Marijuana and Schizophrenia?

The AHA! Team — Fri, 31 May 2024 05:31:56 +0000

Michael Greger M.D. FACLM via Nutrition Facts – The evidence linking cannabis use to psychotic disorders is considered strong enough to warrant a public health warning. “Even as proponents of [cannabis] legalization contend that smoked marijuana is a harmless natural substance that improves the quality of life, a growing body of evidence links it in a small but significant number of users to…the induction or aggravation of psychosis.” “Psychotic disorders are arguably the most serious of mental illnesses, the best known being schizophrenia.” “Schizophrenia, an illness that is characterized by delusions, hallucinations, and odd behavior, is among the top 10 leading causes of disability in the United States. It affects approximately 1% of the general population.” Can cannabis cause it? Schizophrenia… affects approximately 1% of the general population As I discuss in my video Does Marijuana Cause Schizophrenia?, over the last half-century, “nearly 2,000 studies have been published on this topic…and the pro-psychotic effects of cannabis have dominated media reporting about this drug. But how clear is the link?” Population studies have “consistently demonstrated a strong, positive, and dose-dependent association between cannabis use and the risk of psychotic disorders.” Indeed, studies have shown that the more cannabis people use, the more likely they are to be psychotic, as seen in a chart below and at 1:10 in my video. However, that doesn’t mean cannabis is the cause. It could just be a correlation or even a consequence of the disease. “The link between cannabis and psychosis is well established,” but it may be the case that patients with mental health problems self-medicate and “use cannabis to relieve their distress.” The link between cannabis and psychosis is well established… As you can see below and at 1:38 in my video, there isn’t only a link between cannabis and psychosis in snapshot-in-time cross-sectional studies, but in cohort studies as well, where people are followed over time. Research has shown that cannabis use often precedes psychosis, not the other way around. Now, it goes without saying that “the vast majority of people who use cannabis do not develop psychotic disorders such as schizophrenia, and many people diagnosed with such disorders have never used cannabis.” But, overall, these studies are considered to be “strong enough evidence to warrant a public health message that cannabis use can increase the risk of psychotic disorders.” There is another potential explanation: Even though cannabis use precedes schizophrenia, could it be that whichever genes drive schizophrenia also make it more likely you start smoking pot? The biggest strike against the cannabis-schizophrenia link is country-by-country ecological studies that don’t seem to show more disease in areas where there’s more use. And, overall, schizophrenia rates seem to have remained stable or even gone down worldwide since the 1960s, even though there’s been a big bump in cannabis use since then. If about 10 percent of schizophrenia cases are attributable to marijuana use and there’s been a fourfold increase in use, why hasn’t there been a 40 percent increase in the prevalence of schizophrenia? The problem with that argument is “there is little reliable evidence on the temporal [true] trends in the incidence of schizophrenia, so it is difficult to know whether this statement is true or not.” Perhaps it’s more of an issue with potency rather than just cannabis in general. Indeed, “the incidence of schizophrenia is higher in countries…where high-potency cannabis has taken over the market compared with countries…where more traditional forms of cannabis are smoked.” The bottom line is you don’t know until you put it to the test. You can’t just randomize kids to cannabis, but, in a way, Nature set up a natural experiment for us. There are genes that kids randomly get that can increase their likelihood of smoking pot. Do those kids then go on to have a higher risk of schizophrenia? Yes, research “findings strongly support” all of those population studies that suggest “cannabis plays a causal [cause-and-effect] role in the development of schizophrenia.” Okay, but by how much? Let’s break it down. Even if cannabis use doubles the risk, that would mean only going from a 7-in-1,000 chance of developing a psychosis to 14 in 1,000. So, going from a 1 in 140 chance to a 1 in 70 chance. It would be different if schizophrenia runs in your family, where a doubling of risk could mean going from a one-in-ten chance to one in five, but, on a population scale, it could take thousands of cannabis users quitting to prevent a single case of schizophrenia. So, from a public health standpoint, “addiction is a far more common problem.” Researchers “estimate that people who try cannabis are ninefold more likely to become addicted to it”—even though that itself is relatively rare—“than to develop psychosis in their lifetime.” I have an entire series of videos on cannabis, which I originally released in a webinar and downloadable digital DVD. Key Takeaways Although some proponents of cannabis legalization argue that marijuana is a “harmless natural substance that improves the quality of life,” it has been linked “in a small but significant number of users to…the induction or aggravation of psychosis.” Schizophrenia, a psychotic disorder characterized by hallucinations, odd behavior, and delusions, affects about 1 percent of the general population. Studies have found that the more cannabis people use, the more likely they are to be psychotic, but that could just be a correlation or even a consequence of the disease. Individuals with mental health problems may self-medicate and use cannabis to relieve distress, for example. Research has found that cannabis use often precedes psychosis, not the other way around. Overall, there appears to be “strong enough evidence to warrant a public health message that cannabis use can increase the risk of psychotic disorders.” There does not seem to be more disease in regions with greater cannabis use. Overall, schizophrenia rates appear to have remained stable or even declined worldwide since the 1960s, despite a large jump in cannabis use since then. Potency may be a bigger issue. In countries with higher potency cannabis, the incidence of schizophrenia is higher than in countries with “more traditional forms.” Some genes can increase our likelihood of using cannabis, and kids who randomly get them have been found to have a higher risk of schizophrenia. Research suggests that cannabis may have a cause-and-effect role in the development of that psychosis. Even if cannabis use doubles the risk, however, that would just mean a 1-in-70 chance of developing a psychosis without a family history of schizophrenia. From a public health standard, the far more common problem is addiction. To read the original article click here.

