From an evolutionary perspective, homosexuality is a trait that would not be expected to develop and persist in the face of Darwinian natural selection. Previous studies have shown that homosexuality runs in families, leading most researchers to presume a genetic underpinning of sexual preference. However, no major gene for homosexuality has been found despite numerous studies searching for a genetic connection.
In the current study, researchers from the Working Group on Intragenomic Conflict at the National Institute for Mathematical and Biological Synthesis integrated evolutionary theory with recent advances in the molecular regulation of gene expression and androgen-dependent sexual development to produce a biological and mathematical model that delineates the role of epigenetics in homosexuality.
Study co-author Sergey Gavrilets explained that epi-marks constitute an extra layer of information attached to our genes’ backbones that regulate their expression. While genes hold the instructions, epi-marks direct how those instructions are carried out – when, where and how much a gene is expressed during development. Epi-marks are usually produced anew each generation, but recent evidence demonstrates that they sometimes carryover between generations and thus can contribute to similarity among relatives, resembling the effect of shared genes.
The study notes that sex-specific epi-marks produced in early fetal development protect each sex from the substantial natural variation in testosterone that occurs during later fetal development. Sex-specific epi-marks stop girl fetuses from being masculinized when they experience atypically high testosterone, and vice versa for boy fetuses. Different epi-marks protect different sex-specific traits from being masculinized or feminized – some affect the genitals, others sexual identity, and yet others affect sexual partner preference.
However, Gavrilets contends that when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons, such as sexual preference, and similarly a partial masculinization of daughters.
If correct, the new findings may go a long way to explaining the riddle of homosexuality, showing that “sexually antagonistic” epi-marks, which normally protect parents from natural variation in sex hormone levels during fetal development, sometimes carryover across generations and cause homosexuality in opposite-sex offspring. The mathematical modeling in the study demonstrates that genes coding for these epi-marks can easily spread in the population because they always increase the fitness of the parent but only rarely escape erasure and reduce fitness in offspring. “Transmission of sexually antagonistic epi-marks between generations is the most plausible evolutionary mechanism of the phenomenon of human homosexuality,” concluded Gavrilets.
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