title: Acute, short-term, and chronic effects of marijuana on the female primate reproductive function.
abstract: Studies with laboratory animals clearly show that the crude drug marijuana and delta-9-THC, the principal psychoactive ingredient, inhibit secretion of the pituitary hormones LH and FSH as well as prolactin. These changes in pituitary hormone levels produce decreases in sex steroid hormones and cause disruption of ovulation and spermatogenesis. With chronic drug use, disruption of sex accessory organs has also been observed. A principal site of THC action is the hypothalamus, because THC effects on pituitary hormone production can be reversed with hypothalamic releasing factors. It is now known that drug effects in sexually mature animals are reversible when drug treatment stops. In adults, tolerance develops to hormone changes brought on by the use of marijuana. Clinical studies on human subjects generally agree with the animal findings, although conflicting results have been reported as well. It is likely that the differences in results obtained in experiments with laboratory animals and with humans are caused, at least in part, by differences in experimental design. Further, it is not known how much disruption of reproductive hormone levels is necessary for changes in human fertility and sexual function to occur. The use of marijuana by pregnant women or by women who are attempting to become pregnant is cause for special concern. Studies with laboratory animals and retrospective studies on women who have used marijuana during pregnancy show that the risks of pregnancy loss and other adverse effects on the fetus are increased by marijuana use. THC crosses the placental barrier and while the potent teratogenic and mutagenic effects suggested for marijuana some years ago have not been confirmed, significant changes consistent with retardation of fetal growth and development have been observed. Effects of THC on the proper functioning of the placenta may be responsible for these effects on pregnancy. Pregnancy that occurs after the development of tolerance with chronic marijuana use may involve an ovum that has been damaged by exposure to the drug during critical developmental stages. More studies need to be done before the mechanisms of toxic effects on pregnancy and fetal development can be described. While there have been no clinical studies relating marijuana use to adolescent development, studies in laboratory animals show that the developing reproductive system during adolescence is particularly vulnerable.(ABSTRACT TRUNCATED AT 400 WORDS)
mesh_terms: D000818:Animals; D013759:Dronabinol / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004361:Drug Tolerance; D005260:Female; D012739:Gonadal Steroid Hormones / Q000097:blood; D006062:Gonadotropins / Q000097:blood; D066298:In Vitro Techniques; D008253:Macaca mulatta; D008597:Menstrual Cycle / Q000187:drug effects; D009490:Neurosecretory Systems / Q000187:drug effects; D010906:Pituitary Hormone-Releasing Hormones / Q000494:pharmacology; D010907:Pituitary Hormones / Q000097:blood; D011323:Primates / Q000502:physiology*; D011817:Rabbits; D051381:Rats; D012098:Reproduction / Q000187:drug effects*; D013997:Time Factors
chemical_list: D012739:Gonadal Steroid Hormones; D006062:Gonadotropins; D010906:Pituitary Hormone-Releasing Hormones; D010907:Pituitary Hormones; D013759:Dronabinol