The effects of prenatal stress, and of prenatal alcohol and nicotine exposure, on human sexual orientation.
BACKGROUND
Studies of rats have shown that mothers who are subjected to stress during pregnancy are more likely than mothers who are not stressed during pregnancy to have male offspring who exhibit female-typical sexual receptivity postures (lordosis) in the presence of other males following the onset of puberty. More recent animal experiments have indicated that prenatal exposure to alcohol affects the sexual preferences of male offspring in ways that are similar to the effects of prenatal stress. Research with human subjects have thus far yielded inconsistent findings regarding the effects of prenatal stress on male sexual orientation, and no research has yet addressed the possible involvement of prenatal exposure to alcohol or other widely used recreational drugs, such as nicotine.


OBJECTIVE
The present study was undertaken to determine if prenatal stress could be one of the causes of variations in sexual orientation in humans, both singularly and in conjunction with prenatal exposure to alcohol and nicotine.


METHODS
Over 7500 offspring and their mothers provided information regarding the offspring's sexual orientation and the mother's stressful experiences and use of alcohol and nicotine during pregnancy.


RESULTS
Findings indicate that prenatal stress has a modest but significant effect on the sexual orientation of male offspring, particularly when the stress occurred during the first trimester of pregnancy. Regarding prenatal exposure to alcohol, no evidence was found to suggest that it impacted offspring sexual orientation of either males or females. Prenatal nicotine exposure, however, appears to significantly increase the probability of lesbianism among female offspring, especially if the exposure occurred in the first trimester along with prenatal stress in the second trimester.


CONCLUSIONS
The present study is consistent with animal models suggesting that prenatal stress disrupts the typical sex hormonal milieu within which male fetal brains are sexed, thereby feminizing/demasculinizing the male's sexual orientation. However, little support was found for similar effects of prenatal alcohol exposure. In the case of prenatal nicotine, this study is the first to suggest that this drug has masculinizing/defeminizing effects on the sexual orientation of female offspring.
Ellis
L
L
Minot State University, 58707, Minot, ND, USA. ellis@minotstateu.edu
Cole-Harding
S
S
D000328:Adult; D002492:Central Nervous System Depressants / Q000009:adverse effects*; D004347:Drug Interactions; D000431:Ethanol / Q000009:adverse effects*; D005260:Female; D006801:Humans; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D011247:Pregnancy; D011262:Pregnancy Trimester, Second; D011297:Prenatal Exposure Delayed Effects; D012727:Sex Characteristics; D012725:Sexual Behavior / Q000187:drug effects / Q000502:physiology*; D013315:Stress, Psychological / Q000523:psychology*
D002492:Central Nervous System Depressants; D018722:Nicotinic Agonists; D000431:Ethanol; D009538:Nicotine