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{{Short description|Possible causes of homosexuality}}
⚫ Guys, this is fake'''Epigenetic theories of homosexuality''' concerns the study of changes in gene expression or cellular ] caused by mechanisms other than changes in the underlying DNA sequence. ] 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. Instead of affecting the organism's DNA sequence, non-genetic factors cause the organism’s genes to express themselves differently. DNA in the human body is wrapped around histones, which are proteins that package and order DNA into structural units. DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome.<ref> Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013. </ref> 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 environment.
⚫ {{Sexual orientation}}
⚫ 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 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.<ref name="Richards">Richards, Sabrina. The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.</ref> The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert sexual preference in individuals without altering genitalia or sexual identity.<ref>"National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.</ref>
'''Epigenetic theories of homosexuality''' concern the studies of changes in ] or cellular ] caused by mechanisms other than changes in the underlying ], and their role in the development of ].<ref name="Friberg"/><ref>{{cite journal |last1=Rice |first1=William R. |last2=Friberg |first2=Urban |last3=Gavrilets |first3=Sergey |title=Homosexuality via canalized sexual development: A testing protocol for a new epigenetic model |journal=BioEssays |date=September 2013 |volume=35 |issue=9 |pages=764–770 |doi=10.1002/bies.201300033|pmid=23868698 |pmc=3840696 }}</ref><ref>{{cite journal |last1=Rice |first1=William R. |last2=Friberg |first2=Urban |last3=Gavrilets |first3=Sergey |title=Sexually antagonistic epigenetic marks that canalize sexually dimorphic development |journal=Molecular Ecology |date=April 2016 |volume=25 |issue=8 |pages=1812–1822 |doi=10.1111/mec.13490|pmid=26600375 |bibcode=2016MolEc..25.1812R |s2cid=71599 |url=https://liu.diva-portal.org/smash/get/diva2:929171/FULLTEXT01 }}</ref> ] examines the set of chemical reactions that switch parts of the ] on and off at strategic times and locations in the organism's ]. However, epigenetic theories tangle a multiplicity of initiating causes and resulting final effects and will never lead to a single cause or single result. Hence, any interpretation of such theories may not focus on just one isolated reason of a multiplicity of causes or effects.<ref>{{Cite web |url=https://www.volkswagenstiftung.de/de/evolution/ausbildungskonzepte.html |title=Ausbildungskonzept "Integrated approaches to teach and study the role of evolution for the emergence of biological complexity" |access-date=2016-11-28 |archive-url=https://web.archive.org/web/20170701141625/https://www.volkswagenstiftung.de/de/evolution/ausbildungskonzepte.html |archive-date=2017-07-01 |url-status=dead }}</ref>
This research gives support to the hypothesis that homosexuality stems from the under expression of certain genes on the DNA sequence involved with sexual preferences. This theory as well as other concepts involved with epi-marks, twin studies, and fetal androgen signaling will be explored here.

⚫ 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 ]s, which are ]s that package and order DNA into structural units. DNA and histone are covered with ]s known as the ], which shapes the physical structure of the genome.<ref> Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013.</ref> 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 ]s buffering ] ]es and ] fetuses from certain ] exposure and used published data on fetal androgen signaling and ] through non-genetic changes in DNA packaging to develop a new model for homosexuality.<ref name="Richards">Richards, Sabrina. The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.</ref> The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert ] in individuals without altering ] or ].<ref>"National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.</ref> However, a later study found that male homosexuality is not linked to low androgen sensitivity or "sex-reversed" epi-marks.<ref name="Ngun">{{cite book |last1=Ngun |first1=TC |last2=Vilain |first2=E |title=The biological basis of human sexual orientation: is there a role for epigenetics? |chapter=The Biological Basis of Human Sexual Orientation |series=Advances in Genetics |date=2014 |volume=86 |pages=167–84 |doi=10.1016/B978-0-12-800222-3.00008-5 |pmid=25172350|isbn=978-0-12-800222-3 }}</ref>


== Epigenetic marks == == Epigenetic marks ==
{{details|Epigenetics}} {{details|Epigenetics}}


Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. Moreover, epi-marks are modifications of histone proteins.<ref>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}} </ref> 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.<ref>Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis</ref> Epi-marks change how the histones function and as a result, influence the way genes are expressed.<ref name="Friberg">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}}</ref> Epigenetic marks are intended to promote normal sex development while in fetal development, however, they can be passed on to an offspring through the process of mitosis. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to mascunlinization of female offspring and feminization of male offspring.<ref name="LiveScience"> LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.</ref> However, these epi-marks hold no consistency between individuals in regard to strength and variability. Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during ] and after birth. Moreover, epi-marks are modifications of histone proteins.<ref>{{cite journal |last1=Ruthenburg |first1=AJ |last2=Allis |first2=CD |last3=Wysocka |first3=J |title=Methylation of lysine 4 on histone H3: intricacy of writing and reading a single epigenetic mark |journal=Molecular Cell |date=12 January 2007 |volume=25 |issue=1 |pages=15–30 |doi=10.1016/j.molcel.2006.12.014 |pmid=17218268|doi-access=free }}</ref> Epigenetic marks are modifications of the ] and ] groups that bind to DNA histones thereby changing how the proteins function and as a result, alter gene expression.<ref>Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis</ref> Epi-marks change how the histones function and as a result, influence the way genes are expressed.<ref name="Friberg">{{cite journal |last1=Rice |first1=WR |last2=Friberg |first2=U |last3=Gavrilets |first3=S |title=Homosexuality as a consequence of epigenetically canalized sexual development |journal=The Quarterly Review of Biology |date=December 2012 |volume=87 |issue=4 |pages=343–68 |doi=10.1086/668167 |pmid=23397798|s2cid=7041142 }}</ref> Epigenetic marks promote normal ] during ]. However, they can be passed on to ] through the process of ]. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to ] of female offspring and ] of male offspring.<ref name="LiveScience"> LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.</ref> However, these epi-marks hold no consistency between individuals in regard to strength and variability.{{citation needed|date=April 2018}}


== Twin studies == == Twin studies ==


Identical twins have identical DNA, which leads to the perceived conclusion that all identical twins are either 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<ref name="LiveScience"/> Only twenty percent of identical twins are both homosexual which leads to the hypothesis that even though identical twins share the same DNA, homosexuality is created by something else rather than the genes. Epigenetic transformation allows the on and off switch of certain genes, subsequently shaping how cells respond to androgen signaling, which is critical in sexual development.<ref name="Richards"/> ]s have nearly identical DNA, which leads to the perceived conclusion that all identical twins are either ] or homosexual. However, it is evident that this is not the case, consequently leaving a gap in the explanation for homosexuality. Epigenetic modifications act as temporary "switches" that regulate how the genes are expressed.<ref name="LiveScience"/> 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.<ref>Balter, M. (2015). Can epigenetics explain homosexuality puzzle?. https://www.science.org/doi/full/10.1126/science.350.6257.148</ref> 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.<ref name="Richards"/>
Another example of epigenetic consequences is evident in 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.<ref>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}}</ref> Another example of epigenetic consequences is evident in ] in ] (identical) twins. There are pairs of twins that are discordant with multiple sclerosis and do not both show the trait. After ], it was suggested that DNA was identical and that epigenetic differences contributed to the gene difference between identical twins.<ref>{{cite journal |last1=Handunnetthi |first1=L |last2=Handel |first2=AE |last3=Ramagopalan |first3=SV |title=Contribution of genetic, epigenetic and transcriptomic differences to twin discordance in multiple sclerosis. |journal=Expert Review of Neurotherapeutics |date=September 2010 |volume=10 |issue=9 |pages=1379–81 |doi=10.1586/ern.10.116 |pmid=20819009|s2cid=37946401 |doi-access=free }}</ref>


== Effects of fetal androgen exposure == == Effects of fetal androgen exposure ==


While in the fetal stages, hormonal influences of ], specifically ], 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.<ref name="Friberg"/> 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.<ref>Brook, Charles, Gerard S. Conway, and Melissa Hines. "Androgen and Psychosexual Development: Core Gender Identity, Sexual Orientation, and Recalled Childhood Gender Role Behavior in Women and Men with Congenital Adrenal Hyperplasia (CAH)." Journal of Sex Research 41.1 (2004): 75-81. Online {{pmid|15216426}}</ref> While in the fetal stages, hormonal influences of ], specifically ], 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.<ref name="Friberg"/> 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.<ref>{{cite journal |last1=Hines |first1=M |last2=Brook |first2=C |last3=Conway |first3=GS |title=Androgen and psychosexual development: core gender identity, sexual orientation and recalled childhood gender role behavior in women and men with congenital adrenal hyperplasia (CAH). |journal=Journal of Sex Research |date=February 2004 |volume=41 |issue=1 |pages=75–81 |doi=10.1080/00224490409552215 |pmid=15216426|s2cid=33519930 }}</ref>


