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Epigenetic Theories of Homosexuality

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Epigenetic marks

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Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. These markers allows for modifications of histone proteins[1] especially on the methyl and acetyl groups that bind to DNA histones. Such modifications change how the proteins function and alter gene expression.[2] Hence, these changes alter the functions of histone proteins, which subsequently influence the way genes are expressed.[3] Epigenetic marks plays a part in both fetal and sexual development. These marks promote normal sexual development and in the case of fetal development, they can be passed on to offspring through the process of mitosis. When they are transferred from one parent to an offspring of the opposite sex, epigenetic marks can contribute to an altered sexual development, thus leading to masculinization of female offspring and feminization of male offspring. Such alterations were found to be responsible for sexual differences in the human brain[4], which may be related to sexual orientation of humans.

Recent studies suggest that epi-marks may influence the sensitivity of a fetus to testosterone and estrogen in the womb, altering the "masculinity" or "femininity" of humans which may possibly result in same-sex attraction[5]. With an accuracy of 70%, 9 methylation sites are found to possibly be identifications for homosexuality[6]. These regions were found to be associated with transcriptional regulation and axonal transport[7] which serves as the first example of a biomarker for the prediction of sexual orientation.

However, more studies are required to generate consistency for the strength of such a model.

Twins Studies

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Identical twins have identical DNA, which leads to the perceived conclusion that all identical twins are either heterosexual or homosexual. However, not all twins share the same sexual orientation[8], consequently leaving a gap in the explanation for homosexuality. A "gay" gene does not produce homosexuality, rather, epigenetic modifications act as temporary "switches" that regulate how the genes are expressed[9]. Moreover, another study found that only 20% of identical twins are both homosexual[10]. This suggest that homosexuality may not simply be the product of genes alone. Moreover, epigenetic transformation allows for the on-and-off switching of certain genes. including genes responsible for androgen signalling which influences the sexual orientation of one since androgen is critical in sexual development[11].

Twin studies provide potential for the genetic study of homosexuality. For example, in a study, a total of 47 pair of male identical twins' DNA - 37 pairs of discordant twins (meaning one gay and one straight) and 10 pairs who were both gays, were studied for their methlyation patterns in 140,00 regions of their DNA[12]. 5 regions of DNA methylation have been found to be related to one's sexual orientation with one region coding for proteins for nerve conduction and another region coding for proteins involved in the immune system[13]. This suggests and supports the epigenetic mark hypothesis for the effects of epigenetics on homosexuality. However, more extensive research are currently conducted to improve the generalizability of the results[14].

Epigenetics have been found to be involved in many other human differences including multiple sclerosis in monozygotic(identical) twins. There are pairs of twins that are discordant with multiple sclerosis and do not both show the trait. After gene testing, it was suggested that DNA was identical and that epigenetic differences contributed to the gene difference between identical twins.[15] Such studies suggest that epigenetics do play a part in human differences, and may be responsible for the differences in sexual orientation in identical twins[16].

Criticism

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A highly controversial topic, the biological basis of homosexuality is currently still under-researched and more studies are required to generate better consistency and generalizability to the proposed models. While genetic influences are found to be statistically significant, more studies are still neccessary for the generalizability and reliability of these theories[17].

Moreover, most studies placed more emphasis on the research of gays instead of lesbians and bi-sexuals, causing such studies to be less generalizable to homosexuality as a whole.

References

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  1. ^ Ruthenburg, A., C. Allis, and J. Wysocka. "Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark." Molecular Cell 25.1 (2007): 15-30. Print. PMID 17218268 doi:10.1016/j.molcel.2006.12.014
  2. ^ Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
  3. ^ Friberg, Urban, Sergey Gavrilets, and William R. Rice. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology 87.4 (2012): n. pag. Print. PMID 23397798 doi:10.1086/668167
  4. ^ McCarthy, Margaret M.; Nugent, Bridget M. (2015-01-01). "At the frontier of epigenetics of brain sex differences". Frontiers in Behavioral Neuroscience. 9: 221. doi:10.3389/fnbeh.2015.00221. ISSN 1662-5153. PMC 4543874. PMID 26347630.
  5. ^ "Homosexuality may be caused by chemical modifications to DNA". news.sciencemag.org. Retrieved 2015-11-15.
  6. ^ "Epigenetic Marks Tied to Homosexuality | The Scientist Magazine®". The Scientist. Retrieved 2015-11-15.
  7. ^ "EventPilot Web". ep70.eventpilotadmin.com. Retrieved 2015-11-15.
  8. ^ Bailey, J. Michael; Pillard, R. C. (1991-12-01). "A genetic study of male sexual orientation". Archives of General Psychiatry. 48 (12): 1089–1096. doi:10.1001/archpsyc.1991.01810360053008. ISSN 0003-990X. PMID 1845227.
  9. ^ Cite error: The named reference LiveScience2 was invoked but never defined (see the help page).
  10. ^ Bailey, J. Michael; Dunne, Michael P.; Martin, Nicholas G. (2000). "Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample". Journal of Personality and Social Psychology. 78 (3): 524–536. doi:10.1037/0022-3514.78.3.524. PMID 10743878.
  11. ^ Cite error: The named reference Richards was invoked but never defined (see the help page).
  12. ^ Ruthenburg, A., C. Allis, and J. Wysocka. "Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark." Molecular Cell 25.1 (2007): 15-30. Print. PMID 17218268 doi:10.1016/j.molcel.2006.12.014
  13. ^ Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
  14. ^ Handunnetthi, Lahiru, Adam Handel, and Sreeram V. Ramagopalan. Contribution of Genetic, Epigenetic and Transcriptomic Differences to Twin Discordance in Multiple Sclerosis. Ebsco Host. Psyc Info, 2010. Web. PMID 20819009 doi:10.1586/ern.10.116
  15. ^ Handunnetthi, Lahiru, Adam Handel, and Sreeram V. Ramagopalan. Contribution of Genetic, Epigenetic and Transcriptomic Differences to Twin Discordance in Multiple Sclerosis. Ebsco Host. Psyc Info, 2010. Web. PMID 20819009 doi:10.1586/ern.10.116
  16. ^ "Medscape Log In". www.medscape.com. Retrieved 2015-12-01.
  17. ^ Pillard, R. C. & Weinrich, J. D. (1986). Evidence of familial nature of male homosexuality. Arch. Gen. Psychiat. 43, 808–12
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