Posted on 04/01/2013 12:23:05 PM PDT by abigailsmybaby
ABSTRACT Male and female homosexuality have substantial prevalence in humans. Pedigree and twin studies indicate that homosexuality has substantial heritability in both sexes, yet concordance between identical twins is low and molecular studies have failed to find associated DNA markers. This paradoxical pattern calls for an explanation. We use published data on fetal androgen signaling and gene regulation via nongenetic changes in DNA packaging (epigenetics) to develop a new model for homosexuality. reduced androgen sensitivity in XX fetuses and enhanced sensitivity in XY fetuses, and that this difference is most feasibly caused by numerous sex-specific epigenetic modifications (epi-marks) originating in embryonic stem cells. These epi-marks buffer XX fetuses from masculinization due to excess fetal androgen exposure and similarly buffer XY fetuses from androgen underexposure. Extant data indicates that individual epi-marks influence some but not other sexually dimorphic traits, vary in strength across individuals, and are produced during ontogeny and erased between generations. Those that escape erasure will steer development of the sexual phenotypes they influence in a gonad-discordant direction in opposite sex offspring, mosaically feminizing XY offspring and masculinizing XX offspring. Such sex-specific epi-marks are sexually antagonistic (SA-epi-marks) because they canalize sexual development in the parent that produced them, but contribute to gonad-trait discordances in opposite-sex offspring when unerased. In this model, homosexuality occurs when stronger-than-average SA-epi-marks (influencing sexual preference) from an opposite-sex parent escape erasure and are then paired with a weaker-than-average de novo sex-specific epi-marks produced in opposite-sex offspring. Our model predicts that homosexuality is part of a wider phenomenon in which recently evolved androgen-influenced traits commonly display gonad-trait discordances at substantial frequency, and that the molecular feature underlying most homosexuality is not DNA polymorphism(s), but epi-marks that evolved to canalize sexual dimorphic development that sometimes carryover across generations and contribute to gonad-trait discordances in opposite-sex descendants.
(Excerpt) Read more at jstor.org ...
Here is another thought presented by someone here on FR:
The only way you know someone is a homosexual is by self identification or observing the behavior.
If you’re serious, just search using the title. There are several articles that discuss the study.
The latest on Darwinian Evolution, in terms of epigenetics, is that we've found that Lamarckian connection between the genome and the macro-world ~ and it's stranger than we ever imagined it could be.
You'll notice as you get into epigenetics and methylation that just about no one discusses 'evolutionary forces'. That demon demigod is gone from the lexicon. The new one is getting down to molecular formulae!
Most homosexuals are not born that way.
They just get sucked into it.
But as they say with most prenatal screening, don't do it unless you are willing to act (abort) on the information.
If there were an effective screen for these epigenetic markers and a couple could tell if the child was likely to be homosexual - would be find social conservatives suddenly pro-abort, and homosexuals suddenly anti-abortion?
Disturbing findings in this article. Other research has shown brain changes in practicing homosexual adults.
What if the epi-marks tend to resist erasure in those who adopt gay lifestyles at earlier ages?
B.S. It’s a choice and an abomination to the Creator.
Homosexual behavior is a behavior.
Homosexuality is a condition (same sex attraction, orientation).
Learn the English language. -ity denotes a state or condition or essence, not an act.
I suspect that there is something of a simple rationale for homosexuality in basic biology. That is, all people are composed of both dominant and recessive genes. Generally the dominant genes are better, and the recessive genes are “backups”, sometimes defective, but available if the dominant genes “fail” in some way, over a single, or several generations.
This being said, since humans have relatively few offspring, another genetic methodology would be to “load” the first child with a predominance of dominant genes, and give subsequent children increasing numbers of recessive genes, so that they continue in the bloodline.
However, beyond a certain number of recessive genes, and a child may not be viable for reproduction. For this reason, a “safety” is engaged of making them homosexual, since any offspring they had would be genetically worthless.
Importantly, the first theory seems to hold water, because it has been statistically noted.
“In several studies, the observation is that the more older brothers a man has, the greater the probability is that he will have a homosexual orientation. It has sometimes been called the ‘older brother effect’.”
While I haven’t seen any studies about predominance of recessive genes among homosexuals, it is widely known that as a group, homosexuals have far more physical and psychological problems *not* associated with their sexuality, than average. This would seem to support a recessive “loading” “safety” theory.
Importantly, homosexuality should be looked at as just one mechanism by which reproduction is prevented. Non-fertile prostitution, and sexuality in post-menopausal females might be two other ways in which those who should not reproduce are distracted away from those who should.
this is garbage propaganda.
by this logic:
behavior of:
murdering is a behavior that is inherited...
speeding is a behavior that is inherited...
bill clinton cheating is a behavior that is inherited...
lying is a behavior that is inherited...
No, dominant genes are not “better”. Dominant genes have a stronger effect (for good or bad) than recessive genes. This usually has to do with the molecular biology of the resulting protein from the two different alleles.
If wrinkled pods are dominant to smooth pods in a plant - it isn’t because wrinkled pods are better - it is because the allele that specifies wrinkles is sufficient in just one copy to determine that the pods are not smooth.
Pedigree and twin studies indicate that homosexuality has substantial heritability in both sexes, yet concordance between identical twins is low and molecular studies have failed to find associated DNA markers.
Yet the study showing that children adopted by homosexuals are more likely to be homosexual will be ignored, denounced and investigated for fraud.
I am very familiar with epigenetics and I wouldn’t be surprised if it influences propensities but the key is just as with genetics or hormonal influences they are never entirely or even mostly predictive. Twin studies have shown that only 20-39% of those that are identical genetically share the same sexual orientation with the influence on female orientation being the smallest. This means a majority of those where at least one genetically identical twin manifests as homosexual the other twin does NOT manifest as homosexual. This means that environment most certainly plays a dominate role. Unlike intelligence which has a 70% correlation between identical twins sexual orientation is clearly not hardwired where homosexuality is concerned.
Does this mean a cure is to follow?
This is your area of expertise, and not mine, but why wouldn’t dominant genes be “better”?
They’re more likely to be expressed, so they better be of some survival benefit to the organism. I would imagine that gene dominance is not something that is cast in stone, either.
Just the first sentence makes this bogus
Huntington's disease is a dominant trait. It is not a “better” allele than a non-Huntington allele. It is “dominant” in that it only takes one bad copy stacking up in your brain cells and eventually driving you mad and killing you.
Brown eyes are not “better” than blue eyes - but the gene that says “put a lot of brown (melanin) in there” is dominant to the gene that says “don't put that much brown in there”. It is as if you instruct one worker to make a hill and the other to only fill in a hole- the one who fills it up “dominates” over the one who doesn't in that you end up with a hill. He isn't a “better” worker - both followed instructions.
Sometimes a bad copy is recessive in that it doesn't function - but one good copy does the job plenty well. In that case the “dominant” gene is better - but for every example of that there is a contrary example where it only takes one bad copy to mess something up!
If by “cast in stone” you mean determined by the molecular biology of the genes and the proteins they code for - then yes - it is cast in stone.
If by “cast in stone” you mean for every example where a dominant allele is better than the recessive allele there is probably an example where a recessive allele is better than a dominant allele; or neither is objectively better than the other - then no - it is NOT “cast in stone”.
“Male and female homosexuality have substantial prevalence in humans.”
Bad science, bad statistics, worse politics.
Since when did 3% become statistically “substantial”?
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