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Health Czar Shows Amazing Ignorance About Marijuana Facts

You'd think the director of NIH would know a thing or two about the science of cannabis. You'd be wrong.

Photo Credit: Boyan Dimitrov / Shutterstock.com


In the Internet era, members of the general public have unprecedented access to scientific facts and figures. Among the resources now available at one’s fingertips is the National Center for Biotechnology Information database. NCBI is an NIH.gov electronic search engine that allows the public to instantly read the abstracts of hundreds of thousands of peer-reviewed scientific papers on virtually any subject, including an estimated 20,000 papers on cannabis alone.

So why then does the head of the National Institutes of Health purport to know so little about the science of pot?

Speaking publicly last week at a dinner hosted by USA Today and National Geographic, NIH director Francis Collins—known as one of the nation’s top scientists for his leadership of the international Human Genome Project—acknowledged that pot isn’t necessarily “an evil drug that’s going to ruin our civilization.” Nevertheless, he expressed a surprising lack of familiarity with much of the readily available research that has been conducted on the plant and its impact on those who consume it.

"We don't know a lot about the things we wish we did," with respect to the herb, Collins said, seemingly unaware that a keyword search of the agency’s own sponsored website would yield thousands of scientific papers specific to marijuana and its behavioral and health effects. "I've been asked repeatedly, does regular marijuana smoking, because you inhale deeply, increase your risk of lung cancer? We don't know. Nobody's done that study."

Wrong. In fact, the largest case-controlled study ever to investigate the respiratory effects of marijuana smoking reported that cannabis use was not associated with lung-related cancers, even among subjects who reported smoking more than 22,000 joints over their lifetime. Summarizing the finding of the NIH-funded  study to the Washington Post, lead investigator and pulmonologist Donald Tashkin of UCLA affirmed, “We hypothesized that there would be a positive association between marijuana use and lung cancer, and that the association would be more positive with heavier use. What we found instead was no association at all, and even a suggestion of some protective effect."

Writing in 2013 in the scientific journal Annals of the American Thoracic Society, Tashkin reiterated: “Cannabis smoking is not equivalent to tobacco smoking in terms of respiratory risk. Despite the presence in cannabis smoke of known carcinogens, toxic gases, and particulates, cannabis smoking does not seem to increase risk of chronic obstructive pulmonary disease (COPD) or airway cancers. In fact, there is even a suggestion that at low doses, cannabis smoking may be protective for both conditions.”

Yet, according to the head of NIH, no one, including Tashkin, has adequately studied the effects of marijuana on the lungs. In truth, not only has the question already been sufficiently asked and answered; it is NIH that paid for the answers.

One study Collins conveniently was aware of was a July 2012 observational trial published in the Proceedings of the National Academy of Sciences which reported that subjects who use cannabis heavily during adolescence experienced an average drop in IQ of roughly 8 points compared to their non-toking peers. But the NIH director failed to mention that the journal’s editors published a separate analysis just two months later repudiating that paper’s findings, concluding that the original study’s authors failed to adequately control for the subjects’ disparate socioeconomic status.

“The association (between adolescent-onset cannabis use and IQ) 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,” the later study determined. “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.”

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