Are you a heterosexual woman seeking a monogamous relationship? Have you ever wanted to genetically test a prospective partner for his ability to remain happily monogamous?
If so, don't pin your hopes on a study published last week in the Proceedings of the National Academy of Sciences. The study suggests that men with a particular gene variant are twice as likely as men without it to be bad at "pair bonding." Like so many genetic findings about complex human traits, if replicated, this finding would be of genuine interest. But it wouldn't be remotely enough for a new genetic test of infidelity.
Since the early 1990s, researchers have investigated the role that the hormone vasopressin has in the pair-bonding behavior of our evolutionary cousins, the voles. (Voles look like chubby mice.) In 2004 researchers took a vasopressin-related gene from one species of vole known for its monogamy, and transferred it to another species known for its infidelity. Miraculously, the vole Eliot Spitzers became vole Joe Bidens. Leaving aside questions about, for example, what monogamy means in voles, the results of that experiment were intriguing.
The new PNAS study moves from voles to humans. What is the relationship between gene variants associated with the expression of vasopressin in humans, and our pair-bonding behavior?
The researchers found no association between the variants they investigated and pair bonding behavior in women. But they did find that men with two copies of a particular gene variant were less likely than men without it to be engaged in happy monogamous relationships. Specifically, whereas 34 percent of the men with two copies of the gene variant had marital difficulties, only 15 percent of the men with no copies exhibited such difficulties. A gene variant that may confer twice the risk of trouble is interesting, but it's also depressingly easy to over-interpret.
First, it's possible to have the gene variant but to have no marital difficulties. (66 percent of the men with two copies of the variant had no marital trouble.) Second, it's possible to have marital difficulties but not have the gene variant. (Again, 15 percent of the men with no copies of the variant did have trouble.) So, taking the results at face value, if you're a man and have the variant, you're surely not automatically in trouble - and if you don't have the variant, you surely might still be unfaithful. Indeed, in their own argot, the authors of the PNAS piece explicitly acknowledge that their gene variant has "a relatively small effect size."
It wasn't so long ago that geneticists thought they might identify single gene variants that caused complex disorders. After all, in the 1980s and '90s, they found single-gene variants that by themselves caused rare disorders like Huntington's disease and cystic fibrosis. In those heady days, it didn't seem like a stretch to believe that, if single genes could cause rare disorders, they might also cause common disorders like hypertension and depression. Nor did it seem like a stretch to hope that this One-Gene-One-Disorder (or O GOD) model could also illuminate common complex traits like "aggression" or "novelty seeking" - or "pair bonding."
But in the last several years, the O GOD model has died. Editors at Nature bluntly wrote last month that genes are surely involved in the emergence of common psychiatric disorders, "but decades of futile hunting have made it painfully clear that the contribution of any single gene to disease is probably minuscule." Of course the same goes for complex traits like pair bonding: the contribution of any single gene will be small.
It's not that genes are unimportant. Decades of comparing identical and fraternal twins show that the aggregate effects of multiple genes are indeed important in explaining the emergence of virtually all complex diseases and traits.
It's just that years of searching in vain for single genes to explain complex traits has revealed the need for an infinitely more complex model. Common traits and disorders now appear to be the result of myriad genes interacting over time with each other, as well as with myriad other biological and environmental variables.
We should be grateful when we find what might be another small piece of a fabulously complex puzzle. But we should have learned by now to curb our enthusiasm. In a time when start-up companies are beginning to advertise gene scans that purport to help us glimpse our futures, we must remember that very few disorders or character traits - least of all infidelity - are caused by single genes.
Erik Parens, Ph.D., is a senior research scholar at The Hastings Center, a nonpartisan research institution dedicated to bioethics and the public interest. He studies how we use new technologies to shape ourselves, and how emerging science shapes our self-understanding. He is co-editor (with Nancy Press and Audrey Chapman) of "Wrestling with Behavioral Genetics: Science, Ethics and Public Conversation," (Johns Hopkins University Press, 2006).
This article appeared on page B - 9 of the San Francisco Chronicle. See Original article