Epigenetic theories of homosexuality

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Epigenetic theories of homosexuality concern the studies of changes in

DNA sequence, and their role in the development 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. However, epigenetic theories tangle a multiplicity of initiating causes and of resulting final effects and will never lead to a single cause or a single result. Hence, any interpretation of such theories may not focus just one isolated reason of a multiplicity of causes or of effects.[4]

Instead of affecting the organism's DNA sequence, non-genetic factors may cause the organism's genes to express themselves differently. DNA in the human body is wrapped around

chemical tags known as the epigenome, which shapes the physical structure of the genome.[5]
It tightly wraps inactive genes on the DNA sequence making those genes unreadable while loosely wrapping active genes making them more expressive. The more tightly wrapped the gene, the less it will be expressed in the organism. These epigenetic tags react to stimuli presented from the outside world. It adjusts specific genes in the genome to respond to humans' rapidly changing environments. The idea of epigenetics and gene expression has been a theory applied to the origins of homosexuality in humans. One team of researchers examined the effects of
genitalia or sexual identity.[7] However, a later study found that male homosexuality is not linked to low androgen sensitivity or "sex-reversed" epi-marks.[8]

Epigenetic marks

Further information: Epigenetics

Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during

masculinization of female offspring and feminization of male offspring.[11] However, these epi-marks hold no consistency between individuals in regard to strength and variability.[citation needed
]

Twin studies

heterosexual or homosexual. However, it is evident that this is not the case, 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.[11] Of the pairs of identical twins in which one twin is homosexual, the other twin, despite having the same genome, only has a 20-50% chance of being homosexual as well.[12] This leads to the hypothesis that homosexuality is created by something else rather than the genes. 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.[6]
Another example of epigenetic consequences is evident in
gene testing, it was suggested that DNA was identical and that epigenetic differences contributed to the gene difference between identical twins.[13]

Effects of fetal androgen exposure

While in the fetal stages, hormonal influences of androgen, specifically testosterone, cause feminine qualities in regard to sexual development in females and masculine qualities in males. In typical sexual development, females are exposed to minimal amounts of testosterone, thus feminizing their sexual development, while males are typically exposed to high levels of testosterone, which masculinize their development. Epi-marks play a critical role in this development by acting as a buffer between the fetus and androgen exposure. Moreover, they predominantly protect XY fetuses from androgen underexposure while protecting XX fetuses from androgen overexposure.[1] However, when androgen overexposure happens in XX fetuses, research suggests they can show masculinized behavior in comparison to females who undergo normal levels of androgen exposure. The research also suggests that excess androgen exposure in females led to reduced heterosexual interest in adulthood than did females with normal levels of androgen.[14]

Heritability

New epi-marks are usually produced with each generation, but these marks sometimes carry over between

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.[citation needed
]

Limitations of the hypothesis

Epigenetic explanations for sexual orientation are still purely speculative. W. Rice and colleagues say that they "cannot provide definitive evidence that homosexuality has a epigenetic underpinning".[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.[15]

References

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  4. ^ "Ausbildungskonzept "Integrated approaches to teach and study the role of evolution for the emergence of biological complexity"". Archived from the original on 2017-07-01. Retrieved 2016-11-28.
  5. ^ "The Epigenome at a Glance." Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013.
  6. ^ a b Richards, Sabrina. "Can Epigenetics Explain Homosexuality?." The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.
  7. ^ "National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.
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  10. ^ Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
  11. ^ a b "Gene Regulation May Explain How Homosexuality Flourishes." LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.
  12. ^ Balter, M. (2015). Can epigenetics explain homosexuality puzzle?. https://www.science.org/doi/full/10.1126/science.350.6257.148
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