapses, nausea, panic attacks, paranoia, psychotic episodes, restlessness, seizures, sexual dysfunction, suicidal thoughts or behaviors, violent behavior, weight loss, withdrawal symptoms (including deeper depression)

2) Common Adverse Psychological Symptoms of Antidepressant Drug Withdrawal

Depressed mood, low energy, crying uncontrollably, anxiety, insomnia, irritability, agitation, impulsivity, hallucinations or suicidal and violent urges. The physical symptoms of antidepressant withdrawal include disabling dizziness, imbalance, nausea, vomiting, flu-like aches and pains, sweating, headaches, tremors, burning sensations or electric shock-like zaps in the brain

3) Common Symptoms of Minor Tranquilizer Drug Withdrawal

Abdominal pains and cramps, agoraphobia , anxiety, blurred vision, changes in perception (faces distorting and inanimate objects moving), depression, dizziness, extreme lethargy, fears, feelings of unreality, heavy limbs, heart palpitations, hypersensitivity to light, insomnia, irritability, lack of concentration, lack of co-ordination, loss of balance, loss of memory, nightmares, panic attacks, rapid mood changes, restlessness, severe headaches, shaking, sweating, tightness in the chest, tight-headedness

4) Common (Usually Late Onset) Adverse Psychological Symptoms From Anti-Psychotic Drug Use

Blurred vision, breast enlargement/breast milk flow,  constipation, decreased sweating, dizziness, low blood pressure, imbalance and falls, drowsiness, dry mouth, headache, hyperprolactinemia (pituitary gland dysfunction), increased skin-sensitivity to sunlight, lightheadedness, menstrual irregularity (or absence of menstruation), sexual difficulty, (decline in libido, anorgasmia, genital pain).

The lethal adverse effects of antipsychotic drugs include Catatonic decline, Neuroleptic Malignant Syndrome (NMS, a condition marked by muscle stiffness or rigidity, dark urine, fast heartbeat or irregular pulse, increased sweating, high fever, and high or low blood pressure); Torsades de Pointes (a condition that affects the heart rhythm and can lead to sudden cardiac arrest”; Sudden death

5) Late and Persistent Adverse Effects of Antipsychotic Drug Use  (Some of these symptoms may even start when tapering down or discontinuing the drug!)

Aggression, akathisia (inner restlessness, often intolerable and leading to suicidality), brain atrophy (shrinkage), caffeine or other psychostimulant addiction, cataracts, creativity decline, depression, diabetes, difficulty urinating, difficulty talking, difficulty swallowing, fatigue and tiredness, hypercholesterolemia, hypothyroidism, intellectual decline (loss of IQ points), obesity, pituitary tumors, premature death, smoking – often heavy – (nicotine addiction), tardive dyskinesia (involuntary, disfiguring movement disorder), tongue edge “snaking” (early sign of movement disorder), jerky movements of head, face, mouth or neck, muscle spasms of face, neck or back, twisting the neck muscles, restlessness – physical and mental (resulting in sleep difficulty), restless legs syndrome, drooling, seizure threshold lowered, skin rashes (itching, discoloration), sore throat, staring, stiffness of arms or legs, swelling of feet, trembling of hands, uncontrollable chewing movements, uncontrollable lip movements, puckering of the mouth, uncontrollable movements of arms and legs, unusual twisting movements of body, weight gain, liver toxicity

6) Common Symptoms of Antipsychotic Drug Withdrawal

Nausea and vomiting, diarrhea, rhinorrhea (runny nose), heavy sweating, muscle pains, odd sensations such as burning, tingling, numbness,  anxiety, hypersexuality, agitation, mania, insomnia, tremor, voice-hearing

FAA Medical Certification Requirements for Psychotropic Medications

https://www.leftseat.com/psychotropic.htm

Pilots can only take one of four antidepressant drugs – Celexa (Citalopram), Lexapro (Escitalopram), Prozac (Fluoxetine) and Zoloft (Sertraline).

Most psychiatric drugs are not approved under any circumstances.

These include but are not limited to:

  • Abilify (Aripiprazole)
  • Effexor (Venlafaxine)
  • Elavil (Amitriptyline)
  • Luvox (Fluvoxamine Maleate)
  • Monoamine Oxidase Inhibitors
  • Paxil (Paroxetine)
  • Remeron (Mirtazapine)
  • Serzone (Nefazodone)
  • Sinequan (Doxepin)
  • Tofranil (Imipramine)
  • Trazodone
  • Tricyclic Antidepressants
  • Wellbutrin (Bupropion)

To assure favorable FAA consideration, the treating physician should establish that you do not need psychotropic medication. The medication should be discontinued and the condition and circumstances should be evaluated after you have been off medication for at least 60 and in most cases 90 days.

Should your physician believe you are an ideal candidate, you may be considered by the FAA on a case by case basis only. Applicants may be considered after extensive testing and evidence of successful use for one year without adverse effects. Medications used for psychiatric conditions are rarely approved by the FAA. The FAA has approved less than fifty (50) airmen under the FAA’s SSRI protocol.

After discontinuing the medication, a detailed psychiatric evaluation should be obtained. Resolved issues and stability off the medication are usually the primary factors for approval.

Dr Kohls is a retired physician who practiced holistic mental health care for the last decade of his family practice career. He writes a weekly column on various topics for the Reader Weekly, an alternative newsweekly published in Duluth, Minnesota, USA. Many of Dr Kohls’ weekly columns are archived at http://duluthreader.com/articles/categories/200_Duty_to_Warn.

Source:  http://www.globalresearch.ca/the-connections-between-psychotropic-drugs-and-irrational-acts-of-violence/5441484  April 08, 2015

 

CLEARING THE HAZE

….The ugly truth is that Colorado was suckered. It was promised regulation and has been met by an industry that fights tooth and nail any restrictions that limit its profitability.”  Ben Cort, Director of Professional Relations for the Center for Additction Recovery and rehabilitation at the University Of Colorado Hospital

Source:   http://gazette.com/clearingthehaze

 

REGULATION STILL INEFFECTIVE

But how it would work was described only in general terms and sound bites before voters headed to the polls to make a decision Gov. John Hickenlooper later would call “reckless” and “a bad idea” and new Colorado Attorney General Cynthia Coffman declared “not worth it” to dozens of state attorneys general last month.

Source:http://www.washingtonexaminer.com/regulation-still-ineffective/article/2562323?custom_click=rss

 

NO APPROVED MEDICINE IN MARIJUANA

Dr. Stuart Gitlow, a physician serving as president of the American Society of Addiction Medicine, does not mince words: “There is no such thing at this point as medical marijuana,” he said. It’s a point he has made routinely for the past decade, as advocates for marijuana legalization have claimed the drug treats an array of serious illnesses, or the symptoms of illnesses, including cancer, depression, epilepsy, glaucoma and HIV, the virus that causes AIDS.

