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Use of marijuana cannabis

Article archive for my students

Marijuana is not anywhere near as harmless as most students believe it to be.

This is a drug that literally changes how the brain works. As such, one should expect that long term unregulated use could have harmful consequences.

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Is Marijuana as Safe as We Think?
Permitting pot is one thing; promoting its use is another.

By Malcolm Gladwell, The New Yorker, January 14, 2019 Issue

A few years ago, the National Academy of Medicine convened a panel of sixteen leading medical experts to analyze the scientific literature on cannabis. The report they prepared, which came out in January of 2017, runs to four hundred and sixty-eight pages. It contains no bombshells or surprises, which perhaps explains why it went largely unnoticed. It simply stated, over and over again, that a drug North Americans have become enthusiastic about remains a mystery.

For example, smoking pot is widely supposed to diminish the nausea associated with chemotherapy. But, the panel pointed out, “there are no good-quality randomized trials investigating this option.” We have evidence for marijuana as a treatment for pain, but “very little is known about the efficacy, dose, routes of administration, or side effects of commonly used and commercially available cannabis products in the United States.” The caveats continue. Is it good for epilepsy? “Insufficient evidence.” Tourette’s syndrome? Limited evidence. A.L.S., Huntington’s, and Parkinson’s? Insufficient evidence. Irritable-bowel syndrome? Insufficient evidence. Dementia and glaucoma? Probably not. Anxiety? Maybe. Depression? Probably not.

Then come Chapters 5 through 13, the heart of the report, which concern marijuana’s potential risks. The haze of uncertainty continues. Does the use of cannabis increase the likelihood of fatal car accidents? Yes. By how much? Unclear. Does it affect motivation and cognition? Hard to say, but probably. Does it affect employment prospects? Probably. Will it impair academic achievement? Limited evidence. This goes on for pages.

We need proper studies, the panel concluded, on the health effects of cannabis on children and teen-agers and pregnant women and breast-feeding mothers and “older populations” and “heavy cannabis users”; in other words, on everyone except the college student who smokes a joint once a month. The panel also called for investigation into “the pharmacokinetic and pharmacodynamic properties of cannabis, modes of delivery, different concentrations, in various populations, including the dose-response relationships of cannabis and THC or other cannabinoids.”

Figuring out the “dose-response relationship” of a new compound is something a pharmaceutical company does from the start of trials in human subjects, as it prepares a new drug application for the F.D.A. Too little of a powerful drug means that it won’t work. Too much means that it might do more harm than good. The amount of active ingredient in a pill and the metabolic path that the ingredient takes after it enters your body—these are things that drugmakers will have painstakingly mapped out before the product comes on the market, with a tractor-trailer full of supporting documentation.

With marijuana, apparently, we’re still waiting for this information. It’s hard to study a substance that until very recently has been almost universally illegal. And the few studies we do have were done mostly in the nineteen-eighties and nineties, when cannabis was not nearly as potent as it is now. Because of recent developments in plant breeding and growing techniques, the typical concentration of THC, the psychoactive ingredient in marijuana, has gone from the low single digits to more than twenty per cent—from a swig of near-beer to a tequila shot.

Are users smoking less, to compensate for the drug’s new potency? Or simply getting more stoned, more quickly? Is high-potency cannabis more of a problem for younger users or for older ones? For some drugs, the dose-response curve is linear: twice the dose creates twice the effect. For other drugs, it’s nonlinear: twice the dose can increase the effect tenfold, or hardly at all. Which is true for cannabis? It also matters, of course, how cannabis is consumed. It can be smoked, vaped, eaten, or applied to the skin. How are absorption patterns affected?

Last May, not long before Canada legalized the recreational use of marijuana, Beau Kilmer, a drug-policy expert with the rand Corporation, testified before the Canadian Parliament. He warned that the fastest-growing segment of the legal market in Washington State was extracts for inhalation, and that the mean THC concentration for those products was more than sixty-five per cent. “We know little about the health consequences—risks and benefits—of many of the cannabis products likely to be sold in nonmedical markets,” he said. Nor did we know how higher-potency products would affect THC consumption.

