By Dr. Liji Thomas, MDReviewed by Benedette Cuffari, M.Sc.  Aug 28 2024

How much should we worry?

American parents have been warning teenagers about the dangers of marijuana for about 100 years. Teenagers have been ignoring them for just as long. As I write this, a couple of kids are smoking weed in the woods just yards from my office window and about a block and a half from the local high school. They started in around 9 A.M., just in time for class.

Exaggerating the perils of cannabis—the risks of brain damage, addiction, psychosis—has not helped. Any whiff of Reefer Madness hyperbole is perfectly calibrated to trigger an adolescent’s instinctive skepticism for whatever an adult suggests. And the unvarnished facts are scary enough.

We know that being high impairs attention, memory and learning. Some of today’s stronger varieties can make you physically ill and delusional. But whether marijuana can cause lasting damage to the brain is less clear.

A slew of studies in adults have found that nonusers beat chronic weed smokers on tests of attention, memory, motor skills and verbal abilities, but some of this might be the result of lingering traces of cannabis in the body of users or withdrawal effects from abstaining while taking part in a study. In one hopeful finding, a 2012 meta-analysis found that in 13 studies in which participants had laid off weed for 25 days or more, their performance on cognitive tests did not differ significantly from that of nonusers.

But scientists are less sanguine about teenage tokers. During adolescence the brain matures in several ways believed to make it more efficient and to strengthen executive functions such as emotional self-control. Various lines of research suggest that cannabis use could disrupt such processes.

For one thing, recent studies show that cannabinoids manufactured by our own nerve cells play a crucial role in wiring the brain, both prenatally and during adolescence. Throughout life they regulate appetite, sleep, emotion, memory and movement—which makes sense when you consider the effects of marijuana. There are “huge changes” in the concentration of these endocannabinoids during the teenage years, according to neurologist Yasmin Hurd of the Icahn School of Medicine at Mount Sinai, which is why she and others who study this system worry about the impact of casually dosing it with weed.

Brain-imaging studies reinforce this concern. A number of smallish studies have seen differences in the brains of habitual weed smokers, including altered connectivity between the hemispheres, inefficient cognitive processing in adolescent users, and a smaller amygdala and hippocampus—structures involved in emotional regulation and memory, respectively.

More evidence comes from research in animals. Rats given THC, the chemical that puts the high in marijuana, show persistent cognitive difficulties if exposed around the time of puberty—but not if they are exposed as adults.

But the case for permanent damage is not airtight. Studies in rats tend to use much higher doses of THC than even a committed pothead would absorb, and rodent adolescence is just a couple of weeks long—nothing like ours. With brain-imaging studies, the samples are small, and the causality is uncertain. It is particularly hard to untangle factors such as childhood poverty, abuse and neglect, which also make their mark on brain anatomy and which correlate with more substance abuse, notes Nora Volkow, director of the National Institute on Drug Abuse and lead author of a superb 2016 review of cannabis research in JAMA Psychiatry.

To really sort this out, we need to look at kids from childhood to early adulthood. The Adolescent Brain Cognitive Development study, now under way at the National Institutes of Health, should fill the gap. The 10-year project will follow 10,000 children from age nine or 10, soaking up information from brain scans, genetic and psychological tests, academic records and surveys. Among other things, it should help pin down the complex role marijuana seems to play in triggering schizophrenia in some people.

But even if it turns out that weed does not pose a direct danger for most teens, it’s hardly benign. If, like those kids outside my window, you frequently show up high in class, you will likely miss the intellectual and social stimulation to which the adolescent brain is perfectly tuned. This is the period, Volkow notes, “for maximizing our capacity to navigate complex situations,” literally building brainpower. On average, adolescents who partake heavily wind up achieving less in life and are unhappier. And those are things a teenager might care about.

Source: https://www.scientificamerican.com/article/what-pot-really-does-to-the-teen-brain/ December 2017

Abstract

Source: https://www.nature.com/articles/s41467-024-49262-5 June 2024

More than 178 000 people died from excessive alcohol use in the US during 2020 to 2021, surpassing deaths from the overdose epidemic.¹ Excessive drinking is now the leading cause of preventable death in the US.¹ Alcohol use disorder (AUD) most commonly begins during adolescence, although rarely is it identified and treated at this age.² We urgently need interventions that allow us to better identify those young people at risk of developing AUD and alcohol-related complications later in adulthood. In their study of alcohol use among youths with a chronic medical condition (CMC), Weitzman et al³ describe a novel approach for alcohol prevention in a population of youths with medical vulnerability. Youths with a CMC are particularly susceptible to the effects of alcohol and warrant particular attention. Although the rate of alcohol use among these youths is similar to that of their peers, youths with a CMC have higher rates of progression to heavy alcohol use and AUD.⁴ Weitzman et al³ found that high-risk alcohol use occurred in more than 1 of 10 youths (aged 14-18 years) with a CMC seen in the specialty clinics included in their study. These youths also have an increased risk of treatment nonadherence and potential medication reactions with alcohol as a result of the underlying disease, worsening the potential effects of high-risk alcohol exposure in this population.⁴

Given these disparities, Weitzman et al³ designed a randomized clinical trial aimed at evaluating the effects of the Take Good Care (TGC) alcohol use prevention intervention over 12 months among youths with a CMC. In the specialty clinic setting, youths in the intervention group received a brief, personalized intervention consisting of a self-administered slide deck on an electronic tablet. Slides were disease tailored, and they included specific effects of alcohol use on disease processes, treatment safety, and efficacy as well as motivational information on health-protecting decisions and behaviors. Although there was no change among youths reporting no or minimal (low-risk) alcohol use, there was a 40% relative reduction in self-reported frequency of alcohol use among those receiving the TGC intervention who reported high-risk alcohol use at baseline compared with those who received treatment as usual.

The study by Weitzman et al³ highlights the potential importance of brief interventions in changing youth behavior, particularly among a group of youths who are medically vulnerable. Although a shocking 11.5% of youths with a CMC in this study reported high-risk alcohol use at baseline, nationally only a quarter of pediatricians report using validated screening tools to assess alcohol use among adolescents and only 11% of pediatricians correctly use the Screening, Brief Intervention, and Referral to Treatment (SBIRT) tool recommended by the American Academy of Pediatrics.⁵ Despite growing evidence supporting the benefit of SBIRT for pediatric populations, barriers to implementation include insufficient time and need for clinician training⁵; both of these barriers are ameliorated with the use of the self-administered, electronic intervention described by Weitzman et al.³ This study adds to the growing database highlighting the effectiveness of SBIRT in identifying and intervening in instances of substance use among youths. It presents a tool easily adopted by clinicians, with an impact on those youths at greatest risk of developing problematic alcohol use.

Considering the prevalence of alcohol use among youths with CMCs, an important aspect of the study by Weitzman et al³ is its low-touch intervention that can be easily adapted and implemented in a variety of clinical settings. Weitzman et al³ show the value of even simple, low-touch interventions in changing youth behavior. From the patient perspective, the use of an electronic tablet enhances privacy when answering questions and allows for flexibility in time spent on each piece of content. From the clinician perspective, the use of an electronic tablet requires minimal additional effort or training, standardizes the content provided, and allows for intervention completion outside of face-to-face appointment time. Yet despite its simplicity, the low-touch TGC intervention has been shown to exert a substantial effect on adolescent behavior. At 12 months, the reduction in alcohol use frequency among youths with a CMC and high-risk alcohol use represents not only a meaningful behavioral change but also an enduring one.

In contrast with traditional fear-based messages around alcohol prevention, Weitzman et al³ demonstrate the impact of a strengths-based model that engages the normal adolescent quest for independence and the examination of choice in larger contexts. The TGC intervention educated youths with a CMC on disease-specific processes, treatments, and effects of alcohol, thereby encouraging reflection around alcohol-related choices. In presenting this information for youths to consider, the intervention relayed respect for patients’ ability to engage in their own health care and health behaviors. Additionally, disease-tailored content paired with motivational information on health-protecting behaviors encouraged patients’ sense of autonomy and independence. The statistically significant effects of this approach suggest that personalized intervention resonates with youths with CMCs and is an effective tool for behavioral change. Furthermore, this delivery model allows for content to be tailored based on disease or other aspects of youths’ lived experience. Content adjusted to the needs of specific subpopulations of youths creates interventions that they connect with and are thus most greatly affected by, in both depth and longevity of impact.

Finally, key to the study by Weitzman et al³ is the intervention location; utilization of the specialty care setting for an alcohol use prevention intervention is novel and effective. Many youths with a CMC receive the majority of their care in the specialty care setting and, accordingly, often develop stronger therapeutic relationships with their specialty care physician than their primary care physician. In 41.3% of visits to their specialists, youths with a CMC present for routine preventative care,⁶ yet specialists screen for substance use at alarmingly low rates compared with their primary care counterparts (self-reported 8% vs 38%, respectively).⁷ Interventions within the specialty clinic space allow for greater potential to reach more youths with CMCs at critical moments in their health journeys, thereby curbing heavy alcohol use, its associated medication nonadherence, and potential interaction with medications. By doing so, this method of intervention may decrease disease-associated complications and mortality in addition to alcohol-associated complications and mortality among youths with CMCs, and by extension, the adults that they become. The TGC intervention and its broader application represent an exciting new paradigm for future practice.

Source: https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2820973 July 2024

Source: Email from Ed Moses to Drug Watch International drug-watch-international@googlegroups.com August 2017

This is The Drug Report’s Friday Fact report – The rate of violent behavior in daily marijuana users aged 18-34 was nearly twice the violent behavior rate of non-users

The study “Associations of cannabis use, use frequency, and cannabis use disorder with violent behavior among young adults in the United States” was recently published by Nora D. Volkow and the team at NIDA. The study found that the rate of violent behavior in daily marijuana users aged 18-34 was nearly twice the violent behavior rate of non-users.

The study consisted of 113,434 participants, aged 18 to 34, and relied on data from the 2015-2019 National Surveys on Drug Use and Health (NSDUH).

The datasets provided information on the rates of daily marijuana use, whether the participants had Cannabis Use Disorder, and violent behavior. The study found:

The violence behavior rates for both males and females who were daily marijuana users and had Cannabis Use Disorder were close to doubling that of males and females who were non-marijuana users.

Source: Email from Smart Approaches to Marijuana (SAM) reply@learnaboutsam.org May 2024

Bertha Madras, a leading expert on weed, outlines the science linking it to psychiatric disorders, permanent brain damage, and other serious harms.

Young people who smoked marijuana in the 1960s were seen as part of the counterculture. Now the cannabis culture is mainstream. A 2022 survey sponsored by the National Institutes of Health found that 28.8% of Americans age 19 to 30 had used marijuana in the preceding 30 days—more than three times as many as smoked cigarettes. Among those 35 to 50, 17.3% had used weed in the previous month, versus 12.2% for cigarettes.

While marijuana use remains a federal crime, 24 states have legalized it and another 14 permit it for medical purposes. Last week media outlets reported that the Biden administration is moving to reclassify marijuana as a less dangerous Schedule III drug—on par with anabolic steroids and Tylenol with codeine— which would provide tax benefits and a financial boon to the pot industry.

Bertha Madras thinks this would be a colossal mistake. Ms. Madras, 81, is a psychobiology professor at Harvard Medical School and one of the foremost experts on marijuana. “It’s a political decision, not a scientific one,” she says. “And it’s a tragic one.” In 2024, that is a countercultural view.

Ms. Madras has spent 60 years studying drugs, starting with LSD when she was a graduate student at Allan Memorial Institute of Psychiatry, an affiliate of Montreal’s McGill University, in the 1960s. “I was interested in psychoactive drugs because I thought they could not only give us some insight into how the brain works, but also on how the brain undergoes dysfunction and disease states,” she says.

In 2015 the World Health Organization asked her to do a detailed review of cannabis and its medical uses. The 41-page report documented scant evidence of marijuana’s medicinal benefits and reams of research on its harms, from  cognitive impairment and psychosis to car accidents.

She continued to study marijuana, including at the addiction neurobiology lab she directs at Mass General Brigham McLean Hospital. In a phone interview this week, she walked me through the scientific literature on marijuana, which runs counter to much of what Americans hear in the media.

For starters, she says, the “addiction potential of marijuana is as high or higher than some other drug,” especially for young people. About 30% of those who use cannabis have some degree of a use disorder. By comparison, only 13.5% of drinkers are estimated to be dependent on alcohol. Sure, alcohol can also cause harm if consumed in excess. But Ms. Madras sees several other distinctions.

One or two drinks will cause only mild inebriation, while “most people who use marijuana are using it to become intoxicated and to get high.” Academic outcomes and college completion rates for young people are much worse for those who use marijuana than for those who drink, though there’s a caveat: “It’s still a chicken and egg whether or not these kids are more susceptible to the effects of marijuana or they’re using marijuana for self medication or what have you.”

Marijuana and alcohol both interfere with driving, but with the former there are no medical “cutoff points” to determine whether it’s safe to get behind the wheel. As a result, prohibitions against driving under the influence are less likely to be enforced for people who are high. States where marijuana is legal have seen increases in car accidents.

One of the biggest differences between the two substances is how the body metabolizes them. A drink will clear your system within a couple of hours. “You may wake up after binge drinking in the morning with a headache, but the alcohol is gone.” By contrast, “marijuana just sits there and sits there and promotes brain adaptation.”

That’s worse than it sounds. “We always think of the brain as gray matter,” Ms. Madras says. “But the brain uses fat to insulate its electrical activity, so it has a massive amount of fat called white matter, which is fatty. And that’s where marijuana gets soaked up. . . . My lab showed unequivocally that blood levels and brain levels don’t correspond at all—that brain levels are much higher than blood levels. They’re two to three times higher, and they persist once blood levels go way down.” Even if people quit using pot, “it can persist in their brain for a while.”

Thus marijuana does more lasting damage to the brain than alcohol, especially at the high potencies being consumed today. Levels of THC—the main psychoactive ingredient in pot—are four or more times as high as they were 30 years ago. That heightens the risks, which range from anxiety and depression to impaired memory and cannabis hyperemesis syndrome—cycles of severe vomiting caused by long-term use.

There’s mounting evidence that cannabis can cause schizophrenia. A large-scale study last year that examined health histories of some 6.9 million Danes between 1972 and 2021 estimated that up to 30% of young men’s schizophrenia diagnoses could have been prevented had they not become dependent on pot. Marijuana is  worse in this regard than many drugs usually perceived as more dangerous.

“Users of other potent recreational drugs develop chronic psychosis at much lower rates,” Ms. Madras says. When healthy volunteers in research experiments are given THC—as has been done in 15 studies—they develop transient symptoms of psychosis. “And if you treat them with an antipsychotic drug such as haloperidol, those symptoms will go away.”

Marijuana has also been associated with violent behavior, including in a study published this week in the International Journal of Drug Policy. Data from observational studies are inadequate to demonstrate causal relationships, but Ms. Madras says that the link between marijuana and schizophrenia fits all six criteria that scientists use to determine causality, including the strength of the association and its consistency.

Ms. Madras says at the beginning of the interview that she was operating on three hours of sleep after crashing on scientific projects. Yet she is impressively lucid and energized. She peppers her explanations with citations of studies and is generous in crediting other researchers’ work.

Another cause for concern, she notes, is that more pregnant women are using pot, which has been linked to increased preterm deliveries, admissions of newborns into neonatal intensive care units, lower birth weights and smaller head circumferences. THC crosses the placenta and mimics molecules that our bodies naturally produce that regulate brain development.

“What happens when you examine kids who have been exposed during that critical period?” Ms. Madras asks. During adolescence, she answers, they show an increased incidence of aggressive behavior, cognitive dysfunction, and symptoms of ADHD and obsessive-compulsive disorders. They have reduced white and gray matter.

A drug that carries so many serious side effects would be required by the Food and Drug Administration to carry a black-box warning, the highest-level alert for drugs with severe safety risks. Marijuana doesn’t—but only because the FDA hasn’t cleared it.

The agency has selectively approved cannabis compounds for the treatment of seizures associated with Lennox-Gastaut or Dravet syndrome, nausea associated with chemotherapy for cancer, and anorexia associated with weight loss in AIDS patients. But these approved products are prescribed at significantly less potent doses than the pot being sold in dispensaries that are legal under state law.

What about medicinal benefits? Ms. Madras says she has reviewed “every single case of therapeutic indication for marijuana—and there are over 100 now that people have claimed—and I frankly found that the only one that came close to having some evidence from randomized controlled trials was the neuropathic pain studies.” That’s “a very specific type of pain, which involves damage to nerve endings like in diabetes or where there’s poor blood supply,” she explains.

For other types of pain, and for all other conditions, there is no strong evidence from high-quality randomized trials to support its use. When researchers did a “challenge test on normal people where they induce pain and tried to see whether or not marijuana reduces the pain, it was ineffective.”

Ms. Madras sees parallels between the marketing of pot now and of opioids a few decades ago. “The benefits have been exaggerated, the risks have been minimized, and skeptics in the scientific community have been ignored,” she says. “The playbook is always to say it’s safe and effective and nonaddictive in people.”

Advocates of legalization assert that cannabis can’t be properly studied unless the federal government removes it from Schedule I. Bunk, Ms. Madras says: “I have been able to study THC in my research program.” It requires more paperwork, but “I did all the paperwork. . . . It’s not too difficult.”

Instead of bankrolling ballot initiatives to legalize pot, she says, George Soros and other wealthy donors who “catalyzed this whole movement” should be funding rigorous research: “If these folks, these billionaires, had just taken that money and put it into clinical trials, I would have been at peace.”

It’s a travesty, Ms. Madras adds, that the “FDA has decided that they’re going to listen to that movement rather than to what the science says.” While the reclassification wouldn’t make recreational marijuana legal under federal law, dispensaries and growers would be able to deduct their business expenses on their taxes. The rescheduling would also send a cultural signal that marijuana use is normal.

Ms. Madras worries that “it sets a precedent for the future.” She points to the movement in states to legalize psychedelic substances, for whose medicinal benefits there also isn’t strong scientific evidence. Meantime, she says it makes no sense that politicians continuously urge more spending on addiction treatment and harm reduction while weakening laws that prevent people from becoming addicted in the first place.
Her rejoinder to critics who say the war on drugs was a failure? “This is not a war on drugs. It’s a defense of the human brain at every possible age from in utero to old age.”

Ms. Finley is a member of the Journal’s editorial board.

Source: https://www.wsj.com/articles/what-you-arent-reading-about-marijuana-permanent-brain-damage-biden-schedule-iii-9660395e May 2024

Foreword
The National Institute on Drug Abuse (NIDA) is pleased to publish in its Research Monograph series the proceedings of the 48th Annual Scientific Meeting of the Committee on Problems of Drug Dependence, Inc. (CPDD). This meeting was held at Tahoe City, Nevada, in June 1986.

The scientific community working in the drug abuse area was saddened by the untimely death of one of its very productive and active leaders: Joseph Cochin, M.D., Ph.D. Joe was a talented scientist who was greatly admired by his students and colleagues. For the past five years, Joe had served as the Executive Secretary of the CPDD. This monograph includes papers from a symposium on “Mechanisms of Opioid Tolerance and Dependence,” dedicated to his memory. These papers were presented by many of his friends and colleagues, who took the opportunity to express their high esteem for Joe.
The CPDD is an independent organization of internationally recognized experts in a variety of disciplines related to drug addiction. NIDA and the CPDD share many interests and concerns in developing knowledge that will reduce the destructive effects of abused drugs on the individual and society. The CPDD is unique in bringing together annually at a single scientific meeting an outstanding group of basic and clinical investigators working in the field of drug dependence. This year, as usual, the monograph presents an excellent collection of papers. It also contains progress reports of the abuse liability testing program funded by NIDA and carried out in conjunction with the CPDD. 

This program continues to represent an example of a highly successful government/private sector cooperative effort. I am sure that members of the scientific community and other interested readers will find this volume to be a valuable “state-of-the art” summary of the latest research into the biological, behavioral, and chemical bases of drug abuse.

Charles R. Schuster, Ph.D.
Director
National Institute on Drug Abuse

For the full contents, please go to: 

Source: https://babel.hathitrust.org/cgi/pt?id=ien.35557000188076&seq=11 This version September 2023

US DRUG CZAR EXPLAINS CAUSES AND RSDT TOOL TO PREVENT TEEN DRUG USE AND OVERDOSE DEATH INTERVIEW WITH U.S. DRUG CZAR JOHN WALTERS

Introduction:  In response to recent news of a huge increase in drug overdose deaths and arrests for drug trafficking among Fairfax County youths, Fox News TV5 reporter Sherri Ly interviewed U.S. Drug Czar John Walters for his expert views on the cause and potential cure for these horrific family tragedies.  Following is a transcript of that half-hour interview with minor editing for clarity and emphasis added.  The full original interview is available through the 11/26/08 Fox5 News broadcast video available at link:

WALTERS:  Well, as this case shows, while we’ve had overall drug use go down, we still have too many young people losing their lives to drugs, either through overdoses, or addiction getting their lives off track.  So there’s a danger.  We’ve made progress, and we have tools in place that can help us make more progress, but we have to use them. 

Q 1:  You meet with some of these parents whose children have overdosed.  What do they tell you, and what do you tell them?

WALTERS:  It’s the hardest part of my job; meeting with parents who’ve lost a child.  Obviously they would give anything to go back, and have a chance to pull that child back from the dangerous path they were on.  There are no words that can ease their grief.  That’s something you just pray that God can give them comfort.  But the most striking thing they say to me though is they want other parents to know, to act.  And I think this is a common thing that these terrible lessons should teach us.

Many times, unfortunately, parents see signs: a change in friends, sometimes they find drugs; sometimes they see their child must be intoxicated in some way or the other.  Because it’s so frightening, because sometimes they’re ashamed – they hope it’s a phase, they hope it goes away – they try to take some half measures.  Sometimes they confront their child, and their child tells them – as believably as they ever can – that it’s the first time.  I think what we need help with is to tell people; one, it’s never the first time.  The probability is low that parents would actually recognize these signs – even when it gets visible enough to them – because children that get involved in drugs do everything they can to hide it.  It’s never the first time.  It’s never the second time.  Parents need to act, and they need to act quickly.  And the sorrow of these grieving parents is, if anything, most frequently focused on telling other parents, “Don’t wait: do anything to get your child back from the drugs.”

Secondly, I think it’s important to remember that one of the forces that are at play here is that it’s their friends.  It’s not some dark, off-putting stranger – it’s boyfriends, girlfriends.  I think that was probably a factor in this case.  And it’s also the power and addictive properties of the drug.  So your love is now being tested, and the things you’ve given your child to live by are being pulled away from them on the basis of young love and some of the most addictive substances on earth.  That’s why you have to act more strongly.  You can’t count on the old forces to bring them back to safety and health.

Q 2:  When we talk about heroin – which is what we saw in this Fairfax County drug ring, alleged drug ring – what are the risks, as far as heroin’s concerned?  I understand it can be more lethal, because a lot of people don’t know what they’re dealing with?

WALTERS:  Well it’s also more lethal because one, the drug obviously can produce cardiac and respiratory arrest.  It’s a toxic substance that is very dangerous.  It’s also the case that narcotics, like heroin – even painkillers like OxyContin, hydrocodone, which have also been a problem – are something that the human body gets used to.  So what you can frequently get on the street is a purity that is really blended for people who are addicted and have been long time addicted.  So a person who is a new user or a naïve user can more easily be overdosed, because the quantities are made for people whose bodies have adjusted to higher purities, and are seeking that effect that only the higher purity will give them in this circumstance.  So it’s particularly dangerous for new users.  But we also have to remember, it almost never starts with heroin.  Heroin is the culmination here.  I think some of the – and I’ve only seen press stories on this — some of these young people may have gotten involved as early as middle school.

We have tools so that we don’t have to lose another young woman like this– or young men.  We now have the ability to use Random Student Drug Testing (RSDT) because the Supreme Court has, in the last five years, made a decision that says it can’t be used to punish.  It’s used confidentially with parents.  We have thousands of schools now doing it since the president announced the federal government’s willingness to fund these programs in 2004.  And many schools are doing it on their own.  Random testing can do for our children what it’s done in the military, what it’s done in the transportation safety industry– significantly reduce drug use.

First, it is a powerful reason not to start.  “I get tested, I don’t have to start.”  We have to remember, it’s for prevention and not a “gotcha!”  But it’s a powerful reason for kids to say, even when a boyfriend or girlfriend says come and do this with me, “I can’t do it, I get tested.  I still like you, I still want to be your friend; I still want you to like me, but I just can’t do this,” which is very, very powerful and important.  And second, if drug use is detected the child can be referred to treatment if needed.

Q 3:  Is the peer pressure just that much that without having an excuse, that kids are using drugs and getting hooked?

WALTERS:  Well one of the other unpleasant parts of my job is I visit a lot of young people in treatment; teenagers, sometimes as young as 14, 15, but also 16, 17, 18.  It is not uncommon for me to hear from them, “I came from a good family.  My parents and my school made clear what the dangers were of drugs.  I was stupid.  I was with my boyfriend (or girlfriend) and somebody said hey, let’s go do this.  And I started, and before I knew it, I was more susceptible.”

We have to also understand the science, which has told us that adolescents continue to have brain development up through age 20-25.  And their brains are more susceptible to changes that we can now image from these drugs.  So it’s not like they’re mini-adults.  They’re not mini-adults.  They’re the particularly fragile and susceptible age group, because they don’t have either the experience or the mental development of adults.  That’s why they get into trouble, that’s why it happens so fast to them, that’s why it’s so hard for them to see the ramifications.

So what does RSDT do?  It finds kids early–­ if prevention fails.  And it allows us to intervene, and it doesn’t make the parent alone in the process.  Sometimes parents don’t confront kids because kids blackmail them and say “I’m going to do it anyway, I’m going to run away from home.”  The testing brings the community together and says we’re not going to lose another child.  We’re going to do the testing in high school – if necessary, in middle school.  We’re going to wrap our community arms around that family, and get those children help.  We’re going to keep them in school, not wait for them to drop out.  And we’re certainly not going to allow this to progress until they die.

Q 4:  And in a sense, if you catch somebody early, since you’re saying the way teenagers seem to get into drug use is a friend introduces it to a friend, and then next thing you know, you have a whole circle of friends doing it.  Are you essentially drying that up at the beginning, before it gets out of hand?

WALTERS:  That is the very critical point.  It’s not only helping every child that gets tested be safer, it means that the number of young people in the peer group, in the school, in the community that can transfer this dangerous behavior to their friends shrinks.  This is communicated like a disease, except it’s not a germ or a bacillus.  It’s one child who’s doing this giving it behaviorally to their friends, and using their friendship as the poison carrier here.  It’s like they’re the apple and the poison is inside the apple.  And they trade on their friendship to get them to use.  They trade on the fact that people want acceptance, especially at the age of adolescence.  So what you do is you break that down, and you make those relationships less prone to have the poison of drugs or even underage drinking linked to them.  And of course we also lose a lot of kids because of impaired driving.

Q 5:  And how does the drug testing program work, then, in schools– the schools that do have it.  Is it completely confidential?  Are you going to call the police the minute you find a student who’s tested positive for heroin or marijuana or any other illicit drug?

WALTERS:  That’s what is great about having a Supreme Court decision.  It is settled – random testing programs cannot be used to punish, to call law enforcement; they have to be confidential.  So we have a uniform law across the land.  And what the schools that are doing RSDT are seeing is that it’s an enormous benefit to schools for a relatively small cost.  Depending on where you are in the country, the screening test is $10-40.  It’s less than what you’re going to pay for music downloads in one month for most teenage kids in most parents’ lives.  And it protects them from some of the worst things that can happen to them during adolescence.  Not only dying behind the wheel, but overdose death and addiction.

 Schools that have done RSDT have faced some controversy; so you have to sit down and talk to people; parents, the media, young people.  You have to engage the community resources.  You’re going to find some kids and families that do have treatment needs.  But with RSDT you bring the needed treatment to the kids.

I tell, a lot of times, community leaders – mayors and superintendents, school board members – that if you want to send less kids into the criminal justice system and the juvenile justice system, drug test — whether you’re in a suburban area or in an urban area.

What does the testing do?  It takes away what we know is an accelerant to self-destructive behavior: crime, fighting in school, bringing a weapon, joining a gang.  We have all kinds of irrefutable evidence now – multiple studies showing drugs and drinking at a young age accelerate those things, make them worse, make them more violent, as well as increasing their risks of overdose deaths and driving under the influence.  So drug testing makes all those things get better.  And it’s a small investment to make everything else we do work better.

Again, drug testing is not a substitute for drug education or good parenting or paying attention to healthy options for your kid.  It just makes all those things work better.

Q 6:  And I know you’ve heard this argument before, but isn’t that big brother?  Aren’t there parents out there who say to you, “I’m the parent: why are you going to test my child for drugs in school; that’s my job?” 

WALTERS:  I think that is the critical misunderstanding that we are slowly beginning to change by the science that tells us substance abuse is a disease.  It’s a disease that gets started by using the drug, and then it becomes a thing that rewires our brain and makes us dependent.  So instead of thinking of this as something that is a moral failing, we have to understand that this is a disease that we can use the kind of tools for public health – screening and interventions – to help reduce it.

Look, let me give you the counter example.  It’s really not big brother.  It’s more like tuberculosis.  Schools in our area require children to be tested for tuberculosis before they come to school.  Why do they do that?  Because we know one, they will get sicker if they have tuberculosis and it’s not treated.  And we can treat them, and we want to treat them.  And two, they will spread that disease to other children because of the nature of the contact they will have with them and spreading the infectious agent.  The same thing happens with substance abuse.  Young people get sicker if they continue to use.  And they spread this to their peers.  They’re not secretive among their peers about it; they encourage them to use them with them.  Again, it’s not spread by a bacillus, but it’s spread by behavior.

If we take seriously the fact that this is a disease and stop thinking of it as something big brother does because it’s a moral decision that somebody else is making, we can save more lives.  And I think the science is slowly telling us that we need to be able to treat this in our families, for adults and young people.  We have public health tools that we’ve used for other diseases that are very powerful here, like screening – and that’s really what the random testing is.  We’re trying to get more screening in the health care system.  So when you get a check up, when you bring your child to a pediatrician, we screen for substance abuse and underage drinking.  Because we know we can treat this, and we know that we can make the whole problem smaller when we do. 

Q 7:  You have said there were about 4,000 schools across the country now that are doing this random drug testing.  What can we see in the numbers since the Supreme Court ruling in 2002, as far as drug use in those schools, and drug use in the general population?

WALTERS:  Well, what a number of those schools have had is of course a look at the harm from student drug and alcohol use.  Some of them have put screening into place, random testing, because they’ve had a terrible accident; an overdose death; death behind the wheel.  What’s great is when school districts do this, or individual schools do this, without having to have a tragedy that triggers it.  But if you have a tragedy, I like to tell people, you don’t have to have another one.  The horrible thing about a tragic event is that most people realize those are not the only kids that are at risk.

There are more kids at risk, obviously, in our communities in the Washington, DC area where this young woman died.  We know there’s obviously more children who are at risk of using in middle school and high school.  The fact is those children don’t have to die.  We cannot bring this young lady back.  Everybody knows that.  But we can make sure others don’t follow her.  And the way we can do that is to find, through screening, who’s really using.  And then let’s get them to stop – let’s work with their families, and let’s make sure we don’t start another generation of death.  So what you see in these areas is an opportunity to really change the dynamic for the better.

Q 8:  Now, although nationally drug use among our youth is going down – what does it say to you – when I look at the numbers specific to Virginia, the most recent that I could find tells me that 3% of 12th graders, over their lifetime, have used a drug like heroin?  What does it say to you?  To me, that sounds like a lot.

WALTERS:  Yeah, and it’s absolutely true.  I think the problem here is that when you tell people we are taking efforts that are making progress nationwide, they jump to the conclusion that that means that we don’t have a problem anymore.  We need to continue to make this disease smaller.  It afflicts our young people.  It obviously also afflicts adults, but this is a problem that starts during adolescence — and pre-adolescence in some cases — in the United States.  We can make this smaller.  We not only have the tools of better prevention but also better awareness and more recognition of addiction as a disease.  We need to make that still broader.  We need to use random testing.  If we want to continue to make this smaller, and make it smaller in a permanent way, random testing is the most powerful tool we can use in schools.

We want screening in the health care system.  We have more of that going on through both insurance company reimbursement and public reimbursement through Medicare and Medicaid for those who come into the public pay system.  That needs to grow.  It needs to grow into Virginia, it’s already being looked at in DC; it needs to grow into Maryland and the other states that don’t have it.  We are pushing that, and it’s relatively new, but it’s consistent with what we’re seeing – the science and the power of screening across the board.

We need to continue to look at this problem in terms of also continuing to push on supply.  We’re working to reduce the poisons coming into our communities, which is not the opposite of demand; that we have to choose one or the other.  They work together.  Keeping kids away from drugs and keeping drugs away from kids work together.  And where we see that working more effectively, we’ll save more lives.  So again, we’ve seen that a balanced approached works, real efforts work, but we need to follow through.  And the fact that you still have too many kids at risk is an urgent need.  Today, you have kids that could be, again, victims that you have to unfortunately tell about on tonight’s news, that we can save.  It’s not a matter we don’t know how to do this.  It’s a matter of we need to take what we know and make it reality as rapidly as possible.

Q 9:  Where are these drugs coming from?  Where’s the heroin that these kids allegedly got coming from?

WALTERS:  We do testing about the drugs to figure out sources for drugs like heroin.  Principally, the heroin in the United States today has come from two sources.  Less of it’s coming out of Colombia.  Colombia used to be a source of supply on the East Coast, but the Colombian government, as a part of our engagement with them on drugs, has radically reduced the cultivation of poppy and the output of heroin.  There still is some, but it’s dramatically down from what it was even about five years ago.  Most of the rest of the heroin in the United States comes from Mexico.  And the Mexican government, of course, is engaged in a historic effort to attack the cartels.  You see this in the violence the cartels have had as a reaction.  So we have promising signs.  There are dangerous and difficult tasks ahead, but we can follow through on that as well.

Most of the heroin in the world comes from Afghanistan; 90% of it.  And we are working there, of course, as a part of our effort against the Taliban and the forces of terror and Al Qaeda, to shrink that.  The good news is that last year we had a 20% decline in cultivation and a 30% decline in output there.  Most of that does not come here, fortunately.  But it has been funding the terrorists.  It’s been drained out of most of the north and the east of the country.  It’s focused on the area where we have the greatest violence today, in the southwest.  We’re working now – you see Secretary Gates talking to the NATO allies about bringing the counter-insurgency effort together with the counter-narcotics effort to attack both of these cancers in Afghanistan.  We have a chance to change heroin availability in the world in a durable way by being successful in Afghanistan.  We’ve started that path in a positive way.  Again, it’s a matter of following through as rapidly as possible.

Q 10:  Greg Lannes, the father of the girl in Fairfax County who died, told me that one of his main efforts, as you imagined, was to let people know that those drugs, they’re coming from where it is produced, outside our country; that they’re getting all the way down to the street level and into our neighborhoods– something that people don’t realize.  So when you hear that they busted a ring of essentially teenagers who have been dealing, using and buying heroin, what does that say to you as the man in charge of combating drugs in our country?

WALTERS:  Well again, we have tools that can make this smaller.  But we have to use those tools.  And we have multiple participants here.  Yes we need to educate.  And we need to make sure that parents know they need to talk to their children, even when their children look healthy and have come from a great home.  Drugs – we’ve learned, I think, over the last 25 years or more, drugs affect everybody; rich or poor, middle class, lower class or upper class.  Every family’s been touched by this, in my experience, by alcohol or drugs.  They know that reality– we don’t need to teach them that.

What we need to teach them is the tools that we have that they can help accelerate use of.  Again, I think – there is no question in my mind that had this young woman been in a school, middle school or high school that had random testing – since that’s where this apparently started, based on the information I’ve seen in the press – she would not be dead today.  So again, we can’t go back and bring her to life.  But we can put into place the kind of screening that makes the good will and obvious love that she got from her parents, the obvious good intentions that I can’t help but believe were a part of what happened in the school, the opportunities that the community has to have a lot of resources that she didn’t get when she needed them.  And now she’s dead.  Again, we can stop this: we just have to make sure we implement that knowledge in the reality of more of our kids as fast as possible.

Q 11:  Should anyone be surprised by this case?  And that such a hardcore drug like heroin is being used by young people?

WALTERS:  We should never stop being surprised when a young person dies.  They shouldn’t die.  They shouldn’t die at that young age, and we should always demand of ourselves, even while we know that’s sometimes going to happen today, that every death is a death too many.  I think that it is very important not to say we’re going to accept a certain level.  Never accept this.  Never!  That’s my attitude, and I know that’s the president’s  attitude as well here.  Never accept that heroin’s going to get into the lives of our teenagers.  Never accept that our children are going to be able to use and not be protected.  It’s our job to protect them.  They have a role, also, obviously in helping to protect themselves.  But we need to give them the tools that will help protect them.

When I talk to children and young adults in high school or college, they know what’s going on among their peers.  And in some ways, when you get them alone and they feel they can talk candidly, they tell us they don’t understand why we, as adults who say this is serious, don’t act.  They know that we see children who are intoxicated; they know that we must see signs of this, because as kid’s lives get more out of control, they show signs of it.  They want to know why we don’t act.

We can use the tools of screening, and we can use the occasion of a horrible event like this to bring the community together and say it’s time for us to use the shock and the sorrow for something positive in the future.  I haven’t met a parent of a child who’s been lost who doesn’t say I just want to use this now for something positive.  And that’s understandable, and I think we ought to honor that wish.

Q 12:  Well, I guess I’m not asking should we accept that this is in our schools, but is it naïve for people not to understand or realize that these hardcore drugs are in our schools, and in our communities, and in our neighborhoods. 

WALTERS:  Yeah.  Where it is naïve, I think, is to not recognize the extent and access that young people have to drugs and alcohol.  I think we sometimes think that because they come from a home where this isn’t a part of their lives now, that it’s not ever going to be part of their lives.  Look, your viewers should go on the computer.  Type marijuana into the Google search engine and see how many sites encourage them to use marijuana, how to get marijuana, how to grow marijuana, the great fun of marijuana.  Go on YouTube and type in marijuana, and see how many videos come up using marijuana, joking around about marijuana.  And then when you start showing one, of course the system is designed to show you similar things.  Type in heroin.  See what kind of sites come up, and see what kind of videos come up on these sites.  Young people spend more time on these sites than they do, frequently, watching television.  Remember, there is somebody telling your children things about drugs.  And if it’s not you, the chances are they’re telling them things that are false and dangerous.  So there is a kind of naiveté about what the young peoples’ world, as it presents itself to them, tells them about these substances.  It minimizes the danger, it suggests that it’s something that you can do to be more independent, not be a kid anymore. 

We, from my generation — because I’m a baby boomer — unfortunately have had an association of growing up in America with the rebellion that’s been associated with drug use.  That’s been very dangerous, and we’ve lost a lot of lives.  We have to remember that it’s alive and well, and has become part of the technological sources of information that young people have.  I also see young people in treatment centers who got in a chat room and somebody offered them drugs or offered them to come and buy them alcohol and flattered them, and got them involved in incredibly self-destructive behavior.  The computer brings every predator and every dangerous influence into your own child’s home – into their bedroom in some cases, if that’s where that computer exists.  You wouldn’t let your kids go out and play in the park with drug dealers.  If you have a computer and it’s not supervised, those drug dealers are in that computer.  Remember that.  And they’re only a couple of keystrokes away from your child.

Q 13:  And you talk about the YouTube and the computers and all those things.  What about just the overall societal image?  Because we have this whole image with heroin, of heroin chic.  How much does that contribute to the drug use, and how difficult does it make your job, when a drug is being made out to be cool in society by famous people?

WALTERS:  There are still some elements of that.  It was more prominent a number of years ago.  I would say you see less of that now glamorized in the entertainment industry, or among people who are celebrities in and out of entertainment.  You see more cases of real harm.  But it’s still out there.  The one place that I think is replacing that, just to get people ahead of the game here, is prescription pharmaceuticals.  Those have been marketed to kids on the internet as a safe high.  They falsely suggest that you can overcome the danger of an overdose because you can predict precisely the dosage of OxyContin, hydrocodone, Vicodin.  And there are sites that suggest what combination of drugs to use.  We’ve seen prescription drug use as the one counter example of a category of drug use going up among teens.  We’re trying to work on that as well, but that’s something that’s in your own home, because many people get these substances for legitimate medical care.  Young people are going to the medicine cabinet of family or friends, taking a few pills out and using those.  And those are as powerful as heroin, they’re synthetic opioids, and they have been a source of overdose deaths. 

So let’s not forget – while this Fairfax example reminds us of the issues of heroin chic and of the heroin that’s in our communities, the new large problem today is a similar dangerous substance in pill form in our own medicine cabinets.  Barrier to access is zero.  They don’t have to find a drug dealer; they just go find the medicine cabinet.  They don’t have to pay a dime for it because they just take it and they share that with their friends.  We need to remember, that’s another dimension here.  Keep these substances out of reach – under our control when we have them in our home.  Throw them away when we’re done with them.  Make sure we talk to kids about pills.  Because people, again, are telling them that’s the place to go to avoid overdose death, is to take a pill.

Q 14:  When you see a lot of these celebrities checking in and out of rehab, does it sort of glamorize it for kids?  And teach them hey, you can use, you can check into rehab, you can come back, you can – you know.  Is there a mixed message there?

WALTERS:  There is.  Some young people interpret it the way you describe; of it’s something you do and you can get away with it by going into rehab.  We do a lot of research on young people’s attitudes for purposes of helping shape prevention programs in the media, as well as in schools and for parents.  We do a lot with providing material to parents.  I would say that compared to where we’ve been in the last 15 or 20 years, there’s less glamorization today.

I think we should also remember the positive, because we reinforce that.  A lot of young people – obviously not all or we wouldn’t have this death – believe that taking drugs makes you a loser.  They’ve seen that a lot of those celebrities are showing their careers going down the toilet because they can’t get away from the pills and the drugs and the alcohol.  And I think they see that even among some of their peers.  That’s a good thing.  We should reinforce that as parents: teaching our kids that drug and alcohol use may be falsely presented to you as something you do that would make you popular, make you seem like you should have more status in society generally.  But actually, look at a lot of these people; they’ve had enormous opportunities, enormous gifts, and they can’t stop themselves from throwing them away.  And they may not stop themselves from throwing away their lives. 

I think you could use these events as a teachable moment.  It can go two ways.  Help your child understand what the truth is here.  And I tell young people – and I think parents have to start this more directly – this is the way this is going to come to you:  Somebody you really, really want to like you; somebody you really, really like; someone you may even love — or think you love — they’re going to say come and do this with me.  If you can’t find any other reason to not do this with them, say, “Before we do this, let’s go to a treatment center.  Let’s go talk to people who stood where we stood and said it’s not going to happen to me.”  If everybody, when they got the chance to start, thought of an addict or somebody who was dead, they wouldn’t start.  The fact is that does not enter their mind. 

Many people in treatment centers understand that part of the task of recovery is helping other people avoid this.  So they’re willing to talk about it.  In fact, that’s part of their path of staying clean and sober, which not many kids are going to be able to do on their own.  But it makes them think that what presents itself as something overwhelmingly attractive has behind it a horrible dimension, for their friends as well as for themselves.  And more and more, I think kids understand this.

We can use the science of this as a disease, and the experience of many families.  Remember, uncle Joe didn’t used to be like this.  Especially Thanksgiving, when we have families getting together and all of a sudden mom’s going to get loaded and become ugly in the corner.  We also have to remember we have an obligation to reach out to those people, and to get them help.  We can treat them.  Nobody gets sober, in my experience, by themselves.  They have to take responsibility.  But you have to overcome the pushback, and addiction and alcoholism have, as a part of the disease, denial.  When you tell somebody they have a problem, they get angry with you.  They don’t say hey thanks, I want your help.  They don’t hit bottom and become nice.  That’s a myth.  They need to be grabbed and encouraged and pushed.  Almost everybody in treatment is coerced – by a family member, by an employer, sometimes by the criminal justice system.

So remember that, when you find your child using and they want to lie to you up down and sideways saying, “It’s the first time I’ve ever done it.”  No, no, no, no, no, that’s the drugs talking.  That shows you, if anything, you have a bigger problem than you realized and you need to reach out, get some professional help.  But don’t wait!

Source:    National Institute of Citizen Anti-drug Policy (NICAP)

DeForest Rathbone, Chairman, Great Falls, Virginia, 703-759-2215, DZR@prodigy.net

Abstract

Summary

Highlights

Aaron Hernandez was supposed to be the epitome of the American Dream—overcoming childhood setbacks to earn a spot in the NFL on the New England Patriots. Millions of kids across America wish they could be so lucky. But the 2020 documentary on Netflix, “Killer Inside: The Mind of Aaron Hernandez,” takes a deep dive into his life to investigate how his dream unraveled into a nightmare. Convicted of murdering his friend Odin Lloyd and accused of killing two other men (but found not guilty), Hernandez took his own life in a prison suicide in 2017. He was only 27.
The compelling docuseries explores many of the factors that could have contributed to the tragic end of such a promising life—childhood abuse, unstable parenting, hidden bisexuality. And then there was his brain. The docuseries delivers a fascinating look at his troubled brain, but it misses one key factor that may have contributed to Hernandez’ brain dysfunction.

The Brain of Aaron Hernandez
After Hernandez’s death, his brain was delivered to Boston University, where researchers made razor-thin slices for examination. Their findings? His brain was “riddled” with Stage 3 chronic traumatic encephalopathy (CTE). This neurodegenerative disease, which has 4 stages, has been found in athletes like football players, boxers, and soccer players who endure repeated concussions and other blows to the head. It has been associated with memory loss, cognitive dysfunction, and suicidal thoughts and behavior.
A Boston University publication reported that Ann McKee, director of BU’s Chronic Traumatic Encephalopathy Center, said that his brain was the worst case of CTE ever seen in someone so young. “Especially in the frontal lobes, which are very important for decision-making, judgment, and cognition, we could see damage to the inner chambers of the brain,” she said. The frontal lobes are also involved in impulse control, empathy, and learning from past experiences.
The documentary focuses heavily on CTE and the significant role it likely played in Hernandez’ downfall, and for good reason. The filmmakers also hone in on another aspect of his life that may have contributed to his troubles—cannabis use. It is reported that the football player began smoking marijuana regularly in high school and continued to smoke throughout his pro career. The docuseries calls him a “chainsmoker” with a serious habit, but it neglects to connect the dots between marijuana use and brain dysfunction.

