there was a theory that the genes that confer gay men also confer extra fertility for women (and twinning). So keeping the genes in the population via other mechanisms. (I think the research was in Italian families, no link sorry.)
Aside from the inclusive fitness claim, Cochran’s gay germ hypothesis is also consistent with the continued existence of homosexuality: the pathogen co-evolves and so while the genes do get selected against, which genes keeps changing. Unfortunately, his theory still remains something of a ‘germ of the gaps’ theory—no one’s come up with a remotely plausible theory or found decent evidence that homosexuality spikes the fertility of relatives so much as to compensate for the sterility of homosexuals (remember, inclusive fitness decreases fast: if a homosexual has 1.05 rather than 2.1 children, then their siblings have to have 2.1 additional children, their cousins 4.2 additional children, and so on), so a theory which merely isn’t contradicted by any evidence looks pretty good by comparison.
One thing I thought of which would be direct evidence for the infection theory: polygenic scores for homosexuality. It’s somewhat heritable, so given a large sample size like UK Biobank, it should be possible to explain a few % of variance and construct a PGS based on a fairly narrow age cohort like 1 or 2 decades. Then the PGS can be applied longitudinally outside the sample. If it’s pathogenic co-evolution and the relevant genes keep changing, then the homosexuality PGS should show highest predictive validity in the original age bracket, but then decrease steadily as one moves away from the age bracket into the past or toward the present, showing a clear inverted V shape. While polygenic scores can increase or decrease steadily or show sudden shocks for various reasons just like heritabilities can increase/decrease over time (eg education PGS decrease due to dysgenics, height PGS increase and so on), they don’t typically show a distinct V shape, so finding one for homosexuality would be very striking.
My theory and meta-theory: The gay germ theory is pretty silly. But the big myth to which it is a reaction, is the idea that people are simply “born that way”. Cochran has a paranoid intuition that something else is happening, so he posits his gay germ. But what’s really happening is sexual imprinting. A person’s sexuality is greatly shaped by the first conditions under which they experience arousal, orgasm, and emotional bonding. Sexualities are “transmitted” in a way a little like languages. There’s no “German germ” which makes people think and speak auf deutsch, instead there’s some sort of deep learning based on early experience of a German-speaking environment. The acquisition of sexuality might be more like conditioning than learning, but it’s still an acquired trait.
That theory is even worse than the inclusive fitness one because you offer no mechanism whatsoever to offset the huge fitness penalty.
Sexual imprinting is a highly successful evolved mechanism critical to reproductive fitness which does in fact succeed in the overwhelming majority of cases; in many ways, it is more important than trivial details like ‘eating food’ because at least an offspring which immediately starves to death doesn’t drain parental resources and compete with siblings and the parents can try again! There should be a very good reason why such an important thing, found throughout the animal kingdom in far stupider & less sexually-dimorphic organisms, goes wrong in such a consistent way when other complex behaviors work at a higher rate and fail much more bluntly & chaotically. ‘Random imprinting’ is too weak a mechanism to thwart such a critical device, and doesn’t explain why the errors do not rapidly disappear with general or sex-linked adaptations. (Even as a 5% liability-threshold binary trait, a reproductive fitness penalty of 50%, to be generous to a trait which involves active aversion to procreative sex, would imply it should be far lower now than when it first arose*.)
Further, such a random nonshared environment theory doesn’t explain why dizygotic and monozygotic same-sex twins differ in concordance. (They don’t differ in language, so your example is evidence against your imprinting theory.)
* https://www.researchgate.net/profile/J_Bailey2/publication/21311211_A_genetic_study_of_male_sexual_orientation/links/02e7e53c1a72a8a596000000.pdf gives a low end heritability estimate of 0.31; population prevalence among males is usually estimated ~5% giving a liability threshold of ~-1.64; homosexuality is amply documented for the past 2500 years or so, at least back to the ancient Greeks, which at a generation time of ~25 years, means 100 generations. So assuming a fitness penalty of ‘just’ half and that selection started only 100 generations ago (rather than much further back), we would expect the rate of homosexuality to be less than 1/5th what it is.