When it comes to cannabis, the best-case scenario is that we will muddle through, learning more about its true effects as we go along and adapting as needed—the way, say, the once extraordinarily lethal innovation of the automobile has been gradually tamed in the course of its history. For those curious about the worst-case scenario, Alex Berenson has written a short manifesto, “Tell Your Children: The Truth About Marijuana, Mental Illness, and Violence.”

Berenson begins his book with an account of a conversation he had with his wife, a psychiatrist who specializes in treating mentally ill criminals. They were discussing one of the many grim cases that cross her desk—“the usual horror story, somebody who’d cut up his grandmother or set fire to his apartment.” Then his wife said something like “Of course, he was high, been smoking pot his whole life.”

Of course? I said.

Yeah, they all smoke.

Well . . . other things too, right?

Sometimes. But they all smoke.

Berenson used to be an investigative reporter for the Times, where he covered, among other things, health care and the pharmaceutical industry. Then he left the paper to write a popular series of thrillers. At the time of his conversation with his wife, he had the typical layman’s view of cannabis, which is that it is largely benign. His wife’s remark alarmed him, and he set out to educate himself. Berenson is constrained by the same problem the National Academy of Medicine faced—that, when it comes to marijuana, we really don’t know very much. But he has a reporter’s tenacity, a novelist’s imagination, and an outsider’s knack for asking intemperate questions. The result is disturbing.

The first of Berenson’s questions concerns what has long been the most worrisome point about cannabis: its association with mental illness. Many people with serious psychiatric illness smoke lots of pot. The marijuana lobby typically responds to this fact by saying that pot-smoking is a response to mental illness, not the cause of it—that people with psychiatric issues use marijuana to self-medicate. That is only partly true. In some cases, heavy cannabis use does seem to cause mental illness. As the National Academy panel declared, in one of its few unequivocal conclusions, “Cannabis use is likely to increase the risk of developing schizophrenia and other psychoses; the higher the use, the greater the risk.”

Berenson thinks that we are far too sanguine about this link. He wonders how large the risk is, and what might be behind it. In one of the most fascinating sections of “Tell Your Children,” he sits down with Erik Messamore, a psychiatrist who specializes in neuropharmacology and in the treatment of schizophrenia.

Messamore reports that, following the recent rise in marijuana use in the U.S. (it has almost doubled in the past two decades, not necessarily as the result of legal reforms), he has begun to see a new kind of patient: older, and not from the marginalized communities that his patients usually come from. These are otherwise stable middle-class professionals. Berenson writes, “A surprising number of them seemed to have used only cannabis and no other drugs before their breaks. The disease they’d developed looked like schizophrenia, but it had developed later—and their prognosis seemed to be worse. Their delusions and paranoia hardly responded to antipsychotics.”

Messamore theorizes that THC may interfere with the brain’s anti-inflammatory mechanisms, resulting in damage to nerve cells and blood vessels. Is this the reason, Berenson wonders, for the rising incidence of schizophrenia in the developed world, where cannabis use has also increased?

In the northern parts of Finland, incidence of the disease has nearly doubled since 1993. In Denmark, cases have risen twenty-five per cent since 2000. In the United States, hospital emergency rooms have seen a fifty-per-cent increase in schizophrenia admissions since 2006. If you include cases where schizophrenia was a secondary diagnosis, annual admissions in the past decade have increased from 1.26 million to 2.1 million.

Berenson’s second question derives from the first. The delusions and paranoia that often accompany psychoses can sometimes trigger violent behavior. If cannabis is implicated in a rise in psychoses, should we expect the increased use of marijuana to be accompanied by a rise in violent crime, as Berenson’s wife suggested?

Once again, there is no definitive answer, so Berenson has collected bits and pieces of evidence. For example, in a 2013 paper in the Journal of Interpersonal Violence, researchers looked at the results of a survey of more than twelve thousand American high-school students. The authors assumed that alcohol use among students would be a predictor of violent behavior, and that marijuana use would predict the opposite. In fact, those who used only marijuana were three times more likely to be physically aggressive than abstainers were; those who used only alcohol were 2.7 times more likely to be aggressive. Observational studies like these don’t establish causation. But they invite the sort of research that could.

