“MY GENES MADE ME DO IT!”

by Marion Williams

In the early 90s Simon LeVay and Dean Hamer did some much publicised research into the nature of homosexuality. [1] The media and some sections of the gay community have given much attention to these research findings as they suggest homosexuality may have some organic basis. The theoretical framework that has emerged from these and other studies of homosexuals and transgendered people, suggest to the general public that we are finding solid answers in the area of neurology, genetics and endocrinology (brains, chromosomes and hormones). Before giving a critique of these studies as well as the general ‘biological’ theories, it is important that we become familiar with the research, the theorists’ hypotheses and the conclusions that have been drawn from the data. When we take time to sort through the facts, presumptions and conclusions, we find that the ‘born-gay’ argument is shaky, if not inherently flawed. It is modern Western folklore and pseudoscience at its best.

BRAINS

LeVay and Hamer present us the findings of Gorkski in 1978 which show us that a rat’s hypothalamus, a region involved with instinctive behaviours, has a cell group within it known as the medial preoptic region which has been implicated in the generation of sexual behaviour (because of studies done on the same region in monkeys). With rats this region was found to be three times larger in males. Sex differentiation of the brain structure, called sexual dimorphism is said to come about through the influence of hormones. Within this region of the brain are neurons which are rich in receptors for sex hormones, both androgens and estrogens. With males, a surge of testosterone, secreted by the testes around the time of birth, stabilises the numbers of neurons. In females the lack of such a surge causes the neurons to die, thus reducing the size of the brain structure. Gorkski and his colleagues also claim to have found sexually dimorphic structures in the human brain. A cell group named INAH3 within the medial preoptic region has been seen to be three times larger in males.

LeVay in 1990 wanted to investigate whether brain size differed according to sexual orientation so he investigated the brains of 35 men who had died of AIDS; 19 homosexuals and 16 heterosexuals as well as six women. He found the INAH3 group in the heterosexual men to be 2-3 times larger than those of the homosexual men; some of whose were missing altogether. The size of INAH3 was the same for gay men as it was for the women. LeVay theorised that the structural differences arose during the period of brain development and consequently contributes to sexual behaviour (in light of monkey studies). [2]

WHY CAN WE QUESTION THIS CONCLUSION?

·      The studies have not been replicated and the methods proved to be unsound. [3]

·              At the time of death virtually all men with AIDS have decreased testosterone levels and in studies of Mongolian gerbils the size of a structure comparable to the SDN-POA varies with the amount of testosterone present. [4]

·            The brains of monkeys, not rats, were used to identify the origins of sexual behaviour in the medial preoptic region but this region (in monkeys) is the same size for both male and female. [5]

             Other studies carried out on the sexually dimorphic nucleus of the preoptic area (SDN-POA) have shown conflicting results when attempting to identify specific regions which are different in men and women. Also Gorkski and Avendish even found in another study that destroying a rat’s SDN-POA did not impair sexual function at all. [6]

              Genetic males with Androgen Insensitivity Syndrome once called Testicular Feminisation Syndrome, who lacked an enzyme responsible for utilising their androgens and bringing on male genitalia, were raised as girls and grew up as feminine heterosexual women. [7] If they had male brains why would this be possible?

HORMONES

Theorists over the years have suggested that homosexuals and transgendered individuals may have abnormal levels of circulating sex hormones. Popular myths often uphold this idea. Recent theories however, have concentrated more on the Prenatal Hormone Hypotheses which suggests that abnormal levels of hormones, undetectable at birth and in adulthood, have affected the brain of the foetus, which later may predispose an individual to homosexuality.

LeVay suggests that there is interaction between gonadal steroids and the developing drain in that there is a difference in the way brains respond to androgens. He suggests male homosexuals therefore have a feminised brain, not because of the amount of androgens secreted, but because of the receptiveness of the brains to the androgens.

Some suggest that the cause of Gender Identity Disorder is due to levels of hormones present in-utero which are undetectable in adulthood and current interest is in the pre-natal influence of H-Y antigen since it is thought that this antigen may somehow affect the sexual centre in the hypothalamus. [8] Dorner in a study in 1976 found some transsexuals to have raised levels of Lutenizing Hormone and Follicle Stimulating Hormone as well as low Free Plasma Testosterone and therefore concluded that gender disorders were hormonally based. [9]

WHY CAN WE QUESTION THESE CONCLUSIONS?