To be immune to selection because it’s part of intelligence would imply a strong genetic correlation. Aside from the fact that I am doubtful any such genetic correlation will ever be found (there is no noted phenotypic correlation of homosexuality & intelligence that I’ve heard of), this still has the issue that homosexuality ought to be decreasing noticeably over time: while intelligence has apparently been neutral or selected for over the past few millennia and so hypothetically could’ve slowed the selection against homosexuality, intelligence itself has been selected against for at least a century, so that would accelerate the selection now that there are fitness penalties for both homosexuality & intelligence (by a fair bit, because selection on continuous traits is much faster than selection on rare binary traits).
there is no noted phenotypic correlation of homosexuality & intelligence that I’ve heard of
I’ve heard the raw correlation widely claimed, but I think most people interpret it as measuring closeting. Certainly openly gay men have higher income than straight men.
I’d be inclined to suspect closeting too. The better your ability to support yourself, the less you need to worry about repercussions.
Tangential and possibly relevant: I’ve noticed bisexual women appear to be ridiculously common in high-intelligence nerd communities. I don’t know whether I should associate that with the intelligence or the geek/nerd/dork personality cluster, nor do I know which way the causation goes.
You only posit that because your paranoid ignorance of biology.
Cochran has a paranoid intuition that something else is happening, so he posits his gay germ
Bullshit. Cochran wrote down his exact thought process. He thinks that everything is due to germs. Moreover, he measures of the strength of the evidence. Schizophrenia and (male) homosexuality are at the top of the list
OK, let’s talk about proximate causes and ultimate causes. The proximate causes are whatever leads to the formation of a particular human individual’s sexuality. The ultimate causes are whatever it is that brought about the existence of a population of organisms in which a given sexuality is even possible.
My focus has been on proximate causes. I look at the role of fantasy, choice, and culture in shaping what a person seeks and what they can obtain, and the powerful conditioning effect of emotional and sexual reward once obtained, and I see no need at all to posit an extra category of cause, in order to explain the existence of homosexuality. It’s just how some people end up satisfying their emotional and sexual drives.
What I had not grasped, is that the idea of the gay germ is being motivated by consideration of ultimate causes—all this talk of fitness penalties and failure to reproduce. I guess I thought Cochran was a science-jock who couldn’t imagine being gay, and who therefore sought to explain it as resulting from an intruding perturbation of human nature.
I am frankly not sure how seriously I should take the argument that there has to be (in gwern’s words) a “mechanism… to offset the huge fitness penalty”. Humanity evolves through sexual selection, right? And there are lots of losers in every generation. Apparently that’s part of our evolutionary “business model”. Meanwhile I’ve argued that non-reproducing homosexuality is a human variation that arises quite easily, given our overall cognitive ensemble. So maybe natural selection has neither a clear incentive to eliminate it, nor a clear target to aim at anyway.
I agree with what you said, and it is borne out very well by my experience of gay persons. As for gwern’s comment, the silliness is to think that evolution has enough selective power to completely remove that sort of thing. In fact, it would be far easier for evolution to remove a gay gene than for it to prevent things that happen through accidental social circumstances.
Consider this: I am over 40, I do not have children and have never had sex, and I have no intention to do so. Shouldn’t evolution have completely removed the possibility of people like me? I am not even helping other people raise children. I live alone, and consume my own resources.
The answer is that if “people like me” came about because of a specific gene, evolution would indeed have removed the possibility. As it is, it comes about through a vast collection of accidental and social facts, and the most evolution can do is make it rare, which it does. The same is true of homosexuality.
I thought Cochran was a science-jock who couldn’t imagine being gay
Whereas you can imagine it so easily that you didn’t bother to look at the real world, just as you can imagine Cochran so easily you didn’t bother to look at him
how seriously I should take the argument that there has to be (in gwern’s words) a “mechanism… to offset the huge fitness penalty”
90% of biologists don’t believe in evolution, either, but progress comes from those who do.
Are there any ideas about how and when the gay germ is acquired?
If someone hasn’t experienced sex yet, but they already think they are gay, is that because of the gay germ?
Gays generally say that they “always knew they were different” (and there is some evidence that this is not just confabulated memories), so it is probably acquired before age 5, possibly before birth. It is probably something common, like the flu. And there might be multiple infections that cause the same brain changes, as appears to be the case with narcolepsy.
If homosexuality has such a huge fitness penalty, why haven’t we evolved immunity to the gay germ?
You could ask a similar question about any explanation of homosexuality. It is measured to be weakly heritable. So we know that there are genes that protect from it. Given the fitness penalty, why haven’t those genes swept through the population? That wouldn’t necessarily eliminate it, but they would eliminate the heritability.