Berenson looks, too, at the early results from the state of Washington, which, in 2014, became the first U.S. jurisdiction to legalize recreational marijuana. Between 2013 and 2017, the state’s murder and aggravated-assault rates rose forty per cent—twice the national homicide increase and four times the national aggravated-assault increase. We don’t know that an increase in cannabis use was responsible for that surge in violence. Berenson, though, finds it strange that, at a time when Washington may have exposed its population to higher levels of what is widely assumed to be a calming substance, its citizens began turning on one another with increased aggression.

His third question is whether cannabis serves as a gateway drug. There are two possibilities. The first is that marijuana activates certain behavioral and neurological pathways that ease the onset of more serious addictions. The second possibility is that marijuana offers a safer alternative to other drugs: that if you start smoking pot to deal with chronic pain you never graduate to opioids.

Which is it? This is a very hard question to answer. We’re only a decade or so into the widespread recreational use of high-potency marijuana. Maybe cannabis opens the door to other drugs, but only after prolonged use. Or maybe the low-potency marijuana of years past wasn’t a gateway, but today’s high-potency marijuana is. Methodologically, Berenson points out, the issue is complicated by the fact that the first wave of marijuana legalization took place on the West Coast, while the first serious wave of opioid addiction took place in the middle of the country. So, if all you do is eyeball the numbers, it looks as if opioid overdoses are lowest in cannabis states and highest in non-cannabis states.

Not surprisingly, the data we have are messy. Berenson, in his role as devil’s advocate, emphasizes the research that sees cannabis as opening the door to opioid use. For example, two studies of identical twins—in the Netherlands and in Australia—show that, in cases where one twin used cannabis before the age of seventeen and the other didn’t, the cannabis user was several times more likely to develop an addiction to opioids. Berenson also enlists a statistician at N.Y.U. to help him sort through state-level overdose data, and what he finds is not encouraging: “States where more people used cannabis tended to have more overdoses.”

The National Academy panel is more judicious. Its conclusion is that we simply don’t know enough, because there haven’t been any “systematic” studies. But the panel’s uncertainty is scarcely more reassuring than Berenson’s alarmism. Seventy-two thousand Americans died in 2017 of drug overdoses. Should you embark on a pro-cannabis crusade without knowing whether it will add to or subtract from that number?

Drug policy is always clearest at the fringes. Illegal opioids are at one end. They are dangerous. Manufacturers and distributors belong in prison, and users belong in drug-treatment programs. The cannabis industry would have us believe that its product, like coffee, belongs at the other end of the continuum.

“Flow Kana partners with independent multi-generational farmers who cultivate under full sun, sustainably, and in small batches,” the promotional literature for one California cannabis brand reads. “Using only organic methods, these stewards of the land have spent their lives balancing a unique and harmonious relationship between the farm, the genetics and the terroir.”

But cannabis is not coffee. It’s somewhere in the middle. The experience of most users is relatively benign and predictable; the experience of a few, at the margins, is not. Products or behaviors that have that kind of muddled risk profile are confusing, because it is very difficult for those in the benign middle to appreciate the experiences of those at the statistical tails.

Low-frequency risks also take longer and are far harder to quantify, and the lesson of “Tell Your Children” and the National Academy report is that we aren’t yet in a position to do so. For the moment, cannabis probably belongs in the category of substances that society permits but simultaneously discourages. Cigarettes are heavily taxed, and smoking is prohibited in most workplaces and public spaces. Alcohol can’t be sold without a license and is kept out of the hands of children. Prescription drugs have rules about dosages, labels that describe their risks, and policies that govern their availability. The advice that seasoned potheads sometimes give new users—“start low and go slow”—is probably good advice for society as a whole, at least until we better understand what we are dealing with.

Late last year, the commissioner of the Food and Drug Administration, Scott Gottlieb, announced a federal crackdown on e-cigarettes. He had seen the data on soaring use among teen-agers, and, he said, “it shocked my conscience.” He announced that the F.D.A. would ban many kinds of flavored e-cigarettes, which are especially popular with teens, and would restrict the retail outlets where e-cigarettes were available.