Marijuana and the Brain
A growing body of evidence shows that marijuana use impairs brain activity. In the largest known brain imaging study, which appeared in the Journal of Alzheimer’s Disease, scientists from Amen Clinics, Google, Johns Hopkins University, UCLA, and the UC San Francisco evaluated 62,454 brain SPECT scans of more than 30,000 individuals (ages 9 months to 105 years) to investigate factors that accelerate brain aging. SPECT (single-photon emission computed tomography) is a brain imaging technology that measures brain activity and blood flow. The study found that a number of brain disorders and behaviors predicted accelerated aging. Of all the disorders and behaviors analyzed, cannabis abuse ranked as the second-highest brain ager, topped only by schizophrenia.
The study, which included brain scans from 1,000 cannabis users, 25,168 non-cannabis users, and 100 healthy controls, showed reduced cerebral blood flow among the cannabis users compared to non-users and healthy controls. A significant decrease in blood flow was noted specifically in the right hippocampus, an area of the brain that helps with memory formation. This part of the brain is severely affected in those that suffer from Alzheimer’s disease.

Healthy SPECT Scan

Marijuana Affected SPECT Scan

Other research has concluded that marijuana harms the teenage brain in numerous ways. For example, a 2019 review found that it increases the risk of depression and suicidal thoughts and behaviors. And marijuana use at a young age has also been associated with increased impulsivity.
Although pot promoters would argue that most people who smoke marijuana don’t become murderers and don’t die by suicide, it’s important to understand that in vulnerable people it may have negative impacts on brain function that contribute to unhealthy behaviors. Sadly, considering that Hernandez’s brain was so damaged by CTE, marijuana use was likely only making bad brain function worse.

You Can Change Your Brain
Unfortunately, this information is too late to help Hernandez, but it isn’t too late for other football players who have endured years of helmet-to-helmet tackles. A study at Amen Clinics on 30 retired professional football players who had suffered head trauma showed that after following a brain healthy program for 6 months, 80% showed significant improvement in blood flow to the frontal lobes, as well as improvements in overall cognitive functioning, processing speed, attention, reasoning, and memory. Hall of Fame quarterback Terry Bradshaw spoke openly about his own brain rehabilitation after suffering multiple concussions. 
Likewise, it isn’t too late for people who grew up in traumatic households. See how a man named Kevin overcame his traumatic upbringing to enhance his brain health using a variety of innovative therapies. And it isn’t too late for people who have been bad to their brain with drug use. Find out how Arnie broke free from the chains of addiction. It’s never too late to start enhancing brain function.
The world’s largest database of brain scans related to behavior—over 160,000 and growing —shows that when you adopt a brain health program, you can change your brain and change your life for the better.
At Amen Clinics, we take a unique brain-body approach that gets to the root cause of your symptoms. Our comprehensive evaluations include brain SPECT imaging, as well as laboratory testing and assessing other important factors that could be contributing to symptoms. By getting to the root cause of your symptoms, we can create a more effective, personalized treatment plan for you.
If you want to join the tens of thousands of people who have already enhanced their brain health, overcome their symptoms, and improved their quality of life at Amen Clinics, speak to a specialist today at 888-288-9834. If all our specialists are busy helping others, you can also schedule a time to talk.

Source: What the Aaron Hernandez Documentary Missed About His Brain | Amen Clinics Amen Clinics February 2020

One way to deter harmful recreational drug use by teenagers is to treat them like adults. Rather than simply tell them to “Just Say No” to alcohol, tobacco or illicit drugs, it may be more helpful to explain how these substances create unique risks for them risks that arise due to the changing state of the adolescent brain.

It’s an approach recommended by Dr. Robert DuPont, the first director of the National Institute of Drug Abuse, the second White House “drug czar” and the current head of the Institute for Behavior and Health.

Scientists have long recognized that people who use alcohol, tobacco, marijuana and other drugs while adolescents are far more likely to use more dangerous drugs in their 30s and 40s. Back in 1984, researchers writing in the American Journal of Public Health reported that “the use of marijuana is a good predictor of the use of more serious drugs only if it begins early” and that early drinking is a similar “predictor of marijuana use.”

It should come as no surprise, then, that Americans in their 30s and 40s who used recreational drugs as teenagers are the group most severely affected by opioid overdoses today.

Unfortunately, neither the media nor popular culture adequately informs young people about the neurological damage alcohol, nicotine, and marijuana can inflict on the brain. On the contrary, despite strong evidence that early recreational drug use increases the likelihood of future drug addiction, the media and today’s culture often describe marijuana use as an “organic,” “natural” approach to anxiety and stress management. Indeed, Northern Michigan University launched the nation’s first medicinal plant chemistry major, offering students the chance to focus on marijuana-related studies. What message does that send to the still-developing minds of college students?

One group is taking a non-traditional approach to convincing students otherwise.

One Choice is a drug prevention campaign developed for teenagers by the Institute for Behavior and Health. It relies on cutting-edge neuroscience to encourage young Americans to make decisions that promote their brain health.

Pioneered by Dr. DuPont, One Choice specifically advocates that adolescents make “no use of any alcohol, nicotine, marijuana or other drugs” for health reasons. The theory is that adolescents who make the decision not to use alcohol, nicotine, or marijuana at all that make “One Choice” to avoid artificial, chemical brain stimulation are far less likely to wind up addicted to drugs such as opioids later on.

The One Choice approach is evidence-based. In 2017, scientists at Mclean Hospital and Harvard Medical School published their findings on the impact of early substance use on cognitive development. They explained that the brains of teenagers are still developing and can be negatively impacted by substance use. Adolescent brains are still forming the communication routes that regulate motivation, stress and habit-formation well into adulthood. As such, it is easier for substances to hijack and alter those routes in developing brains than in adult brains.

Hindering the vital attributes of habit formation, stress management and motivational behavior can drastically affect a young person’s academic performance. Collectively, and in the long run, that can impair the competitiveness of a national economy. Thus, it is crucial that young Americans learn to prioritize brain health.

The timing for the innovative One Choice approach is propitious. Today’s young Americans are more interested in biology, psychology and health sciences than ever before. According to the National Center for Education Statistics, the field of “health professions and related programs” is the second most popular major among college students, with psychology and biological or biomedical sciences following as the fourth and fifth most popular, respectively. By explaining developmental neuroscience to teenagers, One Choice engages young people on a topic of interest to them and presents the reality of a pressing public health issue, instead of throwing moral platitudes and statistics at them.

Pro-marijuana legalization organizations, such as the Drug Policy Alliance, agree: “The safest path for teens is to avoid drugs, doing alcohol, cigarettes, and prescription drugs outside of a doctor’s recommendations.” And certainly honesty, along with scientific accuracy, is critical if we are to persuade adolescents not to use drugs.

Brain health is critical to the pursuit of happiness. And leveraging scientifically accurate presentations and testimonies to convince young Americans to prioritize their own brain health early on can prevent future substance abuse.

Source: Using Neuroscience to Prevent Drug Addiction Among Teenagers | The Heritage Foundation January 2019

Just one or two joints seem to change the structure of the brain, say researchers from universities around the world, led by senior author and University of Vermont professor of psychiatry Hugh Garavan, PhD, and first author and former UVM postdoctoral fellow Catherine Orr, PhD.
 
The study is part of a long-term European effort called IMAGEN, which has collected brain images from 2,000 children in Ireland, France, and Germany, starting when they were age 14 and continuing through age 23.
 
Researchers compared the brain images of 46 children age 14 who reported having used marijuana once or twice with those of children that age who had not used the drug. The images of the marijuana triers showed greater brain volume in areas with cannabinoid receptors. The biggest differences were in the amygdala, involved in fear and other emotions, and the hippocampus, the site of memory development and spatial abilities.
 
“You’re changing your brain with just one or two joints. Most people would likely assume that one or two joints would have no impact on the brain,” says Dr. Garavan.
 
It is unclear what the extra gray matter in these brain areas means. Normally at age 14, the brain is refining its synaptic connections to make it thinner, not thicker. Dr. Garavan says one possibility is that initial marijuana use in this age group may be disrupting that “pruning” process.
 
The new findings open a new area of focus for future research.
 
Read study abstract here.

Source:  The Marijuana Report  16.01.2019

There is evidence in both patients with psychotic disorders and the general population that cannabis use is associated with adverse effects of psychopathology and cognition.

RESEARCH UPDATE

Substance use comorbidity in schizophrenia has been described as “the rule rather than the exception.”¹ The large Epidemiological Catchment Area study estimated that 47% of patients with schizophrenia also had a lifetime comorbid diagnosis of a substance use disorder.² Substance use comorbidity is also often deleterious to the course of schizophrenia, including potential contributions to medication non-adherence and illness relapse.¹ Cannabis (marijuana) is one of the most commonly used substances by patients with schizophrenia.

There is recent, renewed interest in the endocannabinoid system, which represents a novel potential treatment target in schizophrenia.³ Modulation of this system by the main psychoactive component in marijuana, Δ9-tetrahydro-cannabinol (THC), can induce acute psychosis and cognitive impairment. However, the non-psychotropic plant-derived agent cannabidiol (CBD) may decrease psychotic symptoms and improve cognitive function in schizophrenia.^4-6

Presently, CBD oil is sold at numerous shops throughout the US, with purported benefits that include alleviation of symptoms such as depression, anxiety, insomnia, and pain. However, the purity and safety of CBD is not regulated by the US Food and Drug Administration. CBD may be “contaminated” with some amount of THC and/or other unknown ingredients. In the past decade, there have been a number of systematic reviews regarding associations between cannabis use and psychosis. Therefore, a review of systematic evidence for associations between cannabis use, risk of psychosis, and the clinical course of schizophrenia is of particular relevance to the practicing clinician.

Adverse effects of cannabis on psychosis and cognition

There is evidence from a quantitative review of 15 studies in healthy participants that a single administration of THC (intravenous, oral, or nasal) versus placebo induced positive, negative, and other psychopathology with large effect sizes (ESs).⁷ Furthermore, evidence from 69 studies, comprising 2152 adolescents and young adults who used cannabis and 6575 controls with minimal cannabis exposure, showed that frequent or heavy use was associated with significantly reduced cognitive functioning with a small-to-medium ES = -0.25, although these effects were diminished with abstinence for more than 72 hours.⁸

Cannabis use and risk of psychosis

Moore and colleagues⁹ performed a systematic review of 35 studies of cannabis use and risk of psychotic mental health outcomes. They found that individuals who had used cannabis had a significant, 1.4-fold increased risk of any psychotic outcomes, independent of potential confounding and transient intoxication effects. Findings also provided evidence for a dose-response effect, with even greater, 2.1-fold risk in individuals who used cannabis most frequently.

More recently, Marconi and colleagues¹⁰ performed a meta-analysis of 10 studies, including 66,810 individuals, that investigated the association between the degree of cannabis consumption and risk of psychosis. In all individual studies, higher levels of cannabis use were associated with increased risk of psychosis. They also found evidence for a dose-response relationship, with a 2-fold increase in risk for the average cannabis user, and a 4-fold increase in risk for the heaviest users, compared with non-users. Although these findings do not definitively establish a causal association between marijuana use and psychotic disorders, it nevertheless remains a replicated risk factor for psychosis with a clear dose-dependent relationship.

Cannabis use in patients with psychotic disorders

Koskinen and colleagues¹¹ performed a quantitative review of the rates of cannabis use disorders (CUDs) in clinical samples of patients with schizophrenia. They identified 35 studies for inclusion in the meta-analysis. The median current rate of CUD was 16.0% (Interquartile Range [IQR] 8.6-28.6%), and the median lifetime rate of CUD was 27.1% (IQR=12.2-38.5). The rate of current/lifetime CUDs was markedly higher in first-episode (28.6%/44.4%) versus chronic schizophrenia (22.0%/12.2%), as well as in younger patient samples and samples with a high proportion of males. They concluded that approximately 1 in 4 patients with schizophrenia has a diagnosis of a comorbid CUD.

Hunt and colleagues¹² more recently performed a systematic review of the prevalence of comorbid substance use in patients with schizophrenia spectrum disorders. They identified 69 studies, and the pooled estimate for current or lifetime CUD was 26.2%. Consistent with the review by Koskinen and colleagues,¹¹ the prevalence was significantly higher in individuals with first-episode psychosis (35.6%) versus chronic schizophrenia (20.8%), but did not differ by study setting or patient clinical status.

The substantial prevalence of cannabis use also appears to extend to the psychosis prodrome. There is evidence from 30 studies, including 4205 individuals at ultra high risk (UHR) for psychosis, that there are high rates of current (26.7%) and lifetime (52.8%) cannabis use, and CUDs (12.8%).¹³ Compared with non-users, UHR cannabis users also had higher rates of suspiciousness and unusual thought content.

Furthermore, research suggests that people with substance-induced psychoses will later transition to a diagnosis of schizophrenia. Murrie and colleagues¹⁴ synthesized the results of longitudinal observations studies of transition from substance-induced psychosis to schizophrenia. Six studies with estimates of transition to schizophrenia among 3040 people with cannabis-induced psychosis were included. The risk of transition to schizophrenia in these individuals was 34% (95% CI 25-46%), which was the highest risk among all substances. They concluded that substance-induced psychoses are common reasons for seeking care, and these serious conditions are associated with substantial risk of transition to schizophrenia. Treatment of cannabis-induced psychoses should be considered in the same framework as that for other brief psychotic disorders (i.e., engagement, assessment, and care); this also may help decrease rates of transition to schizophrenia.

Impact of cannabis on psychotic disorders

Large and colleagues¹⁵ conducted a systematic review of the association between cannabis use and the age of onset of psychosis. They included 41 samples, finding that the age of onset of psychosis for those who used cannabis was 2.7 years younger than for non-users, corresponding to a small-to-medium effect size of 0.41. These findings are broadly consistent with a potential causal role for cannabis in the development of psychosis in some patients.

Bogaty and colleagues¹⁶ performed a meta-analysis of 14 studies of neurocognition in lifetime cannabis users and never-users in young patients with psychotic disorders (aged 15 to 45 years). They found that lifetime cannabis users performed significantly worse than never-users on several cognitive domains, including premorbid and current IQ, verbal learning and working memory, and motor inhibition. Effect sizes were small to medium for most domains (0.17-0.40), except for verbal working memory, which showed a large effect size (0.76). Interestingly, patients who use cannabis performed better on tests of conceptual set-shifting. Increasing age exacerbated the between-group differences.

Schoeler and colleagues¹⁷ conducted a systematic review and meta-analysis of the effect of continued versus discontinued cannabis use after the onset of psychosis. They identified 24 studies, including 16,565 patients with pre-existing psychosis and at least a 6 month duration of follow-up. They found that continued cannabis use was associated with a significant: increase in risk of relapse of psychosis compared with non-users (ES=0.36) and discontinued users (ES=0.28); longer hospital admissions than non-users (ES=0.36); and more severe positive, but not negative, symptoms. Krause and colleagues¹⁸ performed a meta-analysis of the efficacy, acceptability, and tolerability of antipsychotics in patients with schizophrenia and comorbid substance use. They included 8 randomized controlled trials in patients with cannabis use comorbidity. Clozapine was superior to other antipsychotics for reduction of substance use and negative symptoms in those who used cannabis. Risperidone was superior to olanzapine for reducing of drug cravings and weight gain.

Conclusions

Premorbid cannabis use is associated with a dose-dependent increased risk of developing a psychotic disorder. There is evidence in both patients with psychotic disorders and the general population that cannabis use is associated with adverse effects of psychopathology and cognition. Cannabis use and CUDs are highly prevalent throughout the clinical course of illness.

Cannabis use is associated with an earlier age of onset of psychosis and more severe impairments in neurocognition. Continued cannabis use after the onset of psychosis is associated with increased risk of illness relapse, longer hospitalizations, and more severe positive psychopathology. There is also evidence for superior efficacy of clozapine for reduction of substance use and negative symptoms in patients with schizophrenia and comorbid cannabis use. Targeted interventions for improved prevention, detection, and treatment are warranted to improve outcomes in this population.

Dr Miller is Professor, Department of Psychiatry and Health Behavior, Augusta University, Augusta, GA. He is the Schizophrenia Section Chief for Psychiatric Times.

The author reports that he receives research support from Augusta University, the National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Stanley Medical Research Institute.

Source: https://www.psychiatrictimes.com/view/novel-insights-cannabis-psychosis July 2020

A new study recently published in Nature Medicine found a stunning association between prenatal THC exposure and development of autism. Using provincial birth registries, Canadian researchers analyzed all live births that occurred in Ontario between April 2007 and March 2012 for a total of 497,821 births.

Investigators found that infants who were prenatally exposed to THC were 57% more likely to develop autism spectrum disorder (ASD) and 35% more likely to develop intellectual disabilities and learning disorders. Previous studies of this type have been difficult to interpret due to polysubstance use among expectant mothers making it difficult to tease out the effects of THC exposure alone. In this study, researchers were able to directly compare unexposed infants to those whose mothers only used marijuana during their pregnancy. Thus, any effects observed in this study can be reliably attributed to prenatal THC exposure since no other substances were used. Results persisted even adjusting for other potential risk factors for ASD such as maternal age, education, psychiatric disorders, socioeconomic status, parity, and race.

The results of this study confirm that of previous research on the harms of prenatal THC exposure. Nevertheless, marijuana is routinely recommended to pregnant women by pot docs as well as dispensary employees with no medical training at all. Given the explosion in marijuana use among pregnant women in states like FL, lawmakers must take immediate action to fund education campaigns and ban marijuana recommendations for pregnant women. How many more lives need to be ruined so that Big Pot and their political allies can line their pockets?

Source:  https://www.dfaf.org/study-finds-link-between-prenatal-thc-exposure-and-autism/ 19.08.20

ABSTRACT

Parental cannabis use has been associated with adverse neurodevelopmental outcomes in offspring, but how such phenotypes are transmitted is largely unknown. Using reduced representation bisulphite sequencing (RRBS), we recently demonstrated that cannabis use is associated with widespread DNA methylation changes in human and rat sperm. Discs-Large Associated Protein 2 (DLGAP2), involved in synapse organization, neuronal signaling, and strongly implicated in autism, exhibited significant hypomethylation (p < 0.05) at 17 CpG sites in human sperm. We successfully validated the differential methylation present in DLGAP2 for nine CpG sites located in intron seven (p < 0.05) using quantitative bisulphite pyrosequencing. Intron 7 DNA methylation and DLGAP2 expression in human conceptal brain tissue were inversely correlated (p < 0.01). Adult male rats exposed to delta-9-tetrahydrocannabinol (THC) showed differential DNA methylation at Dlgap2 in sperm (p < 0.03), as did the nucleus accumbens of rats whose fathers were exposed to THC prior to conception (p < 0.05). Altogether, these results warrant further investigation into the effects of preconception cannabis use in males and the potential effects on subsequent generations.

KEYWORDS: Cannabis, sperm, DNA methylation, autism, heritability

Introduction

Cannabis sativa is the most commonly used illicit psychoactive drug in the United States (U.S.) and Europe [¹]. In the U.S., 11 states and Washington D.C. have legalized the recreational use of cannabis and 33 states have legalized the use of medicinal cannabis [²,³]. Since 1995, cannabis potency (defined as the concentration of the psychoactive cannabis component delta-9-tetrahydrocannabinol, or THC, in the sample [⁴]) has consistently risen from ~4% to as high as 32% in some states [²,⁵,⁶]. Changes in cannabis potency have been accompanied by changes in attitudes about cannabis and patterns of cannabis use. Between 2002 and 2014, the percentage of adults in the U.S. who perceived cannabis use as risky declined from 50% to 33% [⁶]. During this same period, the percentage of U.S. adults who believed cannabis to have no risk rose from 6% to 15% [⁶]. According to a 2015 Survey on Drug Use and Health, 52.5% of men in the U.S. of reproductive age (≥18) have reported cannabis use at some point in their lives, making cannabis exposure especially relevant for potential future fathers [⁷–¹¹].

Given the increased prevalence of cannabis use in the U.S., studies are beginning to focus on the effects of use on the health and development of offspring. Prenatal cannabis exposure via maternal use during pregnancy is associated with decreased infant birth weight, an increased likelihood to require the neonatal intensive care unit, and the potential for an impaired fetal immune system compared to those infants who are not exposed during gestation [¹,¹²]. In rodent studies, rat pups born to parents who were both exposed to THC during adolescence had increased heroin-seeking behaviour later in life, a phenotype that was accompanied by epigenetic changes in the nucleus accumbens [¹³–¹⁵]. These studies and others have begun to highlight the potential for intergenerational consequences of cannabis exposure [¹⁶]. Identifying the mechanism that underlies these changes is critical as cannabis use continues to increase across the U.S.

The environment impacts the integrity and maintenance of the epigenome such that it is now viewed as a molecular archive of past exposures [¹⁷]. While the majority of environmental epigenetic studies are focused on the impact of the inutero environment on the epigenome and health of the child, it has become apparent that the exposure history of the father must also be considered – specifically the impact of his exposures on the sperm epigenome. Studies have shown that exposure to phthalates, pesticides, nutritional deficiencies, and obesity can all induce potentially heritable changes in the sperm epigenome [¹⁸–²⁴]. It is likely that other common and emerging exposures, including cannabis, may also contribute to disruption of sperm DNA methylation in a similar fashion, and that such changes could be transmitted to the subsequent generation.

Using reduced representation bisulphite sequencing (RRBS) our group recently demonstrated that cannabis use in humans, and THC exposure in rats, is associated with decreased sperm concentrations and widespread changes in sperm DNA methylation [²⁵]. Of the regions identified in humans, Discs-Large Associated Protein 2 (DLGAP2) exhibited significant hypomethylation in the sperm of cannabis-exposed men compared to controls (p < 0.05). DLGAP2, a membrane-associated protein located in the post-synaptic density of neurons, plays a key role in synapse organization and neuronal signaling [²⁶]. Dysregulation of DLGAP2 is associated with various neurological and psychiatric disorders, such as autism spectrum disorder (ASD) and schizophrenia [²⁶–²⁹]. In our prior screen, we identified 17 differentially methylated CpG sites within DLGAP2 in the sperm of cannabis-exposed men compared to controls. DLGAP2 was just one of 46 genes with greater than 10 CpG sites showing significantly altered DNA methylation in the sperm of cannabis users compared to controls, out of the 2,077 genes we identified as having altered DNA methylation. The first objective of this study was to validate our preliminary RRBS findings for DLGAP2 using quantitative bisulphite pyrosequencing. Our second objective was to determine the functional association between DNA methylation and gene expression of DLGAP2 to better understand how cannabis use might affect this relationship. To determine the possible intergenerational effects of paternal cannabis use, our third objective was to determine if Dlgap2 was differentially methylated in the sperm of rats exposed to THC versus controls, and if so, whether or not these changes were intergenerationally heritable.

Results

DLGAP2 is hypomethylated in sperm from cannabis users versus controls by Reduced Representation Bisulphite Sequencing (RRBS)

Our prior study [²⁵] revealed 17 differentially methylated sites by RRBS in the sperm of cannabis users compared to controls for the DLGAP2 gene. Table S1 lists all 17 of these sites and their genomic coordinates. ^{Figure 1a} graphically demonstrates the significant hypomethylation of nine of these sites that are clustered together in the seventh intron of this gene. DLGAP2 is schematically shown in ^{Figure 1b}, including the exon-intron structure, position of CpG islands, transcription start site and the region of interest in intron 7 within the context of the gene body, with an inset showing the nucleotide sequence analysed in this study.

Validation of DLGAP2 RRBS methylation data

To confirm the methylation differences that were initially detected using RRBS, we designed a bisulphite pyrosequencing assay for the DLGAP2 intron 7 region (see ^{Figure 1b}) which captures 10 CpG sites, nine of which were identified as significantly differentially methylated using RRBS. We first validated pyrosequencing assay performance using defined mixtures of fully methylated and unmethylated human genomic DNAs. The measured levels of methylation by pyrosequencing showed good agreement between the amount of input methylation levels and the amount of methylation detected (r² = 0.99 and p = 0.0003) (^{Figure 1c}). These results confirmed the linearity of the assay in the ability to detect increasing amounts of DNA methylation at this region across the full range of possible methylation values, and indicate that the assay is suitable for use with biological specimens.

The DLGAP2 intron 7 region is not an imprinting control region (ICR)

DLGAP2 is paternally expressed in the testis, biallelically expressed in the brain, and has low expression elsewhere in the body [³⁰]. Since DLGAP2 is known to be genomically imprinted in testis [³⁰], and since the imprint control region for this gene has not yet been defined, we sought to determine if the region of interest in intron 7 is part of the DLGAP2 imprint control region (ICR). The methylation at ICRs is established during epigenome reprogramming in the primordial germ cells in embryonic development. Male and female gametes exhibit divergent methylation at ICRs, and this methylation profile is maintained through subsequent post-fertilization epigenetic reprogramming and in somatic cells throughout the life course. Therefore, we expected that if the DLGAP2 intron 7 region is an ICR, the diploid testis tissues from human conceptuses would exhibit approximately 50% methylation due to the complete methylation of one allele at this region and the complete lack of methylation at the other allele. Human conceptal testes tissues (n = 3) showed an average of 72.5% methylation at the DLGAP2 intron 7 region (^{Figure 1d}). This finding, of higher than anticipated and variable levels of methylation, is inconsistent with ICR status.

Bisulphite pyrosequencing validates the RRBS methylation data in human sperm

We next performed quantitative bisulphite pyrosequencing on the same sperm DNA samples from cannabis users and controls as those used to generate the RRBS data to confirm the loss of methylation present at the intron 7 region of DLGAP2. All nine CpG sites that were hypomethylated in the cannabis users by RRBS were also found to be hypomethylated by bisulphite pyrosequencing, as well as an additional CpG site that was captured in the assay design (p < 0.05 for all 10 sites) (^{Figure 2}). Following Bonferroni correction of the p value to adjust for multiple comparisons (p < 0.005), CpG sites 1,2,3,5,7,8,9, and 10 remained significant. From this pyrosequencing assay we observed methylation differences of 7–15% between the sperm of the cannabis users (n = 8) compared to controls (n = 7). Correlation of the RRBS and pyrosequencing data for each individual CpG site showed significant agreement at all sites analysed (p < 0.02 for all sites; Figure S1). All CpG sites showed a significant loss of methylation in accordance with the direction of change observed by RRBS for these same CpG sites.

Methylation of DLGAP2 intron 7 is inversely correlated with DLGAP2 expression

Given that we observed significant loss of intron 7 DLGAP2 DNA methylation in sperm of cannabis users relative to non-users, we next examined the relationship between DNA methylation and gene expression in the brain, where this gene’s function is critical. We used 28 conceptal brain tissues to examine the relationship between DNA methylation and mRNA expression. Expression levels were normalized to the lowest expressing sample, and the relationship between DNA methylation and mRNA expression was calculated with a Pearson correlation. We found that as methylation increased in this region, mRNA expression decreased significantly (p < 0.05) (^{Figure 3a}). Knowing that there are sex differences in autism spectrum disorder (ASD), and that dysregulation of DLGAP2 is associated with ASD [²⁶], we sought to determine if there were any sex differences in the methylation-expression relationship in these tissues. To investigate this, we ran the correlation for males (n = 15) and females (n = 13) independently. The inverse relationship between methylation and expression was evident for both males and females, but this relationship was significant only in females (p = 0.006) (^{Figure 3b, c}).

Intergenerational inheritance of altered Dlgap2 DNA methylation

We next sought to investigate Dlgap2 using data obtained from our prior study [²⁵] to determine if there was any differential methylation of Dlgap2 in THC versus control rats that was not initially identified using the imposed thresholds of that study. We were particularly interested in the potential for intergenerational transmission and to determine if route of THC exposure affected DNA methylation at this gene. The pilot study rats [²⁵] were given THC via oral gavage (to mimic oral ingestion of drug) while subsequent studies dosed rats via intraperitoneal injection (to mimic inhalation of drug). From the rats administered THC via oral gavage versus controls, we identified a region of Dlgap2 that showed differential methylation by the RRBS analysis that contains eight CpG sites. This region is in the first intron of Dlgap2, in a CpG island that spans the first exon of this gene as well (schematic of the gene structure and sequence of this region shown in ^{Figure 4a}). We validated the rat Dlgap2 pyrosequencing assay using commercially available rat DNA of defined methylation status. The results showed good agreement between the input methylation and the amount of methylation detected by pyrosequencing (r² = 0.92, p = 0.01) (^{Figure 4b}).

We were able to demonstrate intergenerational inheritance of an altered DNA methylation pattern in Dlgap2. Comparing the average methylation for exposed and unexposed sperm for each CpG site revealed that sites 2,3,4 and 6 of the eight CpG sites analysed were significantly hypomethylated in the sperm of rats exposed via injection to 4mg/kg THC compared to controls (p = 0.03 to p = 0.005) (^{Figure 4c}). CpG site 6 remained significant after Bonferroni correction (p < 0.006). The same region of Dlgap2 was then analysed in the hippocampus and nucleus accumbens of rats whose fathers were exposed to control or 4mg/kg THC. While CpG site 7 was significantly hypomethylated (p < 0.05) in the hippocampus of the offspring (^{Figure 5a}), this site was not identified as differentially methylated in the sperm of THC exposed rats, and therefore we could not conclude that this change was transmitted as the result of changes present in the exposed sperm. In the nucleus accumbens, however, significant hypomethylation (p = 0.02) at CpG site 2 was detected in the offspring (^{Figure 5b}), one of the same sites identified in the sperm of THC exposed rats. We also found that there was an inverse relationship between DNA methylation and expression of Dlgap2 in the nucleus accumbens, though not statistically significant likely due to the small sample size available in this study (n = 6 exposed, n = 8 unexposed; Figure S2).

Discussion

In this study, we examined the effects of regular male cannabis use on human sperm DNA methylation, at DLGAP2. Our RRBS study initially identified 17 CpG sites in DLGAP2 that were differentially methylated in the sperm of cannabis users compared to controls. Of the sites that were initially identified, nine of them all reside together in the seventh intron of this gene, though not in a defined CpG island. To first confirm the RRBS data, we performed quantitative bisulphite pyrosequencing for the nine clustered CpG sites. We were able to capture an additional CpG site with careful assay design for a total of ten CpG sites analysed via bisulphite pyrosequencing. We successfully validated the RRBS findings, confirming that there was significant hypomethylation among these ten sites with cannabis use. We confirmed a significant inverse correlation between methylation and expression at this region in human conceptal brain tissues.

To begin to determine whether or not the effects of cannabis on sperm are heritable, we analysed sperm from THC exposed and control male rats, as well as the hippocampus and nucleus accumbens from offspring of THC exposed and control males for changes in DNA methylation at Dlgap2. Rats exposed to THC were given a dose (4mg/kg THC for 28 days) that is pharmacodynamically equivalent to daily cannabis use to resemble frequent use in humans. We identified significant hypomethylation at Dlgap2 in the sperm of exposed rats as compared to controls. This hypomethylated state was also detected in the nucleus accumbens of rats born to THC exposed fathers compared to controls, supporting the potential for intergenerational inheritance of an altered sperm DNA methylation pattern. While the changes in the degree of methylation are small in the rats (0.5–0.7%), we previously reported that fractional changes in methylation can significantly influence the degree to which the gene’s expression is altered [³¹].

DLGAP2 is a member of the DLGAP family of scaffolding proteins located in the post-synaptic density (PSD) of neurons. The PSD is a protein-dense web that lies under the postsynaptic membrane of neurons and facilitates excitatory glutamatergic signaling in the central nervous system [²⁶,³²]. DLGAP2 functions to transmit neuronal signals across synaptic junctions and helps control downstream signaling events [²⁶,³²]. Due to its important role in PSD signaling, even small changes in the expression of DLGAP2 can have severe consequences [²⁶,³²]. Of particular relevance, DLGAP2 has been linked to schizophrenia and importantly, has been identified as an autism candidate gene [²⁷,²⁸,³³,³⁴]. Differential methylation of DLGAP2 is reported in the brain of individuals with autism, and has been linked to post-traumatic stress disorder in rats [²⁷,³⁵]. Knockout of Dlgap2 in mice results in abnormal social behaviour, increased aggressive behaviour, and learning deficits [³⁶].

Studies are increasingly showing associations between cannabis use and various neuropsychiatric and behavioural disorders including anxiety, depression, cognitive deficits, autism, psychosis, and addiction [²,⁶,⁷,⁹,¹⁴,³⁷–³⁹]. Research looking into the effects of THC exposure found that rat pups born to parents who were exposed to THC during adolescence showed increased effort to self-administer heroin compared to those born to unexposed parents [¹³]. This increase in addictive behaviour was driven by THC-induced changes in DNA methylation, occurring in the striatum, including the nucleus accumbens [¹⁴,¹⁵]. One of the genes whose methylation was altered by parental THC exposure was Dlgap2 [¹⁵]. Recently, a group from Australia analysed datasets from two independent cohorts to examine the relationship between cannabis legalization in the U.S. and ASD incidence. They determined there was a strikingly significant positive association between cannabis legalization and increased ASD incidence. Further, the study authors predicted that there will be a 60% increase in excess ASD cases in states with legal cannabis by 2030, and deemed ASD the most common form of cannabis-associated clinical teratology [⁴⁰].

It is estimated that the ratio of boys with ASD to girls with ASD is 4:1 which led us to stratify our analysis looking at the relationship between DNA methylation and gene expression by sex [⁴¹,⁴²]. The results of our methylation-expression analyses demonstrated a significant association in females but not males. While we don’t know the ASD status of these samples, there are several reasons why this may be the case. First, there are certain genes that confer a stronger ASD phenotype in girls compared to boys [⁴¹,⁴²]. Thus, while we see the trend in both sexes, it is possible that dysregulation of this gene may manifest phenotypically more in girls. Alternatively, it may be that the regulatory relationship between methylation and expression is retained in females while altered methylation further exacerbates an already fragile relationship in males. Overall, this data confirms that the region of DNA methylation within DLGAP2 that was differentially methylated in the sperm of cannabis users compared to controls is functionally important in the brain.

DLGAP2 is an imprinted gene that exhibits paternal expression in the testis, biallelic expression in the brain, and low expression elsewhere in the body [³⁰]. Because the methylation established at imprinted genes resists post-fertilization epigenetic reprogramming [⁴³–⁴⁵], this supports the possibility that changes in methylation at DLGAP2 in sperm could be transmitted to the next generation. However, given that the region in intron 7 is not an ICR, it is unlikely that this would be a potential mechanism for intergenerational inheritance of an altered methylation pattern at this region. However, it has recently been discovered that a subset of genes termed ‘escapees’ are able to escape primordial germ cell (PGC) and post-fertilization reprogramming events [⁴⁶,⁴⁷], providing a mechanism for epigenetic changes incurred by sperm to be passed on to the subsequent generation.

Processes in the PSD are sensitive to endocannabinoids [²⁶,⁴⁸–⁵¹], which suggests that these processes are potentially sensitive to exogenous cannabinoids, such as THC and cannabis. This is especially important as cannabis legalization and use are increasing dramatically across the U.S. It is estimated that 22% of American adults currently use cannabis, of which 63% are regular users (≥1–2 times per month) [⁷–¹⁰]. Among regular users 55% are males and over half of all men over 18 have reported cannabis use in their lifetime [⁷–¹⁰]. Importantly, this age range includes individuals of reproductive age. Since almost half of all pregnancies in the U.S. are unplanned, there is concern that many pregnancies may occur during a time when one, or both, parents are using or are exposed to cannabis [⁵²].

Our results provide novel findings about the effects of paternal cannabis use on the methylation status of an ASD candidate gene, a disorder whose rates continue to climb, but whose precise aetiologies remain unknown. Studies are beginning to show that there is a potential for paternal intergenerational inheritance. In particular, epigenetic changes in umbilical cord blood of babies born to obese fathers were also found in the sperm of obese men. This study is the first to demonstrate that there are changes present in the sperm epigenome of cannabis users at a gene involved in ASD.

The results of this study have several limitations. The sample size was small, which might limit generalization of the study findings. However, even though our sample size was small, we were able to identify common pathways that were differentially methylated in both human and rat sperm, highlighting the potential specificity of these effects [²⁵]. We did not account for a wide variety of potential confounders such as various lifestyle habits, sleep, diet/nutrition, exercise, etc, given that their influence on the sperm DNA methylome is largely unknown. Larger studies are required to confirm these findings. In the conceptal tissues we were only able to analyse whole brain, rather than the areas where DLGAP2 is most highly expressed such as the hippocampus and the striatum, which could have diluted the strength of the results.

Strengths of the study included that we used a highly quantitative method to confirm the methylation status that was measured by RRBS. This study was the first demonstration of the association between cannabis use and substantial hypomethylation of DLGAP2 in human sperm. Additionally, we are able to confirm a functional relationship between methylation and expression in a relevant target tissue, and have shown that the relationship between methylation and expression is weakened in males, which could bear relevance to the sexual dimorphism in the prevalence of autism. This is the first demonstration of potential heritability of altered methylation resulting from preconceptional paternal THC exposure. Given the increasing legalization and use of cannabis in the U.S., our results underscore a need for larger studies to determine the potential for heritability of DLGAP2 methylation changes in the human F1 generation and beyond. It will also be important to examine how cannabis-associated methylation changes relate to neurobehavioral phenotypes

Source:   Epigenetics. 2020; 15(1-2): 161–173.

Published online 2019 Aug 26. doi: 10.1080/15592294.2019.1656158

Source: https://www.sciencedirect.com/science/article/abs/pii/S0165032719320919 May 2020

In what is sure to be a controversial finding among cannabis users and proponents, a review of existing research published this week in The Lancet Psychiatry suggests that a single dose of THC may induce a variety of psychiatric symptoms associated with schizophrenia and other psychiatric disorders.

According to a news release issued by The Lancet on March 17:

A single dose of the main psychoactive component in cannabis, tetrahydrocannabinol (THC), can induce a range of psychiatric symptoms, according to results of a systematic review and meta-analysis of 15 studies including 331 people with no history of psychotic or other major psychiatric disorders, published in The Lancet Psychiatry journal.

The study was funded by the Medical Research Council and was conducted by researchers from Kings College London, South London and the Maudsley NHS Foundation Trust, Imperial College London, Leiden University Medical Hospital, Yale University School of Medicine, Connecticut Mental Health Center, and VA Connecticut Healthcare System.

The study also notes that these psychiatric symptoms are not associated with cannabidiol (CBD), one of the other major active compounds in cannabis. The authors reviewed four studies examining CBD’s effects on the development of the same psychiatric symptoms, and no significant differences were found between the effects of CBD and the effects of a placebo. “In studies that focused on whether CBD counters THC-induced symptoms, one study identified reduced symptoms, using a modest sample, but three larger studies failed to replicate this finding.”

The aforementioned news release quotes King’s College professor Oliver Howes as saying, “As the THC-to-CBD ratio of street cannabis continues to increase, it is important to clarify whether these compounds can cause psychotic symptoms. Our finding that THC can temporarily induce psychiatric symptoms in healthy volunteers highlights the risks associated with the use of THC-containing cannabis products. This potential risk should be considered in discussions between patients and medical practitioners thinking about using cannabis products with THC. This work will also inform regulators, public health initiatives, and policy makers considering the medical use of THC-containing cannabis products or their legalisation for recreational use.” 

There’s an important distinction to note here. Although the researchers found that a dose of THC—which they say is roughly equivalent to a single joint—can induce symptoms that mimic those of certain psychiatric disorders, THC does not in fact cause said disorders in users. 

This will come as little surprise to cannabis users, who are well aware from decades of anecdotal evidence that smoking a joint can make some people a little paranoid, but it has certainly never made anyone schizophrenic.

To put things in perspective, consider that in a commentary he wrote for the Straight last August, author and activist Dana Larsen noted that “every analysis of relative drug harms lists cannabis as one of the safest psychoactive substances there is.”

You can read the paper, which is title “Psychiatric symptoms caused by cannabis constituents: a systematic review and meta-analysis”, at the Lancet Psychiatry website.

Source:  https://www.straight.com/cannabis/1374471/review-studies-suggests-thc-cannabis-could-induce-psychotic-symptoms-healthy-people  19^th March 2020

A meta-analysis of all studies worldwide showing association between marijuana use and schizophrenia:

Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319–328.
http://dirwww.colorado.edu/alcohol/downloads/Cannabis_and_behavior.pdf

“There was an increased risk of any psychotic outcome in individuals who had ever used cannabis…with greater risk in people who used cannabis most frequently. There is now sufficient evidence to warn young people that using cannabis could increase their risk of
developing a psychotic illness later in life.”

The most recent study conducted in the United States (Columbia University, New York), showing a high risk (odds ratio, “OR”) for schizophrenia spectrum disorders, particularly in those who become cannabis-dependent:

Davis GP, Compton MT, Wang S, Levin FR, Blanco C. Association between cannabis use, psychosis, and schizotypal personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Schizophr Res. 2013 Dec;151(1-3):197-202.
“There was a similar dose-response relationship between the extent of cannabis use and schizotypal personality disorder (OR=2.02 for lifetime cannabis use, 95% CI 1.69-2.42; OR=2.83 for lifetime cannabis abuse, 95% CI 2.33-2.43; OR=7.32 for lifetime cannabis dependence, 95% CI 5.51-9.72). Likelihood of individual schizotypal features increased significantly with increased extent of cannabis use in a dose-dependent manner.”

Studies that corrected for general genetic background effects and many non-cannabis environmental variables by comparing siblings. The risk ratios are somewhat lower than general population studies, because genetic predisposition is more or less controlled for:

McGrath J, Welham J, Scott J, Varghese D, Degenhardt L, Hayatbakhsh MR, Alati R, Williams GM, Bor W, Najman JM. Association between cannabis use and psychosis-related outcomes using sibling pair analysis in a cohort of young adults. Arch Gen Psychiatry. 2010; 67(5):440-7.
“Longer duration since first cannabis use was associated with multiple psychosis-related outcomes in young adults… the longer the duration since first cannabis use, the higher the risk of psychosis-related outcomes…
Compared with those who had never used cannabis, young adults who had 6 or more years since first use of cannabis (i.e., who commenced use when around 15 years or younger) were twice as likely to develop a nonaffective psychosis…
This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.”

Giordano GN, Ohlsson H, Sundquist K, Sundquist J, Kendler KS. The association between cannabis abuse and subsequent schizophrenia: a Swedish national co-relative control study.
Psychol Med. 2014 Jul 3:1-8. [Epub ahead of print]
http://journals.cambridge.org/download.php?file=%2FPSM%2FS0033291714001524a.pdf&code=79f795824a92c8eead870197ef071dd8

“Allowing 7 years from initial CA registration to later diagnosis, the risk for schizophrenia in discordant full sibling pairs remained almost twofold….The results of this study therefore lend support to the etiologic hypothesis, that CA is one direct cause of later schizophrenia.”

Those diagnosed with schizophrenia who also use recreational drugs are much more likely to be violent, including those who use cannabis:

Fazel S, Långström N, Hjern A, Grann M, Lichtenstein P. Schizophrenia, substance abuse, and violent crime. JAMA. 2009 May 20;301(19):2016-23.
“The risk was mostly confined to patients with substance abuse comorbidity (of whom 27.6% committed an offense), yielding an increased risk of violent crime among such patients (adjusted OR, 4.4; 95% CI,3.9-5.0), whereas the risk increase was small in schizophrenia patients without substance abuse comorbidity (8.5% of whom had at least 1 violent offense; adjusted OR,1.2; 95% CI, 1.1-1.4; P<0.001 for interaction).”

Fazel S, Gulati G, Linsell L, Geddes JR, Grann M. Schizophrenia and violence: systematic review and meta-analysis. PLoS Med. 2009 Aug;6(8):e1000120. doi: 10.1371/journal.pmed.1000120. Epub 2009 Aug 11.
“The effect of comorbid substance abuse was marked with….. an OR of 8.9” (as compared to the general population)

Arseneault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin Study. Arch Gen Psychiatry. 2000;57(10):979-86.
“for having more than two of these disorders at once…..the OR (odds ratio for violence) was, …..for marijuana dependence plus schizophrenia spectrum disorder, 18.4”

Harris AW, Large MM, Redoblado-Hodge A, Nielssen O, Anderson J, Brennan J. Clinical and cognitive associations with aggression in the first episode of psychosis. Aust N Z J Psychiatry. 2010 Jan;44(1):85-93.
‘The use of cannabis with a frequency of more than fourfold in the previous month was the only factor that was found to be associated with serious aggression’

Self-report of psychotic symptoms by otherwise healthy users (12% to 15%):

Thomas H. A community survey of adverse effects of cannabis use. Drug Alcohol Depend. 1996 Nov;42(3):201-7.
“This survey estimates the frequency of various adverse effects of the use of the drug cannabis. A sample of 1000 New Zealanders aged 18-35 years were asked to complete a self-administered questionnaire on cannabis use and associated problems. The questionnaire was derived from criteria for the identification of cannabis abuse which are analagous to criteria commonly used to diagnose alcoholism. Of those who responded 38% admitted to having used cannabis. The most common physical or mental health problems, experienced by 22% of users were acute anxiety or panic attacks following cannabis use. Fifteen percent reported psychotic symptoms following use.”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%).”

Barkus EJ, Stirling J, Hopkins RS, Lewis S.. Cannabis-induced psychosis-like experiences are associated with high schizotypy Psychopathology 2006;39(4):175-8.
“In the sample who reported ever using cannabis (72%) the means for the subscales from the CEQ were as follows: ……Psychotic-Like Experiences (12.98%).”

