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De novo mutations and male homosexuality


Mr.Zurich92

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Is there a possibility that a minority of male homosexuals are gay cause of rare de novo mutations?

I'm gay I do look very weird. Very often I get insultet with painful words like ''faggot''. I do look very strange. That's why I believe something biological is not running correctly! I also realized that male homosexuality is common. Why that?

I have theories that male homosexality is seperated in three subtypes!

Subtypes 1. : approx. 70% of all gay men, homosexuality is caused by
uncommon hormonal condition in combination of too less gene
activity.

Subtype 2. : 20 % of all gay men, Homosexuality is caused by complex
polygenic interaction which leads to this kind of sexual
orientation

Subtype 3. : 10 % of all gays, Homosexuality is caused by very rare de
novo mutations.


I am sure I do have a de novo mutation which causes my homosexuality. How I can find out which gene is affected?

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I have only read the abstract yet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2427196/

 

Sexual antagonism implies that these genes are persisting rather than being weeded out. My guess is that they heighten androphilic attraction regardless of sex. Homosexual is a "gender binary" term.

 

 

I also realized that male homosexuality is common. Why that?

 

Male and female orientation may be different. If vaginal photoplethysmography accurately measures arousal, then females seem to tend more toward bisexuality relative to men.

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Heredity studies indicate that female homosexuality is not very heritable at all and thus unlikely to be primarily due to genetics. Male homosexuality has varying degrees of heritability and so does have some genetic basis. However, it is clear from these studies that there is also a good deal of environmental factors at work.

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Heredity studies indicate that female homosexuality is not very heritable at all and thus unlikely to be primarily due to genetics. Male homosexuality has varying degrees of heritability and so does have some genetic basis. However, it is clear from these studies that there is also a good deal of environmental factors at work.

I can only hope you don't mean with ''environment'' the social environment later in life. I guess you mean the biological environment in the whomb.

Edited by Mr.Zurich92
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I can only hope you don't mean with ''environment'' the social environment later in life. I guess you mean the biological environment in the whomb.

 

I mean all of it. You're basic hereditary study cannot distinguish between so specific environmental factors, except for the shared and unique environment of the individual. In some of the largest twin studies, genetics accounted for ~34-39% of the variance while the unique environment accounted for ~61-66%, and the shared nearly none. In women its ~18-19% genetic, ~16-17% shared environment, and 64-66% unique environment.

 

I don't see why you should hope for anything, that leads to biased assessment of the data.

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I mean all of it. You're basic hereditary study cannot distinguish between so specific environmental factors, except for the shared and unique environment of the individual. In some of the largest twin studies, genetics accounted for ~34-39% of the variance while the unique environment accounted for ~61-66%, and the shared nearly none. In women its ~18-19% genetic, ~16-17% shared environment, and 64-66% unique environment.

 

Doesn't sexual orientation pose unique problems for a twin study?

Homosexuals are less likely to reproduce, so our parents tend to be heterosexual. Therefore, the twins will typically both inherit heterosexual genetics regardless whether they're identical. That's why it's worth considering that homosexuality often results from a mutation or epigenetic alteration rather than an inherited allele.

I can further the case for de novo mutations for sex-independent androphilia. All males have an X-chromosome (XY), yet the Y-chromosome must do something to make them gynephilic, unlike their androphilic XX counterparts. It's foreseeable that a mutated Y (or a chromosome that interacts with the Y) might cause the male to default to androphilic orientation.

If homosexuality can result from a mutation or epigenetic alteration occuring after the zygote splits, this genetic effect could easily be mistaken for unique environment in a twin study.


 

I do look very strange. That's why I believe something biological is not running correctly!

 

I don't see why an allele for sex-independent androphilia should cause such problems, but perhaps such a mutation (or any mutation, really) might correlate with a higher prevalence of mutations.

Edited by MonDie
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Doesn't sexual orientation pose unique problems for a twin study?