There are only two possibilities: either the fitness penalty is not what it looks like (eg, the sexual antagonism hypothesis); or the environment has changed so that which genes protect has changed.
Germ theory gives a simple explanation for changing environment, The Red Queen Hypothesis: the germ is evolving, so the genes that protect against it are changing. This is the metric that Cochran and Ewald use: multiply the fitness cost by the heritability. The higher that number, the more likely the cause is infection.
There actually is a known replicator that assists the reproduction of gay phenotypes, but it’s a behavior: gay sex! For a recent exposition, see the video that cost “Milo” his job.
No, there is no evidence of such replication. This isn’t really compatible with gays being detectable at age <5. Also, it’s pretty clear that isn’t what happens in sheep, which are highly analogous.
Common infections can have effects on a small population. For example, Barr-Epstein is implicated in at least some cases of narcolepsy, but 95% of the population tests positive for it.
What about pederasty in ancient Greece, what about sex in all-male prisons… in both those cases, you have men who by current definitions are not gay, but rather bisexual. And in both cases you have recruitment into an existing sexual culture, whether through seduction or coercion.
Human sexuality can clearly assume an enormous variety of forms, and I don’t have a unified theory of it. Obviously genes matter, starting with the basic facts of sex determination, and then in a more elusive way, having some effect on sexual dispositions in the mature organism.
And yes, natural selection will be at work. But, in this case it is heavily mediated by culture (which is itself a realm of replicator populations), and it is constrained by the evolvability of the human genome. I continue to think that the existence of nonreproductive sexuality is simply a side effect of our genomic and evolutionary “business model”, of leaky sexual dimorphism combined with Turing-complete cognition.
What about pederasty in ancient Greece, what about sex in all-male prisons… in both those cases, you have men who by current definitions are not gay, but rather bisexual.
Pederasty in ancient Greece was culturally very different from modern homosexual behavior though (or at least, the conventional view thereof; some people would contend that the ‘ancient’ model is very much lurking beneath the surface of even the most modern, ‘egalitarian’ gay relationships!). In that case, there was a very clear demarcation between an active participant (the pederast or erastês) who did behave ‘bisexually’ in some sense, but was really more properly connoted as highly masculine, and a passive participant (the erômenos) who was the only one to be specially connoted as ‘feminine’.
The sexual manifestations of pederasty were also criticized by quite a few philosophers and intellectuals, and the tone of these critiques suggests that pederasty could easily shade into sexually abusive behavior. (Notably, Christian morality also shared this critical attitude—the heavy censure of “homosexuality” and heterosexual “fornication” one finds in the New Testament can really only be understood in the light of Graeco-Roman sexual practices). Sex in all-male prisons also seems to share many of these same features; at the very least, if the common stereotypes of it are to be believed, it doesn’t really feature the ‘egalitarianism’ of modern homosexual relationships!
Yes, the gay uncle hypothesis, that the gay phenotype has positive inclusive fitness, is absurd. But I think Elo was referring to the sexual antagonism hypothesis, that the gene increases fitness in women who carry it and decreases fitness in men. Then we are out of the realm of inclusive fitness and the tradeoff is 1:1. Moreover, if the female variant has 100% penetrance and the male variant only 1⁄3 penetrance, then there is a 3:1 advantage. So if gay men are down a child, female carriers only need to have 1⁄3 of an extra child.
In one sense 1⁄3 of an extra child is small. It would be pretty hard to measure that sisters of gay men have 1⁄6 of an extra child. The claim isn’t immediately inconsistent with the two observations of (1) gay equilibrium; and (2) not particularly fecund relatives. But in another sense, 1⁄3 of an extra child in reach is a huge fitness boost and I would expect natural selection to find another route to this opportunity. So I don’t believe this, either, but it’s a lot better than the gay uncle hypothesis.
Well, maybe. I don’t much like that either since you would expect some sex-linked adaptations to neutralize it in males on the Y chromosome (and you would expect to see low genetic correlation between female homosexuality and male homosexuality if they’re entirely different things) and I don’t think I’ve seen many plausible examples of sexual antagonism in humans. (Actually, none come to mind.) It’s better than overall inclusive fitness but still straining credulity for such a pervasive fitness-penalizing phenomenon.
In one sense 1⁄3 of an extra child is small. It would be pretty hard to measure that sisters of gay men have 1⁄6 of an extra child.
Why is that? 0.33 kids vs a mean of 2.1 and an SD of I dunno, 3 (lots of people have 0 kids, a fair number have 4-6), implies a fairly observable effect size with a sample requirement of n=1300 (power.t.test(power=0.8, d=0.33/3)), even less if you take advantage of within-family comparisons to control away some of that variance, and it doesn’t require a particularly exotic survey dataset—most studies which ask in as much detail as sexual orientation will also collect basic stuff like ‘number of offspring’.
Your power calculation was for an effect size of 1⁄3, which only makes sense if you know exactly which women have the gene.
The obvious test is to look at the children of sisters of gay vs straight men. But then the relationship is 1⁄2, so this cuts down the necessary advantage to 1⁄6. This has been done, but it is not at all standard, and I the sample size was too small. Aunts have the advantage of having being older and thus more likely to have completed their fertility and the disadvantage of being less related.
The fertility of mothers is more commonly measured: the number of siblings. And, indeed, it is often claimed that gay men come from large families, or at least that they have older brothers. But we still don’t know that the mother has the gene. As a warm-up, consider the case of penetrance still 1⁄3, but gays having no children, requiring female carriers to have an extra 2⁄3 to compensate. Then male carriers have 4⁄3 children and female carriers 8⁄3, so the gay man is 2⁄3 likely to have gotten the gene from his mother, 1⁄3 from his straight father. So his expected family size is an extra 4⁄9, which is measurable in a large sample.
Back to my model where gay men have 1 child and female carriers 7⁄3. Then the gay son is 7⁄12 likely to have gotten the gene from his mother, 4⁄12 from his straight father and 1⁄12 from his gay father. So a naive calculation says that his family size should be boosted by 1/3*7/12 and reduced by 1*1/12, thus net increased by 1⁄9, which is very small. (This is naive because the fertility of a gay man conditioning on his having a child probably depends on the exact distribution of fertility. This problem also comes up conditioning on the mother having a child, but with a small fertility advantage it probably doesn’t matter much comparing the mother of a gay and a straight.)
Your power calculation was for an effect size of 1⁄3, which only makes sense if you know exactly which women
Not sure I follow. I wasn’t talking about the gene, I was talking about the net fertility impact which must exist in the sisters to offset their gay brother’s lack of fitness. If you want to see if it exists, all you have to do is compare the sisters of gay men to non-gay men; either the former have enough extra babies to make up for it or not.
have the gene.
There is no single gene for homosexuality otherwise the pedigree studies would look much clearer than they do and not like a liability-threshold sort of thing, the linkage studies would’ve likely already found it, or 23andMe’s GWAS would’ve (homosexuality is so common that a single variant would have to be very common; they probably ran a GCTA since I know they’ve GCTAed at least 100 traits they haven’t published on but not whether they checked the correlation with chromosome length to check for polygenicity). So I’m not sure your calculations there are relevant.
Yes, of course all my calculations are under the simplifying assumption of a single gene. But under that assumption, sisters of gay men have only 1⁄2 chance of having the gene and so their expected additional number of babies is only 1⁄6. If you don’t think that this assumption is appropriate, you can suggest some other model and do a calculation. One thing I can guarantee you is that it won’t produce the number 1⁄3.
If you don’t think that this assumption is appropriate, you can suggest some other model and do a calculation. One thing I can guarantee you is that it won’t produce the number 1⁄3.
I think you’re missing the point. The effect size of the gene or genes is irrelevant, as is the architecture. There can be any distribution as long as there’s enough to be consistent with current genetic research on homosexuality having turned up few or no hits (linkage, 23andMe’s GWAS & GCTA, etc). The important question is merely: do their sisters have enough kids to via inclusive fitness make up for their own lack of kids? If the answer is no, you’re done with the sexual antagonism theory, so you only need to detect that. This is set by the fitness penalty of being homosexual, not by any multiplications. So if homosexuals have 1 fewer kid, then you need to detect 2 kids among their sisters, and so on. From that you do the power calculation.
So if homosexuals have 1 fewer kid, then you need to detect 2 kids among their sisters, and so on. From that you do the power calculation.