Rates of psychotic symptoms in those with cannabis dependence as compared to non-dependent users and nonusers:

Fergusson DM, Horwood LJ, Swain-Campbell NR. Cannabis dependence and psychotic symptoms in young people. Psychol Med. 2003 Jan;33(1):15-21.
“Young people meeting DSM-IV criteria for cannabis dependence had elevated rates of psychotic symptoms at ages 18 (rate ratio = 3.7; 95% CI 2.8-5.0; P < 0.0001) and 21 (rate ratio = 2.3; 95% CI 1.7-3.2; P < 0.0001).”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“more than half of the respondents who were dependent on cocaine (80%), cannabis (63.5%), amphetamines (56.1%), and opiates (53.1%) reported psychotic symptoms. Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%)……. There was also a marked increase in the risk for psychotic symptoms when dependence became moderate or severe for cannabis (OR=25.1, OR=26.8; respectively).”

Studies on the psychotomimetic properties of THC administered to healthy individuals in the clinic:

D’Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH. The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis. Neuropsychopharmacology. 2004 Aug;29(8):1558-72.
“∆-9-THC (1) produced schizophrenia-like positive and negative symptoms; (2) altered perception;(3) increased anxiety; (4) produced euphoria; (5) disrupted immediate and delayed word recall, sparing recognition recall; (6) impaired performance on tests of distractibility, verbal fluency, and working memory (7) did not impair orientation; (8) increased plasma cortisol. These data indicate that D-9-THC produces a broad range of transient symptoms, behaviors, and cognitive deficits in healthy individuals that resemble some aspects of endogenous psychoses.”

Morrison PD, Nottage J, Stone JM, Bhattacharyya S, Tunstall N, Brenneisen R, Holt D, Wilson D, Sumich A, McGuire P, Murray RM, Kapur S, Ffytche DH. Disruption of frontal θ coherence by ∆9-tetrahydrocannabinol is associated with positive psychotic symptoms. Neuropsychopharmacology. 2011;;36(4):827-36.
“Compared with placebo, THC evoked positive and negative psychotic symptoms, as measured by the positive and negative syndrome scale (p<0.001)…… The results reveal that the pro-psychotic effects of THC might be related to impaired network dynamics with impaired communication between the right and left frontal lobes.”

Bhattacharyya S, Crippa JA, Allen P, Martin-Santos R, Borgwardt S, Fusar-Poli P, Rubia K, Kambeitz J, O’Carroll C, Seal ML, Giampietro V, Brammer M, Zuardi AW, Atakan Z, McGuire PK. Induction of psychosis by ∆9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing. Arch Gen Psychiatry. 2012 Jan;69(1):27-36. doi: 10.1001/archgenpsychiatry.2011.161.
“Pairwise comparisons revealed that 9-THC significantly increased the severity of psychotic symptoms compared with placebo (P<.001) and CBD (P<.001).”,

Freeman D, Dunn G, Murray RM, Evans N, Lister R, Antley A, Slater M, Godlewska B, Cornish R, Williams J, Di Simplicio M, Igoumenou A, Brenneisen R, Tunbridge EM, Harrison PJ, Harmer CJ, Cowen P, Morrison PD. How Cannabis Causes Paranoia: Using the Intravenous Administration of ∆9-Tetrahydrocannabinol (THC) to Identify Key Cognitive Mechanisms Leading to Paranoia. Schizophr Bull. 2014 Jul 15. pii: sbu098. [Epub ahead of print]
“THC significantly increased paranoia, negative affect (anxiety, worry, depression, negative thoughts about the self), and a range of anomalous experiences, and reduced working memory capacity.”

For data on dose-response (a very large study by Zammit et al., and another by van Os et al.) and the greater risk for psychosis posed by high strength marijuana (DiForti et al.):

Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G, 2002, Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ. 2002 Nov 23;325(7374):1199. http://www.bmj.com/content/325/7374/1199.full.pdf
“We found a dose dependent relation between frequency of cannabis use and risk of schizophrenia, with an adjusted odds ratio for linear trend across the categories of frequency of cannabis use used in this study of 1.2 (1.1 to 1.4, P < 0.001). The adjusted odds ratio for subjects with a history of heaviest use of cannabis ( > 50 occasions) was 3.1 (1.7 to 5.5)………………Cannabis use is associated with an increased risk of
developing schizophrenia, consistent with a causal relation. This association is not explained by use of other psychoactive drugs or personality traits relating to social integration.”

van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol. 2002 Aug 15;156(4):319-27.
“…..further evidence supporting the hypothesis of a causal relation is demonstrated by the existence of a dose-response relation.. between cumulative exposure to cannabis use and the psychosis outcome……. About 80 percent of the psychosis outcome associated with exposure to both cannabis and an established vulnerability to psychosis was attributable to the synergistic action of these two factors. This finding indicates that, of the subjects exposed to both a vulnerability to psychosis and cannabis use, approximately 80 percent had the psychosis outcome because of the combined action of the two risk factors and only about 20 percent because of the action of either factor alone.”

DiForti M, Morgan C, Dazzan P, Pariante C, Mondelli V, Marques TR, Handley R, Luzi S, Russo M, Paparelli A, Butt A, Stilo SA, Wiffen B, Powell J, Murray RM. High-potency cannabis and the risk of psychosis. Br J Psychiatry. 2009,195(6):488-91.
“78% (n = 125) of the cases group preferentially used sinsemilla (skunk) compared with only 31% (n = 41) of the control group (unadjusted OR= 8.1, 95% CI 4.6–13.5). This association was only slightly attenuated after controlling for potential confounders (adjusted OR= 6.8, 95% CI 2.6–25.4)………. Our most striking finding is that patients with a first episode of psychosis preferentially used high-potency cannabis preparations of the sinsemilla (skunk) variety…… our results suggest that the potency and frequency of cannabis use may interact in further increasing the risk of psychosis.”

DiForti M, Marconi A, Carra E, Fraietta S, Trotta A, Bonomo M, Bianconi F, Gardner-Sood P, O’Connor J, Russo M, Stilo SA, Marques TR, Mondelli V, Dazzan P, Pariante C, David AS, Gaughran F, Atakan Z, Iyegbe C, Powell J, Morgan C, Lynskey M, Murray RM. Proportion of
patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study. Lancet Psychiatry, online February 18, 2015, http://dx.doi.org/10.1016/S2215-0366(14)00117-5.
“In the present larger sample analysis, we replicated our previous report and showed that the highest probability to suffer a psychotic disorder is in those who are daily users of high potency cannabis. Indeed, skunk use appears to contribute to 24% of cases of first episode psychosis in south London. Our findings show the importance of raising awareness among young people of the risks associated with the use of high-potency cannabis. The need for such public education is emphasised by the worldwide trend of liberalisation of the legal constraints on cannabis and the fact that high potency varieties are becoming much more widely available.”

For data on percent of those with marijuana-induced psychosis who go on to receive a diagnosis of a schizophrenia spectrum disorder:

Arendt M, Mortensen PB, Rosenberg R, Pedersen CB, Waltoft BL. Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia. Arch Gen Psychiatry. 2008;65(11):1269-74. http://archpsyc.ama-assn.org/cgi/reprint/65/11/1269
“Approximately half of the subjects who received treatment of a cannabis induced psychosis developed a schizophrenia spectrum disorder within 9 years after treatment…… The risk of schizophrenia after a cannabis-induced psychosis is independent of familial predisposition……. cannabis-induced psychosis may not be a valid diagnosis but an early marker of schizophrenia……. Psychotic symptoms after cannabis
use should be taken extremely seriously.”

Niemi-Pynttäri JA, Sund R, Putkonen H, Vorma H, Wahlbeck K, Pirkola SP. Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. J Clin Psychiatry. 2013 74(1):e94-9.
“Eight-year cumulative risk to receive a schizophrenia spectrum diagnosis was 46% for persons with a diagnosis of cannabis-induced psychosis ….. chances for amphetamine-, hallucinogen-, opioid-, sedative- and alcohol-induced (schizophrenia spectrum diagnoses) were 30%, 24%, 21%, and 5% respectively.”

For cause and effect (which comes first: psychosis or marijuana use):
Arseneault L, Cannon M, Poulton R, Murray R, Caspi A, Moffitt TE, 2002, Cannabis use in
adolescence and risk for adult psychosis: longitudinal prospective study.BMJ. 2002 Nov 23;325(7374):1212-3.
“Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis. Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). Thirdly, risk was specific to cannabis use, as opposed to use of other drugs….”

Henquet C, Krabbendam L, Spauwen J, et al. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ. 2005;330:11–15. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC539839/pdf/bmj33000011.pdf
“Exposure to cannabis during adolescence and young adulthood increases the risk of psychotic symptoms later in life. Cannabis use at baseline increased the cumulative incidence of psychotic symptoms at follow up four years later…but has a much stronger effect in those with evidence of predisposition for psychosis……….Predisposition for psychosis at baseline did not significantly predict cannabis use four years later..”

and also:

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: d738 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021)…………There was no evidence for self medication effects, as psychotic experiences at T2 did not predict incident cannabis use between T2 and T3 (0.8, 0.6 to 1.2; P=0.3).”

For data on those who quit using when psychotic symptoms develop (further evidence against self-medication):

Fergusson DM, Horwood LJ, Ridder EM. Tests of causal linkages between cannabis use and psychotic symptoms. Addiction. 2005;100(3):354-66.

For degree of risk relative to other drugs:

Niemi-Pynttäri JA, Sund R, Putkonen H, Vorma H, Wahlbeck K, Pirkola SP. Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. J Clin Psychiatry. 2013 74(1):e94-9.
“Eight-year cumulative risk to receive a schizophrenia spectrum diagnosis was 46% for persons with a diagnosis of cannabis-induced psychosis ….. chances for amphetamine-, hallucinogen-, opioid-, sedative- and alcohol-induced (schizophrenia spectrum diagnoses) were 30%, 24%, 21%, and 5% respectively.”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“more than half of the respondents who were dependent on cocaine (80%), cannabis (63.5%), amphetamines (56.1%), and opiates (53.1%) reported psychotic symptoms. Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%)……. There was also a marked increase in the risk for psychotic symptoms when dependence became moderate or severe for cannabis (OR=25.1, OR=26.8; respectively).”

Another angle on the potential confound of self-medication: genetic predisposition for schizophrenia does not predict cannabis use:

Veling W, Mackenbach JP, van Os J, Hoek HW. Cannabis use and genetic predisposition for schizophrenia: a case-control study. Psychol Med. 2008 Sep;38(9):1251-6. Epub 2008 May 19.
“BACKGROUND: Cannabis use may be a risk factor for schizophrenia. RESULTS: Cannabis use predicted schizophrenia [adjusted odds ratio (OR) cases compared to general hospital controls 7.8, 95% confidence interval (CI) 2.7-22.6; adjusted OR cases compared to siblings 15.9 (95% CI 1.5-167.1)], but genetic predisposition for schizophrenia did not predict cannabis use [adjusted OR intermediate predisposition
compared to lowest predisposition 1.2 (95% CI 0.4-3.8)].”

For data on potential benefits of cessation:

González-Pinto A, Alberich S, Barbeito S, Gutierrez M, Vega P, Ibáñez B, Haidar MK, Vieta E, Arango C. Cannabis and first-episode psychosis: different long-term outcomes depending on continued or discontinued use. Schizophr Bull. 2011 May;37(3):631-9. Epub 2009 Nov 13. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080669/pdf/sbp126.pdf
“OBJECTIVE: To examine the influence of cannabis use on long-term outcome in patients with a first psychotic episode, comparing patients who have never used cannabis with (a) those who used cannabis before the first episode but stopped using it during follow-up and (b) those who used cannabis both before the first episode and during follow-up….. CONCLUSION: Cannabis has a deleterious effect, but stopping use after the first psychotic episode contributes to a clear improvement in outcome. The positive effects of stopping cannabis use can be seen more clearly in the long term.”

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“The finding that longer exposure to cannabis was associated with greater risk for persistence of psychotic experiences is in line with an earlier study showing that continued cannabis use over time increases the risk for psychosis in a dose-response fashion. This is also in agreement with the hypothesis that a process of sensitisation might underlie emergence and persistence of psychotic experiences as an indicator of liability to psychotic disorder.”

For data on marijuana use resulting in an earlier age of onset of schizophrenia (suggestive of causality), see Dragt et al. and a meta-analysis (see Large et al.,); also: a very extensive (676 schizophrena patients) and therefore more statistically powered analysis (see DeHert paper); two papers showing that the age-of-onset effect may be specific to those without a family history (see Scherr et al. and Leeson et al., papers); two studies that evaluate the age of onset specific to gender (Veen et al. and Compton et al. ) which is important because comparing across genders can be confounded by the greater tendency of males to engage in risky behavior (the conclusions are not the same in terms of gender; the gender distribution was slightly better in the Veen et al. study) and finally, two papers of relevance to specificity of age of onset effect to cannabis, a meta-analysis of published studies on age of onset that shows another drug of abuse (tobacco) is not associated with
a decreased age of onset (Myles et al.) and a study showing that ecstasy, LSD, stimulants, or sedatives did not have an effect to lower age of onset whereas cannabis use did (Barnes et al.) :

Large M, Sharma S, Compton MT, Slade T, Nielssen O. Cannabis Use and Earlier Onset of Psychosis: A Systematic Meta-analysis. Arch Gen Psychiatry. 2011 68(6):555-61. http://www.ncbi.nlm.nih.gov/pubmed/21300939
“The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.”

Dragt S, Nieman DH, Schultze-Lutter F, van der Meer F, Becker H, de Haan L, Dingemans PM, Birchwood M, Patterson P, Salokangas RK, Heinimaa M, Heinz A, Juckel G, Graf von Reventlow H, French P, Stevens H, Ruhrmann S, Klosterkötter J, Linszen DH; on behalf of the EPOS group.Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Acta Psychiatr Scand. 2011 Aug 29. doi: 10.1111/j.1600-0447.2011.01763.x. [Epub ahead of print]
“Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Objective: Numerous studies have found a robust association between cannabis use and the onset of psychosis. Nevertheless, the relationship between cannabis use and the onset of early (or, in retrospect, prodromal) symptoms of psychosis remains unclear. The study focused on investigating the relationship between cannabis
use and early and high-risk symptoms in subjects at clinical high risk for psychosis. Results: Younger age at onset of cannabis use or a cannabis use disorder was significantly related to younger age at onset of six symptoms (0.33 < r(s) < 0.83, 0.004 < P < 0.001). Onset of cannabis use preceded symptoms in most participants. Conclusion: Our results provide support that cannabis use plays an important role in the development of psychosis in vulnerable individuals.”

De Hert M, Wampers M, Jendricko T, Franic T, Vidovic D, De Vriendt N, Sweers K, Peuskens J, van Winkel R.Effects of cannabis use on age at onset in schizophrenia and bipolar disorder. Schizophr Res. 2011 Mar;126(1-3):270-6.

“BACKGROUND: Cannabis use may decrease age at onset in both schizophrenia and bipolar disorder, given the evidence for substantial phenotypic and genetic overlap between both disorders….RESULTS:… Both cannabis use and a schizophrenia diagnosis predicted earlier age at onset. There was a significant interaction between cannabis use and diagnosis, cannabis having a greater effect in bipolar patients….DISCUSSION:…. Our results suggest that cannabis use is associated with a reduction in age at onset in both schizophrenic and bipolar patients. This reduction seems more pronounced in the bipolar group than in the schizophrenia group: the use of cannabis reduced age at onset by on average 8.9 years in the bipolar group, as compared to an average predicted reduction of 1.5 years in the schizophrenia group.”

Scherr M, Hamann M, Schwerthöffer D, Froböse T, Vukovich R, Pit schel-Walz G, Bäuml J.. Environmental risk factors and their impact on the age of onset of schizophrenia: Comparing familial to non-familial schizophrenia. Nord J Psychiatry. 2011 Aug 31. [Epub ahead of print]
“Background and aims: Several risk factors for schizophrenia have yet been identified. The aim of our study was to investigate how certain childhood and adolescent risk factors predict the age of onset of psychosis in patients with and without a familial component (i.e. a relative with schizophrenia or schizoaffective disorder). Results: Birth complications and cannabis abuse are predictors for an earlier onset of schizophrenia in patients with non-familial schizophrenia. No environmental risk factors for an earlier age of onset in familial schizophrenia have been identified.”

Leeson VC, Harrison I, Ron MA, Barnes TR, Joyce EM. The Effect of Cannabis Use and Cognitive Reserve on Age at Onset and Psychosis Outcomes in First-Episode Schizophrenia. Schizophr Bull. 2011 Mar 9. [Epub ahead of print] http://schizophreniabulletin.oxfordjournals.org/content/early/2011/03/09/schbul.sbq153.full.pdf+html
“Objective: Cannabis use is associated with a younger age at onset of psychosis, an indicator of poor prognosis, but better cognitive function, a positive prognostic indicator. We aimed to clarify the role of age at onset and cognition on outcomes in cannabis users with first-episode schizophrenia as well as the effect of cannabis dose and cessation of use……Conclusions: Cannabis use brings forward the onset of psychosis in people who otherwise have good prognostic features indicating that an early age at onset can be due to a toxic action of cannabis rather than an intrinsically more severe illness. Many patients abstain over time, but in those who persist, psychosis is more difficult to treat.”

Veen ND, Selten JP, van der Tweel I, Feller WG, Hoek HW, Kahn RS. Cannabis use and age at onset of schizophrenia. Am J Psychiatry. 2004 Mar;161(3):501-6. http://ajp.psychiatryonline.org/cgi/reprint/161/3/501
“The results indicate a strong association between use of cannabis and earlier age at first psychotic episode in male schizophrenia patients.”

Compton MT, Kelley ME, Ramsay CE, Pringle M, Goulding SM, Esterberg ML, Stewart T, Walker EF. Association of pre-onset cannabis, alcohol, and tobacco use with age at onset of prodrome and age at onset of psychosis in first-episode patients. Am J Psychiatry. 2009 Nov;166(11):1251-7. Epub 2009 Oct 1. http://ajp.psychiatryonlie.org/cgi/reprint/166/11/1251
“Whereas classifying participants according to maximum frequency of use prior to onset (none, ever, weekly, or daily) revealed no significant effects of cannabis or tobacco use on risk of (editor’s note: “timing of”) onset, analysis of change in frequency of use prior to
onset indicated that progression to daily cannabis and tobacco use was associated with an increased risk of onset of psychotic symptoms. Similar or even stronger effects were observed when onset of illness or prodromal symptoms was the outcome. A gender-by-daily-cannabis use interaction was observed; progression to daily use resulted in a much larger increased relative risk of onset of psychosis in females than in males.”

Myles N, Newall H, Compton MT, Curtis J, Nielssen O, Large M. The age at onset of psychosis and tobacco use: a systematic meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2011 Sep 8. [Epub ahead of print]
“Unlike cannabis use, tobacco use is not associated with an earlier onset of psychosis.”

Barnes TR, Mutsatsa SH, Hutton SB, Watt HC, Joyce EM. Comorbid substance use and age at onset of schizophrenia. Br J Psychiatry. 2006 Mar;188:237-42. http://bjp.rcpsych.org/content/188/3/237.full.pdf+html
“Alcohol misuse and any substance use (other than cannabis use) were not significant in relation to age at onset….. those patients in the sample who reported that they had used cannabis had an earlier age at onset of psychosis than other patients who did not report cannabis use but who shared the same profile with regard to the other variables (e.g. comparing men who reported alcohol misuse and use of both cannabis and other drugs with men who had the same characteristics apart from the fact that they had not used cannabis).”

Data from other cultures

Sarkar J, Murthy P, Singh SP. Psychiatric morbidity of cannabis abuse. Indian J Psychiatry. 2003 Jul;45(3):182-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952166/pdf/IJPsy-45-182.pdf
“The paper evaluates the hypothesis that cannabis abuse is associated with a broad range of psychiatric disorders in India, an area with relatively high prevalence of cannabis use. Retrospective case-note review of all cases with cannabis related diagnosis over a 11 -year period, for subjects presenting to a tertiary psychiatric hospital in southern India was carried out. Information pertaining to sociodemographic, personal, social, substance-use related, psychiatric and treatment histories, was gathered. Standardized diagnoses were made according to Diagnostic Criteria for Research of the World Health Organization, on the basis of information available.Cannabis abuse is associated with
widespread psychiatric morbidity that spans the major categories of mental disorders under the ICD-10 system, although proportion of patients with psychotic disorders far outweighed those with non-psychotic disorders. Whilst paranoid psychoses were more prevalent, a significant number of patients with affective psychoses, particularly mania, was also noted.”

Rodrigo C, Welgama S, Gunawardana A, Maithripala C, Jayananda G, Rajapakse S. A retrospective analysis of cannabis use in a cohort of mentally ill patients in Sri Lanka and its implications on policy development. Subst Abuse Treat Prev Policy. 2010 Jul 8;5:16. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910013/pdf/1747-597X-5-16.pdf
”BACKGROUND: Several epidemiological studies have shown that cannabis; the most widely used illegal drug in the world, is associated with schizophrenia spectrum disorders (SSD)……. CONCLUSIONS: Self reported LTC (editor’s note: life time cannabis) use was strongly associated with being diagnosed with SSD (editor’s note: schizophrenia spectrum disorders”.

Population study showing change in incidence rate in young when drug laws are eased

Ajdacic-Gross V, Lauber C, Warnke I, Haker H, Murray RM, Rössler W. Changing incidence of psychotic disorders among the young in Zurich. Schizophr Res. 2007 Sep;95(1-3):9-18. Epub 2007 Jul 16.
“There is controversy over whether the incidence rates of schizophrenia and psychotic disorders have changed in recent decades. To detect deviations from trends in incidence, we analysed admission data of patients with an ICD-8/9/10 diagnosis of psychotic disorders in the Canton Zurich / Switzerland, for the period 1977-2005. The data was derived from the central psychiatric register of the Canton Zurich. Ex-post forecasting with ARIMA (Autoregressive Integrated Moving Average) models was used to assess departures from existing trends. In addition, age-period-cohort analysis was applied to determine hidden birth cohort effects. First admission rates of patients with psychotic
disorders were constant in men and showed a downward trend in women. However, the rates in the youngest age groups showed a strong increase in the second half of the 1990’s. The trend reversal among the youngest age groups coincides with the increased
use of cannabis among young Swiss in the 1990’s.”

Estimates of how many men aged 20-40 would have to avoid regular marijuana use for one year in order to prevent one case of schizophrenia in that same year (but for number relevant to a 20 year avoidance of schizophrenia by avoiding regular marijuana use during
20 years, divide by 20):

Hickman M, Vickerman P, Macleod J, Lewis G, Zammit S, Kirkbride J, Jones P. If cannabis caused schizophrenia–how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations. Addiction. 2009;104(11):1856-61.

“In men the annual mean NNP (number needed to prevent) for heavy cannabis and schizophrenia ranged from 2800 [90% confidence interval (CI) 2018–4530] in those aged 20–24 years to 4700 (90% CI 3114–8416) in those aged 35–39”.

Key studies interpreted to diminish the connection between marijuana and schizophrenia:

Proal AC, Fleming J, Galvez-Buccollini JA, Delisi LE. A controlled family study of cannabis users with and without psychosis. Schizophr Res. 2014 Jan;152(1):283-8.
“The results of the current study, both when analyzed using morbid risk and family frequency calculations, suggest that having an increased familial risk for schizophrenia is the underlying basis for schizophrenia in these samples and not the cannabis use. While cannabismay have an effect on theage of onset of schizophrenia it is unlikely to be the cause of illness.”

Rebuttal: Miller CL. Caution urged in interpreting a negative study of cannabis use and schizophrenia. Schizophr Res. 2014 Apr;154(1-3):119-20.
“The morbid risk reported for the relatives of the non-cannabis-using patients (Sample 3) was actually 1.4-fold higher than the cannabis using patients (Sample 4), but the study did not have enough power to statistically confirm or refute a less than 2-fold difference. An increase in sample size would be required to do so, and if the observed difference were to be confirmed, it would explain not only why the Sample 4 data fits poorly with a multigene/small environmental impact model but also would give weight to the premise that cannabis use significantly contributes to the development of this disease.”

Power RA, Verweij KJ, Zuhair M, Montgomery GW, Henders AK, Heath AC, Madden PA, Medland SE, Wray NR, Martin NG. Genetic predisposition to schizophrenia associated with increased use of cannabis. Mol Psychiatry. 2014 Jun 24. doi: 10.1038/mp.2014.51. [Epub ahead of print] http://emilkirkegaard.dk/en/wp-content/uploads/Genetic%20predisposition%20to%20schizophrenia%20associated%20with%20increased%20use%20of%20cannabis.pdf
“Our results show that to some extent the association between cannabis and schizophrenia is due to a shared genetic aetiology across common variants. They suggest that individuals with an increased genetic predisposition to schizophrenia are
both more likely to use cannabis and to use it in greater quantities.”

Rebuttal: Had this paper been titled “The causal genes for schizophrenia have been discovered” it would never have been published. In the absence of a consistent finding of genes of major effect size for schizophrenia, this study of inconsistently associated genes of low effect size is meaningless.

Buchy L, Perkins D, Woods SW, Liu L, Addington J. Impact of substance use on conversion to psychosis in youth at clinical high risk of psychosis. Schizophrenia Res 156 (2-3): 277–280.
“Results revealed that low use of alcohol, but neither cannabis use nor tobacco use at baseline, contributed to the prediction of psychosis in the CHR sample”.
Rebuttal: The study was small in size and the age range of their subjects at study onset was large (12 to 31) which included both subjects that had not reached the peak age of risk for schizophrenia even by the end of the study as well as subjects who were well past the peak age of onset of schizophrenia. The fact that the study screened out psychotic individuals was problematic for the latter group, in that those who were most vulnerable to the psychosis inducing effects of cannabis would already have converted to psychosis by that age.

Overview of Key Public Health Issues Regarding the Mental Health Effects of Marijuana

For the monetary cost of schizophrenia to the U.S. annually ($63 billion in 2002 dollars):

Wu EQ, Birnbaum HG, Shi L, Ball DE, Kessler RC, Moulis M, Aggarwal J. The economic burden of schizophrenia in the United States in 2002. J Clin Psychiatry. 2005 Sep;66(9):1122-9.

For the trends in adolescent drug, alcohol and cigarette use, showing an upward tick in marijuana use as medical marijuana has become more prevalent, and that the mind-altering drug legal for adults (alcohol) is still more commonly used by teens than is marijuana:

Johnston, L. D., O’Malley, P. M., Bachman, J. G., & Schulenberg, J. E. (2012). Monitoring the Future national results on adolescent drug use: Overview of key findings, 2011. Ann Arbor, MI: Institute for Social Research, The University of Michigan.

For a summary of Sweden’s drug law experience:
Hallam C., 2010, Briefing paper 20, The Beckley Foundation: What Can We Learn from Sweden’s Drug Policy Experience? www.beckleyfoundation.org/pdf/BriefingPaper_20.pdf
“in the case of Sweden, the clear association between a restrictive drug policy and low levels of drug use is striking. In his foreword to the article on Sweden’s Successful Drug Policy, Antonio Maria Costa is frank enough to confess that, “It is my firm belief that the generally positive situation of Sweden is a result of the policy that has been applied to address the problem”.

For data showing the relationship between drug enforcement policies in Europe and drug use, such that Sweden has a zero tolerance policy on drugs and has one of the lowest rates of “last month use” in Europe (1%), 4-fold lower than the Netherlands and 7-fold lower than Spain and Italy, two countries that have liberalized their enforcement policies so that marijuana possession carries no substantive penalty.

European Monitoring Centre for Drugs and Addiction, 2012 Annual report
http://www.emcdda.europa.eu/attachements.cfm/att_190854_EN_TDAC12001ENC_.pdf

Source: Microsoft Word – 2015- Summary of literature on marijuana and psychosis.doc (momsstrong.org) January 2016

Alex Azar
Secretary of Health and Human Services
US Department of Health and Human Services
200 Independence Avenue SW
Washington D.C, 20201
November 5, 2019

Dear Secretary Azar:
This letter is to bring to your attention a study underway at the University of Washington referred to as the “Moms and Marijuana Study” and granted under the title: “Olfactory Activation and Brain Development in Infants with Prenatal Cannabis Exposure.” The Office of Human Research Protections issued a decision against opening a case on this research, and we are asking you, as the Secretary of Health and Human Services, to overturn that decision based on the scientific concerns we outline in this letter.

Women who are in their first trimester of a pregnancy, who are frequent users of marijuana for morning sickness, are being recruited. The study seeks to assess the damage marijuana prenatal exposure may have on the babies by means of various testing, including an MRI scan of the infants at six months of age. The recruited women will receive $300.00 + for their participation. The study is solely funded by NIDA. This study calls into question serious issues over human rights and raises ethical questions, including mandatory reporting pertaining to substance abuse in pregnancy. This open letter seeks to gather support from you in seeing that this study is re-evaluated at the federal level. The study’s website is at the following link: https://depts.washington.edu/klab/infoMM.html

We are of the view that the Kleinhans study does not meet the requirements set forth by the Office of Human Research Protections (https://www.hhs.gov/ohrp/regulations-and-policy/regulations/45-cfr46/ ): “Subpart B presumption that pregnant women may be included in research, provided certain conditions are met. According to Subpart B, the permissibility of research with pregnant women hinges on a judgment of the potential benefits and risks of the research. Approval of proposed research carrying no “prospect of direct benefit” to the woman or fetus requires that the risk to the fetus be judged “not greater than minimal”. Fetal risk that exceeds that standard is permissible only when the proposed research offers a prospect of direct benefit to the pregnant woman, the fetus, or both.

Notably, if the proposed research does not fit within either of those two parameters, Subpart B offers an additional mechanism at the national level for approval by the Secretary of Health and Human Services.”

The federal definition of minimum risk reads: “That the magnitude and probability of harm or discomfort anticipated in the research are not greater in and of themselves than those ordinarily encountered in daily life or during the performance of routine physical or psychological examinations or tests.” Although the primary harm at issue is exposure to marijuana, the use of MRI or fMRI has not yet been proven safe for otherwise healthy infants, where an unknown risk would come with no benefit, as there is no diagnosis being sought. The UW study consent form reads on page 3:“There are no known side effects associated with MRI or fMRI when earphones are used to protect your hearing.” …. “There may be risks associated with the use of magnetic resonance which are not known at this time.” It is precisely questions about the potential for MRI risks that should be investigated in an animal model first. In principle, any study that recruits subjects and then tracks the consequences of drug transfer to a developing fetus should be carried out in animal models first, and not in humans until the animal results point towards safety. The evidence of decades of research on marijuana in pregnancy does not point to safety but rather to risk and harm.

Two basic principles in bioethics are relied upon to determine the merit of research that involves human subjects: Is the study necessary and can the research be done without the use of human subjects? There now exists a significant body of scientific evidence that warrants and justifies warning women not to use marijuana products at pre-conception, while pregnant, or breast-feeding. The University of Washington study is not necessary to conclude that marijuana use is associated with risk to the child (and also the mother). The National Academies, a lead authority, concluded in a scientific literature review in 2017: There is substantial evidence of a statistical association between maternal cannabis smoking and lower birth weight of the offspring. Studies have already shown that prenatal use is associated with a 50 percent increased likelihood of low birth weight. The Surgeon General’s advisory of August 29, 2019 is also relied upon here. What is the “necessity” that this study addresses? The conclusion has already been made by the findings of science – pregnant women should refrain from marijuana use in order to protect the life and health of their child.

Yet, in spite of existing scientific literature of concern, a highly misleading recruitment statement appears on the University of Washington study’s website introductory page: “We do not expect to find anything of medical concern during the infant MRI scans…If you’re interested in helping us learn more about whether cannabis is safe to use for morning sickness, click the Sign Up button and let us know!” Their lack of concern about the potential for adverse medical outcomes directly contradicts the findings of Grewen et al. (2015) which similarly evaluated postnatal outcomes using MRI scans on infants that had been exposed to marijuana in utero. As compared to controls, the exposed infants showed hypoconnectivity between brain regions: ” Marijuana-specific differences were observed in insula and three striatal connections: anterior insula–cerebellum, right caudate–cerebellum, right caudate–right fusiform gyrus/inferior occipital, left caudate–cerebellum. +MJ neonates had hypo-connectivity in all clusters compared with −MJ and CTR groups.” While an imperfect study because the cases included a proportion of women in the case group who used not only marijuana but also alcohol, tobacco, opiates and SSRIs, one of the two control groups was matched to the cases for use of those drugs, while the other was completely drug free. Notably, work in an animal model by Tortoriello et al. (2014) presents a plausible mechanism for the observed effect of marijuana seen between cases and controls. The combined evidence points towards harm, and confirmation could easily be sought in an animal model that parallels the intent of the University of Washington study.

Furthermore, the ethics are clearly different between the Kleinhans et al. and Grewen et al. studies, because unlike the protocol for the former, the study of Grewen et al. did not recruit women while the fetus was developing but recruited shortly before or after the time of birth. Being unaware of marijuana use until the time of birth, the researchers could not intervene to encourage abstinence for the sake of the fetus, whereas the University of Washington team could intervene, but their protocols do not allow them to. As a further point of distinction, the University of Washington protocol states that infants enrolled in the study will be screened and excluded if they have been in an NICU for 24 hours. This will, for obvious reasons, result in a biased outcome in reporting overall harm from marijuana use during pregnancy.

Typical morning sickness affects up to 91% of pregnancies (Castillo and Phillippi, 2015), and is regarded by many medical practitioners as being a reflex protecting against consumption of dangerous foods or beverages, as well as a sign of a healthy pregnancy because the absence of morning sickness is associated with a higher rate of miscarriage (reviewed by Sherman and Flaxman, 2002). The rare condition when morning sickness becomes pathologic, hyperemesis gravidarum, affects on average 1.1% of pregnancies, and is defined as a loss of 5% or more of the pre-pregnancy weight (Castillo and Phillippi, 2015). Maintenance of fluid and electrolyte balance may become problematic in this situation and pharmacologic intervention may become necessary, both for the health of the mother and the baby. To date, the serious documented outcomes include an increased risk for preterm births and low birth weight (Dodds et al., 2006).

Thus, if the Kleinhans study were to be proposing to recruit only those with hyperemesis gravidarum, the ethics might be more favorable. They would, however, have to exclude women whose marijuana use may have triggered the hyperemesis, which may occur in a subset of pregnant users (Alaniz et al., 2015). The study recruitment website is definitely remiss in not making that possibility clear to those interested in enrolling, and the research protocol describes no effort to ascertain if marijuana might be triggering hyperemesis in their study subjects.

In summary, there is already sufficient scientific evidence to answer the question as to whether or not marijuana is safe to use for typical morning sickness. That answer is no. Please see additional references for numerous research publications showing harm at the end of this letter.
Complaints have been filed with NIDA, The University of Washington, The World Medical Association regarding the Helsinki Declaration, The Office of Human Research Protections, and two doctors have filed a human rights complaint on behalf of the children involved. Complaint documents will be forwarded on request.

Thank you for your time in reviewing this serious situation.

Best regards,
Pamela McColl
Child Rights Activist
pjmccoll@shaw.ca

and

Christine L. Miller, Ph.D.
Neuroscientist
MillerBio
6508 Beverly Rd
Baltimore, Maryland 21239
cmiller@millerbio.com

et al.

Correspondence with the OHRP in regards to the University of Washington study began in September
of 2019. On October an email was received from the OHRP to Pamela McColl:
October 25, 2019

Hello,
OHRP has reviewed the study and will not be opening a case.
Sincerely,
Division of Compliance Oversight OHRP

September 25, 2019
“OHRP is now reviewing your complaint and this study. We are currently gathering the information about the research being conducted before a full review is started. Once OHRP completes a full review of the study, the research conducted and the study’s approval process, we will contact you with our findings. Please remember, this does not mean you can’t contact OHRP again before we finish the full review. You can contact us using this email address to update your complaint at any time.
Thank-you,
Division of Compliance Oversight (OHRP)

September 17, 2019
Thank you for contacting the Office for Human Research Protections (OHRP). OHRP has responsibility for oversight of compliance with the U.S. Department of Health and Human Services (HHS) regulations for the protection of human research subjects (see 45 CFR Part 46 at
www.hhs.gov/ohrp/regulations-and-policy/guidance/index.html

In carrying out this responsibility, OHRP reviews allegations of noncompliance involving human subject research projects conducted or supported by HHS or that are otherwise subject to the regulations, and determines whether to conduct a for-cause compliance evaluation. For further details see OHRP’s guidance, “Compliance Oversight Procedures for Evaluating Institutions,” at www.hhs.gov/ohrp/compliance-and-reporting/evaluating-institutions/index.html.

OHRP has jurisdiction only if the allegations involve human subject research (a) conducted or supported by HHS, or (b) conducted at an institution that voluntarily applies its Assurance of Compliance to all research regardless of source of support. Since this requirement appears to be met by the circumstances described in your email, OHRP appears to have jurisdiction.
Sincerely,
Division of Compliance Oversight
cc. Surgeon General Jerome Adams
cc. Director NIDA Dr. Nora Volkow

In-text citations:
Alaniz VI, Liss J, Metz TD, Stickrath E. Cannabinoid hyperemesis syndrome: a cause of refractory nausea and vomiting in pregnancy. Obstet Gynecol. 2015 Jun;125(6):1484-6.
Castillo MJ, Phillippi JC. Hyperemesis gravidarum: a holistic overview and approach to clinical assessment and management. J Perinat Neonatal Nurs. 2015;29(1):12-22.
Dodds L, Fell DB, Joseph KS, Allen VM, Butler B. Outcomes of pregnancies complicated by hyperemesis gravidarum. Obstet Gynecol. 2006;107(2, pt 1):285–292.
Grewen K, Salzwedel AP, Gao W. Functional Connectivity Disruption in Neonates with Prenatal Marijuana Exposure. Front Hum Neurosci. 2015;9:601.
Sherman PW, Flaxman SM. Nausea and vomiting of pregnancy in an evolutionary perspective. Am J Obstet Gynecol. 2002;186(5 Suppl Understanding):S190-7.
The National Academies of Sciences, Engineering, and Medicine, 2017, The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. National Academies Press, Washington, D.C. 20001
Tortoriello G, et al. Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway. EMBO J. 2014;33(7):668-85.

Additional references on specific neonatal outcomes:
Lower birth weight, animal studies
Benevenuto SG et al., Recreational use of marijuana during pregnancy and negative gestational and fetal outcomes: An experimental study in mice. Toxicology. 2017;376:94-101.
“Five minutes of daily (low dose) exposure during pregnancy resulted in reduced birthweight…..females from the Cannabis group presented reduced maternal net body weight gain, despite a slight increase in their daily food intake compared to the control group”

Lower birth weight, human studies
Gunn,JKL, Rosales CB, Center KE, Nunez A, Gibson SJ, Christ C, and Ehiri EJ. Prenatal exposure to cannabis and maternal and child health outcomes: A systematic review and meta-analysis. BMJ Open 2016; 6(4):e009986.
“Infants exposed to cannabis in utero had a decrease in birth weight (low birth weight pOR=1.77: 95% CI 1.04 to 3.01; pooled mean difference (pMD) for birth weight=109.42 g: 38.72 to 180.12) compared with infants whose mothers did not use cannabis during pregnancy. Infants exposed to cannabis in utero were also more likely to need placement in the neonatal intensive care unit compared with infants whose mothers did not use cannabis during pregnancy (pOR=2.02: 1.27 to 3.21).”
Brown SJ, Mensah FK, Ah Kit J, Stuart-Butler D, Glover K, Leane C, Weetra D, Gartland D, Newbury J, Yelland J. Use of cannabis during pregnancy and birth outcomes in an Aboriginal birth cohort: a crosssectional, population-based study. BMJ Open. 2016;6(2):e010286.
“Controlling for education and other social characteristics, including stressful events/social health issues did not alter the conclusion that mothers using cannabis experience a higher risk of negative birth outcomes (adjusted OR for odds of low birth weight 3.9, 95% CI 1.4 to 11.2).”
Fergusson, D. M., L. J. Horwood, and K. Northstone. 2002. Maternal use of cannabis and pregnancy outcome. British Journal of Obstetrics and Gynaecology 109(1):21–27.
“Over 12,000 women expecting singletons at 18 to 20 weeks of gestation who were enrolled in the Avon Longitudinal Study of Pregnancy and Childhood……the babies of women who used cannabis at least once per week before and throughout pregnancy were 216g lighter than those of non-users.”

Preterm birth, animal studies
Wang H, Xie H, Dey SK. Loss of cannabinoid receptor CB1 induces preterm birth. PLoS One. 2008;3(10):e3320.
“CB1 deficiency altering normal progesterone and estrogen levels induces preterm birth in mice…. CB1 regulates labor by interacting with the corticotrophin-releasing hormone-driven endocrine axis.”

Preterm birth, human studies
Luke S, Hutcheon J, Kendall T. Cannabis Use in Pregnancy in British Columbia and Selected Birth Outcomes. J Obstet Gynaecol Can. 2019;41(9):1311-1317.
“Using cannabis in pregnancy was associated with a 47% increased risk of SGA (adjusted OR 1.47; 95% CI 1.33–1.61), a 27% increased risk of spontaneous preterm birth (adjusted OR 1.27; 95% CI 1.14–1.42), and a 184% increased risk of intrapartum stillbirth (adjusted HR [aHR] 2.84; 95% CI 1.18–6.82).”
Corsi DJ, Walsh L, Weiss D, Hsu H, El-Chaar D, Hawken S, Fell DB, Walker M. Association Between Selfreported Prenatal Cannabis Use and Maternal, Perinatal, and Neonatal Outcomes. JAMA. 2019;322(2):145-152.
“In a cohort of 661 617 women…. The crude rate of preterm birth less than 37 weeks’ gestation was 6.1%among women who did not report cannabis use and 12.0% among those reporting use in the unmatched cohort (RD, 5.88% [95%CI, 5.22%-6.54%]). In the matched cohort, reported cannabis exposure was significantly associated with an RD of 2.98%(95%CI, 2.63%-3.34%) and an RR of 1.41 (95% CI, 1.36-1.47) for preterm birth. Compared with no reported use, cannabis exposure was significantly associated with greater frequency of small for gestational age (third percentile, 6.1% vs 4.0%; RR, 1.53 [95%CI, 1.45-1.61]), placental abruption (1.6%vs 0.9%; RR, 1.72 [95% CI, 1.54-1.92]), transfer to neonatal intensive care (19.3%vs 13.8%; RR, 1.40 [95%CI, 1.36-1.44]), and 5-minute Apgar score less than 4 (1.1% vs 0.9%; RR, 1.28 [95%CI, 1.13-1.45]).”
Saurel-Cubizolles MJ, Prunet C, Blondel B. Cannabis use during pregnancy in France in 2010. BJOG. 2014;121(8):971-7.
“Cannabis users had higher rates of spontaneous preterm births: 6.4 versus 2.8%, for an adjusted odds ratio (aOR) of 2.15 (95% CI 1.10–4.18).”
Leemaqz SY, Dekker GA, McCowan LM, Kenny LC, Myers JE, Simpson NA, Poston L, Roberts CT;

SCOPE Consortium. Maternal marijuana use has independent effects on risk for spontaneous preterm birth but not other common late pregnancy complications. Reprod Toxicol. 2016;62:77-86. “continued maternal marijuana use at 20 weeks’ gestation was associated with” spontaneous preterm birth “independent of cigarette smoking status [adj OR2.28 (95% CI:1.45–3.59)] and socioeconomic index (SEI) [adj OR 2.17 (95% CI:1.41–3.34)]. When adjusted for maternal age, cigarette smoking, alcohol and SEI, continued maternal marijuana use at 20 weeks’ gestation had a greater effect size [adj OR 5.44 (95% CI 2.44–12.11)].”

Impacts on the neonatal immune system, animal study
Zumbrun EE et al. Epigenetic Regulation of Immunological Alterations Following Prenatal Exposure to Marijuana Cannabinoids and its Long Term Consequences in Offspring. J Neuroimmune Pharmacol. 2015; 10(2):245-54.
“Data from various animal models suggests that in utero exposure to cannabinoids results in profound T cell dysfunction and a greatly reduced immune response to viral antigens

Impacts on cortical wiring and development, animal studies
Tortoriello G, et al. Miswiring the brain: Δ9-tetrahydrocannabinol disrupts cortical development by inducing an SCG10/stathmin-2 degradation pathway. EMBO J. 2014;33(7):668-85.
“Here, we show that repeated THC exposure disrupts endocannabinoid signaling, particularly the temporal dynamics of CB1 cannabinoid receptor, to rewire the fetal cortical circuitry….these data highlight the maintenance of cytoskeletal dynamics as a molecular target for cannabis”
DiNieri JA, Wang X, Szutorisz H, Spano SM, Kaur J, Casaccia P, Dow-Edwards D, Hurd YL. Maternal cannabis use alters ventral striatal dopamine D2 gene regulation in the offspring. Biol Psychiatry. 2011 Oct 15;70(8):763-9.
“we exposed pregnant rats to THC and examined the epigenetic regulation of the NAc Drd2 gene in their offspring at postnatal day 2, comparable to the human fetal period studied, and in adulthood…. Decreased Drd2 expression was accompanied by reduced D2R binding sites and increased sensitivity to opiate reward in adulthood”
Rodríguez de Fonseca F, Cebeira M, Fernández-Ruiz JJ, Navarro M, Ramos JA. Effects of pre- and perinatal exposure to hashish extracts on the ontogeny of brain dopaminergic neurons. Neuroscience. 1991;43(2-3):713-23.
“Perinatal exposure to cannabinoids altered the normal development of nigrostriatal, mesolimbic and tuberoinfundibular dopaminergic neurons, as reflected by changes in several indices of their activity”.

Impacts on cortical wiring and development, human studies
Grewen K, Salzwedel AP, Gao W. Functional Connectivity Disruption in Neonates with Prenatal Marijuana Exposure. Front Hum Neurosci. 2015;9:601.