Homosexuals are less likely to reproduce, so our parents tend to be heterosexual. Therefore, the twins will typically both inherit heterosexual genetics regardless whether they're identical. That's why it's worth considering that homosexuality often results from a mutation or epigenetic alteration rather than an inherited allele.

I can further the case for de novo mutations for sex-independent androphilia. All males have an X-chromosome (XY), yet the Y-chromosome must do something to make them gynephilic, unlike their androphilic XX counterparts. It's foreseeable that a mutated Y (or a chromosome that interacts with the Y) might cause the male to default to androphilic orientation.

If homosexuality can result from a mutation or epigenetic alteration occuring after the zygote splits, this genetic effect could easily be mistaken for unique environment in a twin study.

 

No, it does not pose any unique challenge to twin studies. Twin studies are meant to measure heredity and the combination of genetic components, not specific genes. Furthermore, if homosexuality is a quantitative trait caused by multiple recessive alleles, then it is unsurprising that the parents would be heterosexual.

 

I really do not like to throw around the term "epigenetic" lightly because "epigenetic" is typically misused by nearly everyone, including many scientists. The proper definition of "epigenetic" is "hertitable differences that are not caused by differences in underlying sequences". "Epigenetics" is not the environment. We have a term for that....the "environment" and when the environment interacts with our genes its called "gene by environment interactions" or as is often stated "GxE". "Epigenetics" was coined by Waddington in the 1950s for a very specific idea, while the fact that GxE interactions has been known since Fisher or earlier in the early 1910s. Epigenetics is also not synonymous with DNA methylation or histone modifications. Most of these variants are actually "genetic" because they are caused by neighboring or underlying genetic variation and thus are not truly "epigenetic". Furthermore, if homosexuality were truly "epigenetic" then it would be heritable and indistinguishable from the genetic component of homosexuality as measured by the standard twin study. Not to say that environmental conditions or variants of DNA methylation cannot underly part or all of homosexuality, just that by a proper definition of epigenetics, its really not epigenetic. I know I am being quite the stickler on this, but I work in epigenetics and it is a pet peeve of mine to see the term thrown around as a catch all for anything and everything that doesn't resemble simple genetics. It makes the field of epigenetics meaningless.

 

De novo mutations will either be shared by twins and thus show up as the genetic component or if not shared, will lead to an underestimation of the genetic component. Its unlikely to be largely due to de novo mutations, however, because you would have to have a very high frequency of similar de novo mutations to reach this sort of frequency in a population. This is especially true of the study populations of the size used in the best twin studies, that include thousands of individuals. There is clearly a quantitative genetic component to homosexuality, however, it really is only in the range of ~34-39% of the phenotypic variance for males and even less for females. It is clear that the largest source of variance in sexuality is the individual's "unique environment". Whether this occurs in the womb, in early childhood, or whatever, I don't know.

 

While it is interesting why some people are homosexual, we should not let our understanding of the biology be predetermined by what we think "it should be" rather than what it is. Homosexuality is clearly a complex trait and like ALL complex traits, there are both genetic and environmental contributions. Human height is a complex trait that is determined by a combination of environment and genetics. So is intelligence. Of course there is going to be variance in the relative contribution of genetics and environment and we should just accept as fact what is fact and not presume that it must be one or the other.

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How did they measure homosexuality? I recall reading the abstract of a twin study... here it is!

http://www.ncbi.nlm.nih.gov/pubmed/1845227

[...] Sexual orientation of relatives was assessed either by asking relatives directly, or when this was impossible, asking the probands. Of the relatives whose sexual orientation could be rated, 52% (29/56) of monozygotic cotwins, 22% (12/54) of dizygotic cotwins, and 11% (6/57) of adoptive brothers were homosexual. Heritabilities were substantial under a wide range of assumptions about the population base rate of homosexuality and ascertainment bias. However, the rate of homosexuality among nontwin biological siblings, as reported by probands, 9.2% (13/142), was significantly lower than would be predicted by a simple genetic hypothesis and other published reports. [...]


