Evidence suggests that human male fertility is impacted by long-term exposure to marijuana. Indeed, endocannabinoids and their receptors are present in the male reproductive tract, further suggesting a functional role in fertility, but there has been no genetic test to clarify mechanisms.
Now, in a paper the February 2009 issue of the journal Biology of Reproduction, Sun et al. characterize the phenotype of mice genetically lacking FAAH, fatty acid amide hydrolase.
Male mice homozygous for the Faah knockout have elevated levels of anandamide, an endocannabinoid, in the reproductive system, and their sperm have decreased ability to fertilize due to poor penetration of the egg's zona pellucida. These results point to previously unsuspected pathways regulating sperm function.
But perhaps more importantly, they are of great clinical significance: because sperm of chronic marijuana users, as well as sperm in Faah-mutant males are exposed to enhanced cannabinoid/endocannbinoid signaling, clinically beneficial effects of anandamide must be weighed against potentially harmful effects on fertility.
(Note: The term anandamide for the endocannabinoid arachidonoylethanolamide was coined by the discoverer of this compound, Dr. Mechoulam; "ananda" means bliss or ecstasy.)
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