Tuesday, April 04, 2006

Homosexuality Part II: What is it with gay men and their mothers?

Part II in a three part series on the biological basis of homosexuality. (Part I can be read here or here)

One pattern has emerged that suggests that male and female homosexuality may have very different causes, a pattern that has been replicated and observed across numerous studies: the fraternal birth order effect. If you are a gay male, there is a greater probability that you have older brothers. In fact, each prior born male increases the probability of subsequent males being homosexual by 33%*, according to the most statistically robust studies. The same effect is not observed in boys with older sisters, or in girls at all. One proposed mechanism suggests that each male pregnancy promotes and reinforces a maternal immune response to certain proteins produced by the Y chomosome (the H-Y complex), meaning that later male pregnancies are subjected to stronger immune responses from the maternal system. This potentially disrupts typical foetal development and prenatal hormone action, or upsets the symmetry of body development, which is significantly correlated with the occurence of homosexuality in both males and females...

Again, there are problems here: there have been no studies in humans illustrating the actual mechanism of maternal immune response or its effect on the foetus. Further, there are youngest brothers that are not gay, and older brothers that are. As a result, this is at best one factor that may influence sexuality in only a subset of genetic males. The studies also don't take into account the possible behavioural effects of older brothers on the development of sexual identity in their younger brothers, although recent research has discounted this possible factor. The pattern is nonetheless informative: the fact that no such effect is found in females again underlies that male and female sexual orientation are probably not mirror images of each other, but rather the result of different developmental and social processes.

All in the family?

Recently, genetic studies on sexual orientation have gained some momentum and favour among researchers. This is in part due to the ability of some types of genetic studies to expose patterns of the heritability of sexual orientation, but also due to the rapid advances in genetic and molecular techniques that have produced such comprehensive studies as the Human Genome Project.

The application of genetic study to sexual orientation has proved more contentious than the application of developmental studies, given the shackling of the discipline to the ghosts of eugenics, genetic engineering, cloning and designer babies. Genetic factors are also assumed to be more deterministic, more rigid, than pre- and post-natal environmental influences, a common but frustrating misconception. Indeed, the study of sexual orientation using genetic techniques - family studies, twin studies and molecular studies - has revealed just as much variation, just as many general trends and probabilities, as our developmental approaches.

Studies across and within generations of have shown a moderate but still significant pattern of the behaviour in some families. That is, patterns of homosexuality do tend to run in certain families (contrary to the assertion of Allan-John Marsh), higher than you would expect by chance alone; if you are homosexual, the probability of one of your siblings also being homosexual is higher than if you are heterosexual. There is evidence to suggest that this statistical relationship is stronger between pairs of gay brothers and pairs of gay sisters than between the gay brother/lesbian sister relationship (which this author incidentally falls into), although that particular relationship is still significantly stronger than a straight brother/lesbian sister or gay brother/straight sister relationship. Again, these are just observable trends, not rules.

Twin studies have proved useful because they allow researchers to tease apart the effect of shared environments from genetic effects within families. Fraternal twins, which share identical environments but are only genetically related to each other to the extent of normal siblings, on average exhibit less shared homosexuality than identical twins, which share identical environments and identical genetic makeup. The difference between the rate of shared sexual orientation allows us to estimate how much of the variation in sexual orientation has a heritable component - estimates which from 14% to 76% depending on which study you look at.

Of course, we need to remember that not all identical twin sets share the same sexual orientation; some members of identical twin sets are gay while their twins are not. This means that even when we control for social and genetic factors, some further factor is influencing sexual orientation. We are again, at best, left with a trend, an estimate, a correlation.

All in the genes?

As previously mentioned, there are no ‘gay genes’, just as there are no ‘schizophrenia’ genes, no ‘alcholic genes’, no ‘violence’ genes. However, modern molecular studies combined with family and pedigree analysis allows us to try and narrow down which particular chomosomal locations, termed loci (singular locus), are associated with the occurrence, though not the cause, of homosexuality.

The most interesting discovery in this field was made in 1993 when a group of genetic researchers based at the National Cancer Institute in Maryland** reported on a familial and molecular study of 40 families of gay men. A certain point on the X chromosome, labelled Xq28 was found to be common to 33 pairs of gay brothers within these 40 families. It was the first definitive study which identified a possible genetic marker of homosexuality in males. No such marker was or has since been found in the familial studies of lesbians. Naturally the press had a field day, and the term ‘gay gene’ was born.

The identification of Xq28 in gay familial studies has been subsequently replicated with varying degrees of statistical significance. What needs to be considered is that, in these studies, not all gay men had Xq28 and not all males who possessed Xq28 were gay. More interestingly, there was a significant pattern of maternal male inheritance. That is, the study suggested that if you were gay, it was more probable that your mother’s brother was gay, rather than your father.

In fact, no paternally inherited chromosomal marker has been identified that is associated with homosexuality. Gay fathers do not statistically produce more gay children of either gender than heterosexual fathers. Similarly, lesbian mothers do not statistically produce more gay children of either gender than heterosexual mothers.

So where do we find ourselves at the end of all this, biologically? What do we think we know, what do we know we don’t?

1. Human sexual orientation is correlated with non-social biological factors. These include pre-natal developmental processes and genetic influences.

2. There is evidence that pre-natal testosterone levels play a role in the development of adult sexual orientation, but this differs both between gay males and lesbian females, and within gay male and lesbian female groups themselves.

3. There is evidence that the causative mechanisms of male and female homosexuality, and sexual orientation in general, are fundamentally disparate.

4. There is evidence that fraternal birth order is correlated with occurrence of homosexuality in males, but not in females.

5. There is a higher sharing of homosexuality between siblings than would be predicted by chance alone. Evidence therefore suggests that there is a familial component associated with homosexuality in both gay males and gay females.

6. Identical twins have a higher sharing of homosexuality than fraternal twins. Evidence therefore suggests that there is heritable component of human sexual orientation.

7. One maternally inherited chromosomal marker has been identified that is statisically but not causatively associated with the occurrence of male homosexuality in some individuals in some families.

8. There is no evidence to suggest that parent sexual orientation has any role in determining, or influencing their childen’s sexual orientation.

Finally, and most importantly: There are exceptions to every trend, link, association and relationship that has been identified. As a result, no line of evidence, alone or in conjunction with any other, or in conjunction with environmental factors, is sufficient as a causative model for human homosexuality in either males or females.

That, in a nutshell, is our understanding of the ‘biological’ basis of human sexual orientation. In essence we have nothing more than theories and hypotheses about some of the developmental mechanisms and genetic patterns that may be involved. We have no hard and fast rules, we have no easy answers. We just have a good idea.

We now face the question: Can we approach the social and ethical issues of homosexuality from a position informed by biology, by nature? If we can, how do we make sense of this sensational mess?

Next Week - Part III: Pink Sperm and Designer Babies

*Ellis L and R Blanchard. 2001. Birth order, sibling sex ratio, and maternal miscarriages in homosexual and heterosexual men and women. Personality and Individual Differences 30(4):543-552

**Hamer DH, Hu S, Magnuson VL, Hu N and AML Pattatucci. 1993. A Linkage Between DNA Markers on the X Chromosome and Male Sexual Orientation. Science 261(5119):321-227