“+MJ (marijuana-exposed) neonates had hypo-connectivity in all clusters compared with –MJ (marijuana unexposed) and CTR (control) groups. Altered striatal connectivity to areas involved in visual spatial and motor learning, attention, and in fine-tuning of motor outputs
involved in movement and language production may contribute to neurobehavioral deficits reported in this at-risk group. Disrupted anterior insula connectivity may contribute to altered integration of interoceptive signals with salience estimates, motivation, decision-making, and later drug use.”
El Marroun H, Tiemeier H, Franken IH, Jaddoe VW, van der Lugt A, Verhulst FC, Lahey BB, White T. Prenatal Cannabis and Tobacco Exposure in Relation to Brain Morphology: A Prospective Neuroimaging Study in Young Children. Biol Psychiatry. 2016;79(12):971-9.
“prenatal cannabis exposure was associated with differences in cortical thickness….. it may be possible that the frontal cortex in cannabis-exposed children undergoes altered neurodevelopmental maturation (i.e., having differences in cortical trajectories) as compared with
nonexposed control subjects”
Wang X, Dow-Edwards D, Anderson V, Minkoff H, Hurd YL. In utero marijuana exposure associated with abnormal amygdala dopamine D2 gene expression in the human fetus. Biol Psychiatry. 2004; 56:909–915.
“Adjusting for various covariates, we found a specific reduction, particularly in male fetuses, of the D(2) mRNA expression levels in the amygdala basal nucleus in association with maternal marijuana use. The reduction was positively correlated with the amount of maternal marijuana intake during pregnancy.”

Received by email

I, Surgeon General VADM Jerome Adams, am emphasizing the importance of protecting our Nation from the health risks of marijuana use in adolescence and during pregnancy. Recent increases in access to marijuana and in its potency, along with misperceptions of safety of marijuana endanger our most precious resource, our nation’s youth.

BE PREPARED. GET NALOXONE. SAVE A LIFE.

Background

Marijuana, or cannabis, is the most commonly used illicit drug in the United States. It acts by binding to cannabinoid receptors in the brain to produce a variety of effects, including euphoria, intoxication, and memory and motor impairments. These same cannabinoid receptors are also critical for brain development. They are part of the endocannabinoid system, which impacts the formation of brain circuits important for decision making, mood and responding to stress.

Marijuana and its related products are widely available in multiple forms. These products can be eaten, drunk, smoked, and vaped. Marijuana contains varying levels of delta-9-tetrahydrocannabinol (THC), the component responsible for euphoria and intoxication, and cannabidiol (CBD). While CBD is not intoxicating and does not lead to addiction, its long-term effects are largely unknown, and most CBD products are untested and of uncertain purity.

Marijuana has changed over time. The marijuana available today is much stronger than previous versions. The THC concentration in commonly cultivated marijuana plants has increased three-fold between 1995 and 2014 (4% and 12% respectively). Marijuana available in dispensaries in some states has average concentrations of THC between 17.7% and 23.2%. Concentrated products, commonly known as dabs or waxes, are far more widely available to recreational users today and may contain between 23.7% and 75.9% THC.

The risks of physical dependence, addiction, and other negative consequences increase with exposure to high concentrations of THC and the younger the age of initiation. Higher doses of THC are more likely to produce anxiety, agitation, paranoia, and psychosis. Edible marijuana takes time to absorb and to produce its effects, increasing the risk of unintentional overdose, as well as accidental ingestion by children and adolescents. In addition, chronic users of marijuana with a high THC content are at risk for developing a condition known as cannabinoid hyperemesis syndrome, which is marked by severe cycles of nausea and vomiting.

This advisory is intended to raise awareness of the known and potential harms to developing brains, posed by the increasing availability of highly potent marijuana in multiple, concentrated forms. These harms are costly to individuals and to our society, impacting mental health and educational achievement and raising the risks of addiction and misuse of other substances.  Additionally, marijuana use remains illegal for youth under state law in all states; normalization of its use raises the potential for criminal consequences in this population. In addition to the health risks posed by marijuana use, sale or possession of marijuana remains illegal under federal law notwithstanding some state laws to the contrary.

Watch the Surgeon General Answer FAQs on Marijuana

Marijuana Use during Pregnancy

Pregnant women use marijuana more than any other illicit drug. In a national survey, marijuana use in the past month among pregnant women doubled (3.4% to 7%) between 2002 and 2017. In a study conducted in a large health system, marijuana use rose by 69% (4.2% to 7.1%) between 2009 and 2016 among pregnant women. Alarmingly, many retail dispensaries recommend marijuana to pregnant women for morning sickness.

Marijuana use during pregnancy can affect the developing fetus.

• THC can enter the fetal brain from the mother’s bloodstream.
• It may disrupt the endocannabinoid system, which is important for a healthy pregnancy and fetal brain development
• Studies have shown that marijuana use in pregnancy is associated with adverse outcomes, including lower birth weight.
• The Colorado Pregnancy Risk Assessment Monitoring System reported that maternal marijuana use was associated with a 50% increased risk of low birth weight regardless of maternal age, race, ethnicity, education, and tobacco use.

The American College of Obstetricians and Gynecologists holds that “[w]omen who are pregnant or contemplating pregnancy should be encouraged to discontinue marijuana use. Women reporting marijuana use should be counseled about concerns regarding potential adverse health consequences of continued use during pregnancy”. In 2018, the American Academy of Pediatrics recommended that “…it is important to advise all adolescents and young women that if they become pregnant, marijuana should not be used during pregnancy”.

Maternal marijuana use may still be dangerous to the baby after birth. THC has been found in breast milk for up to six days after the last recorded use. It may affect the newborn’s brain development and result in hyperactivity, poor cognitive function, and other long-term consequences. Additionally, marijuana smoke contains many of the same harmful components as tobacco smoke. No one should smoke marijuana or tobacco around a baby.

Marijuana Use during Adolescence

Marijuana is also commonly used by adolescents, second only to alcohol. In 2017, approximately 9.2 million youth aged 12 to 25 reported marijuana use in the past month and 29% more young adults aged 18-25 started using marijuana. In addition, high school students’ perception of the harm from regular marijuana use has been steadily declining over the last decade. During this same period, a number of states have legalized adult use of marijuana for medicinal or recreational purposes, while it remains illegal under federal law. The legalization movement may be impacting youth perception of harm from marijuana. 

The human brain continues to develop from before birth into the mid-20s and is vulnerable to the effects of addictive substances. Frequent marijuana use during adolescence is associated with:

• Changes in the areas of the brain involved in attention, memory, decision-making, and motivation. Deficits in attention and memory have been detected in marijuana-using teens even after a month of abstinence.
• Impaired learning in adolescents. Chronic use is linked to declines in IQ, school performance that jeopardizes professional and social achievements, and life satisfaction.
• Increased rates of school absence and drop-out, as well as suicide attempts.

Risk for and early onset of psychotic disorders, such as schizophrenia. The risk for psychotic disorders increases with frequency of use, potency of the marijuana product, and as the age at first use decreases. 

• Other substance use. In 2017, teens 12-17 reporting frequent use of marijuana showed a 130% greater likelihood of misusing opioids23.

Marijuana’s increasingly widespread availability in multiple and highly potent forms, coupled with a false and dangerous perception of safety among youth, merits a nationwide call to action. 

You Can Take Action

No amount of marijuana use during pregnancy or adolescence is known to be safe. Until and unless more is known about the long-term impact, the safest choice for pregnant women and adolescents is not to use marijuana.  Pregnant women and youth–and those who love them–need the facts and resources to support healthy decisions. It is critical to educate women and youth, as well as family members, school officials, state and local leaders, and health professionals, about the risks of marijuana, particularly as more states contemplate legalization.

Science-based messaging campaigns and targeted prevention programming are urgently needed to ensure that risks are clearly communicated and amplified by local, state, and national organizations. Clinicians can help by asking about marijuana use, informing mothers-to-be, new mothers, young people, and those vulnerable to psychotic disorders, of the risks. Clinicians can also prescribe safe, effective, and FDA-approved treatments for nausea, depression, and pain during pregnancy. Further research is needed to understand all the impacts of THC on the developing brain, but we know enough now to warrant concern and action. Everyone has a role in protecting our young people from the risks of marijuana.

Information for Parents and Parents-to-be

You have an important role to play for a healthy next generation.

• Review the facts to understand the risks associated with marijuana use during pregnancy.
• Check out these Frequently Asked Questions  about marijuana use and pregnancy.
• Learn about marijuana safety for children and pregnant and breastfeeding women.
• Start a conversation with your kids: Marijuana: Facts Parents Need to Know.
• Keep your adolescent from using marijuana and other drugs: Keeping Youth Drug Free – PDF.
• Watch the Message to Parents from NIH/NIDA 

Information for Youth:

You have an important role to play for a healthy next generation.

• Want to know how marijuana affects brain development? Get the facts. 
• Learn key techniques on how to resist peer pressure: Above the Influence .
• Learn how to help friends stop using marijuana with Letter to Teens
• Get around-the-clock free advice and referrals: Substance Abuse and Mental Health Administration (SAMHSA) National Helpline (1-800-662-HELP (4357).

Information for States, Communities, Tribes, and Territories:

You have an important role to play for a healthy next generation.

• Learn how communities and schools can act: Preventing Marijuana Use among Youth & Young Adults.
• Find key messages for communities at www.samhsa.gov/marijuana. 
• Get training and educational resources for your community: Prevention Technology Transfer Centers.

Information for Health Professionals:

You have an important role to play for a healthy next generation.

• Learn how you can integrate marijuana education into prenatal care visits: Marijuana Pregnancy & Breastfeeding Guidance – PDF.
• Get advice on talking with adolescents and parents about marijuana use from the American Academy of Pediatrics guidance for clinicians .
• Read the American College of Obstetricians and Gynecologists position on Marijuana use during pregnancy and lactation .

Source: Surgeon General’s Advisory: Marijuana Use & the Developing Brain | HHS.gov August 2019

• Medical Profession.  Many professional organizations have made strong statements warning against widespread cannabis use. e.g. AMA, RACGP, AAP, ACOG, British Lung Foundation.

• Common Pattern.  The almost ubiquitous pattern in which medical cannabis is used today is to treat decades long cannabis addiction, with the other indications serving as mere “tickets” to engage whilst simultaneously avoiding legal censure.

• Parallel Drug Approval Pathway.  It is obvious that whilst all other drugs are held to a strict approvals and regulatory pathway cannabis products are held to no serious control whatsoever with the industry in an effectively unregulated exponential growth phase.

• Limited Benefits. Despite the international rhetoric of many governments and the  cannabis industry there is either nil or very poor evidence for the efficacy of the vast majority of cannabinoid products in the management of  most indications presenting to GPs  (Ref RACGP Review).

• Known Harms.  Alternately, there is increasing direct and indirect evidence from cellular, mechanistic, case data and epidemiological studies of “likely” harm from cannabis, both within and across generations (epigenetics). This is supported by large epidemiological studies, confirming increased cancers and neonatal congenital abnormalities in areas of increased cannabinoid use, not dissimilar from those used to identify links between tobacco or alcohol and morbidities.  Numerous aging pathologies are also accelerated.

• Further Harms.
  1. Gateway role – Into harder drugs and criminal lifestyle is now well established by studies in numerous countries.  Whilst few cannabis users progress to harder drugs, virtually all users of harder drugs have used cannabis, with much higher rates of drug and criminal progression amongst ever users of cannabis.
  2. Adult Brain – Most major psychiatric syndromes have been linked with cannabis viz: sedation, amotivational state, anxiety, PTSD, serious mental disorders, depression, psychosis, bipolar disorder, schizophrenia, suicidal thoughts and completed suicides.  Also linked with homicide and violence and over 70 mass shootings in USA thought to be linked with aggression (seen in both cannabis withdrawal and intoxication), impaired judgement and psychosis
  3. Child Brain – ADHD-like and autism-like features; extreme aggression; impaired cortical processing; learning difficulties; smaller brain; microcephaly; anencephaly (which causes death within hours)
  4. Chest disease – COPD, chronic bronchitis, emphysema, lung cysts, elevated residual volume, premalignant changes in upper and lower airways
  5. Immunomodulation – Both immunosuppression and immunostimulation are described mediated via T-cells, B-cells, NK Cells, T-reg cells, antibodies and cytokines
  6. Endocrinopathy – Central and peripheral hypogonadism, Prolactin elevated
  7. Cardiovascular  – accelerated coronary artery and atherosclerotic disease; strongly arrythmogenic (many tachyarrhythmias both atrial and ventricular)

• Genetic Toxicity.  These include gestationally and neonatal congenital abnormalities, cancers both childhood and adult, and the occurrence of premature age-related morbidities, and powerful direct effects on the aging process etc.

• Known Mechanisms.  These findings are underpinned by clear cellular mechanistic studies on how cannabinoids (both THC and CBD based) can cause the above by interfering  with normal cellular and body functions creating antecedents of disease. This of course is not surprising given the increasing understanding of the role of endogenous cannabinoids in normal development, body functioning, and cellular reproduction and maintenance, chromosomes, gene maintenance and control (epigenome) and that use of large doses or prolonged exogenous cannabinoids can significantly disrupt these functions.

• “Do No Harm.”  Given the aforementioned, it is clear that caution needs to be applied to the medical use of cannabinoids, that although in the most positive interpretation may have a nominal impact managing morbidities, may in turn cause greater harm transgenerationally.

• Multigenerational Impacts Genetic and epigenetic effects are believed to persist for at least three to four generations.  Cannabinoids have been shown to be driving several childhood (and thus cross-generational) cancers including total childhood cancer.  Cannabis, THC and cannabidiol have been shown to be linked with the cancers of the: breast, prostate, ovary and testis showing carcinogenesis to the reproductive organs.  Also many birth defects including the absence of arms and legs and congenital brain, face,  and heart defects.  Also aging of the sperm and ovum themselves in rodents and humans.

• Rigorous Trials – Evidence Base.  It is therefore not only reasonable but essential that each cannabinoid product marketed should be assessed by the established international standards for pharmaceutical development, and to which all other pharmaceutical products, prior to being released and used in populations must conform.  There is need for a robust evidence base.  At present cannabis is not performing impressively in hundreds of clinical trials.  In the case of cannabinoids this must include rigorous and long term tests of genetic, epigenetic and epitranscriptomic toxicity including: genotoxicity, carcinogenicity, mutagenicity, teratogenicity and gametotoxicity in both sexes.

Source: https://pubmed.ncbi.nlm.nih.gov/

Methamphetamine, a well-known psychostimulant drugs of abuse is in a resurgence in people using opioids and others. While many treatment options exist for patients with opioid use disorders, alcohol use disorders, and even tobacco smokers, there are far fewer options for people trying to stop using methamphetamines. No known medical treatments exist for overdose, dependence, craving, relapse, or to reverse all of the effects of methamphetamine binges and dependence. Experts studying substance use disorders recognize that their effects from misuse, especially the misuse of methamphetamine, can linger even after periods of abstinence.

Patients treated for methamphetamine binges, or dependence, for example, often suffer from cognitive impairments, including psychosis. Some of the persistent problems may reflect underlying brain change or even damage. If overlooked, cognitive problems can limit the effectiveness of treatment. They can also create a dangerous hopelessness or relapse cycle. That’s one reason why it’s so important to understand how substances like methamphetamine may alter the brain’s structure.

How Long Do Methamphetamine Brain Changes Last?

Methamphetamine addiction is a growing epidemic worldwide, following on the heels of the opioid crisis. Chronic methamphetamine use has been shown to lead to neurotoxicity in both humans and animals.  Magnetic resonance imaging (MRI) studies in methamphetamine users have shown enlarged striatal volumes, and positron emission tomography (PET) studies have shown decreased brain glucose metabolism (BGluM) in the striatum of abstinent methamphetamine users.

Some features of the methamphetamine toxicity profile are puzzling as well as difficult to treat. In prior work, it’s been noted how psychosis can follow methamphetamine use and last into abstinence. Varying levels of methamphetamine use can induce psychosis, depending in part on an individual’s background, and it can develop quickly or after 20 years of use. This psychosis can be quite similar to Schizophrenia – in some cases, violent behaviors have been connected to methamphetamine psychosis as well.

A study of Japanese prisoners found that a subgroup of methamphetamine users experienced chronic psychosis. Lingering cognitive problems may cause other health complications, difficulty thinking or concentrating at work, and increasingly risky behavior, in addition to higher relapse rates. Furthermore, later-in-life stress can also revive psychotic symptoms. More research on methamphetamine and cognitive problems can help treatment providers understand these hidden tripwires for patients.

One study, by Thanos et. al., looked at brain changes in rats after long-term methamphetamine use. Researchers split rats into 3 groups and gave them methamphetamine daily for 4 months. They dissolved methamphetamine in a saline solution and gave one rat group high methamphetamine doses, one rat group low methamphetamine doses, and the remaining rat group saline. Subsequent testing showed significant changes in the rats’ brains, stemming from higher doses. They also detected changes in brain glucose metabolism across different areas of the brain. These changes affect sleep cycles, face sensory processing, navigation, and memory. Researchers additionally found increases in striatal volume, referring to a part of the brain with a key role in decisions and reward management.

These increases resemble the results of other research, an important part of the study. Cognitive problems in humans taking methamphetamine can exist before substance use. But Thanos et. al. observe that a combination of research on methamphetamine use and this part of the brain, involving humans, monkeys, and rats, all finds similar increases. Unfortunately, this combination indicates that some methamphetamine-induced problems in the brain are prolonged and significant.

Thanos et. al. also start the rats’ substance use in adolescence. They point out that studies of human use in adolescence and adulthood find similar brain problems, adding to the likelihood of long-term damage. Thanos has continued this work with NIDA Director Volkow, looking at damage produced in the brain by methamphetamine. These most current results from their group, corroborate clinical experiences and reports of toxicity and encourage us to further examine the mechanisms behind MA-induced neurotoxicity.

 Why Is This Important?

This kind of study is important because treatment and recovery providers need to understand the full spectrum of issues their patients face. Once the acute problems are resolved, many challenges may remain. Even in abstinence, brain problems after methamphetamine use may become substantial hurdles for patients in recovery.

Psychological and neuropsychological testing may help the clinical team understand what has been lost and what might be done to help. Thanos et. al. also suggest that methamphetamine use may trigger a direct brain injury that we suggested was similar to a concussion or traumatic brain injury. Thanos suggests that methamphetamine targets the dopamine rich pleasure system, undermines it and the residual brain inflammation is both the proof and the cause of the post-drug changes to the health of our dopamine systems. Determining long-term methamphetamine brain changes can be even more useful for setting goals and interventions designed to help patients. Some of the strategies currently used to treat traumatic brain injuries may be helpful, as may use of exercise, dance, and transcranial magnetic stimulation. Post drug abstinence psychoses may not be as reversible by medications used for naturally-occurring psychoses.

Many patients, for example, show subtle changes without clear signs of cognitive difficulties. Testing may reveal real problems. Others present with fears and anxiety or disordered thinking that may have there roots in changes to their brains. And untangling cause and effect can help us better understand when pre-existing cognitive problems, and not substance use, are the main culprits. As with many substance use disorders, we have to remember that a holistic approach based on individual needs is the best way to help.

With methamphetamine this is even more important as medication assisted therapies do not exist. Time of abstinence, rehabilitation with healthy thinking, eating, sleeping, and diet are easier to prescribe or advise than find. Time of abstinence is of the essence as it appears that methamphetamine induces a drug use disorder with binges, relapses and cravings but also with loss of brain function and evidence of something that looks like a traumatic brain injury. Treating it like a neurological injury in addition to traditional addiction treatment, may be an idea worth looking at too.

Source:https://www.addictionpolicy.org/blog/tag/research-you-can-use/examining-brain-health-could-help-fight-methamphetamine-use-disorder    1^st  August 2019

Abstract:

Background: The relationship between cannabis and violence remains unclear, especially amid those with severe mental illnesses (SMI). The objective of this meta-analysis was to investigate the cannabis-violence association in a population of individuals with a SMI.

Method: A systematic search of literature using PubMed, PsychINFO, Web of Science and Google scholar was performed (any time-August 2018). All peer-reviewed publications assessing both cannabis use and the perpetration of violence in an SMI sample were included. Data on several key study characteristics such as the proportion of SMI in the sample as well as the number of cannabis users and violent participants were extracted. Odds ratios (OR) were likewise extracted and aggregated with random-effects models.

Results: Of the potential 2449 articles that were screened for eligibility, 12 studies were analyzed using a random-effect meta-analysis. Results showed a moderate association between cannabis use and violence (OR = 3.02, CI = 2.01–4.54, p = 0.0001). The association was significantly higher when comparing cannabis misuse (OR = 5.8, CI = 3.27–10.28, p = 0.0001) to cannabis use (OR = 2.04, CI = 1.36–3.05, p = 0.001).

Conclusion: These findings are clinically relevant for violence prevention/management and highlight the necessity of further investigations with methodologically-sound studies. Thus, longitudinal studies adjusting for important confounding factors (i.e., psychopathic traits and stimulant use) are warranted

Source: Cannabis use and violence in patients with severe mental illnesses: A meta-analytical investigation – PubMed (nih.gov) April 2019

In March 2014, the Colorado Department of Public Health and Environment (CDPHE) learned of the death of a man aged 19 years after consuming an edible marijuana product. CDPHE reviewed autopsy and police reports to assess factors associated with his death and to guide prevention efforts.

The decedent’s friend, aged 23 years, had purchased marijuana cookies and provided one to the decedent. A police report indicated that initially the decedent ate only a single piece of his cookie, as directed by the sales clerk. Approximately 30-60 minutes later, not feeling any effects, he consumed the remainder of the cookie.

 During the next 2 hours, he reportedly exhibited erratic speech and hostile behaviors. Approximately 3.5 hours after initial ingestion, and 2.5 hours after consuming the remainder of the cookie, he jumped off a fourth floor balcony and died from trauma.

The autopsy, performed 29 hours after time of death, found marijuana intoxication as a chief contributing factor. Quantitative toxicologic analyses for drugs of abuse, synthetic cannabinoid, and cathinones (“bath salts”) were performed on chest cavity blood by gas chromatography and mass spectrometry. The only confirmed findings were cannabinoids (7.2 ng/mL delta-9 tetrahydrocannabinol [THC] and 49 ng/mL delta-9 carboxy-THC, an inactive marijuana metabolite). The legal whole blood limit of delta-9 THC for driving a vehicle in Colorado is 5.0 ng/mL. This was the first reported death in Colorado linked to marijuana consumption without evidence of polysubstance use since the state approved recreational use of marijuana in 2012.

Source:  MMWR Morb Mortal Wkly Rep. 2015 Jul 24;64(28):771-2.

As with any addiction, alcoholism is closely connected with stress. And while plenty of people first started drinking as a way to cope with stress or even just wind down after a long day, developing an alcohol use disorder can end up causing significant stresses of its own. If you’re thinking about pursuing alcohol use disorder treatment for yourself or for a loved one, it can be helpful to understand how alcohol is connected to stress.

Present Stress That Can Lead to Alcohol Use

While stresses from your past can certainly contribute to alcoholism, plenty of people also start to develop alcohol use disorder as they struggle to cope with current stress. Often, people end up turning to alcohol in order to try to manage the stresses of day-to-day life. These can include pressure at work or at school, marriage, and divorce, moving, and financial issues.

Minority stress is also an important consideration. If you’re a minority (either in terms of race/ethnicity or sexual orientation), you face unique stresses. You might stress about being passed over for a promotion at work, and you also might fear harassment or becoming the victim of a hate crime.

It’s important to note that stress alone typically does not cause a substance use disorder. However, significant stresses may place you at higher risk of developing one, and high stress levels in sobriety can also make relapse more likely. High stress is a risk factor for alcoholism, along with the following:

• One or more close relatives who have an alcohol use disorder
• Depression and other mental health disorders
• Heavy drinking over time (which can sometimes result in alcohol-induced dementia)
• Social factors (like the way alcohol is viewed or treated in your community)
• A history of past traumas

Past Stress That Can Lead to Alcohol Use

Unfortunately, it isn’t just current stressful events that can predispose you to drink more. Stresses and traumas from your past can also play a role in alcoholism. Several studies point to childhood abuse and neglect as being a significant factor in the development of an alcohol use disorder. One study found that emotional abuse and neglect were most commonly seen in men and women seeking help for alcoholism. The severity of their alcoholism correlated with the severity of the abuse.

Past traumas, even if they were not experienced in childhood, may also make someone more likely to experience alcoholism. Many people with an alcohol use disorder also have PTSD. As with other mental health diagnoses, the relationship between alcoholism and PTSD becomes a vicious cycle. Alcohol use makes PTSD symptoms worse, and the PTSD symptoms make alcoholism worse.

If you have experienced trauma and are also struggling with alcohol use disorder, it’s easy to feel as though there is no hope. But at Granite Recovery Centers, we offer evidence-based therapies including trauma therapy. In therapy for trauma and PTSD, you will be able to process your trauma and develop healthier coping strategies to help you avoid self-destructive behaviors. With these therapies, you’ll be able to break the cycle of worsening symptoms and experience a greater quality of life.

How Can Alcohol Use Cause Stress?

While it might seem logical that alcohol use can cause stress, there’s also a good bit of biochemical evidence to explain, at least in part, how alcohol shapes your stress response. Even in the short term, alcohol consumption increases levels of cortisol. Cortisol is known as the stress hormone, and your body also releases it during periods of intense anxiety or fear. In the short term, a cortisol release can be helpful — it increases alertness and focus, which was helpful evolutionarily because it helped humans and animals get themselves out of dangerous situations.

However, having elevated cortisol over a long period of time can be detrimental, exhausting, and even dangerous. And in chronic heavy drinkers and those with alcohol use disorder, cortisol isn’t just elevated during intoxication — it stays elevated through withdrawal. In fact, one study even found that cortisol increased as intoxicated people started moving toward withdrawals. If you’ve ever experienced intense anxiety when withdrawing from alcohol, you’ve felt this cortisol surge firsthand.

Because most people with an alcohol use disorder go through a near-constant cycle of intoxication and withdrawal, cortisol can remain elevated for years on end. Chronically elevated cortisol can cause a number of ill health effects:

• Slow healing (of wounds, broken bones, etc.)
• Acne
• Thinning skin
• Weight gain
• Extreme fatigue
• Irritability
• Trouble focusing
• Muscle weakness
• Headaches
• Elevated blood pressure

Chronically elevated cortisol may cause other health problems as well, but more research is needed to determine exactly what these effects are. Of course, the physical stresses of elevated cortisol combined with chronic heavy drinking can mean your body is put through a lot of physical stress as well as emotional stress.

You already know that plenty of people use alcohol to alleviate stress, but over time, alcohol can cause its own significant stresses. As mentioned above, the elevated cortisol you experience while intoxicated and in withdrawal can cause significant emotional distress. When your body is under stress, and elevated cortisol is effectively causing a constant stress response, it becomes significantly more difficult to handle even everyday stresses.

And in some cases (like when you are intoxicated enough to experience blackouts or respiratory suppression), being intoxicated can be a stressful experience in itself. And for many people with an alcohol use disorder, that stressful experience is something they experience on a daily or near-daily basis. Some of the physical effects of heavy drinking — including dizziness, nausea, headaches, and dehydration — can compound the emotional stress you’re already feeling.

Many people also consciously or unconsciously use alcohol to self-medicate psychiatric disorders, including depression and bipolar disorder. However, in many cases, alcohol use worsens the symptoms of mental health issues, which can cause considerably more emotional distress on a daily basis. In some cases, heavy alcohol use can even contribute to the development of new mental health diagnoses.

If you’ve been using alcohol to help manage a mental health diagnosis (or to help manage a mental health issue that has not yet been diagnosed), Granite Recovery Centers’ dual diagnosis treatment program can help you. With this approach, medical and recovery professionals work with you to find better treatments and coping mechanisms for your mental health diagnosis while also helping you manage your alcohol use disorder. In many cases, this treatment approach will greatly improve your quality of life, as you’ll be much better equipped to manage both diagnoses.

Regardless of whether you have a mental health diagnosis or not, heavy alcohol use can begin to cause stress as it starts to affect the rest of your life. For example, you may constantly worry whether someone will smell alcohol on your breath at work, or you may worry about when you can take another drink. For many people with an alcohol use disorder, it can start to feel like leading a double life, which becomes exhausting and highly stressful over time. And as a person starts to drink more, they often become more socially isolated. Feeling isolated can increase stress, and the person may then continue drinking heavily to cope with that stress.

If you struggle with an alcohol use disorder or other substance use disorder, you already know just how stressful day-to-day life can become. If you have to drink to get rid of withdrawal symptoms and can’t control your drinking once you start, it’s easy to feel trapped, which is, of course, a major stress in itself. If you feel this way, you aren’t alone — taking the first steps to get help can free you from the seemingly unending cycle of alcohol use.

How Do I Know If I’ve Developed an Alcohol Use Disorder?

If you have started using alcohol as a way to cope with stress, it can be difficult to tell whether you have developed an alcohol use disorder or if you are beginning to develop one. While you’ll need to consult a medical professional if you’re looking for a definite diagnosis, you can look for some of the common signs:

• Spending a lot of time both drinking and recovering from drinking
• Not being able to control how much you drink once you start
• Continuing to drink even when you experience negative consequences
• Giving up on hobbies or responsibilities in order to drink
• Developing an alcohol tolerance
• Craving alcohol or becoming preoccupied with drinking when you can’t drink
• Experiencing withdrawal symptoms when you don’t drink (or drinking to ensure you avoid these symptoms)
• Using alcohol when it is dangerous to do so (like when you’re driving)

Binge drinking can also be a sign of a developing alcohol use disorder. Binge drinking is defined as consuming five or more standard drinks in two hours for men and consuming four or more standard drinks in two hours for women. On its own, binge drinking doesn’t necessarily indicate an alcohol use disorder, but it could be a sign that one is starting to develop.

It’s important to keep in mind that alcohol use disorders are on a spectrum. Milder cases tend to have fewer symptoms present, while more severe cases have more. Even if you think you only have a mild case, you can still benefit tremendously from treatment. Most cases of alcohol use disorder become progressively worse over time.

How Can Treatment Help?

If you’re unfamiliar with substance use disorder treatment, you may think residential treatment’s only benefit is preventing you from accessing your substance of choice. This couldn’t be further from the truth. A good residential treatment program takes a holistic approach to help you improve your life.

In most cases (and definitely in severe cases), a stay at a residential treatment center begins with a medical detox program. In medical detox, you’ll be supervised by a doctor and likely given medication to prevent seizures and other complications of alcohol withdrawal. Withdrawing from alcohol on your own can be very dangerous, and inpatient detox can ensure that you’re safe. Granite Recovery Centers provides medical detoxification for people who do not need immediate medical intervention, are not a danger to themselves, and are capable of self-evacuation in the event of an emergency.

Once you’re in treatment, you’ll work with counselors and medical professionals to help you identify issues that make you want to drink. These professionals will help you develop healthier coping mechanisms to deal with stress so you’ll be less likely to turn to alcohol in the future. You may get to participate in cognitive behavioral therapy and dialectical behavioral therapy, as well as trauma therapy if needed.

Nutritional deficiencies developed while drinking heavily can add to stress and feeling generally unwell, so residential rehabilitation includes healthy food and ample exercise opportunities. And if you have a co-occurring mental health condition, on-site professionals will help you develop an effective treatment plan.

Ready to Take the Next Step?

Alcohol is an easy answer to stress for many people. But if you have an alcohol use disorder, chances are good that alcohol only causes more stress and worsens the stress you already have. And if the prospect of quitting by yourself seems like too much, don’t worry—the professionals working with Granite Recovery Centers will be helping you every step of the way. If you’re ready to change your life, give us a call at 855-712-7784 today!

Source: https://www.graniterecoverycenters.com/resources/the-connection-between-stress-and-alcoholism/ April 2021

In the September/October 2020 Missouri Medicine, Polocaro and Vettraino raise the important issue of the transgenerational effects of prenatal cannabinoid exposure (PCE) on subsequent generations.¹ The implications of multigenerational toxicity of cannabinoids is very far-reaching with major policy implications.

The picture presented by Polcaro and Vettraino relating to the mental health implications of PCE is correct if too conservative. As they observe the subject is deeply confounded with multiple other factors impacting post-natal neurological development. For these reasons the significant concordance between reports from five longitudinal studies of childhood development relating to impaired indices of concentration, startle, excitability, poor visuospatial processing and executive functioning including ADHD-like and autism-like features are of particular concern.^2–6 Under a legalization paradigm the state effectively condones unlimited all day every day exposure to extremely high concentrations of THC, other cannabinoids and cannabis tars. What is especially concerning about this is that many of the neurotoxic and neurodevelopmental toxicities of cannabis exhibit threshold dose effects above which severe damage becomes commonplace.⁷ In the context of an increasingly solid consensus relating to the harmful impacts of adult and adolescent cannabis exposure⁸ the implications of PCE-neurotoxicity have not been carefully considered. It has been shown that nationwide autism rates are undergoing an exponential rise and indeed New Jersey has been shown to have 4.5% of 8-year-old boys who carry an autism spectrum disorder diagnosis.^9,10 Our space-time and causal inference studies demonstrate that indeed cannabinoid exposure to THC and cannabigerol amongst other fractions of cannabis, is a principal driver of this nationwide epidemic (manuscript submitted).^9,10

A very concerning consensus is now emerging relating to cannabis-induced teratogenesis, embryotoxicity and fetotoxicity. A 2007 Hawaiian study found that 21 birth defects including many cardiovascular defects, Downs syndrome, orofacial clefts, gastroschisis and arm and hand defects were elevated in offspring of women exposed only to cannabis gestationally with odds ratios up to 40-fold and upper confidence intervals to 123-fold.¹¹ A report on Canada found that total congenital defects were three times more common in the northern territories where cannabis is smoked about three times as much.^12,13 In October 2018 Colorado Health reported an excess of 20,152 total birth defects beyond their baseline expected 67,620 defects 2000–2013 across the period of cannabis legalization when the use of other drugs was falling, representing an elevation of 29.8% above background rates.¹⁴ In a high cannabis use area of Australia 13 defects were found to be elevated compared to Queensland, which for methodological reasons is a conservative estimate.¹⁵ Concerningly elevated rates of Downs syndrome in Colorado, Hawaii, Australia and Canada clearly indicate that heritable cannabis genotoxicity can occur at the hundred megabase chromosomal scale.^11,12,14,15 A close association of atrial septal defect (secundum type) with rising patterns of cannabis use across space and time in the US was recently reported, suggesting that the list of known teratological associations of prenatal cannabis exposure is as yet incomplete.¹⁶ This epidemiological literature is closely concordant with studies in experimental animals.^17–19 Again an abrupt rise in genotoxicity with increasing cannabinoid exposure has been demonstrated for many cannabinoids and is of particular concern.^20–23

Links between cannabis and several paediatric cancers including acute lymphoid leukaemia (ALL), acute myeloid leukaemia, rhabdomyosarcoma and neuroblastoma suggest further implications of cannabinoid genotoxicity.^24–28 Since these tumours together encompass the common tumours of childhood, it is at least possible that cannabis is responsible for the 43% elevation in total childhood cancer across US 1975–2017.²⁹ Indeed Downs syndrome is well known to be associated with a 2,000-fold elevated risk of childhood ALL from 2/100,000 to around 5/100.^30,31

This diverse assemblage of highly congruent evidence of severe cannabis-related neurotoxicity and genotoxicity from varied locations can only be described as extremely concerning indeed. In view of its well described epigenetic and chromoanagenetic effects^32–34 and its clearly transgenerational-multigenerational impacts one can only conclude that if the evidence base is not admitted to the cannabis debate and access to fetotoxic and embryotoxic cannabinoids is not immediately restricted the community will inevitably pay a heinous price in terms of avoidable paediatric neurotoxicity, congenital birth defects, heritable cancerogenesis and multigenerational epigenotoxicity.

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7721409/ Nov-Dec 2020 in response to ‘Cannabis in Pregnancy and Lactation – A Review’ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723128/

Source: Preventing Marijuana Use Among Youth & Young Adults (getsmartaboutdrugs.gov) March 2017

Researchers have found that even occasional cigarette use is enough to affect the volume and connectivity of developing brains

After decades of educational programming and advertising, regular cigarette smoking and sales in the United States have declined to their lowest levels in 50 years. But doctors and parents are now racing to deal with another health crisis that has popped up in its place: the meteoric rise of electronic cigarettes (or e-cigarettes) among adolescents.

This nicotine electronic delivery device was originally introduced to the market as a promising tool to aid smoking cessation among already current smokers. Yet, the lack of federal regulations, the appealing flavors available, and perceptions that these devices were less harmful than regular cigarettes have led to a worrying spike in use among U.S. adolescents. One in five U.S. high school students and one in 20 middle school students currently use e-cigarettes.

E-cigarette use among youth has skyrocketed in the past few years

U.S. Surgeon General Jerome Adams has declared e-cigarettes an epidemic among youth, stressing that e-cigarette aerosols containing nicotine increase the risk of addiction to nicotine and other drugs, and impact brain development which can induce mood disorders and lower impulse control. Now, new research led by Dr. Bader Chaarani of the University of Vermont and published in the journal Biological Psychiatry: Cognitive Neuroscience and Neuroimaging has found adolescents that smoked only a few cigarettes had smaller and less connected brain areas than their peers who never smoked. This could mean that adolescent smokers’ brains will develop and function differently, which may affect decision-making and self-control in adulthood. 

Just like regular cigarettes, e-cigarettes contain nicotine, a neuroactive chemical and an addictive component whose main target is the brain. Nicotine acts upon receptors in our brains -through nicotinic acetylcholine receptors (nAChRs)- to promote the release of a neurotransmitter called dopamine. Dopamine is a feel-good chemical, triggering a pleasurable response in our brains. When linked with the action of smoking, it plays a fundamental role in nicotine addiction.

Adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired

Nicotine exposure among adults presents lower risks compared to adolescents. This is because our brains develop throughout our first three decades of life. During this maturation period, the brain circuits are being remodeled, especially those involved in reward function (dopamine) and cognitive function (acetylcholine). Therefore, adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired, making young people even more vulnerable to future addiction. 

Previous studies have shown that adolescent smokers have reduced neural activity and show symptoms of nicotine dependency at lower nicotine levels than adults, and that individuals that begin smoking during adolescence are more likely to develop nicotine dependence than individuals that start in their late 20′s.

Studies of smoking’s effects on the brain have largely focused on adults, not youth – until now

One big gap in research observing the effects of cigarette smoking on brain volume, connectivity, and function to date is that such studies have been mostly performed on adult smokers rather than adolescent smokers. The majority have also focused on daily and heavy smokers, yet have overlooked occasional smokers, which is relevant due to common experimentation behaviors during adolescence. 

The new research by Dr. Chaarani and their team finally addresses these gaps by looking at the brains of adolescent light smokers. They found that just a couple of cigarette puffs can potentially alter the development of adolescent brain. 

The research team recruited over 600 14-year-old adolescents and calculated a cigarette-smoking score for each participant based on how many times, during their lifetime, they had smoked cigarettes. Participants ranged from young people who had never smoked to those who have smoked more than 40 times.

Smoking even a few times is significantly linked to a decreased volume of the gray matter and neuronal connectivity

The researchers also looked at the brain of each of the participants using functional magnetic resonance imaging (fMRI). These images were used to estimate the brain gray matter volume corresponding to the neuron bodies where synapses occur, and white matter connectivity, meaning the “telephone wires” that connect neurons and brain areas by carrying electrical signals. 

Interestingly, Dr. Chaarani and their team found that smoking even a few times was significantly linked to a decreased volume of the gray matter and neuronal connectivity. And the more teens smoked, the more the gray matter volume at the ventromedial prefrontal cortex (vmPFC), and the connectivity at the corpus callosum of their brains was reduced. Scientists have previously linked alterations in the vmPFC volume with a reduction in reward and with an increased risk of anxiety disorders. 

Moreover, reduction in the connectivity could indicate that nicotine induces axonal damage, meaning it may be altering the communication between brain areas. These alterations in brain connection have also been reported in individuals with substance addiction and alcohol dependence. While the research only showed a link between low doses of cigarette smoking and brain alterations, rather than a causal effect, these type of consequences have been consistently reported in many studies on brains of adult smokers.

E-cigarettes may look harmless, but they have lasting effects on developing brains

Although this study focused on adolescents who smoked traditional cigarettes, scientists have demonstrated that such risks are applicable to teenagers who vape using the popular JUUL brand of e-cigarettes since the two methods deliver similar amounts of nicotine.

Researchers are still working to understand the impact of nicotine in the brain of young smokers, particularly now that e-cigarette use among youth has increased rapidly. This new study could play a critical role in educational campaigns, and spur regulatory agencies, parents, and teachers to take an active role in preventing this newest addiction. 

Source:  https://massivesci.com/articles/smoking-vaping-risks-adolescent-brain-function-development-addiction-nicotine/   June 2019

Summary

Source: The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study – The Lancet Psychiatry March 2019

The study by Sadananda et al published in the current issue of the IJMR highlights the neurophysiological basis of altered cognition in subjects with opioid addiction. The study demonstrated aberrant network activity between the default mode network (DMN) and fronto-parietal attentional network (FAN) as a major cause for working memory deficits in drug addiction. Working memory is an important to retain the cognitive information essential for goal directed behaviours. Human beings are endowed with an efficient cognitive faculty of working memory, essential for efficient functioning of the executive network system of the brain. As working memory is the key to carry out any cognitive process involving attention, volition, planning, goal directed behaviour, etc., consciousness is linked largely to working memory processing. The importance of integrating neuroscience knowledge especially the executive functions of human brain in leadership has been taught in neuro-leadership programs as a mean to maximize the human capabilities, productivity, creativity, leadership, wellness, positive attitude.

Aberrant network activities and structural deficits in brain areas of executive functioning impede most of our intellect including mental flexibility, novel problem solving, behavioural inhibition, memory, learning, planning, judgement, emotion regulation, self-control and other social functioning. Deficits in working memory and attention owing to reduced fronto-parietal network (FPN) activity is reported in schizophrenia, autism, attention deficit hyperactive disorder (ADHD) and anxiety disorders. Opioid addiction is reported to impede such dynamicity of the executive system leading to a wide range of deficits in cognition. Opioid addiction alters the network integrity between DMN and FPN networks and weakens the cognitive information processing in cognitively challenging paradigms. Dysfunctional dynamics of DMN activity is believed to contribute to impaired self-awareness, negative emotions and addiction related ruminations. Aberrant DMN activity and reduced medial prefrontal cortical functions are common neural phenotypes of cognitive deficits in conditions like mental illness, drug addiction, sleep deprivation and neurodegenerative disorders. People with substance use disorders develop mental illnesses as a serious comorbidity that in turn, leads to severe behavioural impairments at the social, emotional and cognitive domains. Chronic sleep deprivation associated with drug addiction and substance abuse is another predisposing factor that worsen the behavioural impairments. Over all, drug addiction, substance abuse and the subsequent maladaptive behaviours including mental illness and sleep deprivation trigger a complex set of network instability in the domains of cognition and affect. The euphoria and hallucinating experience of drugs of abuse would soon lead to psychological distress and to cognitive and emotional behavioural impairments due to the disruption of various top down and bottom-up network dynamics.

Substance use disorders are an imminent socio-economic burden and have become a major public health concern worldwide. Despite knowing the harmful effects and consequences of drug use, reports say that the youth especially the adolescents have a tendency to continue the habit. There is a need to have effective measures in place such as educational programmes to improve the self-efficacy of parents and family members to help their children to develop the right behavioural attitude, enhance the capacity building in teachers to strengthen the self-esteem and wellness of students to organize substance use control awareness programmes in coordination with NGOs at educational institutions, involvement of television and other visual and social media platforms to organise substance abuse control programmes and for interactive opportunity for children/youth with educators, researchers and professionals, organization of knowledge dissemination programmes to the public/schools/colleges to highlight the adverse effects of drug abuse on mental health and cognition. Introduction to such knowledge sharing platforms such as the Virtual Knowledge Network (VKN) at NIMHANS, Bengaluru, provide interactive skill building opportunities to safeguard them from substance abuse and addiction. People should have easy access to such services and rehabilitation centers. Various behavioural intervention strategies such as cognitive retraining, psychotherapy, yoga therapy, mindfulness-based intervention programmes etc. are reported to improve cognitive abilities, regulation of negative emotions and restoration of motivational behaviours. A study on single night exposure to olfactory aversive conditioning during sleep helped to quit addiction to cigarette smoking temporarily. Such studies highlight the possibility of learning new behaviours during sleep and its positive impact on wake associated behaviours. Such approaches are quite useful, easily testable and cost-effective. Thanks to the incredible phenomenon of adult brain plasticity, it is possible to re-establish social intelligence, prosocial motivation among people with substance abuse.

Source: Drug addiction – How it hijacks our cognition & consciousness – PMC (nih.gov) October 2021

Abstract

Rates of cannabis use among adolescents are high, and are increasing concurrent with changes in the legal status of marijuana and societal attitudes regarding its use. Recreational cannabis use is understudied, especially in the adolescent period when neural maturation may make users particularly vulnerable to the effects of Δ-9-tetrahydrocannabinol (THC) on brain structure. In the current study, we used voxel-based morphometry to compare gray matter volume (GMV) in forty-six 14-year-old human adolescents (males and females) with just one or two instances of cannabis use and carefully matched THC-naive controls. We identified extensive regions in the bilateral medial temporal lobes as well as the bilateral posterior cingulate, lingual gyri, and cerebellum that showed greater GMV in the cannabis users. Analysis of longitudinal data confirmed that GMV differences were unlikely to precede cannabis use. GMV in the temporal regions was associated with contemporaneous performance on the Perceptual Reasoning Index and with future generalized anxiety symptoms in the cannabis users. The distribution of GMV effects mapped onto biomarkers of the endogenous cannabinoid system providing insight into possible mechanisms for these effects.

SIGNIFICANCE STATEMENT Almost 35% of American 10th graders have reported using cannabis and existing research suggests that initiation of cannabis use in adolescence is associated with long-term neurocognitive effects. We understand very little about the earliest effects of cannabis use, however, because most research is conducted in adults with a heavy pattern of lifetime use. This study presents evidence suggesting structural brain and cognitive effects of just one or two instances of cannabis use in adolescence. Converging evidence suggests a role for the endocannabinoid system in these effects. This research is particularly timely as the legal status of cannabis is changing in many jurisdictions and the perceived risk by youth associated with smoking cannabis has declined in recent years.