They simply asked for orientation, which we all know is a really bad measure of sexual preference. A penile plethysmograph might provide better data.

It looks like they compensated for this, but I can't see what the results were after the correction.


 

While it is interesting why some people are homosexual, we should not let our understanding of the biology be predetermined by what we think "it should be" rather than what it is. Homosexuality is clearly a complex trait and like ALL complex traits, there are both genetic and environmental contributions. Human height is a complex trait that is determined by a combination of environment and genetics. So is intelligence. Of course there is going to be variance in the relative contribution of genetics and environment and we should just accept as fact what is fact and not presume that it must be one or the other.

 

I'm always critical about how to interpret research findings.

 

I don't think my usage of epigenetic was inconsistent with your definition, but I didn't know that the methylations had to be induced by the environment to be epigenetic.

Edited by MonDie
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How did they measure homosexuality? I recall reading the abstract of a twin study... here it is!

 

http://www.ncbi.nlm..../pubmed/1845227

bailey et al said

[...] Sexual orientation of relatives was assessed either by asking relatives directly, or when this was impossible, asking the probands. Of the relatives whose sexual orientation could be rated, 52% (29/56) of monozygotic cotwins, 22% (12/54) of dizygotic cotwins, and 11% (6/57) of adoptive brothers were homosexual. Heritabilities were substantial under a wide range of assumptions about the population base rate of homosexuality and ascertainment bias. However, the rate of homosexuality among nontwin biological siblings, as reported by probands, 9.2% (13/142), was significantly lower than would be predicted by a simple genetic hypothesis and other published reports. [...]

They simply asked for orientation, which we all know is a really bad measure of sexual preference. A penile plethysmograph might provide better data.

It looks like they compensated for this, but I can't see what the results were after the correction.

 

Why is asking someone for their orientation a bad measure of sexual preference?

 

As far as twin studies go, one of the most extensive and best to date used data from all twin-pairs in Sweden, including thousands of individuals. This is what I base my previous figures on. They did not base their assessment on self-reported sexual attraction, but rather on lifetime number of same-sex and opposite-sex partners that a person had ever "sexually" been with, deliberately avoiding using an actual description of sexual intercourse.

 

Bailey and Pillard came up with estimates of ~0.31-0.74 based on that data. While more significant than the .34-.39 figure of the Swedish twin study, the population size was much smaller. Even if we take this upper limit, genetics does not fully account for ones sexual orientation. The fact that there is a higher rate of homosexuality amongst adopted siblings than the general population also suggests a major environmental factor.

 

I'm always critical about how to interpret research findings.

 

Why are you critical about how to interpret these findings? If there is a scientific reason for such criticism, then that is valid and I would love to hear it. Otherwise, one should be careful that one's criticism is not based simply on biases.

 

I don't think my usage of epigenetic was inconsistent with your definition, but I didn't know that the methylations had to be induced by the environment to be epigenetic.

 

I said quite the opposite in fact. I specifically said that "epigenetic" does not mean environmentally induced. Only that it has to be heritable and independent of genetic variation. Most true epigenetic variants appear to be simply due to random gain/loss of methylation, not environment.

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I might comment on the study once I've read it. However, the twin studies are taking us away from the opening subject.

 

 


I have theories that male homosexality is seperated in three subtypes!

 

Subtypes 1. : approx. 70% of all gay men, homosexuality is caused by
uncommon hormonal condition in combination of too less gene
activity.

 

Subtype 2. : 20 % of all gay men, Homosexuality is caused by complex
polygenic interaction which leads to this kind of sexual
orientation

 

Subtype 3. : 10 % of all gays, Homosexuality is caused by very rare de
novo mutations.

