Most mammals do not form long-term pair bonding relationships, but two notable exceptions are prarie voles and humans. The explanation behind these relationships is that the animals have co-opted maternal love for the feelings they have towards their partner. This would explain the male fascination with breasts, which have been decoupled from sex but where stimulation still provides huge releases of the neurotransmitter oxytocin.
But perhaps more interesting is the possibility for genetic control of the varied behavior in pair bonding. Prarie voles show sexual and social fidelity while montane and meadow voles do not; prarie voles contain a 428-base pair sequence in the 5′ flanking region of the avpr1a gene while montane and meadow voles do not. When this gene (including the 428 bp sequence) is encoded transgenically in mice, which are not normally monogomous, they exhibit more social behavior similar to prarie voles. Finally, there is some intraspecific variation in the level of “monogaminity” in prarie voles depending upon polymorphisms in this 5′ flanking region of the avpr1a gene.
It is this last fact that probably tickled the fancy of Walum et al, because they tested to see whether variations in this gene affected pair bonding in humans as well. They designed their own measure behavior called the Pair Bonding Scale which depending on questions of time spent together (”How often are you and your partner involved in common interests outside the family?”), closeness (“I don’t like when other people come too close to me”), and the mushy stuff (“How often do you kiss your mate?”). They then analyzed twins and their offspring from Sweden to reduce variance in unexamined genes.
They tested for the effect of polymorphism in three different repetitive sequences in the human AVPR1A gene in both men and women: the (GT)25 dinucleotide repeat, a complex (CT)4-TT-(CT)8-(GT)24 repeat (RS3), and a (GATA)14 tetranucleotide repeat (RS1). The significant result that they found (it was P<.001 even after correcting for the other 11 hypotheses) was a correlation between having carrying the 334 RS3 allele and having a lower score on the Pair Bonding Scale. The effect sizes were d=0.27 between men who did not carry the 334 allele and 334 heterozygotes, and d=0.38 between men who did not carry it and those who carried 334 homozygotes, meaning that the effect was dose-dependent. The researchers confirmed the effect with further tests of marital instability. A few questions:
1) It is interesting that in this model it is the characteristics of the male that determine the quality of the relationship. Does this fit with our cultural expectations?
2) The 334 allele is associated with increased activity in the amygdala, which is involved in emotionally charged memories. Perhaps those expressing the allele are more likely to remember instances of fights? Or, perhaps they are more likely to remember past instances of infidelity, project them onto the future, and act overprotectively?
3) Should we conduct genetic tests of our partners to determine potential marital stability?
Young LF. 2009 Being human: Love: Neuroscience reveals all. Nature 457: 148. doi:10.1038/457148a.
Walum H, Westerg L, Henningsson S, Neiderhiser JM, Reiis D, Igl W, Ganiban JM, Spotts EL, Pedersen NL, Eriksson E, Lichtenstein P. 2008 Genetic variation in the vasopressin receptor 1a gene (AVPR1A) associates with pair-bonding behavior in humans. PNAS 37:14153-14156. doi: