But how do we know if this is a valid question—if the situation really needs to be explained at all?
Percentage of the population with the condition. (RichardKennaway’s comment explains how you would calculate the ‘expected rate’ from underlying conditions, but here I’ll just use statistical comparisons.)
The rate of major birth defects in the US, as reported by the CDC, is also about 3%.
This comparison is a category error—the comparison isn’t “homosexuality” vs. “all birth defects,” but “homosexuality” vs. “any individual birth defect.” The most common birth defects are in the “1 in 2000” range, not the “1 in 30-50″ range; so what the heck is causing there to be ~40-80 times as many homosexuals?
Embryological development is a complex and fragile process, and there are many ways for it to go wrong. We don’t wonder how it is possible that selection pressure allows anencephaly to occur in 1 in 4859 births.
Note that anencephaly leads to early death, and you might think that in most evolutionarily relevant time periods, the costs of of raising a child to adulthood may have been significantly larger than the costs in bringing a pregnancy to term. A gene that halves your chance of giving birth to a child with anencephaly will have a very tiny impact on your overall fitness, and thus take a long time to spread through the population.
This comparison is a category error—the comparison isn’t “homosexuality” vs. “all birth defects,” but “homosexuality” vs. “any individual birth defect.”
This is true (noted also by Douglas_Knight here). It’s a little weakened by the fact that homosexuality likely has several different possible causes, which should also be considered separately. The loss of fitness due to homosexuality is also much less than that due to severe birth defects. I think given these initial data, the question still deserves a quantitative analysis. But I can’t really judge because I don’t know the relevant math—that’s what I hoped someone would give in response to my post.
Note that anencephaly leads to early death, and you might think that in most evolutionarily relevant time periods, the costs of of raising a child to adulthood may have been significantly larger than the costs in bringing a pregnancy to term. A gene that halves your chance of giving birth to a child with anencephaly will have a very tiny impact on your overall fitness, and thus take a long time to spread through the population.
From the gene’s eye view, an allele isn’t guaranteed to be selected during recombination. It seems to me that after conception, natural selection should operate on the fitness of the actual child as well as the inclusive fitness of the parents affected by raising the child. But I’m just handwaving and guessing here.
Wikipedia on causes of homosexuality says there are “various biological causes”, and quotes:
The American Academy of Pediatrics stated in Pediatrics in 2004:
Sexual orientation probably is not determined by any one factor but by a combination of genetic, hormonal, and
environmental influences. In recent decades, biologically based theories have been favored by experts....
The American Psychological Association states “there are probably many reasons for a person’s sexual orientation and the reasons may be different for different people
We’re interested specifically in the heritable component, which seems to be relatively small. There certainly seem to be some specific genetic loci involved, one on the X chromosome and another probably on chromosome 8.
At least one proposed etiology says the mother’s immune reaction to the fetus affects its sexual determination, so we should be looking at genetic correlations in mothers of homosexual children as well as in the children themselves.
Wikipedia on causes of homosexuality says there are “various biological causes”, and quotes:
I don’t much care about quotes from very prestigious professional bodies; they are always mealy-mouthed and self-serving, where they do not endorse pleasing claims on radically insufficient evidence (eg diet). What’s more relevant is the actual research, like the link to https://en.wikipedia.org/wiki/Biology_and_sexual_orientation ; I’m not too impressed, as it seems to be mostly a laundry list of fairly dubious corrrelations and downstream effects or irrelevant to humans animal research (does anyone think that deleting an entire gene in mice to turn them gay tells us anything relevant about causes in healthy humans?).
Lots of things are simple. If the world is not simple, inference is impossible. Many things turn out to be straightforward; as complex and intricate a phenomenon as AIDS is, ‘HIV causes AIDS’ is much more accurate than ‘AIDS is not determined by any one factor but by a combination of genetic, hormonal, and environmental influences; in recent years, biologically-based theories have been favored by experts...’ In statistical modeling, it’s far from surprising to discover that a few variables have most of the predictive value and that it’s only the last few percent which require extreme complexity to predict or model.
Many small scale biological features are re-used over and over, if they break, many things can break a bit. Primary ciliary dyskinesia is an example if this. In the meantime, many complex adaptive structures (like “the ability to hear”) are caused by more than one subcomponent, so any of several different subcomponents breaking can produce a symptomatically similar disruption of the complex structure.
Biological causes and biological outcomes are in a many-to-many relationship, with lots of “best effort” failover systems as backups. The amount of effort to put into fixing up a structure is itself something that most of the animal kingdom has optimized a bit, for example via the poorly named “heat shock proteins” that suppress mutational expression in good times but reveal the mutations in bad times.