 

Much to my shame, I assumed heritability (sexual antagonism) implies a genetic cause, and I assumed this contradicted the opening post.

 

Homosexuality as a consequence of epigenetically canalized sexual development. (Rice, Friberg, Gavrilets)

Abstract http://www.ncbi.nlm.nih.gov/pubmed/23397798

 

summary of findings on io9.com http://io9.com/5967426/scientists-confirm-that-homosexuality-is-not-genetic--but-it-arises-in-the-womb

 

Their theory is that these epi-marks protect the fetus from androgen fluctuations. These epi-marks are normally erased and replaced with native epi-marks during development in the womb. Sometimes, however, they aren't erased, and non-erased opposite-sex epi-marks may overpower the native epi-marks. Their model suggests that this accounts for most homosexuality. This seems consistent with Mr. Zurich's first subtype, and may even be what he was referring to.

 

 

 


Very often I get insultet with painful words like ''faggot''.

 

My condolences, by the way. I would have said something the first time, but I mysteriously skipped over that part, instead contemplating the "strange" appearance portion, then dismissing it.

Edited by MonDie
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I might comment on the study once I've read it. However, the twin studies are taking us away from the opening subject.

 

 

 

Much to my shame, I assumed heritability (sexual antagonism) implies a genetic cause, and I assumed this contradicted the opening post.

 

Homosexuality as a consequence of epigenetically canalized sexual development. (Rice, Friberg, Gavrilets)

Abstract http://www.ncbi.nlm.nih.gov/pubmed/23397798

 

summary of findings on io9.com http://io9.com/5967426/scientists-confirm-that-homosexuality-is-not-genetic--but-it-arises-in-the-womb

 

Their theory is that these epi-marks protect the fetus from androgen fluctuations. These epi-marks are normally erased and replaced with native epi-marks during development in the womb. Sometimes, however, they aren't erased, and non-erased opposite-sex epi-marks may overpower the native epi-marks. Their model suggests that this accounts for most homosexuality. This seems consistent with Mr. Zurich's first subtype, and may even be what he was referring to.

 

I read that paper when it first came out. Good old PR propaganda and bad science reporting led to a lot of misconceptions. That paper is not a "study", at least not in the traditional sense. They don't produce any data, they don't even conduct an actual meta-study. Rather its more a review, where they make an argument based on actual research against genetic causes and then propose a model for how epigenomic features (epigenomic is different than epigenetic) could be the cause of homosexuality. Quite frankly I don't buy it because epigenomic marks are rarely inherited in mammals and actually proving that epigenomic marks are the cause rather than genetic variants is extremely difficult and has only been done in a limited number of circumstances. Their argument simply boils down to that there is variation between monozygotic twins and as of yet no actual genes have been linked to homosexuality. Neither of which rules out a genetic component. While several studies have been done to measure the heritability of homosexuality, very few studies have actually tried to map the trait and none with the statistical power to detect highly quantitative traits that contribute only a small portion of the heritability. Then there is also the fact that homosexuality seems to carry a high environmental factor, making it even more difficult to find linked or associated genes if it is caused by many common variants with small contributions to an overall genetic component.

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I want to list some facts:

 

There are clearly more homosexual men than homosexual women! Guess 1 to 3 or even 1 to 4

 

They couldn't find a male knockout mouse yet, which shows homosexual sexual preference

 

They could find recently one gene in a female knockout mouse, that leads to homosexual sexual preference. It's a gene that is needed for producing a protein, that eliminates estrogen which can masculinize hypothalamus prenatally.

 

Human brain is female organized generally, it gets masculinized through hormones in the whomb.

 

 

 

What if the complex interactions of hormones and activity doesn't run correctly. I mean what if in a sensitife time span during pregnancy some gene which are needed for testosteron production are simply not active enough for producing enough testosteron JUST BY CHANCE? Or the genes which are needed for testosteron production are active enough but in the brain(during a sensitive time span) the genes which masculinizes nuclei like Bed nucleus of stria terminalis, Inah3 or Amygdala weren't active enough and have then a female volume? Like the aromatase gene which is needed for converting testosteron to estrogen which can masculinize hypothalamus.

