Promoting Good Practice In Prevention
The implications of these findings on the propagation of cannabis genotoxicity and epigenotoxicity to the next generation extremely significant.
Prior to this research, the field was aware of the effects in the male but the work in females is more recent.
To access the full document:
A recent study published in the Journal of Studies on Alcohol and Drugs discusses the history and current state of psychedelic research for the treatment of substance abuse disorders (SUDs).
Psychedelics are consciousness-altering drugs, some of which include lysergic acid diethylamide (LSD), dimethyltryptamine (DMT), psilocybin, and mescaline. Methylenedioxymethamphetamine (MDMA) and ketamine are also considered psychedelics; however, these drugs have different mechanisms of action.
Although psychedelics have been exploited for centuries to induce altered states of consciousness, their use, as opposed to their abuse, has largely been unexplored in modern medicine. In fact, several studies have indicated the potential utility of psychedelics for individuals who have mental illness due to traumatic experiences, false beliefs, and unhealthy behavioral patterns, such as posttraumatic stress disorder (PTSD) and depression.
The recent coronavirus disease 2019 (COVID-19) pandemic led to global changes in the use of methamphetamine, alcohol, and cannabis, as well as a significant increase in opioid overdoses in the United States. Thus, another promising application of psychedelics is their potential use for treating SUDs.
However, restrictive policies, poor funding, lack of equitable and diverse recruitment and access, as well as the multiplicity of small-scale psychedelic research programs have prevented researchers from effectively investigating the effects of psychedelics in the treatment of SUDs.
Over the past seven decades, researchers have become increasingly interested in examining the potential use of psychedelics in traditional medicine. Despite federal policies banning recreational drug use, researchers have elucidated some of the biological effects of psychedelics on the central nervous system (CNS) and their potential role in the treatment of SUDs. Nevertheless, there remains a lack of well-controlled multi-center trials and systematic reviews in this area.
As researchers continue to examine the pharmacological potential of these drugs, it is crucial to address their addiction and abuse potential, the legalization of recreational drugs, and the attempts of pharmaceutical companies to introduce high-selling psychedelics as therapies for mental illness.
Psychedelics like ayahuasca, Peyote, and psilocybin-containing mushrooms have been used throughout history by traditional healers and indigenous communities for both spiritual and health purposes. By recognizing these contributions, researchers can benefit from the potential benefits of traditional usage patterns while investigating the use of these drugs for treating SUDs and other mental health disorders.
For example, a hybridized SUD therapy program in Peru utilizes ayahuasca to treat alcohol and drug use. At one year following treatment, reduced depression and anxiety, higher quality of life, and reduced severity of addiction have been reported.
One notable contribution is the acknowledgment that key experiences of treatment participants might provide more insight than the search for putative “active ingredients” of interventions as complex as psychedelic-assisted treatment.”
Psychedelic use, specifically ayahuasca use, is closely linked to vomiting as a means of purging the body. This is reported to have spiritual, Amazonian, and clinical benefits.
The optimal approach to psychedelic-assisted treatment involves mutual respect for and recognition of the value of both traditional and modern applications. Thus, mixed-methods research is crucial, as traditional approaches may help identify a better therapeutic agent or program than traditional approaches to identifying and isolating active ingredients.
However, it is essential to evaluate and quantify the success rates of traditional approaches to psychedelic use, as well as elucidate the biological mechanisms that may contribute to their therapeutic effects. Researchers must recognize and credit traditional history and practices throughout these efforts to protect these cultures from being exploited, ignored, and suppressed by pharmaceutical industries.
The rush to patent processes in psychedelic treatments of addiction and other psychiatric conditions reflects the enormous greed of private commercial entities to benefit financially from vulnerable patients in need of effective therapies.
Thus, regulatory control of psychedelic therapies is vital to establish rigorous research standards that can lead to the generation of sufficient evidence in this area. Without this type of overview, private corporate interests may seek to exploit governmental support for crucial research needed to address these mental health issues.
Source: https://www.news-medical.net/news/20240828/Psychedelics-A-new-hope-for-substance-abuse-treatment.aspx
A 48-year-old woman in California contracted a potentially deadly meningitis infection in 2016 from smoking her favourite medical marijuana strain three to six times a day, according to a British Medical Journal case study report published last month.
The infection came from a fungus, called cryptococcus, that most people contract from inhaling contaminated dust or eating food that mouse faeces have touched.
Meningitis is the most common illness to develop from exposure to cryptococcus, and causes potentially fatal inflammation in the brain and spinal cord.
Dr Bryan Shapiro, who treated the woman, says that cannabis smokers in California should be sure to know where their marijuana came from, especially if their immune systems are compromised in any way, as meningitis could be lethal for them.
The unnamed woman’s sister brought her to the Cedars-Sinai Medical Center (CSMC) in Los Angeles, California. She had ‘strange symptoms,’ Dr Shapiro said, including being dizzy, tired, struggling to recall even her own name, and behaving aggressively.
In fact, her behaviour had become so erratic that she was fired from her job as an administrative assistant before being admitted to the hospital.
At CSMC, the emergency room team could not figure out what was ailing the otherwise healthy patient. When she assaulted a nurse, the team called in the psychiatric department.
‘We thought it might be catatonia [abnormal movement triggered by mental issues], and it took us some time to rule out a psychiatric illness,’ Dr Shapiro said.
Still unable to diagnose her, they took a sample of her brain fluid, which tested positive for Cryptococcus neoformans, ‘a rare fungal infection usually only seen in people with late stage HIV or transplant patients,’ Dr Shapiro explained.
But the woman was otherwise in reasonably good health. The only things that stood out in her medical history were high blood pressure and a significant marijuana habit.
‘She said she had smoked between three and six marijuana blunts about daily since her teenage years,’ Shapiro said, ‘I’ve never known a patient who smokes that heavily and wondered if there could be a link between her heavy cannabis use for a lifetime.’
They treated the woman for meningitis, but if they hadn’t done so ‘prudently…there is a strong possibility she would have died, she was very, very severe at the time we saw her,’ he says.
As she was recovering, Dr Shapiro and his team investigated her favourite medical marijuana dispensary in Bakersfield where she always purchased one of the shop’s cheaper strains, which was grown locally outdoors.
DNA sequencing of nine samples revealed small amounts of the rare fungus.
‘That lent credibility to the idea that the cryptococcus in the cannabis may have caused the woman’s systemic malfunction, and smoking might actually predispose someone to invasive fungal infection,’ Dr Shapiro said.
Fungus spores are actually grow on cannabis quite commonly.
A study conducted last year identified evidence of mould, pesticides and other contaminants on much of the weed grown in the state.
More than 90 percent of the marijuana plants tested were contaminated with pesticides, and crops from 20 farms were positive for mold.
The soil in Bakersfield and the surrounding Central Valley area is known to be a breeding ground for another fungus called Coccidioides immitis, which is to blame for a slew of cases of an infection, dubbed ‘valley fever.’
Valley fever is a potentially sever lung infection and its symptoms can mirror those of the flu that has killed nearly 100 people in California since the start of the year.
The prevalence of the valley fever fungus – which causes infection when it is inhaled – in the area ‘raised suspicions’ for Dr Shapiro and his team that the soil could harbour cryptococcus as well.
The spores of these fungi are very heat resistant, so they survive even as the weed they are attached to is smoked.
Even so, it is rare for someone with an otherwise healthy immune system to get such an infection, and Dr Shapiro points to other research that has suggested that THC – the psychoactive component of weed – may itself suppress the immune system.
‘So, the more you smoke, the greater the exposure [to the fungus and] the more likely it is that your body is unable to fight off the infection,’ he says.
Dr Shapiro was unable to disclose the name of the particular dispensary that the contaminated marijuana came from, but said that it is under investigation.
This case was the first of its kind that Dr Shapiro or his team had seen, so it’s too early to make formal recommendations, he says, but advises: ‘Make sure you know where your marijuana is coming from.
‘I recommend buying indoor-grown strains and, for people who are immuno-compromised like those with HIV or other infections, I would recommend avoiding inhaled marijuana products,’ he says. Edible products, on the other hand are probably safer for consumption.
Source: https://www.dailymail.co.uk/health/article-5327367/California-woman-caught-meningitis-CANNABIS.html January 2018
Overdose deaths are a widespread problem North Carolinians have been struggling to combat in recent years.
According to the state health department, American Indian/Indigenous and Black communities are the most at risk. From 2019 to 2021, both populations saw reports of overdoses more than double. The number of overdoses is up 117% for the Indigenous population and 139% for Black people. Overdoses increased 53% among white people during the same timeframe.
The problem has only been exacerbated by a rise in illegally manufactured fentanyl.
In Wake County in 2023:
The danger of fentanyl not only lies in its widespread availability state-wide, but in the drug’s potency itself.
When someone’s lungs aren’t told to expand and contract properly, their body starts to lack sufficient oxygen supply.
Without enough oxygen supply, the brain can shut down within minutes. This can then lead to permanent brain damage or death once other organs stop functioning properly due to a lack of blood flow.
The medication naloxone has emerged as a powerful antidote for opioid overdoses.
The CDC reports that naloxone can reduce the effects of several opioids including, fentanyl, morphine, heroin, oxycodone, methadone, hydrocodone, codeine and hydromorphone.
The medication allows for the body’s response system to switch back ‘on’ and restore normal breathing.
During the same timeframe, the state tells WRAL News there were nearly 17,000 overdose reversal reports.
Naloxone will not harm someone who hasn’t taken an opioid, so it is recommended even when it is unclear what kind of drug a person has taken.
More than one dose may be needed because some opioids, like fentanyl, can take a stronger hold on the opioid receptors.
Other states, including Arizona and San Franscico, have since molded similar programs on North Carolina’s success.
Source: https://www.wral.com/amp/21525957/ July 2024
Illicit use of the veterinary tranquilizer xylazine continues to spread across the United States. The drug, which is increasingly mixed with fentanyl, often fails to respond to the opioid overdose reversal medication naloxone and can cause severe necrotic lesions.
A report released by Millennium Health, a specialty lab that provides medication monitoring for pain management, drug treatment, and behavioral and substance use disorder treatment centers across the country, showed the number of urine specimens collected and tested at the US drug treatment centers were positive for xylazine in the most recent 6 months.
As previously reported by Medscape Medical News, in late 2022, the US Food and Drug Administration (FDA) issued a communication alerting clinicians about the special management required for opioid overdoses tainted with xylazine, which is also known as “tranq” or “tranq dope.”
Subsequently, in early 2023, The White House Office of National Drug Control Policy designated xylazine combined with fentanyl as an emerging threat to the United States.
Both the FDA and the Drug Enforcement Administration have taken steps to try to stop trafficking of the combination. However, despite these efforts, xylazine use has continued to spread.
The Millennium Health Signals report showed that the greatest increase in xylazine use was largely in the western United States. In the first 6 months of 2023, 3% of urine drug tests (UDTs) in Washington, Oregon, and California were positive for xylazine. From November 2023 to April 2024, this rose to 8%, a 147% increase. In the Mountain West, xylazine-positive UDTs increased from 2% in 2023 to 4% in 2024, an increase of 94%. In addition to growth in the West, the report showed that xylazine use increased by more than 100% in New England — from 14% in 2023 to 28% in 2024.
Nationally, 16% of all urine specimens were positive for xylazine from late 2023 to April 2024, up slightly from 14% from April to October 2023.
Xylazine use was highest in the East and in the mid-Atlantic United States. Still, positivity rates in the mid-Atlantic dropped from 44% to 33%. The states included in that group were New York, Pennsylvania, Delaware, and New Jersey. East North Central states (Ohio, Michigan, Wisconsin, Indiana, and Illinois) also experienced a decline in positive tests from 32% to 30%.
The South Atlantic states, which include Maryland, Virginia, West Virginia, North and South Carolina, Georgia, and Florida, had a 17% increase in positivity — from 22% to 26%.
From April 2023 to April 2024 state-level UDT positivity rates were 40% in Pennsylvania, 37% in New York, and 35% in Ohio. But rates vary by locality. In Clermont and Hamilton counties in Ohio — both in the Cincinnati area — about 70% of specimens were positive for xylazine.
About one third of specimens in Maryland and South Carolina contained xylazine.
“Because xylazine exposure remains a significant challenge in the East and is a growing concern in the West, clinicians across the US need to be prepared to recognize and address the consequences of xylazine use — like diminished responses to naloxone and severe skin wounds that may lead to amputation — among people who use fentanyl,” said Millennium Health Chief Clinical Officer Angela Huskey, PharmD, in a press release.
The Health Signals Alert analyzed more than 50,000 fentanyl-positive UDT specimens collected between April 12, 2023, and April 11, 2024. Millennium Health researchers analyzed xylazine positivity rates in fentanyl-positive UDT specimens by the US Census Division and state.
Source: https://www.medscape.com/viewarticle/emerging-threat-xylazine-use-continues-spread-across-united-2024a1000d1h July 2024
Studies examining lifestyle and cognitive decline often use healthy lifestyle indices, making it difficult to understand implications for interventions. We examined associations of 16 lifestyles with cognitive decline. Data from 32,033 cognitively-healthy adults aged 50-104 years participating in prospective cohort studies of aging from 14 European countries were used to examine associations of lifestyle with memory and fluency decline over 10 years. The reference lifestyle comprised not smoking, no-to-moderate alcohol consumption, weekly moderate-plus-vigorous physical activity, and weekly social contact. We found that memory and fluency decline was generally similar for non-smoking lifestyles. By contrast, memory scores declined up to 0.17 standard deviations (95% confidence interval= 0.08 – 0.27) and fluency scores up to 0.16 standard deviations (0.07 – 0.25) more over 10 years for those reporting smoking lifestyles compared with the reference lifestyle. We thus show that differences in cognitive decline between lifestyles were primarily dependent on smoking status.
Source: https://www.nature.com/articles/s41467-024-49262-5 June 2024
By Shahirah Hamid: Senior Commissioning Editor at 360info Southeast Asia
26 June 2024
Drugs are at the root of immeasurable human suffering.
Drug use eats away at people’s health and wellbeing. Overdoses claim hundreds of thousands of lives every year.
Meanwhile, synthetic drugs are becoming more lethal and addictive, and the illicit drug market is breaking production records, feeding crime and violence in communities around the world.
At every turn, the most vulnerable people — including young people — suffer the worst effects of this crisis. People who use drugs and those living with substance abuse disorders are victimized again and again: by the drugs themselves, by stigma and discrimination, and by heavy-handed, inhumane responses to the problem.
As this year’s theme reminds us, breaking the cycle of suffering means starting at the beginning, before drugs take hold, by investing in prevention.
Evidence-based drug prevention programmes can protect people and communities alike, while taking a bite out of illicit economies that profit from human misery.
When I was Prime Minster of Portugal, we demonstrated the value of prevention in fighting this scourge. From rehabilitation and reintegration strategies, to public health education campaigns, to increasing investment in drug-prevention, treatment and harm-reduction measures, prevention pays off.
On this important day, let’s recommit to continuing our fight to end the plague of drug abuse and trafficking, once and for all.
Source: https://www.unodc.org/islamicrepublicofiran/en/the-secretary-general-message-on-the-occasion-of-the-international-day-against-drug-abuse-and-illicit-trafficking.html
The epidemic began about 25 years ago when drug and healthcare companies began to enthusiastically promote these very-addictive chemicals, claiming they were effective in relieving suffering and did not cause dependency.
A study published this past May by researchers at the Johns Hopkins Bloomberg School of Public Health found that one out of every three Americans have lost someone – a relative or a friend – to an opioid or other drug overdose. The US National Institute on Drug Abuse found that more than 320,000 American children have lost parents from overdoses in the past decade, and the annual financial costs to the US of the opioid crisis is $1 trillion.
Incredibly, Israelis today are the largest consumers per capita in the world of opioids, and an untold number of them are addicted or have already died. No one knows the fatality figures here, as the causes of death are described as organ failures, seizures, heart attack or stroke – not listed by what really caused them.
Is this another example of a “misconception” – wishful thinking on the scale of the belief by the government, the IDF, and the security forces that Hamas would “behave” if regularly paid off with suitcases full of cash? Is Israel headed to where the US already is? Perhaps. What is clear is that our various health authorities now have to somehow clean up the opioid mess.
The scandal has been indirectly embarrassing for Israel because among the most notorious companies involved in the opioid disaster is the Sackler family, who own the Purdue Pharma company that manufactured and promoted the powerful and addictive opioid OxyContin and who are now drowning in huge lawsuits. Tel Aviv University’s Medical Faculty that was for decades known as the Sackler Faculty has deleted it from its name.
Last year, the Knesset Health Committee met to discuss the rise in opioid consumption here, with testimony from Ben-Gurion University of the Negev School of Public Health dean and leading epidemiologist Prof. Nadav Davidovitch, who is also the principal researcher and chairman of the Taub Center Health Policy Program. He stressed that inappropriate use of strong pain medications leads to addiction and other severe negative consequences and noted that while most of the rise in consumption is among patients of lower socioeconomic status, the well-off are also hooked. Davidovitch called for the launching of serious programs to treat addicted Israelis based on the experiences of other countries with the crisis.
Opioids attach themselves to opioid-receptor proteins on nerve cells in the brain, gut, spinal cord, and other parts of the body. This obstructs pain messages sent from the body through the spinal cord to the brain. While they can effectively relieve pain, they can be very addictive, especially when they are consumed for more than a few months to ease acute pain, out of habit, or from the patients’ feeling of pleasure (they make some users feel “high”). Patients who suddenly stop taking them can sometimes suffer from insomnia or jittery nerves, so it’s important to taper off before ultimately stopping to take them.
The Health Ministry was forced in 2022 to alter the labels on packaging of opioid drugs to warn about the danger of addiction after the High Court of Justice heard a petition by the Physicians for Human Rights-Israel and the patients’ rights organization Le’altar that claimed the ministry came under pressure from the pharmaceutical companies to oppose this. After ministry documents that showed doctors knew little about the addictions caused by opioids were made public by the petitioners, psychiatrist Dr. Paola Rosca – head of the ministry’s addictions department – told the court that the synthetic painkillers cause addiction. She has not denied the claim that the ministry was squeezed by the drug companies to oppose label changes.
In an interview with The Jerusalem Post, Prof. Pinhas Dannon – chief psychiatrist of the Herzog Medical Center in Jerusalem and a leading expert on opioid addiction – noted that anyone with a medical degree can prescribe synthetic painkillers to patients. “There is no special prescription, no time limit, no supervision,” he said.
“A person who undergoes surgery who might suffer from serious pain is often automatically given prescriptions for opioids – not just one but several,” Dannon revealed. “Nobody checks afterwards whether the patient took them, handed them over to others (for money or not), whether they took several kinds at once, or whether they stopped taking them. They are also prescribed by family physicians, orthopedists treating chronic back pain, urologists, and other doctors, not only by surgeons.”
Dannon, who runs a hospital clinic that tries to cure opioid addiction, said there are only about three psychiatric hospitals around the country that have small in-house departments to treat severely addicted patients. “Not all those addicted need inpatient treatment, but when we build our new psychiatry center, we would be able to provide such a service.”
Since opioids are relatively cheap and included in the basket of health services, the four public health funds that pay for and supply them have not paid much attention. Once a drug is in the basket, it isn’t removed or questioned. Only now, when threatened by lawsuits over dependency, have the health funds begun to take notice and try to promote reductions in use.
Dannon declared that the health funds, hospitals, and pharmacies must seriously supervise opioid use by tracking and be required by the ministry to report who is taking them, how much, what ages, and for how long. Opioids are meant for acute pain, not for a long period. “The Health Ministry puts out fires but is faulty in prevention and supervision,” he said.
A Canadian research team has just conducted a study at seven hospital emergency departments in Quebec and Ontario to determine the ideal quantity of prescription opioids to control pain in discharged patients and reduce unused opioids available for misuse.
They recommended that doctors could adapt prescribing quantity to the specific condition causing pain, based on estimates to alleviate pain in 80% of patients for two weeks, with the smallest quantity for kidney or abdominal pain (eight tablets) and the highest for back pain (21 tablets) or fractures (24 tablets), and add an expiry date for them. Since half of participants consumed even smaller quantities, pharmacists could provide half this quantity to further reduce unused opioids available for misuse.
Rosca, who was born in Italy where she studied medicine and came on aliyah in 1983, has worked in the ministry since 2000; in 2006, she became head of the addictions department.
“In Italy, every psychiatrist must learn about alcohol and other drug addictions including opioids,” she said. “Here, there is no mandatory course in any medical school on the subject. We tried to persuade the Israel Medical Association and its Scientific Council, which decides on curricula and specializations, but we didn’t succeed. Maybe now, in the face of the crisis, it will change its mind. We run optional courses as continuing medical education for physicians who are interested.”
Her department wanted pharmacists to provide electronic monitoring of opioid purchases, but “the Justice Ministry opposed it on the grounds that it would violate privacy. I wasn’t asked for my opinion.”
She concedes that the ministry lacks statistics on the number of addicted people, and Arabs have been excluded from estimates until now. “We’re doing a study with Jerusalem’s Myers-JDC-Brookdale Institute to find out how many. Some say one percent, some say five percent. We hope that by December, we will get more accurate figures. Before the COVID-19 pandemic, the ministry set up a committee on what to do about opioids, but its recommendations were never published, and there was no campaign,” Rosca recalled.
In 1988, the government established the statutory Anti-Drug Authority that was located in Jerusalem’s Givat Shaul neighborhood. It was active in fighting abuse and shared research with foreign experts, but seven years ago, its name was changed to the National Authority for Community Safety and became part of the Ministry for National Security, losing much of its budgets – and, according to observers, its effectiveness as well.
The Health Ministry used to be responsible for setting up and operating clinics for drug rehabilitation, but it handed this over in 1997 to a non-profit organization called the Israel Public Health Association, which employs numerous former ministry professionals. Its director-general, lawyer Yasmin Nachum, told the Post in an interview that the IPHA is very active in fighting drug addiction.
“Israel can’t deny anymore that we are in a worrisome opioid epidemic like that in the US: We are there,” he said. “We see patients every day. Some used to take heroin and other street drugs, but with the easy access and low price, they have switched to opioids. If they are hospitalized for an operation and don’t use all the prescriptions they are given, they sell them to others. We want to have representation in every hospital to warn doctors and patients.”
Of a staff of 1,100, the IPHA has 170 professionals – narcotics experts, social workers, occupational therapists, and others working with 3,000 addicted patients every day. Its other activities include mental health, ensuring safety of food and water, and rehabilitation.
“We work in full cooperation with the ministry,” Nachum said. “Our approach is that when opioids are taken for pain for as long as six months, it’s the time to stop taking them. The doctors provide addicted patients with a drug called buprenorphine, sold under the brand name Subutex, which is used to treat opioid-use disorder, acute pain, and chronic pain.”
Buprenorphine is a mixed opioid agonist and antagonist. That means it has some of the effects of opioids but also blocks some of their effects. Before the patient can take it under direct observation, he must have moderate opioid-withdrawal symptoms. The drug relieves withdrawal symptoms from other opioids and induces some euphoria, but it also blocks the efficacy of many other opioids including heroin, to create an effect.
Buprenorphine levels in the blood stay consistent throughout the month. Nachum said the replacement drug is relatively safe, with some side effects, but fortunately, there is no danger of an overdose.
NARCAN (NALOXDONE) is another prescription drug used by some professionals to fight addiction. Not in Israel’s basket of health services, it blocks the effects of opioids by temporarily reversing them, helping the patient to breathe again and wake up from an overdose. While it has saved countless lives, new and more powerful opioids keep appearing, and first responders are finding it increasingly difficult to revive people with it.
Now, US researchers have found an approach that could extend naloxone’s lifesaving power, even in the face of continually more dangerous opioids by using potential drugs that make naloxone more potent and longer lasting. Naloxone is a lifesaver, but it’s not a miracle drug; it has limitations, the team said.
After the Nova massacre on October 7, when significant numbers of participants who were murdered were high on drugs, the IPHA received a huge number of calls. In December, Nachum decided to open a hotline run by professionals about addiction that has been called monthly by some 300 people. “We also hold lectures for pain doctors, family physicians, and others who are interested, because there has been so little awareness.”
All agree that the opioid crisis has been seriously neglected here and that if it is not dealt with seriously and in joint efforts headed by healthcare authorities, it will snowball and add to Israel’s current physical and psychological damage.
Source: https://www.jpost.com/health-and-wellness/article-811126
Everyone knows illicit drug use in Australia is worsening, but wouldn’t it be helpful if we had precise numbers for gauging the scale of the problem? How useful it would be if we could measure consumption, perhaps even knowing just how much of each substance was being used in what locations and how patterns were changing.
In fact, we do have those figures, through analysis of wastewater; we’re just not paying enough attention to them. They show our current means of minimising harm from drug use isn’t working. We must look beyond treating it as a mainly law enforcement problem.
The Australian Criminal Intelligence Commission released its 21st National Wastewater Drug Monitoring Program report last month. It found that ‘more than 16.5 tonnes of methylamphetamine, cocaine, heroin and MDMA combined was consumed between August 2022 and August 2023 representing a 17 per cent increase in consumption of these drugs from the previous year’.
Reports from the commission’s National Wastewater Drug Monitoring Program ought to be the most consequential inputs for developing illicit drug policy and law enforcement strategy in Australia. Seven years ago, on the eve of the release of the first report, one of Australia’s most senior law enforcement leaders at the time confided to this writer that the program would show, as it has shown, that our law enforcement strategy was having no impact on the availability of illicit drugs. It would show a failure of policy and strategy, that officer said.
Yet, the reports generally result in several print media reports and quickly fade from public and policymaking attention.
The program is a sophisticated initiative focused on gathering intelligence about drug consumption patterns across Australia. It involves collecting and analysing sewage samples from various places, including cities and regional areas, to detect and monitor the presence of illicit drugs and pharmaceuticals in wastewater. By examining the levels of substances such as methamphetamine, cocaine, MDMA, and opioids, it offers valuable insights into drug use trends, geographical distribution and changes in consumption patterns.
It uses advanced analytical techniques to quantify the concentration of targeted substances. By monitoring drug use at a population level it should help identify emerging drug threats, assess the effectiveness of existing interventions and guide efficient allocation of resources to address public health concerns related to substance abuse.
The latest report reveals several trends in drug consumption. One is continued high use of methamphetamine in many urban and regional areas, indicating ongoing challenges in reducing its availability. Additionally, the program has detected fluctuations in consumption of other drugs, such as cocaine, MDMA, and prescription opioids. Drug use patterns are dynamic.
The findings underscore the importance of targeted interventions and evidence-based strategies to address substance abuse, especially the need for a comprehensive approach that combines law enforcement efforts with public health initiatives.
The program’s findings are not mere statistics; they are revelations that should reverberate through policymaking and public-health administration. Outstanding performance by our law enforcement and border officers, with their record levels of drug seizures and arrests, is clearly having negligible effect on drug availability, use or price.
Some argue that, if not for these efforts, the problem would be worse. It’s a hollow argument. Our enforcement strategy aims not to prevent things from worsening but to improve them. In short, the Wastewater Monitoring Program provides seven years of evidence of the need for a paradigm shift in our approach to illicit drugs.
The data should empower policymakers to sculpt interventions that transcend rhetoric, go beyond traditional law enforcement and embrace a comprehensive strategy where public health, harm reduction and treatment intertwine.
Alternatives to a strictly law enforcement approach to illicit drugs focus on public health, harm reduction and treatment strategies. Drug possession for personal use should be treated as a civil offence or a minor infraction rather than a crime. This approach aims to reduce the negative consequences of drug use, such as incarceration and stigma, while prioritising public health interventions. It was introduced in Canberra in 2024 and has not resulted in an influx of drug tourists or a marked increase in organised crime.
Harm reduction programs, such as needle exchanges, safe injecting rooms, and pill testing, are crucial. These initiatives improve the wellbeing of drug users and reduce the spread of infectious diseases without necessarily focusing on drug prohibition.
Investing in accessible and effective drug treatment and rehabilitation programs is also necessary. These efforts should include counselling, detoxification services, medication-assisted treatment (such as methadone or buprenorphine for opioid use disorder) and mental health support. Emphasising treatment over punishment can help individuals overcome addiction and reintegrate into society.
Prevention efforts should continue to aim at reducing drug-use initiation and promoting healthy behaviour. This includes education campaigns in schools and communities, raising awareness about the risks of drug use and focusing on harm.
These alternatives often complement each other, forming a comprehensive approach that acknowledges the complexity of drug use and addiction while prioritising public health and harm reduction.
Law enforcement still has a place in our national illicit drug strategy. It must continue to focus on reducing the availability of illicit drugs and disrupting organised crime. Its success here should not be assessed based on arrests and seizures but by the Wastewater Monitoring Program’s evidence base.
The Australian government’s approach to illicit drugs is shaped by a complex interplay of factors, including political dynamics, international obligations, evidence-based practices, resource considerations and public perceptions. Any changes to drug strategies are typically considered within this broader context to ensure a comprehensive and sustainable approach to addressing drug-related challenges. However, we must recognize what the evidence shows.
Young people who smoked marijuana in the 1960s were seen as part of the counterculture. Now the cannabis culture is mainstream. A 2022 survey sponsored by the National Institutes of Health found that 28.8% of Americans age 19 to 30 had used marijuana in the preceding 30 days—more than three times as many as smoked cigarettes. Among those 35 to 50, 17.3% had used weed in the previous month, versus 12.2% for cigarettes.
While marijuana use remains a federal crime, 24 states have legalized it and another 14 permit it for medical purposes. Last week media outlets reported that the Biden administration is moving to reclassify marijuana as a less dangerous Schedule III drug—on par with anabolic steroids and Tylenol with codeine—which would provide tax benefits and a financial boon to the pot industry.
Bertha Madras thinks this would be a colossal mistake. Ms. Madras, 81, is a psychobiology professor at Harvard Medical School and one of the foremost experts on marijuana. “It’s a political decision, not a scientific one,” she says. “And it’s a tragic one.” In 2024, that is a countercultural view.
Ms. Madras has spent 60 years studying drugs, starting with LSD when she was a graduate student at Allan Memorial Institute of Psychiatry, an affiliate of Montreal’s McGill University, in the 1960s. “I was interested in psychoactive drugs because I thought they could not only give us some insight into how the brain works, but also on how the brain undergoes dysfunction and disease states,” she says.
In 2015 the World Health Organization asked her to do a detailed review of cannabis and its medical uses. The 41-page report documented scant evidence of marijuana’s medicinal benefits and reams of research on its harms, from cognitive impairment and psychosis to car accidents.
She continued to study marijuana, including at the addiction neurobiology lab she directs at Mass General Brigham McLean Hospital. In a phone interview this week, she walked me through the scientific literature on marijuana, which runs counter to much of what Americans hear in the media.
For starters, she says, the “addiction potential of marijuana is as high or higher than some other drug,” especially for young people. About 30% of those who use cannabis have some degree of a use disorder. By comparison, only 13.5% of drinkers are estimated to be dependent on alcohol. Sure, alcohol can also cause harm if consumed in excess. But Ms. Madras sees several other distinctions.
One or two drinks will cause only mild inebriation, while “most people who use marijuana are using it to become intoxicated and to get high.” Academic outcomes and college completion rates for young people are much worse for those who use marijuana than for those who drink, though there’s a caveat: “It’s still a chicken and egg whether or not these kids are more susceptible to the effects of marijuana or they’re using marijuana for self-medication or what have you.”
Marijuana and alcohol both interfere with driving, but with the former there are no medical “cutoff points” to determine whether it’s safe to get behind the wheel. As a result, prohibitions against driving under the influence are less likely to be enforced for people who are high. States where marijuana is legal have seen increases in car accidents.
One of the biggest differences between the two substances is how the body metabolizes them. A drink will clear your system within a couple of hours. “You may wake up after binge drinking in the morning with a headache, but the alcohol is gone.” By contrast, “marijuana just sits there and sits there and promotes brain adaptation.”
That’s worse than it sounds. “We always think of the brain as gray matter,” Ms. Madras says. “But the brain uses fat to insulate its electrical activity, so it has a massive amount of fat called white matter, which is fatty. And that’s where marijuana gets soaked up. . . . My lab showed unequivocally that blood levels and brain levels don’t correspond at all—that brain levels are much higher than blood levels. They’re two to three times higher, and they persist once blood levels go way down.” Even if people quit using pot, “it can persist in their brain for a while.”
Thus marijuana does more lasting damage to the brain than alcohol, especially at the high potencies being consumed today. Levels of THC—the main psychoactive ingredient in pot—are four or more times as high as they were 30 years ago. That heightens the risks, which range from anxiety and depression to impaired memory and cannabis hyperemesis syndrome—cycles of severe vomiting caused by long-term use.
There’s mounting evidence that cannabis can cause schizophrenia. A large-scale study last year that examined health histories of some 6.9 million Danes between 1972 and 2021 estimated that up to 30% of young men’s schizophrenia diagnoses could have been prevented had they not become dependent on pot. Marijuana is worse in this regard than many drugs usually perceived as more dangerous. “Users of other potent recreational drugs develop chronic psychosis at much lower rates,” Ms. Madras says. When healthy volunteers in research experiments are given THC—as has been done in 15 studies—they develop transient symptoms of psychosis. “And if you treat them with an antipsychotic drug such as haloperidol, those symptoms will go away.”
Marijuana has also been associated with violent behavior, including in a study published this week in the International Journal of Drug Policy. Data from observational studies are inadequate to demonstrate causal relationships, but Ms. Madras says that the link between marijuana and schizophrenia fits all six criteria that scientists use to determine causality, including the strength of the association and its consistency.
Ms. Madras says at the beginning of the interview that she was operating on three hours of sleep after crashing on scientific projects. Yet she is impressively lucid and energized. She peppers her explanations with citations of studies and is generous in crediting other researchers’ work.
Another cause for concern, she notes, is that more pregnant women are using pot, which has been linked to increased preterm deliveries, admissions of newborns into neonatal intensive care units, lower birth weights and smaller head circumferences. THC crosses the placenta and mimics molecules that our bodies naturally produce that regulate brain development.
“What happens when you examine kids who have been exposed during that critical period?” Ms. Madras asks. During adolescence, she answers, they show an increased incidence of aggressive behavior, cognitive dysfunction, and symptoms of ADHD and obsessive-compulsive disorders. They have reduced white and gray matter.
A drug that carries so many serious side effects would be required by the Food and Drug Administration to carry a black-box warning, the highest-level alert for drugs with severe safety risks. Marijuana doesn’t—but only because the FDA hasn’t cleared it.
The agency has selectively approved cannabis compounds for the treatment of seizures associated with Lennox-Gastaut or Dravet syndrome, nausea associated with chemotherapy for cancer, and anorexia associated with weight loss in AIDS patients. But these approved products are prescribed at significantly less potent doses than the pot being sold in dispensaries that are legal under state law.
What about medicinal benefits? Ms. Madras says she has reviewed “every single case of therapeutic indication for marijuana—and there are over 100 now that people have claimed—and I frankly found that the only one that came close to having some evidence from randomized controlled trials was the neuropathic pain studies.” That’s “a very specific type of pain, which involves damage to nerve endings like in diabetes or where there’s poor blood supply,” she explains.
For other types of pain, and for all other conditions, there is no strong evidence from high-quality randomized trials to support its use. When researchers did a “challenge test on normal people where they induce pain and tried to see whether or not marijuana reduces the pain, it was ineffective.”
Ms. Madras sees parallels between the marketing of pot now and of opioids a few decades ago. “The benefits have been exaggerated, the risks have been minimized, and skeptics in the scientific community have been ignored,” she says. “The playbook is always to say it’s safe and effective and nonaddictive in people.”
Advocates of legalization assert that cannabis can’t be properly studied unless the federal government removes it from Schedule I. Bunk, Ms. Madras says: “I have been able to study THC in my research program.” It requires more paperwork, but “I did all the paperwork. . . . It’s not too difficult.”
Instead of bankrolling ballot initiatives to legalize pot, she says, George Soros and other wealthy donors who “catalyzed this whole movement” should be funding rigorous research: “If these folks, these billionaires, had just taken that money and put it into clinical trials, I would have been at peace.”
It’s a travesty, Ms. Madras adds, that the “FDA has decided that they’re going to listen to that movement rather than to what the science says.” While the reclassification wouldn’t make recreational marijuana legal under federal law, dispensaries and growers would be able to deduct their business expenses on their taxes. The rescheduling would also send a cultural signal that marijuana use is normal.
Ms. Madras worries that “it sets a precedent for the future.” She points to the movement in states to legalize psychedelic substances, for whose medicinal benefits there also isn’t strong scientific evidence. Meantime, she says it makes no sense that politicians continuously urge more spending on addiction treatment and harm reduction while weakening laws that prevent people from becoming addicted in the first place.
Her rejoinder to critics who say the war on drugs was a failure? “This is not a war on drugs. It’s a defense of the human brain at every possible age from in utero to old age.”
Source: https://www.wsj.com/articles/what-you-arent-reading-about-marijuana-permanent-brain-damage-biden-schedule-iii-9660395e
Racial disparities are vast across the nation and in Oregon, a new report shows. But the statistics reveal some surprising differences among states.
In some statistics that measure outcomes for different racial and ethnic groups, Oregon, like Washington, does better than most states. In other measures, it does worse.
For the first time in three years, The Commonwealth Fund, a nonprofit health care research and advocacy group, has issued its state-by-state measurements of health care disparities. The report compiled data on 25 health care measures tracking outcomes, quality, access and use of services by five different racial and ethnic groups — Black, white, Hispanic, American Indian and Alaska Native, as well as Asian American, Native Hawaiian and Pacific Islander. Researchers then aggregated them to create what amounts to a scorecard.
The report is called Advancing Racial Equity in U.S. Health Care: The Commonwealth Fund 2024 State Health Disparities Report. Its findings are similar to earlier research from 2021 that found the performance of Oregon’s health system as experienced by different groups tended to be better in some measures than most states.
But there are still major problems, according to David Radley, the longtime leader of The Commonwealth Fund’s scorecard project. Two years ago he joined the Center for Evidence-Based Policy at Oregon Health & Science University as its director of data and analytics.
“There are still big disparities” in Oregon, he said. “There’s still a lot of improvements to be made.”
For instance? For Black people in Oregon, the rate of deaths before age 75 for causes that are treatable through health care is 141 per 100,000. For white people, however, the rate is slightly less than half that: 69 per 100,000.
Meanwhile, the proportion of people who reported skipping needed health care due to cost was 7% for white people, but double that or more for people who are Black, Hispanic or American Indian and Alaska Native.
The statistics are more complex than they seem on the surface, according to Radley. In effect, they measure not just the provision of health care but the effects of social factors that contribute to health outcomes, such as access to healthy food and stable housing. Other reports, by The Commonwealth Fund as well as the Coalition of Communities of Color in Oregon, have focused on issues like structural racism.
Asked about the study, state Rep. Ricki Ruiz, a Gresham Democrat, said he thinks improvements need to be a priority in access to primary care, affordability and interpreter services. With parents that moved to the United States from Mexico, he served as the family interpreter with health care providers starting when he was six years old — and not exactly fluent in health care terms.
“As a first-generation citizen, one of the things we always struggled to navigate was the health care system,” he said. “Disparities still exist. And that is something that is alarming. That is something we need to continue to study— to be able to minimize that as much as we can.”
The report provides a state-by-state overview of statistics and their rankings among states (and Washington, D.C.) where sufficient data was available in all categories for that group.
It found that Oregon and Washington score similarly to one another when it comes to measures broken down by race and ethnicity. And they do better than most other states.
For people who are Asian American, Native Hawaiian, and Pacific Islander:
For people who are American Indian and Alaska Native:
For people who are Black:
For people who are Hispanic:
For people who are White:
According to Radley, the findings for Oregon call for making health care more affordable, while also focusing on strengthening the state’s provision of primary care.
That includes ensuring access to care with community health workers and providers that speak the same language as the patient.
“That’s one of the best tools we have to fight these kinds of disparities,” he said.
Source: https://www.thelundreport.org/content/oregon-performs-better-health-equity-disparities-remain?
April 24, 2024
The Australian community deserve a clear picture of all persons whose Mental Health has come to the attention of the police, hospitals and the community.
When cannabis genotoxicity effects are added to cannabis neurotoxicity effects the argument against the widespread use of cannabis for everything becomes very robust indeed.
The drug prevention taskforce outlines below our real concerns regarding the Stabbing rampage at Sydney. It does appear that here in Australia our State and Federal Medical Department has been testing toxic factors using blood and not using the much better hair test.
Most of the cannabis (80-90%) is excreted within 5 days as hydroxylated and carboxylated metabolites. See attached (Chemistry and Toxicology of cannabis).
Because 90% of THC is gone in 80 minutes from blood. Please demand hair testing of the subject for marijuana use (blood test may not be positive due to rapid clearance). This is very indicative of cannabis induced psychosis most of the cannabis (80-90%) is excreted within 5 days as hydroxylated and carboxylated metabolites . There are eighteen acidic metabolites as per Goulle JP, Saussereau E, Lacroix C. [Delta-9-tetrahydrocannabinol pharmacokinetics]. Ann Pharm Fr 2008; 66: 232-244. Studies attached.
Drug Free Australia is seeking to bring urgent attention to Australian whether Federal or State, regarding extremely important research relating to Mental Health and cannabis use. It appears that Australian public policies have moved from concern for the health and wellbeing of society – by improving and promoting good health – to pushing unnecessary drug use for profiteers while charging the tab to society-at-large. DFA believes that it is time for governments worldwide to promote research and media publicity which avoids the cherry-picked faux studies used by those wanting to legalise cannabis. Rather, the focus should be on its serious harms to mental and physical health particularly related to early use.
TOP 15 RISKS OF MARIJUANA ON HEALTH https://iasic1.org. The Drug Free Australian paper (MENTAL HEALTH AND CANNABIS USE) see attached. (A Panel Study of the Effect of Cannabis Use on Mental Health, Depression and Suicide in the 50 States)see attached.
EXCLUSIVE: Regular cannabis use in people’s mid-20s can cause permanent damage to the brain development and legalizing the drug has WRONGLY presented it as harmless, drug safety expert Dr Nora Volkow, director of the National Institute on Drug Abuse, warned cannabis use among young adults was a ‘concern’. She called for ‘urgent’ research into the potential health risks of the drug. Several papers have suggested regular use could be damaging mental development and affecting users’ social life
But these often also include people regularly using alcohol and tobacco, making it difficult to deduce whether cannabis is behind the changes. About 48million Americans use cannabis annually, a number that is rising. https://www.dailymail.co.uk/health/article-11138001/Taking-cannabis-mid-20s-damages-cognitive-development-NIH-expert-warns.html
(Illegal Marijuana growers poison forests-these people fight back) https://www.nationalgeographic.com/environment/article/illegal-marijuana-growing-threatens-california-national-forests (Green But Not Green: How Pot Farms Trash the Environment) http://www.slate.com/articles/news_and_politics/uc_breakthroughs_2014/2014/04/green_but_not_green_how_pot_farms_trash_the_environment.html
RECOMMENDATIONS THAT CAN HELP PREVENT THE AUSTRALIAN “LOST GENERATION DYING”
All Australian Governments and community leaders need to take this evidence regarding Mental Health very seriously. The issue of cannabis-caused violence needs to be addressed. For example, the Australian Government must consider organising several Mental Health teams working 24/7 to evaluate the mental health and wellbeing of those involved in animal cruelty, road rage, spousal abuse and child fatalities. These teams should have the authority to place these individuals into detox and rehabilitation centres for three to twelve months according to their progress. They will also need to be constantly reminded that they are very important to the Australian community’s future. Here in Queensland, we have one centre available. .and a third that could be built. They could be equipped at minimum cost and run with existing staff for this mental health program.
The Australian National Drug Strategy 2017-2026 identifies cannabis as a priority substance for action, noting 20% of Australian drug and alcohol treatment services are provided to people identifying cannabis as their principal drug of concern. DFA believes that the number is higher for those under 25 years of age.
We greatly appreciate your time in responding to these extremely important matters in terms of community health, welfare and safety and would value your response early Should you require further information and/or a face-to-face meeting we would be very pleased to accommodate.
Kind Regards
Herschel Baker, International Liaison Director,
>>>>>>>>>>>>>>>>>>>>>>>
Please click on the links below to read the reports:
A new study by NYU Langone, funded by the National Institutes of Health and the National Institute on Drug Abuse, shows how fentanyl has taken over America’s illegal drug supply. It has happened fast.
Law enforcement seizure data shows that illicit fentanyl seizures grew more than 1700% in the 6 year span from 2017 to 2023.
Fentanyl pills specifically made up nearly half of fentanyl seizures in 2023, at 49%. Compare that to 10% in 2017.
As much as 85% of these seizures are happening in the western part of the United States.
A lead researcher on the study, Dr. Joseph Palamar, said that though the numbers are staggering, they’re not surprising given recent trends.
“A couple of years ago, most fentanyl was in powder form. The way it began was fentanyl started creeping up into the heroin supply …then pills started coming around — particularly in the West, and pills introduced fentanyl in a whole different manner to people,” he said.
Related stories:
Palamar says fentanyl in pill-form changes the game, so to speak, in terms of who is now able to obtain it.
Pills are easier to take or to smoke, so there’s no need to figure out how to use a needle. Also, because many fentanyl pills are meant to look like legitimate pills, it’s easier for people who don’t necessarily know they’re taking fentanyl to find it, ingest it and overdose.
“My fear in particular is that there are young people who are trying to get their hands on pills like Adderall or Oxy or Xanax and if they buy them illegally, they don’t know that they could have fentanyl in them — just a few milligrams is enough to kill a teenager,” Palamar said.
Rob Sullivan oversees multiple drug detox programs in northwestern Washington state, and has been in the industry for 20 years.
He says he and his colleagues have noticed that it takes longer for someone to detox from fentanyl — prompting requests to insurance companies to extend detox stays. He also says people have a harder time completing detox, and many times people detox without even realizing they’ve taken fentanyl.
“We see right now, we’re about 66% complete. And 44% don’t complete. Whereas we used to be higher when it was just regular opioids, because people knew what to expect, meaning clients, and also professionals knew what to expect,” Sullivan said.
“Whereas with fentanyl — so different, and so powerful — that it’s really, it’s a different ballgame than what it was,” he said.
Palamar hopes that these findings spark a stronger emphasis on drug use prevention
“We need people to be educated about fentanyl and the associated risks, particularly the people who have not used fentanyl. I worry about people starting fentanyl, and I also worry about people being unintentionally exposed to fentanyl — especially young people.”
Source: https://www.ktvq.com/us-news/new-study-shows-the-rising-prevalence-of-fentanyl-pills
Mary Brett – in memoriam
Mary Brett, Former biology teacher (30 years at Dr Challoner’s Grammar School for boys, Amersham, Buckinghamshire. UK), Trustee of CanSS (Cannabis Skunk Sense), Member of PandA (Centre for Policy Studies) and former Vice President of Eurad. With regret, it is noted that Mary has recently died, in 2024, after a long illness – her expert contribution to the field of drug prevention and education is to be celebrated, and remembered for the quality of her work throughout.
The paper reproduced here below is but one example of Mary’s expert contributions to the field.
Prevention is the policy of this Government but harm-reduction organisations are being consulted for information and evidence—the Advisory Council on Misuse of Drugs (ACMD), Drugscope and the John Moores University Liverpool.
Information on cannabis from these sources is out-of-date, misleading, inaccurate, has huge omissions and is sometimes wrong. It does not stand comparison with current scientific evidence.
Children do not want to take drugs. They want reliable information to be able to refuse them.
Tips on safer usage and “informed choice” have no place in the classroom.
Prevention works.
www.homeoffice.gov.uk/publications/alcohol-drugs/drugs/frank/coke-poster
www.homeoffice.gov.uk/publications/alcohol-drugs/drugs/frank/meow-poster
www.homeoffice.gov.uk/publications/alcohol-drugs/drugs/frank/skunk-poster
My pupils would have used words like: pathetic, patronising, trite, useless and positively encouraging drug use—and so would I.
In an open letter to the ACMD on November 13 he wrote:
January 2012
Source: Home Affairs or visit http://www.parliament.uk/business/committees/committees-a-z/commons-select/home-affairs-committee/publications/
Posted June 4, 2024
“It is the deadliest drug threat our country has ever faced.” says Anne Milgram, Administrator, Drug Enforcement Administration (DEA), referring to the threat of fentanyl in the United States. She should know.
We still have record deaths, and that’s after the DEA seized more than 80 million fentanyl-laced fake pills and nearly 12,000 pounds of fentanyl powder so far in 2024 . The fentanyl seizures represent more than 157.6 million deadly doses; 70% of the counterfeit pills contain a lethal dose of fentanyl. Sometimes, the drug is smoked and as with intravenous injection, speeds access to the brain, further endangering users.
The best new prevention approach, the “One Pill Can Kill” initiative led by the DEA, is amplified by the Community Anti-Drug Coalitions of America (CADCA) and other volunteers educating the public and seeking to prevent flooding of the U.S. with fentanyl and fentanyl-laced fake pills resembling Xanax, Oxycontin, Adderall, Vicodin and other popular prescription medications—but with a deadly twist. The counterfeit pills, more often than not, contain a lethal dose of fentanyl.
“CADCA and its 7,000 coalition members across the nation have worked tirelessly to address the issue of fentanyl-laced fake pills that are poisoning our nation’s youth by planning and implementing comprehensive, data-driven strategies, with multiple public and private partners to address community conditions causing this problem,” said CADCA’s president and CEO, retired Army general Barrye L. Price.
Across the country, fentanyl has largely fueled a more than doubling of overdose deaths among children ages 12-17 since the start of the pandemic. The deaths were inadvertently hidden by “good news” reported by the CDC on May 15, 2024, announcing that there were an estimated 107,543 drug overdose deaths in the U.S. during 2023—a decrease of 3% from the 111,029 deaths estimated in 2022.
Fentanyl is killing adolescents and people of color, many with no idea they are taking fentanyl. The counterfeit drugs are easy to obtain from friends or buy through social media. Sold online for $2 to $10 apiece, their lethal potency caught policy leaders, emergency rooms, addiction experts, family health providers, and pediatricians nationwide by surprise.
Such is the fentanyl crisis as of June 2024. As i will describe in this blog post, there are treatments of last resort and medications designed to reverse the effects of fentanyl when education, prevention, and treatment have failed. An estimated 80,000 deaths per year are attributed to opioid-induced respiratory depression (OIRD) caused by fentanyl alone. Wonder medicines that counter the effects include the widely-used naloxone (Narcan) and much-less-used (but also effective) opioid overdose reversal drug nalmefene (Opvee).
The Life-Saving Role of Naloxone
Naloxone has gained attention as a wonder drug capable of reviving a person who has overdosed, appeared to have died, or nearly died. I adminishtered, intravenously, my first dose of naloxone in 1975 while working in the Yale New Haven Hospital emergency room.. At the time, naloxone was most often given intravenously by anesthesiologists during surgery to reverse the sedative effects of opioids doctors had administered earlier. When naloxone was approved by the FDA in 1971, total drug overdose deaths in the U.S. were 6,771, rare enough that there was no national call to add it to emergency rooms to reverse overdoses. Since then, the number of overdoses has catastrophically escalated.
When Individuals Overdose on Opioids
What are signs of an opioid overdose? They include unconsciousness, very small eye pupils, slow or shallow breathing, vomiting, inability to speak, faint heartbeat, limp arms and legs, pale skin, and purple lips and fingernails. When a person overdoses on opioids, breathing slows or altogether stops. The overdosed person appears sleepy and is unresponsive.
Opioids
interfere with receptors in the brain, slowing breathing so that insufficient oxygen reaches the brain and other vital organs like the heart; the heart rate may slow or even stop. As breathing slows, oxygen levels fall, which may trigger abnormal heart rhythms. Blue lips and fingernails signal the lack of oxygen. Because insufficient oxygen reaches the brain and heart, the consequences are coma, brain damage, or death.
The antidote, naloxone, attaches to opioid receptors, reversing and blocking effects of opioids. Naloxone can quickly restore normal breathing. Naloxone is so safe we give it immediately to anyone with signs of opioid overdose or when an overdose is suspected. However, the drug has no effect on someone with no opioids in their system.
Reversing Respiratory Depression
The specific mechanism that drives opioid death by overdose is stimulation of one class of endogenous opioid receptors—mu-opioid receptors—in cells in the brainstem; it inhibits breathing. Respiratory depression, or decreased (or terminated) breathing, is a direct effect of opioid use, and, in the case of fentanyl, it appears extremely quickly.
Intravenous naloxone is not available in the community, where first responders depend on intranasal or intramuscular administration. Yet naloxone must be administered much sooner for fentanyl than for heroin because the window for saving the overdosed person is much shorter than with heroin. So, the right dose of naloxone must be given by a friend, loved one, or first responder almost immediately.
Other opioid antagonists, like nalmefene, may be expected to do a better job in fentanyl overdoses. After the person recovers, they should be offered long-term treatment resources, including the ability to initiate treatment for opioid use disorder in the emergency department, as Yale’s Brian Fuerhlein described in an earlier blog post.
Renarcotization
Researchers, addiction experts, and other healthcare providers have documented that when fentanyl is taken chronically, the drug may be absorbed into fat tissue and stay there, accumulating and forming a reservoir of fentanyl. Naloxone might reverse a “normal” fentanyl overdose, but due to the “depot effect,” after a person becomes conscious, they may lose consciousness again and stop breathing. This event is called re-narcotization.
If it is suspected that someone has overdosed on fentanyl and they are given naloxone, they may start breathing again and become conscious. With less potent opioids, naloxone can cover someone for 60 minutes. But someone with a supply of fentanyl in body fat depots can renarcotize several times. It is important to call 911. Additional doses of naloxone may be given as the patient is transported to the ER or hospital, where oxygen and other life support is available.
Narcan Nasal Spray
Naloxone can now be administered by non-health professionals via nasal spray to save lives. Intranasal naloxone works within two to three minutes. If the person has not responded after three minutes, another dose should be given. After administering naloxone, it’s very important to always call 911 because experts need to determine whether respiratory support, more naloxone, or other measures are necessary to reverse the overdose.
The FDA approved Narcan (naloxone) as a nasal spray for over-the-counter use because it is safe, easy to use, and saves lives. In 2021, the Food and Drug Administration approved an 8-mg intranasal naloxone product, twice the amount than the usual 4-mg dose. The FDA also granted a second over-the-counter naloxone agent in early 2024. This drug, RiVive, is a generic naloxone nasal spray available from Harm Reduction Therapeutics, a nonprofit pharmaceutical organization. Nasal naloxone is currently available in 3mg (Revive), 4mg (Narcan), and 8mg (Kloxxado) dosages.
Making naloxone available without a prescription expands its availability to people with an opioid-dependent loved one or who themselves have opioid use disorder (OUD). To save someone from an opioid overdose, you need naloxone or nalmefene. Steps for responding to an opioid overdose can be found here.
Another Opioid Overdose Reversal Drug: Nalmefene
Nalmefene has been saving lives from opioid overdoses since May 2023, when the FDA approved nalmefene hydrochloride nasal spray (Opvee). Nalmefene is a long-duration opioid antagonist first approved for injection in 1995. The original injectable nalmefene was removed from the market for commercial reasons in 2008. However, the dramatic rise in opioid overdose deaths and the emergence of powerful synthetic opioids catalyzed the development of an intranasal (IN) form of nalmefene for emergency treatment of opioid, and especially fentanyl, overdoses.
Nalmefene is an opioid receptor antagonist particularly well-suited for fentanyl overdoses. One reason is it has a longer half-life than naloxone, which means it stays in the body longer. This may protect against re-intoxication but may also make withdrawal symptoms last longer in those with opioid use disorders.
Synthetic opioids like fentanyl are now the most common drugs involved in drug overdose deaths in the U.S. Nalmefene is 10 times more potent than naloxone and has an 8- to 10-fold longer half-life (8 to 11 hours), reducing the likelihood of re-overdosing from long-acting opioids.
Xylazine and other adulterants illegally added to opioids in the U.S. have also received attention for generating zombie-like behavior in people. Such additives make overdose reversal more difficult. However, the key to harm reduction is reversing the effects of synthetic opioids on the heart, lungs, and brain.
The efficacy of frontline, community-based reversal of poisoning events with antidotes such as naloxone has been questioned due to the rise of highly potent synthetic opioids, primarily illicitly manufactured fentanyl (IMF), which causes 90% or more of opioid deaths in the U.S.
In many cases today, community-based first responders have improvised or evolved strategies to cope with fentanyl. Typically, multiple naloxone doses are given to individuals who overdosed on opioids. That was definitely not the case when I was giving naloxone to patients in the Yale emergency department in the 1970s or even back when the opioid crisis was primarily either a prescription-opioid or heroin crisis.
However, it’s unclear whether giving opioid overdose patients more doses sequentially is the optimal strategy in dealing with fentanyl. A very nice study by Strauss suggests it’s a good idea to have higher doses of intranasal naloxone available, as it appears that a large first dose at once is superior to the same dose given sequentially.
Some overdoses might be relatively naloxone-resistant and more easily respond to nalmefene. Additional research is needed to determine the optimal naloxone-dosing schedule for fentanyl overdose reversal. Multi-site studies directly comparing nalmefene to naloxone in the community setting are needed.
Conclusion
More than 1 in 8 Americans have had their lives disrupted by a drug overdose. Nearly 49 million Americans (more than 17%) age 12 and older have a substance use disorder. Among young adults aged 18-25, the share jumps to 28%. More than 6 million people had an opioid use disorder, and another 1.8 million had a methamphetamine use disorder in 2022.
The evolving opioid epidemic has morphed into a counterfeit-pill, multi-drug crisis centered on fentanyl, often paired—knowingly or unknowingly—with other illicit drugs. Smoking fentanyl is the newest opioid crisis or problem we have not prevented.
Overdose deaths are only one measure of the drug epidemic’s severity. An estimated 321,566 children lost a parent to drug overdose between 2011 and 2021.
Since 2000, more than 1.1 million overdose deaths have been reported in the U.S. Overdose reversal with intranasal anti-opioids like naloxone and nalmefene has made a big difference but should not be the centerpiece of opioid crisis strategy. Education and prevention are needed and, as we develop new and better treatments for OUDs, so are overdose reversal and relapse prevention. Some very effective means to reverse opioid overdoses are available today, and future research should provide further information on the best medication and dosages for fentanyl overdose situations.
References
Skolnick P. On the front lines of the opioid epidemic: Rescue by naloxone. Eur J Pharmacol. 2018 Sep 15;835:147-153. doi: 10.1016/j.ejphar.2018.08.004. Epub 2018 Aug 7. PMID: 30092179.
Ellison M, Hutton E, Webster L, Skolnick P. Reversal of Opioid-Induced Respiratory Depression in Healthy Volunteers: Comparison of Intranasal Nalmefene and Intranasal Naloxone. J Clin Pharmacol. 2024 Mar 4. doi: 10.1002/jcph.2421. Epub ahead of print. PMID: 38436495.
Crystal R, Ellison M, Purdon C, Skolnick P. Pharmacokinetic Properties of an FDA-approved Intranasal Nalmefene Formulation for the Treatment of Opioid Overdose. Clin Pharmacol Drug Dev. 2024 Jan;13(1):58-69. doi: 10.1002/cpdd.1312. Epub 2023 Jul 27. PMID: 37496452; PMCID: PMC1081801
Source: https://www.psychologytoday.com/us/blog/addiction-outlook/202406/the-fentanyl-death-crisis-in-america
There are several principal pathways to inheritable genotoxicity, mutagenicity and teratogenesis induced by cannabis which are known and well established at this time including the following. These three papers discuss different aspects of these effects.
1. Stops Brain Waves and Thinking
The brain has both stimulatory and inhibitory pathways. GABA is the main brain inhibitory pathway. Brain centres talk to each other on gamma (about 40 cycles/sec) and theta frequencies (about 5 cycles/sec), where the theta waves are used as the carrier waves for the gamma wave which then interacts like harmonics in music. The degree to which the waves are in and out of phase carries information which can be monitored externally. GABA (γ-aminobutyric acid) inhibition is key to the generation of the synchronized firing which underpins these various brain oscillations. These GABA transmissions are controlled presynaptically by type 1 cannabinoid receptors (CB1R’s) and CB1R stimulation shuts them down. This is why cannabis users forget and fall asleep.
2. Blocks GABA Pathway and Brain Formation
GABA is also a key neurotransmitter in brain formation in that it guides and direct neural stem cell formation and transmission and development and growth of the cerebral cortex and other major brain areas. Gamma and theta brain waves also direct neural stem cell formation, sculpting and connectivity. Derangements then of GABA physiology imply that the brain will not form properly. Thin frontal cortical plate measurements have been shown in humans prenatally exposed to cannabis by fMRI. This implies that their brains can never be structurally normal which then explains the long lasting and persistent defects identified into adulthood.
3. Epigenetic Damage
DNA not only carries the genetic hardware of our genetic code but it also carries the software of the code which works like traffic lights along the sequence of DNA bases to direct when to switch the genes on and off. This is known as the “epigenetic code”. Fetal alcohol syndrome is
believed to be due to damage to the software epigenetic code. The long lasting intellectual, mood regulation, attention and concentration defects which have been described after in utero cannabis exposure in the primary, middle and high schools and as college age young adults
are likely due to these defects. Epigenetics “sets in stone” the errors of brain structure made in (2) above.
4. Arterial Damage
Cannabis has a well described effect to damage arteries through (CB1R’s) (American Heart Association 2007) which they carry in high concentration (Nature Reviews Cardiology 2018). In adults this causes heart attack (500% elevation in the first hour after smoking), stroke,
severe cardiac arrhythmias including sudden cardiac death; but in developing babies CB1R’s acting on the developing heart tissues can lead to at least six major cardiac defects (Atrial- ventricular- and mixed atrioventricular and septal defects, Tetralogy of Fallot, Epstein’s deformity amongst others), whilst constriction of various babies’ arteries can lead to serious side effects such as gastroschisis (bowels hanging out) and possibly absent limbs (in at least one series).
5. Disruption of Mitotic Spindle
When cells divide the separating chromosomes actually slide along “train tracks” which are long chains made of tubulin. The tubulin chains are called “microtubules” and the whole football-shaped structure is called a “mitotic spindle”. Cannabis inhibits tubulin formation,
disrupting microtubules and the mitotic spindle causing the separating chromosomes to become cut off in tiny micronuclei, where they eventually become smashed up and pulverized into “genetic junk”, which leads to foetal malformations, cancer and cell death. High rates of
Down’s syndrome, chromosomal anomalies and cancers in cannabis exposed babies provide clinical evidence of this.
6. Defective Energy Generation & Downstream DNA Damage
DNA is the crown jewel of the cell and its most complex molecule. Maintaining it in good repair is a very energy intensive process. Without energy DNA cannot be properly maintained. Cannabis has been known to reduce cellular energy production by the cell’s power plants,
mitochondria, for many decades now. This has now been firmly linked with increased DNA damage, cancer formation and aging of the cells and indeed the whole organism. As it is known to occur in eggs and sperm, this will also damage the quality of the germ cells which go into forming the baby and lead directly to damaged babies and babies lost and wasted through spontaneous miscarriage and therapeutic termination for severe deformities.
7. Cancer induction
Cannabis causes 12 cancers and has been identified as a carcinogen by the California Environmental Protection agency (2009). This makes it also a mutagen. 4 of these cancers are inheritable to children; i.e. inheritable carcinogenicity and mutagenicity. All four studies in
testicular cancer are strongly positive (elevation by three fold). Carcinogen = mutagen = teratogen.
8. Colorado’s Teratology Profile
From the above described teratological profile we would expect exactly the profile of congenital defects which have been identified in Colorado(higher total defects and heart defects, and chromosomal defects) and Ottawa in Canada (long lasting and persistent brain
damage seen on both functional testing and fMRI brain scans in children exposed in utero) where cannabis use has become common. Gastroschisis was shown to be higher in all seven studies looking at this; and including in Canada, carefully controlled studies. Moreover in
Australia, Canada, North Carolina, Colorado, Mexico and New Zealand, gastroschisis and sometimes other major congenital defects cluster where cannabis use is highest. Colorado 2000-2013 has experienced an extra 20,152 severely abnormal births above the rates prior to
cannabis liberalization which if applied to the whole USA would equate to more than 83,000 abnormal babies live born annually (and probably about that number again therapeutically aborted); actually much more since both the number of users and concentration of cannabis have risen sharply since 2013, and cannabis has been well proven to be much more severely genotoxic at higher doses.
9. Cannabidiol is also Genotoxic
Cannabidiol tests positive in many genotoxicity assays, just as tetrahydrocannabinol does.
10. Births defects registry data needs to be open and transparent and public.
At present it is not. This looks too much like a cover up.
Source: By Professor Dr. A. S Reece
(Edith Cowan University & University of Western Australia) 2019
Young people who smoked marijuana in the 1960s were seen as part of the counterculture. Now the cannabis culture is mainstream. A 2022 survey sponsored by the National Institutes of Health found that 28.8% of Americans age 19 to 30 had used marijuana in the preceding 30 days—more than three times as many as smoked cigarettes. Among those 35 to 50, 17.3% had used weed in the previous month, versus 12.2% for cigarettes.
While marijuana use remains a federal crime, 24 states have legalized it and another 14 permit it for medical purposes. Last week media outlets reported that the Biden administration is moving to reclassify marijuana as a less dangerous Schedule III drug—on par with anabolic steroids and Tylenol with codeine— which would provide tax benefits and a financial boon to the pot industry.
Bertha Madras thinks this would be a colossal mistake. Ms. Madras, 81, is a psychobiology professor at Harvard Medical School and one of the foremost experts on marijuana. “It’s a political decision, not a scientific one,” she says. “And it’s a tragic one.” In 2024, that is a countercultural view.
Ms. Madras has spent 60 years studying drugs, starting with LSD when she was a graduate student at Allan Memorial Institute of Psychiatry, an affiliate of Montreal’s McGill University, in the 1960s. “I was interested in psychoactive drugs because I thought they could not only give us some insight into how the brain works, but also on how the brain undergoes dysfunction and disease states,” she says.
In 2015 the World Health Organization asked her to do a detailed review of cannabis and its medical uses. The 41-page report documented scant evidence of marijuana’s medicinal benefits and reams of research on its harms, from cognitive impairment and psychosis to car accidents.
She continued to study marijuana, including at the addiction neurobiology lab she directs at Mass General Brigham McLean Hospital. In a phone interview this week, she walked me through the scientific literature on marijuana, which runs counter to much of what Americans hear in the media.
For starters, she says, the “addiction potential of marijuana is as high or higher than some other drug,” especially for young people. About 30% of those who use cannabis have some degree of a use disorder. By comparison, only 13.5% of drinkers are estimated to be dependent on alcohol. Sure, alcohol can also cause harm if consumed in excess. But Ms. Madras sees several other distinctions.
One or two drinks will cause only mild inebriation, while “most people who use marijuana are using it to become intoxicated and to get high.” Academic outcomes and college completion rates for young people are much worse for those who use marijuana than for those who drink, though there’s a caveat: “It’s still a chicken and egg whether or not these kids are more susceptible to the effects of marijuana or they’re using marijuana for self medication or what have you.”
Marijuana and alcohol both interfere with driving, but with the former there are no medical “cutoff points” to determine whether it’s safe to get behind the wheel. As a result, prohibitions against driving under the influence are less likely to be enforced for people who are high. States where marijuana is legal have seen increases in car accidents.
One of the biggest differences between the two substances is how the body metabolizes them. A drink will clear your system within a couple of hours. “You may wake up after binge drinking in the morning with a headache, but the alcohol is gone.” By contrast, “marijuana just sits there and sits there and promotes brain adaptation.”
That’s worse than it sounds. “We always think of the brain as gray matter,” Ms. Madras says. “But the brain uses fat to insulate its electrical activity, so it has a massive amount of fat called white matter, which is fatty. And that’s where marijuana gets soaked up. . . . My lab showed unequivocally that blood levels and brain levels don’t correspond at all—that brain levels are much higher than blood levels. They’re two to three times higher, and they persist once blood levels go way down.” Even if people quit using pot, “it can persist in their brain for a while.”
Thus marijuana does more lasting damage to the brain than alcohol, especially at the high potencies being consumed today. Levels of THC—the main psychoactive ingredient in pot—are four or more times as high as they were 30 years ago. That heightens the risks, which range from anxiety and depression to impaired memory and cannabis hyperemesis syndrome—cycles of severe vomiting caused by long-term use.
There’s mounting evidence that cannabis can cause schizophrenia. A large-scale study last year that examined health histories of some 6.9 million Danes between 1972 and 2021 estimated that up to 30% of young men’s schizophrenia diagnoses could have been prevented had they not become dependent on pot. Marijuana is worse in this regard than many drugs usually perceived as more dangerous.
“Users of other potent recreational drugs develop chronic psychosis at much lower rates,” Ms. Madras says. When healthy volunteers in research experiments are given THC—as has been done in 15 studies—they develop transient symptoms of psychosis. “And if you treat them with an antipsychotic drug such as haloperidol, those symptoms will go away.”
Marijuana has also been associated with violent behavior, including in a study published this week in the International Journal of Drug Policy. Data from observational studies are inadequate to demonstrate causal relationships, but Ms. Madras says that the link between marijuana and schizophrenia fits all six criteria that scientists use to determine causality, including the strength of the association and its consistency.
Ms. Madras says at the beginning of the interview that she was operating on three hours of sleep after crashing on scientific projects. Yet she is impressively lucid and energized. She peppers her explanations with citations of studies and is generous in crediting other researchers’ work.
Another cause for concern, she notes, is that more pregnant women are using pot, which has been linked to increased preterm deliveries, admissions of newborns into neonatal intensive care units, lower birth weights and smaller head circumferences. THC crosses the placenta and mimics molecules that our bodies naturally produce that regulate brain development.
“What happens when you examine kids who have been exposed during that critical period?” Ms. Madras asks. During adolescence, she answers, they show an increased incidence of aggressive behavior, cognitive dysfunction, and symptoms of ADHD and obsessive-compulsive disorders. They have reduced white and gray matter.
A drug that carries so many serious side effects would be required by the Food and Drug Administration to carry a black-box warning, the highest-level alert for drugs with severe safety risks. Marijuana doesn’t—but only because the FDA hasn’t cleared it.
The agency has selectively approved cannabis compounds for the treatment of seizures associated with Lennox-Gastaut or Dravet syndrome, nausea associated with chemotherapy for cancer, and anorexia associated with weight loss in AIDS patients. But these approved products are prescribed at significantly less potent doses than the pot being sold in dispensaries that are legal under state law.
What about medicinal benefits? Ms. Madras says she has reviewed “every single case of therapeutic indication for marijuana—and there are over 100 now that people have claimed—and I frankly found that the only one that came close to having some evidence from randomized controlled trials was the neuropathic pain studies.” That’s “a very specific type of pain, which involves damage to nerve endings like in diabetes or where there’s poor blood supply,” she explains.
For other types of pain, and for all other conditions, there is no strong evidence from high-quality randomized trials to support its use. When researchers did a “challenge test on normal people where they induce pain and tried to see whether or not marijuana reduces the pain, it was ineffective.”
Ms. Madras sees parallels between the marketing of pot now and of opioids a few decades ago. “The benefits have been exaggerated, the risks have been minimized, and skeptics in the scientific community have been ignored,” she says. “The playbook is always to say it’s safe and effective and nonaddictive in people.”
Advocates of legalization assert that cannabis can’t be properly studied unless the federal government removes it from Schedule I. Bunk, Ms. Madras says: “I have been able to study THC in my research program.” It requires more paperwork, but “I did all the paperwork. . . . It’s not too difficult.”
Instead of bankrolling ballot initiatives to legalize pot, she says, George Soros and other wealthy donors who “catalyzed this whole movement” should be funding rigorous research: “If these folks, these billionaires, had just taken that money and put it into clinical trials, I would have been at peace.”
It’s a travesty, Ms. Madras adds, that the “FDA has decided that they’re going to listen to that movement rather than to what the science says.” While the reclassification wouldn’t make recreational marijuana legal under federal law, dispensaries and growers would be able to deduct their business expenses on their taxes. The rescheduling would also send a cultural signal that marijuana use is normal.
Ms. Madras worries that “it sets a precedent for the future.” She points to the movement in states to legalize psychedelic substances, for whose medicinal benefits there also isn’t strong scientific evidence. Meantime, she says it makes no sense that politicians continuously urge more spending on addiction treatment and harm reduction while weakening laws that prevent people from becoming addicted in the first place.
Her rejoinder to critics who say the war on drugs was a failure? “This is not a war on drugs. It’s a defense of the human brain at every possible age from in utero to old age.”
Ms. Finley is a member of the Journal’s editorial board.
Source: https://www.wsj.com/articles/what-you-arent-reading-about-marijuana-permanent-brain-damage-biden-schedule-iii-9660395e May 2024
The lowered rates of substance use that youth reported after the start of the COVID-19 pandemic remained steady into 2023. However, the rate of fatal drug overdoses among youth, which rose in 2020, remained increased well into 2022.
After the COVID-19 pandemic and its associated school closures began in 2020, youth reported that they were using illicit substances significantly less, according to the 2023 Monitoring the Future survey. Among 12th graders, use of any illicit substances in the previous year fell from 36.8% in 2020 to 32% in 2021. Among 10th graders, the rate fell from 30.4% to 18.7%, while it fell from 15.6% to 10.2% among 8th graders.
Many schools have returned to in-person learning since the fall of 2021, and yet the percentage of students reporting any illicit substance use in 2023 has held steady at the lowered levels reported during the pandemic, according to the most recent Monitoring the Future survey. In 2023, 31.2% of 12th graders, 19.8% of 10th graders, and 10.9% of 8th graders reported any illicit substance use in the past year.
Monitoring the Future has tracked national substance use among 8th, 10th, and 12th graders at hundreds of schools across the country annually since 1975. It is conducted by the University of Michigan and funded by the National Institute on Drug Abuse (NIDA).
