Don't Blame Reefer
Once again, the anti-cannabis forces have seized upon another big lie to demonize the plant.
By Paul Armentano | May 16, 2011
Prohibitionists have a long history of exploiting tragedy to further their own Drug War agenda. Case in point: Members of Congress in the 1980s seized upon the cocaine overdose of basketball star Len Bias to enact sweeping legislative changes that established mandatory-minimum sentencing in drug crimes, random workplace drug-testing for public employees, and the creation of the Drug Czar’s office.
So it was hardly surprising to see the anti-drug zealots return to this tried-and-true playbook in the days immediately following the shooting of Arizona Congresswoman Gabrielle Giffords and 18 others. Only hours after alleged shooter Jared Lee Loughner was taken into custody, pundits on the political right opined that the 22-year-old former pot smoker had been driven mad by weed.
For instance, barely a day after the massacre, former George W. Bush speechwriter David Frum posed the question “Did pot trigger the Giffords shooting?” – to which the longtime conservative commentator answered, “Increasingly, experts seem to be saying ‘yes.’”
Frum’s accusation appeared to gain a modicum of respectability one month later, when the mainstream media highlighted a report in the Archives of General Psychiatry that purported to show a link between marijuana use and psychosis.
“It is increasingly clear that marijuana is a cause of schizophrenia,” the study’s lead researcher, Matthew Large of the Prince of Wales Hospital in New South Wales, Australia, told the website WebMD in February. (In a separate interview, he said he was “horrified” by suggestions that the plant should be legalized and regulated.) Large further insisted that “the schizophrenia caused by cannabis starts earlier than schizophrenia with other causes.”
In fact, this supposedly “new” study contained no new findings at all. Instead, Large and his team simply reviewed previously published research, much of itdecades old.
“There are no new data – I want to emphasize that. This is a meta-analysis, which means it [reviews] the studies that were already out there,” explained SUNY Albany psychology professor Mitch Earleywine, the author of the bookUnderstanding Marijuana: A New Look at the Scientific Evidence, speaking on the NORML Daily Audio Stash several days after the report’s release. “What you’re not hearing in the media is that, in fact, this [reported association] is probably early-onset folks self-medicating [with cannabis].”
There are several published reports to back up Earleywine’s suspicion. For example, a 2005 study of 1,500 subjects appearing in the scientific journalAddiction reported that the development of “psychotic symptoms in those who had never used cannabis before the onset of [such] symptoms … predicted future cannabis use.”
Other studies reinforcing Earleywine’s self-medication theory include a 2008 study published in the International Journal of Mental Health Nursing, which found that schizophrenics typically report using cannabis to reduce anxiety and “improve their mental state.” Indeed, marijuana use has been associated with clinically objective benefits in some schizophrenics. Recently, a 2010 report in the journal Schizophrenia Research found that schizophrenic patients with a history of cannabis use demonstrate higher levels of cognitive performance compared to nonusers. Researchers in that study concluded: “The results of the present analysis suggest that [cannabis use] in patients with SZ [schizophrenia] is associated with better performance on measures of processing speed and verbal skills. These data are consistent with prior reports indicating that SZ patients with a history of [cannabis use] have less severe cognitive deficits than SZ patients without comorbid [cannabis use].”
The clinical literature also casts doubt on Large’s claim that marijuana use accelerates mental illness. In a study published last year, a team of researchers from New York City’s Albert Einstein College of Medicine, Yale University and the National Institute of Mental Health assessed whether lifetime pot use was associated with an earlier onset of symptoms in schizophrenic patients. The researchers concluded: “Although cannabis use precedes the onset of illness in most patients, there was no significant association between onset of illness and [cannabis use] that was not accounted for by demographic and clinical variables.”
Even more significantly, the researchers criticized the findings of earlier studies that purported to show a “pot trigger” for mental illness, noting: “Previous studies implicating cannabis use disorders in schizophrenia may need to more comprehensively assess the relationship …. ”
Apparently, Matthew Large and his team didn’t get the memo.
As for Large’s most serious claim, that juvenile marijuana use “is a cause of schizophrenia,” most experts on the subject – and most scientific reviews of the matter – disagree.
For example, the authors of a 2009 study published in Schizophrenia Researchargued definitively that increased cannabis use by the public has not been followed by a proportional rise in diagnoses of schizophrenia or psychosis. Investigators at the Keele University Medical School in Britain compared trends in marijuana use and the incidence of schizophrenia in the United Kingdom from 1996 to 2005. They reported that the “incidence and prevalence of schizophrenia and psychoses were either stable or declining” during this period, even as cannabis use among the general population was on the rise.
“[T]he expected rise in diagnoses of schizophrenia and psychoses did not occur over a 10-year period,” the researchers 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.”
The study’s results didn’t surprise Dr. Julie Holland, clinical assistant professor of psychiatry at the New York University School of Medicine and editor of The Pot Book: A Complete Guide to Cannabis—Its Role in Medicine, Politics, Science, and Culture. “The bottom line here is, no one knows exactly what causes schizophrenia, and scientists have been looking for decades,” she says. “The best explanation is a ‘stress diathesis’ model, where people have a genetic tendency toward schizophrenic illness and then something triggers its appearance. But unless you have the genes, you won’t get the illness. Cannabis won’t change one’s genetic predisposition.”
Holland does caution that people with a predisposition toward schizophrenia “tend to have a stronger, more psychotic-like reaction to cannabis – but that is different from the idea that pot actually gives you schizophrenia, which is completely untrue.” As for the severity of those potential psychotic symptoms, Holland adds: “When the drug wears off, so do its effects. There is no lasting psychosis from pot.”
Dr. Lester Grinspoon, a retired associate professor of psychiatry at Harvard Medical School, has studied both cannabis and schizophrenia for over 40 years and is the author of such books as Schizophrenia: Psychopharmacology and Psychotherapy and Marihuana: The Forbidden Medicine. His expert opinion largely echoes the views of Earleywine and Holland.
“Schizophrenia is largely a genetically determined disorder,” he explains. “However, not all people who have this genetic makeup develop the disorder. So we have been searching for other variables that must be involved, but so far with little success. Recently, we have seen the publication of a number of papers that point the finger toward cannabis. Because my work in schizophrenia was first undertaken in the 1960s, when marijuana was first observed to be increasingly widely used by young people, I was always careful to include the possibility that the patient had previously smoked marijuana in my history taking. I can’t tell you how many patients this involved, but it was certainly measured in the hundreds – and not once did I find that it could be considered causal. Its use, on a few occasions, seemed like an attempt to alter an insufferable internal environment, much as people with schizophrenia often do with alcohol and tobacco.”
Ultimately, however, even if a causal connection between cannabis use and mental illness were one day established, this finding alone would do little to support the blanket prohibition of pot. In fact, the policy implications of such a finding would be just the opposite: Such health risks should be seen as legitimate reasons not for prohibition, but for regulation. After all, there are numerous adverse health consequences associated with alcohol, and it’s precisely because of these effects that the product is legally regulated and its use restricted to specific consumers and settings.
Similarly, if there are actual mental-health risks associated with the use of cannabis by certain individuals, then a regulated system would best identify and educate these people so they could refrain from its use. Placed in this context, the fearmongering of the Drug War crowd regarding marijuana and mental illness does little to advance the cause of prohibition and instead provides yet more ammunition for its repeal.