A team of international researchers has confirmed that there's no such thing as a gay gene.' But that doesn't mean biology is off the hook in terms of explaining why homosexuality exists in the human population. It's not about genetics, say the researchers, it's about epigenetics the process in which the expression of DNA is influenced by any number of external factors. And in the case of homosexuality, these factors are happening inside the womb.
And indeed, when looking at this issue through a strictly Darwinian lens, it makes no sense for homosexuality to exist in the gene pool. Given the "selfish gene" theory, it couldn't possibly be a beneficial adaptation it's a trait that could never be passed down. But that said, homosexuality is common for men and women in most cultures an observation that clearly demands an explanation.
An added layer of information
Writing in The Quarterly Review of Biology, researchers William Rice, a professor at the University of California, Santa Barbara, and Urban Friberg, a professor at Uppsala University in Sweden, believe that homosexuality can be explained by the presence of epi-marks temporary switches that control how our genes are expressed during gestation and after we're born.
Specifically, the researchers discovered sex-specific epi-marks which, unlike most genetic switches, get passed down from father to daughter or mother to son. Most epi-marks don't normally pass between generations and are essentially "erased." Rice and Friberg say this explains why homosexuality appears to run in families, yet has no real genetic underpinning.
Epigenetic mechanisms can be seen as an added layer of information that clings to our DNA. Epi-marks regulate the expression of genes according to the strength of external cues. Genes are basically the instruction book, while epi-marks direct how those instructions get carried out. For example, they can determine when, where, and how much of a gene gets expressed.
Moreover, epi-marks are usually produced from scratch with each generation but new evidence is showing that they can sometimes carryover from parent to child. It's this phenomenon that gives the impression of having shared genes with relatives.
Masculinization and feminization
To reach this conclusion, Rice and Friberg created a biological and mathematical model that charted the role of epigenetics in homosexuality. They did so by applying evolutionary theory to recent advances in the molecular regulation of gene expression and androgen-dependent sexual development.
Normally, sex-specific marks that are triggered during early fetal development work to protect boys and girls in the womb from undergoing too much natural variation in testosterone, which should normally happen later in a pregnancy. Epigenetic processes prevent female fetuses from becoming masculinized when testosterone exposure gets too high, and vice versa for males.
Moreover, epi-marks also protect different sex-specific traits from swinging in the opposite direction; some affect the genitals, others sexual identity and others affect sexual orientation. And at the same time, these epi-marks can be transmitted across generations from fathers to daughters, or mothers to sons which can cause reversed effects like the feminization of some traits in boys (like sexual preference), or a partial masculinization of girls.
Essentially, Rice and Friberg have discovered the presence of "sexually antagonistic" epi-marks which sometimes carryover to the next generation and cause homosexuality in opposite-sex offspring.
And importantly in order to satisfy the rules of Darwinian selection the researchers noted through their mathematical modeling that these epigenetic characteristics can easily proliferate in the population because they increase the fitness of the parent; these epi-marks normally protect parents from natural variation in sex hormone levels during fetal development. They also only rarely escape erasure and reduce the fitness of offspring.
The entire study will appear online at The Quarterly Review of Biology later this week and go by the title, "Homosexuality as a consequence of epigenetically canalized sexual development."
i hate JSTOR formatting...