·      Androgens given to a female rat produces mounting behaviour and a male rat deprived of androgens engages in the female behaviour of lordosis (bending of the back). [10] Human sexual behaviour is diverse with many homosexual males taking an active role and lesbians taking a passive role. According to this theory, they would not be homosexual.

·      Money and Mustaph in 1977 showed in some experiments that if male hormones are administered to a homosexual person they only increase the homosexual behaviour. Here we see that sex hormones increase the drive stimuli but do not change the orientation. [11] Others suggest similarly, that at puberty the surge of sex-hormones does not determine the course of adult sexuality; rather it activates the already established patterns. [12]

·         Although there have been many speculations about physiological causes of Gender Identity Disorder, generally it has been found that there is no evidence of biological aetiology. [13] Money found that effeminate boys, ‘tomboys’, transvestites, transsexuals, homosexuals and bisexuals studied appeared to be normal on all six physiological tests used. [14]

·           There are conflicting results in the studies of possible abnormalities in the Hypothalamus-Pituitary Neuroendocrine function. To date there has been no conclusive evidence for the Pre-natal Hormone Hypothesis. There is in fact much more direct evidence which disproves the pre-natal hormone theories of Gender Dysphoria (Gender Identity Disorder). [15]

·          The search for abnormal levels of circulating androgens in transsexuals has for the most, yielded negative. In most investigations there is no evidence of lowered testosterone or higher levels of estrogen as a function of the degree of femininity. [16]

·         Girls exposed to high levels of male hormone during foetal life as a result of either maternal drug treatment or Congenital Adreno Hyperplasia (a genetic disorder leading to a defect in the adrenal gland and hence a high production of androgens), although more ‘tomboyish’, were heterosexual in orientation. [17]

·        If lesbians had been exposed to androgens, which would develop a ‘male’ brain, there would be no increase in the lutenizing hormone which triggers ovulation. Why is it lesbians menstruate and bear children?

 

CHROMOSONES

TWIN STUDIES

Pillard and Weinrich in 1985 in a study of gay men found that 57% of the identical twin brothers; 24% of fraternal twin brothers and 13% of non-twin brothers are also gay. Also maternal uncles had a 7% chance, and sons of maternal aunts had an 8% chance of being gay. For women the ratios are similar. These researchers agreed with another researcher J. Michael Bailey who believes the family clustering of homosexuality suggests the proportion of influence that comes from a genetic component is about 50%. [18]

Hamer et al did a study on nuclear families with 2 gay sons. Out of 40 pairs 33 showed the same marker on the Xq 28 region of the X chromosome. They assume that the gene effects androgen receptors which are the ones responsible for masculinization.

WHY CAN WE QUESTION THESE CONCLUSIONS?

·     Bailey compared the molecular structure of the androgen receptor gene in 197 homosexual and 213 heterosexuals and found there to be no difference in structure. Also the androgen receptor locus turned out to be at the Xq 11 region. This excludes the androgen receptor from playing a role in homosexuality. [19]

·        The Xq 28 region only represents less than 2 % of the total human genome. [20]

·     It also was not mentioned that the Xq 28 region found was not in the same sequence for the 33 sets of twins so the only similarities were between the twins themselves. This region therefore could be representing any characteristic. [21]

·      The study by Pillard failed to reveal that of adopted brothers of homosexuals 11% were gay which is much higher than the average rate of 2.4% of the male population. This seems to indicate an environmental influence. [22]

·         Heterosexuals and women were not studied. [23]

·        Hamer, himself said, “Here the genes serve to predispose rather than pre-determine…whether this fanciful notion contains a grain of truth remains to be seen.” [24]

·         William Byrne in an article, ‘The Biological Evidence Challenged’ in Scientific American (May 1994), as a response to the above material, wrote “Most of the links in the chain of reasoning from biology to sexual orientation and social policy do not hold up under scrutiny…What evidence exists thus far of innate biological traits underlying homosexuality is flawed.” [25]