By G. Wilson and Q. Rahman (Peter Owen, London, July 2005, 176pp.)
The authors are physiological/psychological researchers at the University of East London, and actively publishing in those fields, but there are surprising gaps in their account. In addition the facts within the papers they quote destroy their thesis that those with SSA are born gay.
They ascribe same sex attraction (SSA) to two sources: genes and hormones, which is nothing new, but add a novel twist. They wonder seriously if there are two types of SSA, one caused by hormones, the other by genes, but don't investigate the idea further.
The book looks mainstream academic, with nearly 20 pages of bibliography, but is frankly extreme. The authors argue for a 100% contribution to SSA from genetic and pre-natal hormones, and 0% environmental factors, and I don’t think many other researchers would agree. They base their conclusions mainly on twin studies.
What would you get out of buying this book? A mostly up-to-date survey of the various theories linking various biological factors to SSA, and of course their particular areas of expertise, finger length ratios, fingerprint patterns, and differences in the eye-blink reflexes between lesbian and heterosexual women. The book is fairly clearly written, and there are a few new ideas. However any social factors tend to be dismissed superficially. They argue they have succeeded in “excluding the social acquisitionists from further debate”.
What is new and genuinely interesting? Well, there is an interesting pair of comparison graphs which show that LeVay’s work on SSA-hypothalamus-structure correlation in the early ‘90s could not be duplicated. That is unusually clearly expressed. Their details about intersex studies are usefully full, and cover a few recent cases of possible interest to researchers.
The authors of this book frequently cite one of the foremost twin study researchers, JM Bailey, with approval (unlike many these days in the gay and transsexual communities) but they do not quote his summary of the origin of SSA. Bailey concluded there was a genetic component, but added, on the basis of twin studies, “There must be something in the environment.” The authors are dogmatic and say in their summary “The popular idea that sexual orientation can be influenced by social factors, such as upbringing, contagion or seduction, has no scientific backing”.
The authors primarily use twin studies to argue for a contribution of genes to SSA. Their conclusion is possible, but you might like to consult the caveats in our book My Genes Made Me Do It! (Whitehead & Whitehead 1999).
At this point I should say something about twin studies. If identical twins share the same trait they are said to be “concordant”. If they differ, they are discordant. For sexual orientation it is usual to quote concordances of about 30% from the best twin studies – but this is very misleading. I’ve been guilty of unthinkingly quoting these higher figures myself in the past. These commonly quoted concordances are called “probandwise concordances” but are intended to be subject to further calculations and are different from what are known as "pairwise concordances". Pairwise concordances are drawn from the same original data as probandwise concordances, but pairwise concordances are the ones giving the most intuitively accurate final information on the genetic contribution to SSA. Jones & Yarhouse (2000) re-calculated the pairwise concordance from the original data in Bailey’s paper. They find for identical twins (male or female) that if one has SSA the chances of the second one or co-twin having SSA are 11% for either gender - only 1 time in 9. Here is how the final (pairwise) concordances look:
In other words, it is the overwhelming norm that if one identical twin has SSA, the other usually doesn’t. Since identical twins have identical genes the conclusion is inescapable – we are mostly not born gay, and genes are not much responsible. This is not just a test for the influence of genes, but a test for the influence of any common factors before birth, common womb environment, for example. The effect shown in the figure includes all common factors before birth. Born gay? No.
To say it a different way: for all the biological factors one could list that might affect a child before birth, their effects are summed up in the diagram above. They are in summary, weak. Remarkably, this includes all the factors we don’t know about and are yet to be discovered. Whatever their apparent individual strength, they add up to something quite weak. This must remain true in the future unless Bailey’s results (taken from the Australian twin registry and generally considered the best survey) are totally erroneous, which is highly unlikely because they have good support from other twin work.
Based on twin studies the authors opt for a genetic contribution of 30% (error limits 0-50%). From this, the reader will see there is uncomfortably much variation in the various surveys and models. The genetic contribution might be nearer 0%.
Twin studies try to estimate the relative influence of genetics, shared family environment and unique individual experiences (random factors) on the development of any trait. The authors try to argue that twin studies completely rule out family influence. They don’t. Bailey has shown by interviews with discordant identical twins, that a shared environment may be interpreted quite differently by identical twins, so that different reactions to common family events can show up as random factors. To be fair, however, this work of Bailey is not universally known. The authors seek to put hormonal influences in the random factors category of the twin study model.