Source:http://www.washingtonexaminer.com/no-approved-medicine-in-marijuana/article/2562336

 

LEGALIZATION DIDN’T UNCLOG PRISONS

Of all the misunderstandings about marijuana’s impact on the country, perhaps none is greater than the belief that America’s courts, prisons and jails are clogged with people whose only offense was marijuana use. This is the perception, but statistics show few inmates are behind bars strictly for marijuana-related offenses, and legalization of the drug will do little to affect America’s growing incarceration numbers.

Source:http://www.washingtonexaminer.com/legalization-didnt-unclog-prisons/article/2562326

 

DRUG USE A PROBLEM FOR EMPLOYERS

“This is a very troublesome issue for our industry, but I do not see us bending or lowering our hiring standards,” Johnson said. “Our workplaces are too dangerous and too dynamic to tolerate drug use. And marijuana? In many ways, this is worse than alcohol. I’m still in shock at how we (Colorado) voted. Everyone was asleep at the wheel.”

Source:http://www.washingtonexaminer.com/drug-use-a-problem-for-employers/article/2562334

 

MEDICAL MARIJUANA INDUSTRY STILL GROWING

And amid all the hoopla around legalized recreational pot, its older cousin, the medical marijuana (MMJ) industry — with 505 stores throughout Colorado — quietly continued to grow, adding patients by the thousands who seemingly had no problem finding physicians willing to diagnose what critics say are often phantom medical conditions. Statewide, the number of people on the Medical Marijuana Registry grew 4 percent in 2014 — the first year of legal recreational sales — from 111,030 to 115,467 by year’s end.

Source:http://www.washingtonexaminer.com/medical-marijuana-industry-still-growing-in-colorado/article/2562335

The most obvious characteristic of marijuana-legalisation campaigners – apart from billionaire interests on the scale of Big Tobacco – is that their lobbying and promises are based on theories not facts.

Legalisers regularly use the words “science” and “evidence base” but rarely cite research references. Never has this chasm between theory and fact been so powerfully and conspicuously exposed as in the March analysis by local media in Clearing the Haze of events a year after marijuana was legalised for recreational use in Colorado.

Here in the UK, a decade-long follow up by researchers into Britain’s disastrous 2004 ‘Lambeth experiment’ of depenalisation proved that it led to more crime and hospitalisations not less. The Colorado aftermath of legalisation is on a vaster scale.

CLAIM:“We view our top priority as creating an environment where negative impacts on children from marijuana legalisation are avoided completely,” Colorado’s governor promised.

FACT:There are growing concerns over exposure, potency and availability of marijuana to children. Even before legalisation, Governor John Hickenlooper predicted the need for “a project to analyse the correlation between marijuana use during pregnancy and birth defects” (FYI, here’sa listand one on perils tochildren). Colorado hospitals have admitted more children for marijuana harms. A June 2014 survey of 100 Colorado school officers found that 89 per cent witnessed a rise in marijuana-related incidents since legalisation.

CLAIM:Legalisation will fund prevention, education.

FACT:Colorado budgeted only about $34,000 for its Office of Behavioral Health’s prevention work in the 2014-2105 fiscal year; nothingwas received. Its Department of Public Health and EnvironmentGood to Knowcampaign, crafted with marijuana business owners, tells children how to use pot. “It’s like inviting a tobacco company to help us learn how to use tobacco and develop our next anti-smoking campaign.”

CLAIM:Regulation works.

FACT:How regulation would work was described only in soundbites before voting. Hickenlooper later admitted it was “reckless” and “a bad idea”. This February, Colorado Attorney General Cynthia Coffman declared it “not worth it”. Ben Cort at the University of Colorado Hospital disclosed that “Colorado has been met by an industry that fights tooth and nail any restrictions that limit profitability. Like Big Tobacco, the marijuana industry derives profits from addiction and its survival depends on turning a percentage of kids into lifelong customers.”

CLAIM:Legalisation of marijuana will unclog prisons.

FACT:There aren’t enough offenders in prison for simple possession of pot to unclog the system if they were freed: only 103. In 2011, the federal government convicted only 48 marijuana offenders with under 5,000 grams of marijuana: almost 12,000 joints.

CLAIM:Legalisation will produce new revenue for the general fund.

FACT:Tax revenues failed to meet projections – taxpayers could even get two refunds. The Governor’s Office of Marijuana Coordination director said the first priority for tax revenue is to cover regulatory costs. Moreover, Colorado isn’t equipped to gather cost-benefit analysis to quantify costs linked with cannabis abuse. This is alongside lawsuits against the state, manufacturing hazards, pressured resources for the homeless, concerns over children’s welfare and more: “Voters didn’t understand how difficult, resource-intensive and costly the enforcement of even just marijuana driving laws would be”.

CLAIM:Legalisation of marijuana will hobble drug cartels.

FACT:Cheaper marijuana prices mean cartels turn to ‘harder’ drugs including ‘black tar’ heroin and methamphetamine, as well as cybercrime and continued people-trafficking.

CLAIM:By regulating sales of marijuana, Colorado will make money otherwise locked into the black market.

FACT:Black-market sales are booming so much that they are blamed for cannabis tax revenues falling short of claims. “Don’t buy the argument that regulating sales will eliminate the black market, reduce associated criminal activity and free up law enforcement agencies’ resources,” Coffman urged in February. Worse is that “Colorado is the black market for the rest of the US”: neighbouring Denver suffered an almost 1,000 per cent spike in marijuana seizures.

CLAIM:Legalisation and regulation will see people using lower strengths of drugs.

FACT:Colorado permits one ounce of tetrahydrocannabinol (THC), the active ingredient giving a euphoric high. Many people envision an ounce of dried marijuana plant, about 40 standard cigarettes. But one ounce of concentrated THC equals over 2,800 average-size brownies or candy; an ounce of hash oil is roughly 560 standard ‘vaping’ hits.

CLAIM:Medical marijuana works, only legalisation allows research.

FACT:Treating marijuana – sold in dispensaries without FDA approval and shown to be more carcinogenic than tobacco when combusted – as if exempt from the approval process others drugs must undergo for public safety, is seen as derailing legitimate research on specific parts of the marijuana plant for new clinically-proven medicines without addiction risks. As the prevention charity, Cannabis Skunk Sense, puts it: “it’s like getting penicillin by eating mouldy bread”. Non-legalisation has not stopped 70+ scientific studies on cannabinoids elsewhere, and the National Institutes of Health awarded over $14million for such research.

CLAIM:Marijuana is safer than alcohol.

FACT:“Not when it comes to driving – and officers are seeing people using both substances, which is worse,” revealed one police chief.In the first six months of 2014, 77 per centDUIDs (driving under influence of drugs) involved marijuana. Accident risk doubles with any measurable amount of THC in the bloodstream, rising when alcohol is added.

The tragic fact above all else is that these downsides were predicted by authoritative individuals and organisations – and ignored. The good of many people was sacrificed for the greed of a few: be it for money, power or a drugged delusion. Deirdre Boyd

Source: www.conservativewoman.co.uk 1st April 2015

Several students and visitors from Wesleyan University were hospitalized on February 22 after taking the club drug MDMA. U.S. DEA/HANDOUT VIA REUTERS/REUTERS

At least 11 people from the Wesleyan University campus in Middletown, Connecticut, were hospitalized on Sunday with symptoms consistent with drug overdoses. School officials and emergency responders are blaming MDMA, also known as Molly, a form of the drug ecstasy that medical experts say has become increasingly popular on college campuses.