In the dozen years since e-cigarettes were introduced into the marketplace, they have attracted an enormous amount of attention. There are scores of studies and papers on the subject in the medical and legal literature, grappling with the questions raised by the new technology. Vaping is clearly popular among kids. Is it a gateway to traditional tobacco use? Some public-health experts worry that we’re grooming a younger generation for a lifetime of dangerous addiction. Yet other people see e-cigarettes as a much safer alternative for adult smokers looking to satisfy their nicotine addiction. That’s the British perspective.

Last year, a Parliamentary committee recommended cutting taxes on e-cigarettes and allowing vaping in areas where it had previously been banned. Since e-cigarettes are as much as ninety-five per cent less harmful than regular cigarettes, the committee argued, why not promote them? Gottlieb said that he was splitting the difference between the two positions—giving adults “opportunities to transition to non-combustible products,” while upholding the F.D.A.’s “solemn mandate to make nicotine products less accessible and less appealing to children.” He was immediately criticized.

“Somehow, we have completely lost all sense of public-health perspective,” Michael Siegel, a public-health researcher at Boston University, wrote after the F.D.A. announcement:

Every argument that the F.D.A. is making in justifying a ban on the sale of electronic cigarettes in convenience stores and gas stations applies even more strongly for real tobacco cigarettes: you know, the ones that kill hundreds of thousands of Americans each year. Something is terribly wrong with our sense of perspective when we take the e-cigarettes off the shelf but allow the old-fashioned ones to remain.

Among members of the public-health community, it is impossible to spend five minutes on the e-cigarette question without getting into an argument. And this is nicotine they are arguing about, a drug that has been exhaustively studied by generations of scientists. We don’t worry that e-cigarettes increase the number of fatal car accidents, diminish motivation and cognition, or impair academic achievement. The drugs through the gateway that we worry about with e-cigarettes are Marlboros, not opioids. There are no enormous scientific question marks over nicotine’s dosing and bio-availability. Yet we still proceed cautiously and carefully with nicotine, because it is a powerful drug, and when powerful drugs are consumed by lots of people in new and untested ways we have an obligation to try to figure out what will happen.

A week after Gottlieb announced his crackdown on e-cigarettes, on the ground that they are too enticing to children, Siegel visited the first recreational-marijuana facility in Massachusetts. Here is what he found on the menu, each offering laced with large amounts of a drug, THC, that no one knows much about:

Strawberry-flavored chewy bites
Large, citrus gummy bears
Delectable Belgian dark chocolate bars
Assorted fruit-flavored chews
Assorted fruit-flavored cubes
Raspberry flavored confection
Raspberry flavored lozenges
Chewy, cocoa caramel bite-sized treats
Raspberry & watermelon flavored lozenges
Chocolate-chip brownies.

He concludes, “This is public health in 2018?”

This article appears in the print edition of the January 14, 2019, issue, with the headline “Unwatched Pot.”

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Prenatal Exposure to Cannabis Affects the Developing Brain

Children born to moms who smoked or ingested marijuana during pregnancy suffer higher rates of depression, hyperactivity, and inattention.

By Andrew Scheyer, The Scientist, 1/1/2019

Excerpt

A Lifetime of Consequences?

Large-scale, longitudinal studies of humans whose mothers smoked marijuana once or more per week and experimental work on rodents exposed to cannabinoids in utero have yielded remarkably consistent intellectual and behavioral correlates of fetal exposure to this drug. Some exposed individuals exhibit deficits in memory, cognition, and measures of sociability.

These aberrations appear during infancy and persist through adulthood and are tied to changes in the expression of multiple gene families, as well as more global measures of brain responsiveness and plasticity. Researchers currently consider these perturbations to be mediated by changes to the endocannabinoid system caused by the active compounds in cannabis.

marijuana cannabis cannabinoids fetal explosure

How Cannabis Affects the Function of Neurons

The human body contains two primary cannabinoid receptors: CB1R and CB2R. CB1R is present in the human fetal cerebrum by the first weeks of the second trimester, and is the brain’s most abundant G-protein coupled receptor. Located at the presynaptic terminal of neurons, CB1R is activated by endocannabinoids, which are synthesized from fatty acids in the postsynaptic neuron.