 

Anyway is epigentic the same as gene activity? I thought gene activity and epigenetic isn't the same!

 

 

Let's say there is no god and humans and animals are simply the result of complex biochemical process of million years. So we can say homosexuality is happing mostly because our species is biochemical built in a way with this prenatal hormone(and gene activity) issue which is very ''error-prone''? Contrary to birds where brain masculinisation is happing just by chromosone set and not by hormones.

 

Homosexuality is an biological error because the definition of life is:

 

Homeostasis, Organization, Metabolism, Growth, Adaptation, Response to stimuli and Reproduction. Homosexuals like me can't reproduce directly, because my brain is biological hardwired to be attracted to the same sex. I can't make pregant another man! And here comes the second reason why homosexuality is a biological error:

 

Each organ has its function. My testicles are producing sperm. But for what reason are they producing sperm? Sperms are made to fertilize eggs. But only women have eggs and I'm not attracted to women.

 

My third reason why Homosexuality is an biological error is because:

 

Sexual orientation has its function. A heterosexual man is attracted to tits, vagina or female ass because this signals are indicating something. they are indicating if a woman is procreative and if rate of offspring can be high or if the womn can give milk to the offspring. There is also a reason for this sexual orientation.

 

The same for heterosexual women. they are attracted to muscles because they indicate if a man can protect the woman and can care for the family(tobring food build a house) or women are attracted rather to tall men than small men, simply because small men do indicated weakness compared to tall men. Sexual orientation has its biological reasons. I'm attracted to muscles but for what benefit? I'm a man myself. Do you see what I mean?

 

 

By the way I still believe that there is a de novo mutation in my personal case that causes my homosexuality! And I will investigate it.


 

I read that paper when it first came out. Good old PR propaganda and bad science reporting led to a lot of misconceptions. That paper is not a "study", at least not in the traditional sense. They don't produce any data, they don't even conduct an actual meta-study. Rather its more a review, where they make an argument based on actual research against genetic causes and then propose a model for how epigenomic features (epigenomic is different than epigenetic) could be the cause of homosexuality. Quite frankly I don't buy it because epigenomic marks are rarely inherited in mammals and actually proving that epigenomic marks are the cause rather than genetic variants is extremely difficult and has only been done in a limited number of circumstances. Their argument simply boils down to that there is variation between monozygotic twins and as of yet no actual genes have been linked to homosexuality. Neither of which rules out a genetic component. While several studies have been done to measure the heritability of homosexuality, very few studies have actually tried to map the trait and none with the statistical power to detect highly quantitative traits that contribute only a small portion of the heritability. Then there is also the fact that homosexuality seems to carry a high environmental factor, making it even more difficult to find linked or associated genes if it is caused by many common variants with small contributions to an overall genetic component.

 

 

Sir please! I hardly believe childhood experience, upbringing or social life has any influence on someones sexual orientation! In this case sexual orientation is 100% prenatal or even perinatal biological determinated! Brain masculinisation and defeminisation is prenatal and perhaps perinatal organized! It makes me very angry when heterosexual men like you or Endy0816 are saying that the evironment after birth has an influence on sexual orientation. We are still living in mostly homophobic society. Even here in my country Switzerland and much more in the USA, Homosexuality is still for a lot of people a NO-GO, something they hate. Parents don't want a gay son or a lesbian daughter. Everything is socially constructed than a man has to be attracted to women. So the social influence is from beginning anti-homosexual. So your point that ''evironment'' after birth has an influence on sexual orientation is wrong. So you believe if a young guy is playing baskettball with other guys and has good childhood generally, and also learns to flirt with women he gets heterosexual? That's simply not the case. Sexual orientation is biolgical organized prenatally. Later in life cause of puberty when hormon level rise the sexual drive gets stronger. But the sexual orientation is fixed already in the whomb!


