pubmed.ncbi.nlm.nih.gov

Minireview: Hormones and human sexual orientation - PubMed

Review

. 2011 Aug;152(8):2937-47.

doi: 10.1210/en.2011-0277. Epub 2011 Jun 21.

Affiliations

Review

Minireview: Hormones and human sexual orientation

Jacques Balthazart. Endocrinology. 2011 Aug.

Abstract

Many people believe that sexual orientation (homosexuality vs. heterosexuality) is determined by education and social constraints. There are, however, a large number of studies indicating that prenatal factors have an important influence on this critical feature of human sexuality. Sexual orientation is a sexually differentiated trait (over 90% of men are attracted to women and vice versa). In animals and men, many sexually differentiated characteristics are organized during early life by sex steroids, and one can wonder whether the same mechanism also affects human sexual orientation. Two types of evidence support this notion. First, multiple sexually differentiated behavioral, physiological, or even morphological traits are significantly different in homosexual and heterosexual populations. Because some of these traits are known to be organized by prenatal steroids, including testosterone, these differences suggest that homosexual subjects were, on average, exposed to atypical endocrine conditions during development. Second, clinical conditions associated with significant endocrine changes during embryonic life often result in an increased incidence of homosexuality. It seems therefore that the prenatal endocrine environment has a significant influence on human sexual orientation but a large fraction of the variance in this behavioral characteristic remains unexplained to date. Genetic differences affecting behavior either in a direct manner or by changing embryonic hormone secretion or action may also be involved. How these biological prenatal factors interact with postnatal social factors to determine life-long sexual orientation remains to be determined.

PubMed Disclaimer

Figures

Fig. 1.
Fig. 1.

In mammals, early exposure to testosterone produces a male phenotype: the behavioral characteristics of the male are strengthened (masculinization) and the ability of males to show behavior typical of females is reduced or lost (defeminization). The female phenotype develops in the apparent absence of hormone action (or in the presence of very low estrogen concentrations). These spontaneous differentiation processes occurring during early development of animals can be entirely reproduced by experimental manipulations (via castration, injections of agonists or antagonists) of steroid concentrations in embryonic or newborn animals. The figure shows that after such treatments, neonatally castrated (CX) males behave like females, whereas females treated early in life with testosterone (T) or its aromatized metabolite estradiol (E2) behave like males. Experimental animals considered are those shaded in blue (genetic males) or red (genetic females). Other subjects represent only the test stimuli.

Fig. 2.
Fig. 2.

Theoretical model illustrating how fluctuations around an average concentration of testosterone (T) during embryonic life could lead to a homosexual or heterosexual orientation.

Similar articles

Cited by

References

    1. Kinsey AC, Pomeroy WR, Martin CE. 1948. Sexual behavior in the human male. Philadelphia: W.B. Saunders Co - PMC - PubMed
    1. Goy RW, McEwen BS. 1980. Sexual differentiation of the brain. Cambridge, MA: The MIT Press
    1. Beach FA. 1948. Hormones and behavior. New York: Paul B. Hoeber, Inc
    1. Phoenix CH, Goy RW, Gerall AA, Young WC. 1959. Organizational action of prenatally administered testosterone propionate on the tissues mediating behavior in the female guinea pig. Endocrinology 65:369–382 - PubMed
    1. Arnold AP, Chen X. 2009. What does the “four core genotypes” mouse model tell us about sex differences in the brain and other tissues? Front Neuroendocrinol 30:1–9 - PMC - PubMed

Publication types

MeSH terms

Substances