Androgens are steroid hormones of which testosterone is one and which is the most powerful in males (Rommerts, 1998 in Christiansen, 2001). Pre- and peri-natally, a surge of testosterone determines that a brain will be male (and consequently lack of a surge will create a female brain). Post-natally androgens have also been seen to affect male sexual behaviour (e.g. Salmimies et al, 1982 in Christiansen, 2001). More specifically, Gorski’s study on sexual dimorphism in the preoptic area showed that “although male and female rats initially have about the same numbers of neurons in the medial preoptic area, a surge of testosterone secreted by the testes of male fetuses around the time of birth acts to stabilise their neuronal population. In females the lack of such a surge allows many neurons in their cell group to die, leading to the typically smaller structure” (LeVay & Hamer, p.44). McGivern and Handa (1996) would argue strongly with the ecological validity of animal studies in generalising to human sexual orientation. They suggest that animal models of homosexuality are inherently inadequate for at least two reasons: it has not been explained how homosexual behaviour arises in rats when steroids have not been given, and normal male rats showing low levels of typical male sex behaviour do not in fact show increased same-sex mounting behaviour or lordosis. Further objection exists to the use of rats in the study of sexual dimorphism and sexual orientation: Merkx (1984, in McGivern and Handa, 1996) suggests that (p.78) “in fact, male preference behavior for an estrous female rat does not appear to be influenced by perinatal androgen exposure ”. Although Gorski had not in fact made a connection between his rat studies on sexual dimorphism and sexual orientation, as shall be seen next his work has been used to this end and therefore the previous methodological criticisms remain valid.
Gorski and Allen (in LeVey & Hamer, 1994) also found that a cell group called INAH3 was sexually dimorphic and that it differed within sex as well as between sex. LeVay (1991 in LeVay & Hamer, 1994) extended this finding to show that specifically there was a difference in size of the INAH3 structure between straight and gay men. As has been noted however (Byne, 1994; Christiansen, 2001; Pinel, 2000), it is very difficult to establish a causal relationship between hormones (especially prenatal action) and behaviour in humans because levels cannot be manipulated and human behaviour is far more complicated than in animals. Indeed it may be that being homosexual actually causes small changed in the size of the INAH3 region, or there may be a third variable. It can be said therefore that there is very weak evidence for implicating sexual dimorphism in sexual orientation.
LeVay and Hamer (1994) nevertheless suggest that this may be relevant to a prenatal influence on sexual orientation in the following way. If, as it has been found, the “sexually dimorphic cell group in the medial preoptic area appears plastic in its response to androgens during early brain development but then is largely resistant to change” (p.47), then the size of INAH3 in men may in fact influence sexual orientation. A further methodological issue is that their sample used men who had had AIDS and therefore this factor may have been involved.
LeVay and Hamer (1994, p.47) go on to ask the following question: “Assuming that some of the structural differences related to sexual orientation were present at birth in certain individuals, how did they arise?” They suggest two possibilities, both of which involve prenatal hormonal influence. The first proposal which they believe to be less likely is that atypical levels of gonadal androgens cause some people to develop into homosexuals. The explanation which they propose to be more likely is that “intrinsic differences in the way individual brains respond to androgens during development, even when the hormone levels are themselves no different” may create homosexuality.
Interestingly, an experiment on frogs may show that even if pre- or perinatal hormones could be shown to influence sexual orientation it may not be possible to separate out social influences. The rigorous experiment (Burmeister & Wilczynski, 2001, p.550) involved manipulation of hormones and found that “variation in androgens did not explain variation in evoked call rate. These data indicate that androgens influence the motivation to call [courtship behaviour], but that, when socially stimulated, androgens are necessary but insufficient for calling”. So it seems that if there were intrinsic differences in responsiveness to androgens (and this has not been studied in humans) then this would not necessarily determine sexual behaviour.
An example of another mediating factor in sexual orientation may come from the following study of a correlation between prenatal stress, nicotine and alcohol use and sexual orientation (Ellis & Cole-Harding S, 2001). The findings were consistent with animal models suggesting that prenatal stress disrupts the normal hormone circulation and sex determination process. 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 females.
The implication of this last statement is that genes are ultimately responsible for homosexuality. As LeVay and Hamer (1994) point out, the idea of a gay gene would seem to completely contradict the mechanisms of reproduction. What they suggest however is that a gene may exist that “sway” rather than determine homosexuality. The evidence (through traditional methods of twin and family studies) is relatively strong for some sort of heritability for homosexuality: the concordance rate for male twins is 57% (pooled data, in LeVay & Hamer, 1994). Attempts to find the gene which predisposes people to homosexuality have yielded mixed and unconvincing results. Initially a region was found that correlated with homosexuality but this has not been replicated (Hamer et al, 1993 in LeVay & Hamer, 1994). LeVay and Hamer also point out that it is not know how quantitatively important that region might be in influencing sexual orientation. Looking at genes for androgen receptors and INAH3 has found no significant correlations for the former and mapping has not found any relationship yet for the latter (LeVay & Hamer, 1994).
As William Byne (1994, p.50) noted in an introduction to a challenge on biological studies of sexual orientation: “The salient question about biology and sexual orientation is not whether biology is involved but how it is involved.” Sexual dimorphism has been well supported by experimental evidence. The mechanisms of androgens have also been well supported by evidence from non-human experiments. The link between prenatal androgenisation and homosexuality has not been proved and although some intuitively appealing hypotheses exist it is possible that they will remain very difficult to confirm simply because hormone levels cannot be manipulated and even if they could it is still not known to what extent social and cultural factors play in sexual orientation.
Bibliography
Burmeister, S.S. & Wilczynski, W. (2001). Social Context Influences Androgenic Effects on Calling in the Green Treefrog (Hyla cinerea). Hormones & Behaviour, 40 (4), 550-8
Byne, W. (1994). The biological evidence challenged. Scientific American, 270 (5), 26-31.
Christiansen, K. (2001). Hormones and Sport. Journal of Endocrinology, 170, 39-48.
Ellis, L. & Cole-Harding, S. (2001). The effects of prenatal stress, and of prenatal alcohol and nicotine exposure, on human sexual orientation. Physiology & Behaviour, 74 (1-2), 213-26.
LeVey, S. and Hamer, D.H. (1994). Evidence for a biological influence in male homosexuality. Scientific American, 270 (5), 20-25.
McGivern, R.F. & Handa, R.J. (1996). Prenatal exposure to drugs of abuse: methodological considerations and effects on sexual differentiation. NIDA Research Monograph, 164, 78-124.
Pinel, J.P.J. (2000). Biopsychology. 4th ed. Boston: Allyn and Bacon.