== Heritability == == Heritability ==


New epi-marks are usually produced with each generation, but it is believed that these marks sometimes carry over between generations. Sex-specific epi-marks are produced in early fetal development that protect each sex from the natural disparity in testosterone that occurs during later stages of fetal development. Different epi-marks protect different sex-specific traits from being masculinized or feminized—some affect the genitals, others affect sexual identity, and yet others affect sexual preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons and similarly a partial masculinization of daughters. Furthermore, the reversed effects of feminization and masculinization can lead to a reversed sexual preference. For example, sex-specific epi-marks normally prevent female fetuses from being masculinized through exposure of atypically high testosterone, and vice versa for male fetuses. Sex-specific epi-marks that are normally erased and not passed between generations, can lead to an altered sexual preference when they escape erasure and are transferred from a father's genes to a daughter or from a mother's genes to a son.<ref name="Friberg"/> 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 mismatched sexual preference in offspring. New epi-marks are usually produced with each generation, but these marks sometimes carry over between ]s. Sex-specific epi-marks are produced in early fetal development that protect each sex from the natural disparity in testosterone that occurs during later stages of fetal development. Different epi-marks protect different sex-specific traits from being masculinized or feminized—some affect the genitals, others affect sexual identity, and yet others affect sexual preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons and similarly a partial masculinization of daughters. Furthermore, the reversed effects of feminization and masculinization can lead to a reversed sexual preference. For example, sex-specific epi-marks normally prevent female fetuses from being masculinized through exposure of atypically high ], and vice versa for male fetuses. Sex-specific epi-marks are normally erased and not passed between generations. However, they can sometimes escape erasure and are then transferred from a father's genes to a daughter or from a mother's genes to a son. When this happens, this may lead to an altered sexual preference.<ref name="Friberg"/> 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 ] 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|date=October 2015}}

== 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".<ref name="Friberg"/> 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.<ref name="Ngun"/>
== Possible applications for sexual orientation change ==
Also, a report of a study of 34 male monozygotic twin pairs discordant for sexual orientation revealed no support for the epigenetic hypothesis.<ref name="Bocklandt">{{cite journal |last1=Bocklandt |first1=Sven |last2=Lin |first2=Wen |last3=Sehl |first3=Mary E. |last4=Sánchez |first4=Francisco J. |last5=Sinsheimer |first5=Janet S. |last6=Horvath |first6=Steve |last7=Vilain |first7=Eric |title=Epigenetic Predictor of Age |journal=PLOS ONE |date=22 June 2011 |volume=6 |issue=6 |pages=e14821 |doi=10.1371/journal.pone.0014821|pmid=21731603 |pmc=3120753 |bibcode=2011PLoSO...614821B |doi-access=free }}</ref>
⚫ {{Main|Sexual orientation change efforts}}
Following a late 2012 publication on possible epigenetic origins of homosexuality,<ref>{{cite news|url=http://www.sciencedaily.com/releases/2012/12/121211083212.htm|title=Epigenetics may be a critical factor contributing to homosexuality, study suggests|publisher=Science Daily|date=11 December 2012}}</ref> some people {{who ?|date=September 2014}} have suggested that it might be possible to alter one's sexual orientation with ],<ref>{{cite news|author=Tim Spector|title=Why Does the Search for a Gay Gene Freak Everyone Out?|url=http://www.slate.com/blogs/outward/2014/02/18/gay_gene_research_why_does_it_make_people_freak_out.html|work=Slate|date=February 18, 2014}}</ref> similarly to treatment of ], ] or ]. Prenatal ] may also be used to reduce the probability of homosexuality in females by compensating the effects of androgen overexposure.<ref>{{cite news|author=Shari Roan|title=Medical treatment carries possible side effect of limiting homosexuality|url=http://articles.latimes.com/2010/aug/15/science/la-sci-adrenal-20100815|work=Los Angeles Times|date=August 15, 2010}}</ref>


== References == == References ==
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Latest revision as of 00:45, 28 June 2024

Possible causes of homosexuality
Sexual orientation
Sexual orientations
Related terms
Research
Animals
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Epigenetic theories of homosexuality concern the studies of changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence, and their role in the development of homosexuality. 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 resulting final effects and will never lead to a single cause or single result. Hence, any interpretation of such theories may not focus on just one isolated reason of a multiplicity of causes or effects.

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 histones, which are proteins that package and order DNA into structural units. DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome. 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 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. The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert sexual preference in individuals without altering genitalia or sexual identity. However, a later study found that male homosexuality is not linked to low androgen sensitivity or "sex-reversed" epi-marks.

