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)
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)