Though some reports said 11 people had received medical treatment, Wesleyan President Michael S. Roth put the number at 12 in an email to students on Monday. That includes 10 students and two visitors.

“I ask all students: Please, please stay away from illegal substances, the use of which can put you in extreme danger. One mistake can change your life forever,” Roth wrote. “And please keep those still hospitalized in your hearts and minds. Please join me in supporting their recovery with your prayers, thoughts and friendship.”

In a statement on Monday, a Middletown Police Department spokeswoman, Lieutenant Heather Desmond, wrote that her department would be involved in an investigation into “the origin of the drugs taken” and to “determine the extent of the criminal involvement in the case.”

A spokeswoman for Middlesex Hospital tells Newsweek it treated 11 people, three of whom are still there and four of whom were airlifted by helicopter to Hartford Hospital. She could not comment on the conditions of the three patients there. A spokeswoman for Hartford Hospital confirmed that four people were there. She too could not speak to their conditions. The police spokeswoman wrote that two individuals are in critical condition and two are in serious condition.

Middletown Fire Chief Robert Kronenberger tells Newsweek his department made seven runs to Wesleyan related to the incident on Sunday after receiving calls between 7:30 a.m. and 1:30 p.m. It rendered aid to eight individuals, including two people in a single dorm room. “We saw the trend and we worked with the university and the police department to notify them of the trend,” Kronenberger says. “We’ve never had anything to this extent,” he says, referring to health and safety issues at Wesleyan. “A couple of them were in some serious dire straits,” he says about the students, adding that they were cooperative. “As a parent of two college-age students, this definitely concerns me and hopefully something to this extent will open eyes,” he says.

Wesleyan’s student newspaper, The Wesleyan Argus, first reported about the incident on its website on Sunday after the school’s vice president for student affairs, Michael Whaley, sent a series of emails to students.

Medical experts say MDMA use on college campuses has grown in recent years, and while there have been reports of bad reactions to the drug, it appears the Wesleyan incident is the most widespread.

In 2013, a University of Virginia sophomore collapsed at a nightclub after taking MDMA and later died. Students at Syracuse University in Syracuse, New York; Plymouth State University in Plymouth, New Hampshire; and Texas State University in San Marcos, Texas have also died after taking the drug. In 2013, organizers of the Electric Zoo music festival in New York City cut the event short after two people died while taking MDMA, including a University of New Hampshire student.

“This age group is a risk-taking group that is willing to follow their friend wherever they go, and if the person next to them is popping a pill, then they’re going to do it too,” says Dr. Mark Neavyn, director of medical toxicology at Hartford Hospital, who treats patients there for MDMA overdoses.

“I think the popular culture engine kind of made it seem safer in some way,” Neavyn says, referring to references to the drug by the singers Miley Cyrus and Madonna that made headlines.

But when it comes to MDMA, people are rarely taking what they think they’re taking, the doctor says.

According to Neavyn, symptoms of an MDMA overdose include fast heart rate, high blood pressure, delirium, elevated body temperature and alterations in consciousness. Extreme cases could involve cardiac arrhythmia and seizures.

Wesleyan, which has about 2,900 full-time undergraduate students and 200 graduate students, also apparently dealt with MDMA-related issues last semester. As the Argus reported, the school’s Health Services Department emailed students on September 16 following a series of MDMA-related hospitalizations.

One former Wesleyan student from the class of 2011, who requested anonymity when discussing drug use, says the news is not surprising, given the prevalence of drugs on campus. “Anything you can imagine…would be readily available there,” the person says. “I don’t think at Wesleyan you need [a campus event] to take drugs. If it’s sunny, there’s probably a good percentage of people that are taking something.”

The campus activities calendar did not show any major events scheduled for Saturday or Sunday.

Another former Wesleyan student from the class of 2012, who also requested anonymity, says the drug culture at Wesleyan is comparable to that at similar schools. “It’s one of those things where, much like at those schools, you kind of have an understanding of where you can go to get it and who had it,” the person says. “If there’s a will there’s a way.”

www.newsweek.com weds Feb. 2015

When you smoke marijuana, there’s an almost immediate effect on your brain, sense of perception, and heart rate. There may be long-term effects as well.

 

The Effects of Marijuana on the Body

Marijuana comes from the Cannabis plant. The flowers, seeds, leaves, and stems of the plant must be shredded and dried before they can be used. Most people who use marijuana smoke it, but it can be mixed into food, brewed into tea, or even used in a vaporizer. One of the ingredients in marijuana is a mind-altering chemical called delta-9-tetrahydrocannabinol (THC).

When you inhale marijuana smoke into your lungs, it is quickly released into your bloodstream on its way to your brain and other organs. It takes a little longer to be absorbed when you eat or drink it.

The effects of marijuana on the body are immediate. Longer-term effects may depend on how you take it, how much you take, and how often you use it. Since its use has long been illegal in the United States, large-scale studies have been difficult to manage.

In recent years, the medicinal properties of marijuana are gaining acceptance in mainstream America. Medical marijuana is now legal in 23 states and the District of Columbia. THC and another ingredient called cannabidol (CBD) are the main substances of therapeutic interest. National Institutes of Health-funded research into the possible medicinal uses of THC and CBD is ongoing.

In addition to medicinal use, recent legislation has made marijuana a legal recreational drug in Colorado and Washington State. With the potential for increased recreational use, knowing the effects that marijuana can have on your body is as important as ever.

Respiratory System

 

Much like tobacco smoke, marijuana smoke is made up of a variety of toxic chemicals that can irritate your bronchial passages and lungs. If you’re a regular smoker, you’re more likely to wheeze, cough, and produce phlegm. You’re also at increased risk of bronchitis and lung infections. Marijuana may aggravate existing respiratory illnesses like asthma and cystic fibrosis.

Marijuana smoke contains carcinogens. It has the potential to elevate your risk of developing lung cancer. However, studies on the subject have had mixed results. According to the National Institute of Drug Abuse(NIDA), there is no conclusive evidence that marijuana smoke causes lung cancer. More research is needed.

Circulatory System

THC moves from your lungs into your bloodstream and throughout your body. Within minutes, your heart rate may increase by 20 to 50 beats per minute, according to the NIDA. That rapid heartbeat can continue for up to three hours. For people with heart disease, this faster heartbeat could raise the risk of heart attack.

One of the telltale signs of recent marijuana use is bloodshot eyes. They look red because marijuana causes blood vessels in the eyes to expand or dilate. Marijuana may help stop the growth of blood vessels that feed cancerous tumors.

 Central Nervous System

 

When you inhale marijuana smoke into your lungs, it doesn’t take long for THC to enter your bloodstream. From there, it is quickly transported to your brain and the rest of your organs. When you get marijuana from food or drink, it is absorbed a little more slowly.