“This is encouraging news,” said Anish Dube, M.D., M.P.H., chair of APA’s Council on Children, Adolescents, and Their Families. “Peers have a huge influence on young people and the types of decisions they make. For better or worse, the pandemic limited the amount of time young people physically spent with their peers, and this may be at least one reason why we saw less risk-taking behavior among youth.”
Youth who responded to the survey most commonly reported drinking alcohol, vaping nicotine, and using cannabis in the past year. Compared with 2022 levels, past-year use of alcohol fell among 12th graders and remained stable for 10th and 8th graders. Nicotine vaping declined among 12th and 10th graders and remained stable among 8th graders. Finally, cannabis use remained stable among students in all three grades.
Simultaneously, however, in recent years the rate of fatal overdoses among youth has increased. A 2022 study published in JAMA found that, beginning in 2020 until June 2021, adolescents experienced a greater relative increase in overdose mortality compared with the overall population. An analysis by NIDA published last December found that the upward trends previously reported continued into the summer of 2022. Between the end of 2019 and the beginning of 2020, the rate of unintentional overdose deaths per 100,000 population among youth aged 15 to 19 rose from 0.89 to 1.32. The rate has not declined since that increase. In the summer of 2022, the rate was 1.63.
“In my own clinical experience, one of the biggest challenges has been the widespread availability of fentanyl and its derivatives, their lethality, and the ease with which they can be laced into other substances that young people are trying,” Dube said.
The illicit substances available now are highly addictive and can provide a quick and intense high, said Oscar Bukstein, M.D., M.P.H. That is part of the reason the rate of overdose deaths among adults is so high, and the same is likely true for youth.
“Young people in particular are usually novice drug users,” Bukstein pointed out. Just like younger adolescents are more likely to experience alcohol poisoning, youth who are using other illicit substances may similarly be unaware of the true danger of what they are using, he explained. Bukstein is a member of APA’s Council on Children, Adolescents, and Their Families and a professor of psychiatry at Harvard Medical School.
Bukstein also noted that, because Monitoring the Future surveys youth in schools, those who are not in school due to high-risk behaviors such as truancy or dropping out are less likely to be included. That means the survey may not capture youth who are at the highest risk for substance use. These youth need far more resources than are available to them, such as residential treatment for those who need more than intensive outpatient care, Bukstein said.
Overall, Bukstein is optimistic about Generation Z, he added. “I’ve noticed that there’s a greater sense among the general adolescent population that they want something out of life,” he said. “They know these substances are dangerous, that they are not going to get them where they want to go, and they don’t need them.”
Source: https://psychnews.psychiatryonline.org/doi/10.1176/appi.pn.2024.03.3.10
The United States is knee-deep in what some experts call the opioid epidemic’s “fourth wave,” which is not only placing drug users at greater risk but is also complicating efforts to address the nation’s drug problem.
These waves, according to a report from Millennium Health, were the crisis in prescription opioid use, followed by a significant jump in heroin use, then an increase in the use of synthetic opioids like fentanyl.
The latest wave involves using multiple substances at the same time, combining fentanyl mainly with either methamphetamine or cocaine, the report found. “And I’ve yet to see a peak,” said one of the co-authors, Eric Dawson, vice president of clinical affairs at Millennium, a specialty laboratory that provides drug-testing services to monitor use of prescription medications and illicit drugs.
The report, which takes a deep dive into the nation’s drug trends and breaks usage patterns down by region, is based on 4.1 million urine samples collected from January 2013 to December 2023 from people receiving some kind of drug-addiction care.
Its findings offer staggering statistics and insights. Its major finding is how common polysubstance use has become. According to the report, an overwhelming majority of fentanyl-positive urine samples — nearly 93% — contained additional substances. “That is huge,” said Nora Volkow, director of the National Institute on Drug Abuse at the National Institutes of Health.
The most concerning, Volkow and other addiction experts said, is the dramatic increase in the combination of methamphetamine and fentanyl use. Meth, a highly addictive drug often in powder form that poses several serious cardiovascular and psychiatric risks, was found in 60% of fentanyl-positive tests last year. That is an 875% increase since 2015.
“I never, ever would have thought this,” Volkow said.
Among the report’s other key findings:
But Jarratt Pytell, an addiction medicine specialist and assistant professor at the University of Colorado’s School of Medicine, warned these declines shouldn’t be interpreted as a silver lining.
A lower level of heroin use “just says that fentanyl is everywhere,” Pytell said, “and that we have officially been pushed by our drug supply to the most dangerous opioids that we have available right now.”
“Whenever a drug network is destabilizing and the product changes, it puts the people who use the drugs at the greatest risk,” he said. “That same bag or pill that they have been buying for the last several months now is coming from a different place, a different supplier, and is possibly a different potency.”
In the illicit drug industry, suppliers are the controllers. It may not be that people are seeking out methamphetamine and fentanyl but rather that they’re what drug suppliers have found to be the easiest and most lucrative product to sell.
“I think drug cartels are kind of realizing that it’s a lot easier to have a 500-square-foot lab than it is to have 500 acres of whatever it takes to grow cocaine,” Pytell said.
Dawson said the report’s drug use data, unlike that of some other studies, is based on sample analysis with a quick turnaround — a day or two.
Sometimes researchers face a months-long wait to receive death reports from coroners. Under those circumstances, you are often “staring at today but relying on data sources that are a year or more in the past,” said Dawson.
Self-reported surveys of drug users, another method often used to track drug use, also have long lag times and “often miss people who are active for substance use disorders,” said Jonathan Caulkins, a professor at Carnegie Mellon University. Urine tests “are based on a biology standard” and are good at detecting when someone has been using two or more drugs, he said.
But using data from urine samples also comes with limitations. For starters, the tests don’t reveal users’ intent.
“You don’t know whether or not there was one bag of powder that had both fentanyl and meth in it, or whether there were two bags of powder, one with fentanyl in it and one with meth and they took both,” Caulkins said. It can also be unclear, he said, if people intentionally combined the two drugs for an extra high or if they thought they were using only one, not knowing it contained the other.
Volkow said she is interested in learning more about the demographics of polysubstance drug users. “Is this pattern the same for men and women, and is this pattern the same for middle-age or younger people? Because again, having a better understanding of the characteristics allows you to tailor and personalize interventions.”
All the while, the nation’s crisis continues. According to the Centers for Disease Control and Prevention, more than 107,000 people died in the U.S. in 2021 from drug overdoses, most because of fentanyl.
Caulkins said he’s hesitant to view drug use patterns as waves because that would imply people are transitioning from one to the next.
“Are we looking at people whose first substance use disorder was an opioid use disorder, who have now gotten to the point where they’re polydrug users?” he said. Or, are people now starting substance use disorders with methamphetamine and fentanyl, he asked.
One point was clear, Dawson said: “We’re just losing too many lives.”
Source: https://lexingtonky.news/2024/02/24/opioid-epidemic-is-in-a-fourth-wave-with-multiple-substances-being-used-at-the-same-time-and-fentanyl-is-the-most-common/
Why Do People Relapse? Understanding and Overcoming Relapse in Substance Abuse Recovery: Embarking on the journey of addiction recovery is a tough, but worthwhile goal. However, it is not uncommon for you to face setbacks in the form of relapse during your recovery journey.
In this blog post, we will explore the reasons why people relapse in drug addiction, explore the various stages of relapse, and discuss effective strategies for preventing relapse. Understanding these aspects is crucial for you, your family members, and addiction treatment programs to help you best achieve recovery.
The biggest stumbling block people face on the path of recovery is when they slip up. Knowing why relapse happens is critical for those working on getting clean and those helping them out. Let’s dive into the four big causes of going back to drugs during recovery – how mental health problems, ineffective ways of dealing with stress or emotions, intense withdrawal symptoms, and not setting solid limits work together to trip people up.
Mental health challenges often coexist with substance abuse. Attending a dual diagnosis treatment program, which addresses both mental health issues and substance use disorder, can significantly increase the effectiveness of your recovery efforts.
Your dual diagnosis treatment team understands how substance use disorders are a chronic disease and will work to give you the tools you need to successfully tackle recovery and lay the groundwork for a sober life.
Many individuals turn to drugs or alcohol as a coping strategy to deal with negative emotions, stress, conflict in relationships, and peer pressure. As the Marlatt and Gordon model establishes, the seeds of relapse are planted in a high-risk scenario and nurtured by unhealthy coping skills.
If you are facing elevated stress levels, coupled with poor coping skills, you are at a much greater risk for addiction relapse. Negative emotions like anger, depression, anxiety, and boredom can also increase your risk for returning to drug and alcohol use for comfort.
Simply put, without effective coping skills, relapse rates drastically increase.
The physical discomfort experienced during withdrawal can be overwhelming, leading your to turn to substance use to alleviate these symptoms. All will to stay sober can easily vanish in the face of intense cravings and physical pain, even if you are fully aware of the consequences.
The vulnerability during the withdrawal phase, coupled with the desire to avoid physical and mental distress, underscores the importance of comprehensive support and coping strategies to navigate this critical stage of the recovery journey successfully.
A strong contributor to relapse is your social environment- the people you surround yourself with. Having friends or family members who engage in drug abuse and significantly challenge your recovery and your resolve to stay sober. Even just being around them can trigger intense cravings, heightening your risk of relapse.
Establishing and maintaining well-defined boundaries is crucial for preventing relapse. Without clear boundaries, individuals may find themselves in situations that trigger drug use.
A relapse can happen in many ways. What is commonly seen as a “traditional” relapse happens when you consciously decide to consume alcohol or use drugs. This might involve choosing to smoke marijuana to reduce stress after a substantial period of sobriety or having a glass of wine with friends, believing you can handle it without spiraling into excessive use.
On the flip side, a “freelapse” is the informal term for an accidental relapse, which occurs when you unintentionally use drugs or alcohol.
At times, the path toward a relapse unfolds without you even realizing it, manifesting in actions taken weeks or months before using drugs or alcohol. Specific thoughts, emotions, and events can act as triggers, sparking cravings and urges for drug use. If not effectively addressed, these triggers can significantly elevate the risk of relapse, which is why it is extremely important to proactively manage these risk factors in the recovery process.
The onset of the emotional relapse stage before actually picking up a drug or sipping a drink. In this phase, you may find yourself struggling to manage your negative emotions in a healthy manner. Rather than addressing your feelings openly, there might be a tendency to bottle them up, withdraw from social interactions, deny the existence of problems, and overlook self-care.
Although the thought of drug and alcohol use may not be at the forefront of your mind during this stage, the avoidance of confronting emotional pain and challenging situations sets the stage for potential relapse in the future. Recognizing and addressing these early signs becomes crucial in preventing future relapse and fostering a healthier recovery journey.
In the mental relapse phase, you may struggle with conflicting emotions surrounding sobriety. Within this stage, there is an internal struggle: one side strives to remain sober, while the other wrestles with cravings, harboring secret thoughts about a potential relapse.
Mental relapse goes beyond mere internal conflict; it includes romanticizing past drug use, downplaying the negative feelings and consequences, and actively seeking opportunities for using drugs or alcohol. This intricate mental struggle highlights the delicate balance you have to maintain between your substance addiction and your will to recover.
The physical relapse stage is where the actual addiction relapse occurs. What starts out as an initial slip, perhaps with just a few sips of a drink or or hit of a drug, can quickly escalate into a full-blown relapse, characterized by a complete loss of control over your actions and total drug dependence.
The importance of recognizing early warning signs and implementing effective strategies to prevent progression towards physical relapse in the ongoing journey of drug recovery.
Whether you have relapsed before or not, knowing what to do if you slip back into the throws of drug abuse is critical for getting back on track and preventing future relapse. No relapse is insurmountable and there’s always an opportunity for recovery.
If you have experienced a relapse, quickly follow these proactive steps to minimize the negative effects of drug use and prevent further substance use.
1. Ask for help. Seeking assistance from family members, friends, and other addicts in the recovery process can significantly help you navigate the challenges of relapse. Create a sober support system and immerse yourself in it. The worst thing you can do in early recovery is suffer in silence.
2. Find support groups near you. Both traditional twelve-step support groups like Alcoholics Anonymous (AA) and Narcotics Anonymous (NA), as well as science-based alternatives like SMART Recovery, offer nonjudgmental spaces for you to discuss substance abuse relapses openly. With meetings available on a daily basis, you can quickly find a support group that’s right for you, allowing you to talk about your relapse experiences within 24 hours of it happening.
3. Avoid triggers at all costs. Being around people, places, situations, etc… that are triggering to you, in the aftermath, of a relapse can be detrimental to your recovery, and actually intensify your cravings. By putting distance between yourself and your triggers helps to create an environment ripe for addiction recovery.
4. Establish healthy boundaries. In all stages of substance abuse recovery, but especially shortly after a relapse, it’s vital to set boundaries to protect yourself from threats against your sobriety. A key component to maintaining firm personal boundaries is steering clear of people who are not completely onboard with your choice to be sober. These people will only try to pressure you back into a lifestyle of using drugs or alcohol, so surrounding yourself with your sober support system is the only way to remain sober after a relapse.
5. Prioritize your self-care. Both your mental and physical well-being should be taken care of, especially in the wake of a relapse, and is one of the key components of recovery, and it gives you a way to relieve tension and reduce stress.
6. Self-reflect about why the relapse happened. Rather than seeing a relapse as a setback, you can see it as a learning tool. Dedicate time to reflect on the circumstances leading to the relapse. Explore the events that unfolded before the relapse occurred. Did you try out any other coping mechanisms prior to resorting to substance use? Think about potential alternatives to using or drinking that you could have used.
Asking yourself these questions offers insights into what you can do differently, encouraging a constructive approach to managing challenges that arise along your path to substance use disorder recovery.
7. Come up with a relapse prevention plan. This is a guide designed to be a steadfast companion to help you maintain sobriety. It should be as detailed as possible, and easy to follow when needed.
Acting promptly after a relapse significantly increases your chances of a quick recovery with minimal negative consequences. It is important to remember that recovery is not linear or bound by time constraints. It is never too late to regain control after a relapse.
If early recovery seems too overwhelming, seek drug addiction treatment to help manage the task. Some treatment centers offer an inpatient program with medical detox and behavioral therapies to help you regain your footing and relapse prevention classes to help you assimilate back into your daily life with the help of addiction specialists.
Preventing relapse in addiction recovery involves a complex approach that addresses both the physical and psychological aspects of your substance use.
To start off, recognizing the specific situations or emotions that may lead to relapse and developing effective coping strategies, whether through therapy, mindfulness, or healthy activities, is paramount in navigating through moments of weakness. Building and maintaining a strong support system, made up of supportive friends, family, and possibly support groups, provides a crucial safety net.
Additionally, the creation of a personalized relapse prevention plan, including detailed strategies for recognizing and managing triggers, is vital to staying sober. Regular self-reflection and adjustments to the plan over time ensure its continued effectiveness, empowering you to maintain lifelong sobriety.
Creating a personalized plan to prevent addiction relapse is a crucial component of substance abuse recovery. This plan should include strategies for recognizing triggers and coping with cravings. It should also outline your specific triggers for drug use, as well as at least 3 positive coping skills that work for you.
Additionally, your relapse prevention plan should list specific people who are in your sober support system, with their phone numbers, who you can call for help when you are feeling the urge to use. You should also compile a list of local addiction support groups that can be there for you in your time of need.
Regularly consulting and revising this plan is instrumental, making sure it stay relevant to your evolving life experiences and fortifying your commitment to a sober life.
Building a strong support system and fostering a supportive environment are key factors in maintaining long-term sobriety. Creating a nurturing atmosphere involves not only external factors but also the changes you make within yourself.
Most addicts relapse because they do not change both the people they hang around with, as well as the way they approach situations in life after completing an addiction treatment program and in the early stages of recovery. By attending a local support group meeting, you can meet and befriend people who are going through the same things you are and you can be pillars of strength for each other.
Further, you may find it helpful to make a list of fun activities that do not involve drinking alcohol or using drugs. This list may be helpful when you are experiencing cravings and need to divert your attention.
Cultivating a positive mindset not only enhances your motivation and resilience during challenging times but also reinforces your belief in yourself and your capacity for personal growth and living a fulfilling, sober life. Your positive outlook serves as a powerful ally in overcoming obstacles, nurturing a sustainable foundation for lasting recovery.
Prioritizing self-care, including healthy habits and activities, contributes to overall well-being and reduces the risk of relapse. Self-care encompasses a range of activities that bring you pleasure without causing harm, including but not limited to yoga, meditation, exercise, reading, journaling, and eating healthy foods.
Recovery from drug addiction is a complex journey that requires dedication, resilience, and ongoing support. By understanding the reasons behind relapse, implementing effective treatment programs, and adopting preventative strategies, you can increase your chances of achieving and maintaining long-term sobriety.
Remember, relapse does not signify failure but rather serves as an opportunity for growth and reinforcement of your commitment to recovery.
Source: https://www.hippocraticpost.com/addiction/understanding-and-overcoming-substance-abuse-relapse/
Cannabis is harmful to the lungs, but in a different way to tobacco, causing significant respiratory symptoms such as bronchitis with evidence to suggest it can result in destructive lung disease – sometimes referred to as ‘bong lung’ – in heavy cannabis users.
These are the key findings from a review of research on the effects of smoking cannabis on the lungs undertaken by respiratory specialists, Professor Bob Hancox, from the University of Otago’s Department of Preventive and Social Medicine and Dr Kathryn Gracie, from Waikato Hospital’s Respiratory Department.
Cannabis is the second-most commonly smoked substance after tobacco and the most widely-used illicit drug world-wide. Although cannabis remains illegal in most countries, many countries – like New Zealand – are considering decriminalising or legalising its use.
Professor Hancox explains that much of the debate about legalising cannabis appears to revolve around the social and mental health effects. Both he and Dr Gracie believe policies around the liberalisation of cannabis should consider the wider health effects of smoking cannabis.
“The potential for adverse effects on respiratory health from smoking cannabis has had much less attention than the social and mental health effects,” Professor Hancox says.
“We believe policies around the liberalisation of cannabis should consider the potential impacts on the lungs.
“Whether liberalising availability will lead to further increases in cannabis use remains to be seen, but it is likely that patterns of cannabis use will change, with resulting health consequences.”
Because cannabis has been an illegal and unregulated substance and the fact most cannabis users also smoke tobacco, making the effects difficult to separate, Dr Gracie explains that it has been difficult to carry out research on cannabis and its direct impact on the lungs.
“Perhaps, most importantly, the individuals who are extremely heavy users of cannabis may not be well represented in the existing epidemiological research. Most case reports of cannabis-related destructive lung disease document very heavy cannabis consumption.
“Despite these limitations there is sufficient evidence that cannabis causes respiratory symptoms and has the potential to damage both the airways and the lungs.”
“Cannabis may also increase the risk of lung cancer, but there is not enough evidence to be sure of this yet,” Dr Gracie says.
Professor Hancox says there is still a lot to learn about cannabis, but there is sufficient evidence to show that smoking cannabis is not harmless to the lungs.
A combination of smoking both cannabis and tobacco is likely to result in poorer health outcomes.
“Many people smoke both cannabis and tobacco and are likely to get the worst of both substances.”
Source: https://www.otago.ac.nz/news/news/smoking-cannabis-causes-bronchitis-and-changes-to-lung-function May 2020
Vienna (Austria), 22 March 2024 — The 67th session of the Commission on Narcotic Drugs (CND) concluded today, after a two-day high-level segment focusing on the Midterm Review of the 2019 Ministerial Declaration and five days of discussions focused on the implementation of international drug control treaties and drug policy commitments.
In his closing remarks, H.E. Philbert Johnson of Ghana, Chair of the CND at its 67th session, thanked all delegations for contributing to the biggest gathering of the Commission ever, with 140 Member States of the United Nations represented as well as representatives of 18 intergovernmental organizations, 141 non-governmental organizations, and nine UN entities. More than 2500 participants attended in total.
Ghada Waly, Executive Director of the United Nations Office on Drugs and Crime (UNODC), in her closing remarks acknowledged that a fundamental truth had emerged from this year’s high-level segment – that even in times of division and fractures, common ground can be found, as embodied in the High-Level Declaration adopted at the opening session.
The Executive Director made the following pledge on behalf of UNODC as part of the Chair’s Pledge4Action initiative: “UNODC pledges to support a paradigm shift towards much stronger frameworks for prevention in Member States, whether to prevent drug use and harmful behaviours, to prevent illicit economies from exploiting and expanding, or to prevent violence associated with the illicit drug trade, with a focus on children and adolescents, as well as those who are in settings of vulnerability.”
She continued: “We will strive to provide and improve low-cost and accessible tools that build prevention skills, identify and share best practices for prevention in different contexts, and encourage and support far greater investment in prevention nationally and globally, to build the resilience of individuals and communities.”
The Commission decided to place one benzodiazepine, one synthetic opioid, two stimulants, one dissociative-type substance, sixteen precursors of amphetamine-type stimulants and two fentanyl precursors under international control. The scheduling of the two series of amphetamine-type stimulant precursors is part of – for the first time – the taking of a pre-emptive measure to address the proliferation of closely related designer precursors with no known legitimate use.
During the 67th session of the CND, four resolutions were also adopted, covering topics including: alternative development; rehabilitation and recovery management programmes; improving access to and availability of controlled substances for medical purposes; and preventing and responding to drug overdose.
In accordance with the 2019 Ministerial Declaration, Commission conducted a midterm review of progress made in the implementation of all international drug policy commitments during the two-day High-Level Segment, consisting of a General Debate and two multi-stakeholder round-table discussions on the topics “Taking stock: work undertaken since 2019” and “The way forward: the road to 2029”. The final review is planned for 2029.
As part of the General Debate, 66 countries pledged concrete actions towards addressing and countering the world drug problem as part of the Chair’s Pledge4Action initiative.
The CND is the policymaking body of the United Nations with prime responsibility for drug control and other drug-related matters. The Commission is the forum for Member States to exchange knowledge and good practices in addressing and countering the world drug problem.
Source: https://www.unodc.org/unodc/en/frontpage/2024/March/twenty-three-new-substances-precursors-placed-under-international-control-four-resolutions-passed-at-67th-session-of-the-commission-on-narcotic-drugs.html
Nowadays, teaching your child to make healthy choices is crucial for their development and well-being. Understanding the importance of nutritious eating and an active lifestyle can set the foundation for a lifetime of health and happiness. This article, which has been developed by www.recoveryproud.com links to a number of sites which can help young people to keep control of their lifestyles. Additionally, a large body of generic information can be derived by visiting the National Drug Prevention Alliance.
Make your home a haven for healthy choices. Keep nutritious snacks within easy reach and involve your child in meal preparation. This not only makes healthy eating more appealing but also instills a sense of responsibility and appreciation for wholesome food. It’s a practical way to teach them about nutrition and the benefits of eating well. By letting them assist in simple cooking tasks and making choices about the meals, you empower them with knowledge and skills that foster a lifetime of healthy eating habits.
Talking to your kids about drugs is a crucial aspect of parenting that can help safeguard their future. Engaging in open and honest conversations about the dangers of drug use builds a foundation of trust and awareness. It empowers children with the knowledge to make informed decisions and resist peer pressure. This dialogue should be age-appropriate, focusing on the health risks, legal implications, and the impact on mental and emotional well-being. By fostering a supportive environment where children feel comfortable discussing their fears and curiosities about drugs, parents can guide their children towards healthy choices and provide them with coping strategies for dealing with life’s challenges.
Limiting screen time is more crucial now than ever. Encourage your child to embrace physical activities, which are essential for their health and happiness. Present alternatives that divert their attention from screens, like outdoor adventures or sports. This not only fosters physical well-being but also teaches them to value real-world experiences over digital engagements.
Instilling the value of good nutrition in your child’s mind is vital. Explain how choosing foods wisely fuels both their body and brain, supporting their growth, learning, and play. This foundation of understanding encourages them to make healthy decisions that contribute to their overall well-being. By discussing the roles of different nutrients and how they affect the body, you can make the concept of eating well more tangible and engaging for them.
Don’t Forget to Declutter
Teaching your kids about decluttering offers numerous benefits that extend well beyond a tidy home. It instills in them the value of organization and cleanliness, fostering an environment where they can think clearly and focus better on their tasks. So the next time you’re cleaning, get your kids involved. This process also nurtures decision-making skills, as children learn to differentiate between what is necessary and what is superfluous. Additionally, decluttering with your kids encourages mindfulness and appreciation for what they have, promoting a lifestyle of minimalism and sustainability. By understanding the importance of decluttering, children can develop healthier habits that contribute to their overall well-being and success in life.
Water is the body’s best friend. It keeps everything running smoothly, from digestion to maintaining a healthy temperature. Encouraging kids to drink water throughout the day is pivotal to their overall health. Simple reminders and having water easily accessible can make all the difference.
Encouraging your child to explore new foods is a journey of discovery. Introduce them to the diverse world of fruits, vegetables, and whole grains, highlighting how each contributes to their health. This exploration is not just about tasting new flavors; it’s about teaching them the benefits of a varied diet, rich in nutrients, that powers their body and mind. By making this journey exciting, you help them develop a love for foods that are good for them.
A consistent bedtime routine is key to your child’s health. Establish rituals that promote relaxation and signal to their body that it’s time to rest. Emphasizing the importance of quality sleep can help them understand how it supports their growth and readiness for daily activities, ensuring they prioritize it as part of their healthy lifestyle. This can include activities like dimming the lights, reading a story together, or practicing some gentle yoga, which can all aid in transitioning from the day’s excitement to a peaceful night’s sleep.
Teaching healthy choices to kids lays the foundation for a lifetime of wellness. By leading by example and fostering an environment where making healthy decisions is both encouraged and celebrated, parents can significantly influence their children’s habits. This journey, while requiring patience and consistency, promises a rewarding outcome for the entire family.
Further guidance can be obtained by referring to www.recoveryproud.com and to the National Drug Prevention Alliance.
Source: www.recoveryproud.com
Cannabis and cannabinoids are implicated in multiple genotoxic, epigenotoxic and chromosomal-toxic mechanisms and interact with several morphogenic pathways, likely underpinning previous reports of links between cannabis and congenital anomalies and heritable tumours. However the effects of cannabinoid genotoxicity have not been assessed on whole populations and formal consideration of effects as a broadly acting genotoxin remain unexplored. Our study addressed these knowledge gaps in USA datasets. Cancer data from CDC, drug exposure data from National Survey of Drug Use and Health 2003–2017 and congenital anomaly data from National Birth Defects Prevention Network were used. We show that cannabis, THC cannabigerol and cannabichromene exposure fulfill causal criteria towards first Principal Components of both: (A) Down syndrome, Trisomies 18 and 13, Turner syndrome, Deletion 22q11.2, and (B) thyroid, liver, breast and pancreatic cancers and acute myeloid leukaemia, have mostly medium to large effect sizes, are robust to adjustment for ethnicity, other drugs and income in inverse probability-weighted models, show prominent non-linear effects, have 55/56 e-Values > 1.25, and are exacerbated by cannabis liberalization (P = 9.67 × 10 –43 ,2.66 × 10 –15 ). The results confirm experimental studies showing that cannabinoids are an important cause of community-wide genotoxicity impacting both birth defect and cancer epidemiology at the chromosomal hundred-megabase level.
Source: https://www.nature.com/articles/s41598-021-93411-5.epdf July 2021
Democratic Gov. Tina Kotek signed legislation Monday to recriminalize the possession of small amounts of certain drugs as the state grapples with a major overdose crisis, ending a legalization experiment backed by voters four years ago.
The new law makes keeping drugs such as heroin or methamphetamine a misdemeanor punishable by up to six months in prison. It also enables police to confiscate the drugs and crack down on their use on sidewalks and in parks.
Back in 2020, voters backed Measure 110, which made minor possession of personal-use amounts of certain drugs a non-criminal violation on par with a traffic ticket.
It took effect in February 2021, making Oregon the first state to officially decriminalize minor drug possession. Since then, the Beaver State has seen a significant uptick in homelessness, homicides and overdose deaths.
In 2020, unintentional opioid overdose deaths clocked in at 472 and hit at least 628 in 2023, according to state data.
In 2022, Portland set a new record for murders with 101 — breaking the mark of 92 set the previous year. Back in January, Kotek declared a fentanyl state of emergency in the city, saying at the time: “Our country and our state have never seen a drug this deadly and addictive, and all are grappling with how to respond.”
The new law, which will take effect Sept. 1, will let local law enforcement decide whether to give violators the chance to pursue treatment before booking them into jail .
Another bill Kotek signed Monday, Senate Bill 5204, allocates $211 million to mobilize resources for behavioral health and education programs, including expanded access to substance abuse treatment and prevention education.
“Success of this policy framework hinges on the ability of implementing partners to commit to deep coordination at all levels,” Kotek emphasized in a letter to legislative leaders.
The governor further called on the Department of Corrections to ensure a “consistent approach for supervision when an individual is released” from detention and to “exhaust non-jail opportunities for misdemeanor sanctions.”
Source: Oregon recriminalizes drugs after upswing in overdose deaths (nypost.com)
Pregnant women who smoke cannabis almost double the risk of their baby being born autistic, warns a new study.
In the largest ever study of its kind, researchers found that children whose mothers reported using cannabis during pregnancy were at greater risk of autism.
The incidence of autism was four per 1,000 person-years among children exposed to cannabis in pregnancy, compared to 2.42 among unexposed children.
‘There is evidence that more people are using cannabis during pregnancy,’ said senior study author Professor Mark Walker, of the University of Ottawa in Canada.
‘This is concerning, because we know so little about how cannabis affects pregnant women and their babies.
‘Parents-to-be should inform themselves of the possible risks, and we hope studies like ours can help.’
A Canadian study found that rates of autism were twice as high among the children of women who used marijuana during pregnancy, compared to rates among children of mothers who did not use the drug (file)
The researchers reviewed data from every birth in Ontario between 2007 and 2012, before recreational cannabis was legalised in Canada.
Of the half a million women in the study, about 3,000 (0.6 per cent) reported using cannabis during pregnancy.
Importantly, these women reported using only cannabis.
The team had previously found that cannabis use in pregnancy was linked to an increased risk of premature birth.
In that study, they found that women who used cannabis during pregnancy often used other substances including tobacco, alcohol and opioids.
The findings, published in the medical journal Nature Medicine. showed that babies born to this group still had an increased risk of autism compared to those who didn’t use cannabis.
The researchers do not know exactly how much cannabis the women were using, how often, at what time during their pregnancy, or how it was consumed.
But as cannabis becomes more socially acceptable, doctors are concerned that some parents-to-be might think it can be used to treat morning sickness.
Dr Daniel Corsi, an epidemiologist at The Ottawa Hospital, said: ‘In the past, we haven’t had good data on the effect of cannabis on pregnancies.’
He added: ‘This is one of the largest studies on this topic to date.
‘We hope our findings will help women and their health-care providers make informed decisions.’
Autism is fairly common, but still poorly understood.
In the US, about one in every 59 children born will fall somewhere on the autism spectrum.
About one in every 66 children in Canada are autistic and, globally, the rate is approximately one in every 160 children.
Research suggests that there is likely some genetic basis for autism, which is about four-times more common among boys than girls.
But scientists believe exposures in the womb likely play a role as well.
The effects of cannabis are similarly poorly understood to the origins of autism.
Although doctors caution against it, cannabis use has not been linked to miscarriages in humans (though animal studies have suggested an increased risk) and evidence on the link between weed and low birth-weight is mixed.
Marijuana use during pregnancy has been linked, however, to up to 2.3 times greater risks of stillbirth.
The Ottawa Hospital study did not investigate how exactly marijuana use in pregnancy might lead to autism in a child, but scientists believe that the drug’s interaction with the so-called endocannabinoid system within the nervous system could play a role in the development of the behavioral condition.
Source: Autism is twice as common in children whose mothers used cannabis in pregnancy | Daily Mail Online
Research suggests that smoking marijuana carries many of the same cardiovascular health hazards as smoking tobacco.
Credit…Gracia Lam
Do you have the heart to safely smoke pot? Maybe not, a growing body of medical reports suggests.
Currently, increased smoking of marijuana in public, even in cities like New York where recreational use remains illegal (though no longer prosecuted), has reinforced a popular belief that this practice is safe, even health-promoting.
“Many people think that they have a free pass to smoke marijuana,” Dr. Salomeh Keyhani, professor of medicine at the University of California, San Francisco, told me. “I even heard a suggestion on public radio that tobacco companies should switch to marijuana because then they’d be selling life instead of selling death.”
But if you already are a regular user of recreational marijuana or about to become one, it would be wise to consider medical evidence that contradicts this view, especially for people with underlying cardiovascular diseases.
Compared with tobacco, marijuana smoking causes a fivefold greater impairment of the blood’s oxygen-carrying capacity, Dr. Keyhani and colleagues reported.
In a review of medical evidence, published in January in the Journal of the American College of Cardiology, researchers described a broad range of risks to the heart and blood vessels associated with the use of marijuana.
The authors, led by Dr. Muthiah Vaduganathan, cardiologist at Brigham and Women’s Hospital in Boston, point out that “marijuana is becoming increasingly potent, and smoking marijuana carries many of the same cardiovascular health hazards as smoking tobacco.”
Edible forms of marijuana have also been implicated as a possible cause of a heart attack, especially when high doses of the active ingredient THC are consumed.
With regard to smoking marijuana, Dr. Vaduganathan explained in an interview, “The combustion products a tobacco smoker inhales have a very similar toxin profile to marijuana, so the potential lung and heart effects can be comparable. When dealing with patients, we really have to shift our approach to the use of marijuana.”
His team reported, “Although marijuana is smoked with fewer puffs, larger puff volumes and longer breath holds may yield greater delivery of inhaled elements.” In other words, when compared to tobacco smoking, exposure to chemicals damaging to the heart and lungs may be even greater from smoking marijuana.
Dr. Vaduganathan said he was especially concerned about the increasing number of heart attacks among marijuana users younger than 50. In a registry of cases created by his colleagues, in young patients suffering a first heart attack, “marijuana smoking was identified as one factor that was more common among them.” The registry revealed that, even when tobacco use was taken into account, marijuana use was associated with twice the hazard of death among those under age 50 who suffered their first heart attack.
Other medical reports have suggested possible reasons. A research team headed by Dr. Carl J. Lavie of the John Ochsner Heart and Vascular Institute in New Orleans, writing in the journal Missouri Medicine, cited case reports of inflammation and clots in the arteries and spasms of the coronary arteries in young adults who smoke marijuana.
Another damaging effect that has been linked to marijuana is disruption of the heart’s electrical system, causing abnormal heart rhythms like atrial fibrillation that can result in a stroke. In one survey of marijuana smokers, the risk of stroke was increased more than threefold.
These various findings suggest that a person need not have underlying coronary artery disease to experience cardiovascular dysfunction resulting from the use of marijuana. There are receptors for cannabinoids, the active ingredients in marijuana, on heart muscle cells and blood platelets that are involved in precipitating heart attacks.
Cannabinoids can also interfere with the beneficial effects of various cardiovascular medications, including statins, warfarin, antiarrhythmia drugs, beta-blockers and calcium-channel blockers, the Boston team noted.
The researchers found that in an analysis of 36 studies among people who suffered heart attacks, the top three triggers were use of cocaine, eating a heavy meal and smoking marijuana. And 28 of 33 systematically analyzed studies linked marijuana use to an increased risk of what are called acute coronary syndromes — a reduction of blood flow to the heart that can cause crushing chest pain, shortness of breath or a heart attack.
“In settings of an increased demand on the heart, marijuana use may be the straw on the back, the extra load that triggers a heart attack,” Dr. Vaduganathan said. He suggested that the recent decline in cardiovascular health and life expectancy among Americans may be related in part to the increased use of marijuana by young adults.
“We should be screening and testing for marijuana use, especially in young patients with symptoms of cardiovascular disease,” Dr. Vaduganathan urged.
He expressed special concern about two recent practices: the vaping of marijuana and the use of more potent forms of the drug, including synthetic marijuana products.
“Vaping delivers the chemicals in marijuana smoke more effectively, resulting in increased doses to the heart and potentially adverse effects that are more pronounced,” the cardiologist said. “Marijuana stimulates a sympathetic nervous system response — an increase in blood pressure, heart rate and demands on the heart that can be especially hazardous in people with preexisting heart disease or who are at risk of developing it.”
Dr. Vaduganathan’s team estimated that more than two million American adults who say they have used marijuana also have established cardiovascular disease, according to data from the National Health and Nutrition Examination Surveys in 2015 and 2016.
According to Dr. Keyhani, who works at the San Francisco VA Medical Center, the combination of marijuana smoking and pre-existing heart disease is especially concerning because inhaling particulate matter of any kind can harm the heart and blood vessels.
“Marijuana is a leafy green, and combustion of any plant is probably toxic to human health if the resulting products are inhaled,” she explained. “Unfortunately, the research base is inadequate because marijuana hasn’t been studied in randomized clinical trials.”
A major problem in attempts to clarify the risks of marijuana is its classification by the U.S. Drug Enforcement Administration as a Schedule I drug, making it illegal to study it rigorously in controlled clinical trials.