Recently published material (after Born Gay) in which the entire human genome was scanned found no significant associations with SSA. No SSA genes at all! (Mustanski et al 2005, including Hamer as author). Perhaps closer tests will eventually show something, but at present the gene hypothesis is not supported, and any genetic contribution should be nearer 0% than 50%. Also, Hamer’s own previous work suggesting an SSA-gene association is not supported by a second attempt to replicate his original findings.
The authors argue for a roughly 30% genetic contribution to SSA, then say that the remaining influences (70%) are prenatal exposure to hormones. Unfortunately their case falls down, as most do, on those same twin studies. In twin studies “genetic” includes all the prenatal common factors, so the only way for hormones to be responsible for an additional 70% would be if hormones affected onetwin and not the other. However it is well known that opposite-sex twins in the same womb influence each other hormonally, so therefore extremely unlikely that identical twins would not. We could argue for some very hypothetical and unlikely extreme exposure to sex-hormones (originating, say, in a transient benign sex-hormone-secreting tumour in one identical twin) that might affect only that twin, but both identical twins should be affected by the diffusion of those hormones in the intimate womb environment. It is almost inconceivable that one twin only would be affected. But this puts hormonal factors back in the “30% common factors” class, they are not a 70% add-on. In fact hormones must be quite a minor contributor.
One would expect such a book to give a reasoned derivation for the estimate of the supposed 70% hormonal contribution, but it doesn't. The authors only say it is “largely determined” without giving numerical supporting evidence. Obviously you cannot move from a statement as vague as that to entitling your book Born Gay. But they do.
They also mention the classic book by Bell, Weinberg and Hammersmith (1981), but don’t mention the bulk of that work, which was Path Analysis. Van Wyk and Geist (1984) who got similar results, pointed out that both sets of Path Analysis studies showed family effects were definitely involved to a significant degree, by all usual statistical criteria, though Bell, Weinberg and Hammersmith were reluctant to say so for some non-scientific reason. Both studies also showed strong random effects.
So family effects are significant, but the authors of Born Gay have not studied this corner of the field properly.
“It is hard to see why parents should influence the sexuality of their children,” the authors say. No, it is not hard, and this shows surprising ignorance of the literature on conventional stages of the development of heterosexuality in youngsters. A lot is known scientifically about this – why do activists consistently portray the origins of heterosexuality and homosexuality as a vast mystery?
Spitzer’s study on gays who have changed their sexual orientation is treated poorly. The authors do not really give the inescapable main point of the study – change is possible for at least some people. It is also attacked in a way which would be considered extreme if applied to any other therapy, demanding a ridiculous standard of proof. Frankly any reasonable scientist would conclude that Spitzer’s result is well supported. Spitzer’s study is the best recently available for establishing that at least some with SSA can change profoundly. But the authors next state that Spitzer’s results must be wrong because sexual orientation cannot be changed! (No references given). This is abysmal argument, and I wonder if they would let their graduate students be as sloppy as this.
The authors also think that many of those who approach therapists for help are “coerced”, but have obviously not encountered the surveys which reveal clients’ motives are primarily rejection of the gay life style, and they are not coerced.
Therapy methods are described as “…draconian – no evidence that they work”. They do not cite examples, nor can they. This betrays a surprising lack of knowledge about what is going on currently in therapy.
“There is no evidence that feelings of inadequacy predispose towards homosexuality”, but some mental health professionals will know many for whom this was an obvious factor.
The authors spend several pages trying to say bisexuals do not exist, to bolster their case for simple origins for SSA. This is topical at present because Bailey (2005) could not find people in whom same- and opposite-sex attraction were evenly balanced. He found that in those with both orientations, either heterosexuality is about 4x as strong as homosexual attraction, or vice versa. So, yes, there could easily be a tendency or pressures to gravitate to one side or the other, but according to Bailey, people with mixed orientations definitely exist.
Born Gay? Sorry guys. Don’t think so.
Bailey (2005) See article in New York Times, July 5, by Benedict Carey.
Bell, AP, Weinberg, MS & Hammersmith , SK (1981) Sexual Preference: Its Development in Men and Women. Indiana University Press, Bloomington , Indiana .
Jones, SL and Yarhouse , MA (2000) Homosexuality. The Use of Scientific Research in the Church’s Moral Debate. IVP, Downer’s Grove, Illinois .
Mustanski, BS, DuPree, MG, Nievergelt, CM, Bocklandt, S, Schork , NJ , Hamer, DH (2005) A genomewide scan of male sexual orientation. Human Genetics. On line, unpaged.
Van Wyk, PH & Geist, CS (1984). Psychosocial development of heterosexual, bisexual and homosexual behavior.Archives of Sexual Behavior 13:505-544.
Whitehead, NE & Whitehead, BK (1999) My Genes Made Me Do It!.