If being a gay man is an inborn, inherent trait with some genetic basis–as the massive, overwhelming, credible, sound, tenable, probable, corroborating, confirming, affirmative collection of scientific evidence states–why are there gay men at all? It’s a trait that strongly discourages procreative sex. Less sex with women means less babies and therefore less spreading of the gay genes.

These alleles should drop out of the population.

Huh.

Well, what is known about gay men and their family members?

i. Gay men are everywhere, persisting in every culture and in every human population at more-or-less the same frequency–regardless of how much a culture loves gay men.

ii. The sisters, mothers and aunts of gay men have more babies than those without a gay brother, son or nephew–but only if the relation is through the gay man’s mother.

iii. A gay man’s male relatives are more likely to be gay–but only if related again through the gay man’s mother.

Well, we can come up with a few possible explanations, and see what best fits these observations.
1. Kin Selection.

The idea? A gay man in the family can only help make the heterosexual relatives pop out more kids and have the kids do better after birth. Babysitting, sexual counseling, consoling, food preparation, hunting…. it’s all gotta be good for making kids, right? Even if the gay uncle, brother or son doesn’t have babies himself, all those related babies are so much better off, the gay alleles survive to make future gay men!

Sadly, this appears to not be the explanation.

2. Overdominance.

This is the gay-is-like-sickle-cell-anemia argument. If having two gay alleles makes you gay, and therefore less prone to baby-making, perhaps having one gay allele makes you such a better straight man. Therefore, straight men carrying one gay and one straight allele do better than their all straight allele counterparts. So, the gay alleles survive.

3. Maternal effects

In other words, the ever popular mom-made-you-gay theory. Genetically this time. For almost all genes, we get one copy from mom and one copy from dad. For a few of these genes, one of these copies is always turned off from the mom or dad, called genetic imprinting. For example, while dad tend to want the biggest babies possible, mothers tend to prefer surviving childbirth–genetically speaking here. So, the mother’s copies of the genes for growing big tend to be turned off in the baby. Perhaps the same thing is going on for genes that make boys straight.

4. Sexually antagonistic selection.

This is the general blame-women theory. Perhaps the gene for making a gay man (not so good for future reproductive prospects) is super good for straight women (making baby making more likely and easier).

Ok, well which is it? Andrea Camperio Ciani, Paolo Cermelli, Giovanni Zanzotto recently published a possible answer in PlosONE.

Running the available empiric data about gay men through a whole bunch of models of these possibilities, they discovered one combination that best fit reality and a few aren’t really possible at all.

Overdominance seems really unlikely. None of the models including this idea fit the data all that well. Nor did the models based on maternal effects. It appears that mom cannot make you gay. Sorry.

The best fits neededtwo genetic loci (two genes), with at least one of these loci on the X chromosome. Recall, while women get two X-chromosomes, men only get one. Additionally, at least one of these alleles must be sexually antagonistic–in favor of women reproducing if they have it, even if it makes you gay as a boy.

Or, as the authors of the study stated:

Our analysis allows us to draw several conclusions that clarify the basic evolutionary dynamics of the genetic factors influencing human male homosexuality and the related female fecundity increase, resolving a number of open questions. As a main point, we can exclude the GFMH propagation mechanisms based on overdominance (male heterozygote advantage), because none of the models (1b), (5a), (5b) account satisfactorily for the sexual-orientation asymmetries of requirement (B1). At this level of genetic analysis, we can also exclude maternal effects, including maternal genomic imprinting, as they lead too easily to GFMH extinction or fixation, against requirement (A). Only the hypothesis that the GFMH are characterized by sexually antagonistic selection (i.e. the GFMH favor one sex and disfavor the other) produces viable population genetic models (see the case (4) above) leading to the persistence of the trait at low frequencies and capable of accounting for the related pedigree asymmetries. For this reason, predictions of possible widespread diffusion of male homo- or bisexuality in human populations are not warranted, as stable low levels of this character are actually compatible with a broad range of parameters in population genetic models.

For what could this allele be? Well, an obvious choice is digging dudes. If a woman has an allele that really makes her like guys, she’s more likely to have babies than a woman who has a less guy-loving allele for this gene. If she passes on this dude loving allele to her son, via the X-chromosome, perhaps he’ll be gay. But since she’s having more babies, it’s a wash.

Neat.

(Updated for clarity and some more details.)