The receptors’ activation modulates the presynaptic release of neurotransmitters, thereby affecting synaptic function and a range of downstream signaling agents, from glutamate, dopamine, and serotonin to neuropeptides and hormones. The function of CB2Rs in the brain is still poorly understood, but there is some evidence that they exist both pre- and post-synaptically, as well as on glia and astrocytes. One recent paper suggests that, like CB1Rs, CB2Rs regulate neurotransmitter release (Synapse, 72:e22061, 2018).

When people smoke or ingest marijuana, exogenous cannabinoids enter the nervous system and activate these receptors. Stimulation by these high-affinity agonists results in stronger binding and greater activation of CB1R, triggering the process of receptor downregulation. Specifically, the greater binding causes the receptors to be internalized and degraded, such that they are no longer as available for cannabinoid signaling, and can thereby alter neuronal firing and other downstream events.

neurons marijuana cannabis cannabinoids fetal explosure presynaptic

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Does Marijuana Use Cause Schizophrenia?

As the drug becomes more popular, concerns have been raised that its use can lead to psychotic disorders. Here’s what scientists know for sure, and what they don’t.

By Benedict Carey, The New York Times, 1/17/2019

Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone.

Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient.

The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science.

Can heavy use cause schizophrenia or other syndromes?

That is the big question, and so far the evidence is not strong enough to answer one way or the other. Even top scientists who specialize in marijuana research are divided, drawing opposite conclusions from the same data.

“I’ve been doing this research for 25 years, and it’s polarizing even among academics,” said Margaret Haney, a professor of neurobiology at Columbia University Medical Center. “This is what the marijuana field is like.”

The debate centers on the distinction between correlation and causation. People with psychotic problems often use cannabis regularly; this is a solid correlation, backed by numerous studies. But it is unclear which came first, the cannabis habit or the psychoses. Children who later develop schizophrenia often seem to retreat into their own world, stalked periodically by bizarre fears and fantasies well outside the range of usual childhood imagination, and well before they are exposed to cannabis. Those who go on to become regular marijuana users often use other substances as well, including alcohol and cigarettes, making it more difficult for researchers to untangle causation.

Consider cigarettes, the least mind-altering of these substances. In a 2015 study, a team led by Dr. Kenneth S. Kendler of Virginia Commonwealth University analyzed medical data on nearly two million people in Sweden. The data followed the individuals over time, from young adulthood, when most schizophrenia diagnoses occur, to middle age. Smoking was a predictor for later development of the disorder, and in what doctors call a dose-response relationship: the more a person smoked, the higher the risk.

Yet nicotine attracts nowhere near the concern that cannabis does, in part because the two drugs are so different in their everyday effects: mildly stimulated versus stoned. Indeed, some scientists have studied nicotine as a partial treatment for schizophrenia, to blunt the disorders effects on thinking and memory.

Is it biologically plausible that cannabis could cause a psychotic disorder?

Yes. Brain scientists know very little about the underlying biology of psychotic conditions, other than that hundreds of common gene variants are likely involved. Schizophrenia, for instance, is not a uniform disorder but an umbrella term for an array of unexplained problems involving recurrent psychosis, and other common symptoms.

Even so, there is circumstantial evidence for a biological mechanism. Psychotic disorders tend to emerge in late adolescence or early adulthood, during or after a period of rapid brain development. In the teenage years, the brain strips away unneeded or redundant connections between brain cells, in a process called synaptic pruning. This editing is concentrated in the prefrontal cortex, the region behind the forehead where thinking and planning occur — and the region that is perturbed in psychotic conditions.

The region is rich with so-called CB1 receptors, which are involved in the pruning, and are engaged by cannabis use. And alterations to the pruning process may well increase schizophrenia risk, according to recent research at the Broad Institute of M.I.T. and Harvard. In a 2016 analysis, scientists there found that people with the disorder often have a gene variant that appears to accelerate the pruning process.

What does this mean for me?

Experts may debate whether cannabis use can lead to psychotic disorders, but they mostly agree on how to minimize one’s risk.

Psychotic conditions tend to run in families, which suggests there is an inherited genetic vulnerability. Indeed, according to some studies, people prone to or at heightened risk of psychosis seem to experience the effects of cannabis differently than peers without such a history. The users experience a more vivid high, but they also are more likely to experience psychosis-like effects such as paranoia.