Back when you did the power calculation for 1⁄3 rather than 2, you didn’t believe that. This number 2 is wrong for three reasons:
Inclusive fitness is irrelevant to the antagonistic selection hypothesis. (factor of 2)
It ignores penetrance, which is clearly not 100%; it doesn’t matter how many children homosexuals have, but rather how many children (male) carriers of the gene(s) have. (factor of 3)
It ignores the fact that siblings only are only 1⁄2 related. The relevant gene(s) should only elevate the fertility of carriers, not all sisters. (factor of 2)
there was a theory that the genes that confer gay men also confer extra fertility for women (and twinning). So keeping the genes in the population via other mechanisms. (I think the research was in Italian families, no link sorry.)
Aside from the inclusive fitness claim, Cochran’s gay germ hypothesis is also consistent with the continued existence of homosexuality: the pathogen co-evolves and so while the genes do get selected against, which genes keeps changing. Unfortunately, his theory still remains something of a ‘germ of the gaps’ theory—no one’s come up with a remotely plausible theory or found decent evidence that homosexuality spikes the fertility of relatives so much as to compensate for the sterility of homosexuals (remember, inclusive fitness decreases fast: if a homosexual has 1.05 rather than 2.1 children, then their siblings have to have 2.1 additional children, their cousins 4.2 additional children, and so on), so a theory which merely isn’t contradicted by any evidence looks pretty good by comparison.
One thing I thought of which would be direct evidence for the infection theory: polygenic scores for homosexuality. It’s somewhat heritable, so given a large sample size like UK Biobank, it should be possible to explain a few % of variance and construct a PGS based on a fairly narrow age cohort like 1 or 2 decades. Then the PGS can be applied longitudinally outside the sample. If it’s pathogenic co-evolution and the relevant genes keep changing, then the homosexuality PGS should show highest predictive validity in the original age bracket, but then decrease steadily as one moves away from the age bracket into the past or toward the present, showing a clear inverted V shape. While polygenic scores can increase or decrease steadily or show sudden shocks for various reasons just like heritabilities can increase/decrease over time (eg education PGS decrease due to dysgenics, height PGS increase and so on), they don’t typically show a distinct V shape, so finding one for homosexuality would be very striking.
My theory and meta-theory: The gay germ theory is pretty silly. But the big myth to which it is a reaction, is the idea that people are simply “born that way”. Cochran has a paranoid intuition that something else is happening, so he posits his gay germ. But what’s really happening is sexual imprinting. A person’s sexuality is greatly shaped by the first conditions under which they experience arousal, orgasm, and emotional bonding. Sexualities are “transmitted” in a way a little like languages. There’s no “German germ” which makes people think and speak auf deutsch, instead there’s some sort of deep learning based on early experience of a German-speaking environment. The acquisition of sexuality might be more like conditioning than learning, but it’s still an acquired trait.
That theory is even worse than the inclusive fitness one because you offer no mechanism whatsoever to offset the huge fitness penalty.
Sexual imprinting is a highly successful evolved mechanism critical to reproductive fitness which does in fact succeed in the overwhelming majority of cases; in many ways, it is more important than trivial details like ‘eating food’ because at least an offspring which immediately starves to death doesn’t drain parental resources and compete with siblings and the parents can try again! There should be a very good reason why such an important thing, found throughout the animal kingdom in far stupider & less sexually-dimorphic organisms, goes wrong in such a consistent way when other complex behaviors work at a higher rate and fail much more bluntly & chaotically. ‘Random imprinting’ is too weak a mechanism to thwart such a critical device, and doesn’t explain why the errors do not rapidly disappear with general or sex-linked adaptations. (Even as a 5% liability-threshold binary trait, a reproductive fitness penalty of 50%, to be generous to a trait which involves active aversion to procreative sex, would imply it should be far lower now than when it first arose*.)
Further, such a random nonshared environment theory doesn’t explain why dizygotic and monozygotic same-sex twins differ in concordance. (They don’t differ in language, so your example is evidence against your imprinting theory.)
* https://www.researchgate.net/profile/J_Bailey2/publication/21311211_A_genetic_study_of_male_sexual_orientation/links/02e7e53c1a72a8a596000000.pdf gives a low end heritability estimate of 0.31; population prevalence among males is usually estimated ~5% giving a liability threshold of ~-1.64; homosexuality is amply documented for the past 2500 years or so, at least back to the ancient Greeks, which at a generation time of ~25 years, means 100 generations. So assuming a fitness penalty of ‘just’ half and that selection started only 100 generations ago (rather than much further back), we would expect the rate of homosexuality to be less than 1/5th what it is.
