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Scientists Call Out Bad Data Linking Weed to Psychosis
That marijuana causes the onset of psychosis is a claim commonly employed to demonstrate the dangers of the drug, but studies touting the theory often lack the evidence to support it.
In a recent letter to the prestigious journal the Lancet, co-authors Dr. Charles Ksir and Dr. Carl Hart explained how researchers overstate the link between psychosis and cannabis by failing to account for variables that may cause co-occurring substance use and mental health disorders.
Speaking to HIGH TIMES, Hart explained that the Lancet has a habit of perpetuating this theory without the evidence to back it.
“Charlie [Ksir, his co-author] and I are concerned that the Lancet and its subsidiary journals have become the journal of marijuana psychosis,” he said.
In their letter, Ksir and Hart—who published their own review of the research on the topic in January—explained that clinical trials have failed to prove causality between marijuana use and psychosis, but researchers draw conclusions suggesting as much regardless.
A month after Ksir and Hart’s study was published, another review of the research by Tabea Schoeler and colleagues at Kings College London found that people already experiencing psychosis can improve outcomes by reducing or eliminating marijuana use, but continuing to use can worsen the severity of symptoms.
Hart and Ksir say this meta-analysis relied solely on “correlational studies”—which, as a rule, do not prove causation— to suggest that a causal relationship between marijuana and psychosis.
Despite the lack of causality in the literature, researchers exhibit “a strong tendency... to accept cannabis use as a so-called component cause of psychosis,” Hart and Ksir wrote.
In response to the criticism, Schoeler and her colleagues countered with another article in the Lancet, stating that while they agree they could not draw conclusions regarding causality, doing as much was not the focus of the study because previous research already "implicates cannabis use as a 'component cause' for psychotic symptomatology."
Hart disputes this defense, arguing that to establish a component cause, one must control for other variables that may have caused both marijuana use and psychosis.
“Schoeler and colleagues stated that rates of cannabis use in patients with psychosis are ‘higher than…those of people with other psychiatric diagnoses’,” Hart and Ksir wrote, adding that to support this claim, the opposing researchers cited an article (by Vito Agosti and colleagues) which concluded that other substance misuse and mental health disorders had stronger associations with psychosis than cannabis.
“They did not report any association between cannabis and psychosis, presumably because of the low frequency of psychosis in the participants studied," Hart and Ksir wrote of this study.
Schoeler and colleagues disputed this point in their reply, writing, “In this regard, we should point out that contrary to the authors’ assertion, Agosti and colleagues did in fact find an increased risk…of psychosis in patients dependent on cannabis.”
Hart retorted, “These people are dishonest. Our point was simply the following (as Agosti and colleagues themselves wrote): 'Alcohol dependence, antisocial personality disorder, and conduct disorder had the strongest associations with cannabis dependence, followed by anxiety and mood disorders.'"
“The cannabis-psychosis link was weaker than these other relationships, even though the authors set out to explore the psychosis-cannabis link. This is the point that we made,” Hart explained.
Indeed, in their review of the literature on cannabis and psychosis, Hart and Ksir found that the association between cannabis-users and people diagnosed with psychosis was caused by a variety of other factors that put certain populations at an increased risk for substance misuse and mental disorders. Put simply, the THC in cannabis did not cause the correlation between marijuana and psychosis, nor did psychosis cause cannabis use.
“After reviewing the scientific literature, we found evidence that bipolar disorder, anxiety disorder, and mood disorder have all been correlated with cannabis use, and reported that psychosis has been correlated with heavy tobacco smoking, heavy alcohol use, stimulant misuse, and sedative misuse. We found no clear evidence for a causal relation between cannabis and psychosis,” Hart and Ksir wrote.
According to their “shared vulnerability hypothesis,” people more vulnerable to substance misuse and mental health disorders are more likely to continue using marijuana and to have recurring episodes of psychosis, but not because one causes the other. Rather, mental health disorders are correlated with a variety of substance misuse, and there is no special link between cannabis and psychosis.
In their reply, Schoeler and her colleagues wrote that “Ksir and Hart suggest that the association between continued cannabis use and psychotic relapse is the result of a ‘shared-vulnerability,' presumably genetic," adding that recent research shows “only modest” overlap in genetic vulnerability for psychosis and marijuana use.
Hart categorically denies any insinuation of genetics, saying instead that "they misread our meaning of ‘shared vulnerability.' To interpret it as ‘genetic’ demonstrates their less-than-careful reading of our paper and also the literature in general.’”
Research into treatment informed by the idea that cannabis causes psychosis further disproves the causal connection, according to Hart and Ksir, who note, that two studies using treatment strategies (like cognitive behavioral therapy) that focused on marijuana use “found no beneficial effect on psychotic symptoms or amount of cannabis use.”
If treatments informed by marijuana use as a cause of psychosis offer no benefit, they argue, continued focus on the marijuana-causes-psychosis theory is a distraction from real solutions that may actually improve public health.
“Our greatest concern is not that someone might be advised to stop using cannabis,” Hart and Ksir wrote. “We are concerned that a misunderstanding of the relation between cannabis use and psychotic behavior leads to an oversimplification of the complex developmental nature of substance use and mental disorders.”
http://www.hightimes.com/read/scientists-call-out-bad-data-linking-weed-psychosis
That marijuana causes the onset of psychosis is a claim commonly employed to demonstrate the dangers of the drug, but studies touting the theory often lack the evidence to support it.