The evidence so far indicates that one’s familial risk for psychotic disorders outweighs any added effect of cannabis use. In a 2014 study, a team led by Ashley C. Proal and Dr. Lynn E. DeLisi of Harvard Medical School recruited cannabis users with and without a family history of schizophrenia, as well as non-users with and without such a history. The researchers made sure the cannabis users did not use other drugs in addition, a factor that muddied earlier studies. The result: there was a heightened schizophrenia risk among people with a family history, regardless of cannabis use.

“My study clearly shows that cannabis does not cause schizophrenia by itself,” said Dr. DeLisi. “Rather, a genetic predisposition is necessary. It is highly likely, based on the results of this study and others, that cannabis use during adolescence through to age 25, when the brain is maturing and at its peak of growth in a genetically vulnerable individual, can initiate the onset of schizophrenia.”

Because marijuana has been illegal for so long, research that could settle the question has been sorely lacking, although that has begun to change. The National Institutes of Health have launched a $300 million project that will track thousands of children from the age of 9 or 10 through adolescence, and might help clarify causation.

For the near future, expert opinions likely will be mixed. “Usually it is the research types who are doing ‘the sky is falling’ bit, but here it is switched,” said Dr. Jay Geidd, a professor of psychiatry at the University of California, San Diego. “The researchers are wary of overselling the dangers, as was clearly done in the past. However, clinicians overwhelmingly endorse seeing many more adolescents with ‘paranoia’” of some kind.

In short: Regularly using the new, high-potency cannabis may indeed be a risk for young people who are related to someone with a psychotic condition. On that warning, at least, most experts seem to agree.

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Daily Marijuana Use And Highly Potent Weed Linked To Psychosis

NPR, 3/19/2019, by Rhitu Chatterjee

Several past studies have found that more frequent use of pot is associated with a higher risk of psychosis — that is, when someone loses touch with reality. Now a new study published Tuesday in the The Lancet Psychiatry shows that consuming pot on a daily basis and especially using high-potency cannabis increases the odds of having a psychotic episode later.

“This is more evidence that the link between cannabis and psychosis matters,” says Krista M. Lisdahl, a clinical neuropsychologist at the University of Wisconsin, Milwaukee, who wasn’t involved in the study.

The study authors consider high-potency cannabis to be products with more than 10 percent tetrahydrocannabinol or THC, the compound responsible for the drug’s psychoactive effects. The fact that consuming high-THC cannabis products has a greater risk is concerning, Lisdahl says, because these products are more common in the market now.

The study also shows that three European cities — London, Paris and Amsterdam — where high-potency weed is most commonly available actually have higher rates of new cases of psychosis than the other cities in the study.

The researchers identified 901 people aged 18 to 64 who were diagnosed with their first episode of psychosis between May 2010 and April 2015, at a mental health facility anywhere in 11 cities, including London, Paris, Amsterdam, Barcelona, other cities across Europe and one site in Brazil.

The researchers then asked these individuals and a control group of 1,200-plus other healthy people about their habits, including their use of weed. “We asked people if they used cannabis, when did they start using it and what kind of cannabis,” explains study author Marta Di Forti, a psychiatrist and clinician scientist at King’s College London.

People reported the names of weed strains they used, such as skunk in the U.K. or the Dutch Nederwiet, which allowed the researchers to identify the THC content in each product through data gathered by the European Monitoring Center for Drugs and Drug Addiction and national data from the different countries.

The study found that those who used pot daily were three times more likely to have a psychotic episode compared with someone who never used the drug.

Those who started using cannabis at 15 or younger had a slightly more elevated risk than those who started using in later years.

Use of high-potency weed almost doubled the odds of having psychosis compared with someone who had never smoked weed, explains Di Forti.

And for those who used high-potency pot on a daily basis, the risk of psychosis was even greater — four times greater than those who had never used.

The easy availability of high-THC weed is a recent phenomenon, she notes. “Almost 20 years ago, there wasn’t much high-potency cannabis available [in the market].”

One recent study showed that high-potency cannabis is increasingly dominating markets. It found that the average potency of weed in Europe and the U.S. in 2017 was 17.1 percent, up from 8.9 percent in 2008.

And some products can be even more potent. For example, in the Netherlands, the THC content of one product that’s gained popularity, locally produced Dutch resin Nederhasj, can be as high as 67 percent.

