Genetic determinism: infidelity edition

New York Times columnist Richard Friedman is writing about hormones, genetics, and infidelity.  This paragraph is about recently-published research by Brendan Zietsch and colleagues (the NYT tries to link, but the URL is wrong)

His study, published last year in Evolution and Human Behavior, found a significant association between five different variants of the vasopressin gene and infidelity in women only and no relationship between the oxytocin genes and sexual behavior for either sex. That was impressive: Forty percent of the variation in promiscuous behavior in women could be attributed to genes.

If you didn’t read carefully you might think this was a claim that the  vasopressin gene association explained the “Forty percent” and that the percentage was lower in men. In fact, the vasopressin gene associations are rather weaker than that, and the variation attributed by the researchers to genes is 62% in men.

But it gets worse. The correlation with genetics was only seen in identical twins. That is, pairs of identical twins had fairly similar cheating behaviour , but there was no similarity at all between pairs of non-identical twins (of any gender combination) or between non-twin siblings.  If that’s not due to chance (which it could be), it’s very surprising. It doesn’t rule out a genetic explanation — but it means the genetics would have to be weird.  You’d need either a variant that had opposite effects with one versus two copies, or a lot of variants that only had effects with two copies and no effect with one, or an effect that switched on only when you had variant copies of multiple genes, or an effect driven by new mutations not inherited from parents.  The results for the vasopressin gene don’t have this kind of weird.

The story is all “yes, it’s surprising that you’d get this sort of effect in a complex social behaviour, but genetics! And voles!”. I’ll give him the voles, but if anything, the strong correlation between identical twins (only) argues against vasopressin gene variants being a major driver in humans, and the research paper is much more cautious on this point.