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New UCI-Led Study Finds Links Between Circadian Rhythms, Metabolism and Addiction

AHA Publisher — Wed, 16 Mar 2022 07:00:58 +0000

University of California, Irvine via Newswise – Irvine, Calif., March 11, 2022 — A new University of California, Irvine-led study establishes important conceptual connections between the fields of circadian rhythms, metabolism, and addiction. Going beyond current studies on substance use disorders, which focus on the impact of addictive drugs on the brain, this new research highlights an existing connection between specific neurons and peripheral organs. The study, titled “Dopamine D2 receptor signaling in the brain modulates circadian liver metabolomic profiles,” was published today in the Proceedings of the National Academy of Sciences. “Our findings provide a link to substance use disorders and metabolic dysfunctions,” explained Emiliana Borrelli, PhD, professor of Microbiology & Molecular Genetics at UCI School of Medicine who, for this study, collaborated with the late Paolo Sassone-Corsi, PhD, professor of Biological Chemistry at UCI. “Through our research we explored how the disruption of normal neuronal functions affects metabolic activity and may move the body to an altered state away from homeostasis, which could contribute to the drug seeking behaviors exhibited by people with substance use disorders.” By analyzing the liver metabolome of mice deficient in the expression of the dopamine D2 receptor (D2R) in striatal medium spiny neurons, the researchers found profound changes in the liver circadian metabolome compared to control mice. In addition, they found that activation of dopaminergic circuits by acute cocaine administration reprograms the circadian liver metabolome. “D2R signaling in medium spiny neurons is key for striatal output and is essential for regulating the first response to the cellular and rewarding effects of cocaine,” said Borrelli. “Thus, our results suggest that changes in dopamine signaling in specific striatal neurons evoke major changes in liver physiology. Dysregulation of liver metabolism could contribute to an altered allostatic state and therefore be involved in continued use of drugs.” The circadian clock is tightly intertwined with metabolism and relies heavily on multifaceted interactions between organ systems to maintain proper timing. Genetic and/or environmental causes can disrupt communication between organs and alter rhythmic activities. Substance use leads to altered dopamine signaling followed by reprogramming of circadian gene expression and metabolism in the reward system. This study shows that dopamine D2 receptors (D2R) in striatal medium spiny neurons (MSNs) play a key role in regulating diurnal liver metabolic activities. In addition, drugs that increase dopamine levels, such as cocaine, disrupt circadian metabolic profiles in the liver, which is exacerbated by loss of D2R signaling in MSNs. These results uncover a strict communication between neurons/brain areas and liver metabolism as well as the association between substance use and systemic deficits,” said Borrelli. Substance use disorders affect millions of people worldwide. The rewarding properties of substances, such as alcohol, nicotine, opioids, and psychostimulants, are linked to their ability to increase dopamine levels in brain areas that control emotions and induce pleasure. Drug intake modifies neuronal plasticity and is at the start of the process of addiction, which leads vulnerable individuals to continually seek and abuse these substances despite the adverse consequences on their lives. This study was funded by grants from the National Institutes of Health under Award Number DA035600 and by the French Institut National de la Sante et de la Recherche Medicale (INSERM). Future studies will examine whether the alterations in the specific metabolites identified in this study contribute to susceptibility to drug use. To read the original article click here.

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Marijuana and Schizophrenia?

New UCI-Led Study Finds Links Between Circadian Rhythms, Metabolism and Addiction