Food for thought...
Marihuana and sex: a critical survey.Abel EL.
Marihuana usage is associated with a life-style that involves earlier and more frequent sexual activity. Marihuana usage does not affect human male testosterone levels significantly, but does adversely affect sperm production. Animal studies have not found consistent changes in weights of male sexual organs but have corroborated the adverse effects of cannabinoid compounds on sperm production. The biological significances of these effects on sperm production are unclear, however, since there is no evidence that human marihuana users or male animals given cannabinoid compounds are less fertile or are at risk for dominant lethal mutations. Cannabinoid compounds reliably inhibit ovulation in animals and are associated with depressed luteinizing hormone (lh - leutenizing hormone - ) levels in both female and male animals. The decreased lh - leutenizing hormone - levels appear to be due to both hypothalamic and ovarian sites of action. Treatment with cannabinoid compounds is also associated with lower testosterone levels in male and lower prolactin levels in female animals. Effects on progesterone levels are inconclusive. Cannabinoid compounds do not possess estrogenic activity. Despite some consistencies in the data in virtually every study conducted with animals, there has been a basic confounding between direct drug action and secondary effects resulting from drug-induced decreases in food and water consumption and attendant weight loss. Almost all of the adverse effects of cannabinoid exposure on reproductive organs can be attributed to these secondary effects.
Marijuana: interaction with the estrogen receptor.
Sauer MA, Rifka SM, Hawks RL, Cutler GB Jr, Loriaux DL.
Crude marijuana extract competed with estradiol for binding to the estrogen receptor of rat uterine cytosol. Condensed marijuana smoke also competed with estradiol for its receptor. Pure delta 9-tetrahydrocannabinol, however, did not interact with the estrogen receptor. Ten delta 9-tetrahydrocannabinol metabolites also failed to compete with estradiol for its receptor. Of several other common cannabinoids tested, only cannabidiol showed any estrogen receptor binding. This was evident only at very high concentrations of cannabidiol. Apigenin, the aglycone of a flavinoid phytoestrogen found in cannabis, displa high affinity for the estrogen receptor. To assess the biological significance of these receptor data, estrogen activity was measured in vivo with the uterine growth bioassay, using immature rats. Cannabis extract in large doses exhibited neither estrogenic nor antiestrogenic effects. Thus, although estrogen receptor binding activity was observed in crude marijuana extract, marijuana smoke condensate and several known components of cannabis, direct estrogenic activity of cannabis extract could not be demonstrated in vivo.
The often heard assertion that THC causes gynecomastia is not related to estrogenic activity of the compound, but rather to the ability of THC to suppress luteinizing hormone (lh - leutenizing hormone - ). A number of studies have shown this (1) (2) (3). Other studies have failed to show an effect (4).
As with evidence supporting the theory behind marijuana induced gynecomastia, there are conflicting studies about whether there is even a correlation between marijuana use and gynecomastia. There is a much stronger correlation between alcoholism and gynecomastia than between weed and gynecomastia.
(1) NIDA Res Monogr 1984;44:46-64
Endocrine effects of marijuana in the male: preclinical studies.
(2) Drug Alcohol Depend 1992 Apr;30(1):59-63
Chronic effects of marihuana smoking on luteinizing hormone, follicle-stimulating hormone and prolactin levels in human males.
(3) : J Pharmacol Exp Ther 1986 Jun;237(3):862-6
Marihuana smoking suppresses luteinizing hormone in women.
(4) 1: Drug Alcohol Depend 1991 Aug;28(2):121- 8
Effects of chronic marijuana use on testosterone, luteinizing hormone, follicle stimulating hormone, prolactin and cortisol in men and women.