Discussion

We present evidence of GMV differences in adolescents associated with only one or two instances of cannabis use. Although novel, this work is consistent with reports of a dose–response effect of cannabis on behavioral and brain measures following heavier use (Lorenzetti et al., 2010; Silins et al., 2014). We identified significantly greater GMV in adolescents who reported only one or two instances of cannabis use relative to cannabis naive controls in large medial temporal clusters incorporating the amygdala, hippocampus, and striatum, extending into the left prefrontal cortex. Significantly greater GMV was also observed in the lingual gyri, posterior cingulate, and cerebellum. The regions identified in this whole-brain, VBM approach replicated previous findings of differences in volume (Yücel et al., 2008; Ashtari et al., 2011; Schacht et al., 2012) and shape (Gilman et al., 2014; Smith et al., 2014, 2015) associated with cannabis use in ROI studies and with the spatial distribution of the eCB system (Burns et al., 2007). Although cannabis use has been associated with reduced brain volumes, studies typically report on adults with heavy substance use histories (cf. Ashtari et al., 2011). Gilman et al. (2014), however, have reported gray-matter density increases in the amygdala and nucleus accumbens of young adult recreational users and Medina et al. (2007) observed hippocampal enlargement in cannabis using adolescents. Our results are also consistent with the Avon Longitudinal Study of Parents and Children (French et al., 2015), which showed a trend for greater cortical thickness in male adolescents with <5 instances of cannabis use relative to THC-naive controls.

Converging evidence suggests that these effects may be a consequence of cannabis exposure. GMV differences could not be explained by group differences in demographic, personality, psychopathology, or other substance use factors. Examination of THC-naive 14-year-olds who later used cannabis showed no GMV differences, even using a more liberal ROI test, suggesting that the differences do not precede cannabis use and are not because of unidentified factors in those predisposed to use. Finally, the spatial distribution of GMV effects was associated with the eCB system, suggesting cannabis exposure may cause these findings.

The preclinical literature presents a number of possible mechanisms by which low levels of cannabis exposure could result in greater GMV relative to THC-naive controls. Adolescent rats treated with cannabinoid agonist showed altered gliogenesis in regions including the striatum and greater preservation of oligodendroglia relative to control animals (Bortolato et al., 2014). Zebra finches treated with cannabinoid agonist showed greater dendritic spine densities (Gilbert and Soderstrom, 2011); critically, these effects were observed in late-prenatal but not adult animals. Of particular relevance to this study, a single dose of Δ9THC transiently abolished eCB-mediated long-term depression (LTD) in the nucleus accumbens and hippocampus of adolescent mice (Mato et al., 2004). Suspension of LTD may interrupt maturation-related neural pruning and preserve gray matter. Future studies should assess whether these processes operate in human adolescents and whether they produce persisting alterations in GMV.

These findings should be interpreted in light of the study’s limitations. The IMAGEN sample is racially and ethnically homogenous so it remains to be determined whether the findings generalize to youth from more diverse backgrounds. Substance use was assessed using self-report and we do not have standard dose units of cannabis nor information on mode of use or a measure of drug metabolites. Combining images from different sites and imaging platforms remains controversial and is not completely controlled by including site as a covariate. Future studies should replicate the present results using images acquired at the same site on the same scanner or with equal numbers of cases and controls per scanner. We also note that the CNR1 gene expression (Hawrylycz et al., 2012) and CB₁ receptor density (D’Souza et al., 2016) maps were generated in independent samples of adults and may not accurately represent the eCB system in our sample of adolescents. Although we report significant spatial associations between GMV effects and both CNR1 gene expression and CB₁ receptor density, the effect sizes were small and any suggestion that these associations represent mechanisms for the effects we observe is speculative and requires further investigation.

We adopted a whole-brain, VBM approach to detect effects that were not limited by anatomical boundaries and to allow exploration of spatial relationships between GMV effects and the eCB system. There is evidence, however, that brain perfusion can influence VBM measures of local volume (Franklin et al., 2013, 2015; Ge et al., 2017; cf. Hawkins et al., 2018) so future studies should combine VBM with other measures of brain structure to provide confirmatory evidence. In particular, shape analysis has been shown to be sensitive to brain structural differences associated with cannabis use (Gilman et al., 2014; Smith et al., 2014, 2015; Weiland et al., 2015). Moreover, combining morphometry metrics allows for testing of associations between them, which can identify different relationships between shape deformations and local volume (Gilman et al., 2014) providing evidence of further differences between cannabis users and controls.

One source of variability in the human findings on brain structural correlates of cannabis use may be comorbid substance use (Weiland et al., 2015; Gillespie et al., 2018). Given recent evidence of different patterns of functional connectivity in groups using alcohol, nicotine, and cannabis alone and in combination (Vergara et al., 2018), it will be important to account for any possible interaction effects of cannabis with other psychoactive substances. This issue is particularly important considering the ways in which comorbid substance use has been addressed in two recent, widely cited studies. Gilman et al. (2014) covaried for alcohol and nicotine use and found gray-matter density increases and shape deformations associated with cannabis use. Weiland et al. (2015) matched groups on alcohol and nicotine use and reported no morphometric differences associated with cannabis use, concluding that previously reported differences associated with cannabis may instead be attributable to alcohol use. The participants in Weiland et al.’s (2015) study, however, were using alcohol and nicotine at higher levels than those in Gilman et al.’s (2014) study. It is possible that cannabis, alcohol, and nicotine have differential effects on brain morphometry; specifically, recreational cannabis use has been associated with volume increases, whereas alcohol has been associated with volume reductions. In the current study, we matched the groups on alcohol and nicotine use and, within the cannabis using group, neither alcohol nor nicotine use was associated with individual differences in GMV, suggesting that the GMV differences we report are associated with cannabis use.

We note individual differences in GMV effects: although regional GMV was greater at the group level for adolescents with low levels of cannabis exposure, the distributions showed a high degree of overlap such that many cannabis users had GMV equivalent to that of controls. None of the tested demographic, personality, or substance use factors stratified GMV in the cannabis users. We note evidence that an association between cannabis use and cortical thickness was stratified by genetic risk for schizophrenia (French et al., 2015) and that an association between cannabis use and hippocampal shape was stratified by dopamine-relevant genes (Batalla et al., 2018). Some adolescents may be vulnerable to GMV effects at extremely low levels of cannabis use and it will be critical to identify those at risk as these structural brain changes may be associated with individual risk for psychopathology and deleterious effects on mood and cognition.

Of the behavioral variables tested, only sensation seeking and agoraphobia differed between the cannabis users and controls and these factors were not related to GMV differences. In the cannabis using participants, GMV in the medial temporal clusters was associated with PRIQ and psychomotor speed such that greater GMV in these regions was associated with reduced performance. The finding that right medial temporal GMV predicted generalized anxiety symptoms at follow-up for those participants who had used cannabis should be interpreted with caution given the small sample size and that we were not able to identify factors that drove the individual differences in cannabis effects on GMV at baseline. These findings are notable, however, as panic and anxiety symptoms are frequently reported side effects by naive and occasional cannabis users (Hall and Solowij, 1998). We also note fMRI evidence of hypersensitivity of the amygdala to signals of threat in a partly overlapping sample of cannabis using adolescents (Spechler et al., 2015) and a relationship between adolescent cannabis use and future mood complaints (Wittchen et al., 2007), even with comparatively low levels of use (Cheung et al., 2010).

We have revealed greater GMV in adolescents with only one or two instances of cannabis use in regions rich in CB₁ receptors and CNR1 gene expression. Critically, we were able to control for a range of demographic and substance use effects, to confirm that these structural brain effects were not associated with comorbid psychopathology, and to demonstrate that these effects were unlikely to precede cannabis use. The pattern of results is characterized by individual differences in GMV effects in the cannabis users; these individual differences were associated with PRIQ and with vulnerability to future symptoms of generalized anxiety. Given the increasing levels of cannabis use among adolescents today, we suggest that studying the effects of recreational use early in life is an area of particular importance that should be addressed in the future by large scale, prospective studies.

Source: Grey Matter Volume Differences Associated with Extremely Low Levels of Cannabis Use in Adolescence | Journal of Neuroscience (jneurosci.org) March 2019

This article is distilled from a paper given at the Recovery Plus conference in London on 26^th June 2018 by Peter Stoker, Director of the National Drug Prevention Alliance.

References available on request.

Prevention, the word and meaning, comes from the Latin “praevenire” which means “to come before”. In other words, to act pre-the event – not during it or after it. Any action later than pre-the event is not prevention, it is repair. And both are required.   When it comes to funding, Prevention is the Cinderella service, and reasons why could include that Treatment has more workers with a resulting vigour; Treatment is easier to count, pleasing accountant-oriented funders; Prevention is (falsely) depicted as inhibiting Human Rights, and libertarian campaigners have always had deeper pockets that Prevention ever had.

INTERNATIONAL HISTORY

Early responses to the drug problem were characterised by being reactive rather than proactive, often with a legal or enforcement flavour.

There was also a tendency to focus on transmission of knowledge, sometimes coupled with a challenging of the users’ attitudes – unintended consequences could follow, for example:

• if you give knowledge to a user you may produce a knowledgeable user, and
• if you challenge a user’s attitude you may produce a knowledgeable user with an attitude.

In due course a more complete model was developed using the simple synonym – KAB, meaning you should address a mixture of Knowledge, Attitudes and Behaviour. (And focus on encouraging positive behaviour, rather than punishment).

Libertarians spotted the educational arena as fertile ground for their campaigns; their speculative allegation that the so-called ‘war on drugs’ was failing was the launchpad for harm reduction (HR1) – this was later augmented by inclusion of human rights (HR2). I witnessed all this being promoted vigorously at the 2009 UNGASS/CND conference in Vienna – we were emphasising ‘Whole Health’ as a goal, but throughout the proceedings there was an apparently innocuous and almost irresistible request from ACLU delegates that human rights should be included in all clauses. It wasn’t evident at this moment that they would later insist that using drugs was itself a “human right”, which therefore meant that prevention was, in effect, a breach of human rights. This activism was bankrolled by George Soros’ Open Society.

You can explore people’s thinking on this every day, in the Google Alerts, but remember what H.L.Mencken had to say: “For every complex problem there is a simple solution … and it doesn’t work”.

Exemplary practice can be observed in several initiatives. There are too many to cover them all, but here are some indicative examples and source materials:

DFAF – Drug Free America Foundation – www.dfaf.org – internationally active, establishing conferences in Europe and the Americas. Publishes a learned journal, and holds an enormous library.

NFIA – National Families In Action – Atlanta USA – www.nationalfamilies.org – countless years of detailed research and practice. Many learned papers. They have just published a very useful technical paper called ‘The MJ File’ – requires reading.

CADCA  – www.cadca.org – Community Anti-Drug Coalitions of America – until recently under direction of Major General Arthur Dean, US Army retired. CADCA is well-resourced; in 2016 alone it trained over 8,000 youth.

A very useful publication by NIDA/CSAP www.drugabuse.gov (Center for Substance Abuse Prevention) is ‘Preventing Drug Abuse’ – a slim volume, its first edition in 1997, revised in 2003 … about due for an update, one might say!

DARE – www.dare.org –  has suffered attacks in recent years but has survived, to the extent that it is signing new client organisations at the rate of about 200 a year even now.

DWI – Drug Watch International –  www.drugwatch.org a long-standing forum of experts in America and abroad. Membership by invitation only.

Straight – peer-led youth rehab service, now closed. Featured in the movie ‘Not My Kid’ starring George Segal and Stockard Channing.  Straight came in for criticism from the liberal left, and eventually closed, but not for this reason. I asked Bill Oliver, Chief Executive for many years, what caused the collapse of Straight. He told me “We were very good drug workers but lousy accountants”. A salutory comment!

SAM – Smart Approaches to Marijuana – www.sam.org . One of the most potent bodies in recent years, in the legalisation battle zone. Under the direction of Kevin  Sabet, a former policy adviser in the  US drug czar’s office. Senior staffers include former Congressman Patrick Kennedy. Their approach is soundly based on scientific evidence.

 And NDPA – National Drug Prevention Alliance – based in Slough, near Heathrow, and almost 30 years old. NDPA has provided support and training for parents, young people, drugs professionals and teachers. It has provided counselling and referral for users, and has done a large amount of work in the broadcast and print media,. It runs two websites – one for drugs professionals www.drugprevent.org.uk and one – more accessible in its presentation –  for parents – www.pinpoints.org.uk The websites include thousands of technical papers as well as other advisory publications. The websites are regularly visited internationally, several hundred thousand visits per year, and readers include our own Home Office.

EXAMPLES OF SUCCESS

Perhaps the earliest example was almost 40 years ago, in the late 1980s. Increased drug use sparked large numbers of parents to press academics into action, with the most memorable campaign being ‘Just Say No’ – under Ronald Regan’s wife Nancy. It was ridiculed by the left, but the campaign was very much more than a slogan, included detailed trainings for parents and youth, plus media activism, and the hard evidence is that it reduced prevalence by more than 60% – 11 million fewer users. Any other health-related campaign today would kill for such a result.

Perhaps the best example of this in recent years has been around the use of tobacco. Historically tobacco was used freely everywhere. Even doctors said it was good for you – it would soothe your throat, for example. Advertising sold it vigorously. Such protests as were made, were largely ignored. And if any people suggested that smoking had made them ill, the rest of us felt that that was their own fault and nothing to do with the us – they were getting what they deserved

Then, one day, the US Surgeon General announced that tobacco smoking by one person could give other persons cancer (through passive smoking). This was a game-changing announcement; we could no longer ignore what these drug users were doing – now it was affecting all of us. Anti-smoking articles and adverts appeared in the media; doctors advised strongly against it, schools told their pupils to avoid it, offices prohibited smoking in the premises, causing those who still were dependent on cigarettes to huddle in unpleasant external doorways, and the newly emerging Health and Safety brigade put in their six-pennorth. In due course the government reacted, producing new and influential legislation, banning smoking in many places. Before long the culture changed markedly, and in consequence so did the prevalence.

But if you want a bang up-to-date success, story you need look no further than Iceland. Comparing latest European figures with a couple of decades ago, teen drinkers have dropped from 42% to 5%, cannabis use has dropped from 17% to 7%, and tobacco smoking from 23% to 3%. The emphasis is on providing stimulating activities for youth, and on schooling parents in now to be more engaged with their families. Countries are following the Icelandic model, and research shows Risk factors and Protective Factors are pretty much the same everywhere.

There are localised examples of how to get ahead of the game – for example, one effective program was run in New York – called ‘Fixing Broken Windows’ the approach was to keep the streets and buildings clean and tidy – it reduced drug abuse and other social aspects.

In society as a whole, what promises the best results? In essence, the most effective  strategy will come from changing the culture.

Balanced prevention policy and strategy

I have yet to find a better definition what we should do than that written by a leading expert in the prevention field, based in Arizona – William Lofquist:

“We need to get beyond the notion that prevention is stopping something happening, to a more positive approach which creates conditions which promote the well-being of people”.

Lofquist found the importance of treating youth as resources, rather than objects or recipients of project work. He also emphasised that it should engage the whole of society, not in some rigid formulaic way but in a fluid, proactive approach which is alive to changes in society and always works to stay ahead of the game.

An assembly of this co-ordinated strategy and policy might include the following:

We can also learn much from the science of ‘Behaviour Modification’  – as practised by, inter all, Professor Brian Sheldon of the Royal Holloway University.

Constructive selfishness …

The tobacco example above describes what I mean by this expression. We should not shrink from recognising that selfishness is a powerful driving force across society. And since it is a powerful driving force, we should seek to drive it to our advantage.

We have yet to wake up to the potential of defining and communicating to society at large the various ways in which one person’s drug misuse adversely affects the rest of us.

Establishing readiness for prevention – CULTURAL CHANGE

What influences culture?

• Peer group influence
• Personal perceptions
• Income versus cost of any action
• Health issues
• Moral structure
• Spiritual structure
• Family values
• Attraction of risk-taking
• Media
• Mental state
• Legislation
• Economy – the well-off or the poor
• Employment – job or no job

CSAP found in their comparison of practices that the best prevention results come through co-ordinated prevention efforts, offering multiple strategies, and providing multiple points of access.

*                 *                   *                 *                  *

This is but a quick canter through the jungle of Prevention. There is much more to it, but I hope I have whetted your appetite – and you may even see the sense in building prevention into your work spectrum. (As co-operators rather than competitors with other agencies).

Don’t fear that prevention will reduce your treatment client base – as treatment workers, you are going to be in demand for a long time yet! Whilst some will be prevented from drug and alcohol abuse, and some will manage to cure themselves, most people need expert help.

We are, after all, working towards the same objective.  I once saw a cartoon in which a drug worker was asking a guru how to solve the drug problem. ‘Why do people use drugs?’ asked the guru. ‘To escape reality’ said the worker. ‘Then the solution is obvious’. Said the guru. ‘Improve reality’

Abstract

Three decades ago, I would have been over the moon to see marijuana legalized. It would have saved me a lot of effort spent trying to avoid detection, constantly looking for places to hide a joint. I smoked throughout my teens and early 20s. During this period, upon landing in a new city, my first order of business was to score a quarter-ounce. The thought of a concert or a vacation without weed was simply too bleak.

These days it’s hard to find anybody critical of marijuana.

The drug enjoys broad acceptance by most Americans — 63 percent favoured ending cannabis prohibition in a recent Quinnipiac poll — and legislators on both sides of the aisle are becoming more likely to endorse than condemn it. After years of loosening restrictions on the state level, there are signs that the federal government could follow suit: In April, Senate Minority Leader Charles E. Schumer (D-N.Y.) became the first leader of either party to support decriminalizing marijuana at the federal level, and President Trump (his attorney general notwithstanding) promised a Republican senator from Colorado that he would protect states that have legalized pot.

And why not? The drug is widely thought to be either benign or beneficial. Even many of those apathetic toward its potential health benefits are ecstatic about its commercial appeal, whether for personal profit or state tax revenue. Legalization in many cases, and for many reasons, can be a good thing. I’m sympathetic.

But I am also a neuroscientist, and I can see that the story is being oversimplified. The debate around legalization — which often focuses on the history of racist drug laws and their selective enforcement — is astoundingly naive about how the widespread use of pot will affect communities and individuals, particularly teenagers. In our rush to throw open the gate, we might want to pause to consider how well the political movement matches up with the science, which is producing inconveniently alarming studies about what pot does to the adolescent brain.

Marijuana for sale at a Colorado dispensary.    (Matthew Staver/Bloomberg Creative Photos)

I took a back-door route to the science of marijuana, starting with a personal investigation of the plant’s effects. When I was growing up in South Florida in the 1980s, pot was readily available, and my appreciation quickly formed the basis for an avid habit. Weed seemed an antidote to my adolescent angst and ennui, without the sloppiness of alcohol or the jaw-grinding intensity of stimulants.

Of the many things I loved about getting high, the one I loved best was that it commuted the voice in my head — usually peevish or bored — to one full of curiosity and delight. Marijuana transformed the mundane into something dramatic: family outings, school, work or just sitting on the couch became endlessly entertaining when I was stoned.

Like any mind-altering substance, marijuana produces its effects by changing the rate of what is already going on in the brain. In this case, the active ingredient delta-9-THC substitutes for your own natural endocannabinoids and mimics their effects. It activates the same chemical processes the brain employs to modulate thoughts, emotions and experiences. These specific neurotransmitters, used in a targeted and judicious way, help us sort the relentless stream of inputs and flag the ones that should stand out from the torrent of neural activity coding stray thoughts, urges and experience. By flooding the entire brain, as opposed to select synapses, marijuana can make everything, including the most boring activities, take on a sparkling transcendence.

Why object to this enhancement? As one new father told me, imbibing made caring for his toddler much more engrossing and thus made him, he thought, a better parent. Unfortunately, there are two important caveats from a neurobiological perspective.

As watering a flooded field is moot, widespread cannabinoid activity, by highlighting everything, conveys nothing. And amid the flood induced by regular marijuana use, the brain dampens its intrinsic machinery to compensate for excessive stimulation. Chronic exposure ultimately impairs our ability to imbue value or importance to experiences that truly warrant it.

In adults, such neuro-adjustment may hamper or derail a successful and otherwise fulfilling life, though these capacities will probably recover with abstinence. But the consequences of this desensitization are more profound, perhaps even permanent, for adolescent brains. Adolescence is a critical period of development, when brain cells are primed to undergo significant organizational changes: Some neural connections are proliferating and strengthening, while others are pared away.

Although studies have not found that legalizing or decriminalizing marijuana leads to increased use among adolescents, perhaps this is because it is already so popular. More teenagers now smoke marijuana than smoke products with nicotine; between 30 and 40 percent of high school seniors report smoking pot in the past year, about 20 percent got high in the past month, and about 6 percent admit to using virtually every day. The potential consequences are unlikely to be rare or trivial.

The decade or so between puberty and brain maturation is a critical period of enhanced sensitivity to internal and external stimuli. Noticing and appreciating new ideas and experiences helps teens develop a sense of personal identity that will influence vocational, romantic and other decisions — and guide their life’s trajectory. Though a boring life is undoubtedly more tolerable when high, with repeated use of marijuana, natural stimuli, like those associated with goals or relationships, are unlikely to be as compelling.

It’s not surprising, then, that heavy-smoking teens show evidence of reduced activity in brain circuits critical for  flagging newsworthy experiences, are 60 percent less likely to graduate from high school, and are at substantially increased risk for heroin addiction and alcoholism. They show alterations in cortical structures associated with impulsivity and negative moods; they’re seven times more likely to attempt suicide.

Recent data is even more alarming: The offspring of partying adolescents, specifically those who used THC, may be at increased risk for mental illness and addiction as a result of changes to the epigenome — even if those children are years away from being conceived. The epigenome is a record of molecular imprints of potent experiences, including cannabis exposure, that lead to persistent changes in gene expression and behavior, even across generations. Though the critical studies are only now beginning, many neuroscientists prophesize a social version of Rachel Carson’s “Silent Spring,” in which we learn we’ve burdened our heirs only generations hence.

Might the relationship between marijuana exposure and changes in brain and behavior be coincidence, as tobacco companies asserted about the link between cancer and smoking, or does THC cause these effects? Unfortunately, we can’t assign people to smoking and nonsmoking groups in experiments, but efforts are underway to follow a large sample of children across the course of adolescent development to study the effects of drug exposure, along with a host of other factors, on brain structure and function, so future studies will probably be able to answer this question.

In the same way someone who habitually increases the volume in their headphones reduces their sensitivity to birdsong, I followed the “gateway” pattern from pot and alcohol to harder drugs, leaping into the undertow that eventually swept away much of what mattered in my life. I began and ended each day with the bong on my nightstand as I floundered in school, at work and in my relationships. It took years of abstinence, probably mirroring the duration and intensity of my exposure, but my motivation for adventure seems largely restored. I’ve been sober since 1986 and went on to become a teacher and scholar. The single-mindedness I once directed toward getting high came in handy as I worked on my dissertation. I suspect, though, that my pharmacologic adventures left their mark.

Now, as a scientist, I’m unimpressed with many of the widely used arguments for the legalization of marijuana. “It’s natural!” So is arsenic. “It’s beneficial!” The best-documented medicinal effects of marijuana are achieved without the chemical compound that gets users high. “It’s not addictive!”  This is false, because the brain adapts to marijuana as it does to all abused drugs, and these neural adjustments lead to tolerance, dependence and craving — the hallmarks of addiction.

It’s true that a lack of benefit, or even a risk for addiction, hasn’t stopped other drugs like alcohol or nicotine from being legal, used and abused. The long U.S. history of legislative hypocrisy and selective enforcement surrounding mind-altering substances is plain to see. The Marihuana Tax Act of 1937, the first legislation designed to regulate pot, was passed amid anti-Mexican sentiment (as well as efforts to restrict cultivation of hemp, which threatened timber production); it had nothing do with scientific evidence of harm. That’s true of most drug legislation in this country. Were it not the case, LSD would be less regulated than alcohol, since the health, economic and social costs of the latter far outweigh those of the former. (Most neuroscientists don’t believe that LSD is addictive; its potential benefits are being studied at Johns Hopkins and New York University, among other places.)

Still, I’m not against legalization. I simply object to the astounding lack of scepticism about pot in our current debate. Whether or not to legalize weed is the wrong question. The right one is: How will growing use of delta-9-THC affect individuals and communities?

Though the evidence is far from complete, wishful thinking and widespread enthusiasm are no substitutes for careful consideration. Instead of rushing to enact new laws that are as nonsensical as the ones they replace, let’s sort out the costs and benefits, using current scientific knowledge, while supporting the research needed to clarify the neural and social consequences of frequent use of THC. Perhaps then we’ll avoid practices that inure future generations to what’s really important.

                                       By Judith Grisel,    May 25, 2018

Source:  https://www.washingtonpost.com/ posteverything/wp/2015/04/30/yes-pot-should-be-legal-but-it-shouldnt-be-sold-for-a-profit/   

Substance use has often been described as “bad learning” linked with impairments in reward processing and decision-making, but there is little substantial research to support this idea. A recent study by Byrne et al. suggests that substance misuse not only promotes harmful habit formation, which might undermine survival, but also makes it difficult to stop using.

Model-free vs. Model-based Learning

The “Dual Systems” theory of reinforcement learning defines two distinct systems:

1. The model-based, or goal-directed system, where actions are planned and purposeful, and we learn about the connection between actions and outcomes, and how to modify our behavior to achieve the desired outcome. This system requires more cognitive processing and is more flexible and controlled.

2. The model-free, or habit-based system, where learning is informed by reflexive responses to stimuli – like compulsive substance use and cravings. This system of learning is less flexible and is more controlled by automatic processing.

The differences between the two systems of learning have been highlighted by researchers in relation to harmful habitual behaviors such as substance use. One school of thought suggests that learning informed by the model-free system, with more of a focus on instinctual response to stimuli and less of a focus on conscious and informed decision-making, sets a person up to be more likely to engage in detrimental behaviors like substance use.

There is evidence that progressing from first use to misuse and addiction is paralleled by a shift from planned, purposeful, and goal-directed behavior to behavior that is habitual and reflexive. This progression and subsequent loss of control has been discussed by National Institutes on Drug Abuse Director Dr. Nora Volkow in her keynote speech at the APA and in her blog about free will. Model-free, conditioned learning means it is harder for a person to engage their frontal lobes, the part of the brain that helps us prioritize healthy, long-term and rational decisions. Repeated problematic substance use initiates a process where humans begin to respond more instinctually to the substance, wanting more and more of it over time. Use begets use, which leads to maladaptive behaviors centered around obtaining and using the substance to trigger the very same dopamine response that drives and reinforces model-free, habitual learning.

Substance Use and Reward Devaluation

Reward devaluation is a process that occurs in the brain where the value of a desirable outcome, like singing in a band, mentoring, or maintaining sobriety is reduced significantly. This process plays into why improving treatment outcomes can be so hard – treatment for addiction is not as “reinforcing” in the brain as substance use. Compulsive drug use is considered “highly pleasurable” by the parts of the brain that control decision-making when people are heavily addicted and feel as though they need the substance to survive. But treatment? not so much — long-term treatment is difficult to complete without continual support and a long-term treatment plan. Many patients stop attending treatment and/or support groups, and taking prescribed medications unless they are compelled to follow a set treatment plan and have adequate supports in place to help keep them on track.

Addiction is correlated to a considerable decrease in a person’s ability to devalue or disengage from habits learned through the model-free system. This means that problematic substance use affects our ability to make decisions and as the disorder progresses, we begin to put less value on long-term rewards and more value on immediately satisfying a need. Gradually, short term needs, like substance use, override long-term needs, like maintaining employment or investing in personal relationships.

Goals of Study

1. To examine the associations between model-based and model-free learning with a wide array of substance use behaviors. The process used to determine this was measuring individual variations in eye-blink rate, an indirect proxy for dopamine functioning, a key neural process related to model-free learning.

2. To assess whether problematic substance use predicted reward disengagement.

Why is This Important?

Patients with substance use disorders are driven to use despite harmful consequences, and although addiction is understood more and more as an acquired brain disease, many are still mystified as to why those suffering can’t manage to break their “habit.” This study helps foster a greater understanding of the mechanisms that explain why. Use may be thought of as “recreational” by the user, but it poses a challenge to the brain, reinforcement systems, and reward hierarchies, which can change a person quickly and in a way that is hard for those around them to understand. Once reward-outcome associations are well established— i.e., taking drugs makes a person “feel good”— individuals with substance use disorders have changed the most basic mechanisms in their brain, and will have more difficulty disengaging from the habitual tendencies. It is not clear how individual experiences, genetics, trauma, and other factors change the speed of these changes. That said, the results of this study are consistent with previous data depicting how alcohol dependence indicates a greater likelihood that a person has habit-based learning strategies over goal-directed strategies. The results do not, however, provide us with more information about whether biological recovery is possible, and how we could make recovery more likely and sustainable for patients.

Authors state that current findings highlight how problems with substance use go beyond the realms of habit formation: they also influence the process of disengaging or “breaking” habits by making it more difficult for individuals with substance use disorders to stop using substances. A better understanding of the mechanisms in the brain that take over once substance use becomes problematic may help us create more effective prevention campaigns and treatments once substance use progresses to a harmful habit.

Source: Why are habits so hard to break? (addictionpolicy.org) May 2019, updated October 2022

Tell Your Children:
The Truth About Marijuana, Mental Illness, and Violence
by alex berenson
free press, 272 pages, $26

The smoking of marijuana, with its careful preparation of the elements and the solemn passing around of the shared joint, was the unholy communion of the counterculture in the late 1960s, when our present elite formed its opinions. Many of them allowed their children to follow their bad examples, and resent that this exposes their young to a (tiny) risk of persecution and career damage. As a result, those who still disapprove of marijuana are much disliked. The book I wrote on the subject six years ago, The War We Never Fought, received a chilly reception and remains so obscure that I don’t think Alex ­Berenson, whose book has received much friendlier coverage, even knows it exists. As a writer who naturally covets readers and sales, I find this mildly infuriating.

But let me say through clenched teeth that it is of course very good news that a fashionable young metropolitan person such as Mr. ­Berenson is at last prepared to say openly that marijuana is a dangerous drug whose use should be severely discouraged. For, as ­Berenson candidly admits, he was until recently one of the great complacent mass of bourgeois bohemians who are pretty relaxed about it. He confesses in the most important passage in the book that he once believed what most of such people believed. He encapsulates this near-universal fantasy thus:

Marijuana is safe. Way safer than alcohol. Barack Obama smoked it. Bill Clinton smoked it too, even if he didn’t inhale. Might as well say it causes presidencies. I’ve smoked it myself, I liked it fine. Maybe I got a little paranoid, but it didn’t last. Nobody ever died from smoking too much pot.

These words are a more or less perfect summary of the lazy, ignorant, self-serving beliefs of highly educated, rather stupid middle-class metropolitans all over the Western world in such places as, let’s just say for example, the editorial offices of the New York Times. Thirty years from now (when it’s too late), they will look as crass and irresponsible as those magazine advertisements from the 1950s in which pink-faced doctors wearing white coats recommended certain brands of cigarettes. But just now, we are in that foggy zone of consciousness where the truth is known to almost nobody except those with a certain kind of direct experience, and can be ignored by everyone else.

One of the experienced ones, thank heaven, is Alex ­Berenson’s wife Jacqueline. She is a psychiatrist who specializes in evaluating mentally ill criminals. One evening, the Berensons were discussing one of her cases, a patient who had committed a terrible, violent act. Casually, Jacqueline remarked, “Of course he was high, been smoking pot his whole life.” Alex doubtfully interjected, “Of course?,” and she replied, “Yeah, they all smoke.” (She didn’t mean tobacco.) And she is right. They all do. You don’t need to be a psychiatrist to know this. You just have to be able to do simple Internet searches.

Most violent crime is scantily reported, since local newspapers lack the resources they once had. The exceptions are rampage mass killings by terrorists (generally in Europe) and non-political crazies (more common in the United States). These crimes are intensively reported, to such an extent that news media find things out they were not even looking for, such as the fact that the perpetrator is almost always a long-term marijuana user. Where he isn’t (and it is almost always a he), some other legal or illegal psychotropic, such as steroids or “antidepressants,” is ­usually in evidence. But you do have to look, and most people don’t. Then you have to see a pattern, one that a lot of important, influential people specifically do not want to see.

That husband-and-wife conversation in the Berenson apartment is the whole book in a nutshell, the epiphany of a former apostle of complacency from the college-­educated classes who suddenly discovers what has been going on around him for years. What he repeats over and over again is very simple: Marijuana can make you permanently crazy. (This is a long-term cumulative effect, not the effect of immediate intoxication.) And once it has made you crazy, it can make you violent, too.

You’ll only find out if you’re susceptible by taking it. It is not soft. It is not safe. It is one of the most dangerous drugs there is, and we are on the verge of allowing it to be advertised and put on open sale. Berenson has gotten into predictable trouble for asserting that the connection is pretty much proved. Alas, this is not quite so. But the correlation is hugely powerful. The chance that it is meaningful is great. Who would be surprised if a drug with powerful psychotropic effects turned out to be the cause of mental illness in its users? Correlation is not causation, but it is one of the main tools of ­epidemiology. Causation, ­especially in matters of the brain, is extraordinarily difficult to prove, and so we may have to base our actions, or our refusals to take action, on something short of total certainty.

Tell Your Children is filled with persuasive, appalling individual case histories of wild violence, including the abuse of small children. It also lists and explains the significance of powerful, large-scale surveys of Swedish soldiers and New Zealand students, which connect the drug to mental illness and lowered school performance. Berenson provides facts and statistics about violent crime in places where marijuana is widely available, and anecdotes so repetitive that they cease to be anecdotes. The puzzle remains as to why it is necessary to say all this repeatedly when a sensible person would listen the first time.

Perhaps it is because of the large, and very well-funded, campaigns for marijuana legalization described by Berenson. People who drink fair-trade coffee and eat vegan, who loathe other greed lobbies—such as pharmaceuticals, tobacco, fast food, or sugary drinks—smile on this campaign to make money from the misery of others.

Berenson shows how mental illness has grown in our midst without being noticed in public statistics. A comparable growth in, say, measles or tuberculosis would have shown up. But deteriorating mental health does not, thanks to privacy concerns, and to the fact that mental illness is not easily classified. It is also a sad truth that rich, advanced Western societies nowadays begrudge money for the mental hospitals needed to house and protect those who have overthrown their own minds. They are reluctant to record the existence and prevalence of the very real suffering that ought to be treated in the hospitals they have sold off, demolished, or never built.

Berenson also witheringly describes the propaganda devised by those who want to legalize the drug, from the mind-expanding zealots who view drug use as liberating to the hard-headed entrepreneurs and political professionals. Argue against them at your peril. Your audience may learn something, but your opponents will not. Wilful ignorance is the most powerful barrier to communication. It seals the human mind up like a fortress. You might as well read the works of Jean-Paul Sartre to a hungry walrus as try to debate with such people. I have attempted it. They don’t hear a word you say, but they hate you for getting in their way.

Berenson gives a fairly thorough account of the “medical marijuana” campaign, an almost comically absurd attempt to portray a poison as a medicine. This campaign is so bogus that it will vanish from the earth within days of full legalization, because in truth there is very little evidence that marijuana-based medicines are of much use. Berenson quotes one refreshingly candid marijuana defender as admitting, “Six percent of all marijuana users use it for medical purposes. Medical marijuana is a way of protecting a subset of society from arrest.”

In the U.S., legalizers are poised to win the modern civil war over the legalization of marijuana which has been dividing the country for half a century. It looks now as if marijuana will soon be legalized, on general sale, advertised and marketed and taxed. This worrying process has already begun in Canada. The United States has approached the issue sideways, conceding states’ rights in a way that would have delighted the Confederates.

The United Kingdom has taken a similar route: It pretends to maintain the law and, when asked, insists it has no plans to change it. But the police and the courts have gradually ceased to enforce it, so that it is now impossible to stroll through central London without nosing the reek of marijuana. Europe has gone the same way, with minor variations. Among the free law-governed nations, only Japan and South Korea still actively and effectively enforce their drug possession laws, and benefit greatly from it. But how long can they hold out?

The legalization campaigners are working like termites to undo the 1961 U.N. Convention that is the basis of most national laws against narcotics, using all the money and dishonesty at their command. They have plenty of both. So, besides the two disastrous, irrevocably legal poisons of alcohol and tobacco, we shall before long have a third—and probably a fourth and fifth not long afterward. If marijuana is legal, how will we keep cocaine and ecstasy illegal for long? Next will come heroin and LSD.

One reason for the default in favor of legalization and non-enforcement is the false association made by so many between marijuana and liberty. The belief that a dangerous, stupefying drug is an element of human liberty has taken hold of two, perhaps three generations. They should know better. Aldous Huxley warned in his much-cited but infrequently read dystopian novel Brave New World that modern men, appalled by the disasters of war and social conflict, would embrace a world where thinking and knowledge were obsolete and pleasure and contentment were the aims of a short life begun in a test-tube and ended by euthanasia. He predicted that they would drug themselves and one another to banish the pains of real life, and—worst of all—come to love their own servitude. In one terrible scene, the authorities spray protesting low-caste workers with the pleasure drug soma, and the workers end up hugging one another and smiling vaguely before returning to their drudgery. (Soma, unlike its real-life modern equivalents, is described as harmless, something easier to achieve in fiction than in reality.) What ruler of a squalid, wasteful, unfair, and ugly society such as ours would not prefer a stupefied, flaccid population to an angry one? Yet somehow, the freedom to stupefy oneself is held up quite seriously by educated people as the equal of the freedoms of thought, speech, and assembly. This is the way the world ends, with a joint, a bong, and a simper.

Whatever was wrong with my intense little segment of the 1960s revolutionary generation (and plenty was wrong with it), we believed that when we saw injustice we should fight it, not dope ourselves into a state of mind where it no longer mattered. But my tiny strand of puritan Bolsheviks was long ago absorbed into a giggling mass of cultural revolutionaries, who scrawled “Sex, Drugs, and Rock and Roll” on their banners instead of “Liberty, Equality, and Fraternity,” or even “Workers of All Lands, Unite!”

While Berenson’s facts are devastating, his own response to the crisis is feeble. He opposes marijuana legalization—and what intelligent person does not? He babbles of education and warning our children. But he declares that “decriminalization is a reasonable compromise.” Actually, it is not. It cannot be sustained. If matters are left as they are, legalization—first de facto and then de jure—will follow, because there will be no impetus to resist it. Unless the law decisively disapproves of and discourages the actual use of the drug, it is neither morally consistent nor practically effective.

The global drug trade would be nowhere without the dollars handed over to it by millions of individuals who are the end-users. We search for Mr. Big and never catch him. But we ignore or even indulge Mr. Small, regarding him as a victim, when in truth he keeps the whole thing going. In the end, the logic leads relentlessly to the stern prosecution and deterrent punishment of individual users. It is because I recognize this grim necessity that I remain a pariah. It is because he doesn’t that Alex Berenson is still just about acceptable in the part of the Western world that believes marijuana is a torch of ­freedom. 

Peter Hitchens is a columnist for The Mail on Sunday.

Source:  https://www.firstthings.com/article/2019/05/reefer-sadness

Kevin Sabet was a drug control policy adviser in the White House for both Republicans and Democrats

When most people talk about Canada’s impending legalization of marijuana, they talk about the future. When Kevin Sabet talks about it, he worries about history repeating. 

“There are huge misconceptions, I often feel like we’re living in 1918, not 2018,” he said.” When I say 1918, I mean 1918 for tobacco when everyone thought that smoking cigarettes was no problem and we had a new industry that was just starting.”

In 1918, soldiers returning home from the trenches of the First World War brought cigarettes home with them and unwittingly sowed the seeds of one of 20th century’s biggest health epidemics. 

“We hadn’t had tobacco related deaths before the 20th century because we hadn’t had a lot of cigarettes, which actually gave us the most deadly form of tobacco we’ve ever seen. I feel like we’re like that with marijuana.”

A former drug control policy adviser to the White House under both the Democrats and Republicans, Sabet is the President and CEO of Smart Approaches to Marijuana, a public health organization opposed to marijuana legalization and commercialization in the United States. 

He said the sudden about-face by Ontario’s newly-elected Progressive Conservative government away from a public monopoly on marijuana sales to a mixed public-private is “a really bad move.” 

“When I see the government monopoly being tossed out the window in favour of a private program that really puts private profit over public health.. I worry about that,” he said. “I think it’s a really bad move.” 

“They are moving from a government monopoly to private retail and that’s going to open the door to all the marketing and promotion and normalization that already is a huge problem for our already legal drugs.”

“We’ve seen how that turned out for pharmaceuticals like opiates, which are highly dangerous and we’ve seen how that turned out for tobacco and alcohol.”

Big investors lining up to cash-in on pot

Source: Ontario’s new retail pot plan ‘puts profit over public health’ says former Obama drug adviser | CBC News August 2018

• Teenagers who smoke have thicker matter in certain parts of their brains
• This was found in areas involved with emotions, memory, fear and panic
• Adolescent brains are typically thinning and being refined during this period
• Experts said ‘most people would assume one or two joints would have no impact’

Just one or two joints is enough to change the structure of a teenager’s brain, scientists have warned.

And the drug could cause changes affecting how likely they are to suffer from anxiety or panic, according to a study.

Researchers found 14-year-old girls and boys exposed to THC – the psychoactive chemical in cannabis – had a greater volume of grey matter in their brains.    

This means the tissue in certain areas is thicker, and it was found to be in the same areas as the receptors which marijuana affects.

Experts said thickening of brain tissue is the opposite of what usually happens during puberty, when teenagers’ brain matter gets thinner and more refined.

Researchers did scans of teenagers’ brains and discovered those who had been exposed to small amounts of marijuana (top row) had thicker regions of the brain (indicated by more orange and yellow tissue) than those who had never smoked cannabis (bottom row)

Researchers from the University of Vermont scanned the brains of teenagers from England, Ireland, France and Germany to study marijuana’s effects. 

They found differences in the volume of grey matter in the amygdala and the hippocampus.

These sections are involved with emotions, fear, memory development and spatial skills – changes to them suggests smoking cannabis could affect these faculties.    

Scientists said theirs is the first evidence to suggest structural brain changes and cognitive effects of just one or two uses of cannabis in young teenagers.

And it suggests as teenagers brains are still developing, they may be particularly vulnerable to the effects of THC.

THC, full name tetrahydrocannabinol, is the chemical in marijuana which makes people high and is what makes it illegal in the UK. 

‘Consuming just one or two joints seems to change grey matter volumes in young adolescents,’ said study author Professor Dr Hugh Garavan.

‘The implication is that this is potentially a consequence of cannabis use. You’re changing your brain with just one or two joints.

‘Most people would likely assume that one or two joints would have no impact on the brain.’

What changes the increased brain volume directly causes is unclear, but the researchers said it is important to understand cannabis’s effects in detail.

This is especially so in the US, where more states are legalising the drug and a view of it being harmless is spreading, they said.

Professor Garavan said cannabis use appears to produce the opposite effect on brain matter of what usually happens during puberty. 

He said a typical adolescent brain undergoes a ‘pruning’ process in which  it gets thinner, rather than thicker, as it refines its connections. 

‘One possibility is they’ve actually disrupted that pruning process,’ he said. 

Previous studies have focused on heavy marijuana users later in life and compared them against non-users. 

Few have looked at the effects of the first few uses of a drug.

Another of the study’s authors, Catherine Orr, now a lecturer at Swinburne University of Technology in Australia said: ‘Rates of cannabis use among adolescents are high and are increasingly concurrent with changes in the legal status of marijuana and societal attitudes regarding its use.

‘Recreational cannabis use is understudied, especially in the adolescent period when neural maturation may make users particularly vulnerable to the effects of THC on brain structure.’

The study, part of a long-term European project known as IMAGEN, involved 46 teenagers who used recreational marijuana once or twice by the age of 14.

They reported how many joints they had smoked and had brain scans.

It also involved 69 teenagers who used the drug at least 10 times between the ages of 14 and 16, and 69 who had not touched the drug by age 16.

Scientists also assessed them for signs of various mental disorders including ADHD, anxiety, depression and panic disorder.    

Dr Orr said: ‘Of the behavioural variables tested, only sensation seeking and agoraphobia differed between the cannabis users and controls. And these factors were not related to greater grey matter differences.’ 

The researchers said the area of the brain which cannabis interacts with is particularly important for brain development in adolescence, suggesting teenagers could be particularly affected by THC. 

Dr Orr concluded: ‘Almost 35 per cent of American 10th graders have reported using cannabis and existing research suggests that initiation of cannabis use in adolescence is associated with long-term neurocognitive effects.

‘We understand very little about the earliest effects of cannabis use, however, as most research is conducted in adults with a heavy pattern of lifetime use.

‘This study presents evidence suggesting structural brain and cognitive effects of just one or two instances of cannabis use in adolescence.’  

The study was published in The Journal of Neuroscience.

Source: Smoking weed just ONCE could change a teenager’s brain | Daily Mail Online January 2019

Abstract

Keywords: attention; cannabis; intellect; intrauterine; memory; perception.

Source: Effects of prenatal marijuana exposure on neuropsychological outcomes in children aged 1-11 years: A systematic review – PubMed (nih.gov) November 2018

Radula complanata, a cannabinoid moss. Henri Koskinen/Shutterstock

Most of us know that the cannabis plant produces compounds that react with the human body. That’s because we have our own system that makes similar compounds, cannabinoids, that have a wide range of actions from appetite control to immune function. Cannabis contains a cannabinoid called THC that interacts with the brain, resulting in euphoria and relaxation, as well as increased hunger and anxiety. It was long thought that there was no other natural source of cannabinoids – and along with a long list of supposed medical uses the mythical power of cannabis, and the psychoactive properties of THC, has grown.

But as it turned out, another plant contains something similar: a compound that has the structural hallmarks for it to act on the brain in a similar way to THC. The discovery of this lost twin, called cis-PET (perrottetinene), or PET, was tucked away in specialist chemistry journals in papers published in 1994 and 2002, with no subsequent research confirming its biological activity. But in a new study, published in Science Advances, a group of Swiss scientists have delved into the mechanism by which PET may be acting on the brain.

The particular liverwort in question, Radula, is endemic to New Zealand and Tasmania and is used as a herbal medicine by the Maori people. Preparations using this plant are also sold as a THC-like legal high on the internet.