Scientists must then resort to the next best research method: prospective cohort studies in which large groups of people with known habits and risk factors are followed for long periods to assess their health status. “The challenge is to recruit a cohort of daily cannabis users,” Dr. Keyhani said. “It’s absolutely important to look at the health effects of cannabis now that the prevalence of daily use is increasing. The absence of evidence is not evidence of absence.”
While there are currently no official guidelines, Dr. Vaduganathan’s team urged that anyone known to be at increased risk of cardiovascular disease should be advised to minimize the use of marijuana or, better yet, quit altogether.
Source: https://www.nytimes.com/2020/10/26/well/live/marijuana-heart-health-cardiovascular-risks.html October 2020
Despite stereotypical images of addicts injecting heroin and then dying, new government research finds that smoking drugs such as fentanyl is now the leading cause of fatal overdoses.
In the new research, published Thursday in Morbidity and Mortality Weekly Report, scientists from the U.S. Centers for Disease Control and Prevention found the percentage of overdose deaths between January 2020 and December 2022 linked to smoking increased 73.7% — going from from 13.3% to 23.1% — while the percentage of overdose deaths linked to injection decreased 29.1% — going from from 22.7% to 16.1%.
These changes were most pronounced when fentanyl was the drug of choice: In those cases, the percentage with evidence of injection decreased 41.6%, while the percentage with evidence of smoking increased 78.9%.
CDC officials explained in their report that they decided to tackle the topic after seeing reports from California suggesting that smoking fentanyl was becoming the preferred way to use the deadly drug.
Some early research has suggested that smoking fentanyl is somewhat less deadly than injecting it, and any reduction in injection-related overdose deaths is a positive, report author Lauren Tanz, a CDC senior scientist who studies overdoes, told the Associated Press.
However, “both injection and smoking carry a substantial overdose risk,” and it’s not clear if a shift toward smoking fentanyl will lower the number of U.S. overdose deaths, Tanz said.
Fentanyl is a powerful drug that, in powder form, is cut into heroin or other drugs. In recent years, it’s been fueling the U.S. overdose epidemic. Drug overdose deaths climbed slightly in 2022 after two big leaps during the pandemic, and provisional data for the first nine months of 2023 suggests it inched up again last year, the AP reported.
Smoked fentanyl is not as concentrated as fentanyl in a syringe, but some users see upsides to smoking, Kral explained, including the fact that people who inject drugs often deal with pus-filled abscesses on their skin and risk infections with hepatitis and other diseases.
“One person showed me his arms and said, ‘Hey, look at my arm! It looks beautiful! I can now wear T-shirts and I can get a job because I don’t have these track marks,’” Kral said.
In the new report, investigators were able to cull data from the District of Columbia and 27 states for the years 2020 to 2022. From there, they tallied how drugs were taken in about 71,000 of the more than 311,000 total U.S. overdose deaths over those three years.
By late 2022, 23% of the deaths occurred after smoking, 16% after injections, 16% after snorting and 14.5% after swallowing, the researchers reported.
Kral noted the study has some limitations.
It can be difficult to determine the exact cause of an overdose death, especially if no witness was present, he said, and injections might be more reported more often because it is easy to spot needle marks on the body. To detect smoking as a cause of death, “they likely would need to find a pipe or foil on the scene and decide whether to write that down,” he said.
Kral added that many people who smoke fentanyl use a straw, and it’s possible investigators saw a straw and assumed it was snorted.
By Robin Foster HealthDay Reporter
SOURCE: Morbidity and Mortality Weekly Report, Feb. 16, 2024; Associated Press
More information
The National Institute on Drug Abuse has more on drug overdose deaths.
To Whom it may concern
On behalf of Drug Free Australia and our coalition of drug prevention researchers, we wish to commend to you, research that could well be a game-changer in informing and preventing a large proportion of Australia’s substance use issues.
The research is in various stages of development and a synopsis of current and emerging research, being done by Dr Stuart Reece and Professor Gary Hulse should be of genuine interest for all Australian Health Professionals. However, it appears that, to date, too many of the world’s researchers have placed this important research in the ‘too hard’ basket, similar to the way the NHS in the United Kingdom did with research into Pandemics.
At present the COVID-19 pandemic and how it is being addressed, should be a ‘wakeup call’ to Australian health authorities that prevention is the single most important goal. A ‘Harm Minimisation’ only approach, fails to achieve best-practice primary prevention outcomes. The passive discounting of the primary pillar of the National Drug Strategy – Demand Reduction over the last 30 years (and particularly the last 10) has seen a very large increase in illegal drug use in this nation.
The only exception to this has been seen in the correct and full use of both demand and supply reduction on the drug Tobacco. There has been little or no use of harm reduction mechanisms and a relentless and unified approach to abstinent/cessation modelling and it has worked spectacularly well, seeing Australia with, arguably, the lowest daily tobacco use in the world.
The research, that we now summarise, should not be placed in Australia’s ‘too hard’ basket. Rather, it warrants recognition by all Australian Health authorities for the world break-through that it is. Such evidence-based data offers timely insights that should promote and resource primary prevention and demand reduction.
Synopsis of the research:
1. Canadian Cannabis Consumption and Patterns of Congenital Anomalies: An Ecological Geospatial Analysis Albert Stuart Reece, MBBS(Hons), FRCS(Ed), FRCS(Glas), FRACGP, MD(UNSW), and Gary Kenneth Hulse, BBSc(Hons), MBSc, PhD
https://journals.lww.com/journaladdictionmedicine/Abstract/publishahead/Canadian_Cannabis_Consumption_and_Patterns_of.99248.aspx
Status
Mapping showed cannabis use was more common in the northern Territories of Canada in the Second National Survey of Cannabis Use 2018. Total congenital anomalies, all cardiovascular defects, orofacial clefts, Downs syndrome and gastroschisis were all found to be more common in these same regions and rose as a function of cannabis exposure.
When Canada was dichotomized into high and low cannabis use zones by Provinces v Territories the Territories had a higher rate of total congenital anomalies 450.026 v 390.413 (O.R.=1.16 95%C.I. 1.08-1.25, P=0.000058; attributable fraction in exposed 13.25%, 95%C.I. 7.04–19.04%). In geospatial analysis in a spreml spatial error model cannabis was significant both alone as a main effect (P<2.0×10-16) and in all its first and second order interactions with both tobacco and opioids from P<2.0×10-16.
Conclusion:
These results show that the northern Territories of Canada share a higher rate of cannabis use together with elevated rates of total congenital anomalies, all cardiovascular defects, Down’s syndrome and gastroschisis. This is the second report of a significant association between cannabis use and both total defects and all cardiovascular anomalies and the fourth published report of a link with Downs syndrome and thereby direct major genotoxicity.
The correlative relationships described in this paper are confounded by many features of social disadvantage in Canada’s northern territories. However, in the context of a similar broad spectrum of defects described both in animals and in epidemiological reports from Hawaii, Colorado, USA and Australia they are cause for particular concern and indicate further research.
139 References – click on this link to access.
https://journals.lww.com/journaladdictionmedicine/Abstract/publishahead/Canadian_Cannabis_Consumption_and_Patterns_of.99248.aspx
2. Cannabis Consumption Patterns Parallel the East-West Gradient in Canadian Neural Tube Defect Incidence – An Ecological Study
https://www.researchgate.net/publication/337911618_Cannabis_Consumption_Patterns_Explain_the_East-West_Gradient_in_Canadian_Neural_Tube_Defect_Incidence_An_Ecological_Study
Status:
Whilst a known link between prenatal cannabis exposure (PCE) and anencephaly exists, the relationship of PCE with neural tube defects (NTD’s) generally has not been defined. Published data from Canada Health and Statistics Canada was used to assess this relationship. Both cannabis use and NTDs were shown to follow an east-west and north-south gradient. Last year cannabis consumption was significantly associated (P<0.0001; Cannabis use: time interaction P<0.0001). These results were confirmed when estimates of termination for anomaly were used. Canada Health population data allowed the calculation of an NTD O.R.=1.27 (95%C.I. 1.19-1.37; P<10-11) for high risk provinces v. the remainder with an attributable fraction in exposed populations of 16.52% (95%C.I. 12.22-20.62). Data show a robust positive statistical association between cannabis consumption as both a qualitative and quantitative variable and NTDs on a background of declining NTD incidence. In the context of multiple mechanistic pathways these strong statistical findings implicate causal mechanisms.
82 References – click on this link to access.
https://www.researchgate.net/publication/337911618_Cannabis_Consumption_Patterns_Explain_the_East-West_Gradient_in_Canadian_Neural_Tube_Defect_Incidence_An_Ecological_Study
3. Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study. Response to Lane
https://bmjopen.bmj.com/content/6/11/e011891.responses
Status:
We wish to thank Dr Lane for his interest in our study. We are pleased to see statistical input to the issues of cannabis medicine as we feel that sophisticated statistical methodologies have much to offer this field.
Most of the concerns raised are addressed in our very detailed report. As described our research question was whether, in our sizeable body of evidence (N=13,657 RAPWA studies), we could find evidence for the now well-described cannabis vasculopathy and what such implications might be. As this was the first study of its type to apply formal quantitative measures of vascular stiffness to these questions it was not clear at study outset if there would be any effect, much less an estimate of effect size. In the absence of this information power calculations would be mere guesswork. Nor indeed are they mandatory in an exploratory study of this type. Similarly the primary focus of our work was on whether cannabis exposure was an absolute cardiovascular risk factor in its own right, and how it compared to established risk factors. Hence Table 2 contains our main results. The role of Table 1 is to illustrate the bivariate (uncorrected) comparisons which can be made, show the various groups involved, and compare the matching of the groups. It is not intended to be a springboard for effect-size-power calculations which are of merely esoteric interest.
Calculations detailing the observed effect size are clearly described in our text being 11.84% and 8.35% age advance in males and females respectively.
Mixed-effects models are the canonical way to investigate longitudinal data given a usual random error structure 1. We agree with Lane that unusual error structures can affect significance conclusions. Diagnostic tests run on our models confirm that the residuals had the usual spheroidal error structure so that the application of mixed-effects models in the classical way is quite satisfactory. Another way to investigate this issue is that of incremental model building comparing models with and without cannabis exposure terms. If one considers regression equations from our data with cannabis use treated either as a categorical (RA/CA ~ Days_Post-Cannabis * BMI + * Cannabis_Category) or a continuous (RA/(CA*BMI) ~ Cigs*SP + * Cannabis_Use +Chol+DP+HDL+HR+CRH) variable one notes firstly that terms including cannabis use remain significant in final models (after model reduction) and secondly that models which include cannabis exposure are significantly better than ones without (Categorical: AIC = 1088.56 v. 1090.22, Log.Ratio = 19.62, P = 0.0204; Continuous: AIC = 412.33 v. 419.73, Log.Ratio = 9.37, P = 0.0022). Unfortunately formatting rules for BMJ Rapid Responses do not allow us to include a detailed table of regression results in each model in the present reply. We also note that AIC’s are little used in our report, and simply indicate the direction of the ANOVA results comparing models linear, quadratic and cubic in chronological age. They also appear routinely in the display of mixed-effects model results. Their use in such contexts is methodologically unremarkable. Control groups are also spelled out in fine detail in Table 1, in all our Figures and in the text.
We are aware that various algorithms for vascular age have been reported in the literature. The list proposed by Lane is correct but non-exhaustive. Such algorithms are generally derived from known cardiovascular risk factors. As clearly stated in our report the algorithm for vascular age we employed is derived from the proprietary software used. As such its details have not been publicized and indeed are commercially protected information.
We have however been assured by AtCor on many occasions that it includes measures of chronological age, sex, arterial stiffness and height (which is important as it dictates distance and thus speed parameters for the reflected and augmented central arterial pressure waves) and is very well validated and tested. AtCor recently advised that their algorithm is based on a very large series of studies done with arterial stiffness published in 2005 2. As such it has distinct advantages over algorithms which do not include indices of arterial stiffness. The AtCor website includes a very interesting, informative and educative animated loop which clearly illustrates the complex relationship between chronological and vascular age as a function of arterial stiffness and vascular tone 3
We are keen to see advanced statistical methods applied to such questions. We are becoming interested in geospatial and spacetime analyses and its application to the important questions of cannabis epidemiology 4. We find the very breadth of the organ systems impacted by cannabis to be quite remarkable with effects on the brain, cardiovasculature, liver, lungs, testes, ovaries, gastrointestinal, endocrine, reproductive and immune systems being well described and constituting most of the body’s major systems 5 6. Testicular and several pediatric cancers have also been described as being cannabis-associated 5. Such a multisystem generality of toxicity suggests to us that some basic cellular functions may be deleteriously affected – as implied by its well described mitochondriopathy 7, its heavy epigenetic footprint 8, accelerated aging as described in our present report 9 or some multi-way interaction between these and other processes. Given that the cannabis industry is presently entering a major commercialization growth phase, and given the multigenerational implications of mitochondriopathy-epigenotoxicity (by direct: substrate supply including ATP, NAD+ and acetate; and indirect: RNA transfer and malate-aspartate and glycerol-3-phosphate shuttle; pathways 10) further study and elucidation of these points is becoming an increasingly imperative international research priority.
Apropos of the recent Covid-19 pandemic emergency it is also worth noting that since cannabis is immunosuppressive, is known to be damaging to lungs and airways and often carries chemical, microbial and fungal contaminants cannabis use and cannabis vaping is also likely to have a deleterious effect on the coronavirus epidemic. Such data implies an untoward convergence of two public health epidemics. Appropriate controls on cannabis use imply improved public health management of SARS-CoV-2.
10 References – click on this link to access. https://bmjopen.bmj.com/content/6/11/e011891.responses
4. Cannabis Teratology Explains Current Patterns of Coloradan Congenital Defects: The Contribution of Increased Cannabinoid Exposure to Rising Teratological Trends.
https://www.researchgate.net/publication/334368364_Cannabis_Teratology_Explains_Current_Patterns_of_Coloradan_Congenital_Defects_The_Contribution_of_Increased_Cannabinoid_Exposure_to_Rising_Teratological_Trends/link/5d2d4d39a6fdcc2462e3097c/download
Status
Rising Δ9-tetrahydrocannabinol concentrations in modern cannabis invites investigation of the teratological implications of prenatal cannabis exposure.
Data from Colorado Responds to Children with Special Needs (CRCSN), National Survey of Drug Use and Health, and Drug Enforcement Agency was analyzed. Seven, 40, and 2 defects were rising, flat, and falling, respectively, and 10/12 summary indices rose. Atrial septal defect, spina bifida, microcephalus, Down’s syndrome, ventricular septal defect, and patent ductus arteriosus rose, and along with central nervous system, cardiovascular, genitourinary, respiratory, chromosomal, and musculoskeletal defects rose 5 to 37 times faster than the birth rate (3.3%) to generate an excess of 11 753 (22%) major anomalies. Cannabis was the only drug whose use grew from 2000 to 2014 while pain relievers, cocaine, alcohol, and tobacco did not. The correlation of cannabis use with major defects in 2014 (2019 dataset) was R = .77, P = .0011. Multiple cannabinoids were linked with summary measures of congenital anomalies and were robust to multivariate adjustment.
66 References – click on this link to access
https://www.researchgate.net/publication/334368364_Cannabis_Teratology_Explains_Current_Patterns_of_Coloradan_Congenital_Defects_The_Contribution_of_Increased_Cannabinoid_Exposure_to_Rising_Teratological_Trends/link/5d2d4d39a6fdcc2462e3097c/download
5. Impacts of cannabinoid epigenetics on human development: reflections on Murphy et. al. ‘cannabinoid exposure and altered DNA methylation in rat and human sperm’ epigenetics 2018; 13: 1208-1221.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773386/pdf/kepi-14-11-1633868.pdf
Status
ABSTRACT Recent data from the Kollins lab (‘Cannabinoid exposure and altered DNA methylation in rat and human sperm’ Epigenetics 2018; 13: 1208–1221) indicated epigenetic effects of cannabis use on sperm in man parallel those in rats and showed substantial shifts in both hypo- and hyper-DNA methylation with the latter predominating. This provides one likely mechanism for the transgenerational transmission of epigenomic instability with sperm as the vector. It therefore contributes important pathophysiological insights into the probable mechanisms underlying the epidemiology of prenatal cannabis exposure potentially explaining diverse features of cannabis-related teratology including effects on the neuraxis, cardiovasculature, immune stimulation, secondary genomic instability and carcinogenesis related to both adult and pediatric cancers. The potentially inheritable and therefore multigenerational nature of these defects needs to be carefully considered in the light of recent teratological and neurobehavioural trends in diverse jurisdictions such as the USA nationally, Hawaii, Colorado, Canada, France and Australia, particularly relating to mental retardation, age-related morbidity and oncogenesis including inheritable cancerogenesis.
Increasing demonstrations that the epigenome can respond directly and in real time and retain memories of environmental exposures of many kinds implies that the genome-epigenome is much more sensitive to environmental toxicants than has been generally realized. Issues of long-term multigenerational inheritance amplify these concerns. Further research particularly on the epigenomic toxicology of many cannabinoids is also required.
206 References – click on this link to access
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6773386/pdf/kepi-14-11-1633868.pdf
6. Canadian Cannabis Consumption and Patterns of Congenital Anomalies: An Ecological Geospatial Analysis.
https://www.ncbi.nlm.nih.gov/pubmed/32187114
Status:
These results show that the northern Territories of Canada share a higher rate of cannabis use together with elevated rates of total congenital anomalies, all cardiovascular defects, Down’s syndrome and gastroschisis. This is the second report of a significant association between cannabis use and both total defects and all cardiovascular anomalies and the fourth published report of a link with Downs syndrome and thereby direct major genotoxicity. The correlative relationships described in this paper are confounded by many features of social disadvantage in Canada’s northern territories. However, in the context of a similar broad spectrum of defects described both in animals and in epidemiological reports from Hawaii, Colorado, USA and Australia they are cause for particular concern and indicate
further.
139 references – click on this link to access https://www.ncbi.nlm.nih.gov/pubmed/32187114
7. The Potential Association Between Prenatal Cannabis use and Congenital Anomalies
https://journals.lww.com/journaladdictionmedicine/Citation/9000/The_Potential_Association_Between_Prenatal.99243.aspx
Status:
Rates of prenatal cannabis use are likely to rise with legalization, increasing social tolerability, and promotion in social media. Cannabis consumption does not appear to be a benign activity, and there may be significant risk factors to the developing fetus when used in pregnancy. Even as epidemiological data continue to emerge, The American College of Obstetricians and Gynecologists and The Society of Obstetricians and Gynecologists of Canada recommend that women avoid the use of cannabis during pregnancy.14 Whether we will definitively establish the risk of prenatal cannabis use on congenital anomalies using epidemiological approaches remains unclear; however, combing data from ecological and patient-level approaches will be crucial. Patient engagement and increasing awareness of the health implications of cannabis are critical first steps to highlight the potential risks of cannabis use in pregnancy.
14. References – click on this link to access
https://journals.lww.com/journaladdictionmedicine/Citation/9000/The_Potential_Association_Between_Prenatal.99243.aspx
8. America Addresses Two Epidemics – Cannabis and Coronavirus and their Interactions: An Ecological Geospatial Study
Status: Embargoed until publication.
Question: Since cannabis is immunosuppressive and is frequently variously contaminated, is its use associated epidemiologically with coronavirus infection rates?
Findings: Geospatial analytical techniques were used to combine coronavirus incidence, drug and cannabinoid use, population, ethnicity, international flight and income data. Cannabis use and daily cannabis use were associated with coronavirus incidence on both bivariate regression and after multivariable spatial regression with high levels of statistical significance. Cannabis use quintiles and cannabis legal status were also highly significant.
Meaning: Significant geospatial statistical associations were shown between cannabis use and coronavirus infection rates consistent with mechanistic reports and environmental exposure concerns.
Extracts from Abstract:
Results. Significant associations of daily cannabis use quintile with CVIR were identified with the highest quintile having a prevalence ratio 5.11 (95%C.I. 4.90-5.33), an attributable fraction in the exposed (AFE) 80.45% (79.61-81.25%) and an attributable fraction in the population of 77.80% (76.88-78.68%) with Chi-squared-for-trend (14,782, df=4) significant at P<10-500. Similarly when cannabis legalization was considered decriminalization was associated with an elevated CVIR prevalence ratio 4.51 (95%C.I. 4.45-4.58), AFE 77.84% (77.50-78.17%) and Chi-squared-for-trend (56,679, df=2) significant at P<10-500. Monthly and daily use were linked with CVIR in bivariate geospatial regression models (P=0.0027, P=0.0059). In multivariable additive models number of flight origins and population density were significant. In interactive geospatial models adjusted for international travel, ethnicity, income, population, population density and drug use, terms including last month cannabis were significant from P=7.3×10-15, daily cannabis use from P=7.3×10-11 and last month cannabis was independently associated (P=0.0365).
Conclusions and Relevance. Data indicate CVIR demonstrates significant trends across cannabis use intensity quintiles and with relaxed cannabis legislation. Recent cannabis use is independently predictive of CVIR in both bivariate and multivariable adjusted models and intensity of use is significant in several interactions. Cannabis thus joins tobacco as a SARS2-CoV-2 risk factor.
Summary and Conclusions
The above research clearly shows the links with substance use and Mental illness, Autism, Congenital anomalies and Paediatric cancer including testicular cancer with marijuana use and abuse. Drug Free Australia respectfully and urgently requests a Position Statement and proposed actions from your Department regarding this research and how it can be further promoted and supported within Australia. We look forward to your timely response.
You can find a list of list of Ngo’s and Medical Professional who written support for Drug Free Australia’s Response to the commercialization of Cannabis/Marijuana/CBD in Australia
https://drugfree.org.au/images/pdf-files/homepagepdf/DRReeceSupport2020_updated6May2020.pdf.
Yours sincerely
Major Brian Watters AO B.A.
President
Drug Free Australia
PO Box 379
Seaford, SA 516
Objectives: Many reports exist of the cardiovascular toxicity of smoked cannabis but none of arterial stiffness measures or vascular age (VA). In view of its diverse toxicology, the possibility that cannabis-exposed patients may be ageing more quickly requires investigation.
Design: Cross-sectional and longitudinal, observational. Prospective.
Setting: Single primary care addiction clinic in Brisbane, Australia.
Participants: 11 cannabis-only smokers, 504 tobacco-only smokers, 114 tobacco and cannabis smokers and 534 non-smokers.
Exclusions: known cardiovascular disease or therapy or acute exposure to alcohol, amphetamine, heroin or methadone.
Intervention: Radial arterial pulse wave tonometry (AtCor, SphygmoCor, Sydney) performed opportunistically and sequentially on patients between 2006 and 2011.
Main outcome measure: Algorithmically calculated VA.
Secondary outcomes: other central haemodynamic variables.
Results: Differences between group chronological ages (CA, 30.47±0.48 to 40.36±2.44, mean±SEM) were controlled with linear regression. Between-group sex differences were controlled by single-sex analysis. Mean cannabis exposure among patients was 37.67±7.16 g-years. In regression models controlling for CA, Body Mass Index (BMI), time and inhalant group, the effect of cannabis use on VA was significant in males (p=0.0156) and females (p=0.0084). The effect size in males was 11.84%. A dose-response relationship was demonstrated with lifetime exposure (p<0.002) additional to that of tobacco and opioids. In both sexes, the effect of cannabis was robust to adjustment and was unrelated to its acute effects. Significant power interactions between cannabis exposure and the square and cube of CA were demonstrated (from p<0.002).
Conclusions: Cannabis is an interactive cardiovascular risk factor (additional to tobacco and opioids), shows a prominent dose-response effect and is robust to adjustment. Cannabis use is associated with an acceleration of the cardiovascular age, which is a powerful surrogate for the organismal-biological age. This likely underlies and bi-directionally interacts with its diverse toxicological profile and is of considerable public health and regulatory importance.
Keywords: Accelerated aging; Biological age; Biomarkers of aging; Cannabis and aging.
Source: Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study – PubMed (nih.gov) November 2016
In a study published this week, researchers asked tens of thousands of individuals over 12 years of age about their use of tobacco products, e-cigarettes, and their health, and conducted follow-up questions over three years.1 They found the development of lung problems like emphysema, bronchitis, asthma, and chronic obstructive pulmonary disease in individuals who had used e-cigarettes in the past or currently use them. Combined use of e-cigarette and tobacco products dramatically increased lung disease risks by an incredible 330 percent. The researchers concluded that, “Use of e-cigarettes is an independent risk factor for respiratory disease in addition to combustible tobacco smoking.” The study’s senior author, Stanton Glantz, told CNN, “I was a little surprised that we could find evidence on incident lung disease in the longitudinal study, because three years is a while but most studies that look at the development of lung disease go over 10 to 20 years.”
The Centers for Disease Control (CDC) reports that, as of December 10, 2019, there are 2,409 hospitalization cases of vaping-related lung injuries in the U.S., resulting in 52 deaths across 26 states and Washington, D.C.2 The FDA has found THC in most of the samples it’s studying from these cases and has highlighted Vitamin E acetate as a chemical linked to some of the lung injuries. But the CDC warns that it still does not know how many other chemicals and products may be involved, and says that, “the best way for people to ensure that they are not at risk while the investigation continues is to consider refraining from the use of all e-cigarette, or vaping, products.” NIDA just reported that 3.5 percent of 12th graders and 3 percent of 10th graders say they vape on a daily basis, with 14 percent of 12th graders also saying that they vaped marijuana in the previous month. That figure is twice as large as it was last year.
Though federal officials have reportedly backed away from banning flavored vaping products3, some states have implemented such restrictions. And other national lawmakers are still considering similar options to confront the vaping epidemic.4 Dr. Scott Gottlieb, the former FDA Commissioner, has now recommended banning all cartridge-based e-cigarette products, which would include popular devices like Juul.5 Gottlieb, along with other experts, is worried about the epidemic of youth vaping, nicotine use and dependence which can lead to the use of tobacco-based products, the number one cause of preventable death, and other substances later in life.
Stories about vaping-related severe lung diseases, the epidemic of youth use, and public policy responses are important for patients, families, medical professionals, and consumers to follow. But we should also continue to monitor research that paints an even more distressing picture of e-cigarette products. In a recent study, researchers looked at the association between e-cigarette use and cancer.
What did this study find about e-cigarette use and cancer in mice?
This study found that exposure to e-cigarettes led to tumors and precancerous growths in the lungs and bladders of mice. The nicotine vapor from e-cigarettes damaged DNA in the exposed mice’s organs.
When tobacco burns, it can change nicotine into carcinogens called nitrosamine ketone. In individuals who use electronic cigarettes, these carcinogens in saliva and urine are 95 percent lower than they are individuals who smoke tobacco. That’s why the UK government says that electronic cigarettes are 95 percent safer than tobacco products. But it’s not as certain that nicotine from e-cigarettes gets turned into these carcinogens, so it’s also not clear if their levels in saliva and urine of individuals using e-cigarettes are a good guide to possible damage. The body can also absorb these carcinogens in other ways, as harmful to DNA. This study looked at DNA damage in mice to see if e-cigarettes might cause lung and bladder cancer, instead of carcinogenic impact in blood and urine. It’s also important to note that no experts suggest that vaping or smoking is good for you.
Researchers exposed the full bodies of 40 mice to e-cigarette vapor for 54 weeks. 22.5 percent of these mice developed lung tumors and, in their bladders, 57.5% ended up with precancerous growths. 20 mice in a control group, subjected to e-cigarette vapor but not nicotine, did not develop tumors. E-cigarette exposure in this study is comparable to human e-cigarette use over three to six years. The study’s authors believe that the results probably indicate e-cigarette aerosol nicotine reaching far into lung tissue and causing DNA damage. They also say that, “The public should not equate the risk of ECS [e-cigarette smoke] with that of TS [tobacco smoke]. Our data simply suggest, on the basis of experimental data in model systems, that this issue warrants in-depth study in the future.” This study also had limitations. It used a small sample size and did not focus on the inhalation of e-cigarette nicotine vapor. And animal studies are not necessarily clear guides for related effects in humans.
Why is this important?
This is the first study finding an association between e-cigarette use and cancer. Though the authors are careful to offer caveats about the research’s limitations, not drawing inferences about the relative safety of e-cigarettes and tobacco products, and the need for more extensive studies, this is still a significant and troubling result. It took many decades for experts to agree that tobacco smoke caused cancer. It seems more logical to assume that smoking and vaping are dangerous until proven otherwise. Some countries have seen enough and banned e-cigarettes completely, such as Argentina, Saudi Arabia, and Singapore. Others do not think it is safe but consider e-cigarettes as part of a harm reduction strategy. The study’s lead, New York University’s Dr. Moon-Shong Tang told CNBC, “It’s foreseeable that if you smoke e-cigarettes, all kinds of disease comes out. Long term, some cancer will come out, probably. E-cigarettes are bad news.” He also suggested that because e-cigarette products have only existed for a relatively short period of time, it may take a while for more research to measure their health effects more comprehensively—possibly up to a decade.
It’s always appropriate for researchers to be cautious about their findings and to point to countervailing factors and the need for supplemental work and corroborating studies. Even experts can be surprised. But more studies continue to indicate the dangers of e-cigarette use. It’s also worth pointing out that there are dangers beyond these studies: inhaling nicotine vapors is likely to stimulate its own continued use, while costing time, energy and money. The cost of a pack of cigarettes is quite cheap even with current taxes. Actual costs are difficult to understand. In general, we assume smoking two packs of cigarettes a day for 20 years is more expensive than the $75,000 for the cost of the cigarettes. The long-term costs are closer to $2 million, after factoring in treatments for tobacco-related cancer, lung and heart disease, and the reduction in lifespan and productivity of the individual using cigarettes.
Prevention of adolescent smoking initiation is a very important health goal, one that we were much closer to attaining before vaping. Experts warn that vaping is causing a new nicotine addiction epidemic.6 They estimate, for example, that, because of vaping, almost 500,000 individuals between the ages of 12 and 29 who used e-cigarettes also end up using tobacco products.7 Use of e-cigarettes paves the way for use of tobacco-based cigarettes, as research suggests.8 If the full costs to society were included at the point of purchase, each pack of cigarettes would cost at least $75. Very few people would choose to spend $75/pack. Similarly, we could find a price at which vaping is less attractive to consumers. The science, in other words, is clear about the risks, and tobacco-like public health-related tax initiatives may be appropriate. Vermont recently passed a 92% wholesale tax on vaping and e-cigarette products. Federal lawmakers are also considering tax changes.
Keeping in mind that it took decades, if not centuries, to prove that cigarette smoking causes cancer, these new e-cigarette studies suggest that the products aren’t just understudied and possibly dangerous, but increasingly just dangerous, associated more frequently with chronic disease, heart problems, and even cancer.9 This study is also interesting in its full-body exposure of mice to e-cigarette vapor, which suggests that secondhand vaping may be dangerous, too. Other reports are coming out suggesting that e-cigarette inhalation is dangerous for everyone, include individuals who do not use the products but may be exposed to them. Mounting evidence shows that e-cigarette use is a highly risky proposition for current and potential consumers and that officials and experts are justified in pursuing ways to curb use. Reversing use trends will require a great deal of work given the near exponential increases in youth vaping.
References:
Bhatta, D.N., Glantz, S.A. (2019) Association of E-Cigarette Use With Respiratory Disease Among Adults: A Longitudinal Analysis. American Journal of Preventive Medicine
Centers for Disease Control and Prevention (CDC). (2019) Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products. Retrieved from https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html
Karni, A., Kaplan, S. (2019) Trump Warns a Flavor Ban Would Spawn Counterfeit Vaping Products. New York Times. Retrieved from https://www.nytimes.com/2019/11/22/health/trump-vaping.html
Hellmann, J. (2019) House Democrats to vote on flavored e-cigarettes ban next year. The Hill. Retrieved from https://thehill.com/policy/healthcare/474184-house-democrats-to-vote-on-flavored-e-cigarettes-ban-next-year
Florko, N. (2019) Former FDA commissioner calls for a full ban on pod-based e-cigarettes. Stat. Retrieved from https://www.statnews.com/2019/11/12/gottlieb-ban-pod-based-e-cigarettes/
Dinardo, P., Rome, E.S. (2019) Vaping: The new wave of nicotine addiction. Cleve Clin J Med.
Soneji, S., Wills, T.A. (2019) Challenges and Opportunities for Tobacco Control Policies in the 21st Century. JAMA Pediatr
National Academies of Sciences, Engineering, and Medicine. (2018) Public health consequences of e-cigarettes. The National Academies Press, Washington, DC
Proctor, R.N. (2012) The history of the discovery of the cigarette-lung cancer link: evidentiary traditions, corporate denial, global toll. Tob Control
Citation:
1. Tang, M., et al. (2019) Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice. PNAS
Source: https://pubmed.ncbi.nlm.nih.gov/
Cannabis hyperemesis syndrome (CHS) is nothing new, but nonetheless lacks a diagnosis code. This means that nobody—including the Centers for Disease Control and Prevention, which is meant to track such things—knows the prevalence of the condition. It is, however, relatively rare. Medical sources say that it’s likely, as you’d expect, to become more common as nationwide cannabis use increases.
No one claims that CHS is lethal, but it is uncomfortable—and in an emergency room situation requires such medications as haloperidol, an antipsychotic, to relieve vomiting and pain. Business Insider recently reported the story of 29-year-old Alice Moon, who began using cannabis regularly to treat pain and nausea. She did so without problems for five years, but then began experiencing CHS symptoms monthly, and eventually weekly.
People who use any substance deserve access to relevant health information, without exaggeration in either direction. “Marijuana is somehow making millions violently sick” and “Mysterious Syndrome Related To Marijuana Use Begins To Worry Doctors” are two CHS-related news headlines from the past month alone. But CHS likely doesn’t affect millions, and it is less mysterious than some imply.
So this isn’t a Reefer Madness story, designed to scare people, nor a head-in-the-sand story, designed to appeal to those who see cannabis as a risk-free panacea.
Even pro-cannabis advocates agree that CHS exists. “It’s a diagnosis of exclusion,” Peter Grinspoon, MD, a primary care physician at an inner-city clinic in Boston, told Filter. Grinspoon is also on staff at Massachusetts General Hospital, teaches at Harvard Medical School, and authored the memoir Free Refills: A Doctor Confronts His Addiction (2016). “I’m not sure how you can really differentiate it from cyclic vomiting syndrome (CVS), idiopathic [unknown cause] vomiting, or just something else causing the vomiting—except for a cannabis history.”
Experts believe that the action of the cannabinoid THC on our CB1 receptors, which are found all over the body but mainly in the brain, produces the symptoms of CHS—though the amounts of THC required, the duration of use in months or years, and why some people experience CHS and not others, are still unexplained.
One thing everyone seems to agree on: CHS is caused by heavy long-term use of cannabis—i.e., it’s not a result of overdose or acute toxicity. And it has one unusual manifestation: People afflicted like to take many hot baths or showers for relief.
A study published last month, based on emergency room visits in a Colorado hospital, also found that CHS is more likely to be associated with smoked than edible cannabis. Of 2,567 ER visits that were at least partly attributed to cannabis use, 18 percent of patients who inhaled it were said to have CHS, versus 8.4 percent of those who ate it.
Emergency Physicians’ Experiences
“It’s very dramatic—patients are sometimes writhing on the floor, and they’re vomiting so much. It’s a horrible syndrome,” said Andrew C. Meltzer, MD, associate professor in the Department of Emergency Medicine and Clinical Research Director of GWU School of Medicine and Health Sciences. “It’s very different from any other kind of vomiting thing, and very disruptive to the ED.”
And in the worst cases, “repeated aggressive vomiting can cause tears in the esophagus.”
Unlike gastroenteritis, with CHS there is no diarrhea, no fever and more of a hypersensitivity to pain in the abdomen, Meltzer told Filter. There is an “overlap” with cyclical vomiting syndrome (CVS), in that many symptoms are the same. Blood work might be needed to rule out pancreatitis and hepatitis, and some patients get radiology.
Toxicology testing, on the other hand, is not very useful, because so many people use marijuana without showing these symptoms. Rather, it’s important to get a history of the extent and duration of marijuana use from the patient, said Meltzer. “Confusion exists in the medical literature,” he noted. In addition, he believes there is a pervasive failure to recognize chronic cannabis use as a possible cause of vomiting.
“We’re still trying to figure out how to make them feel better,” said Meltzer of CHS patients. “Typical anti-emetics like Phenergan and Zofran don’t work. Instead, we use antipsychotics, like haloperidol.” In fact, if the haloperidol works, Meltzer views that as diagnostic of CHS in some ways. The heat from capsaicin rubbed on the abdomen also provides some relief from pain.
In the patients Meltzer has seen with CHS, all “would qualify as addicted” to cannabis, he said. He doesn’t recommend using morphine for CHS pain because of what he sees as the addiction risk in this population.
Some CHS patients can’t be treated with emergency room management alone. Meltzer said he had to admit one patient for dehydration, fluids replacement, renal insufficiency, and other problems. “But now we’re getting more used to how to manage this with haloperidol and even Ativan. They are sedated, they sleep, and they go home.”
“I don’t care what people do in their free time, but in the medical history I try to include things that are pertinent.”
Ryan Marino, MD, an emergency medicine physician and medical toxicologist at the University of Pittsburgh, sees CHS about two-to-three times a month—but acknowledges it could be more, because sometimes it’s hard to be sure.