My guess is that it’s somehow a spandrel of intelligence.
To be immune to selection because it’s part of intelligence would imply a strong genetic correlation. Aside from the fact that I am doubtful any such genetic correlation will ever be found (there is no noted phenotypic correlation of homosexuality & intelligence that I’ve heard of), this still has the issue that homosexuality ought to be decreasing noticeably over time: while intelligence has apparently been neutral or selected for over the past few millennia and so hypothetically could’ve slowed the selection against homosexuality, intelligence itself has been selected against for at least a century, so that would accelerate the selection now that there are fitness penalties for both homosexuality & intelligence (by a fair bit, because selection on continuous traits is much faster than selection on rare binary traits).
I’ve heard the raw correlation widely claimed, but I think most people interpret it as measuring closeting. Certainly openly gay men have higher income than straight men.
I’d be inclined to suspect closeting too. The better your ability to support yourself, the less you need to worry about repercussions.
Tangential and possibly relevant: I’ve noticed bisexual women appear to be ridiculously common in high-intelligence nerd communities. I don’t know whether I should associate that with the intelligence or the geek/nerd/dork personality cluster, nor do I know which way the causation goes.
You only posit that because your paranoid ignorance of biology.
Bullshit. Cochran wrote down his exact thought process. He thinks that everything is due to germs. Moreover, he measures of the strength of the evidence. Schizophrenia and (male) homosexuality are at the top of the list
OK, let’s talk about proximate causes and ultimate causes. The proximate causes are whatever leads to the formation of a particular human individual’s sexuality. The ultimate causes are whatever it is that brought about the existence of a population of organisms in which a given sexuality is even possible.
My focus has been on proximate causes. I look at the role of fantasy, choice, and culture in shaping what a person seeks and what they can obtain, and the powerful conditioning effect of emotional and sexual reward once obtained, and I see no need at all to posit an extra category of cause, in order to explain the existence of homosexuality. It’s just how some people end up satisfying their emotional and sexual drives.
What I had not grasped, is that the idea of the gay germ is being motivated by consideration of ultimate causes—all this talk of fitness penalties and failure to reproduce. I guess I thought Cochran was a science-jock who couldn’t imagine being gay, and who therefore sought to explain it as resulting from an intruding perturbation of human nature.
I am frankly not sure how seriously I should take the argument that there has to be (in gwern’s words) a “mechanism… to offset the huge fitness penalty”. Humanity evolves through sexual selection, right? And there are lots of losers in every generation. Apparently that’s part of our evolutionary “business model”. Meanwhile I’ve argued that non-reproducing homosexuality is a human variation that arises quite easily, given our overall cognitive ensemble. So maybe natural selection has neither a clear incentive to eliminate it, nor a clear target to aim at anyway.
I agree with what you said, and it is borne out very well by my experience of gay persons. As for gwern’s comment, the silliness is to think that evolution has enough selective power to completely remove that sort of thing. In fact, it would be far easier for evolution to remove a gay gene than for it to prevent things that happen through accidental social circumstances.
Consider this: I am over 40, I do not have children and have never had sex, and I have no intention to do so. Shouldn’t evolution have completely removed the possibility of people like me? I am not even helping other people raise children. I live alone, and consume my own resources.
The answer is that if “people like me” came about because of a specific gene, evolution would indeed have removed the possibility. As it is, it comes about through a vast collection of accidental and social facts, and the most evolution can do is make it rare, which it does. The same is true of homosexuality.
Whereas you can imagine it so easily that you didn’t bother to look at the real world, just as you can imagine Cochran so easily you didn’t bother to look at him
90% of biologists don’t believe in evolution, either, but progress comes from those who do.
I believe in evolution, I just don’t believe in the gay germ.
But regardless of belief… I have some questions which I think are fair questions.
Are there any ideas about how and when the gay germ is acquired?
Are there any ideas about its mechanism of action?
If homosexuality has such a huge fitness penalty, why haven’t we evolved immunity to the gay germ?
If someone hasn’t experienced sex yet, but they already think they are gay, is that because of the gay germ?
Gays generally say that they “always knew they were different” (and there is some evidence that this is not just confabulated memories), so it is probably acquired before age 5, possibly before birth. It is probably something common, like the flu. And there might be multiple infections that cause the same brain changes, as appears to be the case with narcolepsy.
