Scare-mongering headlines touting the alleged adverse effects of marijuana’s impact on brain appear in the mainstream media almost daily. But a careful investigation of the relevant science reveals many of these fears to be overblown at best and illegitimate at worst.
Pot Permanently Damages the Brain
“Even occasional marijuana can change your brain.” So claimed the headlines surrounding a highly publicized 2014 study by researchers at Northwestern University’s Feinberg School of Medicine and the Massachusetts General Hospital Center for Addiction Medicine. Authors took images of the brains of college-aged cannabis users and non-users and acknowledged differences in the brain morphology of the two groups.
However, because the study was based on a single set of images, researchers had no way to determine whether the differences predated subjects cannabis use or whether they would remain if they ceased using pot. Further, investigators failed to assess either groups’ cognitive or academic performance to ascertain whether these changes were associated with any adverse real-world outcomes. (All of the participants in the study were enrolled in higher education and none of the participants met criteria for drug dependence.) Nonetheless, investigators pronounced that the observed differences were “abnormal” and indicated that such ‘brain alterations’ would likely lead to more serious drug abusing behaviors down the road.
Or not. In fact, when a separate team of scientists tried to replicate these results in a larger, better-controlled cohort of subjects, they couldn’t.
“We acquired high-resolution MRI scans, and investigated group differences in gray matter using voxel-based morphometry, surface-based morphometry, and shape analysis in structures suggested to be associated with marijuana use, as follows: the nucleus accumbens, amygdala, hippocampus, and cerebellum,” researchers summarized last year in the The Journal of Neuroscience. “No statistically significant differences were found between daily users and nonusers on volume or shape in the regions of interest. Effect sizes suggest that the failure to find differences was not due to a lack of statistical power, but rather was due to the lack of even a modest effect.”
Further, authors theorized that the observed differences reported in 2014 were likely due to the participants’ consumption of alcohol, not pot. They concluded: “[T]he results indicate that, when carefully controlling for alcohol use, gender, age, and other variables, there is no association between marijuana use and standard volumetric or shape measurements of subcortical structures. … [I]t seems unlikely that marijuana use has the same level of long-term deleterious effects on brain morphology as other drugs like alcohol.”
Marijuana Lowers IQ
Smoking cannabis leads to an eight-point drop in intelligence quotient. So says the US National Institute on Drug Abuse on their webpage ‘Marijuana: Get the Facts.’ But the facts in this instance are far from definitive.
NIDA’s claim, which has since been repeated by numerous pundits and anti-drug reform groups is taken from a Duke University study published in 2012 in The Proceedings of the National Academy of Sciences. The study’s authors reported that the persistent use of cannabis by those in their early teens, but not others, was associated with as high as an eight-point drop in IQ by age 38. However, a separate, far less publicized review of the data that appeared later in the same journal suggested that the results were likely because of socioeconomic differences, not subjects’ use of cannabis. It determined: “The association [between heavy adolescent marijuana use and lower IQ by middle age] is given a causal interpretation by the authors, but existing research suggests an alternative confounding model based on time-varying effects of socioeconomic status on IQ. A simulation of the confounding model reproduces the reported associations from the Dunedin cohort, suggesting that the causal effects estimated in Meier et al. are likely to be overestimates, and that the true effect could be zero.”
More recent analyses further support the notion that cannabis use alone does not have an adverse causal effect on either IQ or academic performance. A 2015 study by Meier and colleagues published in the journal Drug and Alcohol Dependence reports that the effects of persistent adolescent cannabis use on academic performance is “non-significant after controlling for persistent alcohol and tobacco use.” Similarly, a study published this month in the Journal of Psychopharmacologyconcludes that cumulative teen pot use is not associated with lower IQ scores or with poorer educational performance once adjustments are made for confounding variables, specifically cigarette smoking. “[T]hose who had used cannabis [greater than or equal to] 50 times did not differ from never-users on either IQ or educational performance,” investigators determined.
Cannabis Adversely Effects Cognition
Indeed, some stupid people may smoke pot. But the relevant science suggests that they were stupid long before ever coming in contact with the herb.
Specifically, Boston University researchers performed a battery of cognitive tests on a cohort of marijuana-using twins and their non-using co-twins. They reported “an absence of marked long-term residual effects of marijuana use on cognitive abilities.”