THC triggers your brain to release large amounts of dopamine, a naturally occurring “feel good” chemical. That’s what gives you a pleasant “high.” It may heighten your sensory perception, as well as your perception of time. In the hippocampus, THC changes the way you process information, so your judgment may be impaired. It may also be difficult to form new memories when you’re high.

Changes also take place in the cerebellum and basal ganglia, upsetting your balance, coordination, and reflex response. All those changes mean that it’s not safe to drive.

Very large doses of marijuana or high concentrations of THC can cause hallucinations or delusions. According to the NIDA, there may be an association between marijuana use and some mental health problems like depression and anxiety, but more research is needed to understand the connection. In people who have schizophrenia, marijuana use can make symptoms worse.

When you come down from the high, you may be tired or feel a bit depressed. In some people, marijuana can cause anxiety. About nine percent of marijuana users develop an addiction, according to the NIDA. Symptoms of withdrawal may include irritability, insomnia, and loss of appetite.

In young people whose brains are not yet fully developed, marijuana can have a lasting impact on thinking and memory skills. If you use marijuana when pregnant, it can affect the brain of your unborn baby. Your child may be more prone to trouble with memory, concentration, and problem-solving skills.

THC can lower pressure in the eyes, which can ease symptoms of glaucoma for a few hours. According to theAmerican Academy of Ophthalmology, more research is needed to understand the active ingredients in marijuana and whether or not it’s a good treatment for glaucoma.

The pharmacologic effect of marijuana extends throughout the central nervous system. It is thought to ease pain and inflammation. It may also be of use in controlling spasms and seizures.

Digestive System

 

Smoking marijuana can cause stinging or burning in your mouth and throat. When you take oral THC, it is processed in your liver. Marijuana can ease nausea and vomiting. It can also increase appetite, which can be useful to people living with cancer or AIDS.

Immune System

Some research indicates that THC affects the immune system. Studies involving animals showed that THC might damage the immune system, making you more vulnerable to illness. Further research is needed.

The family of a Tulsa man who shot himself Saturday night in Keystone is blaming his suicide on his ingestion of edible marijuana candies.

It was completely a reaction to the drugs,” Kim Goodman said about her son Luke’s Saturday night suicide.

Luke Goodman’s death is now the third death in Colorado linked to marijuana edibles.

The 23-year-old college graduate was in the midst of a two-week ski and snowboard vacation with family members. Saturday afternoon he and his cousin, Caleb Fowler, took a bus from Keystone to Silverthorne where Fowler says they bought $78 worth of edibles and marijuana.

He was excited to do them,” Fowler told CBS4.

When the young men got back to Keystone, Fowler said they began ingesting the edible pot. He said his cousin favored some peach tart candies, each piece of candy containing 10 mg of the active ingredient in marijuana, the recommended dose for an adult consuming an edible.

But when Goodman consumed several and experienced no immediate effects he kept gobbling them up. “Luke popped two simultaneously” after the first two didn’t seem to do anything, said Fowler.

Then he said Goodman took a fifth candy, five times the recommended dose. His mother says her son likely didn’t see the warning on the back of the container which says, “The intoxicating effects of this product may be delayed by two or more hours … the standardized serving size for this product includes no more than 10 mg.”

Several hours later Fowler said his cousin became “jittery” then incoherent and talking nonsensically. “He would make eye contact with us but didn’t see us, didn’t recognize our presence almost. He had never got close to this point, I had never seen him like this,” Fowler said.

Fowler says Goodman became “pretty weird and relatively incoherent. It was almost like something else was speaking through him.” When family members left the condo Goodman refused to join them. After they left he got a handgun that he typically traveled with for protection, and turned it on himself.

Summit County Coroner Regan Wood says the preliminary cause of death is a self-inflicted gunshot wound. As for the impact of the marijuana edibles, she said, “That’s what we’ve heard consistently.” She said the impact the edibles had on Goodman will be more clear when toxicology results come back in a few weeks. “It’s still under investigation,” said Wood.

While definitive answers may be weeks away, Kim Goodman, Luke Goodman’s mother, told CBS4 she knows why her son took his own life. “It was 100 percent the drugs,” she said. “It was completely because of the drugs — he had consumed so much of it.” She said her son was well adapted, well-adjusted and had no signs of depression or suicidal thoughts. “It was completely out of character for Luke … there was no depression or anything that would leave us being concerned, nothing like that.”

Caleb Fowler echoed the feeling saying he fully believed the ingestion of so much marijuana laced candy triggered the suicide. “He was the happiest guy in the world. He had everything going for him.”

A year ago a Wyoming college student jumped to his death from a Denver hotel balcony after eating a marijuana cookie. Witnesses said Levy Thamba Pongi was rambling incoherently after eating the cookie. The Denver coroner ruled “marijuana intoxication” was a significant factor in Pongi’s death.

Richard Kirk of Denver faces first-degree murder charges stemming from the fatal shooting of his wife in Denver last year. Before her death his wife called 911 and said her husband had eaten marijuana candy and taken prescription medication and was hallucinating.

Kristine Kirk and Richard Kirk (credit CBS)

Luke Goodman’s family is now planning a memorial service for Friday in Tulsa. His mother says she remembers her last interaction with her son.

We both said ‘I love you’ and I said ‘Have a great week.’ ”

Kim Goodman told CBS4 she believes marijuana edibles should be removed from store shelves.

I would love to see edibles taken off the market … I think edibles are so much more dangerous.”

Source: CBS4 26th March 2015

Several independent scientific study’s using the latest Brain Scan technologies have confirmed without a doubt that marijuana abuse causes great harm and devastation to the human brain. Some of the the most recent studies reported are:

And now we have another important scientific study regarding the damage that marijuana abuse does to the human brain; by the Institute of Experimental Medicine of the Hungarian Academy of Sciences (KOKI).

Hungarian Scientists Prove Devastating Effect Cannabis Use Has On The Brain

Smoking cannabis dramatically reduces the number of molecules ensuring the fine-tuning of brain functions and can significantly interfere in the two-way communication between neurons, according to the result of research spanning several years carried out by the Institute of Experimental Medicine of the Hungarian Academy of Sciences (KOKI), published in the world’s most highly acclaimed neuroscience journal, Nature Neuroscience.

A statement issued by the Hungarian Academy of Sciences reminds that a study arriving at the same conclusion, authored by Hungarian neuroscientists István Katona and Tamás Freund, deputy chairman of the Academy (MTA) and head of the Institute of Experimental Medicine), had already been published in the U. S. Journal of Neuroscience in 1999.

According to the latest results of Mr. Katona’s team, recreational cannabis gravely interferes with the two-way communication between neurons.

The discovery, revealing the gravity of the effect cannabis use has on a molecular level, shocked both the researchers and their colleagues, Mr. Katona said, adding that decision-makers must seriously consider the permitted THC content of cannabis products during increasingly widespread legalisation of the drug.

Research has shown that the number of receptors in synapses receiving endocannabinoid molecules decreased dramatically, by around 85 per cent, after a six-day THC treatment, with total regeneration taking as long as six weeks, the MTA statement reads.