But while similar to THC, does PET actually produce the same effects that THC does at a cellular and molecular level? Does it mimic the physiological effects? And is it different in ways that could give it therapeutic advantage or disadvantage? Some 24 years after its first discovery, the team of chemists and biochemists behind the new study have teased some of the answers out.

Their research was no mean feat. It required a new synthesis method to produce enough PET to do meaningful experiments. Once this was achieved, the researchers looked at two mirror versions of the two compounds, cis (the version found in the liverwort) and trans (a version they artificially created in the lab). In chemistry, the cis and trans terms tell us which side of the carbon chain the functional groups are (the bit of the molecule that does the work).

The researchers wanted to find out if these two versions of PET were able to interact with the two receptors found in humans that mediate the psychoactive effects of cannaboids – CB1, the receptor that produces the “high” effect from THC, and CB2 – in the same way as THC (how strongly they bound and how much is needed to produce an effect).

The researchers found intriguing similarities between the two versions in PET and THC. For both PET and THC, the trans versions (the abundant THC version found in cannabis and the lab-synthesised version found in liverwort) bound to the CB1 receptor better than the cis versions.

THC and PET side by side. Oliver Kayser

What’s interesting about this is that while the levels of cis-PET found in the liverwort plant are too low to produce the “high” effects produced by THC (hence why smoking PET won’t produce a high), it could explain why PET might still have a medicinal effect (similar to the effect produced by lower dose THC). However, any methods to extract and concentrate the liverwort compound could lead to the same problems as THC.

But what about CB2, the other cannabinoid receptor? This receptor plays a role in immune responses. Here the Swiss scientists found that the cisversions of both THC and PET bound this receptor better than the transversions. The implications of this are yet to be explored, but it again hints at a potential medicinal benefit worth exploring further.

The authors of the study then went on to test whether the binding of the CB1 receptors in the brains of mice had the same recognisable THC effects. Usually when THC binds with this receptor it produces four key effects: reduced body temperature, muscle rigidity, reduced movement and decreased sensitivity to pain. In this behavioural test, all four effects were also achieved in the mice using cis-PET, albeit in a much bigger amount.

But there was one notable difference. Inflammation in the brain is mediated by molecules called prostaglandins that can be derived from metabolic pathways involving our own body cannabinoids or plant-derived trans-THC. In contrast, the production of these mediators was reduced by cis-PET. It remains to be seen whether this is a good thing or a bad thing.

So while the study is just a start in understanding the mechanisms and effects of PET on the brain, there’s much we still don’t know. What we do know now, however, is that the levels of PET that are found in the natural liverwort plant are too low to produce the recognised effects of THC, so smoking it is unlikely to lead to a high. But it is also interesting that this compound could well have medicinal benefits without the high – one of the key reasons that THC has previously been dismissed as a medicine. Illegal trading and cultivation has confounded much meaningful clinical research, but this is changing and this new compound will add to the treasure trove of plant-derived cannabinoids that we still have much to understand.

Source: https://theconversation.com/liverwort-could-have-medicinal-benefits-of-cannabis-thc-without-the-high  Oct.24^th 2018

* Correspondence:

Albert Stuart Reece  

A leading perspectives piece in the New England Journal of Medicine recently observed the salience of assessing drug safety in children and emphasized that effects experienced in childhood can have long lasting impacts as they interfere with maturation and growth of the organism into later life.  Senior researchers from the National Institute of Drug Abuse have frequently drawn attention to the implications of adolescent cannabis exposure.  The effects of gestational exposure are even more far reaching.  These factors are given further urgency by studies showing 25% of Californian teenage mothers in California use cannabis.

Cannabis-related neuroteratology appears to clearly fall on a spectrum of deficits.

With the obvious caveats that many of the longitudinal studies of prenatal cannabis exposure (PCE) have been conducted in very different populations, that it is not easy to control for other sociodemographic factors frequently associated with drug use, and that the concentration of cannabis commonly used in the older studies was much lower, findings which together engender a fair degree of heterogeneity in the published reports, a remarkably consistent thread runs through the PCE literature.  Three major longitudinal studies have followed children exposed prenatally from white middle class Ottawa from the late 1970’s; from predominantly African-American Pittsburgh from 1982; and from the Netherlands from 2001.  Reductions in birth weight of 200-300g, slightly smaller head circumferences (2.8mm), and body length are reported in weekly users with several studies reporting dose-response effects.

In terms of neurobehavioural functioning increased neonatal startle response were seen, with specific cognitive defects in grade school, increased impulsivity, hyperactivity and depression at age 10, poor school achievement, adolescent delinquency, increased violence and aggression amongst girls, increased use of tobacco and cannabis in teens, and in the early 20’s in the longest running study, deficits in short term memory, visuospatial memory and motor impulse control.  These defects have been linked with ADHD and with autism.  Microcephaly was also noted in a large Hawaiian study.  Increased neonatal startle and later cognitive defects are also seen in rodents after PCE.

These findings are clinically significant, and may assume public health significance when one notes that autism is increasing in all USA states where it is measured, paralleling rising rates of cannabis use across the country.

Two reports from C.D.C. indicate an almost doubling of the rate of anencephaly following PCE R.R.=1.9 (95%C.I. 1.1-3.2).  In the context of the foregoing findings this major datum implies that cannabis has the unusual distinction of being a neurotoxin which interferes with brain development to the point of chemically amputating the forebrain.  Hence there is clear evidence of a graded spectrum of deficits following PCE from subtle ASD- and ADHD- like neurobehavioural defects, to smaller heads, to microcephaly and to anencephaly including foetal neurological and neonatal death.

In the context of indicative epidemiology consideration of pathophysiological mechanisms is pertinent to address the Hill principles of causality.

There are numerous compelling mechanisms by which PCE can be related to subsequent teratogenic outcomes.

Importantly the cerebellum, midbrain, diencephalon and forebrain express moderate to high levels of type 1 cannabinoid receptors (CB1R) from early in gestation.

It was recently powerfully demonstrated that opposing gradients of the ligand-receptor guidance pairs slit-Roundabout (robo) and the notch ligand dll control and determine mammalian corticogenesis in diverse organisms including snakes, birds, mice and human organoids by controlling the switch for cortical neurogenesis from directly via radial glia cells to a more indirect and proliferative pathway via intermediate progenitors (Figure 1).   Cannabinoids have been shown to reverse this natural gradient for dll, and acting via a 2AG / CB2R / slit2 / Robo1 / 2AG / CB1R / JNK / ERK pathway to stimulate robo.

Neurexin-neuroligin is a trans-synaptic ligand-receptor pair which directly induces and maintains synapse formation, and has been shown to be inhibited by cannabinoids.

Axon guidance is also controlled by robo-slit and by stathmin-induced tubulin polymerization, which are sensitive to cannabinoids.

White matter disconnection is well documented following adolescent and prenatal cannabis use, and in autism, and oligodendrocytes have CB1R’s and CB2R’s.

Mitochondria possess both CB1R’s and cannabinoid signal transduction machinery and are known to be highly sensitive to cannabinoids and interact with DNA maintenance pathways by several routes.

Cannabinoids have also been shown to alter signaling via the neurotransmitters: glutamate, GABA, opioids, dopamine, serotonin and enkephalin.

Cannabinoids have demonstrated intergenerational epigenetic effects on the medium spiny neurons of the nucleus accumbens and amygdala and also on immune cells which sculpt dendritic networks and prune synapses.

Acting via CB1R, GPR55, and vanilloid type 1 receptors cannabis has been linked with arteritis with likely downstream actions on neurogenic and other stem cell niches.

Endocardial cushions also carry high levels of CB1R’s and the American Academy of Pediatrics has a position statement noting the increased incidence of Ebstein’s syndrome and ventricular septal defect (VSD) after PCE.  Both syncytiotrophoblast and placental arteries carry high concentrations of CB1R’s and abnormalities of uterine blood flow have been documented.

Cannabinoids interfere with tubulin polymerization and mitotic spindle function and thereby act as indirect genotoxins. The implication of cannabis with four inheritable cancers implies malignant teratogenicity and genotoxicity.

Colorado reports dramatic rises of total congenital anomalies, microcephaly, VSD, ASD, Down’s syndrome and chromosomal defects, all of which are relatively straightforward to quantify.

Colorado legislators have also moved to declare a state of crisis related to an autism rate presently growing by 30% 2012-2014.  Similarly in northern California a coincident hotspot of cannabis use, gastroschisis and autism has been reported.  In New Jersey 4.5% of 8 year old boys are autistic.

The above findings comprehend both positive and negative association along with multiple plausible biological pathways linking causality.

As rising rates of community cannabis use augment rising cannabis concentrations and intersect often asymptotic cannabinoid dose-response genotoxicity curves, increased clinical teratogenesis is to be expected.  Of these anomalies the neurobehavioural teratology will likely be the most common, is arguably the most costly and severe, and is also most difficult to quantify.

Are we prepared?

Source:  Paper by Albert Stuart Reese sent to Elinore.Mccance-katz@samhsa.hhs.gov  2018

Abstract

Keywords: AUDIT; alcohol consumption; alcohol use disorder; expression QTL; fMRI; genome-wide association study.

Source: Problematic alcohol use associates with sodium channel and clathrin linker 1 (SCLT1) in trauma-exposed populations – PubMed (nih.gov) September 2018

Abstract

(Reuters Health) – Cannabis use by mothers or fathers during pregnancy, or even only before pregnancy, is associated with an increased risk of psychotic-like episodes in their children, a Dutch study suggests.

Because pot use by mothers and fathers carried similar risk, and a mother’s use before pregnancy had the same effect as use during pregnancy, the study team speculates that parental pot use is likely a marker for genetic and environmental vulnerability to psychotic experiences rather than a cause, and could be useful for screening kids at risk for psychosis later in life.

Babies exposed to cannabis in the womb do have an increased risk of being underweight and unusually small when they’re born and developing cognitive and behavior problems early in life, the researchers note in Schizophrenia Research. Cannabis can also cause hallucinations in adults, particularly with frequent use and at high doses, but less is known about the potential for infants exposed to the drug in the womb to develop psychotic-like symptoms.

For the study, researchers examined data from questionnaires asking 3,692 10-year-olds whether they had symptoms that are similar to what adults might experience with psychosis: hearing voices that nobody else detects, seeing things others don’t see, and having thoughts that others might find strange.

They also examined mothers’ reports on their own marijuana use as well as any use by their partners, and they also looked at lab tests for signs of cannabis in mothers’ urine.

When mothers used marijuana during pregnancy, children were 38 percent more likely to have these psychotic-like symptoms than the children of mothers who abstained from use during pregnancy, the study found. But children of mothers who used pot only before, but not during, pregnancy also had a 39 percent higher risk than the kids of mothers who didn’t use it.

Fathers’ cannabis use during pregnancy, meanwhile, was associated with a 44 percent greater likelihood of psychotic-like experiences in their kids.

“Some children with psychotic experiences are at increased risk to develop psychosis or other psychiatric disorders,” said lead study author Dr. Koen Bolhuis, a researcher at Erasmus Medical Center Rotterdam in the Netherlands.

“Unfortunately very little is known about how to treat psychotic experiences in children, or to prevent them from getting worse,” Bolhuis said by email.

Psychotic-like experiences aren’t disabling or frequent enough to be classified as psychosis, a severe mental health disorder in which patients’ thoughts and emotions are impaired on such a regular basis that they routinely experience delusions and hallucinations that make it impossible to know what’s real and what isn’t.

Psychosis can be caused by schizophrenia, and it can also happen as a result of some other medical conditions and as a side effect of certain prescription medications or illegal drugs.

In the current study, mothers who used cannabis during pregnancy were more likely than other women to smoke and drink during pregnancy, which can both independently influence the risk of emotional and behavioral health problems in children. They were also more likely to have partners who used cannabis while they were pregnant.

The study wasn’t a controlled experiment designed to prove whether or how cannabis exposure might directly cause psychotic experiences in children.

Researchers also lacked data on how much of infants’ cannabis exposure came from parent’s smoking versus ingesting pot.

With inhaled cannabis, it’s difficult to separate the impact of the drug itself from the effect of carbon monoxide also released in the smoke, noted Marcel Bonn-Miller of the University of Pennsylvania Perelman School of Medicine in Philadelphia.

“Carbon monoxide is a known toxicant which causes hypoxia, or oxygen deprivation, which has several well-known and well-studied detrimental effects on pregnancy and offspring development,” Bonn-Miller, who wasn’t involved the study, said by email.

Still, the current study results add to evidence that there’s no safe amount of cannabis exposure for babies in the womb, said Dr. Nathaniel DeNicola of George Washington University in Washington, D.C.

“We have sufficient data and biologic plausibility that marijuana use during pregnancy increases the risk of preterm birth and growth restricted babies,” DeNicola, who wasn’t involved the study, said by email. “The data is mixed on stillbirth, but still cause for concern.”

Source: Pot smoking by parents tied to risk of psychotic episodes in kids | Reuters August 2018

Abstract

Source: https://bmjopen.bmj.com/content/8/2/e019605 February 2018

Abstract

Keywords: Addiction; Alcohol abuse; Dentate gyrus; Granule cells; Hippocampus; Human; Neurogenesis; Neurons.

Source: Hippocampal granule cell loss in human chronic alcohol abusers – PubMed (nih.gov) December 2018

Free-marketeers are ignoring the devastating harm it can do as they champion consumer rights.

Four men had to be rescued last weekend from England’s highest mountain, Scafell Pike, after becoming “incapable of walking due to cannabis use”. Said Cumbria police: “Words fail us.”

Well, yes. Does everyone agree that these men placed an irresponsible burden on a public service? Apparently so. Does everyone agree that the use of cannabis should be discouraged to reduce its irresponsible burden on society? Well, no; quite the opposite.

Last week Prince William raised the “massive issue” of drug legalisation. Although he expressed no opinion, merely to raise it was inescapably to express one, since the only people for whom it is a “massive issue” are those who promote it.

At the Labour Party conference yesterday the comedian Russell Brand called for drugs to be decriminalised. At next week’s Conservative conference, the free-market Adam Smith Institute will be pushing for the legalisation of cannabis. Legalisation means more users. That means more harm, not just to individuals but to society. The institute, however, describes cannabis as “a low-harm consumer product that most users enjoy without major problems”. What? A huge amount of evidence shows that far from cannabis being less harmful than other illicit drugs, as befits its Class B classification, its effects are far more devastating. Long-term potheads display on average an eight-point decline in IQ over time, an elevated risk of psychosis and permanent brain damage.

Cannabis is associated with a host of biological ill-effects including cirrhosis of the liver, strokes and heart attacks. People who use it are more likely than non-users to access other illegal drugs. And so on.

Ah, say the autonomy-loving free-marketeers, but it doesn’t harm anyone other than the user. Well, that’s not true either. It can destroy relationships with family, friends and employers. Users often display more antisocial behaviour, such as stealing money or lying to get a job, as well as a greater association with aggression, paranoia and violent death. According to Stuart Reece, an Australian professor of medicine, cannabis use in pregnancy has also been linked to an epidemic of gastroschisis, in which babies are born with intestines outside their abdomen, in at least 15 nations including the UK.

Long-term potheads display on average an eight-point drop in IQ

The legalisers’ argument is that keeping cannabis illegal does not control the harm it does. Yet wherever its supply has been liberalised, its use and therefore the harm it does have both gone up. In 2001 Portugal decriminalised illegal drugs including cocaine, heroin and cannabis. Sparked by a report by the American free-market Cato Institute, which claimed this policy was a “resounding success”, Portugal has been cited by legalisers everywhere as proof that liberalising drug laws is the magic bullet to erase the harm done by illegal drugs.

The truth is very different. In 2010 Manuel Pinto Coelho, of the Association for a Drug Free Portugal, wrote in the BMJ: “Drug decriminalisation in Portugal is a failure . . . There is a complete and absurd campaign of manipulation of facts and figures of Portuguese drug policy . . .”

According to the Portuguese Institute for Drugs and Drug Addiction, between 2001 and 2007 drug use increased by 4.2 per cent, while the number of people who had used drugs at least once rose from 7.8 per cent to 12 per cent. Cannabis use went up from 12.4 per cent to 17 per cent.

The latest evidence about Portugal, a study by the Intervention Service for Addictive Behaviours and Dependencies, shows “a rise in the prevalence of every illicit psychoactive substance from 8.3 per cent in 2012 to 10.2 per cent in 2016-17”, with most of that rise down to increased cannabis use.

For free-marketeers, this evidence of devastating harm to individuals and society is irrelevant. Nothing can be allowed to dent their dogmatic belief that all human life is a transaction, market forces are a religion and the rights of the consumer are sacrosanct. Says the Adam Smith Institute about cannabis legalisation: “The object isn’t harm elimination, it’s not even harm reduction alone, it’s utility maximisation.” In other words, they want as many people as possible to be puffing on those spliffs.

Free-market libertarians are nothing if not consistent. They oppose policies to reduce social harm across the board. Smoking curbs, mandatory seat-belts, speed cameras, gambling restrictions, controls to end unmanageable immigration — they’ve been against them all.

Despite how they are viewed, there’s nothing conservative about the free-marketeers. Far from conserving legal or social constraints, they want to tear them down in the name of consumer choice. The classical political thinkers they quote in support of applying market principles to every aspect of society never in fact subscribed to such a doctrine. Far from putting the autonomous self on a pedestal, Adam Smith himself in his Theory of Moral Sentiments put personal rights last and the interests of others first.

The distortion of such thinking is why Russell Brand and the Adam Smith Institute are soul mates. In a fearful symmetry, both the left and the free-market right deny the importance of conserving the social good. One calls it paternalism, the other the nanny state. Both are radically irresponsible and destructive. The only difference is the gender. And even that, in our current lifestyle free-for-all, is now surely up for grabs.

Source: Thinking is warped on cannabis legalisation (thetimes.co.uk) September 2017

This Notice of Liability Memo and attached Affidavit of Harms give formal notification to all addressees that they are morally, if not legally liable in cases of harm caused by making toxic marijuana products legally available, or knowingly withholding accurate information about the multiple risks of hemp/marijuana products to the Canadian consumer.  This memo further gives notice that those elected or appointed as representatives of the people of Canada, by voting affirmatively for Bill C45, do so with the knowledge that they are breaching international treaties, conventions and law.  They do so also with the knowledge that Canadian law enforcement have declared that they are not ready for implementation of marijuana legalization, and as they will not be ready to protect the lives of Canadians, there may arise grounds for a Charter of Rights challenge as all Canadian citizens are afforded a the right to security of self.

Scientific researchers and health organizations raise serious questions about the safety of ingesting even small amounts of cannabinoids. Adverse effects include risk of harm to the cardio-vascular system, respiratory tract, immune system, reproductive and endocrine systems, gastrointestinal system and the liver, hyperemesis, cognition, psychomotor performance, psychiatric effects including depression, anxiety and bipolar disorder, schizophrenia and psychosis, a-motivational syndrome, and addiction.  The scientific literature also warns of teratogenicity (causing birth deformities) and epigenetic damage (affecting genetic development) and clearly establishes the need for further study. The attached affidavit cites statements made by Health Canada that are grounded in scientific evidence that documents many harms caused by smoking or ingesting marijuana.  

Putting innocent citizens in “harm’s way” has been a costly bureaucratic mistake as evidenced by the 2015 Canadian $168 million payout to victims of exposure to the drug thalidomide. Health Canada approved thalidomide in 1961 to treat morning sickness in pregnant women but it caused catastrophic birth defects and death.

It would be instructive to reflect on “big tobacco” and their multi-billion-dollar liability in cases of misinformed sick and dead tobacco cigarette smokers. Litigants won lawsuits for harm done by smoking cigarettes even when it was the user’s own choice to obtain and smoke tobacco. In Minnesota during the 1930’s and up to the 1970’s tobacco cigarettes were given to generally healthy “juvenile delinquents’ incarcerated in a facility run by the state.  One of the juveniles, now an adult, who received the state’s tobacco cigarettes, sued the state for addicting him. He won.

The marijuana industry, in making public, unsubstantiated claims of marijuana safety, is placing itself in the same position, in terms of liability, as the tobacco companies.
In 1954, the tobacco industry published a statement that came to be known during Minnesota’s tobacco trial as the “Frank Statement.” Tobacco companies then formed an industry group for the purposes of deceiving and confusing the public.

In the Frank Statement, tobacco industry spokesmen asserted that experiments linking smoking with lung cancer were “inconclusive,” and that there was no proof that cigarette smoking was one of the causes of lung cancer. They stated, “We believe the products we make are not injurious to health.” Judge Kenneth Fitzpatrick instructed the Minnesota jurors: “Jurors should assume in their deliberations that tobacco companies assumed a “special duty” by publishing the ad (Frank Statement), and that jurors will have to determine whether the industry fulfilled that duty.” The verdict ruled against the tobacco industry.

Effective June 19, 2009, marijuana smoke was added to the California Prop 65 list of chemicals known to cause cancer. The Carcinogen Identification Committee (CIC) of the Office of Environmental Health Hazard Assessment (OEHHA) “determined that marijuana smoke was clearly shown, through scientifically valid testing according to generally accepted principles, to cause cancer.”

Products liability and its application to marijuana businesses is a topic that was not discussed in the Senate committee hearings. Proposition 65, requires the State to publish a list of chemicals known to cause cancer, birth defects or other types of reproductive harm. Proposition 65 requires businesses to provide their customers with notice of these cancerous causing chemicals when present in consumer products and provides for both a public and private right of action.

The similarities between the tactics of “Big Tobacco” and the “Canadian Cannabis Trade Alliance Institute” and individual marijuana producers would seem to demand very close scrutiny. On May 23, a witness testified before the Canadian Senate claimed that marijuana is not carcinogenic. This evidence was not challenged.

The International Narcotics Control Board Report for 2017 reads: “Bill C-45, introduced by the Minister of Justice and Attorney General of Canada on 13 April 2017, would permit the non-medical use of cannabis. If the bill is enacted, adults aged 18 years or older will legally be allowed to possess up to 30 grams of dried cannabis or an equivalent amount in non-dried form. It will also become legal to grow a maximum of four cannabis plants, simultaneously for personal use, buy cannabis from licensed retailers, and produce edible cannabis products. The Board wishes to reiterate that article 4 (c) of the 1961 Convention restricts the use of controlled narcotic drugs to medical and scientific purposes and that legislative measures providing for non-medical use are in contravention of that Convention….

The situation pertaining to cannabis cultivation and trafficking in North America continues to be in flux owing to the widening scope of personal non-medical use schemes in force in certain constituent states of the United States. The decriminalization of cannabis has apparently led organized criminal groups to focus on manufacturing and trafficking other illegal drugs, such as heroin. This could explain why, for example, Canada saw a 32 per cent increase from 2015 to 2016 in criminal incidents involving heroin possession….The Canadian Research Initiative in Substance Misuse issued “Lower-risk cannabis use guidelines” in 2017. The document is a health education and prevention tool that acknowledges that cannabis use carries both immediate and long-term health risks.”

https://www.incb.org/documents/Publications/AnnualReports/AR2017/Annual_Report_chapters/Chapter_3_Americas_2017.pdf

Upon receipt of this Memo and Affidavit, the addressees can no longer say they are ignorant or unaware that promoting and/or distributing marijuana cigarettes for recreational purposes is an endangerment to citizens. Receipt of this Memo and Affidavit removes from the addressees any claim of ignorance as a defense in potential, future litigation.

Pamela McColl www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

AFFIDAVIT May 27, 2018

I, Pamela McColl, wish to inform agencies and individuals of known and potential harm done/caused by the use of marijuana (especially marijuana cigarettes) and of the acknowledgement the risk of harm by Health Canada. 

Marijuana is a complex, unstable mixture of over four hundred chemicals that, when smoked, produces over two thousand chemicals.  Among those two thousand chemicals are many pollutants and cancer-causing substances.  Some cannabinoids are psychoactive, all are bioactive, and all may remain in the body’s fatty tissues for long periods of times with unknown consequences. Marijuana smoke contains carcinogenic (cancer-causing) substances such as benzo(a)pyrene, benz(a)anthracene, and benzene in higher concentrations than are present in tobacco smoke.  The mechanism by which benzo(a)pyrene causes cancer in smokers was demonstrated scientifically by Denissenko MF et al. Science 274:430-432, 1996. 

Health Canada Consumer Information on Cannabis reads as follows:  “The courts in Canada have ruled that the federal government must provide reasonable access to a legal source of marijuana for medical purposes.”

“Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of cannabis for therapeutic purposes, or of marijuana generally, by Health Canada.”

“Serious Warnings and Precautions: Cannabis (marihuana, marijuana) contains hundreds of substances, some of which can affect the proper functioning of the brain and central nervous system.”

“The use of this product involves risks to health, some of which may not be known or fully understood. Studies supporting the safety and efficacy of cannabis for therapeutic purposes are limited and do not meet the standard required by the Food and Drug Regulations for marketed drugs in Canada.”

Health Canada – “When the product should not be used: Cannabis should not be used if you:-are under the age of 25 -are allergic to any cannabinoid or to smoke-have serious liver, kidney, heart or lung disease -have a personal or family history of serious mental disorders such as schizophrenia, psychosis, depression, or bipolar disorder-are pregnant, are planning to get pregnant, or are breast-feeding -are a man who wishes to start a family-have a history of alcohol or drug abuse or substance dependence Talk to your health care practitioner if you have any of these conditions. There may be other conditions where this product should not be used, but which are unknown due to limited scientific information.

Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of this product, or cannabis generally, by Health Canada.”

Prepared by Health Canada Date of latest version: February 2013, accessed May 2018. https://www.canada.ca/en/health-canada/services/drugs-health-products/medical-use-marijuana/information-medical-practitioners/information-health-care-professionals-cannabis-marihuana-marijuana-cannabinoids.html

A report published by survey company RIWI Corp. (RIWI.com) can be found at: https://riwi.com/case-study/measuringcanadians-awareness-of-marijuanas-health-effects-may-2018

The report measures Canadians’ awareness of marijuana’s health effects as determined by Health Canada and published on Health Canada’s website. RIWI data indicates: 1. More than 40% of those under age 25 are unaware that marijuana impacts safe driving. Further, 21% of respondents are not aware that marijuana can negatively impact one’s ability to drive safely. Health Canada: “Using cannabis can impair your concentration, your ability to make decisions, and your reaction time and coordination. This can affect your motor skills, including your ability to drive.” 2. One in five women aged 25-34 believes marijuana is safe during pregnancy, while trying to get pregnant, or breastfeeding. • RIWI: “For women of prime childbearing age (25-34), roughly one in five believe smoking marijuana is safe during pregnancy, planning to get pregnant, and breastfeeding.” • Health Canada: “Marijuana should not be used if you are pregnant, are planning to get pregnant, or are breastfeeding. … Long-term use may negatively impact the behavioural and cognitive development of children born to mothers who used cannabis during pregnancy.” 3. One in three Canadians do not think that marijuana is addictive. • Health Canada: “Long term use may result in psychological dependence (addiction).” 4. One in three Canadians believe marijuana aids mental health. • Health Canada: “Long term use may increase the risk of triggering or aggravating psychiatric and/or mood disorders (schizophrenia, psychosis, anxiety, depression, bipolar disorder).” 5. One in two males were unaware that marijuana could harm a man’s fertility • “Marijuana should not be used if you are a man who wishes to start a family.”

ClearTheAirNow.org, a coalition of concerned Canadians commissioned the survey.

Affiant is willing to provide further sources of information about the toxicity of marijuana.

Pamela McColl

www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

Source: From email sent to Drug Watch International May 2018

Damage is caused in several different ways.
BRAIN: Messages are passed from cell to cell (neurons) in the brain by chemicals called neurotransmitters which fit by shape into their own receptor sites on specific cells.
The neurotransmitter, anandamide, an endo-cannabinoid (made in body) whose job is to control by suppression the levels of other neurotransmitters is mimicked and so replaced by a cannabinoid (not made in body) in cannabis called THC (Tetrahydrocannabinol). THC is very much stronger and damps down more forcefully the release of other neurotransmitters. Consequently the total activity of the
brain decreases. Chaos ensues.

Neurotransmitters delivering messages to the hippocampus, the area for learning and memory don’t receive enough stimulation to reach it, so signals are lost for ever.
Academic performance plummets and IQs fall by about 8 points. Neurons can be lost permanently. This is brain damage. No child using cannabis even occasionally will achieve their full potential.
Because signalling is slowed down, reaction times increase. Driving becomes hazardous and fatal accidents are rising in legalised USA states. Alcohol plus cannabis in drivers is 16 times more dangerous.
Since THC is fat-soluble, it stays in cells for weeks, constantly ensuring this decrease in brain activity. In the sixties/seventies the THC content was around 1-3%, now in London only ‘skunk’ at 16-20% THC is available. Professor Sir Robin Murray has said that, ‘users will be in a state of low-grade intoxication most of the time’. The Dopamine neurotransmitter has no receptor sites for anandamide and so THC
doesn’t affect it. But the inhibitory Gaba neurotransmitter has. Gaba normally suppresses dopamine but since it is itself suppressed by THC, levels of dopamine quickly increase. Excess dopamine is found in the brains of psychotics, and even schizophrenics if they have a genetic vulnerability. Anyone taking enough THC at one sitting will suffer a psychotic episode which could become permanent. Aggression, violence, even homicides, suicides and murders have resulted from cannabis-induced psychosis. The first research paper linking THC with psychosis was published in 1845. Cannabis-induced schizophrenia costs the country around £2 billion/year. Some of these mentally ill people will spend the rest of their lives in psychiatric units.
THC also depletes the levels of the ‘happiness’ neurotransmitter Serotonin. This can cause depression which may lead to suicide. THC causes dependence. This will affect 1 in 6 using adolescents and 1 in 9 of the general population. Since THC replaces anandamide, there is no need for its production which reduces and eventually stops so the receptor sites are left empty.
Withdrawal then sets in with irritability, sleeplessness, anxiety, depression, even violence until anandamide production resumes. Rehab specialists have told us that adolescent pot addiction is the most challenging to treat.
Cannabis can also act as a gateway drug – it can ‘prime’ the brain for the use of other drugs. Professor David Fergusson (NZ) in longitudinal studies from birth found that ‘The use of cannabis in late adolescence and early adulthood emerged as the strongest risk factor for later involvement in other illicit drug use’.
THC inhibits the vomiting reflex. If a person has drunk too much alcohol, they are often sick and get rid of it. An overdose of alcohol can kill (respiratory muscles stop working) so using cannabis together with alcohol can be fatal.
The signalling of endo-cannabinoids is crucial in brain development. They guide the formation, survival, proliferation, motility and differentiation of new neurons. THC badly interferes with these essential processes. Chaos ensues among the confused brain signals and a cannabis personality develops. Users can’t think logically. They have fixed opinions and answers, can’t find words, can’t take criticism – it’s always someone else’s fault, and can’t plan their day. Families suffer from their violent mood swings – houses get trashed. Anxiety, panic and paranoia may ensue. At the same time users are lonely, miserable and feel misunderstood.

Respiratory System:
Cannabis smoke has many of the same constituents as tobacco smoke but more of its carcinogens – in cancer terms a joint equals 4/5 cigarettes. More tar is deposited in the lungs and airways. Coughing, wheezing, emphysema, bronchitis and cancers have been seen in the lungs.

Heart:
Heart rates rise and stay high for 3-4 hours after a joint. Heart attacks and strokes have been recorded. Some teenagers had strokes and died after bingeing on cannabis.

Hypothalamus:
The hypothalamus is a region of the brain known to regulate appetite. Endocannabinoids in this area send ‘I’m hungry’ messages. When you take THC, that message is boosted. This is called ‘the munchies’. Nabilone, (synthetic THC) can be used to stimulate the appetite in AIDS patients.

DNA and Reproduction:
THC affects the DNA in any new cells being made in the body. It speeds up the programmed cell death (apoptosis) of our defence white blood cells, so our immune system is diminished. There are also fewer sperm. Infertility and impotence have been reported as far back as the 1990s.
An Australian paper published in July 2016 explains this phenomenon. THC can disrupt the actual process of normal cell division mitosis and meiosis (formation of sperm and eggs). In mitosis, the chromosomes replicate and gather together at the centre of the cell. Protein strands (microtubules) are formed from the ends of the cell to pull half of the chromosomes to each end to form the 2 new cells. Unfortunately THC disrupts microtubule formation. Chromosomes can become isolated, rejoin other bits of chromosome and have other abnormalities. Some will actually be shattered into fragments (chromothripsis).
This DNA damage can also cause cancers. Oncogenes (cancer-causing genes) may be activated, and tumour suppressant genes silenced. Chromosome fragments and abnormal chromosomes are frequently seen in cancerous tissues. This would account for other cancers, leukaemia, brain, prostate, cervix, testes and bladder etc, reported in regions of the body not exposed to the smoke. Pregnant users see a 2-4
fold increase in the number of childhood cancers in their offspring. The DNA damage has also been associated with foetal abnormalities – low birth weight, pre-term birth, spontaneous miscarriage, spina bifida, anencephaly (absence of brain parts), gastroschisis (babies born with intestines outside the body) cardiac defects and shorter limbs. All these defects bear in common an arrest of cell growth and cell migration at critical development stages consistent with the inhibition of mitosis noted with cannabis.
DNA damage at meiosis results in fewer sperm as we have seen. Increased errors in meiosis have the potential for transmission to subsequent generations. The zygote (fertilised egg) death rate rises by 50% after the first division. In infants, birth weight is lower and they may be born addicted. Children may have problems with behaviour and cognitive functions as they grow. Childhood cancers are
more common. Intensive care for newborns doubles. The younger they start using cannabis, the more likely they are to remain immature, become addicted, suffer from mental illnesses or progress to other drugs. Average age of first use is 13. Regular cannabis users have worse jobs, less than average money, downward social mobility, relationship problems and antisocial behaviour.

References:
Cannabis Skunk Website www.cannabisskunksense.co.uk Cannabis: A survey of its
harmful effects by Mary Brett is available on DOWNLOADS. It is a 300+ page report
written in 2006 and kept up to date.

Chromothripsis and epigenomics complete causality criteria for cannabis- and
addiction-connected carcinogenicity, congenital toxicity and heritable genotoxicity

Book: Adverse Health Consequencies of Cannabis Use. Jan Ramstrom National Institute of Public Health Sweden www.fhi.se

Source: https://www.cannabisskunksense.co.uk/uploads/site-files/ty,Chromothripsis,CarcinogenicityandFetotoxicity,MR-FMMM.pdf March 2020

Abstract

• Cannabis is responsible for 91% of drug addiction cases involving teenagers
• Skunk – high-potency herbal cannabis – causing more people to seek treatment 
• Backs up research that skunk is having detrimental impact on mental health

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:

• Over the past decade, the number of under-18s treated for cannabis abuse in England has jumped 40 per cent – from 9,043 in 2006 to 12,712 in 2017;
• Treatment for all narcotics has increased by 20 per cent – up from 11,618 to 13,961;
• The proportion of juvenile drug treatment for cannabis use is up from four in five cases (78 per cent) to nine in ten (91 per cent);
• There has been a ‘sharp increase’ in cocaine use among 15-year-olds, up 56 per cent from 16,700 in 2014 to 26,200 in 2016.

Last night, Lord Nicholas Monson, whose 21-year-old son Rupert Green killed himself last year after becoming hooked on high-strength cannabis, said: ‘These figures show the extent of the damage that high-potency cannabis wreaks on the young.

‘The big danger for young people – particularly teens – is that their brains can be really messed up by this stuff because they are still developing biologically. If they develop drug-induced psychosis – as Rupert did – the illness can stick for life.’

The large rise in the number of youngsters treated for cannabis abuse comes despite the fact that total usage is falling slightly.

The report concludes: ‘While fewer people are using cannabis, those who are using it are experiencing greater harm.’

Almost all cannabis on Britain’s streets is skunk, which is four times more powerful than types that dominated the market until the early 2000s. It can even trigger hallucinations.

Lord Monson said: ‘We really need Ministers to get a grip and launch a major publicity campaign about the dangers.’ 

Nine in ten teens at drug clinics are being treated for marijuana use  | Daily Mail Online April 2018

Abstract

The molecular composition of the cannabinoid type 1 (CB1) receptor complex beyond the classical G-protein signaling components is not known. Using proteomics on mouse cortex in vivo, we pulled down proteins interacting with CB1 in neurons and show that the CB1 receptor assembles with multiple members of the WAVE1 complex and the RhoGTPase Rac1 and modulates their activity. Activation levels of CB1 receptor directly impacted on actin polymerization and stability via WAVE1 in growth cones of developing neurons, leading to their collapse, as well as in synaptic spines of mature neurons, leading to their retraction. In adult mice, CB1 receptor agonists attenuated activity-dependent remodeling of dendritic spines in spinal cord neurons in vivo and suppressed inflammatory pain by regulating the WAVE1 complex. This study reports novel signaling mechanisms for cannabinoidergic modulation of the nervous system and demonstrates a previously unreported role for the WAVE1 complex in therapeutic applications of cannabinoids.

Fig 1. CB1 physically interacts with members of the WAVE1 signaling complex in mouse brain and colocalizes with WAVE1 in neurons. 

(A) Expression of EGFP-tagged CB1 (CB1-EGFP) in mouse brain 4 wk after cortical injection of rAAVs. Injection site is marked with a white arrow, and medial longitudinal fissure with a yellow asterisk. Scale bar represents 0.5 mm. (B) Validation of solubilization and pulldown of CB1 by immunoprecipitation using GFP-nanotrap on membrane fractions derived from cortex of mice expressing either CB1-EGFP or GFP alone (as control). Immunoblotting (IB) experiments show that anti-GFP antibody pulls down endogenous CB1 and CB1-EGFP from CB1-EGFP-expressing mice, but not from GFP control mice. The successful pulldown shows the high molecular weight form of CB1 (black arrows), the CB1-EGFP monomer (yellow arrow) and endogenous CB1 (blue arrow head). (C) Summary of MS analysis of GFP nanotrap-immunoprecipitates from the cortex of CB1-EGFP-expressing mice or GFP-expressing control mice (n = 5). rPQ is relative peptide query score. Values for rPQ > 4 indicates specific purification in comparison over negative control. (D) Schematic representation of activation of the WAVE1 complex by GTP-bound (activated) Rac1. (E) Immunoblotting on GFP-nanotrap-immunoprecipitates showing that cytoplasmic FMR1 interacting protein 2 (CYFIP2), NCK-associated protein 1 (NCKAP1), WAVE1 and Rac1 are coimmunoprecipitated with GB1-EGFP, but not with GFP, from the mouse cortex. (F) Immunoblotting on α-CB1-immunoprecipitates showing that WAVE1 is coimmunoprecipitated with CB1 from cortical lysates derived from wild-type mice, but not in lysates from CB1-deficient mice (CB1^-/-). (G) Colocalization of WAVE1 and EGFP-tagged CB1 in growth cones (magnified in inset) of developing cortical neurons with pyramidal morphology. The actin cytoskeleton is counterstained with Phalloidin (growth cone magnified in inset). Scale bars represent 10 μm.

Fig 2. Increased localization of colocalization of WAVE1 and CB1-EGFP at the cell membrane in heterologously-transfected COS7 cells upon ACEA treatment. 

(A) Distribution of heterologously-transfected WAVE1 in cells cotransfected with either GFP (control, upper panels) or CB1-EGFP (lower panels) following treatment with vehicle (DMSO 1:30,000) or CB1 agonist (ACEA 100 nM) for 45 min. Scale bar represents 5 μm. (B) Quantitative summary of intensity of WAVE1-immunoreactivity relative to Phalloidin-stained actin at the plasma membrane in GFP- or CB1-EGFP-coexpressing COS7 cells treated with vehicle (white bars) or ACEA (red bars). (C) Quantitative summary of CB1-EGFP-WAVE1 colocalization in vehicle- or ACEA-treated cells calculated as a fraction of the total intensity of CB1-EGFP fluorescence. Values in panels B and C represent the mean ± SEM and are derived from analyses on at least 15 COS7 cells each over several independent culture experiments. *p < 0.05 one way ANOVA followed by posthoc Tukey’s test.

Fig 3. Cannabinoids directly modulate Rac1 activity and WAVE1 phosphorylation by Rac1 Activation and WAVE1 Phosphorylation via CB1. 

(A) Schematic representation of the Raichu-Rac1 FRET-biosensor employed to measure Rac1 activity. (B) Real-time images representing changes in Rac1 activity in developing mouse cortical neurons following treatment with a CB1 agonist (ACEA; 100 nM) and an inverse agonist at CB1 (AM251; 600 nM). The FRET signal intensity is represented as a pseudocoloured heat map, and insets show magnified view of growth cones. Scale bars (white) represent 20 μm, and scale bars in the inset (yellow) represent 5 μm. (C) Quantitative summary of normalized FRET ratios over the growth cone area at various time points after addition of ACEA, AM251, NGF (100 ng/ml), or vehicle normalized to the average FRET ratio value over the same area prior to addition of pharmacological agents in developing neurons derived from wild-type mice. (D) Preserved effect of NGF and loss of effects of ACEA as well as AM251 on Rac1 activity in developing cortical neurons derived from CB1^-/- mice. Values in panels C and D represent the mean ± SEM and are derived from analyses on 10–16 neurons per group over at least three independent culture experiments. (E, F) Immunoblot analyses showing changes in phosphorylation state of Serine 397 (pSer397) in WAVE1 upon treatment with ACEA (100 nM) or AM251 (600 nM) as compared to vehicle treatment in cortical neurons derived from wild-type mice without pretreatment (E), with overnight pertussis toxin (PTX) (100 ng/ml) pretreatment or from CB1^-/- mice (F). (G) Quantitative summary of cannabinoid-induced modulation of pSer397 WAVE1 levels normalized to βIII-tubulin in the above groups (n = 5–6 independent culture experiments). All graphs represent mean values ± SEM *p < 0.05, two-way ANOVA for repeated measures (C, D) or one-way (G) ANOVA followed by posthoc Tukey’s test. N.s. stands for not significant.

Fig 4. Visualization of cannabinoidergic modulation of actin dynamics in neuronal growth cones mediated by CB1 and WAVE1. 

(A) Real time images of wild-type developing cortical neurons transfected to express LifeAct-GFP, a biosensor for levels of F-actin prior to and at different time points following treatment with ACEA (100 nM), AM251 (600 nM), or vehicle. Scale bar represents 10 μm. (B, C) Analysis on the F-actin dynamics based on cannabinoid-induced changes in LifeAct-GFP intensity (B) and area (C) over time in growth cones of cultured cortical neurons derived from wild-type mice (n = 15–17 neurons per group from 5 independent culture experiments). (D, E) However, no changes in LifeAct intensity (D) nor area of the growth cones (E) were observed with cultured cortical neurons derived from CB1^-/- mice (n = at least 4 neurons per group from 2 independent culture experiments) after treatment. (F, G) Similarly, cultured cortical neurons with down-regulated WAVE1 showed no changes in LifeAct intensity (F) or area of growth cones (G) after cannabinoid treatment (n = at least 4 neurons per group). (H, I) Moreover, the abrogation of the effects after cannabinoid treatment can be contributed to the down-regulation state of WAVE1, since cultured cortical neurons nucleofected with scrambled siRNA, in turn show changes in LifeAct intensity (H) and area (I) of the growth cone following cannabinoid treatment (n = at least 4 neurons per group). (J, K) Immunoblot representation of WAVE1 down-regulation upon siRNA delivery in developing cortical neurons (J) and the corresponding quantification (K) (n = 6). All graphs represent mean values ± SEM *p < 0.05, two-way ANOVA (B-I) or one-way ANOVA (K) for random measures followed by posthoc Tukey’s test.

Fig 5. Cannabinoids regulate growth cone morphology via CB1-Gi-Rac1-WAVE1 signaling. 

(A) Characterization of changes in growth cone morphology in developing cultured cortical neurons immunostained with anti-pGAP43 to recognize normal or enlarging growth cones and Phalloidin to label actin. Insets show normal, enlarged, or collapsed morphology in developing cortical neurons; scale bar represents 10 μm in all images and insets. (B) Bidirectional modulation of the proportion of growth cones with collapsed or enlarged morphology upon treatment with ACEA (100 nM), AM251 (600 nM) or vehicle (DMSO 1:30,000) for 1 h in neurons derived from wild-type mice (n = 10 independent culture experiments), but not in neurons from CB1^-/- mice (n = 4). (C–F) Lack of modulation of cannabinoidergic modulation of growth cone morphology upon treatment in the presence of PTX (100 ng/ml), Rac1 inhibitor, CAS 1090893-12-1 (50 μM) or in neurons with siRNA-mediated downregulation of WAVE1; control siRNA-transfected neurons showed significant cannabinoidergic modulation (n = 4). All graphs represent mean values ± SEM. *p < 0.05, one-way ANOVA followed by posthoc Tukey’s test. N.s. stands for not significant.

Fig 6. CB1 receptor is expressed in axonal as well as dendritic compartments of primary neurons matured over 4 wk in vitro. 

(A) Coimmunostaining against CB1 receptor and dendritic marker MAP2 on 28 days in vitro (DIV) cortical neurons derived from wild-type mouse embryos (upper panels) shows the distribution of CB1 receptor in the axonal compartments (MAP2-negative) as well as dendritic compartments (MAP2-positive). The rabbit anti-CB1 antibody used throughout this experiment did not yield substantial staining in cortical neurons cultured from CB1-deficient mouse embryos at 28 DIV (lower panels). (B) Magnified images represent white boxed areas from main images. (C) CB1 receptor colocalizes with CamKII-GFP and the synaptic protein PSD95 in dendritic compartments, including several spine heads (white arrow heads), indicating postsynaptic localization. (D) Heterologously-expressed CB1-EGFP in mature cultured cortical neurons shows axonal and dentritic localization upon costaining with MAP2. Phalloidin is used to counterstain the entire actin cytoskeleton. Phall. stands for Phalloidin. (E) Dendritic (arrows) ad axonal (arrowhead) localization of endogenous CB1 in cortical neurons cultured from wild-type mice and matured at 28 DIV. White scale bars represent 20 μm and yellow scale bars represent 5 μm.

