Sep 18, 2023 03:22 PM
(This post was last modified: Sep 18, 2023 03:23 PM by C C.)
https://www.theguardian.com/science/2023...rientation
EXCERPTS: Last century, when things were a whole lot worse for gay people than they are today [...] For this reason, the occasional report of a “gay” gene was welcomed by many progressive people. ... Indeed, gay genes were perhaps the only example where many left-leaning people heartily embraced genetic determinism.
Awkwardly, like cold fusion, reports of genes that “cause” human homosexuality (and many other human behaviours) have failed to stand up to scrutiny – there is no “gay gene” in the sense that no one has identified genetic markers or genes that reliably predict sexual orientation in humans. Moreover, since homosexuality would generally be reckoned to reduce reproductive output of an individual, an allele (a gene variant) that directly causes homosexuality is unlikely to spread in a population.
Nonetheless [...] The widespread occurrence of homosexuality in humans and other animals, together with its high heritability but unpredictable genetics and lack of genetic markers, is a significant biological puzzle. There are three leading hypotheses for the common existence of homosexuality in human populations, one based on kin selection, one on sexually antagonistic alleles, and one on epigenetic inheritance.
Briefly, the kin selection idea is that a gene that promotes homosexual behaviour can spread in a population if homosexual people contribute significantly to the reproduction of close relatives. Although this idea is plausible, the lack of any genetic marker that is reliably associated with sexual orientation is a strong argument against it.
The “antagonistic alleles” idea is that there are certain genes that are selected in different directions, that is, positively selected in males, but negatively selected in females and vice versa...
[...] The epigenetic hypothesis for the widespread occurrence of human homosexuality is based on the possibility of epigenetic inheritance of adjustments to a foetus’s testosterone sensitivity. Like most other epigenetic marks, sex-specific epigenetic marks are established anew in the early embryo following fertilisation.
Thus, most of the sex-specific epigenetic marks on genes that are involved in testosterone sensitivity are scrubbed off and re-established in a reliably sex-specific pattern well before the gonads become differentiated into either testes or ovaries. However, not all epigenetic marks are completely erased during embryo development, and it is therefore possible that there is some transgenerational transfer of epigenetic settings for testosterone sensitivity. This could affect sexual phenotype, sexual identity and sexual attraction.
This is a potentially important idea because it may explain the strong tendency for twins to have similar sexual preferences, but for this tendency to be no stronger between identical twins than it is between non-identical twins. This suggests epigenetic inheritance from one or other parent, but not genetic inheritance. If it were solely genetic, we would expect identical twins to be much more likely to share their sexual preferences than non-identical twins... (MORE - missing details)
EXCERPTS: Last century, when things were a whole lot worse for gay people than they are today [...] For this reason, the occasional report of a “gay” gene was welcomed by many progressive people. ... Indeed, gay genes were perhaps the only example where many left-leaning people heartily embraced genetic determinism.
Awkwardly, like cold fusion, reports of genes that “cause” human homosexuality (and many other human behaviours) have failed to stand up to scrutiny – there is no “gay gene” in the sense that no one has identified genetic markers or genes that reliably predict sexual orientation in humans. Moreover, since homosexuality would generally be reckoned to reduce reproductive output of an individual, an allele (a gene variant) that directly causes homosexuality is unlikely to spread in a population.
Nonetheless [...] The widespread occurrence of homosexuality in humans and other animals, together with its high heritability but unpredictable genetics and lack of genetic markers, is a significant biological puzzle. There are three leading hypotheses for the common existence of homosexuality in human populations, one based on kin selection, one on sexually antagonistic alleles, and one on epigenetic inheritance.
Briefly, the kin selection idea is that a gene that promotes homosexual behaviour can spread in a population if homosexual people contribute significantly to the reproduction of close relatives. Although this idea is plausible, the lack of any genetic marker that is reliably associated with sexual orientation is a strong argument against it.
The “antagonistic alleles” idea is that there are certain genes that are selected in different directions, that is, positively selected in males, but negatively selected in females and vice versa...
[...] The epigenetic hypothesis for the widespread occurrence of human homosexuality is based on the possibility of epigenetic inheritance of adjustments to a foetus’s testosterone sensitivity. Like most other epigenetic marks, sex-specific epigenetic marks are established anew in the early embryo following fertilisation.
Thus, most of the sex-specific epigenetic marks on genes that are involved in testosterone sensitivity are scrubbed off and re-established in a reliably sex-specific pattern well before the gonads become differentiated into either testes or ovaries. However, not all epigenetic marks are completely erased during embryo development, and it is therefore possible that there is some transgenerational transfer of epigenetic settings for testosterone sensitivity. This could affect sexual phenotype, sexual identity and sexual attraction.
This is a potentially important idea because it may explain the strong tendency for twins to have similar sexual preferences, but for this tendency to be no stronger between identical twins than it is between non-identical twins. This suggests epigenetic inheritance from one or other parent, but not genetic inheritance. If it were solely genetic, we would expect identical twins to be much more likely to share their sexual preferences than non-identical twins... (MORE - missing details)