“The big issue is [CHS] is under-recognized,” said Marino, agreeing with Meltzer. “So a lot of patients get unnecessary testing.” For someone who comes in with a lot of nausea and vomiting, and is young and otherwise healthy, he says it’s important to ask about their marijuana use.
“I try to be as non-judgemental as possible” in asking those questions, he said. “I don’t care what people do in their free time, but in the medical history I try to include things that are pertinent.”
With emergency patients, the differential diagnosis is crucial and must be done quickly. “When there’s belly pain, you worry about things that need surgery, like appendicitis and the gallbladder,” said Marino. “CVS is kind of similar [to CHS], but people aren’t using cannabis.” So asking about marijuana use history can clearly help.
“The main thing seems to be people who use heavily and regularly: daily use or near-daily use,” said Marino. “With the rise of medical cannabis, more people have access to it, so maybe there are more presentations now than there used to be. But with no ICD [International Classification of Diseases] code, I don’t think you’d be able to say whether you can find prevalence.”
Marino acknowledges that there’s a fine line to tread in questioning patients, especially in situations where they are worried about law enforcement, and some healthcare providers are better than others at getting honest histories. “There are going to be people on the provide side who don’t get the truth out of patients, and there are patients who won’t disclose. This is why the way we treat patients is important.”
Gastroenterologists’ Perspectives
Whether they’re called in to consult in the emergency department or see a person in their office, gastroenterologists have a big role to play for CHS patients. CHS has been known about since 2004, but a seminal 2011 Current Drug Abuse Reviews article put gastroenterologists on the alert.
A year ago, Healio interviewed gastroenterologist Joseph Habboushe, MD for an article titled “Cannabinoid hyperemesis syndrome: What GIs should know.” Habboushe had surveyed 155 patients in an emergency department who reported smoking marijuana frequently and found that 32.9 percent of them met criteria for CHS. He concluded that the syndrome is vastly underreported.
“I would definitely ask” about marijuana use in the case of an otherwise-healthy, vomiting patient, said Lisa Gangarosa MD, AGAF, FACP, professor of Medicine at the UNC Division of Gastroenterology and Hepatology, speaking for the American Gastroenterological Association. “The diagnosis is largely made on the history.”
There is no clear test. “Basically, if the history fits, and if the patient stops smoking and gets better, that’s what it was.”
Some testing would be done to exclude other problems, such as stomach cancer, a large ulcer or gallstones, Gangarosa told Filter. It’s also important to conduct basic lab testing, such as for pregnancy, and then, if all of that testing comes back negative, to think about endoscopy and ultrasound of the gallbladder.
Gangarosa has only seen CHS in patients who have been “smoking pot,” not in anyone who has been prescribed dronabinol, which is synthetic THC.
There is no clear test for the syndrome. “In some cases you can say your impression is suspected marijuana-induced hyperemesis,” she said. “Basically, if the history fits, and if the patient stops smoking and gets better, that’s what it was.”
Surprisingly, many patients who use cannabis haven’t heard of CHS, said Gangarosa. For others, they don’t want to stop smoking, “and they don’t want to believe that this is the cause of their problems. It’s the same thing with pancreatitis—just because of the health harms, doesn’t mean people want to give up drinking.”
The Hot Bath Phenomenon
Andrew Meltzer, the ED physician, said that some of his patients have taken six-to-eight warm baths a day to relieve symptoms.
This reminds me of a personal experience. A member of my family had acute gastritis at the age of six, with a lot of vomiting, and was hospitalized for a week. All she wanted to do was lie in the hospital bathtub with the water as hot as possible. There was no marijuana involved, but bells went off in my head when I heard about the hot shower “cure.” Could this be a common way of responding to extreme vomiting and pain in general?
Experts stress that the hot shower treatment is anecdotal, and can’t be used as a sure sign of CHS. “But it’s something I ask people,” said Ryan Marino. “It seems as if most people have figured out” that it works. “It might be that they’re so symptomatic they try anything, and find the one thing that works.”
Like the capsaicin, which provides heat, and heating pads, heat from the hot shower on the belly might relieve the pain, said Marino. However, “I don’t think anyone has a good reason for the link” between CHS and hot showers.
A Researcher’s View
The National Institute on Drug Abuse (NIDA) referred Filter to Kiran Vemuri, PhD, a research assistant professor at Northeastern University in Boston, who has a grant from the agency to find an antidote for synthetic cannabinoid intoxication.
That, of course, is a very different issue from CHS. But as an organic chemist, Vemuri has studied emesis from a CB1 antagonist perspective. He is aware of the paradox with THC: The synthetic version, dronabinol, is approved by the FDA to treat the nausea and vomiting associated with chemotherapy, as well as to increase appetite in wasting associated with AIDS, and for many other conditions.
How would the same substance that treats nausea induce it?
“This only happens in people who have been consuming cannabis for a long time,” Vemuri said. But he noted that most information in the literature is anecdotal and based on case histories. “People try to come up with a number”— how much cannabis, for how long—“but you can never really tell as to what causes the hyperemesis. Is it the dose, is it the strain?”
“If you know the CB1 receptor is implicated … the best treatment option would be an antagonist.” Except there isn’t one.
Vemuri has studied antagonists which induce nausea, with the CB1 receptor the biological target. CB1 receptors are all over the body, but most are in the brain, he said.
If you want to know everything the top researcher in emesis (vomiting) knows about the topic, look up the work of Linda Parker. It’s hard to study in animals, because not all of them even vomit.
There is no antidote for emesis itself, said Vemuri. “But if you know that the CB1 receptor is implicated, and the patient is presenting with an overdose of THC or synthetic cannabinoids, the best treatment option would be an antagonist.” Except there isn’t one.
As for the hot showers, CB1 receptors could indeed be involved, but there is no “concrete connection” to CHS or its treatment, said Vemuri.
And he cautions that “‘overdose’ is a big word when it comes to THC.” The dose, the strain, the route of administration all matter, he said. And because THC can reside in fat, and build up, it makes sense that some of the side effects could be worse in people who have consumed THC over a long period of time. “At the end of the day, anything in excess is not good.”
No Easy Cure
There was one medication which briefly showed promise for CHS—ribonabant—but it was removed from the market due to psychiatric side effects (suicidal ideation). “The target is so new,” Vemuri said. “But NIDA is definitely interested, and no one ever gave up on the target, and no one ever gave up on cannabis, and no one ever gave up on the antagonists. Recently I was at a conference where I got to know companies that are pursuing both CB1 and CB2.”
While hot showers may provide temporary relief, and anti-emetics and intravenous hydration can help “someone in the throes of repetitive vomiting,” for now, the best way for CHS patients to avoid further symptoms for good is to stop using cannabis, said Lisa Gangarosa, the gastroenterologist.
“That is always the recommendation,” agreed Marino. “It seems to be the only thing that makes it better or makes it go away. But it’s not always the easiest thing. It’s easy for me to say.”
The implications of quitting for people who use cannabis for medical reasons—and the difficulties for people who are addicted—are clear. But for now, the unknown minority of cannabis users unfortunate enough to experience cannabis hyperemesis syndrome have no other reliable recourse.
Source: https://www.dbrecoveryresources.com/2019/04/what-is-cannabis-hyperemesis-syndrome/ April 2019
The doctors told Regina Denney and her son Brian Smith Jr. what was causing his severe vomiting and abdominal pain.
Neither the teenager nor his mother believed what they said: smoking weed.
Smoking marijuana, the two knew, was recommended to cancer patients to spur the appetite. How could it lead to Brian’s condition?
As the months went by and the pounds slipped off Brian’s once healthy frame, it was clear that whatever was causing his stomach troubles had just the opposite effect.
Brian kept smoking. The symptoms continued on and off.
Last October, after another severe bout of vomiting, the teenager died. He was 17 years old.
Five months later, as Denney pored over a coroner’s report for answers, she finally accepted that marijuana played a pivotal role in her son’s death. The autopsy report, which Denney received in March, attributed her son’s death to dehydration due to cannabinoid hyperemesis syndrome.
“We had never heard about this, had never heard about marijuana causing any vomiting. He and I were like, ‘Yeah, I think it’s something else,’ ” Denney said. “Brian did not believe that was what it was because of everything we had ever been told about marijuana. … It didn’t make any sense.”
Cannabinoid hyperemesis syndrome, also known as CHS, can arise in response to long-term cannabis use. The syndrome consists of vomiting, nausea and abdominal pain, which can often be alleviated by taking hot showers.
Doctors say CHS is on the rise, but they are not certain why. Marijuana is more available than in years past, and it is more potent.
Rarely does CHS result in death.
Denney didn’t like the fact that her teen son started smoking at 13, but she figured the situation could be worse. Brian and she had a strong relationship, and he always had been honest with her about his use of marijuana.
For the most part, Brian was a good kid who had a tightknit group of friends who called themselves the GBS, Gimber Block Savages, after the south side street where many of them lived. Although they called themselves a gang, Denney said, they never caused any trouble.
“Basically, they smoked weed,” she said.
About two years after Brian started smoking, he began using a lot more, perhaps to help deal with depression, Denney said. He dropped out of school after ninth grade and started working full-time with an uncle who had a tree-trimming business. Brian helped clear brush.
The job provided enough money to support his marijuana habit, another reason Denney felt there was no reason for her to intervene. After all, many of Brian’s peers were using heroin or methamphetamine.
“I thought, ‘OK, if that’s all he’s doing, smoking marijuana, pick and choose your battles,’ ” she said. “If this is the worst thing he’s doing, I’m OK. He’s not in any trouble legally. He’s not playing with guns, robbing people and stealing things. He’s supporting his own habit. I thought, ‘OK, this is what it is.’ ”
Denney had no reason to be concerned about cannabinoid hyperemesis syndrome. She, like many others, had never heard of it.
A few years ago, many doctors had no idea this condition existed. First described 15 years ago, CHS symptoms follow heavy cannabis use and include intense stomach pain, bouts of vomiting and debilitating nausea.
A study published last year in the journal Basic & Clinical Pharmacology & Toxicology surveyed urban emergency room patients who smoked marijuana 20 or more days a month. Of the 155 who said yes, almost a third experienced CHS symptoms.
“A lot of papers prior to mine would say it’s very rare,” said Joseph Habboushe, one of the study’s authors and a clinical associate professor of emergency medicine at NYU Langone Health in New York City, who saw his first case five or six years ago. “Emergency room doctors on the front-line lines, we know that it’s a totally underdiagnosed entity.”
On the other side of the country, Dr. Jeff Lapoint and his colleagues saw an influx of patients with CHS symptoms about six years ago. Lapoint is the director of the division of medical toxicology at Kaiser Permanente Southern California and practices in San Diego, which he said is home to both craft beer and craft marijuana.
Many of Lapoint’s patients returned time after time when the next bout hit, seeking relief from their stomach woes.
“We would see lots of it. We would see an alarming amount of it,” Lapoint said. “People were coming in all the time, and physicians didn’t know what to do with them.”
Op-ed: Vaping deaths and booming black market: Pot experiment will fail without better oversight
Lapoint said he and his colleagues have seen fewer such cases lately.
Habboushe concluded in his study that as many as 2.75 million regular cannabis users may suffer from symptoms of CHS, though many of them may be mild. Mild symptoms can serve as a warning to discontinue cannabis use to avoid more severe distress down the line, Habboushe said.
A study this year in the Journal of Forensic Science described two people in Canada who died from CHS and a third for whom the condition contributed to death.
Brian was Denney’s baby, her boy after two girls. From the time he was a child, he suffered from acid reflux and often took medicine to ease the symptoms.
Brian, who loved sports and the movie “Twilight,” was close to his family and called himself his mother’s “snuggle bunny.” He was beloved uncle BubBub to his toddler nephew, Zayden. He was a loyal friend, once giving up his bed so a buddy who was homeless had a place to sleep. As a teen, he split time between Denney’s home and that of his father.
In April 2018, Brian felt ill. At first everyone, including his pediatrician, thought his acid reflux was acting up. He lost 40 pounds and frequently complained of nausea that led him to avoid food.
A few days into the illness, he called his mother and told her he couldn’t stop vomiting. Denney drove to his father’s house to take him to the hospital. On the way to Franciscan St. Francis Health, Denney had to stop multiple times for Brian to vomit.
The 1st tied to a weed shop: Another death is linked to vaping. This time, it’s in Oregon
Brian complained of tingling in his face. When they got to the hospital, half his face was numb, the muscles in his hands and legs constricted and froze, and he projectile vomited.
Denney assumed he was having a stroke.
Within a few minutes, he was hooked up to oxygen and a heart monitor. Medical staff placed IVs in each arm. Tests revealed his kidneys were failing, and many of his other lab values were abnormal. No one could tell what was behind the attack, though they knew the frequent vomiting left him dehydrated.
Another emergency room doctor poked her head in the door and asked two questions: Do you smoke marijuana often? Do you take frequent hot showers?
Yes, Brian said. Yes.
You have CHS, the doctor said.
The following day, Brian was discharged with an appointment to follow up with a gastroenterologist in July.
Although neither Denney nor Brian accepted the diagnosis completely, she urged him to consider not smoking as a process of elimination. He agreed, but he struggled with nausea and was too sick to work.
The GI doctor took a tube of blood, did no further testing and confirmed the earlier diagnosis: CHS.
Denney remained unconvinced, thinking the specialist was too quick to accept the emergency room doctor’s diagnosis without doing any confirmatory testing.
“Going to the GI doctor, I thought we’re going to finally get an answer. We’re going to finally know what we need to do to make him better,” she said. “Then when they didn’t run any other tests, it was like, ‘OK, so why are we not doing them?’ It makes no sense.”
After that visit, Brian returned to his dad – and started smoking again.
He told Denney he had symptoms the whole time he wasn’t smoking, so what was the point of quitting?
Experts aren’t 100% sure what’s behind the relatively sudden advent of this condition. They suspect that more potent cannabis may be to blame, along with several states’ decision to legalize the drug for medicinal purposes or altogether.
In the 1970s, THC concentration in most marijuana would be about 7%, Lapoint said. The mean concentration has risen to 15% to 30%, and it’s possible to make extracts with 99% THC.
“Marijuana was the joke of the toxicology world when it was 7%,” Lapoint said. “People never got sick. … But now if you make the concentration 99%, it’s just like if a 17-year-old kid goes to a frat party and has a beer. That’s a lot different than drinking shots of Everclear 151. Just like anything, the dose makes the poison.”
Vaping lung illness:: What we know about the recent spate of cases and deaths
The best treatment for CHS is to stop using cannabis entirely, Habboushe said.
Once a person develops the condition, he or she has probably done something permanent. Further exposure to cannabis highly increases risk of recurrence. Persuading patients to accept this can be difficult, Habboushe said.
“There’s a lot of denial,” he said. “A lot of patients are really heavy marijuana smokers, and they really don’t want to believe that it’s related to cannabis and hard for them to believe because they have been using cannabis forever.”
In July Brian moved back in with Denney. She knew he was not going to give up smoking, but she thought being around his nephew would encourage him to smoke less.
A few months passed. Brian did not put back the weight, but he seemed to be a bit better.
Then came Oct. 7. Brian started feeling ill again. Denney and her daughters had concert tickets, so she went to buy him Gatorade and popsicles to stem the nausea and asked his father to come and stay with him.
When they returned from the concert, he started vomiting nonstop. They rushed to the St. Francis emergency room, where doctors transferred him to Riley Hospital for Children. Once more, Brian was rehydrated.
Denney said her son cut back on smoking, but a few weeks later, he went to visit his cousins. “I know they smoked,” Denney said. “That’s just what he did.”
When she picked him up Oct. 21, he felt a little nauseated but had not been vomiting.
Three days later, Denney woke up around 5 a.m. to find her son sitting in the living room and clutching his stomach.
He told her it was his acid reflux but he was fine. Then he started vomiting again.
“He was throwing up so much,” Denney said. “I was taking the bucket in there and holding it for him because he didn’t have the energy to hold it.”
For the first time, Brian told her he was going to quit smoking.
He grabbed his lower back, saying it hurt bad.
Remembering his kidneys had suffered in his previous attacks, Denney called 911.
Before the paramedics arrived, she found her son lying on his side.
She rolled him over. He was not breathing.
Denney screamed. She started doing chest compressions. Her daughter’s boyfriend ran across the street to get their neighbor, a Navy veteran.
“I kept telling him, ‘Fight, B, fight. I need you. Don’t give up.’ I begged God to take me instead,” Denney said.
The paramedics arrived and worked on Brian for about 45 minutes to no avail. On Oct. 24, Brian died.
Because he died at home, detectives had to investigate, and the coroner prepared a report. It took five months for Denney to receive a copy. It arrived on her birthday in early March.
Soon after Brian’s death, Denney found edibles in his backpack.
She asked herself again and again what she should have done. Should she have forced him to go to rehab?
Denney devoted herself to helping raise awareness about CHS. She started a Facebook group in Brian’s name. She talks about Brian and CHS every chance she gets. She keeps Brian close to her, wherever she is.
Photos of her son hang on the walls in her bedroom. On her dresser sits a dark urn emblazoned with a gold marijuana leaf that contains Brian’s ashes. His sister chose it. She knew her brother would have liked it.
Source: Indiana boy, 17, died from smoking weed. CHS is to blame. What is CHS? (usatoday.com) September 2019
DENVER — When Colorado legalized marijuana, it became a pioneer in creating new policies to deal with the drug.
Now the state’s surgeons, nurses and anesthesiologists are becoming pioneers of a different sort in understanding what weed may do to patients who go under the knife.
Their observations and initial research show that marijuana use may affect patients’ responses to anesthesia on the operating table — and, depending on the patient’s history of using the drug, either help or hinder their symptoms afterward in the recovery room.
Colorado makes for an interesting laboratory. Since the state legalized marijuana for medicine in 2000 and allowed for its recreational sale in 2014, more Coloradans are using it — and they may also be more willing to tell their doctors about it.
Roughly 17% of Coloradans said they used marijuana in the previous 30 days in 2017, according to the National Survey on Drug Use and Health, more than double the 8% who reported doing so in 2006. By comparison, just 9% of U.S. residents said they used marijuana in 2017.
“It has been destigmatized here in Colorado,” said Dr. Andrew Monte, an associate professor of emergency medicine and medical toxicology at the University of Colorado School of Medicine and UCHealth. “We’re ahead of the game in terms of our ability to talk to patients about it. We’re also ahead of the game in identifying complications associated with use.”
One small study of Colorado patients published in May found marijuana users required more than triple the amount of one common sedation medicine, propofol, as did nonusers.
Those findings and anecdotal reports are prompting additional questions from the study’s author, Dr. Mark Twardowski, and others in the state’s medical field: If pot users indeed need more anesthesia, are there increased risks for breathing problems during minor procedures? Are there higher costs with the use of more medication, if a second or third bottle of anesthesia must be routinely opened? And what does regular cannabis use mean for recovery post-surgery?
But much is still unknown about marijuana’s impact on patients because it remains illegal on the federal level, making studies difficult to fund or undertake.
It’s even difficult to quantify how many of the estimated 800,000 to 1 million anesthesia procedures that are performed in Colorado each year involve marijuana users, according to Dr. Joy Hawkins, a professor of anesthesiology at the University of Colorado School of Medicine and president of the Colorado Society of Anesthesiologists. The Colorado Hospital Association said it doesn’t track anesthesia needs or costs specific to marijuana users.
As more states legalize cannabis to varying degrees, discussions about the drug are happening elsewhere, too. On a national level, the American Association of Nurse Anesthetists recently updated its clinical guidelines to highlight potential risks for and needs of marijuana users. American Society of Anesthesiologists spokeswoman Theresa Hill said that the use of marijuana in managing pain is a topic under discussion but that more research is needed. This year, it endorsed a federal bill calling for fewer regulatory barriers on marijuana research.
Why Should Patients Disclose Marijuana Use?
No matter where patients live, though, many nurses and doctors from around the country agree: Patients should disclose marijuana use before any surgery or procedure. Linda Stone, a certified registered nurse anesthetist in Raleigh, N.C., acknowledged that patients in states where marijuana is illegal might be more hesitant.
“We really don’t want patients to feel like there’s stigma. They really do need to divulge that information,” Stone said. “We are just trying to make sure that we provide the safest care.”
In Colorado, Hawkins said, anesthesiologists have noticed that patients who use marijuana are more tolerant of some common anesthesia drugs, such as propofol, which helps people fall asleep during general anesthesia or stay relaxed during conscious “twilight” sedation. But higher doses can increase potentially serious side effects such as low blood pressure and depressed heart function.
Limited airway flow is another issue for people who smoke marijuana. “It acts very much like cigarettes, so it makes your airway irritated,” she said.
To be sure, anesthesia must be adjusted to accommodate patients of all sorts, apart from cannabis use. Anesthesiologists are prepared to adapt and make procedures safe for all patients, Hawkins said. And in some emergency surgeries, patients might not be in a position to disclose their cannabis use ahead of time.
Even when they do, a big challenge for medical professionals is gauging the amounts of marijuana consumed, as the potency varies widely from one joint to the next or when ingested through marijuana edibles. And levels of THC, the chemical with psychoactive effects in marijuana, have been increasing in the past few decades.
“For marijuana, it’s a bit of the Wild West,” Hawkins said. “We just don’t know what’s in these products that they’re using.”
Marijuana’s Effects On Pain After Surgery
Colorado health providers are also observing how marijuana changes patients’ symptoms after they leave the operating suite — particularly relevant amid the ongoing opioid epidemic.
“We’ve been hearing reports about patients using cannabis, instead of opioids, to treat their postoperative pain,” said Dr. Mark Steven Wallace, chair of the pain medicine division in the anesthesiology department at the University of California-San Diego, in a state that also has legalized marijuana. “I have a lot of patients who say they prefer it.”
Matthew Sheahan, 25, of Denver, said he used marijuana to relieve pain after the removal of his wisdom teeth four years ago. After surgery, he smoked marijuana rather than using the ibuprofen prescribed but didn’t disclose this to his doctor because pot was illegal in Ohio, where he had the procedure. He said his doctor told him his swelling was greatly reduced. “I didn’t experience the pain that I thought I would,” Sheahan said.
In a study underway, Wallace is working with patients who’ve recently had surgery for joint replacement to see whether marijuana can be used to treat pain and reduce the need for opioids.
But this may be a Catch-22 for regular marijuana users. They reported feeling greater pain and consumed more opioids in the hospital after vehicle crash injuries compared with nonusers, according to a study published last year in the journal Patient Safety in Surgery.
“The hypothesis is that chronic marijuana users develop a tolerance to pain medications, and since they do not receive marijuana while in the hospital, they require a higher replacement dose of opioids,” said Dr. David Bar-Or, who directs trauma research at Swedish Medical Center in Englewood, Colo., and several other hospitals in Colorado, Texas, Missouri and Kansas. He is studying a synthetic form of THC called dronabinol as a potential substitute for opioids in the hospital.
Again, much more research is needed.
“We know very little about marijuana because we’ve not been allowed to study it in the way we study any other drug,” Hawkins said. “We’re all wishing we had a little more data to rely on.”
Source: If You Smoke Pot, Your Anesthesiologist Needs To Know – KFF Health News August 2019
As states have begun to legalize marijuana, its use has been more openly discussed. While the effects of other commonly used drugs, such as alcohol, have been studied extensively, the effects of marijuana – especially on developing babies during pregnancy – have been much less studied and less widely publicized. This relative silence from the scientific community has affected the public’s opinion on the safety of marijuana: 70 percent of U.S. women think there is “slight or no risk of harm” to the baby from using marijuana during pregnancy. Expectant mothers may use marijuana rather than prescription drugs during pregnancy to relieve pain because they feel “natural” or home remedies are a safer option than prescription drugs. However, just because something is “natural” doesn’t mean it is any safer or a better alternative to well-studied prescription drugs. This seems to be the case for marijuana. Given that marijuana is the most commonly used illicit drug during pregnancy, understanding its risks and impacts on the developing fetus is important.
Three large-scale longitudinal studies tracked how maternal cannabis use affected their child’s development, and they have had surprisingly consistent results. The Ottawa Prenatal Prospective Study surveyed 700 pregnant women who used marijuana in 1978 and has followed about 200 of those children into adulthood. The U.S.-based Maternal Health Practices and Child Development Study has studied 580 children of marijuana users from pregnancy through age 14. The Generation R study is tracking almost 8,000 children in the Netherlands.
Children of marijuana users were more impulsive and hyperactive, and exhibited behavioral issues, lower IQ scores, and memory problems when compared to children of non-users. These mental health problems persisted through their teenage years, where they were significantly more likely to have attention problems and depression. Marijuana-exposed children were also almost twice as likely to display delinquent behavior, such as drug use, by the age of 14 and were more than twice as likely to regularly use marijuana and tobacco as adults. The very consistent results between mice and human studies (summarized in the infographic from The Scientist below) highlights an increasing understanding of the impacts of marijuana use on development.
It’s important to note that some behavioral outcomes may not be completely related to fetal marijuana exposure. Children of marijuana users may have grown up in a different social environment with more lax views on drugs, contributing to their increased drug use.
As marijuana continues to be legalized, we should expect to see more studies on its health effects and safety.
Source: https://sitn.hms.harvard.edu/flash/2019/marijuana-exposure-affects-developing-babies-brains/
ANDRI TAMBUNAN FOR THE WALL STREET JOURNAL
Last year, members of Congress introduced a bill that would add the veterinary tranquilizer xylazine to a list of controlled substances. The drug has worsened the fentanyl crisis as it has been showing up in drug users’ fentanyl supply at an alarming pace.
Fentanyl is a heavily regulated legal medication, prescribed largely for pain relief in cancer patients, postsurgery and for people with chronic pain who have developed tolerance for other opioids.
When prescribed by a doctor, fentanyl can be given as a shot, a patch that is placed on a person’s skin, as lozenges that are sucked like cough drops or film that sits between the cheek and gum, according to the American Society of Health-System Pharmacists Inc. It also can be sprayed in the nose or under the tongue.
The illicit form of fentanyl, a powder that is often mixed into other drugs, has overtaken the drug market in the U.S. Fentanyl is made in clandestine labs in Mexico from easily sourced chemicals.
 |
Xylazine is a veterinary tranquilizer that has increasingly been showing up in illicit drugs, including in fentanyl. The drug, which is authorized only for animals, has been complicating overdoses and producing severe wounds for users that can lead to serious infection and amputation.
Dealers may mix xylazine into fentanyl to save money, federal law-enforcement authorities have said. The drug—known as “tranq” among some users—can be purchased at low prices from Chinese suppliers and offset some of the opioid in the mix.
Drug users often don’t know that xylazine is being mixed into their fentanyl batch and unknowingly become hooked on both substances. Drug users say xylazine can prolong a high from fentanyl but that also often means being unconscious, sometimes for hours at a time.
In February, the FDA said it would restrict imports of xylazine and more carefully scrutinize shipments of the drug into the U.S. to check that they are bound for legitimate use in animals.
The Drug Enforcement Administration said in March that about 23% of seized fentanyl powder and 7% of fentanyl pills contained xylazine last year. The Senate and House bills introduced in March would make xylazine a Schedule III drug, a category that includes ketamine. The bill would require producers and distributors to report order volumes to the DEA.
Drug test results also show xylazine is spreading throughout the U.S. About 43% of fentanyl-positive urine samples in Pennsylvania from April to July contained xylazine, according to Millennium Health, a drug-testing laboratory. The rate in North Carolina was second-highest at 40%. Rates in Ohio and Maryland were close behind.
 |
Fentanyl is often found mixed into heroin, cocaine and methamphetamine, according to the CDC. The drug is also made into fabricated pills that are often indiscernible from commonly prescribed medications such as Percocet (the narcotic oxycodone), Xanax (the sedative alprazolam) or even Adderall (an amphetamine).
Chinese chemical companies are making more ingredients for illegal fentanyl than ever, including N-Phenyl-4-piperidinamine, which Mexican cartels purchase to make into fentanyl.
Drug manufacturers in Mexico also mix illicit fentanyl with other materials, such as baking soda, starch and sugar, to create a powder that can be smoked or dissolved into liquid and injected, a process called “cooking,” or fabricated pills purchased on the illicit market.
Fentanyl is so powerful that in pure form the amount in roughly two sugar packets can provide a year’s supply for a user. When drug suppliers mix fentanyl into drugs or press it into illicit pills, a few grains too many can be enough to trigger a fatal overdose. It is unclear why fentanyl is showing up in such a large array of drugs. Evidence that fentanyl is showing up in more places comes from laboratory tests of drug seizures, toxicology testing and death certifications that take months to complete, according to the National Institute on Drug Abuse. Law-enforcement officials believe that in some cases, the drug is mixed in accidentally by drug manufacturers working with multiple white powders in the same lab, while at other times, drug manufacturers are experimenting in the attempt to create new psychoactive substances.
 |
Fentanyl has infiltrated virtually every channel of the illicit drug supply, according to U.S. law officials. The proportion of seized counterfeit pills in the U.S. containing a potentially lethal dose of fentanyl increased to 60% in 2022 from 10% in 2017, according to samples analyzed by the DEA.
Tainted drugs are so common in cities across the country, including Columbus, Ohio, that the city offers a program for distribution of fentanyl testing strips to users so they can determine whether substances are contaminated with the drug.
In New York City, authorities have been warning of the risks of unknowingly taking fentanyl in cocaine and of its increased presence in cocaine seized by police. Of 980 cocaine deaths in 2020, 81% involved fentanyl, according to recent New York City health department data.
People who use methamphetamine are also sometimes accidentally exposed to fentanyl. But many users are intentionally using meth and opioids simultaneously or in sequence in search of balancing or offsetting effects, researchers say. The drug combination is becoming an emerging driver of U.S. overdoses.
Fentanyl works by binding to the body’s opioid receptors—found in the areas of the brain that control pain and emotions, according to the National Institute on Drug Abuse. Some of the effects of fentanyl include euphoria, relaxation, pain relief, drowsiness and sedation, among others, according to the DEA. With repeated use, the brain adapts to the drug, making it hard to feel pleasure without it. Stopping the use of fentanyl leads to withdrawal, or “dope sickness,” which can include extreme anxiety, vomiting, muscle pain, chills, racing heartbeat and profuse sweating. Many chronic users have long since stopped feeling the euphoric effects of fentanyl and use it to avoid feeling sick.
Drug users who are accustomed to using heroin or prescription pain pills say illicit fentanyl’s effect can be more dramatic and shorter lasting than other opioids, making it more difficult to hold down a job as they seek out drugs every few hours.
 |
Fentanyl slows the body down and reduces respiration but becomes deadly when it suppresses breathing to such slow shallow breaths that a person can’t sustain life and their heart stops. If someone is unconscious, awake but unable to talk, or their breathing slows sharply, that could be an early sign of an overdose. According to the New York State Department of Health, that person’s skin may soon turn bluish purple or ashen. In some cases, a person overdosing will have a faint heartbeat. An overdose can also lead to hypoxia, the decrease in oxygen to the brain, according to neuropsychopharmacologists.
Still, it can be difficult to tell if a person is just very high or experiencing an overdose, according to the National Harm Reduction Coalition. People who are high may display slurred speech or seem dazed, but still be able to respond to a loud noise or someone lightly shaking them, the group says.
Naloxone is an antidote to opioids that can reverse the effects of an overdose within two to three minutes, according to the Mayo Clinic. Naloxone has virtually no effect in people who haven’t taken opioids, according to the World Health Organization.
Recently, the U.S. Food and Drug Administration encouraged pharmaceutical companies to apply for approval for over-the-counter versions of overdose-reversal medications such as Narcan to help address a swelling overdose crisis from bootleg versions of the powerful opioid fentanyl.
The FDA on March 29 approved Emergent BioSolutions Inc.’s Narcan brand of naloxone nasal spray for over-the-counter sale. The company said its nasal spray-version of the medication will likely become available on store shelves by late summer.
The pharmaceutical nonprofit Harm Reduction Therapeutics Inc. has already received priority review from the agency to make an inexpensive naloxone nasal spray for use without a prescription. The company said the FDA gave it a target approval date of April 28.
 |
Harm reduction is a public-health strategy aimed at reducing as much harm as possible to people while they are using drugs, rather than stopping them from taking substances altogether.
Groups that practice harm reduction for drug users teach about using clean needles to prevent infection and the spread of disease. Some groups provide fentanyl test strips so that users can test drugs for fentanyl and hand out naloxone to prevent deaths from overdose. An increasing number of groups supervise drug consumption. The Biden administration is the first to name harm reduction as a priority for drug policy.
Disparities in access to treatment are driving up overdose rates among Black and Native American people, the CDC has said. Overdose deaths per 100,000 people increased 44% for Black people and 39% for Native Americans in 2020 from a year earlier, compared with a 22% increase among white people, according to a study in which the CDC analyzed 25 states and Washington, D.C.
Deaths from fentanyl have affected every age group, but particularly the 25-to 34-year-old and 35-to 44-year-old populations. These two groups combined made up more than half of all synthetic opioid overdose deaths in 2021, according to preliminary CDC data.
Young children have also been directly affected by fentanyl. There were 133 opioid-related deaths among children younger than 3 last year, according to federal mortality data.
Overdose rates were higher in areas with more opioid-treatment programs than average, a finding that the study’s authors said demonstrated other barriers to access for some people. Overdose rates were also higher in counties with higher income inequality, according to the study. The findings show how the escalating overdose crisis is exacting a mounting toll on minority groups that are in some cases marginalized by the healthcare system, CDC researchers said.
Some prisons and jails have programs that dispense antiaddiction medications to help put inmates who are addicted to opioids on a path to sobriety and curb overdose rates. The Biden administration has said it wants medication available for drug users in federal custody and at half of state prisons and jails by 2025.
This explanatory article may be periodically updated.
Brian Spegele, Margot Patrick, Arian Campo-Flores and Jon Kamp contributed to this article.
SOURCE: https://www.wsj.com/health/healthcare/what-is-fentanyl-drug-opioid-health-safety-explained-11658341650
As with any addiction, alcoholism is closely connected with stress. And while plenty of people first started drinking as a way to cope with stress or even just wind down after a long day, developing an alcohol use disorder can end up causing significant stresses of its own. If you’re thinking about pursuing alcohol use disorder treatment for yourself or for a loved one, it can be helpful to understand how alcohol is connected to stress.
Present Stress That Can Lead to Alcohol Use
While stresses from your past can certainly contribute to alcoholism, plenty of people also start to develop alcohol use disorder as they struggle to cope with current stress. Often, people end up turning to alcohol in order to try to manage the stresses of day-to-day life. These can include pressure at work or at school, marriage, and divorce, moving, and financial issues.
Minority stress is also an important consideration. If you’re a minority (either in terms of race/ethnicity or sexual orientation), you face unique stresses. You might stress about being passed over for a promotion at work, and you also might fear harassment or becoming the victim of a hate crime.
It’s important to note that stress alone typically does not cause a substance use disorder. However, significant stresses may place you at higher risk of developing one, and high stress levels in sobriety can also make relapse more likely. High stress is a risk factor for alcoholism, along with the following:
Past Stress That Can Lead to Alcohol Use
Unfortunately, it isn’t just current stressful events that can predispose you to drink more. Stresses and traumas from your past can also play a role in alcoholism. Several studies point to childhood abuse and neglect as being a significant factor in the development of an alcohol use disorder. One study found that emotional abuse and neglect were most commonly seen in men and women seeking help for alcoholism. The severity of their alcoholism correlated with the severity of the abuse.
Past traumas, even if they were not experienced in childhood, may also make someone more likely to experience alcoholism. Many people with an alcohol use disorder also have PTSD. As with other mental health diagnoses, the relationship between alcoholism and PTSD becomes a vicious cycle. Alcohol use makes PTSD symptoms worse, and the PTSD symptoms make alcoholism worse.
If you have experienced trauma and are also struggling with alcohol use disorder, it’s easy to feel as though there is no hope. But at Granite Recovery Centers, we offer evidence-based therapies including trauma therapy. In therapy for trauma and PTSD, you will be able to process your trauma and develop healthier coping strategies to help you avoid self-destructive behaviors. With these therapies, you’ll be able to break the cycle of worsening symptoms and experience a greater quality of life.
How Can Alcohol Use Cause Stress?
While it might seem logical that alcohol use can cause stress, there’s also a good bit of biochemical evidence to explain, at least in part, how alcohol shapes your stress response. Even in the short term, alcohol consumption increases levels of cortisol. Cortisol is known as the stress hormone, and your body also releases it during periods of intense anxiety or fear. In the short term, a cortisol release can be helpful — it increases alertness and focus, which was helpful evolutionarily because it helped humans and animals get themselves out of dangerous situations.
However, having elevated cortisol over a long period of time can be detrimental, exhausting, and even dangerous. And in chronic heavy drinkers and those with alcohol use disorder, cortisol isn’t just elevated during intoxication — it stays elevated through withdrawal. In fact, one study even found that cortisol increased as intoxicated people started moving toward withdrawals. If you’ve ever experienced intense anxiety when withdrawing from alcohol, you’ve felt this cortisol surge firsthand.
Because most people with an alcohol use disorder go through a near-constant cycle of intoxication and withdrawal, cortisol can remain elevated for years on end. Chronically elevated cortisol can cause a number of ill health effects:
Chronically elevated cortisol may cause other health problems as well, but more research is needed to determine exactly what these effects are. Of course, the physical stresses of elevated cortisol combined with chronic heavy drinking can mean your body is put through a lot of physical stress as well as emotional stress.
You already know that plenty of people use alcohol to alleviate stress, but over time, alcohol can cause its own significant stresses. As mentioned above, the elevated cortisol you experience while intoxicated and in withdrawal can cause significant emotional distress. When your body is under stress, and elevated cortisol is effectively causing a constant stress response, it becomes significantly more difficult to handle even everyday stresses.
And in some cases (like when you are intoxicated enough to experience blackouts or respiratory suppression), being intoxicated can be a stressful experience in itself. And for many people with an alcohol use disorder, that stressful experience is something they experience on a daily or near-daily basis. Some of the physical effects of heavy drinking — including dizziness, nausea, headaches, and dehydration — can compound the emotional stress you’re already feeling.
Many people also consciously or unconsciously use alcohol to self-medicate psychiatric disorders, including depression and bipolar disorder. However, in many cases, alcohol use worsens the symptoms of mental health issues, which can cause considerably more emotional distress on a daily basis. In some cases, heavy alcohol use can even contribute to the development of new mental health diagnoses.
If you’ve been using alcohol to help manage a mental health diagnosis (or to help manage a mental health issue that has not yet been diagnosed), Granite Recovery Centers’ dual diagnosis treatment program can help you. With this approach, medical and recovery professionals work with you to find better treatments and coping mechanisms for your mental health diagnosis while also helping you manage your alcohol use disorder. In many cases, this treatment approach will greatly improve your quality of life, as you’ll be much better equipped to manage both diagnoses.
Regardless of whether you have a mental health diagnosis or not, heavy alcohol use can begin to cause stress as it starts to affect the rest of your life. For example, you may constantly worry whether someone will smell alcohol on your breath at work, or you may worry about when you can take another drink. For many people with an alcohol use disorder, it can start to feel like leading a double life, which becomes exhausting and highly stressful over time. And as a person starts to drink more, they often become more socially isolated. Feeling isolated can increase stress, and the person may then continue drinking heavily to cope with that stress.
If you struggle with an alcohol use disorder or other substance use disorder, you already know just how stressful day-to-day life can become. If you have to drink to get rid of withdrawal symptoms and can’t control your drinking once you start, it’s easy to feel trapped, which is, of course, a major stress in itself. If you feel this way, you aren’t alone — taking the first steps to get help can free you from the seemingly unending cycle of alcohol use.
How Do I Know If I’ve Developed an Alcohol Use Disorder?
If you have started using alcohol as a way to cope with stress, it can be difficult to tell whether you have developed an alcohol use disorder or if you are beginning to develop one. While you’ll need to consult a medical professional if you’re looking for a definite diagnosis, you can look for some of the common signs:
Binge drinking can also be a sign of a developing alcohol use disorder. Binge drinking is defined as consuming five or more standard drinks in two hours for men and consuming four or more standard drinks in two hours for women. On its own, binge drinking doesn’t necessarily indicate an alcohol use disorder, but it could be a sign that one is starting to develop.
It’s important to keep in mind that alcohol use disorders are on a spectrum. Milder cases tend to have fewer symptoms present, while more severe cases have more. Even if you think you only have a mild case, you can still benefit tremendously from treatment. Most cases of alcohol use disorder become progressively worse over time.
How Can Treatment Help?
If you’re unfamiliar with substance use disorder treatment, you may think residential treatment’s only benefit is preventing you from accessing your substance of choice. This couldn’t be further from the truth. A good residential treatment program takes a holistic approach to help you improve your life.
In most cases (and definitely in severe cases), a stay at a residential treatment center begins with a medical detox program. In medical detox, you’ll be supervised by a doctor and likely given medication to prevent seizures and other complications of alcohol withdrawal. Withdrawing from alcohol on your own can be very dangerous, and inpatient detox can ensure that you’re safe. Granite Recovery Centers provides medical detoxification for people who do not need immediate medical intervention, are not a danger to themselves, and are capable of self-evacuation in the event of an emergency.
Once you’re in treatment, you’ll work with counselors and medical professionals to help you identify issues that make you want to drink. These professionals will help you develop healthier coping mechanisms to deal with stress so you’ll be less likely to turn to alcohol in the future. You may get to participate in cognitive behavioral therapy and dialectical behavioral therapy, as well as trauma therapy if needed.
Nutritional deficiencies developed while drinking heavily can add to stress and feeling generally unwell, so residential rehabilitation includes healthy food and ample exercise opportunities. And if you have a co-occurring mental health condition, on-site professionals will help you develop an effective treatment plan.
Ready to Take the Next Step?
Alcohol is an easy answer to stress for many people. But if you have an alcohol use disorder, chances are good that alcohol only causes more stress and worsens the stress you already have. And if the prospect of quitting by yourself seems like too much, don’t worry—the professionals working with Granite Recovery Centers will be helping you every step of the way. If you’re ready to change your life, give us a call at 855-712-7784 today!
Source: https://www.graniterecoverycenters.com/resources/the-connection-between-stress-and-alcoholism/ April 2021
The title of “Cannabis in Medicine: An Evidence-Based Approach” contains an irony. In chapter after chapter in this multi-authored book written predominately by providers associated with mainstream medical facilities in Colorado, the authors point out the inadequacy of the evidence we have and the absence of the evidence we need to determine how – or even if – cannabis has medical legitimacy. The foreword’s title, “Losing Ground: The Rise of Cannabis Culture,” sets the tone. David Murray, a senior fellow at the Hudson Institute, argues convincingly that “the current experiment with cannabis, underway nationwide [is] leading us towards a future of unanticipated consequences, a future already established in the patterns of use ‘seeded’ in the population but as yet unmanifested.” In other words, the cannabis horse has not only fled the barn but has been breeding prolifically to the point that we couldn’t get rid of it and its progeny if we wanted to!
The 20 chapters following the foreword are divided into basic science (three chapters) and clinical evidence (17 chapters) sections. Over and over in the clinical evidence chapters, individual authors remind the reader of the lack of quality control in production, the dearth of strong evidence from adequately designed research trials, and the intensifying potency of cannabis with attendant dangers, particularly for youth. The organization of this section lacks consistency in that some chapters focus on specialty (e.g. pulmonary medicine), others on patient groups (e.g. the pediatric and adolescent population), others on physiological implications (e.g. clinical cardiovascular effects; neuropsychiatric effects), others on specific diseases (e.g. gastrointestinal disorders; ocular conditions), and still others on public health topics (e.g. cannabis-impaired driving). While all are relevant, a specialty or organ system focus, with a separate public health section might lend the book more coherence. It would also be worth exploring how “cannabis culture” has become in essence a parallel medical system, with many of cannabis’s most ardent proponents as dropouts from establishment medicine after its nostrums for diagnoses like chronic pain, anxiety, and depression have failed to bring them relief.
I would have liked a chapter specifically grappling with the porous boundary between federal and state jurisdictions over cannabis as medicine and marijuana as recreational substance. Lawyer David G. Evans’ admirable chapter on “The Legal Aspects of Marijuana as Medicine” moves in that direction when he writes that, “‘medical marijuana’ is not a ‘states’ rights’ issue.” To wit, for no other drug than cannabis has the federal government ceded regulatory responsibility to states that are variably (but mostly not) equipped to handle it. The truth, complex in its contradictions and inconsistencies, is that in the United States, marijuana remains a Schedule I drug without recognized medical value; the Federal Drug Administration overseeing American pharmaceuticals throws roadblocks in the way of studying it, thereby interfering with the development of a robust evidence base; the federal government has looked the other way and even colluded with the states as one after another has legalized cannabis medically, recreationally, or both; and physicians risk their federal licenses to prescribe if they do more than recommend this drug. In a nutshell, any effort to impose logic is doomed because the American scene vis-à-vis cannabis is seemingly irretrievably illogical.
The editor of this volume, Kenneth Finn, MD, a PMR and pain management specialist in Colorado Springs, Colorado, is to be commended for encouraging individual chapter authors to develop encyclopedic bibliographies. The book can thus serve as a resource for practitioners wishing to delve into a vast and growing literature that continues to offer little that is conclusive. The book can also serve as a primer on what is known about cannabis as medicine, keeping in mind a slant throughout – not necessarily unjustified, at least from an allopathic or osteopathic perspective – that cannabis is neither legitimate as medicine nor safe, even for recreational use.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723137/ Sept-Oct 2020
Limited information exists on marijuana use and male reproductive health. A recent study from Duke University evaluated differences in sperm quality resulting from tetrahydrocannabinol (THC) exposure in both rats and humans. Findings suggest that paternal marijuana use, prior to conception, may present epigenetic risks to potential offspring.
…
Public perceptions pertaining to marijuana have evolved radically over the past 2 decades. While marijuana remains criminalized at the federal level, 33 states and the District of Columbia have legalized marijuana, in some capacity, for either medical or recreational use. According to the most recent National Survey on Drug Use and Health, nearly 26 million Americans, over the age of 12, currently use marijuana. While the gender gap is narrowing, men remain significantly more likely to use marijuana than women (11.7% vs. 7.3%, respectively).
In 2017, approximately 1.9 million men, between the ages of 26 and 29, reported using marijuana in the past month. Given that the average age of first-time fathers in the U.S. is around 30, these findings suggest that a substantial number of “fathers-to-be” are using marijuana at the time of conception. Little is known, however, about the impact of paternal marijuana use on reproductive outcomes.
Epigenetics, which literally translates to “above” or “on top of” genetics, refers to the biological mechanism through which genes are activated and expressed. This process acts like a light switch, turning on or off how cells read certain heritable traits written within an individual’s unique genetic code. Sperm matures continually throughout adulthood, making it particularly vulnerable to potential epigenetic modifications, such as DNA methylation, that may result from marijuana use. This study explores differences in sperm profiles, based on cannabis exposure in both humans and rats, to better understand potential heritable effects.
Key Findings
Individuals who used marijuana can have higher and also can have significantly lower sperm concentrations, compared to those who did not, posing potential complications for fertility.
THC-exposed sperm was associated with significantly altered DNA, in both rat and human samples.
*Associations were even stronger among individuals with higher levels of THC in their urine, implying a “dose-response relationship” such that chronic marijuana users may be impacted more severely.
Authors identified three unique potential genetic pathways modified by THC exposure.
Looking to the Future
Past research suggests that offspring born to rats exposed to THC during adolescence demonstrate significant DNA alterations in their brains, display heightened drug-seeking behavior, and are at increased risk of developing opioid dependency over time, compared to controls. The present study is the first to extend this line of research to men of childbearing age, lending additional evidence for potential intergenerational, heritable consequences, resulting from paternal marijuana use. Just as other environmental triggers, such as air pollution, cigarette smoking, certain pesticides (i.e. DDT), and exposure to radiation are known to affect sperm health, THC may also increase the potential for genetic mutations.
For Clinicians
Primary care physicians and healthcare professionals, both inside and outside of substance use disorder treatment landscapes, should take time to educate patients about the impact of THC on sperm so individuals may consider potential implications for fertility and children conceived during periods of active use.
For Researchers
This article adds to a growing literature on the potential epigenetic impact of paternal marijuana use prior to conception. Findings must first be replicated in larger samples. Additionally, future longitudinal studies are necessary to explore the extent to which THC induced DNA alterations in sperm are passed down to offspring, as well as their long-term consequences.
For Policymakers
Marijuana potency continues to increase rapidly, with THC level increasing 300% over the past 20 years. Within the current political landscape and shift towards increased access to medical and recreational marijuana, policymakers should work closely with scientists to stay informed on the extent to which increased THC levels and evolving public attitudes impact men’s reproductive health.
For General Public
The full impact of passing THC-related DNA modifications onto offspring, and whether or not these changes are reversible is still unknown. Evidence of DNA alterations to existing Hippo signaling and Cancer genetic pathways may disrupt growth, enhance the potential for miscarriage, or impede healthy embryo development.
Methods
The authors employed a quantitative genome-scale approach, referred to as reduced representation bisulfite sequencing, to compare DNA methylation alterations in sperm across human and rat samples. A number of factors including, time since last ejaculation, semen volume, pH, morphology, and motility were controlled for across participants. Pyrosequencing, a DNA synthesizing method that relies on light detection, was implemented to identify genes with significant methylation differences. Data were then analyzed to uncover specific genetic pathways potentially impacted by paternal, preconception cannabis use.
Study Limitations
A relatively small sample size of human subjects, limiting the generalizability of study findings.
*24 males, age 18-40 years: (12 marijuana users & 12 non-users)
The methodological approach may fail to identify epigenetic modifications that affect multiple genes simultaneously.
Source: What you should know about Marijuana and Sperm (addictionpolicy.org) March 2019, updated October 2022
Alexandria, VA) – A new study released yesterday in the Annals of Internal Medicine found that the rise in marijuana use in Colorado since the state legalized the drug has led to increased emergency room visits. The study found that 9,973 marijuana-related emergency room visits occurred from 2012-2016, more than triple the number that occurred prior to legalization. Additionally, the study found that 10.7% of visits at UCHealth were due to the ingestion of high potency marijuana edibles.
“Evidence continues to build the case that marijuana legalization results in harmful impacts on public health and safety,” said Dr. Kevin Sabet, founder of Smart Approaches to Marijuana and a former senior drug policy advisor to the Obama Administration. “Marijuana is no longer the weed of Woodstock. The industry is churning out new, highly potent candies, gummies, sodas, and ice creams as well as concentrates and vape pens that contain up to 99% THC. These kid-friendly products are regularly getting into the hands of children, whose developing brains are incredibly susceptible to permanent damage from this highly potent pot.”
The study found that 17% of emergency room visits were due to uncontrolled vomiting that was associated with the smoked form of the drug. Previous research has labeled this phenomenon as “scromiting,” or Cannabinoid Hyperemesis Syndrome. 12% of the visits were for acute psychosis and this was associated with high potency edibles. 8% of visits were associated with cardiovascular issues such as irregular heartbeat or even heart attacks after ingestion of edibles.
Another recent study found that the use of high potency edibles was directly linked with increases in severe mental illness, such as psychosis, and stated that if higher potency concentrates and edibles were removed from the market, instances of psychosis would be reduced by a third.
“Lawmakers rushing to legalize marijuana need to slow down and consider the implications it could bring upon their state,” continued Dr. Sabet. “They are certainly not receiving information such as this from the pot industry’s army of lobbyists. This is why organizations such as SAM are so important. We work tirelessly to combat the industry narrative that marijuana is harmless.
Email from SAM https://www.learnaboutsam.org March 2019
Radula complanata, a cannabinoid moss. Henri Koskinen/Shutterstock
Most of us know that the cannabis plant produces compounds that react with the human body. That’s because we have our own system that makes similar compounds, cannabinoids, that have a wide range of actions from appetite control to immune function. Cannabis contains a cannabinoid called THC that interacts with the brain, resulting in euphoria and relaxation, as well as increased hunger and anxiety. It was long thought that there was no other natural source of cannabinoids – and along with a long list of supposed medical uses the mythical power of cannabis, and the psychoactive properties of THC, has grown.
But as it turned out, another plant contains something similar: a compound that has the structural hallmarks for it to act on the brain in a similar way to THC. The discovery of this lost twin, called cis-PET (perrottetinene), or PET, was tucked away in specialist chemistry journals in papers published in 1994 and 2002, with no subsequent research confirming its biological activity. But in a new study, published in Science Advances, a group of Swiss scientists have delved into the mechanism by which PET may be acting on the brain.
The particular liverwort in question, Radula, is endemic to New Zealand and Tasmania and is used as a herbal medicine by the Maori people. Preparations using this plant are also sold as a THC-like legal high on the internet.
But while similar to THC, does PET actually produce the same effects that THC does at a cellular and molecular level? Does it mimic the physiological effects? And is it different in ways that could give it therapeutic advantage or disadvantage? Some 24 years after its first discovery, the team of chemists and biochemists behind the new study have teased some of the answers out.
Their research was no mean feat. It required a new synthesis method to produce enough PET to do meaningful experiments. Once this was achieved, the researchers looked at two mirror versions of the two compounds, cis (the version found in the liverwort) and trans (a version they artificially created in the lab). In chemistry, the cis and trans terms tell us which side of the carbon chain the functional groups are (the bit of the molecule that does the work).
The researchers wanted to find out if these two versions of PET were able to interact with the two receptors found in humans that mediate the psychoactive effects of cannaboids – CB1, the receptor that produces the “high” effect from THC, and CB2 – in the same way as THC (how strongly they bound and how much is needed to produce an effect).
The researchers found intriguing similarities between the two versions in PET and THC. For both PET and THC, the trans versions (the abundant THC version found in cannabis and the lab-synthesised version found in liverwort) bound to the CB1 receptor better than the cis versions.
THC and PET side by side. Oliver Kayser
What’s interesting about this is that while the levels of cis-PET found in the liverwort plant are too low to produce the “high” effects produced by THC (hence why smoking PET won’t produce a high), it could explain why PET might still have a medicinal effect (similar to the effect produced by lower dose THC). However, any methods to extract and concentrate the liverwort compound could lead to the same problems as THC.
But what about CB2, the other cannabinoid receptor? This receptor plays a role in immune responses. Here the Swiss scientists found that the cisversions of both THC and PET bound this receptor better than the transversions. The implications of this are yet to be explored, but it again hints at a potential medicinal benefit worth exploring further.
The authors of the study then went on to test whether the binding of the CB1 receptors in the brains of mice had the same recognisable THC effects. Usually when THC binds with this receptor it produces four key effects: reduced body temperature, muscle rigidity, reduced movement and decreased sensitivity to pain. In this behavioural test, all four effects were also achieved in the mice using cis-PET, albeit in a much bigger amount.
But there was one notable difference. Inflammation in the brain is mediated by molecules called prostaglandins that can be derived from metabolic pathways involving our own body cannabinoids or plant-derived trans-THC. In contrast, the production of these mediators was reduced by cis-PET. It remains to be seen whether this is a good thing or a bad thing.
So while the study is just a start in understanding the mechanisms and effects of PET on the brain, there’s much we still don’t know. What we do know now, however, is that the levels of PET that are found in the natural liverwort plant are too low to produce the recognised effects of THC, so smoking it is unlikely to lead to a high. But it is also interesting that this compound could well have medicinal benefits without the high – one of the key reasons that THC has previously been dismissed as a medicine. Illegal trading and cultivation has confounded much meaningful clinical research, but this is changing and this new compound will add to the treasure trove of plant-derived cannabinoids that we still have much to understand.
Source: https://theconversation.com/liverwort-could-have-medicinal-benefits-of-cannabis-thc-without-the-high Oct.24th 2018
Smoking kills. No other habit has been so strongly tied to death.
In addition to inhaling burned tobacco and tar, smokers breathe in toxic metals like cadmium and beryllium, as well as metallic elements like nickel and chromium — all of which accumulate naturally in the leaves of the tobacco plant.
It’s no surprise, then, that much of the available evidence suggests that vaping, which involves puffing on vaporized liquid nicotine instead of inhaling burned tobacco, is at least somewhat healthier. Some limited studies have suggested that reaching for a vape pen instead of a conventional cigarette may also help people quit smoking regular cigarettes, but hard evidence of that remains elusive.
Very few studies, however, look at how vaping affects the body and brain. Even fewer specifically examine the Juul, a popular device that packs as much nicotine in each of its pods as a standard pack of cigarettes.
But a handful of studies published in the past few months have begun to illuminate some of the potential health effects tied to vaping. They are troubling.
With that in mind, the Food and Drug Administration outlined a new policy on Thursday morning designed to eventually curb the sale of e-cigs and reign in their appeal to young people.
Most recently, researchers at the Stanford University School of Medicine surveyed young people who vaped and found that those who said they used Juuls vaped more frequently than those who used other brands. The participants appeared to be insufficiently aware of how addictive the devices could be.
Researchers took a look at the compounds in several popular brands of e-cigs (not the Juul) this spring and found some of the same toxic metals (such as lead) inside the device that they would normally find in conventional cigarettes. For another study published around the same time, researchers concluded that at least some of those toxins appeared to be making their way through vapers’ bodies, as evidenced by a urine analysis they ran on nearly 100 study participants.
In another study published this summer, scientists concluded that there was substantial evidence tying daily e-cig use to an increased risk of heart attack. And this week, a small study in rats suggested that vaping could have a negative effect on wound healing that’s similar to the effect of regular cigarettes.
In addition to these findings, of course, is a well-established body of evidence about the harms of nicotine. The highly addictive substance can have dramatic impacts on the developing brains of young adults.
Brain-imaging studies of adolescents who begin smoking traditional cigarettes (not e-cigs) at a young age suggest that those people have markedly reduced activity in the prefrontal cortex and perform less well on tasks related to memory and attention, compared with people who don’t smoke. Those consequences are believed to be a result of the nicotine in the cigarettes rather than other ingredients.
Nicholas Chadi, a clinical pediatrics fellow at Boston Children’s Hospital, spoke about the Juul at the American Society of Addiction Medicine’s annual conference this spring. He said these observed brain changes were also linked to increased sensitivity to other drugs as well as greater impulsivity. He described some anecdotal effects of nicotine vaping that he’d seen among teens in and around his hospital.
“After only a few months of using nicotine,” Chadi said, the teens “describe cravings, sometimes intense ones.” He continued: “Sometimes they also lose their hopes of being able to quit. And interestingly, they show less severe symptoms of withdrawal than adults, but they start to show them earlier on. After only a few hundred cigarettes — or whatever the equivalent amount of vaping pods — some start showing irritability or shakiness when they stop.”
The Juul, which is made by the Silicon Valley startup Juul Labs, has captured more than 80% of the e-cig market and was recently valued at $15 billion. But the company is facing a growing backlash from the FDA and scientists who say the company intentionally marketed to teens.
On Tuesday, the company responded to some of these concerns — first by announcing that they’d be temporarily banning the sale of their flavored products at retailers and by deleting their social media accounts, which some research suggests has allured more young customers.
Yet very little research about e-cigs has homed in on the Juul specifically.
So for a study published this week, researchers from the Stanford University School of Medicine surveyed young people who vaped and asked them whether they used the Juul or another e-cigarette.
Their results can be found in a widely accessible version of the Journal of the American Medical Association called JAMA Open. Based on a sample of 445 high-school students whose average age was 19, the researchers observed that teens who used the Juul tended to say they vaped more frequently than those who used other devices. Juul users also appeared to be less aware of how addictive the devices could be compared with teens who vaped other e-cigs.
“I was surprised and concerned that so many youths were using Juul more frequently than other products,” Bonnie Halpern-Felsher, a professor of pediatrics who was a lead author of the study, said in a statement.
“We need to help them understand the risks of addiction,” she added. “This is not a combustible cigarette, but it still contains an enormous amount of nicotine — at least as much as a pack of cigarettes.”
Source: https://www.businessinsider.com/vaping-e-cigs-juul-health-effects-2018-10 October 2018
Source: Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016 – The Lancet August 2018
This Notice of Liability Memo and attached Affidavit of Harms give formal notification to all addressees that they are morally, if not legally liable in cases of harm caused by making toxic marijuana products legally available, or knowingly withholding accurate information about the multiple risks of hemp/marijuana products to the Canadian consumer. This memo further gives notice that those elected or appointed as representatives of the people of Canada, by voting affirmatively for Bill C45, do so with the knowledge that they are breaching international treaties, conventions and law. They do so also with the knowledge that Canadian law enforcement have declared that they are not ready for implementation of marijuana legalization, and as they will not be ready to protect the lives of Canadians, there may arise grounds for a Charter of Rights challenge as all Canadian citizens are afforded a the right to security of self.
Scientific researchers and health organizations raise serious questions about the safety of ingesting even small amounts of cannabinoids. Adverse effects include risk of harm to the cardio-vascular system, respiratory tract, immune system, reproductive and endocrine systems, gastrointestinal system and the liver, hyperemesis, cognition, psychomotor performance, psychiatric effects including depression, anxiety and bipolar disorder, schizophrenia and psychosis, a-motivational syndrome, and addiction. The scientific literature also warns of teratogenicity (causing birth deformities) and epigenetic damage (affecting genetic development) and clearly establishes the need for further study. The attached affidavit cites statements made by Health Canada that are grounded in scientific evidence that documents many harms caused by smoking or ingesting marijuana.
Putting innocent citizens in “harm’s way” has been a costly bureaucratic mistake as evidenced by the 2015 Canadian $168 million payout to victims of exposure to the drug thalidomide. Health Canada approved thalidomide in 1961 to treat morning sickness in pregnant women but it caused catastrophic birth defects and death.
It would be instructive to reflect on “big tobacco” and their multi-billion-dollar liability in cases of misinformed sick and dead tobacco cigarette smokers. Litigants won lawsuits for harm done by smoking cigarettes even when it was the user’s own choice to obtain and smoke tobacco. In Minnesota during the 1930’s and up to the 1970’s tobacco cigarettes were given to generally healthy “juvenile delinquents’ incarcerated in a facility run by the state. One of the juveniles, now an adult, who received the state’s tobacco cigarettes, sued the state for addicting him. He won.
The marijuana industry, in making public, unsubstantiated claims of marijuana safety, is placing itself in the same position, in terms of liability, as the tobacco companies.
In 1954, the tobacco industry published a statement that came to be known during Minnesota’s tobacco trial as the “Frank Statement.” Tobacco companies then formed an industry group for the purposes of deceiving and confusing the public.
In the Frank Statement, tobacco industry spokesmen asserted that experiments linking smoking with lung cancer were “inconclusive,” and that there was no proof that cigarette smoking was one of the causes of lung cancer. They stated, “We believe the products we make are not injurious to health.” Judge Kenneth Fitzpatrick instructed the Minnesota jurors: “Jurors should assume in their deliberations that tobacco companies assumed a “special duty” by publishing the ad (Frank Statement), and that jurors will have to determine whether the industry fulfilled that duty.” The verdict ruled against the tobacco industry.
Effective June 19, 2009, marijuana smoke was added to the California Prop 65 list of chemicals known to cause cancer. The Carcinogen Identification Committee (CIC) of the Office of Environmental Health Hazard Assessment (OEHHA) “determined that marijuana smoke was clearly shown, through scientifically valid testing according to generally accepted principles, to cause cancer.”
Products liability and its application to marijuana businesses is a topic that was not discussed in the Senate committee hearings. Proposition 65, requires the State to publish a list of chemicals known to cause cancer, birth defects or other types of reproductive harm. Proposition 65 requires businesses to provide their customers with notice of these cancerous causing chemicals when present in consumer products and provides for both a public and private right of action.
The similarities between the tactics of “Big Tobacco” and the “Canadian Cannabis Trade Alliance Institute” and individual marijuana producers would seem to demand very close scrutiny. On May 23, a witness testified before the Canadian Senate claimed that marijuana is not carcinogenic. This evidence was not challenged.
The International Narcotics Control Board Report for 2017 reads: “Bill C-45, introduced by the Minister of Justice and Attorney General of Canada on 13 April 2017, would permit the non-medical use of cannabis. If the bill is enacted, adults aged 18 years or older will legally be allowed to possess up to 30 grams of dried cannabis or an equivalent amount in non-dried form. It will also become legal to grow a maximum of four cannabis plants, simultaneously for personal use, buy cannabis from licensed retailers, and produce edible cannabis products. The Board wishes to reiterate that article 4 (c) of the 1961 Convention restricts the use of controlled narcotic drugs to medical and scientific purposes and that legislative measures providing for non-medical use are in contravention of that Convention….
The situation pertaining to cannabis cultivation and trafficking in North America continues to be in flux owing to the widening scope of personal non-medical use schemes in force in certain constituent states of the United States. The decriminalization of cannabis has apparently led organized criminal groups to focus on manufacturing and trafficking other illegal drugs, such as heroin. This could explain why, for example, Canada saw a 32 per cent increase from 2015 to 2016 in criminal incidents involving heroin possession….The Canadian Research Initiative in Substance Misuse issued “Lower-risk cannabis use guidelines” in 2017. The document is a health education and prevention tool that acknowledges that cannabis use carries both immediate and long-term health risks.”
Upon receipt of this Memo and Affidavit, the addressees can no longer say they are ignorant or unaware that promoting and/or distributing marijuana cigarettes for recreational purposes is an endangerment to citizens. Receipt of this Memo and Affidavit removes from the addressees any claim of ignorance as a defense in potential, future litigation.
Pamela McColl www.cleartheairnow.org
AFFIDAVIT May 27, 2018
I, Pamela McColl, wish to inform agencies and individuals of known and potential harm done/caused by the use of marijuana (especially marijuana cigarettes) and of the acknowledgement the risk of harm by Health Canada.
Marijuana is a complex, unstable mixture of over four hundred chemicals that, when smoked, produces over two thousand chemicals. Among those two thousand chemicals are many pollutants and cancer-causing substances. Some cannabinoids are psychoactive, all are bioactive, and all may remain in the body’s fatty tissues for long periods of times with unknown consequences. Marijuana smoke contains carcinogenic (cancer-causing) substances such as benzo(a)pyrene, benz(a)anthracene, and benzene in higher concentrations than are present in tobacco smoke. The mechanism by which benzo(a)pyrene causes cancer in smokers was demonstrated scientifically by Denissenko MF et al. Science 274:430-432, 1996.
Health Canada Consumer Information on Cannabis reads as follows: “The courts in Canada have ruled that the federal government must provide reasonable access to a legal source of marijuana for medical purposes.”
“Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of cannabis for therapeutic purposes, or of marijuana generally, by Health Canada.”
“Serious Warnings and Precautions: Cannabis (marihuana, marijuana) contains hundreds of substances, some of which can affect the proper functioning of the brain and central nervous system.”
“The use of this product involves risks to health, some of which may not be known or fully understood. Studies supporting the safety and efficacy of cannabis for therapeutic purposes are limited and do not meet the standard required by the Food and Drug Regulations for marketed drugs in Canada.”
Health Canada – “When the product should not be used: Cannabis should not be used if you:-are under the age of 25 -are allergic to any cannabinoid or to smoke-have serious liver, kidney, heart or lung disease -have a personal or family history of serious mental disorders such as schizophrenia, psychosis, depression, or bipolar disorder-are pregnant, are planning to get pregnant, or are breast-feeding -are a man who wishes to start a family-have a history of alcohol or drug abuse or substance dependence Talk to your health care practitioner if you have any of these conditions. There may be other conditions where this product should not be used, but which are unknown due to limited scientific information.
Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of this product, or cannabis generally, by Health Canada.”
Prepared by Health Canada Date of latest version: February 2013, accessed May 2018. https://www.canada.ca/en/health-canada/services/drugs-health-products/medical-use-marijuana/information-medical-practitioners/information-health-care-professionals-cannabis-marihuana-marijuana-cannabinoids.html
A report published by survey company RIWI Corp. (RIWI.com) can be found at: https://riwi.com/case-study/measuringcanadians-awareness-of-marijuanas-health-effects-may-2018
The report measures Canadians’ awareness of marijuana’s health effects as determined by Health Canada and published on Health Canada’s website. RIWI data indicates: 1. More than 40% of those under age 25 are unaware that marijuana impacts safe driving. Further, 21% of respondents are not aware that marijuana can negatively impact one’s ability to drive safely. Health Canada: “Using cannabis can impair your concentration, your ability to make decisions, and your reaction time and coordination. This can affect your motor skills, including your ability to drive.” 2. One in five women aged 25-34 believes marijuana is safe during pregnancy, while trying to get pregnant, or breastfeeding. • RIWI: “For women of prime childbearing age (25-34), roughly one in five believe smoking marijuana is safe during pregnancy, planning to get pregnant, and breastfeeding.” • Health Canada: “Marijuana should not be used if you are pregnant, are planning to get pregnant, or are breastfeeding. … Long-term use may negatively impact the behavioural and cognitive development of children born to mothers who used cannabis during pregnancy.” 3. One in three Canadians do not think that marijuana is addictive. • Health Canada: “Long term use may result in psychological dependence (addiction).” 4. One in three Canadians believe marijuana aids mental health. • Health Canada: “Long term use may increase the risk of triggering or aggravating psychiatric and/or mood disorders (schizophrenia, psychosis, anxiety, depression, bipolar disorder).” 5. One in two males were unaware that marijuana could harm a man’s fertility • “Marijuana should not be used if you are a man who wishes to start a family.”
ClearTheAirNow.org, a coalition of concerned Canadians commissioned the survey.
Affiant is willing to provide further sources of information about the toxicity of marijuana.
Pamela McColl
Source: From email sent to Drug Watch International May 2018
Recent widespread legalization changes have promoted the availability of marijuana and its increased potency and perceived safety. The limited evidence on reproductive and perinatal outcomes from marijuana exposure is enough to warrant concern and action. The objective of this review is to provide a current and relevant summary of the recent literature surrounding this topic.
The available published studies on the effect of marijuana exposure on reproductive health and pregnancy outcomes are conflicting. Human studies are often observational or retrospective and confounded by self-report and polysubstance use. However, the current, limited evidence suggests that marijuana use adversely affects male and female reproductive health. Additionally, prenatal marijuana exposure has been reported to be associated with an increased risk of preterm birth and small for gestational age infants.
With the increasing prevalence of marijuana use, there is an urgent need for evidence-driven recommendations and guidelines for couples interested in conception, affected by infertility or who are expecting. At this time, no amount of marijuana use during conception or pregnancy is known to be well tolerated and the limited available evidence suggests that the safest choice is to abstain.
Source: Effects of marijuana on reproductive health: preconception a… : Current Opinion in Endocrinology, Diabetes and Obesity (lww.com) December 2021
Reproductive and Cancer Hazard Assessment Branch Office of Environmental Health Hazard Assessment California Environmental Protection Agency
PREFACE
The Safe Drinking Water and Toxic Enforcement Act of 1986 (Proposition 65, California Health and Safety Code 25249.5 et seq.) requires that the Governor cause to be published a list of those chemicals “known to the state” to cause cancer or reproductive toxicity. The Act specifies that “a chemical is known to the state to cause cancer or reproductive toxicity … if in the opinion of the state’s qualified experts the chemical has been clearly shown through scientifically valid testing according to generally accepted principles to cause cancer or reproductive toxicity.”
The lead agency for implementing Proposition 65 is the Office of Environmental Health Hazard Assessment (OEHHA) of the California Environmental Protection Agency. The “state’s qualified experts” regarding findings of carcinogenicity are identified as the members of the Carcinogen Identification Committee (CIC) of the OEHHA Science Advisory Board (Title 27 Cal. Code of Regs. §25301; formerly Title 22, Cal. Code of Regs. §12301). OEHHA announced the selection of marijuana smoke as a chemical for consideration for listing by the CIC in the California Regulatory Notice Register on December 12, 2007, subsequent to consultation with the Committee at their November 19, 2007 meeting.
At that meeting, the Committee advised OEHHA to prepare hazard identification materials for marijuana smoke. The December 12th notice also marked the start of a 60-day public request for information relevant to the assessment of the evidence on the carcinogenicity marijuana smoke. No information was received as a result of this request. This document was released as a draft document in March 2009 for a 60-day public comment period. No public comments were received.
The draft document provided the Committee with the available scientific evidence on the carcinogenic potential of this chemical. The current document is the final version of the document that was discussed by the Committee at their May 29, 2009 meeting. At their May 29, 2009 meeting the Committee, by a vote of five in favor and one against, found that marijuana smoke had been “clearly shown through scientifically valid testing according to generally accepted principles to cause cancer.” Accordingly, marijuana smoke was placed on the Proposition 65 list of chemicals known to the state to cause cancer.
EXECUTIVE SUMMARY
Marijuana smoke is formed when the dried flowers, leaves, stems, seeds and resins of plants in the genus Cannabis are burned. Marijuana smoke aerosol contains thousands of organic and inorganic chemicals, including psychoactive cannabinoids, which are unique to Cannabis plants. Inhaling marijuana smoke for its psychotropic properties became popular in western cultures in the 1960s, though marijuana has been used for medicinal and psychotropic purposes in other parts of the world for thousands of years. In California, use of marijuana for physician recommended purposes has been legal under state law since 1996 when Proposition 215, the Compassionate Use Act, was passed by state voters. However, the vast majority of marijuana use continues to be for recreational purposes, which remains illegal.
Marijuana smoke and tobacco smoke share many characteristics with regard to chemical composition and toxicological properties. At least 33 individual constituents present in both marijuana smoke and tobacco smoke are already listed as carcinogens under Proposition 65. In examining the potential carcinogenicity of marijuana smoke, a range of information was evaluated. Studies of cancer risk in humans and laboratory animals exposed to marijuana smoke were reviewed. Other relevant data, including studies investigating genotoxicity and effects on endocrine function, cell signalling pathways, and immune function caused by marijuana smoke, were all considered. Also of interest were the similarities in chemical composition and in toxicological properties between marijuana smoke and tobacco smoke, and the presence of numerous carcinogens in marijuana smoke. The findings of all these reviews are summarized below.