You could ask a similar question about any explanation of homosexuality. It is measured to be weakly heritable. So we know that there are genes that protect from it. Given the fitness penalty, why haven’t those genes swept through the population? That wouldn’t necessarily eliminate it, but they would eliminate the heritability.
There are only two possibilities: either the fitness penalty is not what it looks like (eg, the sexual antagonism hypothesis); or the environment has changed so that which genes protect has changed.
Germ theory gives a simple explanation for changing environment, The Red Queen Hypothesis: the germ is evolving, so the genes that protect against it are changing. This is the metric that Cochran and Ewald use: multiply the fitness cost by the heritability. The higher that number, the more likely the cause is infection.
There actually is a known replicator that assists the reproduction of gay phenotypes, but it’s a behavior: gay sex! For a recent exposition, see the video that cost “Milo” his job.
No, there is no evidence of such replication. This isn’t really compatible with gays being detectable at age <5. Also, it’s pretty clear that isn’t what happens in sheep, which are highly analogous.
Common infections can have effects on a small population. For example, Barr-Epstein is implicated in at least some cases of narcolepsy, but 95% of the population tests positive for it.
What about pederasty in ancient Greece, what about sex in all-male prisons… in both those cases, you have men who by current definitions are not gay, but rather bisexual. And in both cases you have recruitment into an existing sexual culture, whether through seduction or coercion.
Human sexuality can clearly assume an enormous variety of forms, and I don’t have a unified theory of it. Obviously genes matter, starting with the basic facts of sex determination, and then in a more elusive way, having some effect on sexual dispositions in the mature organism.
And yes, natural selection will be at work. But, in this case it is heavily mediated by culture (which is itself a realm of replicator populations), and it is constrained by the evolvability of the human genome. I continue to think that the existence of nonreproductive sexuality is simply a side effect of our genomic and evolutionary “business model”, of leaky sexual dimorphism combined with Turing-complete cognition.
Pederasty in ancient Greece was culturally very different from modern homosexual behavior though (or at least, the conventional view thereof; some people would contend that the ‘ancient’ model is very much lurking beneath the surface of even the most modern, ‘egalitarian’ gay relationships!). In that case, there was a very clear demarcation between an active participant (the pederast or erastês) who did behave ‘bisexually’ in some sense, but was really more properly connoted as highly masculine, and a passive participant (the erômenos) who was the only one to be specially connoted as ‘feminine’.
The sexual manifestations of pederasty were also criticized by quite a few philosophers and intellectuals, and the tone of these critiques suggests that pederasty could easily shade into sexually abusive behavior. (Notably, Christian morality also shared this critical attitude—the heavy censure of “homosexuality” and heterosexual “fornication” one finds in the New Testament can really only be understood in the light of Graeco-Roman sexual practices). Sex in all-male prisons also seems to share many of these same features; at the very least, if the common stereotypes of it are to be believed, it doesn’t really feature the ‘egalitarianism’ of modern homosexual relationships!
Yes, the gay uncle hypothesis, that the gay phenotype has positive inclusive fitness, is absurd.
But I think Elo was referring to the sexual antagonism hypothesis, that the gene increases fitness in women who carry it and decreases fitness in men. Then we are out of the realm of inclusive fitness and the tradeoff is 1:1. Moreover, if the female variant has 100% penetrance and the male variant only 1⁄3 penetrance, then there is a 3:1 advantage. So if gay men are down a child, female carriers only need to have 1⁄3 of an extra child.
In one sense 1⁄3 of an extra child is small. It would be pretty hard to measure that sisters of gay men have 1⁄6 of an extra child. The claim isn’t immediately inconsistent with the two observations of (1) gay equilibrium; and (2) not particularly fecund relatives. But in another sense, 1⁄3 of an extra child in reach is a huge fitness boost and I would expect natural selection to find another route to this opportunity. So I don’t believe this, either, but it’s a lot better than the gay uncle hypothesis.
Well, maybe. I don’t much like that either since you would expect some sex-linked adaptations to neutralize it in males on the Y chromosome (and you would expect to see low genetic correlation between female homosexuality and male homosexuality if they’re entirely different things) and I don’t think I’ve seen many plausible examples of sexual antagonism in humans. (Actually, none come to mind.) It’s better than overall inclusive fitness but still straining credulity for such a pervasive fitness-penalizing phenomenon.