 

 

De novo mutations will either be shared by twins and thus show up as the genetic component or if not shared, will lead to an underestimation of the genetic component. Its unlikely to be largely due to de novo mutations, however, because you would have to have a very high frequency of similar de novo mutations to reach this sort of frequency in a population. This is especially true of the study populations of the size used in the best twin studies, that include thousands of individuals. There is clearly a quantitative genetic component to homosexuality, however, it really is only in the range of ~34-39% of the phenotypic variance for males and even less for females. It is clear that the largest source of variance in sexuality is the individual's "unique environment". Whether this occurs in the womb, in early childhood, or whatever, I don't know.

 

 

 

 

Do you read what I wrote? I wrote a minority of gay men like 10% or less of all male homosexuals do have a defective gene that causes their homosexuality. And de novo mutation are the cause of such defective genes. I think I belong to this minority of gay men. That's also why linkage studies or genome wide association studies do not run, because only a very small fraction of gay men do really have a genetic cause for their homosexuality.

 

by the way 23andme is doing a GWAS of sexual orientation: http://blog.23andme.com/wp-content/uploads/2012/11/Drabant-Poster-v7.pdf

 

In the table you can see that some male homosexual do tendencially cry much faster than heterosexual men. do you know that amygdala are responsible for emotions! And science has proven that male homosexuals do have female like organized amygdalas.

Edited by Mr.Zurich92
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You can have children biologically speaking. Generally people manage to conform with society's expectations as far as reproduction goes.

 

It is also possible that it is indirect acting. Increasing the well-being of an opposite-sexed couple's children.

 

With more modern day means you could reasonably purchase an egg, have it artificially inseminated and then have it implanted in a birth mother. Likewise sperm donation is an option.

 

Some stuff down the line would allow Lego Genetics(male eggs, female sperm). You and a partner certainly contain all the necessary chromosomes, just a matter of switching cell characteristics around. Artificial means of growing the embryo are likewise being looked into.

Edited by Endy0816
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You can have children biologically speaking. Generally people manage to conform with society's expectations as far as reproduction goes.

 

It is also possible that it is indirect acting. Increasing the well-being of an opposite-sexed couple's children.

 

With more modern day means you could reasonably purchase an egg, have it artificially inseminated and then have it implanted in a birth mother. Likewise sperm donation is an option.

 

Some stuff down the line would allow Lego Genetics(male eggs, female sperm). You and a partner certainly contain all the necessary chromosomes, just a matter of switching cell characteristics around. Artificial means of growing the embryo are likewise being looked into.

I'm gay but I don't want to live with another man neither I want to see gay parade. I'm also not interested for entering into the gay scene.

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I'm gay but I don't want to live with another man neither I want to see gay parade. I'm also not interested for entering into the gay scene.

 

You don't need to define yourself in anyone's terms but your own. Throw off the shackles of society's opinion and all that jazz.

 

 

If it is genetic, maybe it did/does have some benefit which resulted in it being passed along or maybe it is just an option that will bear fruit in the future as tech-assisted reproduction becomes more common place. Who's to say? Don't try to outguess the human genome keeping its options open. Nothing is good/bad, it is only judged based on how it contributes to fitness.

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Let's say there is no god and humans and animals are simply the result of complex biochemical process of million years. So we can say homosexuality is happing mostly because our species is biochemical built in a way with this prenatal hormone(and gene activity) issue which is very ''error-prone''? Contrary to birds where brain masculinisation is happing just by chromosone set and not by hormones.