There is evidence from some epidemiological studies of people exposed to marijuana smoke suggestive of increased cancer risk from both direct and parental marijuana smoking. However, this evidence is limited by potential biases and small numbers of studies for most types of cancer. Studies reporting results for direct marijuana smoking have observed statistically significant associations with cancers of the lung, head and neck, bladder, brain, and testis. The strongest evidence of a causal association was for head and neck cancer, with two of four studies reporting statistically significant associations. The evidence was less strong but suggestive for lung cancer, with one of three studies conducted in populations that did not mix marijuana and tobacco reporting a significant association. Suggestive evidence also was seen for bladder cancer, with one of two studies reporting a significant association. For brain and testicular cancers, the single studies conducted of each of these endpoints reported significant associations.
Among the epidemiological studies that reported results for parental marijuana smoking and childhood cancer, five of six found statistically significant associations. Maternal and paternal marijuana smoking were implicated, depending on the type of cancer. Childhood cancers that have been associated with maternal marijuana smoking are acute myeloid leukaemia, neuroblastoma, and rhabdomyosarcoma. Childhood cancers that have been associated with paternal marijuana smoking are leukaemia (all types), infant leukaemia (all types), acute lymphoblastic leukaemia, acute myeloid leukaemia, and rhabdomyosarcoma. A limitation common to the epidemiologic studies was potential bias from under-reporting of marijuana smoking due to its illegality, social stigma, lack of privacy during oral interviews, and subject desire to please interviewers, and possibly different degrees of under-reporting between cancer patients and healthy controls. Another limitation of several studies was that they were conducted in geographic locations where marijuana and tobacco are commonly mixed before smoking (e.g., three of six lung cancer studies and one of two bladder cancer studies were conducted in northern Africa, and two of four oral cancer studies were conducted in England). Thus, the results of those studies may have been confounded by the effects of exposure to tobacco smoke.
In animal studies, increases in squamous cell papilloma of the skin were reported in mice exposed dermally to marijuana smoke condensate. Malignant mesenchymatous tumors were reported following six subcutaneous injections of marijuana smoke condensate to newborn rats. In a marijuana smoke inhalation study in female rats, benign tumors of the ovary (serous cytoma and follicular cysts) and benign and malignant tumors of the uterus (adenofibroma, adenosarcoma, and telengiectatic cyst and polyps) were observed. Marijuana smoke condensate also exhibited tumor promoting activity in a mouse skin tumor initiation-promotion assay.
Evidence indicating that marijuana smoke is genotoxic includes findings that marijuana smoke induces mutations in Salmonella, and several small cytogenetic studies in humans suggesting that exposure to marijuana smoke may be associated with increased mutations and chromosomal abnormalities. While the data on the genotoxicity of marijuana smoke per se are limited, many individual smoke constituents have been shown to form DNA adducts, induce gene mutations, and damage chromosomes. Evidence indicating that marijuana smoke alters endocrine function includes findings for a number of different hormonal pathways. Marijuana smoke condensate has been shown to have estrogenic effects, including findings that it can activate the estrogen receptor (ER). Marijuana smoke also has been shown to have anti-estrogenic effects, through the induction of cytochrome P450 1A1 and the resultant increase in estrogen (E2) metabolism and through the inhibition of aromatase, an enzyme that converts testosterone to E2.
Other studies indicate that marijuana smoke condensate has anti-androgenic effects, inhibiting binding of dihydrotestosterone (DHT) to the androgen receptor (AR). Studies of ∆9 -tetrahydrocannabinol (∆9 -THC) and other cannabinoids provide evidence for disruption of the hypothalamic-pituitary-gonadal axis, including evidence that ∆9 -THC inhibits the release of follicle stimulating hormone, luteinizing hormone, prolactin, growth hormone, thyroid-stimulating hormone, and corticotrophin. These alterations in endocrine function can affect the growth of hormone responsive tissues, and might increase the risk of certain cancers (e.g., testes, ovary, uterus, and breast).
Evidence suggesting that marijuana smoke alters cell signalling pathways involved in cell cycle control comes from studies of the effects of ∆9 -THC and other cannabinoids on protein kinases. Depending upon the cell type and the dose administered, ∆9 -THC and other cannabinoids may either stimulate or inhibit cell proliferation. There is evidence that marijuana smoke suppresses the innate and adaptive immune response. The bactericidal activity of rat alveolar macrophages was reduced by marijuana smoke in vivo and in vitro. Tumoricidal and bactericidal activities were reduced in alveolar macrophages from marijuana smokers, compared to non-smokers. In addition, in one study smoking marijuana was associated with a more rapid progression of human immunodeficiency virus infection to acquired immunodeficiency syndrome. ∆9 -THC and other cannabinoids present in marijuana smoke have also been shown to suppress host resistance to microbial infection, macrophage function, natural killer and T cell cytolytic activity, cytokine production by macrophages and T cells, and to decrease antigen presentation by dendritic cells. These immunosuppressive effects could lead to an increased risk of cancer by reducing immunosurveillance capacity against neoplastic cells.
Prolonged exposures to marijuana smoke in animals and humans cause proliferative and inflammatory lesions in the lung, such as cellular disorganization, squamous metaplasia, and hyperplasia of basal and goblet cells (observed in the bronchial epithelial tissues of marijuana smokers). In summary, there is some evidence from studies in humans that marijuana smoke is associated with increased cancer risk. Studies in animals also provide some evidence that marijuana smoke induces tumors, with benign and malignant tumors observed in rats exposed via inhalation, malignant tumors in rats exposed via subcutaneous injection as newborns, and benign tumors in mice exposed dermally. Studies investigating the genotoxicity, immunotoxicity, and effects on endocrine function and cell signalling pathways provide additional evidence for the carcinogenicity of marijuana smoke. Finally, the similarities in chemical composition and in toxicological activity between marijuana smoke and tobacco smoke, and the presence of numerous carcinogens in marijuana (and tobacco) smoke, provide additional evidence of carcinogenicity.
Source: Evidence on the Carcinogenicity of Marijuana Smoke August 2009
Damage is caused in several different ways.
BRAIN: Messages are passed from cell to cell (neurons) in the brain by chemicals called neurotransmitters which fit by shape into their own receptor sites on specific cells.
The neurotransmitter, anandamide, an endo-cannabinoid (made in body) whose job is to control by suppression the levels of other neurotransmitters is mimicked and so replaced by a cannabinoid (not made in body) in cannabis called THC (Tetrahydrocannabinol). THC is very much stronger and damps down more forcefully the release of other neurotransmitters. Consequently the total activity of the
brain decreases. Chaos ensues.
Neurotransmitters delivering messages to the hippocampus, the area for learning and memory don’t receive enough stimulation to reach it, so signals are lost for ever.
Academic performance plummets and IQs fall by about 8 points. Neurons can be lost permanently. This is brain damage. No child using cannabis even occasionally will achieve their full potential.
Because signalling is slowed down, reaction times increase. Driving becomes hazardous and fatal accidents are rising in legalised USA states. Alcohol plus cannabis in drivers is 16 times more dangerous.
Since THC is fat-soluble, it stays in cells for weeks, constantly ensuring this decrease in brain activity. In the sixties/seventies the THC content was around 1-3%, now in London only ‘skunk’ at 16-20% THC is available. Professor Sir Robin Murray has said that, ‘users will be in a state of low-grade intoxication most of the time’. The Dopamine neurotransmitter has no receptor sites for anandamide and so THC
doesn’t affect it. But the inhibitory Gaba neurotransmitter has. Gaba normally suppresses dopamine but since it is itself suppressed by THC, levels of dopamine quickly increase. Excess dopamine is found in the brains of psychotics, and even schizophrenics if they have a genetic vulnerability. Anyone taking enough THC at one sitting will suffer a psychotic episode which could become permanent. Aggression, violence, even homicides, suicides and murders have resulted from cannabis-induced psychosis. The first research paper linking THC with psychosis was published in 1845. Cannabis-induced schizophrenia costs the country around £2 billion/year. Some of these mentally ill people will spend the rest of their lives in psychiatric units.
THC also depletes the levels of the ‘happiness’ neurotransmitter Serotonin. This can cause depression which may lead to suicide. THC causes dependence. This will affect 1 in 6 using adolescents and 1 in 9 of the general population. Since THC replaces anandamide, there is no need for its production which reduces and eventually stops so the receptor sites are left empty.
Withdrawal then sets in with irritability, sleeplessness, anxiety, depression, even violence until anandamide production resumes. Rehab specialists have told us that adolescent pot addiction is the most challenging to treat.
Cannabis can also act as a gateway drug – it can ‘prime’ the brain for the use of other drugs. Professor David Fergusson (NZ) in longitudinal studies from birth found that ‘The use of cannabis in late adolescence and early adulthood emerged as the strongest risk factor for later involvement in other illicit drug use’.
THC inhibits the vomiting reflex. If a person has drunk too much alcohol, they are often sick and get rid of it. An overdose of alcohol can kill (respiratory muscles stop working) so using cannabis together with alcohol can be fatal.
The signalling of endo-cannabinoids is crucial in brain development. They guide the formation, survival, proliferation, motility and differentiation of new neurons. THC badly interferes with these essential processes. Chaos ensues among the confused brain signals and a cannabis personality develops. Users can’t think logically. They have fixed opinions and answers, can’t find words, can’t take criticism – it’s always someone else’s fault, and can’t plan their day. Families suffer from their violent mood swings – houses get trashed. Anxiety, panic and paranoia may ensue. At the same time users are lonely, miserable and feel misunderstood.
Respiratory System:
Cannabis smoke has many of the same constituents as tobacco smoke but more of its carcinogens – in cancer terms a joint equals 4/5 cigarettes. More tar is deposited in the lungs and airways. Coughing, wheezing, emphysema, bronchitis and cancers have been seen in the lungs.
Heart:
Heart rates rise and stay high for 3-4 hours after a joint. Heart attacks and strokes have been recorded. Some teenagers had strokes and died after bingeing on cannabis.
Hypothalamus:
The hypothalamus is a region of the brain known to regulate appetite. Endocannabinoids in this area send ‘I’m hungry’ messages. When you take THC, that message is boosted. This is called ‘the munchies’. Nabilone, (synthetic THC) can be used to stimulate the appetite in AIDS patients.
DNA and Reproduction:
THC affects the DNA in any new cells being made in the body. It speeds up the programmed cell death (apoptosis) of our defence white blood cells, so our immune system is diminished. There are also fewer sperm. Infertility and impotence have been reported as far back as the 1990s.
An Australian paper published in July 2016 explains this phenomenon. THC can disrupt the actual process of normal cell division mitosis and meiosis (formation of sperm and eggs). In mitosis, the chromosomes replicate and gather together at the centre of the cell. Protein strands (microtubules) are formed from the ends of the cell to pull half of the chromosomes to each end to form the 2 new cells. Unfortunately THC disrupts microtubule formation. Chromosomes can become isolated, rejoin other bits of chromosome and have other abnormalities. Some will actually be shattered into fragments (chromothripsis).
This DNA damage can also cause cancers. Oncogenes (cancer-causing genes) may be activated, and tumour suppressant genes silenced. Chromosome fragments and abnormal chromosomes are frequently seen in cancerous tissues. This would account for other cancers, leukaemia, brain, prostate, cervix, testes and bladder etc, reported in regions of the body not exposed to the smoke. Pregnant users see a 2-4
fold increase in the number of childhood cancers in their offspring. The DNA damage has also been associated with foetal abnormalities – low birth weight, pre-term birth, spontaneous miscarriage, spina bifida, anencephaly (absence of brain parts), gastroschisis (babies born with intestines outside the body) cardiac defects and shorter limbs. All these defects bear in common an arrest of cell growth and cell migration at critical development stages consistent with the inhibition of mitosis noted with cannabis.
DNA damage at meiosis results in fewer sperm as we have seen. Increased errors in meiosis have the potential for transmission to subsequent generations. The zygote (fertilised egg) death rate rises by 50% after the first division. In infants, birth weight is lower and they may be born addicted. Children may have problems with behaviour and cognitive functions as they grow. Childhood cancers are
more common. Intensive care for newborns doubles. The younger they start using cannabis, the more likely they are to remain immature, become addicted, suffer from mental illnesses or progress to other drugs. Average age of first use is 13. Regular cannabis users have worse jobs, less than average money, downward social mobility, relationship problems and antisocial behaviour.
References:
Cannabis Skunk Website www.cannabisskunksense.co.uk Cannabis: A survey of its
harmful effects by Mary Brett is available on DOWNLOADS. It is a 300+ page report
written in 2006 and kept up to date.
Chromothripsis and epigenomics complete causality criteria for cannabis- and
addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity
Book: Adverse Health Consequencies of Cannabis Use. Jan Ramstrom National Institute of Public Health Sweden www.fhi.se
Source: https://www.cannabisskunksense.co.uk/uploads/site-files/ty,Chromothripsis,CarcinogenicityandFetotoxicity,MR-FMMM.pdf March 2020
The aim was to examine cross-sectional association between moderate alcohol consumption and total brain volume in a cohort of participants in early middle-age, unconfounded by age-related neuronal change. 353 participants aged 39 to 45 years reported on their alcohol consumption using the AUDIT-C measure. Participants with alcohol abuse were excluded. Brain MRI was analyzed using a fully automated method. Brain volumes were adjusted by intracranial volume expressed as adjusted total brain volume (aTBV). AUDIT-C mean of 3.92 (SD 2.04) indicated moderate consumption. In a linear regression model, alcohol consumption was associated with smaller aTBV (B = – 0.258, p < .001). When sex and current smoking status were added to the model, the association remained significant. Stratified by sex, the association was seen in both males (B = – 0.258, p = 0.003) and females (B = – 0.214, p = 0.011). Adjusted for current smoking, the association remained in males (B = – 0.268, p = 0.003), but not in females. When alcohol consumption increased, total brain volume decreased by 0.2% per one AUDIT-C unit already at 39-45 years of age. Moderate alcohol use is associated with neuronal changes in both males and females suggesting health risks that should not be overlooked.
Figure 1
Cannabis is responsible for 91 per cent of cases where teenagers end up being treated for drug addiction, shocking new figures reveal.
Supporters of the drug claim it is harmless, but an official report now warns the ‘increased dominance of high-potency herbal cannabis’ – known as skunk – is causing more young people to seek treatment.
The revelation comes amid growing concerns that universities – and even some public schools – are awash with high-strength cannabis and other drugs.
The findings also back up academic research, revealed in The Mail on Sunday over the past three years, that skunk is having a serious detrimental impact on the mental health of the young. At least two studies have shown repeated use triples the risk of psychosis, with sufferers repeatedly experiencing delusional thoughts. Some victims end up taking their own lives.
The latest UK Focal Point on Drugs report, drawn up by bodies including Public Health England, the Scottish Government and the Home Office, found that:
Last night, Lord Nicholas Monson, whose 21-year-old son Rupert Green killed himself last year after becoming hooked on high-strength cannabis, said: ‘These figures show the extent of the damage that high-potency cannabis wreaks on the young.
‘The big danger for young people – particularly teens – is that their brains can be really messed up by this stuff because they are still developing biologically. If they develop drug-induced psychosis – as Rupert did – the illness can stick for life.’
The large rise in the number of youngsters treated for cannabis abuse comes despite the fact that total usage is falling slightly.
The report concludes: ‘While fewer people are using cannabis, those who are using it are experiencing greater harm.’
Almost all cannabis on Britain’s streets is skunk, which is four times more powerful than types that dominated the market until the early 2000s. It can even trigger hallucinations.
Lord Monson said: ‘We really need Ministers to get a grip and launch a major publicity campaign about the dangers.’
Nine in ten teens at drug clinics are being treated for marijuana use | Daily Mail Online April 2018
Veterans are twice as likely as non-veterans to die from accidental overdoses involving prescription opioids. In an effort to lower opioid intake, some veterans are turning to hemp products, like CBD oil, to treat chronic pain and PTSD. Now some veterans are saying they want more research and access, reports CBS News correspondent Nancy Cordes.
They are not your typical lobbyists. They’re veterans whose lives were nearly ruined — first by their injuries, and then by their meds.
“I was at a higher than likely rate of committing suicide from pain,” Navy veteran Veronica Wayne told lawmakers. She took opioids for 17 years after an airplane maintenance hatch hit her head.
“I basically became a walking zombie,” Wayne said.
She tried medical marijuana, but still felt impaired. That’s when she heard about hemp.
“It’ll still kill all the pain symptoms and give you the relief that you need, but you’re not going to feel high,” Wayne said.
Now she uses CBD oil. But, she notes, “You can’t get it from the VA. It’s not, it’s not legal.”
Like marijuana, hemp is derived from the cannabis plant. But hemp does not contain THC, the chemical that makes you high. Still both hemp and marijuana are classified as Schedule 1 controlled substances, restricting the VA and other federally funded entities from conducting research. The American Legion is leading the push to change that.
“Anything that makes a veteran feel better — especially something that’s non-toxic — is something we’re going to support,” said Louis Celli, national director of Veterans Affairs and rehabilitation at the American Legion.
Currently hemp products are marketed as unregulated supplements, which makes many doctors reluctant to recommend them.
“We’re not exactly sure how to use them, what the right dose is, how they interact,” said Wayne Jonas, the former director of the NIH office of alternative medicine.
But lawmakers on both sides are pushing to change the law.
“I’m actually cautiously optimistic if we get something on the floor, that it will pass,” Rep. Earl Blumenauer, D-Ore., said.
Until then, Army reservist Dale Rider said many of his buddies are wary of the product that he said helps his back pain.
“For them, they’re all worried that because it’s so closely related to marijuana, that it could pop up on a drug test randomly,” Rider said.
The industry has a powerful ally in Senate Majority Leader Mitch McConnell, who represents Kentucky, where hemp is seen as a potential cash crop. Last month he introduced a bill in the Senate that has bipartisan support to legalize hemp as an agricultural commodity.
Veterans push lawmakers to legalize hemp products – CBS News April 2018
There is a strong association between cannabis use and schizophrenia but the underlying cellular links are poorly understood. Neurons derived from human-induced pluripotent stem cells (hiPSCs) offer a platform for investigating both baseline and dynamic changes in human neural cells. Here, we exposed neurons derived from hiPSCs to Δ9-tetrahydrocannabinol (THC), and identified diagnosis-specific differences not detectable in vehicle-controls. RNA transcriptomic analyses revealed that THC administration, either by acute or chronic exposure, dampened the neuronal transcriptional response following potassium chloride (KCl)-induced neuronal depolarization. THC-treated neurons displayed significant synaptic, mitochondrial, and glutamate signaling alterations that may underlie their failure to activate appropriately; this blunted response resembles effects previously observed in schizophrenia hiPSC- derived neurons. Furthermore, we show a significant alteration in THC-related genes associated with autism and intellectual disability, suggesting shared molecular pathways perturbed in neuropsychiatric disorders that are exacerbated by THC.
The authors declare that they have no conflict of interest.
Fig. 1. THC treatment regulates genes involved in mitochondrial and glutamate pathways.
Fig. 2. Postsynaptic density and ion channel genes are regulated by THC treatment.
Fig. 3. Genes altered by THC treatment in hiPSC-derived neurons are significantly associated with autism and intellectual disability.
Fig. 4. THC treatment results in neuronal hypo-excitability similar to observations using schizophrenia-associated neurons.
We aimed to describe and correlate the hospital panorama of psychotic disorders (PD) with cannabis use (CU) trends in all Portuguese public hospitals.
We conducted a retrospective observational study that analysed all hospitalizations that occurred in Portuguese public hospitals from 2000 to 2015. Hospitalizations with a primary diagnosis of PD or schizophrenia were selected based on Clinical Classification Software diagnostic single-level 659. Episodes associated with CU were identified by the International Classification of Diseases Version 9, Clinical Modification code 304.3/305.2 that correspond to cannabis dependence/cannabis abuse.
The number of hospitalizations with a primary diagnosis of PD and schizophrenia associated with CU rose 29.4 times during the study period, from 20 to 588 hospitalizations yearly (2000 and 2015, respectively) with a total of 3,233 hospitalizations and an average episode cost of €3,500. Male patients represented 89.8% of all episodes, and the mean/median age at discharge were 30.66/29.00 years, respectively. From all hospitalizations with a primary diagnosis of PD or schizophrenia, the ones with a secondary diagnosis of CU rose from 0.87% in 2000 to 10.60% in 2015.
The increase on secondary diagnosis coding and the change on cannabis patterns of consumption in Portuguese population with an increasing frequency of moderate/high dosage cannabis consumers may explain the rise on PD hospitalizations
A life-threatening heart infection afflicts a growing number of people who inject opioids or meth. Costly surgery can fix it, but the addiction often goes unaddressed.
Dr. Thomas Pollard, a cardiothoracic surgeon in Knoxville, Tenn., and his team working to replace heart valves that had been damaged from endocarditis, an infection the patient developed from injecting drugs. Shawn Poynter for The New York Times
OAK RIDGE, Tenn. — Jerika Whitefield’s memories of the infection that almost killed her are muddled, except for a few. Her young children peering at her in the hospital bed. Her stepfather wrapping her limp arms around the baby. Her whispered appeal to a skeptical nurse: “Please don’t let me die. I promise, I won’t ever do it again.”
Ms. Whitefield, 28, had developed endocarditis, an infection of the heart valves caused by bacteria that entered her blood when she injected methamphetamine one morning in 2016. Doctors saved her life with open-heart surgery, but before operating, they gave her a jolting warning: If she continued shooting up and got reinfected, they would not operate again.
With meth resurgent and the opioid crisis showing no sign of abating, a growing number of people are getting endocarditis from injecting the drugs — sometimes repeatedly if they continue shooting up. Many are uninsured, and the care they need is expensive, intensive and often lasts months. All of this has doctors grappling with an ethically fraught question: Is a heart ever not worth fixing?
“We’ve literally had some continue using drugs while in the hospital,” said Dr. Thomas Pollard, a veteran cardiothoracic surgeon in Knoxville, Tenn. “That’s like trying to do a liver transplant on someone who’s drinking a fifth of vodka on the stretcher.”
The problem has consumed Dr. Pollard, a calm Texan who got his Tennessee medical license in 1996, just after the widely abused opioid painkiller OxyContin hit the market. He has seen an explosion of endocarditis cases, particularly among poor, young drug users whose hearts can usually be salvaged, but whose addiction goes unaddressed by a medical system that rarely takes responsibility for treating it.
Certain cases haunt him. A little over a year ago, he replaced a heart valve in a 25-year-old man who had injected drugs, only to see him return a few months later. Now two valves, including the new one, were badly infected, and his urine tested positive for illicit drugs. Dr. Pollard declined to operate a second time, and the patient died at a hospice.
“It was one of the hardest things I’ve ever had to do,” he said.
The Treatment Gap
As cases have multiplied around the country, doctors who used to only occasionally encounter endocarditis in patients who injected drugs are hungry for guidance. A recent study found that at two Boston hospitals, only 7 percent of endocarditis patients who were IV drug users survived for a decade without reinfection or other complications, compared with 41 percent of patients who were not IV drug users. Those hospitals are among a small but growing group trying to be more proactive.
Dr. Pollard has been lobbying hospital systems in Knoxville to provide addiction treatment for willing endocarditis patients, at least on a trial basis, after their surgery. If the hospitals offered it, he reasons, doctors would have more justification for turning away patients who refused and in the long run, hospitals would save money.
Addiction has long afflicted rural east Tennessee, where the rolling hills and mountains are woven with small towns suffering from poverty and poor health. Prescribing rates for opioids are still strikingly high, and the overdose death rate in Roane County, where Ms. Whitefield lives, is three times the national average. Jobs go unfilled here because, employers say, applicants often cannot pass a drug test.
Across Tennessee, some 163,000 poor adults remain uninsured after state lawmakers refused to expand Medicaid under the Affordable Care Act. For them, and even for many covered by Medicaid, as Ms. Whitefield is, evidence-based opioid addiction treatment remains meager. More common are cash-only clinics, or abstinence-based programs that bank on willpower instead of the addiction medications that have proved more effective.
Treatment for endocarditis usually involves up to six weeks of intravenous antibiotics, often in the hospital because doctors are wary of sending addicted patients home with IV lines for fear they would use them to inject illicit drugs. Many, like Ms. Whitefield, also need intricate surgery to repair or replace damaged heart valves. The cost can easily top $150,000, Dr. Pollard said.
Advice from specialty groups, like the American Association for Thoracic Surgery and the American College of Cardiology, about when to operate remains vague. For now, “it’s just a lot of anecdote — surgeons talking to each other, trying to determine when we should and when we shouldn’t,” said Dr. Carlo Martinez, who is one of Dr. Pollard’s partners and who operated on Ms. Whitefield at Methodist Medical Center of Oak Ridge.
Their practice, owned by Covenant Health, will almost always operate on someone with a first-time case of endocarditis from injecting drugs, Dr. Pollard said. But repeat infections, when the damage can be more extensive and harder to fix, make it a tougher call. Dr. Mark Browne, Covenant’s senior vice president and chief medical officer, said, “Each patient is evaluated individually and decisions regarding the appropriate course of care are determined by their attending physician.”
In the nearly two years since she got sick, Ms. Whitefield has felt physically diminished and been prone to illness. She also feels harshly judged by a medical system that saved her life but often treats her with suspicion and disdain.
Over the same stretch of time, Dr. Pollard has grown increasingly disillusioned with hospitals that consider addiction treatment beyond their purview, and haunted by the likelihood that many of his drug-addicted patients will die young whether they get heart surgery or not. He set up a task force in 2016 to address the problem but has faced obstacles, especially concerning cost and, he believes, a societal reluctance to spend money on people who abuse drugs.
“Everybody has sympathy for babies and children,” he said. “No one wants to help the adult drug addict because the thought is they did this to themselves.”
Dr. Pollard has been consumed by the problem of endocarditis among drug users whose addiction goes unaddressed. “We’ve literally had some continue using drugs while in the hospital,” he said. Joe Buglewicz for The New York Times
____
Ms. Whitefield, a talkative young woman with brooding eyes, goes by the nickname Shae. She started on opioid painkillers as a teenager suffering from endometriosis, a disorder of the uterine tissue, and interstitial cystitis, a painful bladder condition. She got the opioids from doctors for years, and eventually from friends.
She and her high school boyfriend, Chris Bunch, had three children by the time she was 26. She trained to become a licensed practical nurse but dropped out of the program when her oldest son, Jayden, got seriously ill as a baby. The family lives in a tiny town that Mr. Bunch, now Ms. Whitefield’s husband, described as “country, country, country.”
In 2015, after their daughter, Kyzia, was born, Ms. Whitefield sank into postpartum depression. She was obsessively worried about shielding Kyzia from sexual abuse and other traumas she had experienced as a child. She started injecting crushed opioid pills and occasionally meth, savoring the needle’s sting — she had an old habit of cutting herself to provide relief from emotional pain — at least as much as the high.
After sharing a needle with one of her brothers that day in June 2016, Ms. Whitefield started shivering and sweating. A fever soon followed, and she lay for almost a week on the couch, thinking she had a kidney infection. She was delirious by the time Jayden, then 8, woke her stepfather one morning and told him to call 911.
She arrived at Methodist Medical Center of Oak Ridge with full-blown sepsis, floating in and out of consciousness. Her organs had started to shut down.
At home, she had stared at a picture on the wall of her grandmother faintly smiling, a source of reassurance, for days. When the first nurse leaned over her in the emergency room, she thought she smelled her grandmother’s perfume.
Her stepfather, Brian Mignogna, remembers being stunned when a doctor who initially assessed her said that if it were up to him, he would not go to great lengths to save her.
“He said once someone’s been shooting up, you go through all this money and surgery and they go right back to shooting up again, so it’s not worth it,” Mr. Mignogna recalled. “I was just dumbfounded.”
Dr. Martinez was the on-call heart surgeon a few days later, though, and felt strongly about taking Ms. Whitefield’s case. Her children and stepfather had been constants at her bedside, and unlike some patients he had seen, she had readily admitted to her drug use. He believed her when she said she had not been injecting for long and wanted to stop.
“She was a young mother and her family was involved; her father was there,” he said. “To me, it seemed she had that social support that patients need once they recover from this.”
Ms. Whitefield also had health coverage through Medicaid, the government insurance program for the poor, because she has young children. It paid for her care, whereas if she were uninsured, the hospital would have had to cover the cost.
Antibiotics cleared the infection that initially led her to the hospital, but she ended up needing surgery two months later. Her mitral valve was so damaged that she had begun showing signs of heart failure. Dr. Martinez was compassionate, but he stressed that the surgery would be “a one-time deal,” Mr. Mignogna recalled.
“The way he put it was, ‘You relapse and end up with another infection, we won’t treat you again,’” Mr. Mignogna said.
Dr. Martinez repaired Ms. Whitehead’s mitral valve in a three-hour operation. It involved sawing open her breastbone, connecting her to a bypass machine to keep blood flowing through her body, and then stopping her heart and fixing the valve. He reinforced it with a small plastic ring before restarting her heart and closing her up.
She had written a note to each of her children — wise Jayden, kind Elijah, strong-willed Kyzia — in case she never woke up. Two weeks later, she was well enough to go home. She soon began seeing a counselor at a clinic unaffiliated with the hospital system and taking buprenorphine, a medication that diminishes opioid cravings and has been found to reduce the risk of relapse and fatal overdose.
Ms. Whitefield has had occasional cravings since the surgery but says she has not used drugs again, traumatized by the memory of her ordeal.
“I know next time God might not save me,” she said quietly. “They will not treat me for a second time if I have track marks or anything like that.”
As she recuperated, Ms. Whitefield started thinking about returning to school, aspiring to become a drug and alcohol counselor or real estate agent, or both.
She has also started serving as an advocate of sorts for others in her community who get endocarditis or other infections from injecting, driving them to the emergency room or sharing every detail of the protocol that saved her. She smarts at the thought of providing only “comfort care” — antibiotics but no surgery — even if a patient refuses addiction treatment.
“When do you stop wanting to save a life?” she asked. “If you have that ability, who’s to say you shouldn’t use it? I see it from their standpoint — not wanting to repeat the same game. But it’s hard, you know? This isn’t an easy disease to break away from.”
____
Dr. Pollard, a quietly driven high school valedictorian, used to have no empathy for drug-addicted patients.
“I was like everyone else: ‘They do it to themselves, they deserve what they get,’” he said. “But then when you see their children, and hear about friends my kids went to school with who have died, it’s closer to home.”
When he became president of the Knoxville Academy of Medicine in 2015, he came up with the idea of the city’s hospital systems teaming up to offer addiction treatment to endocarditis patients. He had the perfect platform to push for it, he thought.
So the following year, he set up a task force that included people from each hospital system — his own, Covenant Health; the University of Tennessee Medical Center; and Tennova Healthcare — as well as from two drug treatment centers and some community groups.
At a task force meeting last August, about a year after Ms. Whitefield’s surgery, Dr. Pollard clicked through a PowerPoint presentation full of data a research nurse had compiled. From 2014 through 2016, the three hospital systems in Knoxville had provided valve surgery to 117 patients diagnosed with endocarditis from injecting drugs. Ten had received a second surgery after becoming reinfected; of those, two had received a third.
Just over half the patients were uninsured, and only 1 percent had private coverage. From the data, it was impossible to know if anyone had been reinfected but turned away by doctors. But at least 21 people — 18 percent — had died since their heart surgery, typically from sepsis or respiratory failure, which Dr. Pollard said indicated reinfection.
The group discussed Dr. Pollard’s proposal for Cornerstone of Recovery, an addiction treatment center here, to admit a handful of endocarditis patients as soon as they were cleared for discharge. Cornerstone would provide several months of inpatient treatment and up to a year’s worth of Vivitrol, a monthly $1,000 shot that blocks cravings and helps prevent relapse.
Buprenorphine, the medication Ms. Whitefield takes, is less expensive. But Cornerstone does not provide it because it is an opioid itself and “is trading one for the other,” said Webster Bailey, its executive director of marketing. Many addiction experts have called that view “grossly inaccurate.” They say it is weaker than drugs like oxycodone and heroin, activating the brain’s opioid receptors enough to ease cravings but not enough to provide a high in people who are already dependent on opioids.
Patients would sign an agreement stating that if they returned to abusing drugs after addiction treatment, they might not be considered a candidate for future heart surgery. The total cost per patient: perhaps $55,000, which Dr. Pollard hopes that government and private funding would help cover if the program expanded.
“This should be part of the treatment, just like antibiotics are,” he told the group.
A surgeon from Tennova dryly pointed out: “Not everybody in that group is going to say, ‘This is for me, I’m going to do it.’”
Still, the group decided Dr. Pollard should take the next step, pitching the pilot plan to each system’s top executives.
“We are competing systems, but this is a common enemy that unites us all,” he said afterward. “We need a united policy.”
Source: https://www.nytimes.com/2018/04/29/health/drugs-opioids-addiction-heart-endocarditis.html April 2018
Smoking during pregnancy has well-documented negative effects on birth weight in infants and is linked to several childhood health problems. Now, researchers at the University at Buffalo Research Institute on Addictions have found that prenatal marijuana use also can have consequences on infants’ weight and can influence behavior problems, especially when combined with tobacco use.
“Nearly 30 percent of women who smoke cigarettes during pregnancy also report using marijuana,” says Rina Das Eiden, PhD, RIA senior research scientist. “That number is likely to increase with many states moving toward marijuana legalization, so it’s imperative we know what effects prenatal marijuana use may have on infants.”
Through a grant from the National Institute on Drug Abuse, Eiden studied nearly 250 infants and their mothers. Of these, 173 of the infants had been exposed to tobacco and/or marijuana during their mothers’ pregnancies. None were exposed to significant amounts of alcohol.
Eiden found that infants who had been exposed to both tobacco and marijuana, especially into the third trimester, were smaller in length, weight and head size, and were more likely to be born earlier, compared to babies who were not exposed to anything. They also were more likely to be smaller in length and weight compared to babies exposed only to tobacco in the third trimester. The results were stronger for boys compared to girls.
“We also found that lower birth weight and size predicted a baby’s behavior in later infancy,” Eiden says. “Babies who were smaller were reported by their mothers to be more irritable, more easily frustrated and had greater difficulty calming themselves when frustrated. Thus, there was an indirect association between co-exposure to tobacco and marijuana and infant behavior via poor growth at delivery.”
Furthermore, women who showed symptoms of anger, hostility and aggression reported more stress in pregnancy and were more likely to continue using tobacco and marijuana throughout pregnancy. Therefore, due to the co-exposure, they were more likely to give birth to infants smaller in size and who were more irritable and easily frustrated. The infants’ irritability and frustration is also linked to mothers who experienced higher levels of stress while pregnant.
“Our results suggest that interventions with women who smoke cigarettes or use marijuana while pregnant should also focus on reducing stress and helping them cope with negative emotions,” Eiden says. “This may help reduce prenatal substance exposure and subsequent behavior problems in infants.”
The study appeared in the March/April issue of Child Development and was authored by Pamela Schuetze, PhD, Department of Psychology, Buffalo State College, with co-authors Eiden; Craig R. Colder, PhD, UB Department of Psychology; Marilyn A. Huestis, PhD, Institute of Emerging Health Professions, Thomas Jefferson University, Philadelphia; and Kenneth E. Leonard, PhD, RIA director.
Source: Prenatal marijuana use can affect infant size, behavior, study finds — ScienceDaily May 2018
Cannabis use increased among parents who smoke cigarettes, as well as among non-smoking parents, according to a latest study from researchers at Columbia University’s Mailman School of Public Health and City University of New York. Cannabis use was nearly four times more common among cigarette smokers compared with non-smokers. Until now, little had been known about current trends in the use of cannabis among parents with children in the home, the prevalence of exposure to both tobacco and cannabis, and which populations might be at greatest risk. The findings will be published online in the June issue of Pediatrics.
“While great strides have been made to reduce children’s exposure to second-hand cigarette smoke, those efforts may be undermined by increasing use of cannabis among parents with children living at home,” said Renee Goodwin, PhD, in the Department of Epidemiology at the Mailman School of Public Health, and corresponding author.
Analyzing data from the National Survey on Drug Use and Health from 2002 to 2015, the researchers found past-month cannabis use among parents with children at home increased from 5 percent in 2002 to 7 percent in 2015, whereas cigarette smoking declined from 28 percent to 20 percent. Cannabis use increased from 11 percent in 2002 to over 17 percent in 2015 among cigarette-smoking parents and from slightly over 2 percent to 4 percent among non-cigarette-smoking parents. Cannabis use was nearly 4 times more common among cigarette smokers versus nonsmokers (17 percent vs 4 percent), as was daily cannabis use (5 percent vs 1 percent). The overall percentage of parents who used cigarettes and/or cannabis decreased from 30 percent in 2002 to 24 percent in 2015.
“While use of either cigarettes or cannabis in homes with children has declined, there was an increase in the percent of homes with both. Therefore, the increase in cannabis use may be compromising progress in curbing exposure to secondhand smoke,” noted Goodwin, who is also at the Graduate School of Public Health and Health Policy at CUNY.
Cannabis use was also more prevalent among men who also smoked compared to women (10 percent vs 6 percent) and among younger parents with children in the home (11 percent) compared with those 50 and older (4 percent). The strength of the relationship between current cannabis use and cigarette smoking was significant and similar for all income levels.
