Humans show variation in sexual behaviour which includes the presence of same-sex partner preferences in a minority. This manifestation of human sexual variation has been and is subject to moral censure in certain (sub)cultures, which has led to a charged debate about the naturalness or otherwise of homosexuality. Perhaps, if it can be established that some people are born gay, moralising conservatives can be silenced because a gay person cannot be expected to violate his or her inherent nature.
Now male-specific mating behaviours and preferences are thought to be programmed into the brain by in utero exposure to androgens (male sex hormones, e.g. testosterone) and some brain regions show differences between the sexes. But a recent rodent study published in the journal Nature (here; summary here; both require access) suggests that we need a radical rethink. Kimchi et al. worked with mice that carried null mutations in a gene, Trpc2, that codes for an ion channel expressed in the vomeronasal organ (VNO). The VNO, also known as Jacobson’s organ, is a small inclusion above the buccal (mouth) cavity that contains pheromone-detecting receptors and which receives its input from the nasal cavity via a duct. And, because the Trpc2 ion channel constitutes a shared component in the signalling pathways of many pheromone receptors, ablating the Trpc2 gene (which is what the null mutation does) renders the VNO inoperative and prevents pheromone detection.
Before this recent study it was known that Trpc2 knockout male mice were unable to distinguish between the sexes, indiscriminately mounting newly introduced males and females and failing to show the usual aggressive response towards intruder males. Kimchi et al. show that female Trpc2 knockout mice also failed to distinguish the sex of introduced mice, but the nature of their responses to them was surprising. The knockout females showed male-typical sexual and soliciting behaviours towards all comers of either sex (see videos here; requires access); they attempted to mount them, they thrusted towards them during mounting, they probed the anogenital region and they emitted complex ultrasonic vocalisations. This led the authors to suggest that these male-typical behaviour patterns are latent in normal females and are normally repressed by pheromonal signalling through the VNO.
An obvious conflating factor in interpreting these results in this way is that ablation of the Trpc2 gene might have effects earlier in development rather than in adult animals. But Kimchi et al. also removed the VNO from adult animals (taking care to prevent blood clots forming that might block olfaction altogether or excluding data when this was shown to have occurred post-mortem). In this way they were able to replicate their findings that loss of VNO functioning results in activation of male-specific behaviours in adult females. This effect was also robust to whether females were sexually naive or experienced and to whether experiments took place in cages or in semi-natural conditions.
Now the VNO is probably vestigial in humans and the TRPC2 gene is a pseudogene in catarrhine primates (Old World monkeys and the apes). In general the role of olfaction (of both odours and odourless pheromones) seems to have decreased in the Old World versus the New World monkeys and all the more so in humans versus all other primates. So although there is some evidence for expression of a pheromone receptor gene in the human olfactory epithelium, we might reasonably expect humans to exhibit rather different dependencies between pheromones and sex. It is obviously too early to conclude that Kimchi et al.’s findings bear directly on human sexual behaviour. And their experiments did not demonstrate the converse case by eliciting female-specific behaviours in males – these may or may not be latent in male mice.
However, I believe it is worth entertaining the hypothesis that in humans male- and female-specific behaviours can be activated by various cues and that developmental perturbations might result in altered sex-typical behaviours during adulthood. There are two important caveats to this: 1. adopting behaviour typical of the other sex is not the same as homosexuality (and the mice in this study seemed to be altogether lacking in partner preferences) and 2. latent sexual proclivites do not negate the possibility that variation in sexual behaviour is genetically influenced. Indeed the Nature study showed that either surgical intervention or genetic modification could release male-typical behaviours in females and they used this to establish that male/female differences were not localised in sexually dimorphic brain regions, but are instead achieved by a switch mechanism in adults. Mice can still be born with this switch set to a particular position.
But I think that the discovery of this mechanism should increase our expectation that environmental effects might be significant in the development of homosexual behaviours. This is because it puts disinhibition in a causal role. It is easier to imagine a range of environmental effects that could interfere with and thereby disinhibit sexual programmes than it is to envisage environmental perturbations that can reorganise sexual behaviour de novo.
Finally allow me to add that I believe that the question of the heritablity of sexual behaviour need have no bearing on moral judgements. This should be evident from two examples. First, I would guess that many would agree with me that paedophilia, or at least paederasty, is a moral problem regardless of whether experience or genes tend to explain more of the variation in this trait because in either case children are likely to suffer harm. Second, I imagine that the fact that some gentleman prefer blondes, even if this could be shown to be a culturally mediated preference, would not be a cause for alarm because this trait is not associated with violation of consent or with causing harm. For full clarity – I do not believe that homosexual behaviour is harmful or wrong, any more so than heterosexual behaviour.