The primary authors of the study published in Nature Neuroscience are junior MTA researcher Barna Dudok, László Barna, leader of the Nikon-KOKI Microscope Centre and Italian guest researcher Marco Ledri.

Source: http://hungarytoday.hu

http://www.nature.com March 2015

Marijuana Use and Mania

 As the debate continues to rage over the possible risks or advantages of smoking marijuana, new research out of Britain’s Warwick University has found a “significant link” between marijuana use and mania, which can range from hyperactivity and difficulty sleeping to aggression, becoming delusional and hearing voices.

Published in the Journal of Affective Disorders, the study of more than 2,000 people suggested potentially alarming consequences for teenagers who smoke the herb. 

“Cannabis [marijuana] is the most prevalent drug used by the under-18s,” said lead researcher Dr Steven Marwaha. “During this critical period of development, services should be especially aware of and responsive to the problems cannabis use can cause for adolescent populations.”

Researchers examined the effect of marijuana on individuals who had experienced mania, a condition that can include feelings of persistent elation, heightened energy, hyperactivity and a reduced need for sleep. On the other side of the coin, mania can make people feel angry and aggressive with extreme symptoms including hearing voices or becoming delusional.

“Previously it has been unclear whether cannabis use predates manic episodes,” Dr Marwaha said. “We wanted to answer two questions:

1.      Does cannabis use lead to increased occurrence of mania symptoms or manic episodes in individuals with pre-existing bipolar disorder?

2.      “But also, does cannabis use increase the risk of onset of mania symptoms in those without pre-existing bipolar disorder?”

Dr Marwaha found that marijuana use tended to precede or coincide with episodes of mania. Representing what the lead researcher referred to as “a significant link,” there was a strong association with new symptoms of mania, suggesting that these are caused by marijuana use.

The researchers also found that marijuana significantly worsened mania symptoms in people who had previously been diagnosed with bipolar disorder. “There are limited studies addressing the association of cannabis use and manic symptoms which suggests this is a relatively neglected clinical issue,” Dr Marwaha said.

However, our review suggests cannabis use is a major clinical problem occurring early in the evolving course of bipolar disorder.   More research is needed to consider specific pathways from cannabis use to mania and how these may be effected by genetic vulnerability and environmental risk factors.”

These findings add to a body of previous studies that have linked marijuana to increased rates of mental health problems including anxiety, depression, psychosis and schizophrenia, and have suggested that the herb is addictive and opens the door to hard drugs.

A study which was published in the journal Neuroscience earlier this month nevertheless found that marijuana could be used to treat depression.

Scientists at the University of Buffalo’s Research Institute on Addictions said molecules present in marijuana could help relieve the depression resulting from long-term stress.

 Source: Journal of Affective Disorders Feb 2015

The main points are that it seems to target teens and college students and could easily be abused by underage persons. Powdered alcohol comes in packets and can be hidden from parents and  teachers, and sneaked into homes, schools, parties, bars, etc. The product may be abused by making it with less liquid (concentrating the alcohol), possibly snorting it. Underage drinking prevention is the main concern. Senator Flores is sponsoring senate bill 536 which would ban Palcohol/ powdered alcohol. Several other states have already banned it. AG Pam Bondi wants it banned. 

The makers of powdered alcohol, Palcohol, say it will be available for sale soon, but several states are already moving to ban the product. So far, Alaska, Delaware, Louisiana, South Carolina and Vermont have banned Palcohol – even though it is not yet available – and Florida, New York, Virginia and several other states are also considering a ban. Florida Attorney General Pam Bondi publicly announced that prohibiting the product is one of her legislative priorities this year. Bondi said, “We want to flat-out ban it in our state.” 

Palcohol is powdered alcohol, developed by Mark Phillips. Phillips said he wanted a “refreshing adult beverage” after engaging in activities such as biking or kayaking, where carrying large bottles of alcohol was not possible. He then spearheaded the creation of powdered alcohol. The product is available either in V powder, which is quadruple-distilled vodka, or R powder, which is premium Puerto Rican rum. Simply add water to the powder and you have an alcoholic beverage.

According to the Palcohol website, Palcohol will be sold in one ounce packages that contain the equivalent of one shot of alcohol each. Each bag is about 80 calories and is gluten-free. The website also notes that Palcohol is “for the legitimate and responsible enjoyment by lawful consumers.” The website explains it can be used by “outdoors enthusiasts such as campers, hikers and others who wanted to enjoy adult beverages responsibly without having the undue burden of carrying heavy bottles of liquid.” Or “adult travlers journeying to destinations far from home could conveniently and lawfully carry their favorite cocktail in powder format.”

Phillips is known in the wine community for producing and hosting the television show, “Enjoying Wine with Mark Phillips” and his book, “Swallow This: The Progressive Approach to Wine.” He also served as a wine expert to the Smithsonian.
However, Palcohol has faced difficulty almost from the beginning. Last April, the Alcohol and Tobacco Tax and Trade Bureau approved the product. However, 13 days later, it rescinded its approval and said it had issued the approval “in error.” The TTB announced, “Those label approvals were issued in error and have since been surrendered.”

As soon as the product hit the media headlines, criticism exploded over the possibility of minors gaining access to the product and users snorting the powdered alcohol. Palcohol dismisses these concerns and counters them on its web site. It notes that snorting the product is “painful” and “impractical…It takes approximately 60 minutes to snort the equivalent of one shot of vodka. Why would anyone do that when they can do a shot of liquid vodka in two seconds?”

The company also says it is not easier to “sneak into venues” and because it does not dissolve instantly, it can’t be used to spike a drink. Finally, the company says kids will not have easier access to powdered alcohol than to regular alcohol.
Unfortunately, however, early versions of the Palcohol web site did not help its cause. SB Nation reported that Palcohol’s website originally included the following wording:
Let’s talk about the elephant in the room….snorting Palcohol. Yes, you can snort it. And you’ll get drunk almost instantly because the alcohol will be absorbed so quickly in your nose. Good idea? No. It will mess you up. Use Palcohol responsibly.
Palcohol subsequently removed that wording and explained, “There was a page visible on this site where we were experimenting with some humorous and edgy verbiage about Palcohol. It was not meant to be our final presentation of Palcohol.”
Despite the controversy, the company says it will be available this Spring. It also is planning to introduce powdered cocktails, including Cosmopolitan, Mojito, and “Powderita,” which it says takes like a Margarita, and Lemon Drop.
However, so far, it is unclear where exactly you will be able to buy it.

 Source:  http://www.commdiginews.com/life/controversy-brews-over-powdered-alcohol-34291/   January 31, 2015 

Not magic at all of course, but a consequence of the fact that substance use problems are closely related to other problems which often develop at early ages when substance use is just not on the agenda. The 2010 English national drug strategy and corresponding public health plans seemed to recognise this, breaking with previous versions to focus attention on early years parenting in general, and particularly among vulnerable families. 