“What this paper has done that’s really nice is they look at rates of psychosis and cannabis use in lots of different places where underlying rates of psychosis are different,” says Suzanne Gage, a psychologist and epidemiologist at the University of Liverpool, who wrote a commentary linked to the study in The Lancet Psychiatry.

This allowed the researchers to compare incidence of psychosis with the availability and use of high-THC cannabis in the different cities, she says.

The study found that the three European cities — London, Paris and Amsterdam — had the highest rates of new diagnoses of psychosis — 45.7 per 100,000 person-years in London, 46.1 in Paris and 37.9 in Amsterdam.

These are also cities where high-potency weed is most easily available and commonly used.

Other European cities in Spain, Italy and France on the other hand have less than 10 percent THC content in most popular cannabis products on the market. These cities also have lower rates of new psychosis diagnosis, according to the study.

“One of the things that’s really novel is that they could show that variation of use and potency of cannabis was related to rates of first-episode psychosis,” Lisdahl says.

One critique of the theory that weed contributes to psychosis risk has been that while more people are using weed worldwide, there hasn’t been a corresponding rise in rates of psychosis, Gage explains. But the new study shows that cities with more easily available high-THC weed do have a higher rate of new diagnoses of psychosis.

“That’s a really interesting finding, and that’s not something anyone has done before,” she adds.

However, the study doesn’t prove causality, cautions Dr. Diana Martinez, a psychiatrist and addiction researcher at Columbia University. “You can’t say that cannabis causes psychosis,” she says. “It’s simply not supported by the data,” she says.

Lisdahl agrees. In order to show causality, one would have to follow people over time — before they started using weed to years later when they have their psychotic episodes, she says. “You need twins in the studies, you need genetic information,” among all other kinds of data, she says.

Psychotic disorders such as schizophrenia and bipolar are complicated, “multifaceted disorders,” Gage notes.

“In all psychotic disorders, there is this multiple hit hypothesis,” Martinez says. Many factors influence whether and how these disorders manifest.

Genetics is known to play a major role, as are a host of environmental factors. “Children who have risk of schizophrenia but grow up in stable homes … they may not go on to develop schizophrenia,” she adds.

The Adolescent Brain Cognitive Development study, which is funded by the U.S. National Institutes of Health, is attempting to tease out the various influences, Lisdahl says. “The NIH has now invested in that question.”

In the meantime, the new findings should be of interest to anyone using cannabis, says study author Di Forti. “There are people across the world who use cannabis for a variety of reasons,” she says. “Some of them recreationally, some of them for medicinal purposes.” They should be aware that using high-potency cannabis comes with a risk, she says.

“They need to know what to look for and ask for help, if they come across characteristics of a psychotic disorder,” she adds.

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In response to The contribution of cannabis use to variation in the incidence of psychotic disorder across Europe (EU-GEI): a multicentre case-control study , Suzanne H. Gage, in Cannabis and psychosis: triangulating the evidence, writes

…It is perfectly possible that the association between cannabis and psychosis is bidirectional, as suggested by other work using genetic variables as proxies for the exposures of interest in a Mendelian randomisation design. Di Forti and colleagues’ study adds a new and novel study design to the evidence available, which consistently indicates that for some individuals there is an increased risk of psychosis resulting from daily use of high potency cannabis. Given the changing legal status of cannabis across the world, and the associated potential for an increase in use, the next priority is to identify which individuals are at risk from daily potent cannabis use, and to develop educational strategies and interventions to mitigate this.

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Research articles

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, 3/19/2019, By Marta Di Forti, the EU-GEI WP2 Group, et al.
DOI:https://doi.org/10.1016/S2215-0366(19)30048-3

Cannabis use and the risk of developing a psychotic disorder, World Psychiatry, 2008 Jun; 7(2): 68–71.

Cannabis Users Have 500% Increased Risk for Schizophrenia, Increased Risk from Alcohol and Other illegal Drugs Too

BDNF overexpression prevents cognitive deficit elicited by adolescent cannabis exposure and host susceptibility interaction. Human Molecular Genetics Vol 26

Cannabis and schizophrenia: New evidence unveiled. Medical News Today.

