New Theory: Homosexuality Is a Mistake of Nature
James R. Aist
Homosexuality is believed to be caused by some combination of biological and environmental factors. Several biological theories have been offered, the most feasible being the genetic, the hormonal and the epigenetic theories. In 2012, a new theory was introduced that combines aspects of the genetic theory with the hormonal theory. This is the epigenetic theory. Epigenetics is a relatively new and vigorously investigated field of biological science that deals with the regulation of gene expression (production of proteins) in cells. The components of chromosomes that regulate genes are called “epi-marks.” These include such things as methylated DNA and variously modified histone proteins, but do not include changes in the DNA sequences themselves that code for specific proteins.
Rice et al. (2012) published a review article presenting a speculative and hypothetical model (theory) to explain the development of homosexuality in both male and female homosexuals. Their goal was to develop a model that would explain why 1) molecular studies have failed to conclusively identify “gay genes” and 2) concordance for homosexuality between identical twins is low (click HERE). The theory draws on research supporting the hormonal theory as well as known properties and functions of epi-marks. The model would explain homosexuality on the basis of epi-mark-controlled prenatal testosterone (a sex hormone) levels, to the virtual exclusion of a role for either a strictly genetic influence or post-natal environmental influences.
Normally, epi-marks regulating sexual orientation are “erased” after they have produced the intended sexual development (i.e., heterosexual males and females). But, occasionally, a mistake is made, and the epi-mark is not erased but is, instead, passed on to the next generation. According to the model, when this mistake is made, epi-mark regulated testosterone overexposure in a female fetus would result in a masculinized female who will prefer females (a lesbian), whereas epi-mark regulated testosterone underexposure in a male fetus would result in a feminized male who will prefer males (a gay). The low concordance in twin studies would be explained not by a low-level genetic influence, as is usually assumed, but by the occasional passing of testosterone-enhancing epi-marks from father to daughter (creating a lesbian) and of testosterone-limiting epi-marks from mother to son (creating a gay man).
It is interesting to note that this model posits homosexuality as an aberrant accident of nature, in which normal prenatal development of a fetus produces the intended effect (heterosexuality), and abnormal prenatal development produces an unintended effect (homosexuality) by mistake. Abnormal prenatal development results when a mistake is made and an epi-mark in a parent is not erased, but is, instead, passed on to the offspring, where its effect (homosexuality) is seen in the subsequent generation. Thus, according to this theory, homosexuality is a mistake of nature.
Although this model is highly speculative and presently has very little, if any, direct experimental support, it does have merit as a scientific hypothesis, because 1) it would explain both male and female homosexuality, 2) it could explain the low concordance for homosexuality found in twin studies, 3) it seems to provide a feasible explanation for the long-term survival of a reproductively deleterious trait in the human population, and 4) it is, at least to some extent, testable. Only further research will determine whether or not this theory will join the many previous theories purporting to represent an almost exclusive influence on the development of homosexuality, all of which have failed.
Twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epigenetics, hormones, etc.) on the development of homosexuality in adults is only weak to weakly moderate (click HERE). Thus, post-natal influences (e.g., cultural, social and experiential factors) are far more influential than is epigenetics in the development of homosexuality (click HERE).
Rice, G., et al. 2012. Homosexuality as a Consequence of Epigenetically Canalized Sexual Development. Quarterly Review of Biology 87:343-368.
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