 

Homosexuality is an biological error because the definition of life is:

 

Homeostasis, Organization, Metabolism, Growth, Adaptation, Response to stimuli and Reproduction. Homosexuals like me can't reproduce directly, because my brain is biological hardwired to be attracted to the same sex. I can't make pregant another man! And here comes the second reason why homosexuality is a biological error:

 

Each organ has its function. My testicles are producing sperm. But for what reason are they producing sperm? Sperms are made to fertilize eggs. But only women have eggs and I'm not attracted to women.

 

I'm not interested in whether one considers "homosexuality" an "error" or not. The morality of it is not something that particularly interests me. I don't think homosexuality is more or less moral whether it is genetic or environmental or more likely some mix of the two. I am not homosexual, so the morality as it pertains to me personally is something I consider irrelevant. Beyond that, if it does not cause others harm, then I consider the morality of it to be none of the business of anyone not participating in the act. I'm pretty simple like that. My interest in it extends to the biology only, in particular the genetics, because I love genetics. The use of terminology like "biological error" is meaningless to me. We are all "mutants" and the products of "mutants" and so to me defining things as "error" becomes rather meaningless. If homosexuality has the effect of improving the survival of relatives, as some have suggested as an evolutionary explanation, then low levels of homosexuality can actually be seen as advantageous. I don't particularly agree with this because I think the evidence for it is very weak, but that is the only reason I do not agree with it. Otherwise....I don't care. Again, I'm pretty simple in usually only caring about what the biology says as long as it doesn't cause harm to others.

 

I say all this in case you think I have some agenda in this argument, I don't. I disagree with your arguments purely based on evidence, not morals, religion, or any other non-scientific reason. I'll address your arguments later, I just wanted to clarify that because you seem to think that I might be arguing from a non-scientific standpoint.

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I'm looking at that Scandinavian twin study. By the way, Chan, your link broke. :o

Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden
(Niklas Långström, Qazi Rahman, Eva Carlström, and Paul Lichtenstein)
http://faculty.bennington.edu/~sherman/sex/samesex%202010.pdf

"From this, we constructed the two variables any lifetime same-sex partner and total number of lifetime same-sex partners (divided into seven categories to minimize the impact of outliers; 0, 1, 2, 3–5, 6–10, 11–20, and 21 or more partners) based on prior work (Kirk, Bailey, Dunne, & Martin, 2000). (Langstrom et al)"

"In men, the full twin model suggested heritability estimates of 39% for any lifetime same-sex partner (95% CI: 00–59%) and 34% for total number of same-sex partners (95% CI: 00–53%) (Langstrom et al)"

The study would have been vastly improved (for our purposes) if they had looked at relative number of same-sex and opposite-sex partners. Instead, they just look at total number of same-sex partners, which is influenced by promiscuity. What if both twins really are gay, but one is choosing abstinence while the other is choosing orgies, or one is far more attractive, or in the closet?

"The average number of same-sex sexual partners among those reporting any such partner was 12.86 in men and 3.53 in women, (Langstrom et al)"

variance???

Post Edit: (Edited a lot)

"Furthermore, while this study focused on same-sex sexual behavior, assessment of sexual attraction or fantasies and even romantic attractions would more fully capture the complexity of sexual orientation. However, both behavioral measures of sexual orientation (any same-sex sexual partner and total number of same-sex partners) correlated strongly with self-reported same-sex sexual attraction (r = .70–.75) upon cross-validation in a contemporary referred sample (n = 555) of age-matched adult men in Toronto, Canada (data available upon request). (Langstrom et al)"

The bolding is mine.

I'm sure they do correlate, but for our purposes it's useless to distinguish between someone with 3-5 same-sex partners and someone with 21+ since they're both probably gay and know it. One isn't more gay because he's more promiscuous. Alas, I don't know the math. With the right data, they could have corrected their results to approximate sexual preference by giving each category a weighted value, but they don't appear to have even wanted to do this—they're concerned about homosexual behavior.