Fig 7. Visualization of disassembly of F-actin by cannabinoid agonists in in dendritic spines on mature cortical neurons, leading to reduction in the density of mature spines. 

(A) Representative real time images of FRAP experiments. Localized photobleaching over single, individual postsynaptic spines (red circles), led to loss of LifeAct-mCherry labeling of F-actin and progressive recovery of fluorescence with actin polymerization, which was inhibited by ACEA as compared to vehicle control. (B & C) Summary of FRAP values as a function of time expressed as one phase exponential function curves fitted to the respective data sets from neurons treated with ACEA or vehicle either from wild-type cultured cortical neurons (B) or with siRNA-mediated WAVE1 knockdown (C) (13–15 dendritic spines/group from 4 independent culture experiments). (D) Immunoblot example of WAVE1 down-regulation 3 d following siRNA delivery in mature cultured cortical neurons and the corresponding quantification (seven independent culture experiments). (E) Quantitative summary of the magnitude of F-actin recovery in the dendritic spine after photobleaching in neurons from the diverse treatment groups (five independent culture experiments). (F) Representative confocal images of mature cortical neurons transduced with rAAV-CamK-II-GFP virions and treated with ACEA (100 nM) or vehicle for 24 h. GFP-labelled dendritic spines were morphologically classified (lower panels) and quantified. Yellow bars represent 50 μm and white bars represent 5 μm. (G) Quantitative summary of average density of dendritic spines of varying morphology in cortical neurons treated with ACEA (100 nM) or vehicle (n = 20–21 dendrites analyzed from three cultures/group). All graphs represent mean values ± SEM *p < 0.05 as compared to control group and †p < 0.05 as compared to WT neurons, two-way ANOVA (E) or one-way ANOVA (D & G) followed by posthoc Tukey’s test. N.s. stands for “not significant.”

Fig 8. Intrathecal delivery of ACEA inhibits mechanical nociceptive hypersensitivity and nociceptive activity-induced structural plasticity of dendrites on spinal dorsal horn neurons in inflammatory pain conditions in vivo. 

(A) Frequency of paw withdrawal responses to mechanical force via plantar application of graded von Frey hairs recorded prior to and 24 h after hind paw intraplantar injection of CFA. Leftward shift in response curves following CFA (indicative of hypersenstivity) is diminished in mice treated intrathecally with ACEA (2 pmol) over 24 h as compared to mice intrathecally receiving vehicle (n = at least 8 per group). (B) Traced images of Golgi-stained large pyramidal-like neurons in laminae II and V of the spinal dorsal horn and dendritic spines (insets) in mice represented in (A). Scale bars represent 10 μm in all panels. (C) Quantitative summary of dendritic spine density in spinal neurons from mice represented in (A) and (B); CFA-induced enhancement in spine density does not occur in mice receiving intrathecal ACEA (n = 12–16 neurons counted from over 4 mice per group). (D, E) Mice with hind paw inflammation show reduced levels of pSer397 WAVE1, quantified over βIII-tubulin as loading control, in spinal lumbar segments L3-L5 at 24 h post-CFA, which is partially and significantly reversed by intrathecal ACEA as compared to vehicle. An example of western blot analysis and quantitative summary from seven mice per group is shown in (D) and (E), respectively. All graphs represent mean values ± SEM *p < 0.05 as compared to basal values within the group and †p < 0.05 as compared to corresponding values in the vehicle group, two-way (A) and one-way (C, E) ANOVA for repeated measures followed by posthoc Tukey’s test.

Fig 9. Role of spinally-expressed WAVE1 in nociceptive activity-induced structural plasticity, inflammatory pain, and cannabinoidergic analgesia in vivo. 

(A, B) An immunoblot example and quantitative data from western blot analysis showing down-regulation of WAVE1 in spinal cord segments L3–L5 after intrathecal in vivo application of WAVE1 siRNA as compared to control siRNA. (C) Normal basal spine density but lack of CFA-induced spine remodeling in lamina II/V lumbar spinal neurons at 24 h post-CFA in mice intrathecally injected with WAVE1 siRNA as compared to control siRNA (n = 16–17 spines counted over four mice per group). (D) Frequency of paw withdrawal responses to mechanical force via plantar application of graded von Frey hairs recorded prior to (dashed lines) and 24 h after hind paw intraplantar injection of CFA (solid lines). Leftward shift in response curves following CFA (indicative of hypersensitivity) is diminished with intrathecal siRNA-mediated WAVE1 knockdown (red symbols) as compared to mice intrathecally injected with control siRNA (black symbols). (E) Mechanical hypersensitivity at 24 h post-CFA is significantly reduced by intrathecal ACEA injection over 24 h in mice intrathecally treated with control siRNA (black squares in E, upper graph), but not in mice intrathecally treated with WAVE1 siRNA (red squares in E, lower graph). (F) Quantitative summary of dendritic spine density in laminae II or V neurons in L3–L5 segments of mice which were tested behaviorally in panels animals in (E). Intrathecal ACEA reduces spine density in control siRNA-injected CFA-inflamed mice, but not in WAVE1 siRNA-treated CFA-inflamed mice (16–18 neurons counted from over four mice per group). All graphs represent mean values ± SEM, n = 7–9 mice per group in panels D & E. *p < 0.05 as compared to basal values within the group and †p < 0.05 as compared to corresponding control, two-way (D, E) and one-way (B, C and F) ANOVA for repeated measures followed by posthoc Tukey’s test.

Source: https://pubmed.ncbi.nlm.nih.gov/26496209 October 2015

Child Neglect and Violence by Marijuana Impaired Parents are the Leading Causes

WASHINGTON, DC, US, April 23, 2018 /EINPresswire.com/ — Parents Opposed to Pot (POP), a nonprofit dedicated to exposing the dangers of marijuana, counts 106 child abuse deaths related to marijuana since states voted to legalize it in November 2012. POP cautions that the normalization of marijuana should be a primary concern to parents and child protection agencies. April is Child Abuse Prevention Awareness Month, and April 25 is Child Abuse Prevention Awareness Day.

Parents Opposed to Pot found local newspaper reports of the incidents online, and the number of deaths could actually be much higher. Some states are more likely than other states to report when marijuana drug use is involved. The deaths have occurred in 30 states, and the counts are higher in states that have legalized pot. The problem is serious enough that when the National Alliance for Drug-Endangered Children ran a conference last summer, much of it focused on marijuana. Nationally, approximately 1700 child abuse deaths occur each year, and substance abuse is a major risk factor.

The earliest deaths after 2012 that POP recorded seemed to be from neglect: toddlers who drowned, died in fires, or infants who were left in hot cars when parents smoked pot and forgot about them. However, many deaths related to marijuana were caused by domestic violence, because parents became angry or psychotic from pot use and had paranoid delusions. The potency of marijuana is several times stronger than it was in the 1990s.The public has not been educated well about how marijuana can trigger psychosis and/or schizophrenia, as stated in the 2017 National Academy of Sciences report.

Shortly after Colorado commercialized marijuana in 2014, stories of three tragic deaths of toddlers related to their parents’ use of marijuana emerged. The month Washington legalized possession of marijuana, a two-year-old drank from his mother’s bong and died. After investigating, state officials determined that the toddler had ingested lethal amounts of both THC and meth, enough to kill an adult.

“As articles in popular magazines such as Cosmopolitan and Oprah Winfrey’s ‘O’ portray cannabis as the ‘it’ drug, parents are being led to believe that a serving of marijuana is no more dangerous than a glass of beer or wine,” explains Dr. Ken Finn, a medical advisor to PopPot.org. “However, three sets of twins died in fires when parents abandoned these toddlers for reasons related to their marijuana use.”

The promotion of marijuana as a way to relax is inappropriate for parents or caregivers of small children, and the promotion of marijuana for pregnant women with morning sickness is a dangerous trend.

Marijuana use impairs executive functioning — which led to poor judgement and forgetfulness in many of these deaths. Greater acceptance means more use, and more use means more addiction.

Eleven deaths occurred in Colorado, while 10 took place in California. In both states, at least one child died where butane hash oil (BHO) labs operated, and numerous children were injured in BHO fires. The two most recent deaths in Colorado occurred last summer when a mother followed a cult leader to a marijuana farm. No one knows how long the two girls had been dead when they were discovered locked in a car covered in tarp last September. They were starved to death. An unusual death in California occurred when a babysitter went to her cousin’s car to smoke pot, leaving a 16-month-old boy inside. The toddler eventually came outside and the visiting car ran over him.

Many ER treatments followed the accidental ingestion of marijuana candies and cookies. A medical journal reported last year that an 11-month-old baby suffered from an enlarged heart muscle and couldn’t be revived a few days after ingesting marijuana in Colorado. However, it’s usually not edibles that kill children, but other acts of neglect and violent behavior.

In Florida, three children drowned when parents or babysitters smoked pot and forgot about them. At least 10 deaths occurred when parents left small children in hot cars while they smoked cannabis. The most common forms of death by neglect when parents use cannabis are fires, 15, drownings, 10 and hot cars, 10.

During the intense debate over medical marijuana in Pennsylvania, the number of pot-related child abuse deaths seemed to increase. Much drama was used to discuss children with seizures, while five other children died due to adult pot use between April and December, 2016.

POP is not the only organization to notice the uptick in child deaths related to marijuana. Yvapil County District Attorney Sheila Polk reported that, in 2013, 62 deaths of children in Arizona were associated with cannabis , and that it was the substance most often related to accidental deaths in the state.

Nationally, parents cause about three quarters of child abuse deaths and most child abuse deaths occur because of neglect. When there’s marijuana in the picture, violence or violent neglect are just as likely to cause death. Boyfriends of the mothers caused 14 such deaths, most often from violence, with the moms in these instances often using pot too. One recent death was the beating death of a three-year-old. The stepfather, who was charged, kept marijuana in the house. Research shows that cannabis can trigger negative thoughts and violent behavior. But, we haven’t included this case our list because it’s not clear what role the drug played in this death.

In four cases, children died because babysitters’ neglected the child, while in four different instances a relative was responsible for the deaths.

POP published 18 blog articles on Child Endangerment that explain some of facts surrounding the deaths. A downloadable fact sheet available on the PopPot.org webpage simplifies the statistics.

Parents Opposed to Pot is a 501c3 nonprofit based in Merrifield, Virginia.

Source: Over 100 Child Abuse Deaths Found Related to Cannabis, with Rise of Commercial Industry (einpresswire.com) April 2018

Abstract

Abstract 

We note the report on the rising gastroschisis incidence 3.1 times 1995-2012

The 20-fold variation across California mirrors the ten-fold variation across Canada here the distribution pattern closely mirrors cannabis consumption, and from where cannabis-related adjusted O.R.= 3.54 (95%C.I. 2.22-5.63) has been reported .

Several clues suggest cannabis is likely involved also in California.  Statewide gastroschisis rose 2.84-fold 2005-2012, whilst last month cannabis use in northern California rose 2.56-fold from 8.41% to 21.55% 2006-2008 to 2014-2016 in the National Survey of Drug Use and Health.

Combining the midrange county rates supplied  with published birth, population and NSDUH data it can be shown that the gastroschisis rate in the NSDUH 1R northern 15 counties rose O.R.=2.33 (95%C.I. 1.91-2.83) compared to the rest of the state for the whole period 1995-2012.

Anderson found rurality was a risk factor for cannabis use which fits with the burgeoning cannabis industry.  Timber production was a probable surrogate marker, and the Federal parks are known to accommodate substantial cannabis plantations.

Moreover as various potent herbicides and rodenticides including carbofuran are used in commercial operations and contaminate the water table these also need to be considered as novel indirect toxins.

Gastroschisis follows cannabis use in many places including Australia, Canada, Mexico, North Carolina, and Washington state.  Mechanistically this is consistent with the appearance of cannabinoid type 1 receptors (CB1R) on the omphalovitelline vessels from the ninth week of gestation, and documented occurrence of cannabis arteritis .

The real possibility clearly needs to be considered that the global rise in cannabis use may underlie the dramatic rise in gastroschisis in many locations.  Indeed since heart and brain defects including anencephaly and brain impairments consistent with autistic deficits are also well described in the congenital cannabis exposure literature, together with Downs syndrome, it may be that a wide variety of defects could be related to the budding industry.

The potential link with the autism spectrum including cannabis-dependent, dose-related and rampant neurexin- neurologin-mediated synaptic dehiscence is of particular concern.  The rapidly growing autism epidemic in Colorado is matched by an autism hotspot in the northern cannabis zone of California which has likely become even hotter since that study was conducted.

Careful substance-spatiotemporal analyses of positive and negative correlation are indicated to investigate causal relationships.

The possibility of worldwide multiorgan cannabis-induced CB1R-mediated severe clinical teratology has not been widely canvassed.

Source:  email: stuart.reece@bigpond.com  

Abstract

At the Tip of an Iceberg: Prenatal Marijuana and Its Possible Relation to Neuropsychiatric Outcome in the Offspring – PubMed (nih.gov) September 2015

Abstract

Source: It’s All in the Rhythm: The Role of Cannabinoids in Neural Oscillations and Psychosis – PubMed (nih.gov) December 2015

Abstract

Keywords: ADHD; Attention deficit disorder; adolescence; drug abuse.

Conflict of interest statement

Source: https://www.ncbi.nlm.nih.gov/pubmed/29315559 June 2018

Legalization advocates and the weed industry can support necessary reforms while being honest about the risks of marijuana use, the study’s author says.

Source: Marijuana Users Report High Rates Of Dependence In Global Drug Survey | HuffPost UK Health (huffingtonpost.co.uk) May 2018

Smoking during pregnancy has well-documented negative effects on birth weight in infants and is linked to several childhood health problems. Now, researchers at the University at Buffalo Research Institute on Addictions have found that prenatal marijuana use also can have consequences on infants’ weight and can influence behavior problems, especially when combined with tobacco use.

“Nearly 30 percent of women who smoke cigarettes during pregnancy also report using marijuana,” says Rina Das Eiden, PhD, RIA senior research scientist. “That number is likely to increase with many states moving toward marijuana legalization, so it’s imperative we know what effects prenatal marijuana use may have on infants.”

Through a grant from the National Institute on Drug Abuse, Eiden studied nearly 250 infants and their mothers. Of these, 173 of the infants had been exposed to tobacco and/or marijuana during their mothers’ pregnancies. None were exposed to significant amounts of alcohol.

Eiden found that infants who had been exposed to both tobacco and marijuana, especially into the third trimester, were smaller in length, weight and head size, and were more likely to be born earlier, compared to babies who were not exposed to anything. They also were more likely to be smaller in length and weight compared to babies exposed only to tobacco in the third trimester. The results were stronger for boys compared to girls.

“We also found that lower birth weight and size predicted a baby’s behavior in later infancy,” Eiden says. “Babies who were smaller were reported by their mothers to be more irritable, more easily frustrated and had greater difficulty calming themselves when frustrated. Thus, there was an indirect association between co-exposure to tobacco and marijuana and infant behavior via poor growth at delivery.”

Furthermore, women who showed symptoms of anger, hostility and aggression reported more stress in pregnancy and were more likely to continue using tobacco and marijuana throughout pregnancy. Therefore, due to the co-exposure, they were more likely to give birth to infants smaller in size and who were more irritable and easily frustrated. The infants’ irritability and frustration is also linked to mothers who experienced higher levels of stress while pregnant.

“Our results suggest that interventions with women who smoke cigarettes or use marijuana while pregnant should also focus on reducing stress and helping them cope with negative emotions,” Eiden says. “This may help reduce prenatal substance exposure and subsequent behavior problems in infants.”

The study appeared in the March/April issue of Child Development and was authored by Pamela Schuetze, PhD, Department of Psychology, Buffalo State College, with co-authors Eiden; Craig R. Colder, PhD, UB Department of Psychology; Marilyn A. Huestis, PhD, Institute of Emerging Health Professions, Thomas Jefferson University, Philadelphia; and Kenneth E. Leonard, PhD, RIA director.

Source: Prenatal marijuana use can affect infant size, behavior, study finds — ScienceDaily May 2018

They were the mind-altering drugs of the Sixties, but now lysergic acid diethylamide (better known as LSD), magic mushrooms and a range of other banned psychedelic drugs are making a comeback.

Not on the party scene, but as the focus of researchers who believe they could treat a variety of mental health problems, including depression.

British researchers are at the forefront of this renaissance of hallucinogenics. But, as Good Health can reveal, a key organisation funding their work is a pressure group with a parallel agenda.

Source: How you have paid to help legalise lethal party drugs | Daily Mail Online May 2018

As the federal government prepares to legalize the recreational use of marijuana, an Ontario judge has ruled that cannabis-induced psychosis led a man to a seemingly hate-filled attack on a family, in what appears to be the first case of its kind in Canadian criminal courts.

The man who committed the attack, Mark Phillips, is a Toronto lawyer with an otherwise clean record, and the great-grandson of Nathan Phillips, a former mayor after whom the civic square in front of Toronto City Hall is named. The 37-year-old pleaded guilty Tuesday to assault causing harm in the Dec. 7 incident in St. Thomas, in southwestern Ontario, in which he cracked a man’s rib with a baseball bat.

Sergio Estepa was with his wife, Mari, teenage son and a family friend, speaking Spanish in the parking lot of a St. Thomas mall when a stranger, Mr. Phillips, approached and told them to stop speaking French, according to evidence in court.

He then came at them with a baseball bat, repeatedly screaming “ISIS,” saying he was arresting the family, and calling for help. The family also called for help.

Ontario Court Justice John Skowronski said that, in ordinary circumstances, such an attack would call for a penitentiary sentence ­– that is, at least two years in federal prison. But he accepted the recommendation of defence lawyer Steven Skurka that Mr. Phillips be given a conditional discharge, on the condition that he complete three years of probation. A conditional discharge means that, once his probation is successfully finished, Mr. Phillips will not have a criminal record.

Addressing the family, whose members had told the court in emotional victim-impact statements about the nightmares and anxiety they had experienced, Justice Skowronski said he wanted them to know that what happened to them was an aberration for the country. “Canada is a country of immigrants, different nations, skin colours, accents, names,” he said, adding that his name had not come from this country.

“This is something that took place because of a mental illness.”

Although Crown prosecutor Lisa Defoe had urged a suspended sentence and probation, which would have left Mr. Phillips with a criminal record, she, too, had accepted the defence argument that the attack was caused by cannabis-induced psychosis.

“At first blush this may appear to be a hate crime,” she told Justice Skowronski, “but it’s important for the Crown not to react emotionally.”

Mr. Skurka had told the court that Peter Collins, a forensic psychiatrist at the Centre for Addiction and Mental Health in Toronto, had uncovered after several sessions with Mr. Phillips that he had been smoking marijuana heavily, including three or four joints earlier on the day of the attack.

With marijuana legalization on the horizon, the case raises questions about mental-health risks and new challenges for the legal system. According to Mr. Skurka, Dr. Collins warned that higher levels than in the past of tetrahydrocannabinol (THC), the active ingredient in cannabis, is creating a higher incidence of drug-induced psychosis.

Mr. Phillips’s parents said he had been having irrational fears about Nazis, Muslims and terrorists. In one incident the same day as the attack, he shouted about North Korea and was kicked out of Air Canada Centre in Toronto.

Dr. Collins ­found that Mr. Phillips’s actions were not those of a hate crime, but of cannabis-induced psychosis.

“In my professional opinion, Mark Aaron Phillips suffered from a drug-induced psychosis in and around the time of the event that led to his arrest,” he wrote in his report.

Mr. Skurka had also read to the court from a medical journal that said that paranoid and grandiose delusions similar to those caused by schizophrenia can also be caused by cannabis use.

“This is someone without any history of discrimination, racism or violence,” Mr. Skurka said in an interview outside the courtroom, after sentencing.

Mr. Estepa said in an interview that he could not understand how a man of Mr. Phillips’s education and training as a lawyer could have been unaware of the effects of marijuana before using it.

“I can’t believe that in 2018, people don’t know that marijuana can affect your mind-state,” he said.

When asked by Justice Skowronski whether he had anything to say, Mr. Phillips replied, “I’m very, very sorry for what happened.”

Mr. Phillips withdrew from his practice of personal injury law after the incident, but hopes to resume working as a lawyer. He will need the Law Society of Ontario’s approval to do so.

Mr. Estepa met his wife after they moved to Canada separately from Colombia in the early 2000s. In his victim-impact statement, he described the pain of hearing his son treated as an outsider.

“Here in his home country, someone told him, ‘You don’t belong here.’ ”

Source: Marijuana-induced psychosis behind Toronto lawyer’s bat attack, judge rules – The Globe and Mail April 2018

High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other.

The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found.

The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient.

Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity.

“If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts.

“The difference is there whether you have psychosis or not, and we think this is strictly related to the potency of the cannabis,” she added. Details of the study are reported in the journal Psychological Medicine.

The scans found that daily users of high-potency cannabis had a slightly greater – by about 2% – “mean diffusivity” in the corpus callosum. “That reflects a problem in the white matter that ultimately makes it less efficient,” Dazzan told the Guardian. “We don’t know exactly what it means for the person, but it suggests there is less efficient transfer of information.”

The study cannot confirm that high levels of THC in cannabis cause changes to white matter. As Dazzan notes, it is may be that people with damaged white matter are more likely to smoke skunk in the first place.

“It is possible that these people already have a different brain and they are more likely to use cannabis. But what we can say is if it’s high potency, and if you smoke frequently, your brain is different from the brain of someone who smokes normal cannabis, and from someone who doesn’t smoke cannabis at all,” she said.

But even with the uncertainty over cause and effect, she urged users and public health workers to change how they think about cannabis use. “When it comes to alcohol, we are used to thinking about how much people drink, and whether they are drinking wine, beer, or whisky. We should think of cannabis in a similar way, in terms of THC and the different contents cannabis can have, and potentially the effects on health will be different,” she said.

“As we have suggested previously, when assessing cannabis use, it is extremely important to gather information on how often and what type of cannabis is being used. These details can help quantify the risk of mental health problems and increase awareness of the type of damage these substances can do to the brain,” she added.

In February, Dazzan and others at the Institute of Psychiatry reported that the ready availability of skunk in south London might be behind a rise in the proportion of new cases of psychosis being attributed to cannabis.

Source: Smoking high-strength cannabis may damage nerve fibres in brain | Drugs | The Guardian November 2015

Yasmin L. Hurd, Olivier J. Manzoni, Mikhail V. Pletnikov, Francis S. Lee, Sagnik Bhattacharyya and Miriam Melis

Abstract

Keywords: adolescence; cannabis; cognition; perinatal; psychiatric disorders; reward.

Source: Cannabis and the Developing Brain: Insights into Its Long-Lasting Effects – PubMed (nih.gov) October 2019

Judith Grisel

Occasionally during my love affair with marijuana I would experience perceptual disruptions profound enough to freak me out. One time I was driving along a crowded road when my car seemed a little wobbly and then listed towards the centre, an alarming thud-thud emanating from the back end. In the middle of a densely populated spot without a hard shoulder, I crept slowly across a few lanes of traffic and pulled to a stop. Concentrating very hard, I got out of the car to assess and hopefully change the flat tyre. I rarely got paranoid from smoking weed; neither did it typically make me sleepy. Instead, I was among the lucky ones, as the drug made everyday activities such as gardening, waiting on tables and talking to my family bearable if not interesting. So I was shocked and embarrassed to find, after a few minutes of close inspection amid the honking horns, that there was nothing wrong with the car.

At the time I took hallucinations as evidence of a good score. Now, as an ex-smoker and neuroscientist whose focus is addictive drugs, I know that my resilient response to this stressful experience was contingent on having a neurotypical brain. Neural pathways are forged by finely orchestrated signals for synapse growth and pruning; disruptions can result in atypical neural connections that increase the risk of psychosis. The liability may be unmasked by environmental conditions that can essentially be reduced to an ambiguous but well-recognised bogeyman: stress.

A new study in the Lancet Psychiatry journal has attempted to shed light on the relationship between cannabis and psychosis. The authors assessed symptoms such as trouble telling the difference between real and unreal experiences, having false ideas about what is taking place, or who one is, nonsense speech, lack of emotion, and social withdrawal – all core features of the debilitating disorder schizophrenia. Replicating and extending earlier studies, the authors were able to connect cannabis use to increased risk for psychosis.

As anyone who has ever taken a general psychology course well knows, correlation does not mean causation. We would need an experiment to prove this link unequivocally – for example, taking a large group of people and randomly assigning them to using and non-using groups, following them for a number of years and then assessing them for psychotic symptoms. Obviously, that would be unethical. Nevertheless, this study strongly supports the notion that schizophrenia can be precipitated by consuming weed, with high-potency strains a particular concern.

This drug is an increasingly ubiquitous part of modern, socially liberal life. A majority of Americans think it is at least harmless, if not beneficial. The plant contains more than 100 pharmacologically active compounds, called cannabinoids. Of these, the two of primary interest to researchers and consumers are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).

In 1964 we learned that THC is responsible for the drug’s recreational high. Two key discoveries followed. First, THC produces its effects (perceptual distortions, changes in thinking and euphoria, for example) by interacting with a particular class of cell receptors. These CB1 receptors are present in virtually every synapse – the point at which brain cells convey information to each other. Such wide distribution indicates that they play a critical role in most, if not all, brain activity. That’s not because we evolved to enjoy smoking weed. It’s because those plants happen to mimic signalling molecules found in our bodies – endocannabinoids – just like morphine mimics our endorphins. It seems that one role of endocannabinoids is to help highlight especially important communication. When something meaningful happens, the release of these molecules helps ensure that relevant circuits in the brain take note.

The primary difference between THC and our brain’s own cannabinoids is dosing. Neurotransmission occurs in a targeted, local manner appropriate to specific demands. After using cannabis, all brain circuits are flooded with THC, so the process of sorting meaning from the mundane is disrupted. Everyday occurrences such as eating a meal, listening to music, watching television or driving a car become soaked with import. For someone with hearty neural connections who is resilient to stress, this can be a real treat, but for those whose ability to cope and sort is naturally less robust, including those with a susceptibility schizophrenia, it can be a threat.

Well designed, placebo-controlled studies on cannabis are still lacking. In particular, we need more research to distinguish between the effects of THC and those of CBD. The latter compound counteracts the effects of THC and has therapeutic promise for a number of health conditions. There seems no reason therefore not to make CBD widely available, but plenty to suggest careful consideration before embracing THC.

We are swept up in a backlash against overly restrictive and unscientific regulation of cannabis. While it is well past time to loosen restrictions, promote research and consider the data that emerges, the Lancet study provides evidentiary warning about the inherent dangers – to some – of our quest to mitigate reality.

Most societies take it upon themselves to provide appropriate assistance for those with disability; they ought also to take reasonable measures to prevent those disabilities occurring, when possible. Addiction and psychosis are similar in that they are the result of biological vulnerability combined with a stressful environment. Some are more predisposed than others, and this should provoke ethical and moral obligation – particularly from those of us who are not at risk – to protect the unlucky ones for whom the use of cannabis may be permanently detrimental.

• Judith Grisel is a behavioural neuroscientist and author of Never Enough: The Neuroscience and Experience of Addiction

Source: Can we all chill out about cannabis? Not quite yet | Judith Grisel | The Guardian 24^th March 2019

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

It’s no secret that substance use disorders (SUDs) can negatively impact the individual struggling, even putting their life in jeopardy.

“For persons with SUDs, their brain is telling them this lie that, ‘You’ve got to use to stay alive,'” said Sterling Shumway, chair of the Texas Tech University Department of Community, Family & Addiction Sciences and director of the Institute for the Study of Addiction, Recovery & Families.

Likewise, groundbreaking new research now indicates that the same thing is happening in the brains of the people caring for those with addiction.

“To further understand the etiology of SUDs and their associations with family systems, research must expand beyond examining the individual struggling with an SUD,” said Shumway, co-principal investigator (P.I.) for the ongoing project. “This includes research that helps us understand the neurological impact of stress, fear and the impairment found in the family system.”

The original hypothesis was that if the person struggling with an SUD’s brain is compelling them to use as a survival mechanism, perhaps the family member’s brain is doing the same thing as it relates to their loved one’s survival, thus leading to the mostly ineffective and compulsive attempts to rescue their loved one.

“It’s really first-of-a-kind research,” Shumway said, “looking to see if the person and their family member have become similarly, what we call, ‘co-impaired.'”

Looking inside the brain

Over the last four years, Shumway and co-P.I. Spencer Bradshaw, director of the Center for Addiction Recovery Research and an assistant professor in the department, have been using functional near-infrared spectroscopy (fNIR) to monitor reactions in the frontal cortex of both those in recovery from an SUD and family members as they participate in a research protocol presenting certain audio and visual cues meant to stimulate the prefrontal cortex (PFC).

“For the person who struggles with alcoholism, this protocol involves sounds and a variety of images that evoke strong emotional responses, including images associated with alcohol. We look at how their brain lights up differently in response to these various images,” Shumway said. “When family members come in, they aren’t presented a picture of a glass of alcohol, they see instead a current image of their loved one seeking recovery. That’s what makes this research groundbreaking, in that a family member’s PFC lights up in a similar way when looking at their addicted loved one as the PFC of someone with an SUD when looking at their substance of choice.”

When the fNIR results showed that family members often exhibited similar impairment and decision-making difficulties as those with an SUD, Shumway and Bradshaw realized they needed to look deeper inside the brain to explain this phenomenon.

“This is the next step in our research: to look at the family member brain at the level of the midbrain – a much deeper, more primitive part of the brain – and compare it with the brains of those struggling with an SUD,” Shumway said. “We want to know if a similar process is also occurring there with respect to these deeper brain structures and their interaction with the PFC.”

Now, with the help of the Texas Tech Neuroimaging Institute, the two are using functional magnetic resonance imaging (fMRI) to do just that.

“What comes from the midbrain is what causes addicts to use – it’s this intense pain associated with craving. Craving is the means by which the brain compels a person to do something they wouldn’t normally do as part of a survival response – that is, to use despite harmful consequences,” Shumway said. “In relation to a person struggling with an SUD, their brain is telling them, ‘You must use drugs and alcohol, or you’re going to die.'”

This message becomes so intrusive that it overrides the more rational frontal cortex, which is attempting to get them to consider the negative consequences. Unfortunately, when the disease of addiction is present, the midbrain wins the battle.

“With family members, particularly those who’ve been fighting the longest to keep their loved one alive, we believe similarly that their midbrain begins to compel them toward behaviors that may enable rather than resolve SUD behavior,” Shumway said. “In other words, they’re reacting to keep their loved one alive. They may know it’s not helping, but they’re going to do it anyway just like the person with an SUD is going to find and use their substance. This, because the midbrain is requiring it of them out of a perceived need for survival.”

Testing the hypothesis

Shumway and Bradshaw will use the fMRI to examine different parts of the brain, how they are connected to one another and which parts are being activated by different activities or presentations.

“Brain structures, their connectivity and their functioning are key to what we now understand about the brain of the person with an SUD and are what we are similarly interested in examining with respect to the family member brain,” Bradshaw said.

As before, Shumway and Bradshaw intend to include a control group.

“With a control group, we’ll be able to compare those who have never been around addiction, never been impacted by addiction, and never have had to make the difficult decisions like those in families where addiction is present,” Bradshaw said.

Shumway emphasized the research is likely one-of-a-kind.

“We’re probably the only ones, perhaps in the world, who have looked at the frontal cortex of family members related to the way it is responding,” he said. “And we probably will be one of the first to look at family members and functioning of the midbrain when given certain stimuli.”

‘They need help, too.’

One of the biggest reasons for this research is to try to help the family members of those with an SUD find their own recovery, which also gives their loved one a better chance

.

“You’ve got two brains – the family member’s and the loved one’s brain –that are trying to keep one person alive. The problem is the family members also suffer

,” Shumway said. “They don’t take care of themselves, and they struggle as well. We’re not very good at taking care of those who struggle with substance use disorders; we’re even worse at taking care of the family members.”

Because dynamics differ between families, the person who is the primary caregiver differs as well – and sometimes that role switches between people within a family.

“It’s often those who have cared for these people the longest who have the most personal investment in their lives and their success,” Bradshaw said. “This person could, at times, be a grandparent, a parent or even a sibling. While we usually find this person to be a close family member, it may include a wide umbrella of people who care about this person.”

This so-called “systems approach” to addiction recovery values everybody in the system. The idea is that if the parents, siblings, etc., are doing well, the person with the disorder has a better chance of doing well. And, reciprocally, if the person with the disorder is doing well, that helps the others in the system do well.

“With SUDs and recovery, it’s a team sport,” Shumway said. “The more people on the team who are healthy makes a big difference in terms of the trajectory of success.”

While the researcher say society if often most concerned about the identified patient with the SUD, and that’s important, it’s not the whole story.

“The health of every family member is important,” Bradshaw said. “Research shows that when family members are impacted by the stress of addiction, they go to the doctor more often, they have higher medical claims and services and they get diagnosed with higher rates of depression.”

Therefore, resources are needed for both the loved one with the SUD and the family member.

“Both deserve happiness and quality of life,” Bradshaw said.

Brain Research: In the Same Way Addiction Sufferers Crave Substances, Their Family Members Crave Them | Texas Tech Today | TTU

Abstract

Background

Epigenetic modifications of a gene have been shown to play a role in maintaining a long‐lasting change in gene expression. We hypothesize that alcohol’s modulating effect on DNA methylation on certain genes in blood is evident in binge and heavy alcohol drinkers and is associated with alcohol motivation.

Methods

Methylation‐specific polymerase chain reaction (PCR) assays were used to measure changes in gene methylation of period 2 (PER2) and proopiomelanocortin (POMC) genes in peripheral blood samples collected from non-smoking moderate, non-binging, binge, and heavy social drinkers who participated in a 3‐day behavioral alcohol motivation experiment of imagery exposure to either stress, neutral, or alcohol‐related cues, 1 per day, presented on consecutive days in counterbalanced order. Following imagery exposure on each day, subjects were exposed to discrete alcoholic beer cues followed by an alcohol taste test (ATT) to assess behavioral motivation. Quantitative real‐time PCR was used to measure gene expression of PER2 and POMC gene levels in blood samples across samples.

Results

In the sample of moderate, binge, and heavy drinkers, we found increased methylation of the PER2 and POMC DNA, reduced expression of these genes in the blood samples of the binge and heavy drinkers relative to the moderate, non-binge drinkers. Increased PER2 and POMC DNA methylation was also significantly predictive of both increased levels of subjective alcohol craving immediately following imagery (p < 0.0001), and with presentation of the alcohol (2 beers) (p < 0.0001) prior to the ATT, as well as with alcohol amount consumed during the ATT (p < 0.003).

Conclusions

These data establish significant association between binge or heavy levels of alcohol drinking and elevated levels of methylation and reduced levels of expression of POMC and PER2 genes. Furthermore, elevated methylation of POMC and PER2 genes is associated with greater subjective and behavioral motivation for alcohol.

Source:  https://doi.org/10.1111/acer.13932  31^st December 2018

We are pleased to announce that a new online course at Auburn University Outreach will feature The Marijuana Report website and e-newsletter. Titled “The Harmfulness of Marijuana Use and Public Policy Approaches to Address the Challenges,” the three-week course will be taught by Paula Gordon, PhD, who has worked as a staff member and/or consultant to several federal agencies concerned about addiction treatment and prevention. Course topics will address:

• The need to defend the brain while nurturing mental and physical well-being: fostering a mental and public health approach to addressing the challenges of drug use and addiction.
• An extraordinary look at the addiction cycle: the lessons and insights from an October 30, 2013, videotaped exchange between Dr. Nora Volkow and the Dalai Lama in Dharamshala, the morning of Day 3 of the workshop series (See the link here).
• Comprehensive coordinated strategies aimed at stopping the use of marijuana and other psychoactive and addictive substances in the US: proposed comprehensive and coordinated public health oriented strategies involving all sectors of society, including government, the justice system, and educational institutions.

Register here

Source: Email from National Families In Action The Marijuana Report The Marijuana Report.Org August 2017

The authors compare the clinical features of idiopathic psychosis (eg, schizophrenia) with cannabis-induced psychosis.

As cannabis consumption rises, there has been significant emerging evidence for cannabis-related risks. Here: a comparison of the clinical features of idiopathic psychosis (eg, schizophrenia) versus cannabis-induced psychosis (CIP). Scroll through the slides for 8 distinguishing features

Source: https://www.psychiatrictimes.com/view/8-distinguishing-features-primary-psychosis-versus-cannabis-induced-psychosis August 2017

In a pre-clinical study, researchers from Western University in Ontario, Canada, studied the effects of long-term exposure to THC in both adolescent and adult rats.

They found changes in behavior as well as in brain cells in the adolescent rats that were identical to those found in schizophrenia. These changes lasted into early adulthood long after the initial THC exposure.

The young rats were “socially withdrawn and demonstrated increased anxiety, cognitive disorganization, and abnormal levels of dopamine, all of which are features of schizophrenia,” according to the article. The same effects were not seen in the adult rats.

“With the current rise in cannabis use and the increase in THC content, it is critically important to highlight the risk factors associated with exposure to marijuana, particularly during adolescence,” the researchers warn.

Read Medical News Today story here. Read study abstract in the journal Cerebral Cortex here.

Email from Monte Stiles, National Families in Action January 2016

A University of Pittsburgh Medical Center study published in the journal Psychology of Addictive Behaviors last September found that chronic marijuana use during adolescence did not lead to depression, anxiety, psychosis, or asthma by mid-life.

The U.K.’s Independent was one of many newspapers that celebrated the news, scoffing at the National Health Service help page that warns: “Your risk of developing a psychotic illness is higher if you start using cannabis in your teens.”
 
Now, however, the journal has run a correction. It turns out that the researchers misinterpreted their data. They checked it again after criticism of their study and found that there was a two-and-one-half-fold increase in psychotic disorders in midlife after chronic marijuana use that began in adolescence.
 
The director of the Maryland chapter of SAM (Smart Approaches to Marijuana) caught the error and notified the journal which lead to the correction. SAM is calling on all media who reported the original incorrect story to correct their account of it now.
 
Read Independent story here.  Read SAM account of the correction here.

Source: Email from Monte Stiles, National Families in Action, January 2016

Two recent studies, one in Great Britain and this one from the University of Southern California, contradict the findings of a rigorous 25-year-long study done with a birth cohort in Dunedin, New Zealand a few years ago. That study found that persistent marijuana use that continued into adulthood resulted in an 8-point drop in IQ. The two new studies find the opposite.

The UCLA study looked at 789 pairs of adolescent twins from two ongoing studies—one in Los Angeles and one in Minnesota—who enrolled between ages 9 and 11. Over 10 years, five IQ tests were administered along with confidential surveys of marijuana use. Marijuana-using twins lost 4 IQ points, but so did their non-using twins, leading researchers to conclude that something other than marijuana was lowering IQ.

The other study compared teens who reported daily marijuana use for six months or longer with teens who used the drug less than 30 times and found no difference in IQ.
 
But critics say both studies are flawed in that they did not measure heavy marijuana use over a long 25-year period like the Dunedin study did.
 
Dr. Madeline Meier, lead researcher of the Dunedin study, writes, “Our 2012 study (Meier et al. PNAS 2012) reported cognitive decline among individuals with a far more serious and far more long-term level of cannabis use. That is, we found cognitive decline in individuals followed up to age 38 who started cannabis use as a teen and who thereafter remained dependent on cannabis for many years as an adult. This new study is different; the two papers report about completely different doses of cannabis, and about participants 2 decades apart in age.  The new study reports cognitive test scores for individuals followed up to only age 17-20, fewer than half of whom had used cannabis more than 30 times, and only a fifth of whom used cannabis daily for > 6 months. This new study and our prior study agree and both report the same finding: no cognitive decline in short-term low-level cannabis users. The message from both studies is that short-term, low-level cannabis use is probably safer than very long-term heavy cannabis use. The big problem remains that for some teens, short-term low-level teenaged cannabis use leads onward to long-term dependence on cannabis when they become adults. That is what is cause for concern.”
 
Read Science story here. Read Dr. Meier’s rebuttal here.

Source: Email from Monte Stiles, National Families in Action January 2016

Almost all cannabis sold on British streets can cause psychosis after weaker forms were driven from the market.

The most potent “skunk” accounts for 94 per cent of all cannabis seized by police, up from half in 2005, according to the first study for almost a decade.

Dealers are thought to be pushing higher-strength products to get recreational users hooked, with the milder hashish form barely available, researchers say.

Teenager cannabis smokers have been told that skunk is more dangerous and that they must watch out for paranoia and other symptoms of psychosis.

Skunk, also known as sinsemilla, is made from unpollinated cannabis and contains higher levels of THC, a psychoactive compound, than herbal marijuana or resin, also known as hashish.

A Home Office study of police seizures in 2005 found that 51 per cent were skunk and 43 per cent resin. Three years later skunk seemed to be becoming stronger and more common, but the study has not been repeated since 2008.

Now researchers at King’s College London have analysed almost 1,000 samples seized by police in London, Merseyside, Derbyshire, Kent and Sussex. Resin accounted for just 6 per cent of samples, falling to 3 per cent in London, and even that had become stronger since 2008, according to results published in Drug Testing and Analysis.

“The increase of high-potency cannabis on the streets poses a significant hazard to users’ mental health,” said Marta Di Forti, senior author of the paper. “It’s a big worry. It’s pretty much the only kind of cannabis you can buy out there.”

Her previous work suggests that skunk users are five times more likely to develop psychosis than non-users, while there is no extra risk for hash smokers. Britain is largely self-sufficient in skunk as farms take over from hash grown in Morocco and Dr Di Forti said that the stronger product could be a deliberate policy by gangs.

“If high potency is more likely to induce dependence, that’s an advantage for the drug dealer because he wants people to come back as much as possible, rather than recreational users who only use at the weekend when they’re listening to music or going to a party,” she said.

Skunk has not got stronger since 2005, which she said could be because users could not tolerate higher THC concentrations without side-effects.

About 2.2 million people are estimated to have smoked cannabis in the past year, a million of them aged 16-24.

While there is some evidence that users can partially detect higher strength cannabis and cut back, Ian Hamilton, a lecturer in mental health at the University of York, said: “If the cannabis market is saturated with higher potency cannabis this increases the risk of younger and more naive users developing problems as they are less likely to adjust the amount of cannabis they ingest than more experienced users.”

Source: https://www.thetimes.co.uk/edition/news/mental-illness-risk-as-skunk-drives-out-milder-cannabis-wgd58b56l# February 2018 

Abstract
Marijuana is currently a growing risk to the public in the United States. Following expanding public opinion that marijuana provides little risk to health, state and federal legislatures have begun changing laws that will significantly increase accessibility of marijuana. Greater marijuana accessibility, resulting in more use, will lead to increased health risks in all demographic categories across the country. Violence is a well-publicized, prominent risk from the more potent, current marijuana available.
We present cases that are highly popularized storylines in which marijuana led to unnecessary violence, health risks, and, in many cases, both. Through the analysis of these cases, we will identify the adverse effects of marijuana use and the role it played in the tragic outcomes in these and other instances. In the analysis of these cases, we found marijuana as the single most common, correlative variable in otherwise diverse populations and circumstances surrounding the association of violence and marijuana.

Conclusion
According to research studies, marijuana use causes aggressive behavior, causes or exacerbates psychosis and produce paranoias. These effects have been illustrated through case studies of highly publicized incidents and heightened political profiles.
These cases contain examples of repeated illustrations of aggression, psychosis and paranoia by marijuana users and intoxication.
Ultimately, without the use and intoxication of marijuana, the poor judgment and misperceptions displayed by these individuals would not have been present, reducing the risk for actions that result in senseless deaths.

Import to these assertions, is that the current marijuana is far more potent in THC concentrations, the psychoactive component. Accordingly, and demonstrated in direct studies, more potent marijuana results in a greater risk for paranoid thinking and psychosis.
In turn, paranoid behavior increases the risk for paranoid behaviors and predictably associated with aggressive and violent behaviors. Marijuana use causes violent behavior through increased aggressiveness, paranoia and personality changes (more suspicious, aggressive and anger).
Recent illicit and “medical marijuana” (especially grown by care givers for medical marijuana) is of much high potency and more likely to cause violent behavior. Marijuana use and its adverse effects should be considered in cases of acts of violence as its role is properly assigned to its high association.
Recognize that high potency marijuana is a predictable and preventable cause of tragic violent consequences.

Source: https://www.omicsonline.org/open-access/marijuana-violence-and-law-2155-6105-S11-014.pdf January 2017

Researchers at the University of Exeter and UCL (University College London) have identified a gene which can be used to predict how susceptible a young person is to the mind-altering effects of smoking cannabis. The finding could help identify otherwise healthy users who are most at risk of developing psychosis.

The research, funded by the Medical Research Council and published in Translational Psychiatry, also show that female cannabis smokers are potentially more susceptible to short-term memory loss than males. Previous studies in this field have looked at people who already have psychosis, but this is the first study to look at healthy people and to examine their acute response — or how the drug affects their minds.

Previous research has found a link between the AKT1 gene and people who have gone on to develop psychosis. In the new study, Celia Morgan, Professor of Psychopharmacology at the University of Exeter and Professor Val Curran and her team from UCL found that young people with variation in the ‘AKT1’ gene experienced visual distortions, paranoia and other psychotic-like symptoms more strongly when they were under the influence of cannabis.

Around one per cent of cannabis users develop psychosis. Although low in number, the impact can be devastating and long lasting. It is known that smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, but it has been difficult to establish who is most vulnerable. Researchers have previously found a high prevalence of one variant of the AKT1 genotype in cannabis users who went on to develop psychosis as a result of their use. This is the first research that shows the link between the same gene and the effects of smoked cannabis in healthy young people.

It is hoped that it will help identify those most at risk of the negative effects of cannabis smoking and may aid the development of genotype targeted medication.

Professor Morgan said: “These findings are the first to demonstrate that people with this AKT1 genotype are far more likely to experience strong effects from smoking cannabis, even if they are otherwise healthy. To find that having this gene variant means that you are more prone to mind-altering affects of cannabis when you don’t have psychosis gives us a clue as to how it increases risk in healthy people. Putting yourself repeatedly in a psychotic or paranoid state might be one reason why these people could go on to develop psychosis when they might not have done otherwise. Although cannabis-induced psychosis is very rare, when it happens it can have a terrible impact on the lives of young people. This research could help pave the way towards the prevention and treatment of cannabis psychosis.”