Though studies are few compared to approaches such as drug education in schools, this renewed emphasis on the early years has a strong theoretical rationale and some research backing. Child development and parenting programmes which do not mention substances at all (or only peripherally) have recorded some of the most substantial prevention impacts. Though mainly targeted at the early years, some extend to early teenage pupils and their families. The rationale for intervention rests partly on strong evidence that schools which develop supportive, engaging and inclusive cultures, and which offer opportunities to participate in school decision-making and extracurricular activities, create better outcomes across many domains, including non-normative substance use. As well as facilitating bonding with the school, such schools are likely to make it easier for pupils to seek and receive the support they need.

Understandably, such findings do not derive from random allocation of pupils to ‘good’ versus ‘bad’ schools, so are vulnerable to other influences the study was unable to account for. More convincing if more limited in intervention scope are studies which deliberately intervene and test what happens among young people randomly allocated to the focal intervention versus a comparator. An early example was a seminal Dutch drug education study of the early ’70s which had a profound impact in Britain. For the practitioners of the time, it was a warning about the dangers of the dominant ‘scare them’ approach, but it might as well have been a lesson about the approach which outperformed the warnings – classroom discussions which simply gave teenage pupils a structured chance to discuss the problems of adolescence, leaving it up to them whether drugs cropped up.

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Among the most prominent and promising of current approaches is the Good Behavior Game classroom management technique for the first years of primary schooling  illustration. Well and consistently implemented, by age 19–21 it was estimated that this would cut rates of alcohol use disorders from 20% to 13% and halve drug use disorders among the boys. In the Effectiveness Bank you can read about the study and read a practitioner-friendly account of the research from the researchers themselves. The same programme has been combined with parenting classes, leading to reductions in the uptake and frequency of substance use over the next three years.

Another primary school example is the Positive Action programme which focuses on improving school climate and pupil character development. In Hawaii and then the more difficult schools of Chicago, it had substantial and, in Chicago, lasting preventive impacts.

In Britain perhaps best known is the Strengthening Families Programme, a family and parenting programme which in the early 2000s impressed British alcohol prevention reviewers. It features parent-child play sessions, during which parents are coached in how to enjoy being with their children and to reinforce good behaviour. At first the accent is on building up the positives before tackling the more thorny issues of limit-setting and discipline. Though the potential seems great, later research has not been wholly positive, and the earlier results derived from the minority of families prepared or able to participate in the interventions and complete the studies.

A final example comes from Norway, where a study raised the intriguing possibility that taking measures to effectively reduce bullying in schools helps prevent some of the most worrying forms of substance use.

Isolating these and other similar studies is not possible via our normal search facilities, so we have specially identified and coded them. They may prove to be the future for drug prevention, as traditional drug education struggles for credibility as a prevention tool. See how this future is shaping up today by running this hot topic search.

Source:  www.findings.org     3rd March 2015

To go or not to go? That is the question when invited to take part in supposedly objective drugs conferences and television investigations, behind which  looms the constant presence of one Sir Richard Branson. Two seemingly flattering invitations to drugs policy events came my way this month.

The first was to be invited to a Home Affairs Select Committee event at the University of Cambridge’s Homerton College on March 12th.  At first sight, it felt a welcome recognition of my longstanding work in the field of drug addiction, and of my new recovery solutions service (DB Recovery Resources). Moreover, it seemed like an opportunity to guide and inform public opinion – even as far as the United Nations. But I was torn for days on whether to accept or not. Finally, I regretfully declined.

Why? The Home Affairs Select Committee’s invitation was entitled “The International Conference on Drugs Policy” and its findings at the end of the day were to be fed into the influential UNGASS, the United Nations General Assembly’s Special Session on world drug problems in 2016. Tempting. But a closer look raised concerns. What exactly was a Parliamentary select committee doing hosting a drugs policy conference? Why had they chosen deputy prime minister Nick Clegg who, at the time of my invitation, was scheduled to chair it? He is a recognised proponent of drugs legalisation, going so far as to include it in his election pledge.

So I was aware of the agenda and bias of the conference before I was invited.  The list of speakers spoke for itself. Every single speaker bar one  – Sarah Graham, an addiction therapist – turned out to be  a high-profile legalisation campaigner, several from organisations funded by the convicted insider trader and fomenter  George Soros. Only after I had publicised the biased agenda on my daily newsletter did HASC kindly invited me to attend. They also at the same time added a second ‘non-legalisation’ speaker to their invite list: Professor Neil McKeganey. But I could see it was still skewed. We would be the minority underdog against high-profile and well-funded legalisation campaigners, like Dr Julian Huppert MP, Baroness Molly Meacher, Roberto Dondisch from Mexico, Danny Kushlick of Transform, Professor David Nutt, who famously said taking ecstasy was less risky than horse riding, former policeman and cannabis activist Tom Lloyd, and last but not least Mike Trace, who was forced to resign his UN role when the Daily Mail revealed him to be the driving force behind an effort to disband the world’s anti-drug laws by stealth.

What chance would I have to support my colleagues? Would this be like National Treatment Agency meetings I had attended too many times in the past (before it was abolished)  where vested-interest findings and recommendations were written before the meeting and then presented as an impartial consensus of all those present – and absent?

Would it be like the self-styled United Kingdom Drug Policy Commission meetings (before it closed) which exploited the names of attendees as supporting its predetermined ‘consensus agreement’, when in reality there was a dearth of support? Was I confident that any anti-legalisation points would be included in the final report to UNGASS? That I sadly declined the invitation gives you the answer.

No. The worry is now that UNGASS may believe this Home Affairs Select Committee report, that UK taxpayers are unwittingly funding, to be impartial.  Better to blog, I thought, and hopefully open their eyes to the truth.

The second ‘flattering’  invitation was to appear on Channel 4’s Cannabis Live programme on 3 March. Although warned in advance about its inherent bias – it was funded by both C4 and Soros-supported organisations, and known legalisation proponents were booked as its speakers – I decided to accept in the hope I would be able to capture some airtime for anti-legalisation views.

(Declaration: my view is informed by the basic laws of supply and demand: increased availability leads to increased consumption. In addition there is, to my very real knowledge, so much disinformation about pot in the public domain that few people can make an informed choice). It was the right decision; although it was questionable whether there was a need for a programme experimenting ‘live’ with substances that are already known to have significant and very negative side effects. It was also worrying that Professor Nutt was  an “independent” scientific expert on it, given his obsession with cannabis legalisation and his well known insistence that it is less harmful than alcohol.

A plus turned out to be Jon Snow’s and Andrew Marr’s very negative experiences when skunk was tested on them. Perhaps that’s why presenter Snow carefully inched my neighbour off his seat to interview me, allowing time for me to make some pivotal points.  These were particularly in response to Branson’s call for regulation [legalisation] of cannabis as a solution to the world’s drug problems. I pointed out  that tobacco is regulated yet kills  more people than any other drug in the world;   that alcohol, benzos and methadone are all regulated but follow tobacco in killing more people each than illicit drugs.

I also pointed out that the first paper linking cannabis and psychosis was published 170 years ago –  in 1845  – so this is not new. All my points were transmitted unedited. A number of ‘silent’ audience members in Narcotics Anonymous introduced themselves and thanked me as we were leaving the studio.  It reminded  me of  US drug czar Michael Botticelli’s recent comment: “I do wish the recovery community was much more involved in anti-legalisation efforts.