Regardless, the leeway afforded by the less than 1 correlation (r = .70–.75) indicates that twin concordance, and hence both additive genetic influences and common environment influences, may be overestimated or underestimated if one interprets these findings in terms of same-sex attraction (self-reported or actual). Whether genetic influences would be under- or over- estimated depends on the relative size of genetic contributions for traits like promiscuity, attractiveness, closetedness, or anything else that could have influenced the measure. I can't do the math, but if I had to guess...

r = 0.70
A = 0.39 ± (0.39 * (1 - 0.70) * ~0.8)
therefore CI (confidence interval): 0.30-0.48 with regard to additive genetic influences on self-reported preference (assuming the Canadian sample was alike to the Scandinavian sample in all relevant respects).



There are clearly more homosexual men than homosexual women! Guess 1 to 3 or even 1 to 4


I want to see the source of this information. Experts disagree about the prevalence of homosexuality among men and women, and their estimates for men alone range from about 6% to 10%, although a larger subsample will report at least one same-sex experience.



You can have children biologically speaking. Generally people manage to conform with society's expectations as far as reproduction goes.

[snipped]


Interestingly, as compared to androphilic men, gynephilic men may generally be more turned off by the non-preferred sex. See the bottom row of Table 4 on page 114.
http://www.researchgate.net/publication/233747536_Heterosexuality_Homosexuality_and_Erotic_Age_Preference

Edited by MonDie
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[snipped]

 

Parents don't want a gay son or a lesbian daughter. Everything is socially constructed than a man has to be attracted to women. So the social influence is from beginning anti-homosexual. So your point that ''evironment'' after birth has an influence on sexual orientation is wrong. So you believe if a young guy is playing baskettball with other guys and has good childhood generally, and also learns to flirt with women he gets heterosexual? That's simply not the case. Sexual orientation is biolgical organized prenatally. Later in life cause of puberty when hormon level rise the sexual drive gets stronger. But the sexual orientation is fixed already in the whomb!

 

[/snipped]

 

Mr. Zurich, I agree that sexual preference can't be that simple. If it were that simple, we would find that children raised by same-sex couples are more likely to turn out gay. AFAIK they aren't, which is consistent with the extremely low contributions from "common environment" influences.

 

I want to explain to you how a twin study works. If anyone knows more than I, they're free to correct me.

 

Basically, the researchers are measuring the frequency and degree of differences between twins, while distinguishing between identical (monozygotic) twins and non-identical (dizygotic) twins. I only learned what I know from the Methods section of this Wikipedia article, but it's very informative.

https://en.wikipedia.org/wiki/Twin_study

 

Most studies only calculate the relative contributions of three categories of factors, denoted as A, C, and E.

A = "additive genetic"

C = "common environment"

E = "unique environment"

However, these terms are deceptively simplistic, so I'm going to invent my own terms.

A-factors are common among monozygotic twins, but variant among dizygotic twins (for example, genetics).

C-factors are shared by twins regardless (they're shared or "common" factors).

E-factors vary among twins regardless.

 

This can get confusing. If something is purely determined by family environment, for example, it will obviously be a C-factor. However, what if it's family environment interacting with genetic factors such as a genetic susceptibility? Such a factor would vary between dizygotic twins, who have different genetics, so it would involve A- and C-factors.

 

We can rule out some possibilities given the small or non-existent contributions from C-factors. It isn't significantly influenced by any shared environmental factors, whether in the womb, from parental suggestion, from stressors, from diet, etc. (unless the shared influence is shared by all people and not just the twin pairs).

However, any such influences that aren't shared are still possible. If these influences interact with genetics, they will be A-factors. If they're randomized effects that are determined independently for each twin, they will be E-factors. The large contributions from "unique environment" (E) could indicate that sexual orientation is determined by randomized variables, whether in the womb, during imaginative role play, or whatever. All I would infer is that parents have almost no control over it—the Swedish twin study, albeit its limited methodology, says 39% for heritability and 61% for unique environment. Do the math!

Edited by MonDie
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