Like meadow voles, some men just don't seem to be built for monogamy, whereas others, like swans, mate for life. New research hints that some of the difference might be due to a single genetic variation.
The gene in question, AVPR1a, governs a receptor that regulates the brain's production of vasopressin, a hormone that contributes to attachment behavior with mates and offspring. A few years ago, scientists found that when they added extra copies of the AVPR1a gene to the brains of promiscuous meadow voles, the animals began acting more like monogamous prairie voles, spending more time with partners and grooming offspring. A similar role for the AVPR1a gene has been observed in chimps and bonobos.
Might such a simple switch be found in humans? A team led by Hasse Walum of the Karolinska Institute in Stockholm, Sweden, sequenced the AVPR1a gene in about 500 pairs of adult same-sex Swedish twins, all of them married or cohabiting for at least 5 years, and their partners. One variation of the gene was particularly common; about 40% of males had either one or two copies of a version--or allele--of the gene known as "334."
Although not simply an analog to the polymorphism found in prairie voles, allele 334 seems to have a similar effect on the stability of human relationships, as measured in interviews and questionnaires. The tests included a Partner Bonding Scale containing items that reflect affection and cooperation, such as "How often do you kiss your mate?" and "How often are you and your partner involved in common interests outside the family?"
Scores on the test were significantly lower for the men carrying either one or two copies of allele 334 than for those without it, the researchers report online this week in the Proceedings of the National Academy of Sciences. The highest score possible is 66; those without the allele scored an average of 48, whereas carriers of one copy of allele 334 scored an average of 46.3. Carriers of two 334 alleles had the lowest scores of all, averaging 45.5. Although the score differences seem small, Walum says they are statistically significant. (No connection was observed in females.)
More striking were the answers to questions as to whether the men had experienced a marital crisis or threat of divorce during the prior year. More than one-third of carriers of two 334 alleles said yes, compared with only 15% of those with no 334 allele. What's more, 32% of those with two alleles were unmarried, compared with 17% of those who didn't carry the allele. Evaluations of the relationship by the men's partners tended to correspond with assessments reported by the men themselves.
The behavior appears to be somewhat heritable. Because the researchers were dealing with a population of twins, they were able to separate genetic and environmental influences. They found that about 28% of the behavior could be chalked up to inheritance, which is similar to what other studies have estimated for the heritability of marital satisfaction and of divorce.
Larry Young of Emory University in Atlanta, Georgia, whose team found the association between the vasopressin polymorphism and pair bonding in voles (ScienceNOW, 9 June 2005), says that assuming the finding can be replicated, it shows how a brain system developed early in mammalian evolution has been retained over the millennia and continues to play "a critical role in social relationships in both rodents and man." Geneticist Simon Easteal of the Australian National University in Canberra adds that "the effects of the ... polymorphism may be greater than these results indicate" because the study didn't cover single men, who presumably are less inclined to fidelity than those in relationships.