In a recent letter to the prestigious journal the Lancet, co-authors Dr. Charles Ksir and Dr. Carl Hart explained how researchers overstate the link between psychosis and cannabis by failing to account for variables that may cause co-occurring substance use and mental health disorders.
Speaking to HIGH TIMES, Hart explained that the Lancet has a habit of perpetuating this theory without the evidence to back it.
“Charlie [Ksir, his co-author] and I are concerned that the Lancet and its subsidiary journals have become the journal of marijuana psychosis,” he said.
In their letter, Ksir and Hart—who published their own review of the research on the topic in January—explained that clinical trials have failed to prove causality between marijuana use and psychosis, but researchers draw conclusions suggesting as much regardless.
A month after Ksir and Hart’s study was published, another review of the research by Tabea Schoeler and colleagues at Kings College London found that people already experiencing psychosis can improve outcomes by reducing or eliminating marijuana use, but continuing to use can worsen the severity of symptoms.
Hart and Ksir say this meta-analysis relied solely on “correlational studies”—which, as a rule, do not prove causation— to suggest that a causal relationship between marijuana and psychosis.
Despite the lack of causality in the literature, researchers exhibit “a strong tendency... to accept cannabis use as a so-called component cause of psychosis,” Hart and Ksir wrote.
In response to the criticism, Schoeler and her colleagues countered with another article in the Lancet, stating that while they agree they could not draw conclusions regarding causality, doing as much was not the focus of the study because previous research already "implicates cannabis use as a 'component cause' for psychotic symptomatology."
Hart disputes this defense, arguing that to establish a component cause, one must control for other variables that may have caused both marijuana use and psychosis.
“Schoeler and colleagues stated that rates of cannabis use in patients with psychosis are ‘higher than…those of people with other psychiatric diagnoses’,” Hart and Ksir wrote, adding that to support this claim, the opposing researchers cited an article (by Vito Agosti and colleagues) which concluded that other substance misuse and mental health disorders had stronger associations with psychosis than cannabis.
“They did not report any association between cannabis and psychosis, presumably because of the low frequency of psychosis in the participants studied," Hart and Ksir wrote of this study.
Schoeler and colleagues disputed this point in their reply, writing, “In this regard, we should point out that contrary to the authors’ assertion, Agosti and colleagues did in fact find an increased risk…of psychosis in patients dependent on cannabis.”
Hart retorted, “These people are dishonest. Our point was simply the following (as Agosti and colleagues themselves wrote): 'Alcohol dependence, antisocial personality disorder, and conduct disorder had the strongest associations with cannabis dependence, followed by anxiety and mood disorders.'"
“The cannabis-psychosis link was weaker than these other relationships, even though the authors set out to explore the psychosis-cannabis link. This is the point that we made,” Hart explained.
Indeed, in their review of the literature on cannabis and psychosis, Hart and Ksir found that the association between cannabis-users and people diagnosed with psychosis was caused by a variety of other factors that put certain populations at an increased risk for substance misuse and mental disorders. Put simply, the THC in cannabis did not cause the correlation between marijuana and psychosis, nor did psychosis cause cannabis use.
“After reviewing the scientific literature, we found evidence that bipolar disorder, anxiety disorder, and mood disorder have all been correlated with cannabis use, and reported that psychosis has been correlated with heavy tobacco smoking, heavy alcohol use, stimulant misuse, and sedative misuse. We found no clear evidence for a causal relation between cannabis and psychosis,” Hart and Ksir wrote.
According to their “shared vulnerability hypothesis,” people more vulnerable to substance misuse and mental health disorders are more likely to continue using marijuana and to have recurring episodes of psychosis, but not because one causes the other. Rather, mental health disorders are correlated with a variety of substance misuse, and there is no special link between cannabis and psychosis.
In their reply, Schoeler and her colleagues wrote that “Ksir and Hart suggest that the association between continued cannabis use and psychotic relapse is the result of a ‘shared-vulnerability,' presumably genetic," adding that recent research shows “only modest” overlap in genetic vulnerability for psychosis and marijuana use.
Hart categorically denies any insinuation of genetics, saying instead that "they misread our meaning of ‘shared vulnerability.' To interpret it as ‘genetic’ demonstrates their less-than-careful reading of our paper and also the literature in general.’”
Research into treatment informed by the idea that cannabis causes psychosis further disproves the causal connection, according to Hart and Ksir, who note, that two studies using treatment strategies (like cognitive behavioral therapy) that focused on marijuana use “found no beneficial effect on psychotic symptoms or amount of cannabis use.”
If treatments informed by marijuana use as a cause of psychosis offer no benefit, they argue, continued focus on the marijuana-causes-psychosis theory is a distraction from real solutions that may actually improve public health.
“Our greatest concern is not that someone might be advised to stop using cannabis,” Hart and Ksir wrote. “We are concerned that a misunderstanding of the relation between cannabis use and psychotic behavior leads to an oversimplification of the complex developmental nature of substance use and mental disorders.”
http://www.hightimes.com/read/scientists-call-out-bad-data-linking-weed-psychosis
