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cbd oil testicular cancer

“Our study is not the first to suggest that some aspect of a man’s lifestyle or environment is a risk factor for testicular cancer, but it is the first that has looked at marijuana use,” said Stephen Schwartz, an epidemiologist and author on the study.

The findings suggest that smoking the drug before the age of 18 raises the cancer risk by coaxing immature cells in the testes to become tumours later in life.

The researchers asked 369 testicular cancer patients if they had any history of marijuana use. A further 979 healthy men were asked about their use of the drug.

Ecstasy remains class A

Being an existing cannabis user raised the risk of cancer by 70%, while men who had used the drug regularly from puberty were twice as likely to develop the disease than those who had not used the drug.

After accounting for any family history of the cancer and lifestyle factors, such as smoking and drinking alcohol, the study found cannabis use emerged as a significant, separate risk factor for the disease.

Men naturally produce a cannabinoid-like substance that is thought to protect the testes against tumours. But smoking cannabis may disrupt this and so raise the risk of cancer, the study speculates.

Scientists at the Fred Hutchinson Cancer Research Centre in Seattle investigated the possibility of a link after learning that the testes were one of the few organs in the body to contain receptors for the main psychoactive substance in the drug, tetrahydrocannabinol (THC). There has also been a rise in testicular cancer cases that has mirrored the rise in marijuana use since the 1950s, they said.

References were collected and logged in EndNote vX7.1 (Thomson Reuters, New York, U.S.A.). Duplicate records were removed prior to further analysis. Abstracts were screened by one reviewer (JG) to remove irrelevant studies, with a 10 % random sample of these verified by a second reviewer (VS). Any disagreements about inclusion were resolved by referral to a third reviewer (DS). The full text of all remaining papers was obtained and assessed by two reviewers (JG and VS) to identify those which met our inclusion criteria.

Methods

The primary psychoactive component of the cannabis plant – delta-9-tetrahydrocannabinol, or THC – stimulates neural cannabinoid receptors, mimicking the action of endogenous cannabanoids (termed endocannabanoids). The position of these cannabinoid receptors in the basal ganglia, hippocampus, cerebellum and neocortex explains the common neurophysiological effects of cannabis ingestion; however, these receptors are also expressed in peripheral locations, including the testis [22].

Meta-analysis results

The second major weakness for two of the three included studies was low and differential response rates. In one study, the response rate was substantially lower among the controls than the cases [9]. If the reported cannabis use was different among those controls who responded compared with those who did not, and if the same differential is not present for the cases who responded and cases who did not respond, this will result in biased OR. For example, if the controls who responded had lower rates of cannabis use than non-responding controls, this will lead to an overestimate of the cannabis-TGCT association. Unusually in a second study, the control group had a substantially higher response rate than the case group [7]. In this study, the controls were friends of the cases, which may explain their willingness to participate in the study. However it is not clear why the response rate among cases was so low. For this latter study, it may be reasonable to assume that cannabis use might have been more similar between cases and controls than if unrelated controls were used. If this is true, we might expect that the ORs in this study would be biased towards the null. Reassuringly, the results of all three studies were reasonably consistent despite the different potential sources of selection bias.