Similarly, a study published in the journal Archives of General Psychiatry found that long-term cannabis smokers (identified as consumers who had smoked cannabis at least 5000 times during their lives) who abstained from pot for several weeks showed virtually no significant differences from control subjects (those who had smoked marijuana less than 50 times in their lives) on ten distinct neuropsychological tests. “]T]here were virtually no significant differences among the groups on any of the test results, and no significant associations between cumulative lifetime cannabis use and test scores,” investigators reported.
Likewise, a 2012 literature review of 11 peer-reviewed studies evaluating pot’s potential long-term impact on cognitive function, involving over 1,000 subjects, concluded, “The results of our meta-analytic study failed to reveal a substantial, systematic effect of long-term, regular cannabis consumption on the neurocognitive functioning of users who were not acutely intoxicated.”
Finally, a separate meta-analysis published in the journal Experimental and Clinical Psychopharmacology concludes that cannabis is not associated with “enduring negative effects” on the cognitive skills in moderate to heavy marijuana consumers. Researchers from the University of Central Florida reviewed various, peer-reviewed studies assessing whether pot use is associated with lasting adverse residual effects on cognition. They reported that chronic cannabis consumption was associated with “small but significant” effects on neurocognitive skills for limited periods of time, but that these effects discontinued following abstinence. Authors reported “no evidence of lasting effects on cognitive performance due to cannabis use” in subjects whose abstention period was at least 25 days. They concluded, “These results fail to support the idea that heavy cannabis use may result in long-term, persistent effects on neuropsychological functioning.”
Marijuana Causes Mental Illness
Claims persist that cannabis use can trigger mental illness, specifically schizophrenia, in otherwise healthy individuals. But data to substantiate these claims is lacking.
Specifically, a 2009 paper in the journal Schizophrenia Research compared trends in marijuana use and incidences of schizophrenia in the United Kingdom from 1996 to 2005. Authors reported that “incidence and prevalence of schizophrenia and psychoses were either stable or declining” during this period, even though pot use among the general population was rising. They concluded: “This study does not therefore support the specific causal link between cannabis use and incidence of psychotic disorders. … This concurs with other reports indicating that increases in population cannabis use have not been followed by increases in psychotic incidence.”
Similarly, a review paper published by a pair of British scientists in the journal Addiction reported that there exists little clinical evidence indicating that marijuana use is casually linked to incidences of schizophrenia or other psychological illnesses. Authors wrote: “We continue to take the view that the evidence that cannabis use causes schizophrenia is neither very new, nor by normal criteria, particularly compelling. … For example, our recent modeling suggests that we would need to prevent between 3000 and 5000 cases of heavy cannabis use among young men and women to prevent one case of schizophrenia, and that four or five times more young people would need to avoid light cannabis use to prevent a single schizophrenia case. … We conclude that the strongest evidence of a possible causal relation between cannabis use and schizophrenia emerged more than 20 years ago and that the strength of more recent evidence may have been overstated.”
More recently, researchers at Harvard University published a study further rebutting the ‘pot equals schizophrenia’ allegation. Writing in 2013 in Schizophrenia Research, investigators compared the family histories of 108 schizophrenia patients and 171 individuals without schizophrenia to assess whether youth cannabis consumption was an independent factor in developing the disorder. Researchers reported that a family history of schizophrenia increased the risk of developing the disease, regardless of whether or not subjects consumed marijuana as adolescents. They concluded: “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 cannabis may have an effect on the age of onset of schizophrenia it is unlikely to be the cause of illness.”
Most recently, a pair of just published commentaries in the journal Nature Neuropsychopharmacology suggests that while THC may be associated with increase psychiatric risks in already vulnerable populations, “there are sufficient reasons to question the causality of this relationship,” such as the possibility of self-medication or shared genetic and environmental risk factors. “To conclude, public perception and popular media often interpret associations shown in longitudinal studies as demonstrating causation, so the scientific community has to consistently emphasize the distinction between association and causation. Given the low odds ratio and evidence that schizophrenia is a neurodevelopmental disorder, the most scientifically conservative stance is that the association between cannabis and psychotic disorders is not causal.”