I was on the Takeaway last week talking about this study:

We examined the role of serotonin transporter (5-HTT) and oxytocin receptor (OXTR) genes in explaining differences in sensitive parenting in a community sample of 159 Caucasian, middle-class mothers with their 2-year-old toddlers at risk for externalizing behavior problems, taking into account maternal educational level, maternal depression and the quality of the marital relationship. Independent genetic effects of 5-HTTLPR SCL6A4 and OXTR rs53576 on observed maternal sensitivity were found. Controlling for differences in maternal education, depression and marital discord, parents with the possibly less efficient variants of the serotonergic (5-HTT ss) and oxytonergic (AA/AG) system genes showed lower levels of sensitive responsiveness to their toddlers. Two-way and three-way interactions with marital discord or depression were not significant. This first study on the role of both OXTR and 5-HTT genes in human parenting points to molecular genetic differences that may be implicated in the production of oxytocin explaining differences in sensitive parenting.

It’s certainly interesting work, and builds on a large body of data showing that perfusing the brain with oxytocin (often via a nasal spray) leads to more generous offers in the ultimatum game, causes prairie voles to instantly pair bond and can, in general, serve as a social lubricant. (In other words, it’s like alcohol without the drunkenness.) This new study found an intriguing correlation between mothers with a less efficient serotonin transporter gene (which modulates the release of oxytocin) and various measures of maternal nurturing, such as the number of times a baby is cuddled. For me, the most interesting aspect of such research is how it demonstrates the sheer difficulty of breaking such damaging social cycles. Let’s say, for instance, that mothers with these genetic variants really are less responsive and sensitive to their children. Other research suggests that infants suffering from childhood neglect suffer from reduced oxytocin and vasopressin levels later on in childhood. The absence of love leaves a biological scar, which is then inflicted on the next generation and so on.

This depressing hypothesis is backed up some even more depressing primate research. As Harry Harlow demonstrated decades ago, baby monkeys forced to live with an unresponsive wire mother didn’t know how to deal with others, sympathize with strangers or behave in a socially acceptable manner. They would start fights without provocation and they wouldn’t stop fighting until one of the monkeys had been seriously injured. They were even vicious to their own children. One monkey raised by a wire-mother bit off the fingers of her child. Another killed her crying baby by crushing its head in her mouth. Most of these scarred mothers, however, just perpetuated the devastating cycle of cruelty. When their babies tried to cuddle, they would push them away. As Harlow would later write, “If monkeys have taught us anything it’s that you’ve got to learn how to love before you learn how to live.”

That said, oxytocin hype is getting out of control. (Just today, Drudge linked to a lame article on how oxytocin can “cure” shyness. So can a six-pack.) It’s become the neurotransmitter-of-the-month, the occult chemical that can make you more moral, romantic and outgoing. By the way, it’s also a potential cure for autism. While there’s been some really interesting research on oxytocin – I’m particularly enamored of the ultimatum game stuff – I think we’re in danger of falling into what I’ll call the serotonin trap. Remember when serotonin was the secret of happiness, the little molecule that, when elevated by an SSRI, could cure depression and make even healthy individuals happier? Well, that neat story is so incomplete it’s wrong. I hope we don’t make the same over-enthusiastic mistake with oxytocin.