However the trouble with Cannabis Live – posing as science when it was exhibitionist entertainment, as one distinguished former Professor of pharmacology commented to me afterwards  – is that it provided a launchpad for the differences between “beneficent” hash and “nightmarish” skunk to be exploited by the legalisation lobbyists. Their hidden agenda. It was worrying that the programme ignored the harms from hash (as opposed to skunk):  yet these include the risk of psychosis, behavioural changes, lack of motivation, lowering of IQ, lung cancer, mouth cancer, motor crashes, lowering of fertility (a mixed blessing) – and the fact that pregnant women using hash can give birth to addicted babies with a range of mental-health problems and medical problems, including leukaemia.

At a press conference the next day, billionaire legalisation campaigner Branson was still calling for regulation (legalisation of cannabis) as a solution despite all the downsides he’d witnessed at Cannabis Live. Of course he did not mention that tobacco is regulated and it kills more people than any other drug in the world, for the simple reason that it is the most widely used drug in the world.

In his cloud cuckoo land, the 80 per cent of cannabis users who use skunk would downgrade to the milder version if they were both legal. I don’t think so. It’s against human nature. Finally, it was left to David Nutt to round up the programme – with his extraordinary recommendation that skunk should remain low in the index of drug harms, in cannabis’s current place, while hash should plummet to the lowest ranking. Maybe he was too close to the skunk factory set up beside his artificial brain in the studio. Had anyone in the audience changed their mind about being pro- or anti-legalisation, asked Snow at the end of the programme? Not one hand went up. I leave you to decide whether this infotainment fulfilled Channel 4’s mission to “keep public service values to the fore”.

Source:   www.the Conservative Woman.co.uk    7th March 2015

Excessive alcohol consumption is a leading cause of premature death in the U.S. and responsible for one in every 10 deaths. The statistics that describe the ways in which we drink ourselves to death are staggering. A study published in the journal Preventing Chronic Disease found that nearly 70% of deaths due to excessive drinking involved working-age adults. The study also found that about 5% of the deaths involved people younger than age 21.  Moreover, excessive alcohol use shortened the lives of those who died by about 30 years. Yes, 30 years.

One strong factor that reinforces the popular culture surrounding drinking is the glamour of advertising. Researchers at the Johns Hopkins Bloomberg School of Public Health examined alcohol-advertising placements to determine whether the alcohol industry had kept its word to refrain from advertising targeting young people. This included television programs for which more than 30% of the viewing audience is likely to be younger than 21 years, the legal drinking age in every state.

The study found that alcohol related advertising increased by 71% in the last decade; this is largely attributed to exposure on cable television. That increase coincided with a reported upsurge of alcohol consumption by high school students. In conclusion, the study suggested that if the National Research Council/Institute of Medicine’s proposed threshold of 15% exposure to advertising was implemented, young viewers would see 54% fewer alcohol ads and society would see a correlating decrease in alcohol related deaths.

What about those “drink responsibly” admonitions on so many commercials? Federal regulations do not require responsibility statements in alcohol advertising. The alcohol industry’s voluntary codes for marketing and promotion emphasize responsibility, but they provide no definition for responsible drinking. So when you see the admonition to “drink responsibly” at the end of an alcohol-related television commercial, there is no idea given as to exactly what that may mean, particularly to someone under the legal drinking age.

David Jernigan, PhD, director of the Center on Alcohol Marketing and Youth at the Johns Hopkins Bloomberg School of Public Health said:

The contradiction between appearing to promote responsible drinking and the actual use of ‘drink responsibly’ messages to reinforce product promotion suggests that these messages can be deceptive and misleading.”

Youth who start drinking before age 15 years are five times more likely to develop alcohol dependence or abuse later in life than those who begin drinking at or after age 21 years according to the Centers for Disease Control and Prevention.

Alcohol advertising influences many people across a wide range of demographics. Regardless of the warning labels on alcohol containers, community prevention programs and general public knowledge of the risks of excessive alcohol consumption, people continue to drink in health-damaging ways. Drinking in public, at sporting events, in parks, during celebrations, etc., is firmly embedded in society as acceptable behavior. At the same time, the large number of alcohol related deaths among all age groups is a concern, especially when this drinking behavior is generally developed while individuals are underage.

Alcohol use is a major public health problem that can lead to social, financial, and health related setbacks and premature death. Talk to health care professional if you or someone close to you is struggling with excessive alcohol consumption.

Source: www.psychcentral.com/science-addiction/2014/10

The polarized legalization debate leads to exaggerated claims and denials about pot’s potential harms. The truth lies in between.

Pretty much everyone who has spent time smoking marijuana knows at least one diehard stoner. The guy whose eyes are always red, the girl who doesn’t use the term “wake and bake” ironically, the person who just can’t seem to ever get it together. These heavy smokers might work at a low-level job or they may be unemployed—but everyone who knows them well knows that they are capable of much more, if only they had any ambition.

Is this really addiction? I believe that it is (and I don’t think that’s an argument against legalization). In fact, the reasons why marijuana is addictive elucidate the true nature of addiction itself.  Addiction is a relationship between a person and a substance or activity; addictiveness is not a simple matter of a drug “hijacking the brain.” In fact, with all potentially addictive experiences, only a minority of those who try them get hooked—and people can even become addicted to apparently “nonaddictive” things, like carrots. Addiction depends on learning, context and psychology, not just neurotransmitters.

With two states having already legalized recreational marijuana use and several more considering doing so, understanding the nature of addiction is more important than ever. Partisans on both sides of the debate have made extreme claims here; some legalizers saying there’s no such thing as marijuana addiction, while some prohibitionists claim “cannabis as addictive as heroin.”

Our concepts of addiction, however, come primarily from cultural experience with alcohol, heroin and, later, cocaine. No one has ever argued that opioids like heroin don’t have the potential to cause addiction because the withdrawal symptoms—vomiting, shaking, pallor, sweating and diarrhea—are objectively measurable. Opioids cause physical dependence that is evident when they become unavailable. The same is true for alcohol, where withdrawal is even more severe and can sometimes even be deadly.

So early researchers focused on these measurable symptoms related to alcoholism and opioid addictions in defining addiction: Using a drug could lead to becoming tolerant to it, tolerance could lead to dose escalation, which could in turn lead to physical dependence, and then the addiction could be driven by the need to avoid the painful symptoms of withdrawal. It was simple and physical.

In this view, however, cocaine and marijuana were not “really” addictive. While people can experience withdrawal symptoms like irritability, depression, craving and sleep problems when quitting these drugs, these are much more subjective and therefore can be dismissed as “psychological” rather than physical. You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

And since most of us like to believe that we have much more control over our minds than we do over physical symptoms, “psychological” addiction is seen as far less serious than the “physical” type. It’s the remnants of this kind of thinking that mainly underlie the idea that marijuana addiction doesn’t exist. Unfortunately, that view of addiction is stuck in the 1970s.