Professor Curran added: “The current study is the largest ever to be conducted on the acute response to cannabis. Our finding that psychotic-like symptoms when young people are ‘stoned’ are predicted by AKT1 variants is an exciting breakthrough as this acute reaction is thought to be a marker of a person’s risk of developing psychosis from smoking the drug.”

The study involved 442 young cannabis users who were tested while under the influence of the drug, and while sober. The researchers measured the extent of the symptoms of intoxication and effect on memory loss and compared it to results seven days later when the young people were drug free. They found that those who with this variation in the AKT1 geneotpye were more likely to experience a psychotic response.

As part of the study, researchers gained permission from the Home Office to analyse the cannabis samples for their make-up and strength. Samples were dropped off at a police station and analysed by the forensic science service.

The research also found that females were more vulnerable than males to impairment in short term memory after smoking cannabis.

“Animal studies have found that males have more of the receptors that cannabis works on in parts of the brain important in short term memory, such as the prefrontal cortex. We need further research in this area, but our findings indicate that men could be less sensitive to the memory impairing effects of cannabis than females,” added Professor Morgan.

Source: https://www.sciencedaily.com/releases/2016/02/160216111357.htm February 2016

• Polly Ross, 32, suffered with Hyperemesis Gravidarum during second pregnancy
• Mother smoked cannabis and magic mushrooms to ease pain, an inquest heard
• ‘Talented and clever’ translator took her life in 2015 after battling with psychosis

A mother-to-be who took cannabis after developing the same morning sickness condition as the Duchess of Cambridge killed herself after developing a drug-induced psychosis, an inquest heard.  

Talented translator Polly Ross, 32, suffered Hyperemesis Gravidarum (HG), the condition which saw Kate Middleton rushed to hospital in August while visiting the queen in Aberdeen.

Hull Coroner’s Court in East Yorkshire was told today how a desperate Mrs Ross took cannabis and magic mushrooms in a bid to tackle the severe bouts of sickness.

However in July 2015, just a year after the birth of her second daughter, she died after stepping out in front of a train.  

A coroner heard Mrs Ross had developed ‘drug induced psychosis’ after taking cannabis to stop symptoms of HG.

Mrs Ross told her GP, Dr Daniella Malesknasr, she had taken cannabis during her pregnancy after visiting the doctors suffering from post natal depression.

Dr Malesknasr told the hearing: ‘She had told me when she was pregnant with her second child that she was taking cannabis and magic mushrooms to help combat HG during her pregnancy – but she was no longer taking it.’

Professor Paul Marks, the senior coroner, questioned: ‘And does taking cannabis actual benefit those suffering from HG?.’

The doctor replied: ‘I can’t possibly comment on that.’

Dr Malesknasr said ‘alarm bells were ringing’ after Polly had told her she wanted to commit suicide on February 13, 2015.

The inquest heard the GP had called in at her home to find her in a psychotic episode and Mrs Ross was sectioned the following month.

By March 18, Dr Malesknasr said Mrs Ross was diagnosed with drug induced psychosis following the amounts of magic mushrooms and cannabis she had been taking.

The GP said she was then given Respiradon to help battle the psychosis.

Mrs Ross tried to take her life three times with self harm and taking an overdose twice in a three month period.

However, the court heard she was remarkably allowed to discharge herself voluntarily following the last attempt to take her own life.

Professor Marks said: ‘So after taking an overdose of paracetamol tablets, Polly was allowed to just leave voluntarily?’

Dr Malesknasr said: ‘I can’t comment on that because it is a hospital matter.’

However, in May 2015 a psychiatrist in the community said that psychosis was no longer a problem and she should come off the anti-psychosis drug Respiradon.

The translator was given help by a crisis team to give her a ‘higher and intense level of support’, but Mrs Ross had refused them entry to her house in Driffield, East Yorkshire.

Mrs Ross died on July 12, 2015, by stepping in front of a train in Hull, East Yorkshire, and ‘death was instant’, Hull Royal Infirmary Consultant Histopathologist Dr Ian Richmond told the hearing.

She had told mental health workers at the women-only care centre at Westlands voluntary care unit in Hull, East Yorkshire, that she was going to the shop.

A statement from Mrs Ross’s aunt Emma May, who cared for her during her final months, read: ‘With the right guidance, medication and support, Mrs Ross could have made a full recovery.

‘There should be systems in place to protect that life especially because there are so many suicides attempts of post natal women.

‘I cannot understand why she was allowed to leave the hospital unit before she died.

‘Polly clearly said many times that she would kill herself, many months before she did.

‘I feel that she posed a significant risk to herself, did not have sufficient capacity to make decision and more should have been done to protect and care for her.’

Mrs Ross, who ran her own ‘very good’ translation business in Paris, was described as ‘an extremely intelligent lady and very driven in her own ambition’, by Mrs May.

She was also described as ‘frighteningly clever’.

She met her English husband Samuel Ross in 2011 in the French capital and the pair quickly married and had two daughters born in June 2012 and June 2014 respectively.

Mrs Ross suffered HG during pregnancy with both children and had post natal depression following the birth of both children.

The inquest, expected to last three days, continues.

WHAT IS HG?

Source: https://www.dailymail.co.uk/news/article-5063227/Pregnant-mum-killed-developing-drug-habit.html November 2017

As more cases turn up, doctors are concerned about the extent to which memory loss may be undetected.

Just over five years ago, a man suffering from amnesia following a suspected drug overdose appeared at Lahey Hospital and Medical Center in Burlington, Massachusetts, a Boston suburb. He was 22, and had injected what he believed to be heroin. When he woke up the next morning, he was extremely confused, repeatedly asking the same questions and telling the same stories. Doctors at Lahey quickly diagnosed the man with anterograde amnesia—the inability to form new memories.

His brain scan revealed why. “I thought it was an extremely strange scan—it was almost hard to believe,” says Jed Barash, a neurologist working at Lahey at the time. In the scan, the twin, seahorse-shaped structures of the man’s hippocampi were lit up against the dark background of the rest of the brain—a clear sign of severe injury to just that one region.

“It was strange because that was all there was,” Barash says.

Memory researchers have known since the late 1950s that the hippocampi are responsible for turning short-term memories into lasting ones, so the amnesia was not surprising. Just how the damage occurred, however, remained a mystery. Lack of oxygen to the brain that would have occurred during the overdose could not be the only explanation. The number of survivors in the state that year could easily have numbered in the thousands, so why was there only one patient with this seemingly unique brain damage?

Along with his colleagues, Barash—now the medical director at the Soldiers’ Home health-care facility in Chelsea, Massachusetts—figured that the opioids must have played a role, and that hunch became only more acute as three more patients—each fitting the same pattern—appeared at Lahey over the next three years. All had the same unique destruction of the hippocampi, all had amnesia, and all were suspected to have overdosed. By that point, the doctors at Lahey faced two fundamental questions: What was causing the strange new syndrome? And precisely how rare was it?

Both questions remain unanswered, but a case report published Tuesday in the Annals of Internal Medicine adds to a growing body of evidence suggesting that the problem is far from isolated, and that a potent opioid variation could be involved. A total of 14 patients have now been identified in Massachusetts, one of whom was first admitted to a hospital in his home state of New Hampshire. The new case study reveals two more patients—one from Virginia, and one from Maryland. Both turned up at a medical facility in West Virginia.

Although many of the patients had taken a variety of drugs, all but one either have a history of opioid use or tested positive for opioids. The most recent case, a 30-year-old man examined last year in West Virginia, is the first patient proven to have taken fentanyl, an extremely potent and dangerous opioid that is rarely tested for in toxicology screens.

There are many barriers to determining the true scope of the problem, from lack of proper testing to the fact that many patients never come to attention in the first place. And amid a larger opioid crisis that some experts say could claim as many as 500,000 lives over the next decade, pinning down the cause of a dozen or so amnesia cases can seem trifling. “It’s sort of like the Titanic going down and you’re worried about some details,” says Alfred DeMaria, the state epidemiologist for Massachusetts.

At the same time, DeMaria suggests that, at the very least, these patients may offer a different route for understanding a disorder, as was the case with a small cluster of patients in the early 1980s who developed Parkinson’s disease after taking contaminated drugs—a misfortune that turned out to be limited to a few people, but which nonetheless gave Parkinson’s researchers a new tool for studying the disease. More worryingly, he also points to several examples of medical investigations that began with a small number of mysterious cases and turned out to have significant public health-implications, such as the appearance of West Nile Virus, or the AIDS epidemic.

Bertha Madras, a psychobiologist at McLean Hospital in Belmont, Massachusetts, and a member of President Donald Trump’s Commission on Combating Drug Addiction and the Opioid Crisis, agreed that getting to the bottom of these amnesia cases is crucial—particularly given that many cases may be going undetected since the type of cognitive testing needed to diagnose amnesia may not be routinely done in overdose survivors. She also suspects that with overdose-antidote drugs like naloxone becoming more widely available, it is possible that more patients, rather than turning up dead, will show up at hospitals.

And with more survivors, Madras said in an email message, “there conceivably will be more cases of brain damage, especially in the very oxygen-sensitive hippocampus, the ‘epicenter’ of initial learning and memory.”

* * *

After encountering more patients following that first one in 2012, Barash contacted the Massachusetts Department of Public Health in 2015, which put out a request to emergency-room physicians, neurologists, and radiologists statewide for information that might identify additional cases. By the end of 2016, a total of 14 people who matched the pattern had been identified. Then, in May of 2017, the DPH made what they called “an unusual amnestic syndrome” with “acute, bilateral hippocampal” damage a reportable disease syndrome—a status that requires any doctor who sees such a case to forward patients’ medical records for review.

As of today, however, DeMaria believes there is no such mechanism in place in other states, and that’s one of the barriers to getting a handle on the prevalence of the amnestic syndrome. Marc Haut, the neuropsychologist who examined the man from Virginia in 2015, and one of the authors on the new Annals paper, had no way of knowing about the investigation in Massachusetts and initially chalked up the damage to cocaine use. At the time, he saw no reason to consider opioids, in part because of the information the patient shared with him. “Patient reports about substance use [are] not always accurate for a couple of reasons, one being the patients themselves,” he says. “And the other being that patients often don’t know what they’re buying and using.”

So it was not until he received an email from Barash that Haut, the chair of the behavioral medicine and psychiatry department at West Virginia University, reconsidered whether opioids could have played a role. To date, only eight of the 16 patients reported in the cluster had cocaine in their system, making opioids a more consistent link than any other drug. Barash, who is also an author on the Annals paper, wonders if fentanyl—considered to be 50 times more potent than heroin—is a key component, in part because the timing and location of the appearance of these amnestic cases parallels the rise of fentanyl overdoses in two of the hardest hit regions in the country. Teasing this out is complicated with the ever-changing landscape of drugs that people are taking, often in combination. “Cocaine overdose deaths are escalating,” said Madras, “along with evidence of combined use of fentanyl, heroin, and cocaine in some deaths.”

And despite the fact that fentanyl abuse has become so common, routine toxicology screens don’t test for the presence of the drug. It was only because Haut had been tipped off that he requested the advanced toxicology screen for the 2017 patient, which found evidence that he had taken fentanyl in addition to cocaine. His MRI scan also revealed the signature hippocampal damage: “bright, big, and intense,” according to Haut.

Source: https://www.theatlantic.com/health/archive/2018/01/fentanyl-overdose-amnesia/551846/ January 2018

This collection of articles has been collated to show how the use of cannabis has been involved in many murders and attacks of violence.

Attacker Smoked Cannabis: suicide and psychopathic violence in the UK and Ireland
“Those whose minds are steeped in cannabis are capable of quite extraordinary criminality.”

What do we want?

Our demands are simple:

· acknowledge that cannabis is a dangerous drug and a prime factor in countless acts of suicide and psychopathic violence, and that no amount of ‘regulation’ will eliminate this danger;
· acknowledge that the alleged medicinal benefits of certain aspects of cannabis are a red herring to soften attitudes to the pleasure drug and ensure that certain corporations are well placed if and when the pleasure drug is legalised;
· admit that since around 1973 cannabis has been decriminalised in all but name, and that this has been a grave mistake;
· begin punishing possession: a caution for a first offence, a mandatory six-month prison sentence and £1000 fine thereafter.

Woman killed by taxi driver ‘might be alive if he had been properly managed’
Shropshire Star | 19 Mar 2018 |

“From the limited evidence which was available to the independent investigation team, it appears possible that, if MB had been fully compliant with anti-psychotic medication and had refrained from misuse of cannabis, then he may not have suffered from a relapse of his psychotic illness.”
Martin Bell had been sectioned for about nine months in August 1999 and was released around six weeks before he killed Gemma Simpson.
The family of a woman who was killed and partially dismembered by a taxi driver who was suffering from a psychotic illness have said she “might still be alive today” if he had been managed properly.
Gemma Simpson’s family were responding to the publication of a report into the treatment of Martin Bell, who killed 23-year-old Miss Simpson in 2000 with a hammer and a knife before sawing her legs off and burying her at a beauty spot near Harrogate, in North Yorkshire.
Bell admitted manslaughter on the grounds of diminished responsibility after leading police to her body 14 years later, and was told he must serve a minimum of 12 years in prison.
Bell had been sectioned in a hospital for about nine months in August 1999 and was released around six weeks before he killed Miss Simpson.
On Monday, NHS England published an independent report into his care and treatment.
The report, which said its authors were severely hampered by a lack of medical records, concluded: “From the limited evidence which was available to the independent investigation team, it appears possible that, if MB had been fully compliant with anti-psychotic medication and had refrained from misuse of cannabis, then he may not have suffered from a relapse of his psychotic illness.
“In these circumstances, the death of Gemma Simpson might have been prevented.”
The new report confirmed that doctors had considered Bell’s cannabis use may have contributed to or exacerbated Bell’s illness and he had smoked the drug on the day he killed Miss Simpson in his Harrogate flat.
But it said that “notwithstanding the failures in service provision outlined in this report, there were no actions that clinicians could have specifically taken to enforce the continuation of medication given MB’s presentation in May 2000, nor to enforce his abstinence from cannabis.”
In a statement issued by the campaign group Hundred Families, Miss Simpson’s family said they broadly welcomed the findings of the report but added: “In 2000 Martin Bell was known to carry a knife, was delusional, and recognised as a real risk to others, yet he was able to be released without any effective package of care, monitoring, or even a proper assessment of how the risks he posed to others would be managed.
“There appear to have been lots of red flags, just weeks and days before Gemma’s death, that should have raised professional concerns.
“We believe that if he had been managed properly, Gemma might still be alive today.”
The family said they understood the pressures on mental health services but said: “We keep hearing that lessons have been learned, but we want to make sure they are truly learned in this case.”
In court in 2013, prosecutors said Bell struck Miss Simpson, who was from Leeds, an “uncountable” number of times with the knife and hammer in a “frenzied” attack before leaving her body for four days in a bath.
He then sawed off the bottom of her legs so she would fit in the boot of a hire car before burying her at Brimham Rocks, near Harrogate.
Bell, who was 30 at the time of the attack, handed himself in at Scarborough police station in 2013 and later took police to where she was buried.

Source: https://www.shropshirestar.com/news/uk-news/2018/03/19/woman-killed-by-taxi-driver-might-be-alive-if-he-had-been-properly-managed/ NHS England report: https://www.england.nhs.uk/north/wp-content/uploads/sites/5/2018/03/independent-investigation-mb-march-18.pdf

On 14 May 2017, Akshar Ali, acting with his friend Yasmin Ahmed, murdered his wife and mother-of-four Sinead Wooding, stabbing her with a knife six times and bludgeoning her with a hammer before dumping her body in a woodland and setting it alight. On 17 January 2018, he and his accomplice were sentenced to 22 years in prison.
One might think the fact that the guilty pair smoked and grew cannabis together would be of interest to reporters, and worthy of at least a fleeting sentence or two, but I have found it mentioned in only two news reports, one in the Yorkshire Evening Post, the other in South African news site IOL.
Of far more interest to some British media, sadly, is the fact that Ali was an ostensible Muslim and Ms Wooding a Muslim convert who had, in the weeks before she was murdered, defied her husband by wearing western clothing and seeing a friend he did not approve of. Some media, including the BBC, the Guardian and, curiously, British media abnormally incurious about the role of cannabis in a gruesome act of uxoricide the Sun managed to avoid mentioning either the matter of Islam or the smoking of cannabis.
Is it, I wonder, an abnormal lack of curiosity that prevents reporters from mentioning the smoking of a powerful psychoactive drug that is a prime factor in countless thousands of similar cases? Or is it a deliberate omission?

An extraordinary murder in Ireland

The following story from Ireland, which occurred ten years ago, is extraordinary for two reasons. First, the 143 injuries the attacker inflicted is, as far as I’m aware, a record. As I have noted many times, a frenzy of violence involving multiple stab wounds is nearly always a sign of a mind unhinged by drugs. 143, though, points to a frightening level of madness, and, as such, the verdict of not guilty by reason of insanity is unsurprising.
But then there is this:
The jury had deliberated for under one hour and had returned during that hour to ask if the fact that Mr Connors had smoked cannabis before the killing was relevant to his culpability.
Mr Justice Birmingham told the jury that consultant psychiatrist, Dr Damien Mohan, had considered whether Mr Connors’ behaviour was attributable to drugs or mental illness and was of the “firm and clear” view that the accused’s mental disorder was the causative factor.
In other words, the fact that the defendant had smoked cannabis before the killing, which occurred around six o’clock in the morning, was not deemed relevant, and the link between his mental disorder and his consumption of cannabis appears to have gone unexplored.

Man found not guilty of murder by reason of insanity
Irish Examiner 4 Feb 2009

A jury has found a Dublin man who killed a stranger with garden shears not guilty of murder by reason of insanity at the Central Criminal Court.
Thomas Connors (aged 25) thought Michael Hughes (aged 30), from Banagher in Offaly, was the embodiment of the devil when he found him sleeping in the stairwell of an apartment block.
Mr Justice George Birmingham told the jury that it had reached “absolutely the right verdict in accordance with the expert evidence”. He thanked it for its careful attention to the case and exempted its members from jury service for seven years.
Mr Connors, of Manor Court, Mount Argos, Harold’s Cross, killed Mr Hughes in a savage attack in the stairwell of an adjacent apartment block, Manor Villa, on the morning of December 15, 2007.
Mr Justice Birmingham said this was a case of “mind boggling sadness” and, were it not for the issue of insanity, would have been a perfectly clear and appalling case of murder.
He said: “Consequent on the special verdict of not guilty by reason of insanity I direct that Mr Connors be committed to a specially designated centre, the Central Mental Hospital, until further order.”
Prosecuting counsel, Paul O’Higgins SC, said Mr Hughes’ family were aware that victim impact evidence would not be heard because the case did not involve the imposition of a sentence.
Mr Justice Birmingham said to the family: “You truly have been through the most appalling experience. Words can’t and don’t describe it and all I can do is express my sympathy.”
The jury had deliberated for under one hour and had returned during that hour to ask if the fact that Mr Connors had smoked cannabis before the killing was relevant to his culpability.
Mr Justice Birmingham told the jury that consultant psychiatrist, Dr Damien Mohan, had considered whether Mr Connors’ behaviour was attributable to drugs or mental illness and was of the “firm and clear” view that the accused’s mental disorder was the causative factor.
Yesterday, the jury heard that Mr Hughes had gone out for a night in Dublin with his cousin and friends. He was to stay at his cousin’s flat in Harold’s Cross but the cousin had gone home early and Mr Hughes was unable to get into the flat when he returned after 4am.
Mr Hughes decided to sleep in the stairwell and sometime after 6am Mr Connors came crashing through the glass doors of the apartment block with garden shears and savagely attacked him, inflicting 143 injuries.
Residents heard screaming and rang gardaí who found Mr Connors walking away from the scene with the shears. He told gardaí that he had fought with the devil and the devil was gone now.
In the days leading up to the killing Mr Connors, a married man with one child, had gone to hospital three times seeking help. He was hearing voices and suffering delusions that his wife was the daughter of the devil. On the second visit he was given tablets. His wife was so frightened by his behaviour that she took their child to a women’s shelter.
On the third occasion, the day before the killing, doctors at Saint Vincent’s Hospital decided Mr Connors should be admitted to Saint James’ but he absconded during the four-hour wait for an ambulance.
In the hours before he killed Mr Hughes, Mr Connors thought the devil was in his apartment and had taken a duvet outside and stabbed it, believing the devil had been hiding in it.
Dr Mohan told the jury that Mr Connors suffered from schizophrenia, as did his father. He had been hospitalised with psychosis in 2004 and 2005 and believed that his father-in-law was the devil.
The victim’s father, Liam Hughes, made a statement outside the Four Courts on behalf of the Hughes family. He said that the family’s thoughts, as always but especially today, were on the 30 years of “love, kindness and generosity of spirit they enjoyed with the deceased”.
Mr Hughes said his son would be remembered by his friends as “a respectful and decent person”. He said a former teacher had contacted the family to pay tribute to Michael as “an honest, kind, sincere, popular and respected person who was a credit to his family and school”.
Mr Hughes said Michael had been a hard-working young man who commuted from Offaly to Dublin each day to work and had recently entered into further education. Mr Hughes said his son had coped admirably with the demands of full-time work and part-time study.
On October 27, 2007, he had become engaged to Deborah Lynch, who was with the family in court. Mr Hughes said his family had shared in their joy at setting up a home together and planning for their future.
He said: “Only seven short weeks later Deborah’s hopes and dreams were shattered.”
He said the Hughes family earnestly hoped that she would find happiness in the future.
Mr Hughes thanked UCD, which had honoured Michael recently on what would have been his conferring day, and his employer, Dublin Bus. He also thanked the team who investigated his son’s death, the Garda family liaison officer and the many friends who had offered comforting words.
He said it had been 13 months since the killing but the pain and horror of it had “scarcely lessened”. He said the natural “role reversal” in the cycle of life could not now happen as he had lost his son.
He said the family was disturbed and saddened by the evidence given in court, but there relieved that the process was over. He asked that the family’s privacy be respected at this time.

Source: https://www.irishexaminer.com/breakingnews/ireland/man-found-not-guilty-of-murder-by-reason-of-insanity-397642.html Posted on May 6, 2019 Leave a comment on An extraordinary murder in Ireland

Jail for man who shot girlfriend 13 times with airgun – before trying to strangle and suffocate her
Leicester Mercury | 27 July 2017 |

Kristian Pole had been smoking cannabis when he ‘flipped out’ and attacked his partner at his home in Leicester
A man who failed to take a chance given by a judge, following an airgun attack on a girlfriend, has been jailed for two years.
Kristian Pole repeatedly fired pellets at close range into his then girlfriend’s face, limbs and body. Then he tried to strangle her and suffocate her with a pillow, Leicester Crown Court was told.
The frightened woman managed to run from Pole’s home in Leicester and alert the police, having suffered bruising and red marks from 13 plastic pellets and being gripped around her neck, in August last year.
Judge Robert Brown gave Pole a chance, in June, by imposing a two-year community order, with rehabilitation requirements, because he had already served several months on remand in custody.
Pole later failed to inform the probation service he had moved address – a condition of the order. He also refused to tell them where he was living with a new partner. This resulted in him being brought back to court, where Judge Brown re-sentenced him on Tuesday.
The judge told 24-year-old Pole, of no known address: “I’ve no choice but to revoke the order and impose custody. You’ve thrown away the chance of a community order by your own actions. When I sentenced you in June, for possessing a BB gun with intent to cause fear of violence and causing actual bodily harm, you’d already served eight or nine months in custody.”
He told Pole, who admitted the offences: “You’d done well on remand and changed your attitude. I was invited to take a chance on you and put you on a community order.
“You’ve failed to engage with the probation service and moved out of your mother’s address, without notifying those concerned about where you were living. This was a serious example of an assault.”
Lynsey Knott, prosecuting, said the assault with the BB gun happened when Pole’s then girlfriend visited his home, where he was smoking cannabis with a male friend.
When the cannabis ran out he erupted in violence, attacking her and shooting “at close range” her face and limbs.
James Varley, mitigating, said: “He’d smoked too much cannabis and flipped out.
“Your Honour will have told many defendants it’s not the harmless drug that many young people think it is.
“It has deleterious effects … what else could explain his conduct other than he was completely out of it when his cannabis supply was cut off.”

Source:https://www.leicestermercury.co.uk/news/leicester-news/jail-man-who-shot-girlfriend-243489

Couple killed friend, set him on fire and then had sex to celebrate, court told
ITV News | 16 Feb 2019 |

Cold-hearted killers who brutally murdered a vulnerable friend before setting him on fire and then having sex will spend at least 28 years in jail.

Evil William Vaill and Deborah Andrews were handed life sentences for killing Skelmersdale dad Eamon Brady in a “brutal and sustained” attack.
Mr Brady was hit in the head with a hammer at least 17 times and repeatedly stabbed and slashed in the neck and body in the early hours of July 21.
Vaill, 37, and Andrews, 44, then wrapped his body in bedding and set it on fire before stealing a PlayStation 4, sound bar, DVD player and bank card belonging to their victim.
Andrews later described the couple as “the new Bonnie and Clyde”.
After the callous killing, the pair went to Beacon Country Park where they burned clothing and hid the weapons. They are also believed to have had sex in a nearby park hours after the attack, the court heard.
They also went on to attempt to sell his PlayStation 4 and use the stolen bank card in a local shop.
The evil couple, who had been friends with Mr Brady for several years, bumped into him by chance after Vaill had attended a funeral. They went back to his flat in Elmridge, Skelmersdale, where they drank and smoked cannabis.
By the time of the murder, Vaill, whose previous convictions include arson and criminal damage, had been drinking for 40 straight hours.
The pair left the flat at around around 4:50am and later told police that Mr Brady was alive and well when they left. But recordings in the police van heard that Andrews was ‘buzzing’ about the murder and describing the pair as the new Bonnie and Clyde.
Vaill, of Evington, Skelmersdale, pleaded guilty to murder and arson last month and was today given a life sentence with a minimum of 28-and-a-half years in prison.
Andrews, of Elmstead, Skelmersdale, was found guilty after a trial and given a life sentence with a minimum of 28 years in prison.
Both appeared emotionless throughout the sentencing at Preston Crown Court while Andrews sat with her hands in her pockets throughout.
Prosecuting, Francis McEntree said Mr Brady was a vulnerable man who was regularly taken advantage of by those around him. He had earlier told family that he wanted to move out of Skelmersdale to escape from people who were ‘leeching off him’.
He knew both of the victims well, having been friends for several years and they had all spent the together socially in a “happy, if noisy” manner.
Mr Brady had been friends with Vaill since their teenage years and an earlier incident in which Vaill stabbed him in the foot with a penknife was considered no more than horseplay after Mr Brady had laughed at him getting hurt when he kicked a lamppost.
An emotional victim statement read on behalf of Mr Brady’s daughter Amy Brady told of the devastating effects she has suffered since the murder of her best friend.
Her father’s death came 17 days short of the second anniversary of her brother Ryan’s death and that after seeing his battered and burnt body, Ms Brady now regularly suffers nightmare and is left “angry with the world”.
“There was a hole in my heart when my brother died that has been made bigger and will never be filled,” it stated.
“My dad was not only my dad, he was my entire being.”
Defending Vaill, Stuart Denney said he had begun cannabis and alcohol use since before he was a teenager and that Skelmersdale was “the worst place in the world for him”.
Michael Lavery, defending Andrews, said she had “limited capabilities and intelligence” and was previously of good character.
Sentencing the pair, Judge Mark Brown said: “Having killed him you set fire to his body to destroy evidence of what had happened and in doing so you committed arson with reckless disregard for the lives of the other residents in the building who were asleep at the time.
“It’s another matter of this case that having just murdered this a man in extremely violent and brutal circumstances that you had sex with each other soon after.”

Source: https://www.itv.com/news/granada/2019-02-16/couple-killed-friend-set-him-on-fire-and-then-had-sex-to-celebrate-court-told/

Teenager found guilty of fatal stabbing of Luke Howard
Liverpool Echo | 22 Jan 2009 |

A LIVERPOOL teenager has been found guilty of killing a friend he stabbed 12 times in a drunk and drug-fuelled rage.

A jury at Liverpool Crown Court found Charlijo Calvert, 15, not guilty of the murder of 16-year-old Luke Howard but unanimously convicted him of manslaughter.
Calvert, of Ronald Street, Old Swan, stabbed Luke, from Dovecot, in the early hours of August 30 at the house of a friend in Ashcombe Road, Knotty Ash.
During the week-long trial, the court heard a group of teenage boys, including the victim and defendant, had gone to the house and drank alcohol, smoked cannabis and snorted cocaine.
Throughout the night, and into the early hours, witnesses said they saw Luke prodding Calvert with a screwdriver and the pair “winding each other up”. At one point, the court heard, they threatened to stab each other but the fatal attack at around 7am.

Source: https://www.liverpoolecho.co.uk/news/liverpool-news/teenager-found-guilty-fatal-stabbing-3462600

Four ‘racist’ killings, two years apart, with one important commonality
1. Skunk addicted schizophrenic fulfils sick fantasy by killing a black woman: ‘Psychiatric reports stated that Maxwell was suffering from paranoid schizophrenia, and his abnormality was so great that it affected his judgment [sic].The reports also said his condition was exacerbated by the heavy use of skunk.’ (3 Apr 2007)
2. Drive caught in gang’s ‘revenge’: ‘The 41-year-old minibus taxi driver was dragged screaming from his cab and beaten to death in July by several white teenagers in Huddersfield… Some of the teenagers had been drinking and smoking cannabis with some girls, who they then persuaded to call up and order the minibus – with fatal consequences.’ (26 Jan 2007)
3. Racist thugs face 30 years in prison for axe murder: ‘The two men who murdered black teenager Anthony Walker were last night each facing up to 30 years in jail after the trial judge ruled the killing was racially motivated, effectively doubling the time they will serve… Anthony Walker wanted to be a lawyer, maybe a judge. He loved God, worked hard at his studies, practised his basketball skills whenever he could, though not on a Sunday if it clashed with church.
Paul Taylor and Michael Barton revelled in the nicknames Chomper and Ozzy. One wanted to be a burglar, the other wanted to join the army, but was too stupid to pass the exams. They spent their time hanging around, smoking cannabis and, in the words of one, “going out robbing”.’ (1 Dec 2005)
4. Asian gang kicked man to death: ‘Three Asian men who kicked a white computer expert to death and bragged: “That will teach an Englishman to interfere in Paki business” were found guilty of murder at the Old Bailey yesterday… The court heard that the three had been drinking all evening in the West End before returning to east London to drink vodka and smoke cannabis.’ (23 Nov 2005)
You know, of course, what the important commonality is, a much more important factor than apparent ‘racism’. I will note here only, as the article does not, that the ‘skunk addicted schizophrenic’ who deliberately targeted a black woman is himself black.

In defence of Peter Hitchens (@ClarkeMicah) and the theory of mental illness

Mail on Sunday columnist Peter Hitchens, author of The War We Never Fought, has received a lot of abuse recently for pointing out in his MoS column of 7 April that the killer of Jo Cox, Thomas Mair, was mentally ill, not a ‘political actor’, and that his mental state was not discussed at his trial (at which Mair himself did not speak).
This matters a great deal, because those who cannot accept that, far from being part of a ‘far-right terrorist plot’, Mair was simply mentally unhinged, and that this mental illness was likely the result of or exacerbated by psychoactive medication, often equally refuse to believe that the prime factor in a particular act of suicide or psychopathic violence isn’t terrorism, Islam, immigration, austerity, video games, gangs, gun laws, ‘depression’, or racism, but cannabis.
Many have cited the following sentencing remarks of the judge in the Mair case, Mr Justice Wilkie, as evidence that Mr Hitchens is barking up the wrong tree:
There is no doubt that this murder was done for the purpose of advancing a political, racial and ideological cause namely that of violent white supremacism and exclusive nationalism most associated with Nazism and its modern forms.
Those who believe that Mair was a ‘terrorist’ are not open to the possibility that the judge is mistaken, nor aware that his remarks are, as Mr Hitchens points out, unusually political in tone. I wonder, then, what such people would make of these sentencing remarks of Judge Findlay Baker, QC, to a man who stabbed his friend’s father to death with a pair of garden shears: “This was an attack of extreme and persistent violence. And I have no doubt it would not have happened if you had not consumed cannabis.”
Or these, of Judge Anthony Niblett, to a man who punched his girlfriend and burnt down her house: “Those whose minds are steeped in cannabis are capable of quite extraordinary criminality. Your mind has been steeped in cannabis for much of your adult life.”
Or these, of Judge Rosalind Coe, QC, to a young man who attempted to murder his infant son: “If any case demonstrates the dangers and potentially tragic consequences of cannabis abuse, such as you had taken part in for many years, this is such a case.”
I could go on.
By contrast, some judges all but shrug and hold up their hands when trying to make sense of a heinous crime. The judge who sentenced 16-year-old Aaron Campbell, for example, said he had “no idea” why Campbell abducted, raped and murdered six-year-old Alesha MacPhail, even though it was noted during the trial that he was high on cannabis when he committed the crime, and knew the MacPhail family from having bought the drug from Alesha’s father. Some judges, like some people, can see the wood amid the trees. Some cannot.

Violence and legalised cannabis in Uruguay: a clarification

I would like to clarify the meaning of a tweet I sent yesterday of a link to an article on violence and homicide in Uruguay, ‘Uruguay gets tough on crime after posting record homicide rate’.
The article reports that in 2018, a year after cannabis went on sale, following legalisation in 2013, there were a record 414 homicides in Uruguay, a small nation of 3.5 million people once famed for its peace and tranquillity. So alarming was this figure (up from 284 in 2017) that 400,000 voters signed a petition calling for exceptional measures against violent crime.
I must stress first that, while it is likely that at least some of these acts of homicide were committed by people whose minds have been damaged by cannabis, I do not say that cannabis legalisation was the cause. I tweeted the article whilst arguing about correlation and causation with a dim-witted young drugs enthusiast who had claimed that an apparent decrease in rates of cannabis consumption amongst teenagers in Washington state was caused by cannabis being legalised there. I have written before that dope heads parrot the phrase ‘correlation does not equal causation’ only when the correlation upsets them. When they find a correlation they like they immediately claim cannabis legalisation as the cause.
Again, I do not say that homicide rate in Uruguay is exceptionally high because cannabis has been legalised. As Peter Hitchens points out in an article on Portugal, ‘The Alleged Portuguese Drug Paradise Examined’, legalisation or decriminalisation nearly always follows years of lax enforcement, making any before-and-after comparison meaningless. By contrast, in his largely excellent book Tell Your Children, Alex Berenson spends too much time, as I write in my review, trying to prove that violent crime has risen in those American states that have legalised cannabis, when he would have done better to expand his section on the alleged ‘war’ on drugs in America and the fact that, contrary to popular opinion, rates of incarceration solely for drugs possession in the USA have been quite low for many years.
I would further add that suggestions that ‘gang warfare’ is involved in Uruguay’s high homicide rate seem similarly erroneous. Drug rivals killing each other makes a good subject for a film or TV series,
but the reality is often a much blander case of a paranoid young man in possession of a weapon killing somebody (often not his ostensible target) out of fear or delusion.

Xixi Bi Llandaff murder: Jordan Matthews jailed for life

He accepted he was smoking “quite a lot” of cannabis at the time and the court heard he felt “insecure” when his girlfriend visited her family in China.

Source: https://www.bbc.co.uk/news/uk-wales-south-east-wales-39026270

‘Cannabis made my boy a killer’

THE mother of a violent schizophrenic who stabbed his best friend to death last night described how her son’s long-term cannabis habit turned him into a monster.
Julie Morgan, formerly from Cardiff, claimed her 20-year-old son Richard Harris’ ‘kind and gentle’ side disappeared not long after he started smoking cannabis from the age of 14.
“Cannabis took my son from me, I have no problem saying that,” said the 45-year-old.

Carl Madigan knifed Sam Cook in heart two weeks after friend slashed man’s stomach open

Facebook accounts show Carl Madigan, 23, and Shaun Bethell, 19, hanging around together and smoking cannabis before the shocking offences which will now define their young lives.
In a dreadful two week period last October, Madigan killed tragic Sam Cook while Bethell, a teenager with a record to rival any career criminal’s, left a man’s bowel hanging out of his body.

Man found guilty of murdering girlfriend’s toddler before claiming he slipped underwater in bath in 999 call

Smith was also found to have a high reading of cannabis in his bloodstream almost six hours after the 999 call – while a makeshift Ribena bottle ‘bong’ and the remains of six cannabis joints were found in a rear annex.
Despite Willett claiming she “always put the kids first,” text messages showed a woman desperate to buy cannabis, even on the night before Teddy’s death.

Cork man, 26, who shattered skull of girlfriend’s infant daughter jailed for eight years
Brendan Kelly, defence barrister, said[…] that the accused appeared to be detached from what was going on and that the defendant had been a long-time cannabis user.

Dad shook baby daughter to death as he was agitated at running out of cannabis
Daily Mirror

A dad who shook his baby daughter to death because he was agitated at running out of cannabis was today jailed for six years.
William Stephens, aged 25, shook daughter Paris so violently she suffered catastrophic head injuries and was bleeding in the eyes.
The thug attacked 16-week-old Paris for crying after he was left to look after her while mum Danah Vince, 19, went to see a doctor.
The little girl died two days later in hospital and one shocked expert said he had never before seen such a severe case of bleeding in the eyes.
Stephens had a history of violence and social services were called in because of his volatile relationship with mum Vince.
A serious case review is being carried out into the way public bodies handled the case.
Stephens – who had serious learning difficulties – was convicted of manslaughter after a seven-week trial.
Vince was cleared of causing or allowing the baby’s death in January.
Passing sentence, the judge Mr Justice Teare told Stephens: “This is a case where a loss of temper and control has resulted in fatal violence to a defenceless baby.
“You will have to live with the fact that you killed your daughter.”
Defence lawyer Ignatious Hughes QC, told the jury: “There is plenty of evidence that he and Danah Vince are likely to have been in a state of agitation due to lack of cannabis.”
Bristol crown court heard Stephens and Vince often fought and argued and social services stepped in to get the pair to sign agreements against domestic violence.
Stephens, from Southmead, Bristol, was given a restraining order to stay away from Vince but defied the ban and continued living with her and their daughter.
He appeared in juvenile court in 2006 for three assaults on a previous girlfriend and received a community order.
Five months later he appeared in front of magistrates for battery and was given the same punishment.
A year later he was given a caution for repeatedly punching a pregnant woman and in November 2008 got another caution for common assault.
In April 2010, he was hauled before magistrates for assaulting a police officer.
The local council is conducting a serious case review which will be published next year.
A spokesman said: “This is an extremely sad case where there has been the tragic loss of a young life.
“If nothing else I hope that today’s verdict offers some small measure of closure.
“An independent Serious Case Review by the Bristol Safeguarding Children Board is being completed, carefully examining the role of public bodies involved in the case to see if there are any lessons to be learnt.
“The complexity of this case will become apparent once that review is published early next year following the conclusion of all relevant legal processes.”
A year later, Danah Vince, the mother of the baby, committed suicide.

Source: https://www.mirror.co.uk/news/uk-news/william-stephens-shook-baby-paris-2923262

Teen faces one year for vicious attack on man outside takeaway

A 17-year-old boy has been warned he faces a one-year sentence for leading a vicious gang attack on a young man who was repeatedly punched and kicked outside a takeaway in Dublin.
The boy, who cannot be named because he is a minor, has pleaded guilty at the Dublin Children’s Court to assault causing harm and violent disorder in connection with the incident on the night of November 14, 2015.
Judge John O’Connor adjourned sentencing to see if the boy’s solicitor can organise a psychological assessment of the teenager whose behaviour, he said, has become more violent and aggressive.
The judge also noted the boy had tragic personal circumstances.
He said it was unacceptable that the boy had started smoking cannabis at the age of 12, and anyone who says it is not addictive “is not living in the real world”.
Garda Dave Jennings had told Judge O’Connor that the victim, a foreign national who is also aged in his late teens, had been at a Chinese takeaway at Kiltalown Way, Tallaght. A group of youths shouted in to him that they were going to rob him when he came out.
When he walked out one of them grabbed the handlebars of his bicycle and the youth then punched him in the side of his face.
The rest of the youths then joined in, grabbing the man, who was repeatedly punched and kicked before his bike was stolen.
The defendant struck the first blow but was not involved in the rest of the attack.
The victim fled back into the takeaway but was followed and had to run into the kitchen area for his safety. Garda Jennings agreed with Damian McKeone, defending, that the attack was not racially motivated.
CCTV footage was shown to Judge O’Connor, who described it as a “vicious assault”.

Source: https://www.irishexaminer.com/ireland/teen-faces-one-year-for-vicious-attack-on-man-outside-takeaway-399847.html

Robbers who held knife to man’s neck before stealing his phone and laptop jailed

Two males who robbed a man at knifepoint at his home in north Belfast have been jailed.
Bennet Donaghy and his accomplice, who at the time of the offence was 16, targeted their victim in the early hours of September 13, 2015.
He managed to escape and ran down the Shore Road in the middle of the night shouting for help.
Donaghy (20), a father-of-one from Cheston Close in Carrickfergus, was handed a 30-month sentence at Belfast Crown Court yesterday. His accomplice, who cannot be named, was given 15 months’ jail.
Both men were informed they would spend half their sentences in custody, with the remainder on licence.
The pair admitted a charge of assault with intent to rob, while the youth also admitted stealing the man’s laptop and mobile phone.
Prior to sentencing, Judge Gordon Kerr QC was informed that the victim was asleep on his sofa at around 4am when he heard persistent knocking at his front door.
He recognised the youth, who he knew from the area, with another young man.
The younger man asked the victim to lend him money, but when he handed them £5 the pair told him: “That’s not enough.”
Crown prosecutor Robin Steer said Donaghy then produced a knife and held it against the occupant’s neck.
The youth, who the man said looked like he was under the influence of drugs, punched the victim a number of times while Donaghy told him he was from the UDA and ordered him to hand over drugs and money.
The man’s home was ransacked, but he escaped and ran down the Shore Road barefoot and with a bruised face, only to be stopped by police.
Officers subsequently called at a house in the area, where they arrested Donaghy and the youth. Also located was a four-inch knife, along with the man’s laptop and mobile phone.
During police interviews, the youth admitted he knew the occupant, but claimed he was unable to remember what had happened because he had smoked a cannabis cigarette.
Like his accomplice, Donaghy claimed to have no recollection of the incident because he too had been smoking drugs.
Mr Steer told Belfast Crown Court there were a number of aggravating factors.
These included the use of violence and threats during the robbery, the presence of a weapon and the fact the victim was targeted in his home in the middle of the night.
Defence barrister Jon Paul Shields, representing the youth, confirmed that his client was under the influence of drugs on the night in question.
He also added that he had since “recognised the seriousness of the offences.”
Telling the court his client knew his behaviour had been unacceptable, Mr Shields said: “At the time, he simply did not give any thought to what he was doing.”
The barrister also told how the young man, who has been working with the Youth Justice Agency, had expressed shame over the incident.
The lawyer said that at the time of the offence, his client had just lost a child, which led to him self-medicating.
Barrister Chris Holmes, acting on behalf of Donaghy, said that his client “apologises profusely to the victim”.
He added that on the night of the robbery, Donaghy was “very, very much under the influence” of drugs.
Mr Holmes also spoke of the defendant’s troubled background, telling the judge his client “didn’t have his sorrows to seek when he was being brought up”, which in turn contributed to poor mental health.

Source: https://www.belfasttelegraph.co.uk/news/northern-ireland/robbers-who-held-knife-to-mans-neck-before-stealing-his-phone-and-laptop-jailed-35560290.html

Sally Hodkin murder: Killer ‘had miscarriage’ prior to fatal stabbing

A patient who murdered a grandmother believed she had suffered a miscarriage and was smoking cannabis in the lead up to the killing, an inquest has heard.
Nicola Edgington virtually decapitated Sally Hodkin with a stolen butcher’s knife in Bexleyheath, in 2011, six years after killing her own mother.
Edgington told hospital staff she needed to be sectioned and felt like killing someone.
A recent report found NHS and police failings led to Mrs Hodkin’s murder.
Edgington, a diagnosed schizophrenic, was discharged from the Bracton Centre mental health facility in 2009 despite an order she be detained indefinitely following the killing of her mother Marion in Forest Row, Sussex, in 2005.
Around two weeks before the killing on 10 October, 2011, Edgington made a number of emergency calls to police about “crackheads” stealing from her flat in early October. She had also been using skunk cannabis, the inquest heard.
On 29 September, she sent a message to her brother telling him about the miscarriage, saying she wanted to reconnect.
The message also mentioned their mother, with Edgington saying: “No-one’s taking care of me like she would.”
Her brother replied on the same day: “You stabbed her to death and left me to find the body. Good news about your miscarriage … do us a favour and slit your wrists.”
On the day of Mrs Hodkin’s murder, Edgington was taken to Oxleas House mental health unit, but was later allowed to walk out of the building.
She got a bus to Bexleyheath, bought a large knife from Asda and stole a steak knife from a butcher’s shop.
Edgington then stabbed Mrs Hodkin and another woman in the street.
Elizabeth Lloyd-Folkard, a forensic social worker who was looking after Edgington, told the inquest that around a week before the killing, she had “no cause of concern about her state of mind”.
Contact with family members, substance misuse, and any issues around pregnancy were noted in reports as high-risk factors that could affect Edgington’s mental health, the inquest heard.
Mrs Hodkin’s son Len Hodkin told the inquest: “All of those risk factors were present in the two to three weeks leading up to October 10.
“It’s not coming with the benefit of hindsight, this information was available to you and other members of the multi-disciplinary team at the time.”
The inquest continues.

Source: https://www.bbc.co.uk/news/uk-england-london-46022330

January 2019 • Volume 48, Number 1 • Alex Berenson
Alex Berenson Author, Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence

The following is adapted from a speech delivered on January 15, 2019, at Hillsdale College’s Allan P. Kirby, Jr. Center for Constitutional Studies and Citizenship in Washington, D.C. </