Epigenetic marks

Further information: Epigenetics

Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. Moreover, epi-marks are modifications of histone proteins. 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. Epi-marks change how the histones function and as a result, influence the way genes are expressed. Epigenetic marks promote normal sexual development during fetal development. However, they can be passed on to offspring through the process of meiosis. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to masculinization of female offspring and feminization of male offspring. However, these epi-marks hold no consistency between individuals in regard to strength and variability.

Twin studies

Identical twins have nearly identical DNA, which leads to the perceived conclusion that all identical twins are either heterosexual or homosexual. However, it is evident that this is not the case, consequently leaving a gap in the explanation for homosexuality. Epigenetic modifications act as temporary "switches" that regulate how the genes are expressed. 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. 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. Another example of epigenetic consequences is evident in 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.

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. 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.

Heritability

New epi-marks are usually produced with each generation, but these marks sometimes carry over between generations. Sex-specific epi-marks are produced in early fetal development that protect each sex from the natural disparity in testosterone that occurs during later stages of fetal development. Different epi-marks protect different sex-specific traits from being masculinized or feminized—some affect the genitals, others affect sexual identity, and yet others affect sexual preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons and similarly a partial masculinization of daughters. Furthermore, the reversed effects of feminization and masculinization can lead to a reversed sexual preference. For example, sex-specific epi-marks normally prevent female fetuses from being masculinized through exposure of atypically high testosterone, and vice versa for male fetuses. Sex-specific epi-marks are normally erased and not passed between generations. However, they can sometimes escape erasure and are then transferred from a father's genes to a daughter or from a mother's genes to a son. When this happens, this may lead to an altered sexual preference. 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.

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

References

  1. ^ Rice, WR; Friberg, U; Gavrilets, S (December 2012). "Homosexuality as a consequence of epigenetically canalized sexual development". The Quarterly Review of Biology. 87 (4): 343–68. doi:10.1086/668167. PMID 23397798. S2CID 7041142.
  2. Rice, William R.; Friberg, Urban; Gavrilets, Sergey (September 2013). "Homosexuality via canalized sexual development: A testing protocol for a new epigenetic model". BioEssays. 35 (9): 764–770. doi:10.1002/bies.201300033. PMC 3840696. PMID 23868698.
  3. Rice, William R.; Friberg, Urban; Gavrilets, Sergey (April 2016). "Sexually antagonistic epigenetic marks that canalize sexually dimorphic development". Molecular Ecology. 25 (8): 1812–1822. Bibcode:2016MolEc..25.1812R. doi:10.1111/mec.13490. PMID 26600375. S2CID 71599.
  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. ^ 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.
  8. ^ Ngun, TC; Vilain, E (2014). "The Biological Basis of Human Sexual Orientation". The biological basis of human sexual orientation: is there a role for epigenetics?. Advances in Genetics. Vol. 86. pp. 167–84. doi:10.1016/B978-0-12-800222-3.00008-5. ISBN 978-0-12-800222-3. PMID 25172350.
  9. Ruthenburg, AJ; Allis, CD; Wysocka, J (12 January 2007). "Methylation of lysine 4 on histone H3: intricacy of writing and reading a single epigenetic mark". Molecular Cell. 25 (1): 15–30. doi:10.1016/j.molcel.2006.12.014. PMID 17218268.
  10. Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
  11. ^ "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
  13. Handunnetthi, L; Handel, AE; Ramagopalan, SV (September 2010). "Contribution of genetic, epigenetic and transcriptomic differences to twin discordance in multiple sclerosis". Expert Review of Neurotherapeutics. 10 (9): 1379–81. doi:10.1586/ern.10.116. PMID 20819009. S2CID 37946401.
  14. Hines, M; Brook, C; Conway, GS (February 2004). "Androgen and psychosexual development: core gender identity, sexual orientation and recalled childhood gender role behavior in women and men with congenital adrenal hyperplasia (CAH)". Journal of Sex Research. 41 (1): 75–81. doi:10.1080/00224490409552215. PMID 15216426. S2CID 33519930.
  15. Bocklandt, Sven; Lin, Wen; Sehl, Mary E.; Sánchez, Francisco J.; Sinsheimer, Janet S.; Horvath, Steve; Vilain, Eric (22 June 2011). "Epigenetic Predictor of Age". PLOS ONE. 6 (6): e14821. Bibcode:2011PLoSO...614821B. doi:10.1371/journal.pone.0014821. PMC 3120753. PMID 21731603.
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