The gay germ theory proposes that there is a pathogen that causes male homosexuality . The reasoning behind this theory is that the fitness hit of homosexuality is too big to allow a genetic explanation. I.e. any genetic variation involved would very quickly be weeded from the gene pool and the occurrence of homosexuality would depend on de novo mutations and be very rare. Pathogens on the other hand, can do with us whatever they want to, because we cannot out-evolve them.
However, there are several indications, that an immune reaction of the mother is somehow involved . Here, the idea would be that embryonic tissue that expresses proteins alien to the immune system is attacked and damaged. This would explain a underdevelopment of a hypothalamic nucleus responsible for a male heterosexual orientation, which expresses male specific genes during masculinization and defeminization in utero.
If we combine both ideas, we end up with a putative pathogen, that might trigger an immune response against male specific proteins. This gives us a hint how to identify the pathogen in question: It would have to be a pathogen that shares an epitope with such a male specific protein. An epitope is a surface of a folded protein, which is recognized by the immune system’s antibody.
Unfortunately identifying epitopes from protein sequences requires a solution to the protein folding problem. So we are not going to be able to do it just by downloading a bunch of genetic sequences.
However, it is entirely possible that there isn’t actually a pathogen involved. The effect of shared environment on sexual orientation, for example, is zero . Pretty weird for an infection. Instead male homosexuality might be a case of what I like to call the “too much of a good thing”-failure mode of evolution. Occasionally evolution finds itself in dead ends, where there is a selection pressure towards a good thing, and a catastrophic failure mode whenever there is too much of the good thing.
One example for this are the trisomies. Here the good thing is having a big ovum . Human egg cells are pretty big and for good reason. After fertilization they have to divide quickly and set up shop in the uterus. If they run out of gas before the placenta is in place, that’s it. One way ova get big is very unequal division in the last two rounds of cell division. One new cell keeps all the cell plasma, the other one is discarded. Very unequal cell division results in a big final cell, but it also increases the likelihood that not all of half of the chromosomes can be stashed in the small cell.
Another example might be autism. One of the symptoms of autism is neural overgrowth in some parts of the cortex . And while the average autist does not do too well on an IQ test, extreme precociousness in children is often accompanied with autism. It seems growing too many neurons and learning too fast has catastrophic failure modes too.
This could be going on with male homosexuality. A strong immune system is nice, but not if it attacks vital parts of you unborn child’s brain. Or conversely, toning down the immune system to accommodate your child is a fine thing, if it doesn’t get one or both of you killed. One could argue that evolution should find some sideway avenue to avoid the failure mode. But it didn’t for the trisomies, nor did it for autism.
 Gay germ theory
 Antibodies against male specific proteins in mothers of gay sons
 Shared environment of homosexuality is zero.
 The ovum is large.
 Brain overgrowth in autism
One thought on “Too much of a good thing”
Hang on… autism doesn’t reduce reproductive success though, does it? Anything with a fitness cost above 1% typically is selected against rather quickly by evolution. Exclusive male homosexuality has a fitness cost as low as 20% (Bell et al 1981) and closer to 80% today (roughly 20% of gay men have biological children). I think the pathogenic model is still more likely. Although, the maternal immune response model could explain it entirely too. Roughly half of pregnancies end in unknown miscarriage… so, evolution not selecting against that would imply that some maternal immune responses would no doubt bring a baby to term, albeit changed in this very specific manner…