After 50 years of rumor, study, and argument in the research community, the National Institute on Drug Abuse (NIDA) has come out squarely behind the assertion that marijuana use in men “may increase their risk for developing testicular cancer.”
But a problem exists. The evidence just isn’t that good. Especially if you base the conclusion on a single small study, as NIDA is apparently doing.
Writing inNIDA Notes for December, 2010, Lori Whitten highlights a study of 369 men from the Seattle area with testicular cancer, and a control group of 979 disease-free men. “The researchers found that the odds of having testicular cancer were 70 percent higher among men who reported current marijuana use compared with nonusers…. They also found that the odds for testicular cancer among men who used marijuana at least weekly were twice that of nonusers.”
The hypothesis supporting this statistical correlation is not terribly robust: Testicular cancer has doubled in the past 50 years in the U.S. So has the percentage of the population that smokes pot. And since cannabinoid receptors are found on the cell membranes of the testes, and chronic marijuana use is associated with decreased testosterone plasma levels and reduced spermatogenesis, marijuana smoking must somehow interfere with the growth of germ cells in the testes. The result: cancer.
But wait, there’s more. Whether or not this contention can be considered true and proven remains quite arguable, but the study does appear to show a statistical association between marijuana use and one particular form of the disease. Marijuana smoking was strongly associated with only one form of testicular cancer, called nonseminomas, a fast growing type representing 40% of all testicular germ cell tumors (TGCT). The other type—seminomas—accounts for the other 60%.
Dr. Sudhansu Dey, a NIDA-funded researcher involved in the study, published in Cancer, told NIDA Notes that the association between marijuana smoking and nonseminomas, but not seminomas, is “difficult to explain.”
Here’s one possibility: Testicular cancer is too rare, and the study in question too small, to be anything but suggestive. It does not show a direct linkage between testicular cancer and pot smoking, and the authors do not claim that it does. In fact, they point to several limitations of their own study. The researchers were only able to directly interview a little more than half of the eligible cases and controls. And the study relied on self-report questionnaires, which, in the case of an illegal drug like marijuana, can skew the results. For example, “patients with cancer may be expected to more accurately admit to the use of an illegal substance than individuals in a control group.”
Specifically, the report states that “the incidence of seminoma from 1973 to 1998 in the US was 64% compared with an increase of only 24% for nonseminoma…. If the increase in nonseminomas was caused in part by an increase in the use of marijuana, then some other increasing exposures must account for the higher incidence of seminomas over time.” The point, as the researchers acknowledge, is that “none of these explanations likely would be specific to nonseminomas. Indeed, if the association is true, then new avenues of research will be needed to address the specificity of the association to nonseminomas.”
In other words, the argument that pot smoking might increase cases of one particular kind of testicular cancer is not accompanied by an explanation of the biological mechanism by which marijuana would be capable of exerting such effects. The primary risk factor for testicular cancer seems to be a family history of the disease, followed by abnormal development of the testicles or undescended testes.
“If these interesting findings are replicated in a large, national representative group of participants,” Dr. Vishnudutt Purohit of NIDA’s Division of Basic Neuroscience and Behavioral Research told NIDA Notes, “then future research should delve into the molecular mechanism underlying the association.”