Nature via Nurture: Genes, experience and what makes us human. Matt Ridley
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The strongest of the instincts, he believed, was love. ‘Of all propensities, the sexual impulses bear on their face the most obvious signs of being instinctive, in the sense of blind, automatic and untaught.’8 But, he insisted, just because sexual attraction was instinctive did not mean it was irresistible. Other instincts, like shyness, prevent us acting upon every sexual attraction.
So let me take James at his word, provisionally at least, and examine the idea of the love instinct in a little more depth. If he is right, there must be some heritable factor, which gives rise to a physical or chemical change in our brains when we fall in love, that change causing, rather than caused by, the emotion of falling in love. Such as this, from the scientist Tom Insel:
A working hypothesis is that oxytocin released during mating activates those limbic sites rich in oxytocin receptors to confer some lasting and selective reinforcement value on the mate.9
Or, to put it more poetically, you fall in love.
What is this oxytocin and why does Insel make such an extravagant claim for it? The story starts in an almost ridiculously unromantic process: urination. Some 400 million years ago, when the ancestors of our species first left the water, they were equipped with a tidy little hormone called vasotocin, a miniature protein made out of a chain of just nine amino acids formed into a ring. Its job was to regulate salt and water balance in the body, and it performed this job by rushing about switching on cells in the kidney or other organs. Fish still use two different versions of vasotocin for this purpose today, and so do frogs. In the descendants of reptiles – and that includes human beings – there are two slightly different copies of the relevant gene lying next to each other, facing different ways (in human beings on chromosome 20). The result today is that all mammals have two such hormones, called vasopressin and oxytocin, that differ at two of the links in the chain.
They still do their old job. Vasopressin tells the kidney to conserve water; oxytocin tells it to excrete salt. But, like vasotocin in modern fish, they also have a role in the regulation of reproductive physiology. Oxytocin stimulates the contraction of muscles in the womb during birth; it also causes milk to be expelled from the ducts in the breast. The GOD is an economiser: having invented a switch for one purpose, he readapts it for other purposes, by expressing the oxytocin receptor in a different organ. But a much greater surprise came in the early 1980s, when scientists suddenly realised that vasopressin and oxytocin had a job to do inside the brain as well as being secreted from the pituitary gland into the bloodstream.
So they tried injecting oxytocin and vasopressin into the brains of rats to see what effect they had. Bizarrely, a male rat injected with intracerebral oxytocin immediately begins yawning and simultaneously gets an erection.10 So long as the dose is low, the rat also becomes more highly sexed: it ejaculates sooner and more frequently. In female rats, intracerebral oxytocin induces the animal to adopt a mating posture. In human beings, meanwhile, masturbation increases oxytocin levels in both sexes. All in all, oxytocin and vasopressin in the brain seem to be connected to mating behaviour.
Now all of this sounds rather unromantic: urine, masturbation, breastfeeding – hardly the essence of love. Be patient. In the late 1980s, Tom Insel was working on the effect of oxytocin on maternal behaviour in rats. Brain oxytocin seemed to help the mother rat form a bond with its young and Insel identified the parts of the rat brain that were sensitive to the hormone. He switched his attention to the pair bond, wondering if there were parallels between a female’s bond to her young and to her mate. At this point he met Sue Carter, who had begun to study prairie voles in the laboratory. She told him how the prairie vole is a rarity among mice for its faithful marriages. Prairie voles live in couples and both father and mother care for the young for many weeks. Montane voles, on the other hand, are more typical of mammals: the female mates with a passing polygamist, separates quickly from him, bears young alone and abandons them after a few weeks to fend for themselves. Even in the laboratory, this difference is clear: mated prairie voles stare into each other’s eyes and bathe the babies; mated montane voles treat their spouses like strangers.
Insel examined the brains of the two species. He found no difference in the expression of the two hormones themselves, but a big difference in the distribution of molecular receptors for them – the molecules that fire up neurons in response to the hormones. The monogamous prairie voles had far more oxytocin receptors in several parts of the brain than the polygamous montane voles. Moreover, by injecting oxytocin or vasopressin into the brains of prairie voles, Insel and his colleagues could elicit all the characteristic symptoms of monogamy, such as a strong preference for one partner and aggression towards other voles. The same injections had little effect on montane voles, and the injection of chemicals that block the oxytocin receptors prevented the monogamous behaviour. The conclusion was clear: prairie voles are monogamous because they respond more to oxytocin and vasopressin.11
In a virtuoso display of scientific ingenuity, Insel’s team has gone on to dissect this effect in convincing detail. They knock the oxytocin gene out of a mouse before birth. This leads to social amnesia: the mice can remember things, but they have no memory of mice they have already met and will not recognise them. Lacking oxytocin in its brain, a mouse cannot recognise a mouse it has just met ten minutes before – unless that mouse was ‘badged’ with a non-social cue such as a distinctive lemon- or almond-scented smell (Insel compares this to an absent-minded professor at a conference who recognises friends by their name tags, not their faces).12 Then by injecting the hormone into just one part of the animal’s brain in later life – the medial amygdala – the scientists can restore social memory to the mouse completely.
In another experiment, using a specially adapted virus, they turn up the expression of the vasopressin receptor gene in the ventral pallidum, a part of a vole’s brain important for reward. Pause here to roll that idea around your mind a few times to appreciate just what science can do these days: they use viruses to turn up the volumes of genes in one part of the brain of a rodent. Even ten years ago such an experiment was unimaginable. The result of turning up the gene’s expression is to ‘facilitate partner preference formation’, which is geekspeak for ‘make them fall in love’. They conclude that for a male vole to pair-bond, it must have both vasopressin and vasopressin receptors in its ventral pallidum. Since mating causes a release of oxytocin and vasopressin, the prairie vole will pair-bond with whatever animal it has just mated; the oxytocin helps in memory, the vasopressin in reward. The montane vole, by contrast, will not react in the same way, because it lacks receptors in that area. Female montane voles express these receptors only after giving birth, so they can be nice to their babies, briefly.
So far I have talked of oxytocin and vasopressin as if they were the same thing, and they are so similar that they probably stimulate each other’s receptors somewhat. But it appears that to the extent that they do differ, oxytocin makes female voles choose a partner; vasopressin makes males choose a partner. The male prairie vole becomes aggressive towards all voles except its mate when vasopressin is injected into his brain. Attacking other voles is a (rather male) way of expressing his love.13
All this is astonishing enough, but perhaps the most exciting result to emerge from Insel’s lab concerns the genes for the receptors. Remember that the difference between the prairie vole and the montane vole lies not in the expression of the hormone, but in the pattern of expression of the hormone’s receptors. These receptors are themselves the products of genes. The receptor genes are essentially identical in the two species, but the promoter regions, upstream of the genes, are very different. Now recall the lesson of chapter 1: that the difference between closely related species lies not in the text of genes themselves,