In the case of male homosexuality, one cause that I recall hearing debate about was that a male child causes a mother’s body to change (current best guess is something immunological), such that later male fetuses appear to have their sexual development mildly disrupted. If I recall correctly, the process looks probabilistically cumulative, so that there’s something like a 1⁄3 chance of homosexuality by the time you get to the fifth or sixth male child from the same mother. Again, if I recall correctly, with modern demography this effect might be enough to account for ~20% of gay men? This is somewhat controversial, but le wik has some of the debate.
Percentage of the population with the condition. (RichardKennaway’s comment explains how you would calculate the ‘expected rate’ from underlying conditions, but here I’ll just use statistical comparisons.)
This comparison is a category error—the comparison isn’t “homosexuality” vs. “all birth defects,” but “homosexuality” vs. “any individual birth defect.” The most common birth defects are in the “1 in 2000” range, not the “1 in 30-50″ range; so what the heck is causing there to be ~40-80 times as many homosexuals?
Note that anencephaly leads to early death, and you might think that in most evolutionarily relevant time periods, the costs of of raising a child to adulthood may have been significantly larger than the costs in bringing a pregnancy to term. A gene that halves your chance of giving birth to a child with anencephaly will have a very tiny impact on your overall fitness, and thus take a long time to spread through the population.
This is true (noted also by Douglas_Knight here). It’s a little weakened by the fact that homosexuality likely has several different possible causes, which should also be considered separately. The loss of fitness due to homosexuality is also much less than that due to severe birth defects. I think given these initial data, the question still deserves a quantitative analysis. But I can’t really judge because I don’t know the relevant math—that’s what I hoped someone would give in response to my post.
From the gene’s eye view, an allele isn’t guaranteed to be selected during recombination. It seems to me that after conception, natural selection should operate on the fitness of the actual child as well as the inclusive fitness of the parents affected by raising the child. But I’m just handwaving and guessing here.
It does?
Wikipedia on causes of homosexuality says there are “various biological causes”, and quotes:
We’re interested specifically in the heritable component, which seems to be relatively small. There certainly seem to be some specific genetic loci involved, one on the X chromosome and another probably on chromosome 8.
At least one proposed etiology says the mother’s immune reaction to the fetus affects its sexual determination, so we should be looking at genetic correlations in mothers of homosexual children as well as in the children themselves.
I don’t much care about quotes from very prestigious professional bodies; they are always mealy-mouthed and self-serving, where they do not endorse pleasing claims on radically insufficient evidence (eg diet). What’s more relevant is the actual research, like the link to https://en.wikipedia.org/wiki/Biology_and_sexual_orientation ; I’m not too impressed, as it seems to be mostly a laundry list of fairly dubious corrrelations and downstream effects or irrelevant to humans animal research (does anyone think that deleting an entire gene in mice to turn them gay tells us anything relevant about causes in healthy humans?).
Fair enough. I should rely less on popularized professional consensus in this kind of thing.
Being who you are, it’s no surprise that you have this attitude (and correctly so).
Since when is anything in biology, neurology, or psychology simple?
Lots of things are simple. If the world is not simple, inference is impossible. Many things turn out to be straightforward; as complex and intricate a phenomenon as AIDS is, ‘HIV causes AIDS’ is much more accurate than ‘AIDS is not determined by any one factor but by a combination of genetic, hormonal, and environmental influences; in recent years, biologically-based theories have been favored by experts...’ In statistical modeling, it’s far from surprising to discover that a few variables have most of the predictive value and that it’s only the last few percent which require extreme complexity to predict or model.
You have explained why inference is hard in biology :-)
A technical term for the “problem” is pleiotropy.
Many small scale biological features are re-used over and over, if they break, many things can break a bit. Primary ciliary dyskinesia is an example if this. In the meantime, many complex adaptive structures (like “the ability to hear”) are caused by more than one subcomponent, so any of several different subcomponents breaking can produce a symptomatically similar disruption of the complex structure.
Biological causes and biological outcomes are in a many-to-many relationship, with lots of “best effort” failover systems as backups. The amount of effort to put into fixing up a structure is itself something that most of the animal kingdom has optimized a bit, for example via the poorly named “heat shock proteins” that suppress mutational expression in good times but reveal the mutations in bad times.
In the case of male homosexuality, one cause that I recall hearing debate about was that a male child causes a mother’s body to change (current best guess is something immunological), such that later male fetuses appear to have their sexual development mildly disrupted. If I recall correctly, the process looks probabilistically cumulative, so that there’s something like a 1⁄3 chance of homosexuality by the time you get to the fifth or sixth male child from the same mother. Again, if I recall correctly, with modern demography this effect might be enough to account for ~20% of gay men? This is somewhat controversial, but le wik has some of the debate.