“The results of our study support the public health gains in reducing overall child secondhand tobacco smoke but raise other public health concerns about child exposure to secondhand cannabis smoke and especially high risk for combined exposures in certain subpopulations,” observed Goodwin.
Noteworthy, according to Goodwin, is that there remains a lack of information on the location of smoking, whether it occurs in the house or in the proximity of children. Unlike cigarettes, smoking cannabis outdoors and in a range of public areas is illegal in most places. Therefore, there is reason to believe that cannabis use is even more likely to occur in the home than cigarette smoking given their differences in legal status.
“Efforts to decrease secondhand smoke exposure via cigarette smoking cessation may be complicated by increases in cannabis use,” said Goodwin. “Educating parents about secondhand cannabis smoke exposure should be integrated into public health education programs on secondhand smoke exposure.”
The study was funded by the National Institutes of Health and National Institute on Drug Abuse (DA20892).
Co-authors are Melanie Wall, Deborah Hasin, and Samantha Santoscoy, Mailman School of Public Health; Keely Cheslack-Postava, Columbia University College of Physicians and Surgeons; Nina Bakoyiannis, CUNY; and Bradley Collins and Stephen Lepore, Temple University.
The popularity of electronic cigarettes continues to grow worldwide, as many people view them as a safer alternative to smoking. But the long-term effects of e-cigarette usage, commonly called “vaping,” are unknown. Today, researchers report that vaping may modify the genetic material, or DNA, in the oral cells of users, which could increase their cancer risk.
The researchers will present their results today at the 256th National Meeting & Exposition of the American Chemical Society (ACS).
“E-cigarettes are a popular trend, but the long-term health effects are unknown,” says Romel Dator, Ph.D., who is presenting the work at the meeting. “We want to characterize the chemicals that vapers are exposed to, as well as any DNA damage they may cause.”
Introduced to the market in 2004, e-cigarettes are handheld electronic devices that heat a liquid, usually containing nicotine, into an aerosol that the user inhales. Different flavors of liquids are available, including many that appeal to youth, such as fruit, chocolate and candy. According to a 2016 report by the U.S. Surgeon General, 13.5 percent of middle school students, 37.7 percent of high school students and 35.8 percent of young adults (18 to 24 years of age) have used e-cigarettes, compared with 16.4 percent of older adults (25 years and up).
“It’s clear that more carcinogens arise from the combustion of tobacco in regular cigarettes than from the vapor of e-cigarettes,” says Silvia Balbo, Ph.D., the project’s lead investigator, who is at the Masonic Cancer Center at the University of Minnesota. “However, we don’t really know the impact of inhaling the combination of compounds produced by this device. Just because the threats are different doesn’t mean that e-cigarettes are completely safe.”
To characterize chemical exposures during vaping, the researchers recruited five e-cigarette users. They collected saliva samples before and after a 15-minute vaping session and analyzed the samples for chemicals that are known to damage DNA. To evaluate possible long-term effects of vaping, the team assessed DNA damage in the cells of the volunteers’ mouths. The researchers used mass-spectrometry-based methods they had developed previously for a different study in which they evaluated oral DNA damage caused by alcohol consumption.
Dator and Balbo identified three DNA-damaging compounds, formaldehyde, acrolein and methylglyoxal, whose levels increased in the saliva after vaping. Compared with people who don’t vape, four of the five e-cigarette users showed increased DNA damage related to acrolein exposure. The type of damage, called a DNA adduct, occurs when toxic chemicals, such as acrolein, react with DNA. If the cell does not repair the damage so that normal DNA replication can take place, cancer could result.
The researchers plan to follow up this preliminary study with a larger one involving more e-cigarette users and controls. They also want to see how the level of DNA adducts differs between e-cigarette users and regular cigarette smokers. “Comparing e-cigarettes and tobacco cigarettes is really like comparing apples and oranges. The exposures are completely different,” Balbo says. “We still don’t know exactly what these e-cigarette devices are doing and what kinds of effects they may have on health, but our findings suggest that a closer look is warranted.”
Source: E-cigarettes can damage DNA — ScienceDaily August 2018
Albert Stuart Reece, MBBS(Hons.), FRCS(Ed.), FRCS(Glas.), FRACGP, MD (UNSW) and Gary Kenneth Hulse, BBSc.(Hons.), MBSc., PhD.
Background: The epidemiology of cannabinoid-related cancerogenesis has not been studied with cutting edge epidemiological techniques. Building on earlier bivariate papers in this series we aimed to conduct pathfinding studies to address this gap in two tumours of the reproductive tract, prostate and ovarian cancer.
Methods: Age-standardized cancer incidence data for 28 tumour types (including “All (non-skin) Cancer”) was sourced from Centres for Disease Control and National Cancer Institute using SEER*Stat software across US states 2001-2017. Drug exposure was sourced from the nationally representative household survey National Survey of Drug Use and Health conducted annually by the Substance Abuse and Mental Health Services Administration 2003-2017 with response rate 74.1%. Federal seizure data provided cannabinoid concentration data. US Census Bureau provided income and ethnicity data. Inverse probability weighted mixed effects, robust and panel regression together with geospatiotemporal regression analyses were conducted in R. E-Values were also calculated.
Results: 19,877 age-standardized cancer rates were returned. Based on these rates and state populations this equated to 51,623,922 cancer cases over an aggregated population 2003-2017 of 124,896,418,350. Inverse probability weighted regressions for prostate and ovarian cancers confirmed causal associations robust to adjustment. Cannabidiol alone was significantly associated with prostate cancer (β-estimate = 1.61, (95%C.I. 0.99, 2.23), P = 3.75 × 10– 7). In a fully adjusted geospatiotemporal model at one spatial and two temporal years lags cannabidiol was significantly independently associated with prostate cancer (β-estimate = 2.08, (1.19, 2.98), P = 5.20 × 10– 6). Cannabidiol alone was positively associated with ovarian cancer incidence in a geospatiotemporal model (β-estimate = 0.36, (0.30, 0.42), P < 2.20 × 10– 16). The cigarette: THC: cannabidiol interaction was significant in a fully adjusted geospatiotemporal model at six years of temporal lag (β-estimate = 1.93, (1.07, 2.78), P = 9.96 × 10– 6). Minimal modelled polynomial E-Values for prostate and ovarian cancer ranged up to 5.59 × 1059 and 1.92 × 10125. Geotemporospatial modelling of these tumours showed that the cannabidiol-carcinogenesis relationship was supra-linear and highly sigmoidal (P = 1.25 × 10– 45 and 12.82 × 10– 52 for linear v. polynomial models).
Conclusion: Cannabinoids including THC and cannabidiol are therefore important community carcinogens additive to the effects of tobacco and greatly exceeding those of alcohol. Reproductive tract carcinogenesis necessarily implies genotoxicity and epigenotoxicity of the germ line with transgenerational potential. Pseudoexponential and causal dose-response power functions are demonstrated.
Keywords: Cannabidiol; Cannabigerol; Cannabinoid; Cannabis; Chromosomal toxicity; Congenital anomalies; Dose-response relationship; Epigenotoxicity; Genotoxicity; Mechanisms; Multigenerational genotoxicity; Oncogenesis; Sigmoidal dose-response; Supra-linear dose response; Transgenerational teratogenicity; Δ9-tetrahydrocannabinol.
Albert Stuart Reece, MBBS(Hons.), FRCS(Ed.), FRCS(Glas.), FRACGP, MD (UNSW) and Gary Kenneth Hulse, BBSc.(Hons.), MBSc., PhD.
Background: As the cannabis-cancer relationship remains an important open question epidemiological investigation is warranted to calculate key metrics including Rate Ratios (RR), Attributable Fractions in the Exposed (AFE) and Population Attributable Risks (PAR) to directly compare the implicated case burden between emerging cannabinoids and the established carcinogen tobacco.
Methods: SEER*Stat software from Centres for Disease Control was used to access age-standardized state census incidence of 28 cancer types (including “All (non-skin) Cancer”) from National Cancer Institute in US states 2001-2017. Drug exposures taken from the National Survey of Drug Use and Health 2003-2017, response rate 74.1%. Federal seizure data provided cannabinoid exposure. US Census Bureau furnished income and ethnicity. Exposure dichotomized as highest v. lowest exposure quintiles. Data processed in R.
Results: Nineteen thousand eight hundred seventy-seven age-standardized cancer rates were returned. Based on these rates and state populations this equated to 51,623,922 cancer cases over an aggregated population 2003-2017 of 124,896,418,350. Fifteen cancers displayed elevated E-Values in the highest compared to the lowest quintiles of cannabidiol exposure, namely (in order): prostate, melanoma, Kaposi sarcoma, ovarian, bladder, colorectal, stomach, Hodgkins, esophagus, Non-Hodgkins lymphoma, All cancer, brain, lung, CLL and breast. Eleven cancers were elevated in the highest THC exposure quintile: melanoma, thyroid, liver, AML, ALL, pancreas, myeloma, CML, breast, oropharynx and stomach. Twelve cancers were elevated in the highest tobacco quintile confirming extant knowledge and study methodology. For cannabidiol RR declined from 1.397 (95%C.I. 1.392, 1.402), AFE declined from 28.40% (28.14, 28.66%), PAR declined from 15.3% (15.1, 15.5%) and minimum E-Values declined from 2.13. For THC RR declined from 2.166 (95%C.I. 2.153, 2.180), AFE declined from 53.8% (53.5, 54.1%); PAR declined from 36.1% (35.9, 36.4%) and minimum E-Values declined from 3.72. For tobacco, THC and cannabidiol based on AFE this implies an excess of 93,860, 91,677 and 48,510 cases; based on PAR data imply an excess of 36,450, 55,780 and 14,819 cases.
Conclusion: Data implicate 23/28 cancers as being linked with THC or cannabidiol exposure with epidemiologically-causal relationships comparable to those for tobacco. AFE-attributable cases for cannabinoids (91,677 and 48,510) compare with PAR-attributable cases for tobacco (36,450). Cannabinoids constitute an important multivalent community carcinogen.
Keywords: Cannabidiol; Cannabigerol; Cannabinoid; Chromosomal toxicity; Congenital anomalies; Dose-response relationship; Epigenotoxicity; Genotoxicity; Mechanisms; Multigenerational genotoxicity; Oncogenesis; Sigmoidal dose-response; Supra-linear dose response; Transgenerational teratogenicity; cannabis; Δ9-tetrahydrocannabinol.
Albert Stuart Reece, MBBS(Hons.), FRCS(Ed.), FRCS(Glas.), FRACGP, MD (UNSW) and Gary Kenneth Hulse, BBSc.(Hons.), MBSc., PhD.
Background: The genotoxic and cancerogenic impacts of population-wide cannabinoid exposure remains an open but highly salient question. The present report examines these issues from a continuous bivariate perspective with subsequent reports continuing categorical and detailed analyses.
Methods: Age-standardized state census incidence of 28 cancer types (including “All (non-skin) Cancer”) was sourced using SEER*Stat software from Centres for Disease Control and National Cancer Institute across US states 2001-2017. It was joined with drug exposure data from the nationally representative National Survey of Drug Use and Health conducted annually by the Substance Abuse and Mental Health Services Administration 2003-2017, response rate 74.1%. Cannabinoid data was from Federal seizure data. Income and ethnicity data sourced from the US Census Bureau. Data was processed in R.
Results: Nineteen thousand eight hundred seventy-seven age-standardized cancer rates were returned. Based on these rates and state populations this equated to 51,623,922 cancer cases over an aggregated population 2003-2017 of 124,896,418,350. Regression lines were charted for cancer-substance exposures for cigarettes, alcohol use disorder (AUD), cannabis, THC, cannabidiol, cannabichromene, cannabinol and cannabigerol. In this substance series positive trends were found for 14, 9, 6, 9, 12, 6, 9 and 7 cancers; with largest minimum E-Values (mEV) of 1.76 × 109, 4.67 × 108, 2.74 × 104, 4.72, 2.34 × 1018, 2.74 × 1017, 1.90 × 107, 5.05 × 109; and total sum of exponents of mEV of 34, 32, 13, 0, 103, 58, 25, 31 indicating that cannabidiol followed by cannabichromene are the most strongly implicated in environmental carcinogenesis. Breast cancer was associated with tobacco and all cannabinoids (from mEV = 3.53 × 109); “All Cancer” (non-skin) linked with cannabidiol (mEV = 1.43 × 1011); pediatric AML linked with cannabis (mEV = 19.61); testicular cancer linked with THC (mEV = 1.33). Cancers demonstrating elevated mEV in association with THC were: thyroid, liver, pancreas, AML, breast, oropharynx, CML, testis and kidney. Cancers demonstrating elevated mEV in relation to cannabidiol: prostate, bladder, ovary, all cancers, colorectum, Hodgkins, brain, Non-Hodgkins lymphoma, esophagus, breast and stomach.
Conclusion: Data suggest that cannabinoids including THC and cannabidiol are important community carcinogens exceeding the effects of tobacco or alcohol. Testicular, (prostatic) and ovarian tumours indicate mutagenic corruption of the germline in both sexes; pediatric tumourigenesis confirms transgenerational oncogenesis; quantitative criteria implying causality are fulfilled.
Keywords: Cannabidiol; Cannabigerol; Cannabinoid; Cannabis; Chromosomal toxicity; Congenital anomalies; Dose–response relationship; Epigenotoxicity; Genotoxicity; Mechanisms; Multigenerational genotoxicity; Oncogenesis; Sigmoidal dose–response; Supra-linear dose response; Transgenerational teratogenicity; Δ9-tetrahydrocannabinol.
Cannabis Use and Health 2014
Introduction
Cannabis is a group of substances from the plant cannabis sativa. Cannabis is used in three main forms: flowering heads, cannabis resin (hashish) and cannabis oil. There are more than 60 psycho-active chemicals in cannabis, including the cannabinoids:
delta-9 tetrahydrocannabinol (THC), which is found in the resin covering the flowering tops and upper leaves of the female plant and which alters mood and produces the feeling of a ‘high’;
and
cannabidiol, which can offset the effects of THC.
Cannabis is usually smoked, either in a hand-rolled cigarette (a ‘joint’) containing the leaf, heads or resin of the plant, or through a water-pipe (a ‘bong’) where water is used to cool the smoke before it is inhaled. In Australia, cannabis is also commonly known as gunja, yarndi, weed and dope.
Patterns of Cannabis Use in Australia and its Public Health Impacts
In 2010, cannabis was the most commonly used illicit drug in Australia. Over one third of Australians (35.4%, approximately 6.5 million) aged 14 years and over had used cannabis at least once in their lifetime, and 1.9 million of these had used cannabis recently (i.e., in the last 12
months). Recent cannabis use among those 14 years and older has increased from 9.1% in 2007 to 10.3% in 2010, though daily users decreased from 14.9% in 2007 to 13% in 2010. In 2010, approximately 247,000 Australians 14 years and over used cannabis daily. For most cannabis users, use is relatively light. Most young people have used it once or twice. However, the younger people start using cannabis, and the greater the frequency with which they use it, the greater the risk of harm.
Based on current use patterns, alcohol abuse and tobacco pose much greater harms to individual and public health in Australia than cannabis. Cannabis-related psychosis, suicide, road-traffic crashes and dependence were estimated to account for 0.2% of the total disease burden in Australia in 2003. This compares to 7.8% of the total burden attributable to tobacco use and 2.3% attributable to alcohol use. In 2004-05, the estimated social costs of cannabis use (including health, crime, road crash and labour costs) was $3.1 billion. Ninety percent of this cost was due to dependent cannabis use. In comparison, the health, crime, road-crash and labour costs of alcohol use in 2004-05 are estimated to be more than three times as much ($9.4 billion).
The Health Effects of Cannabis Use
There is a dose-response relationship between cannabis use and its effects, with stronger effects
expected from larger doses.
Intoxicating effects occur within seconds to minutes and can last for three hours;
Effects last longer with larger doses;
Effects on cognitive function and coordination can last up to 24 hours;
Short-term memory impairment may last for several weeks; and
A single dose in a chronic user can take up to 30 days for the metabolites to be excreted.
Short-term effects of small doses
The most common short-term effects of using cannabis are:
a feeling of euphoria or ‘high’ – with a tendency to talk and laugh more than usual;
impaired balance, reaction time, information processing, memory retention and retrieval, and perceptual-motor coordination;
increased heart rate;
decreased inhibitions such as being more likely to engage in risky behaviour, e.g. unsafe
sexual practice; and
if smoked, increased respiratory problems including asthma.
Short-term effects of large doses
The most common short-term effects of a large dose can include:
hallucinations and changed perceptions of time, sound, colour, distance, touch and other sensations;
panic reactions;
vomiting;
loss of consciousness; and
restlessness and confusion.
The severity of these short-term effects depend on a person’s weight, tolerance to the drug, amount taken, interactions with other drugs, circumstances in which the drug is taken, and the mode of administration.
Long-term effects
The evidence associating regular cannabis use with specific long-term health conditions and adverse effects is of variable quality. Cannabis use is highly correlated with use of alcohol, tobacco and other illicit drugs, all of which have potential adverse health effects. There is sufficient evidence, however, to indicate that cannabis is a risk factor for some chronic health effects and conditions.
Regular and prolonged cannabis use may cause:
cannabis dependence, characterised by impaired control over its use and difficulties in ceasing use; increased tolerance (meaning more of the drug is needed to produce the same effect) and possible withdrawal symptoms, including anxiety, insomnia, appetite disturbance, and
depression;
increased risk of myocardial infarction in those who have already had a myocardial infarction;
and
deficits in verbal learning, memory and attention (in heavy users).
While not conclusive, there is evidence that regular cannabis use can cause chronic bronchitis and impaired immunological competence of the respiratory system. Occasional cannabis use however, is not associated with adverse effects on pulmonary function. Cannabis smoke contains many carcinogens, but there is variable evidence concerning the relationship between cannabis smoking and lung cancer.
Evidence supporting an association between cannabis use and sexual and reproductive effects is weak. However, some studies show an association between cannabis use and increased risk of testicular cancer.
Daily consumption of large quantities of cannabis may lead to the neglect of other important personal and social priorities such as relationships, parenting, careers and community responsibilities.
Pregnant women
Cannabis is the most commonly used illicit drug in women of child-bearing age. Cannabis use during pregnancy has been consistently associated with lower birth-weight babies and pre-term birth, but does not appear to increase the risk of miscarriage or birth abnormalities. Some studies suggest that children exposed to cannabis in utero may have slight impairment in higher cognitive processes such as perceptual organisation and planning. There is insufficient evidence of an association between prenatal cannabis use and postnatal behaviour.
Accidental ingestion by young children
Accidental ingestion of cannabis can cause coma in young children. Cannabis ingestion can be confirmed by positive urine screening for cannabinoids. Cannabis ingestion needs to be considered in toddlers and children with impaired consciousness.
Driving under the influence of cannabis
Cannabis slows reaction time and increases the risk of having a car crash. Other risk factors are blurred vision, poor judgement and drowsiness which can persist for several hours. The effects are increased by alcohol.
Dependence and tolerance
Cannabis dependence is usually defined as impaired control over continued use and difficulty ceasing despite the harms of continued use.19 Dependence can negatively affect personal relationships, education, employment and many other aspects of a person’s life. Data from Australia and other countries indicates that demand for professional help related to cannabis is increasing. Cannabis dependence is the most frequent type of substance-dependence in Australia after alcohol and tobacco. It has been estimated that cannabis dependence will affect around one in ten cannabis users, and around half of those who use it daily. Animal and human studies demonstrate that tolerance to many of the psychological and behavioural responses to cannabis occurs with repeated exposure to the drug. The symptoms of withdrawal from cannabis appear similar to those associated with tobacco, but less severe than withdrawal from alcohol or opiates.
There is a view that the cannabis being used today has a higher THC content and potency than in the past. This may be a perception caused by changes in the mode of use (i.e. through ‘bongs’ rather than ‘joints’, and with more consumption of the heads of the cannabis plant). However, there is some independent evidence that cannabis used today can be of a higher potency. The cannabis in recent street-level seizures in Sydney and the North Coast of NSW has been shown to have a high potency, with around 15% THC, with little or no cannabidiol.
Cannabis as a Gateway Drug
The gateway hypothesis is that cannabis use may act as a causal ‘gateway’ to the use of other illicit drugs such as cocaine and heroin. It is a controversial hypothesis with proponents arguing that because the use of so-called harder drugs is almost always preceded by cannabis use, this means that cannabis use physiologically and/or psychologically causes people to progress to harder drugs. The alternative theory is known as the ‘common cause’ theory whereby a person’s use of cannabis and their later use of other illicit drugs are both seen as effects of common causes such as personal or socio-economic factors, or exposure to illicit drug distribution networks. Evidence for the gateway hypothesis is inconclusive given the difficulties in disentangling the effect of other potential influences in drug use progression. Meta-analyses suggest that the progression in use that has been observed is likely to be due partially to the influence of independent common
causes.
Cannabis and Mental Health
Cannabis and psychosis
Cannabis use is associated with poor outcomes in existing psychosis and is a risk factor for developing psychosis. For those with existing psychosis, using cannabis can trigger further episodes of psychosis, worsen delusions, mood swings, hallucinations and feelings of paranoia, as well as contributing to poor compliance with medication regimes. The research base on cannabis and psychosis has expanded in recent years with studies showing a consistent association between early-aged onset of cannabis use, regular use and a later diagnosis of schizophrenia. Meta-analyses have noted a doubling of the risk of psychotic outcomes in regular cannabis users, and earlier onset (by 2.7 years) among cannabis users who develop psychosis.
There is increasing evidence that the association between cannabis and onset of psychosis is not due to other co-occurring factors. The most plausible view is that cannabis use is a ‘contributory cause’ of psychosis in vulnerable individuals, and that it is one of a number of potential factors that can bring on psychosis (including genetic predisposition)’
Cannabis and depression
The association between cannabis use and depression is weak and insufficient to establish a causal connection. Studies that have found an association are likely to have been affected by confounding variables such as family and personality factors, other drug use and marital status.
There is currently insufficient evidence available to conclude whether cannabis use is associated with suicide. Research is made difficult by confounding factors such as the stresses of an illicit drug-dependent life and pre-existing poor mental health.
Cannabis and anxiety
There is emerging evidence associating cannabis use with anxiety disorders. However, the current level of evidence is not yet sufficient to establish a causal relationship.
Medical Uses Of Cannabis
In addition to psychoactive compounds, cannabis has constituents with other pharmacological effects, including antispastic, analgesic, anti-emetic, and anti-inflammatory actions. These constituents may have therapeutic potential.
Cannabis extracts and synthetic formulations have been licensed for medicinal use in some countries, including Canada, the USA, Great Britain and Germany, for the treatment of severe spasticity in multiple sclerosis, nausea and vomiting due to cytotoxics, and loss of appetite and cachexia associated with AIDS. The synthetic cannabis product Nabiximols (Sativex), which is delivered as a buccal spray and so avoids the harms of cannabis smoke inhalation, is effective in the management of spasticity and pain associated with multiple sclerosis. The psycho-active effects of Nabiximols can also be managed through controlling dosage.
In Australia, the synthetic cannabinoids nabilone and dronabinol are scheduled by authorities for medicinal use. Sativex is also being trialed in Australia for cancer and cannabis withdrawal. Canada has allowed the medical use of smoked cannabis if this is authorised and monitored by a doctor.
There is a growing body of evidence that certain cannabinoids are effective in the treatment of chronic pain, particularly as an alternative or adjunct to the use of opiates, when the development of opiate tolerance and withdrawal can be avoided. Controlled trials have also shown positive effects of cannabis preparations on bladder dysfunction in multiple sclerosis, tics in Tourette syndrome, and involuntary movements associated with Parkinson’s disease. Based on existing data, the adverse events associated with the short-term medicinal use of cannabis are minor.
However, the risks associated with long-term medicinal use are less well understood, particularly the risk of dependence, and any heightened risk of cardiovascular disease. Though there is a growing body of evidence regarding the therapeutic use of cannabinoids, it is still experimental.
Synthetic Cannabis
Synthetic cannabis products have been developed, usually in herbal form for smoking. These products have been marketed in Australia as ‘legal highs’ with product names such as ‘Spice’, ‘K2’, and ‘Kronic’. The psychoactive components are usually THC analogues that bind to cannabinoid receptors in the brain. These analogues are not easily detectable by routine testing, and until recently have not been captured by legislation. These synthetic cannabis products are attractive to their users because they are perceived as safe, are not easily detectable in drug tests, and until recently have not been illegal.
The synthetic cannabis products can not be considered safe given that the synthesized psychoactive substances in them have not been rigorously tested, and little is known about their long or short-term health effects, dependence potential or adverse reactions. Psychotic
symptoms have been associated with use of some synthetic cannabinoids, as well as signs of addiction and withdrawal symptoms similar to those of cannabis. Adverse outcomes have been reported from the use of Kronic in Australia.
The Control of Cannabis Use and Supply
Australian legislation
The possession, cultivation, use, and supply of cannabis is prohibited in all Australian States and Territories. In some Australian jurisdictions there are criminal penalties for the possession, cultivation and use of cannabis, and in others there are less severe civil penalties. Legislation in Australia often distinguishes between possession of small amounts of cannabis (for personal use) possession of larger amounts (trafficable quantities), and possession of even larger “commercially trafficable” quantities. The supplying of cannabis and the possession of large quantities attract criminal penalties in all Australian jurisdictions. All Australian States and Territories have diversionary schemes for minor and early cannabis offenders which require them to undertake educative and treatment programs as an alternative to receiving a criminal penalty.
Criminalisation and health
It is often thought that criminal penalties are a deterrent to cannabis use and, therefore, an effective way to prevent the health impacts and other harms associated with cannabis use. These beliefs have little foundation. A system of criminal prohibition for cannabis use applied in Australia for many years, but the incidence of cannabis use was still significant. The introduction of less serious civil penalties and diversionary alternatives to criminal sanctions did not significantly increase the rates of uptake and use among Australians.
For those who are not deterred from use by criminal penalties, criminalisation can add to the potential health and other risks to which cannabis users are exposed. These include:
exposure of cannabis users, including teenage and occasional users, to ‘harder drugs’. Those who acquire cannabis from large scale illicit drug distribution networks will also become exposed to more harmful drugs, including the direct marketing of those drugs to them;
exposure of cannabis users to criminal networks and activity, including exposure to the threat of violence and the risk of taking part in criminal distribution;
the personal and health-related costs of a criminal conviction. A criminal conviction can negatively impact on a person’s employment prospects and their accommodation and travel opportunities. Limited employment and accommodation prospects can lead to poor health,
including mental health. Individuals with a criminal record are also at a disadvantage in any subsequent criminal proceedings;
a deterrent to individuals seeking health advice, treatment and support regarding their cannabis use;
the inability to collect high quality, reliable data regarding patterns of use and harms.
Harm reduction
A harm-reduction approach is defined as policies and initiatives that aim to reduce the adverse health, social and economic consequences of substance use to individual drug users, their families and the community. Harm reduction considers both the potential harms to individuals using substances like cannabis and the potential harms and negative impacts of the different approaches for controlling the use and supply of these substances. When harm reduction is the primary goal, the key policy focus will be on measures to reduce individuals’ harmful levels of cannabis use, or cannabis use among individuals who are most vulnerable to adverse health impacts, or cannabis use in contexts which involve serious risks to users.
Harm-reduction measures include targeted efforts to reduce the supply of cannabis and to reduce demand for it among vulnerable groups. In certain contexts, and with certain groups, measures emphasizing abstinence may also contribute, in a preventive way, to reducing harms. Policy and legislative approaches that do not effectively address cannabis-related harms or create
significant risks and adverse impacts are not consistent with harm-reduction. Prohibition of cannabis use with criminal penalties has the potential to produce harms and risks. The effectiveness of criminal prohibition of cannabis use in reducing the health-related harms
associated with cannabis use is questionable.
Treatment Options
The number of people seeking treatment for cannabis use is increasing, but most of those who experience cannabis dependence do not seek help. Many regular cannabis users do not believe they need treatment, and there is also a low awareness of the treatment options available and how to access them.
There are fewer treatment options for cannabis dependence than for alcohol or opiate dependence, and limited research on the effectiveness of different cannabis treatment options. Treatments for problematic cannabis use include psychological interventions such as cognitive
behavioural therapy and motivational enhancement, and pharmacological interventions with medications to ease the symptoms of withdrawal or block the effects of cannabis. The research on pharmacological interventions for cannabis is in its infancy, with medications still in the experimental stages of development.
Cognitive behavioural therapy helps the cannabis user develop knowledge and skills to identify risk situations when using cannabis and to modify behaviour accordingly. Motivational enhancement techniques build the cannabis user’s desire to address their problematic use. These counseling interventions are increasingly available online as web-based programs, as well as face-to-face with a counselor. Online programs have the advantage of convenience and anonymity, for those who are concerned about possible stigma. Difficulties in maintaining motivation, and limitations in personalising the programs to individual needs, are drawbacks. According to current research, web-based treatment programs may not be as effective as in-person treatment. Some problematic cannabis users have particular treatment needs, including those with cannabis dependence and mental health issues. These individuals require integrated treatment and coordinated care. General practitioners can play an important role in developing a coordinated care plan to suit the needs of these patients.
The Australian Medical Association Position
The AMA acknowledges that cannabis use is harmful and can lead to adverse chronic health outcomes, including dependence, withdrawal symptoms, early onset psychosis and the exacerbation of pre-existing psychotic symptoms. While the absolute risk of these outcomes is low and those who use cannabis occasionally are unlikely to be affected, those who use cannabis frequently and for sustained periods, or who initiate cannabis use at an early age, or who are susceptible to psychosis, are most at risk.
The AMA also recognises that cannabis use has short-term effects on cognitive and perceptual functioning which can present risks to the safety of users and others. The AMA believes that cannabis use should be seen primarily as a health issue and not primarily as a matter for law enforcement. The most appropriate response to cannabis use should give priority to policies, programs and regulatory approaches that reduce the harms potentially associated with cannabis use, and particularly the health-related harms. The positions outlined below should be read in the light of this harm-reduction principle. The AMA believes the following are the important considerations and central elements in an appropriate harm-reduction response to cannabis use.
Prevention and Early Intervention
As younger people and those who use cannabis frequently are most at risk of harm, prevention and early intervention initiatives to avoid, delay and reduce the frequency of cannabis use in these populations are essential.
All children should have access to developmentally appropriate school-based life-skills programs to assist in preventing or reducing potential substance use problems.
Evidence-based information on the potential risks of cannabis use and where to seek further assistance should be widely available, particularly to young people.
Medical professionals can play an important role in the early identification of patients they believe to be at risk of adverse health outcomes from cannabis use.
When a cannabis user comes into contact with law enforcement or justice administration agencies this should be used as an opportunity to direct them to education, counseling or treatment. This is particularly important with young and first time or early offenders.
Diagnosis and Treatment
Medical professionals have the knowledge and opportunity to screen for and diagnose cannabis-related disorders, including dependence, withdrawal symptoms, and cannabis induced psychosis. Referral networks and linkages should be established within regions between primary care and specialist mental health and drug and alcohol services, to ensure integrated and coordinated treatment support for cannabis use problems.
Medical professionals, particularly general practitioners, have the opportunity to counsel patients who are at risk of cannabis-related harms, and they should be supported to provide education and advice about those potential harms.
Targeted treatment regimens should be developed and resourced for groups with particular needs, including those with dual diagnoses, multiple drug use, young teenage users and culturally appropriate services for Aboriginal peoples and Torres Strait Islanders. Of particular importance are suitable treatment services for cannabis users with mental health needs.
Every effort should be made to address the personal and systemic barriers that cannabis users face in seeking treatment and support when they need it. These include barriers associated with perceptions of stigmatisation, users’ and professionals’ awareness of treatment options, and users’ beliefs that they do not have a health problem.
Doctors should consider accidental cannabis ingestion in the differential diagnosis of children with impaired consciousness.
Cannabis users should have access to the rehabilitative services and support they require to manage associated disorders and particularly the risk of relapse.
Medical Uses of Cannabis
The Australian Medical Association acknowledges that cannabis has constituents that have potential therapeutic uses.
Appropriate clinical trials of potentially therapeutic cannabinoid formulations should be conducted to determine their safety and efficacy compared to existing medicines, and whether their long-term use for medical purposes has adverse effects.
Therapeutic cannabinoids that are deemed safe and effective should be made available to patients for whom existing medications are not as effective.
Smoking or ingesting a crude plant product is a risky way to deliver cannabinoids for medical purposes. Other appropriate ways of delivering cannabinoids for medical purposes should be developed.
Any promotion of the medical use of cannabinoids will require extensive education of the public and the profession on the risks of the non-medical use of cannabis.
Law Enforcement, Cannabis Regulation and Health
In assessing different legislative and policy approaches to the regulation of cannabis use and supply, primary consideration should be given to the impact of such approaches on the health and well-being of cannabis users.
The AMA does not condone the trafficking or recreational use of cannabis. The AMA believes that there should be vigorous law enforcement and strong criminal penalties for the trafficking of cannabis. The personal recreational use of cannabis should also be
prohibited. However, criminal penalties for personal cannabis use can add to the potential health and other risks to which cannabis users are exposed. The AMA believes that it is consistent with a principle of harm reduction for the possession of cannabis for personal
use to attract civil penalties such as court orders requiring counselling and education (particularly for young and first time offenders), or attendance at ‘drug courts’ which divert users from the criminal justice system into treatment.
When cannabis users come into contact with the police or courts, the opportunity should be taken to divert those users to preventive, educational and therapeutic options that they would not otherwise access.
In allocating resources, priority should be given to policies, programs and initiatives that reduce the health-related risks of cannabis use. Law enforcement should be directed primarily at cannabis supply networks.
The AMA believes that the availability and use of synthetic cannabis products (including herbal forms) poses significant health risks, given that the psychoactive chemical constituents of these products are unknown and unpredictable in their effect. There are
particular challenges in regulating these products, and Australian governments must make a concerted effort to develop consistent and effective legislation which captures current and emerging forms of synthetic cannabis.
Research
Further research is needed into the relationship between cannabis use and psychosis and other mental health problems, including the identification of those at greatest risk of cannabis-induced psychosis.
There should be continuing research to identify the risk factors that contribute to individuals developing problematic or early onset cannabis use, and the factors and interventions that can protect against these.
Australian governments should fund research into best practice treatment methods, including suitable pharmacotherapies, for those who are cannabis-dependent or who wish to reduce or cease their use.
There should be systematic ongoing monitoring of the different legislative and policy approaches on cannabis operating in overseas jurisdictions to assess their health and harm-related impacts. The evidence obtained should inform critical reviews of the
approaches that operate in Australia.
Source: 1 (ama.com.au) 2014
Background: Little is known about the relative harms of edible and inhalable cannabis products.
Objective: To describe and compare adult emergency department (ED) visits related to edible and inhaled cannabis exposure.
Design: Chart review of ED visits between 1 January 2012 and 31 December 2016.
Setting: A large urban academic hospital in Colorado.
Participants: Adults with ED visits with a cannabis-related International Classification of Diseases, Ninth or 10th Revision, Clinical Modification (ICD-9-CM or ICD-10-CM), code.
Measurements: Patient demographic characteristics, route of exposure, dose, symptoms, length of stay, disposition, discharge diagnoses, and attribution of visit to cannabis.
Results: There were 9973 visits with an ICD-9-CM or ICD-10-CM code for cannabis use. Of these, 2567 (25.7%) visits were at least partially attributable to cannabis, and 238 of those (9.3%) were related to edible cannabis. Visits attributable to inhaled cannabis were more likely to be for cannabinoid hyperemesis syndrome (18.0% vs. 8.4%), and visits attributable to edible cannabis were more likely to be due to acute psychiatric symptoms (18.0% vs. 10.9%), intoxication (48% vs. 28%), and cardiovascular symptoms (8.0% vs. 3.1%). Edible products accounted for 10.7% of cannabis-attributable visits between 2014 and 2016 but represented only 0.32% of total cannabis sales in Colorado (in kilograms of tetrahydrocannabinol) during that period.
Limitation: Retrospective study design, single academic center, self-reported exposure data, and limited availability of dose data.
Conclusion: Visits attributable to inhaled cannabis are more frequent than those attributable to edible cannabis, although the latter is associated with more acute psychiatric visits and more ED visits than expected.
Primary funding source: Colorado Department of Public Health and Environment.
Flow chart of visit selection and review.
Figure 2.. Exposure to edible and inhalable cannabis products in cannabis-attributable visits at UCHED from 2012 to 2016.
Source: Drugwatch International 2018
Abstract
Background—As an increasing number of states liberalize cannabis use and develop laws and local policies, it is essential to better understand the impacts of neighborhood ecology and marijuana dispensary density on marijuana use, abuse, and dependence. We investigated associations between marijuana abuse/dependence hospitalizations and community demographic and environmental conditions from 2001–2012 in California, as well as cross-sectional associations between local and adjacent marijuana dispensary densities and marijuana hospitalizations.
Source: Drug Alcohol Depend. 2015 September 1; 154: 111–116. doi:10.1016/j.drugalcdep.
There exists sufficient empirical data from cellular to epidemiological studies to warrant caution in the use c