In the 1980s—ironically, not long after Scientific American caused a big controversy by arguing that snorted cocaine is no more addictive than eating potato chips—entrepreneurs began marketing a ready-made smokeable form of the drug. The birth of crack shattered the idea that “physical” dependence is more serious than psychological dependence because people with cocaine addictions don’t vomit or have diarrhea when they quit; while they may appear desperate, it’s not in the physically obvious way of heroin or alcohol withdrawal. And so, if you are going to argue that marijuana is not addictive because you don’t get sick when you quit, you also have to argue the same for crack.

In the 1970s view, cocaine and marijuana were not “really” addictive: You might really want coke or pot, but you didn’t need it like a real junkie, the thinking went.

Good luck with that one, I say. Clearly, crack-addicted people are every bit as compulsive as those with heroin problems—and their criminal involvement if they can’t afford the drug is at least equally likely, though not as common as has been claimed. Crack dealt a deathblow to the “psychological” vs. “physical” distinction—and if it hadn’t, neuroscience was creeping up to show that the psychological and the physical aren’t exactly distinct anyway.

In the ‘70s and ‘80s, researchers also began recognizing that simply detoxing heroin addicts—getting them through the two-week period of intense physical withdrawal symptoms—is not effective treatment. If heroin addiction was driven primarily by the need to avoid withdrawal, addicted people should be out of the woods after they complete cold turkey. But as those of us who have been through it know, that is far from the hardest part.

While kicking heroin isn’t fun, staying off it in the long run is the problem—those “mere” psychological cravings are what drive addiction. Physical dependence isn’t the main problem; it isn’t even necessary. Indeed, we now know that you can actually have physical dependence without any addiction at all: There are some blood pressure medications, for example, that can have deadly withdrawal symptoms if not tapered properly, but people on these meds don’t crave them even though they are quite dependent. Similarly, antidepressants like Paxil have physical withdrawal symptoms, but because they don’t produce a high, you don’t see people robbing drug stores to get them.

So what is addiction, then, if tolerance, withdrawal and physical dependence aren’t essential to it? All of these facts point to one definition that can sum up the problem: Addiction is compulsive use of a substance or engagement in a behavior despite negative consequences. (Put more in neuroscience, addiction is a learned distortion in the brain’s motivational systems that make us persist in pursuing things linked to evolutionary fitness like food and sex.) Anything that causes pleasure via these systems—and that’s basically anything that is possible to enjoy—can be addictive to some person at some time. And that includes marijuana (and, for that matter potato chips).

This doesn’t mean that marijuana addiction is necessarily as severe as cocaine, heroin or alcohol addiction—in fact, it typically isn’t. If given the choice, most families would vociferously prefer having a member addicted to marijuana rather than to cocaine, heroin or alcohol. The negative consequences associated with marijuana addiction tend to be subtler: lost promotions, for example, rather than lostjobsworse relationships, not no relationships. And of course, no risk of overdose death.

Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities.

But this is also what can make it insidious. Marijuana addiction may quietly make your life worse without ever getting bad enough to seem worth addressing; it may not destroy your life but it may make you miss opportunities. With any pattern of regular drug use, it’s important to continually track whether the risks outweigh the benefits, keeping in mind that addiction itself may distort this calculation. This is especially true with marijuana.

However, as with all other drugs, only a minority of marijuana users ever struggle with addiction. Research suggests that about 10% get hooked—and on average, marijuana addiction lasts six years. Even more than other addictions, marijuana addiction seems to be driven by self-medication of mental health problems—90% of people with marijuana addiction also have another addiction or mental illness, typically alcoholism or antisocial personality disorder.

This suggests that exposing more of the population to marijuana won’t necessarily increase the addicted population. First, people with antisocial personality disorder, by definition, tend not to be law abiding, so most have probably already tried it. Second, the percent of people with other pre-existing mental illness will not change because marijuana becomes legal—in fact, in the UK, when they reversed their prior liberalization of marijuana law because of fears related to increased schizophrenia, psychosis rates actually went up. (The link probably wasn’t causal, but it does suggest that legal crackdowns on cannabis don’t prevent related psychosis).

If some people with alcohol, cocaine or heroin addiction switch to marijuana instead, overall harm would be reduced. As I and others have been reporting at least since 2001, using marijuana as an “exit” drug is a real phenomenon, both in cocaine and opioid addiction.

When we consider the risks of various substances, we tend to do so in isolation—but that’s not how choices are made in the real world. Most people would rather their partners have no addictions—but again, some are clearly worse than others. Marijuana craving is rarely as severe as crack craving, as is obvious.

Still, like anything that can be pleasurable, marijuana can be addictive. This doesn’t mean all addictions are the same or that it is as addictive as the currently legal drugs alcohol and tobacco—the data shows it is less so.

Pretending it can’t do any harm at all, however—or that there aren’t people who are addicted to it—does no one any good. If we want better drug policy, as with other types of recovery, we need to avoid denial.

Maia Szalavitz is one of the nation’s leading neuroscience and addiction journalists, and a columnist at Substance.com. She has contributed to Timethe New York TimesScientific American Mindthe Washington Post and many other publications. She has also published five books, including Help at Any Cost: How the Troubled-Teen Industry Cons Parents and Hurts Kids (Riverhead, 2006), and is currently finishing her sixth, Unbroken Brain, which examines why seeing addiction as a developmental or learning disorder can help us better understand, prevent and treat it. Her last column for Substance.com was about why the oft-documented fact that most people age, or grow, out of substance misuse is not common knowledge.

Source: www.substance.com 15th October 2014

Can marijuana use put offspring at heightened risk for opiate addiction, even if the use stops before the offspring are conceived? Recent animal research by NIDA-supported scientists suggests that the answer may be yes.

Dr. Yasmin L. Hurd and colleagues at the Icahn School of Medicine at Mount Sinai in New York City showed that rats whose parents had been exposed as adolescents to the main psychoactive ingredient in marijuana sought heroin more vigorously than the offspring of unexposed animals. Although more research is needed to confirm and explain the findings, they are consistent with other studies suggesting that a parent’s history of drug use, even preconception, may affect a child’s brain function and behavior.

Lasting Imprint

Scientists have known for a while that drugs of abuse produce some of their effects epigenetically—that is, by increasing or decreasing the rates at which the body’s genetic machinery produces certain proteins. Researchers recently reported that some epigenetic changes produced by cocaine appear to be inherited and affect the behavior of subsequent generations. In that experiment, rats whose parents had been exposed to cocaine responded differently when introduced to the drug than did rats whose parents had not been exposed.

Dr. Hurd and colleagues hypothesized that rats whose parents were exposed as adolescents to the main psychoactive ingredient in marijuana (delta-9 tetrahydrocannabinol, or THC) would inherit epigenetic changes that would alter their responses to heroin. To test the hypothesis, the researchers injected adolescent male and female rats with THC for 3 weeks on an intermittent schedule (1.5 milligram per kilogram of body weight every 3 days) that corresponds to the amounts consumed by a typical recreational marijuana user. They waited 2 to 4 weeks for the drug to wash out of the rats’ bodies, then paired and mated them.