Why is that? 0.33 kids vs a mean of 2.1 and an SD of I dunno, 3 (lots of people have 0 kids, a fair number have 4-6), implies a fairly observable effect size with a sample requirement of n=1300 (
power.t.test(power=0.8, d=0.33/3)), even less if you take advantage of within-family comparisons to control away some of that variance, and it doesn’t require a particularly exotic survey dataset—most studies which ask in as much detail as sexual orientation will also collect basic stuff like ‘number of offspring’.Your power calculation was for an effect size of 1⁄3, which only makes sense if you know exactly which women have the gene.
The obvious test is to look at the children of sisters of gay vs straight men. But then the relationship is 1⁄2, so this cuts down the necessary advantage to 1⁄6. This has been done, but it is not at all standard, and I the sample size was too small. Aunts have the advantage of having being older and thus more likely to have completed their fertility and the disadvantage of being less related.
The fertility of mothers is more commonly measured: the number of siblings. And, indeed, it is often claimed that gay men come from large families, or at least that they have older brothers. But we still don’t know that the mother has the gene. As a warm-up, consider the case of penetrance still 1⁄3, but gays having no children, requiring female carriers to have an extra 2⁄3 to compensate. Then male carriers have 4⁄3 children and female carriers 8⁄3, so the gay man is 2⁄3 likely to have gotten the gene from his mother, 1⁄3 from his straight father. So his expected family size is an extra 4⁄9, which is measurable in a large sample.
Back to my model where gay men have 1 child and female carriers 7⁄3. Then the gay son is 7⁄12 likely to have gotten the gene from his mother, 4⁄12 from his straight father and 1⁄12 from his gay father. So a naive calculation says that his family size should be boosted by 1/3*7/12 and reduced by 1*1/12, thus net increased by 1⁄9, which is very small. (This is naive because the fertility of a gay man conditioning on his having a child probably depends on the exact distribution of fertility. This problem also comes up conditioning on the mother having a child, but with a small fertility advantage it probably doesn’t matter much comparing the mother of a gay and a straight.)
Not sure I follow. I wasn’t talking about the gene, I was talking about the net fertility impact which must exist in the sisters to offset their gay brother’s lack of fitness. If you want to see if it exists, all you have to do is compare the sisters of gay men to non-gay men; either the former have enough extra babies to make up for it or not.
There is no single gene for homosexuality otherwise the pedigree studies would look much clearer than they do and not like a liability-threshold sort of thing, the linkage studies would’ve likely already found it, or 23andMe’s GWAS would’ve (homosexuality is so common that a single variant would have to be very common; they probably ran a GCTA since I know they’ve GCTAed at least 100 traits they haven’t published on but not whether they checked the correlation with chromosome length to check for polygenicity). So I’m not sure your calculations there are relevant.
Yes, of course all my calculations are under the simplifying assumption of a single gene. But under that assumption, sisters of gay men have only 1⁄2 chance of having the gene and so their expected additional number of babies is only 1⁄6. If you don’t think that this assumption is appropriate, you can suggest some other model and do a calculation. One thing I can guarantee you is that it won’t produce the number 1⁄3.
I think you’re missing the point. The effect size of the gene or genes is irrelevant, as is the architecture. There can be any distribution as long as there’s enough to be consistent with current genetic research on homosexuality having turned up few or no hits (linkage, 23andMe’s GWAS & GCTA, etc). The important question is merely: do their sisters have enough kids to via inclusive fitness make up for their own lack of kids? If the answer is no, you’re done with the sexual antagonism theory, so you only need to detect that. This is set by the fitness penalty of being homosexual, not by any multiplications. So if homosexuals have 1 fewer kid, then you need to detect 2 kids among their sisters, and so on. From that you do the power calculation.
Back when you did the power calculation for 1⁄3 rather than 2, you didn’t believe that. This number 2 is wrong for three reasons:
Inclusive fitness is irrelevant to the antagonistic selection hypothesis. (factor of 2)
It ignores penetrance, which is clearly not 100%; it doesn’t matter how many children homosexuals have, but rather how many children (male) carriers of the gene(s) have. (factor of 3)
It ignores the fact that siblings only are only 1⁄2 related. The relevant gene(s) should only elevate the fertility of carriers, not all sisters. (factor of 2)