Cannabis use and risk of schizophrenia: a Mendelian randomization study. Molecular Psychiatry volume 23, pages 1287–1292 (2018)

Impact of Cannabis Use on the Development of Psychotic Disorders. Current Addiction Reports

Samuel T. Wilkinson, Rajiv Radhakrishnan, and Deepak Cyril D’Souza write:
The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication; acute psychosis that lasts beyond the period of acute intoxication; and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, delta-9-tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case studies indicate that cannabinoids can induce acute psychosis that lasts beyond the period of acute intoxication but resolves within a month. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood; this association is consistent, temporally related, shows a dose response, and is biologically plausible. However, cannabis is neither necessary nor sufficient to cause a persistent psychotic disorder. More likely, it is a component cause that interacts with other factors to result in psychosis. The link between cannabis and psychosis is moderated by age at onset of cannabis use, childhood abuse, and genetic vulnerability. While more research is needed to better characterize the relationship between cannabinoid use and the onset and persistence of psychosis, clinicians should be mindful of the potential risk of psychosis, especially in vulnerable populations, including adolescents and those with a psychosis diathesis.

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Learning Standards

Massachusetts Comprehensive Health Curriculum Framework

PreK–12 Standard 10: Tobacco, Alcohol, & Substance Use/Abuse Prevention

Students will acquire the knowledge and skills to be competent in making health-enhancing decisions regarding the use of medications and avoidance of substances, and in communicating about substance use/abuse prevention for healthier homes, schools, and communities.

Through the study of Effects on the Body students will
10.5 Describe addictions to alcohol, tobacco, and other drugs, and methods for intervention, treatment, and cessation

10.6 List the potential outcomes of prevalent early and late adolescent risk behaviors related to tobacco, alcohol, and other drugs, including the general pattern and continuum of risk behaviors involving substances that young people might follow
Students generate ideas of what the term “gateway” means in relation to substance abuse and map out a series of behaviors that begin with such “gateway” behaviors

Through the study of Healthy Decisions students will

10.7 Identify internal factors (such as character) and external factors (such as family, peers, community, faith-based affiliation, and media) that influence the decision of young people to use or not to use drugs

10.8 Demonstrate ways of refusing and of sharing preventive health information about tobacco, alcohol, and other drugs with peers. Students research and give an oral report on the effects of second-hand smoke.

By the end of grade 12

Through the study of Effects on the Body students will

10.9 Describe the relationship between multi-drug use and the increased negative effects on the body, including the stages of addiction, and overdose. Students research the increased chances of death from alcohol poisoning when alcohol is combined with marijuana.

10.10 Describe the harmful effects of tobacco, alcohol, and other substances on pregnant women and their unborn children.
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Healthy meal generator

The ingredients can be combined in hundreds of ways, to make a delicious dinner. It takes just 15 minutes of prep, and ten minutes of cooking!

Construct Daily Diet Plant based

Start – pick one protein

Chicken breast or thigh meat, sliced
Vegan chik’n (such as Trader Joe’s or Gardein Chik’n)
Beef strips/tips, sliced
Vegan beef (such as Trader Joe’s or Gardein Beef-less tips)
Tofu (firm)
Tempeh
Gardein Mandarin Orange Crispy Chik’n
Gardein Beefless tips

(If you use real meat, stir fry first for about 4 minutes, then add to the rest of the stir fry. If you use faux meat or tofu, then it all cooks at the same time.)

Pick a carbohydrate to lay your stir fry over

White rice
Brown rice
Quinoa
Spaghetti, or angel hair pasta
Mung bean vermicelli
Rice pasta

Pick a few veggies

Have a different combination each time

Broccoli
Red bell peppers, green bell peppers, yellow or orange bell peppers
Yellow onions, vidalia onions
Summer squash
Bamboo shoots
Miniature corn
Water chestnuts

If you like, add nuts

peanuts
cashews

 

Stir fry sauce

Red curry sauce and coconut milk
Teriyaki sauce
Sesame ginger sauce
Thai Peanut Satay (House of Tsang Bangkok Padang)
Panda Express Orange Sauce
Szechuan Spicy stir fry sauce (House of Tsang)
Island Mango sauce (World Harbors)

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Healthy meal generator