Epigenetics is the expression of genes controlled by short-term transitions known as epi-marks. These epi-marks seem to be an important factor that is often not taken into consideration for contributing to the deep-rooted mystery of why homosexuality exists, and new research says it should.

A new study, published in The Quarterly Review of Biology, reveals that sex-specific epi-marks can contribute to homosexuality. Normally, these epi-marks are not inherited and are thus lost. However when they are not lost, they are able to transfer from father to daughter or mother to son.

From the viewpoint of evolution, homosexuality is a characteristic that does not progress or continue in the process of Darwinian natural selection.

Homosexuality appears in males and females in every culture. Earlier research has established that homosexuality is passed between generations in families, suggesting the root of sexual preference is genetic. Although to date, no gene for homosexuality has been found. Therefore, studies continue to search for a genetic connection.

An earlier study proposed a model using the theory of Darwinian evolution and the presence of male homosexuality in human populations combined with the idea of sexually antagonistic selection.

Researchers from the Working Group on Intragenomic Conflict at the National Institute for Mathematical and Biological Synthesis (NIMBioS) have used the evolution theory combined with current updates in the molecular regeneration of gene expression and androgen-reliant sexual development to create a mathematical and biological model that explains the role of epigenetics in homosexuality.

Epi-marks act as another layer of information fused to our genes that control their expression. Essentially, genes hold the directions, while epi-marks instruct how they are put into motion and completed.

Historically, epi-marks are eliminated and created anew with each generation, but new research shows that they can occasionally pass over between generations, causing similarities within families and appearing as shared genes.

Sex-specific epi-marks are made during early fetal development and serve as security against the considerable natural variation in testosterone that happens in late fetal development. For example, sex-specific epi-marks prevent female fetuses from becoming masculine when there are unusually high testosterone levels present, and vice versa for male fetuses.

Different kinds of epi-marks safeguard different sex-specific characteristics; some protect the genitals, others protect sexual identity, and this study suggests others keep safe sexual partner preference.

When these epi-marks are passed between generations from fathers to daughters or mothers to sons, they have the potential to result in reverse effects. The outcome is feminization of characteristics in sons or masculinization of some characteristics in daughters, occasionally affecting sexual preference.

This study provides an answer to the evolutionary mystery of homosexuality, suggesting that “sexually antagonistic” epi-marks can, at times, pass from generation to generation and result in homosexuality in opposite-sex children. The mathematical modeling shows that the coding of the genes for these epi-marks can spread in the population easily because they invariably raise the fitness of the parent, but are very rarely erased and do not reduce fitness in their children.

The study’s co-author Sergey Gavrilets, NIMBioS’ associate director for scientific activities and a professor at the University of Tennessee-Knoxville, concluded, “Transmission of sexually antagonistic epi-marks between generations is the most plausible evolutionary mechanism of the phenomenon of human homosexuality.”

Written by Kelly Fitzgerald