Epigenetic theories of homosexuality

[1][2][3] Epigenetics examines the set of chemical reactions that switch parts of the genome on and off at strategic times and locations in the organism's life cycle.

DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome.

One team of researchers examined the effects of epi-marks buffering XX fetuses and XY fetuses from certain androgen exposure and used published data on fetal androgen signaling and gene regulation through non-genetic changes in DNA packaging to develop a new model for homosexuality.

[8] Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth.

[9] Epigenetic marks are modifications of the methyl and acetyl groups that bind to DNA histones thereby changing how the proteins function and as a result, alter gene expression.

Epigenetic transformation allows the on and off switching of certain genes, subsequently shaping how cells respond to androgen signaling, which is critical in sexual development.

[1] Epi-marks normally protect parents from variation in sex hormone levels during fetal development, but can carry over across generations and subsequently lead to homosexuality in opposite-sex offspring.

This demonstrates that gene coding for these epi-marks can spread in the population because they benefit the development and fitness of the parent but only rarely escape erasure, leading to same-sex sexual preference in offspring.

[1] Tuck C. Ngun and Eric Vilain published a paper in 2014 in which they evaluated and critiqued the epigenetic model proposed by Rice and colleagues in 2012.

Ngun and Vilain agreed with much of Rice's model, but disagreed that "sex-reversing sensitivity to androgen signaling via epigenetic markers will result in homosexuality in both sexes", noting that non-heterosexuality is far more common in women.

[8] Also, a report of a study of 34 male monozygotic twin pairs discordant for sexual orientation revealed no support for the epigenetic hypothesis.