Matt Ridley

blocking chemical is added to the rat's brain, the rat quickly loses interest in the lever.

In other words, to simplify grossly, dopamine is perhaps the brain's motivation chemical. Too little and the person lacks initiative and motivation. Too much and the person is easily bored and frequently seeks new adventures. Here perhaps lies the root of a difference in personality. As Dean Hamer put it, when he set out to seek the gene for thrill-seeking personalities in the mid-1990s, he was looking for the difference between Lawrence of Arabia and Queen Victoria. Since it takes many different genes to make, control, emit and receive dopamine, let alone to build the brain in the first place, nobody, least of all Hamer, expected to find a single gene controlling exclusively this aspect of personality. Nor did he expect to find that all variation in adventure-seeking is genetic, merely that there would be genetic influences at work among others.

The first genetic difference turned up in Richard Ebstein's laboratory in Jerusalem in the D4DR gene on chromosome 11. D4DR

has a variable repeat sequence in the middle, a minisatellite phrase forty-eight letters in length repeated between two and eleven times.

Most of us have four or seven copies of the sequence, but some people have two, three, five, six, eight, nine, ten or eleven. The larger the number of repeats, the more ineffective is the dopamine receptor at capturing dopamine. A 'long' D4DR gene implies a low responsiveness to dopamine in certain parts of the brain, whereas a 'short' D4DR gene implies a high responsiveness.

Hamer and his colleagues wanted to know if people with the long gene had different personalities from people with the short gene.

This is in effect the opposite procedure from that followed by Robert Plomin on chromosome 6, where he sought to correlate an unknown gene with a known behavioural difference (in I Q ) . Hamer went from the gene to the trait rather than vice versa. He measured the novelty-seeking character of 124 people on a series of set personality tests and then examined their genes.

Bingo. Of the subjects Hamer tested - admittedly not a huge sample 1 6 4 G E N O M E

- people with either one or two long copies of the gene (remember there are two copies of each chromosome in each cell of the adult body, one from each parent) were distinctly more novelty- seeking than people with two short copies of the gene. 'Long' genes were defined as those with six or more repeats of the minisatellite sequence. At first Hamer was worried that he might be looking at what he calls a

'chopstick' gene. The gene for blue eyes is common in people who are bad at using chopsticks, but nobody would dream of suggesting that chopstick skill is genetically determined by the gene for eye colour. It just happens that both blue eyes and chopstick incompetence correlate with non-oriental origin for a blindingly obvious non- genetic reason called culture. Richard Lewontin uses another analogy for this fallacy: the fact that people who are good at knitting tend not to have Y

chromosomes (i.e., they tend to be women) does not imply that knitting is caused by a lack of Y chromosomes.

So, to rule out a spurious correlation of this kind, Hamer repeated the study in the United States with members of one family. Again he found a clear correlation: the novelty-seekers were much more likely to have one or more copy of the long gene. This time the chopstick argument looks increasingly untenable, because any differences within a family are less likely to be cultural ones. The genetic difference may indeed contribute to the personality difference.

The argument goes like this. People with 'long' D4DR genes have low responsiveness to dopamine, so they need to take a more adventurous approach to life to get the same dopamine 'buzz' that short-gened people get from simple things. In search of these buzzes they develop novelty-seeking personalities. Hamer went on to demonstrate a striking example of what it means to be a novelty seeker.

Among heterosexual men, those with the long D4DR genes are six times more likely to have slept with another man than those with the short genes. Among homosexual men, those with the long genes are five times more likely to have slept with a woman than those with the short genes. In both groups, the long-gened people had more sexual partners than the short-gened people.1

We all know people who will try anything, and conversely people P E R S O N A L I T Y 1 6 5

who are set in their ways and reluctant to experiment with something new. Perhaps the first lot have long D4DR genes and the second lot have short ones. It is not quite that simple. Hamer claims to explain no more than four per cent of novelty seeking by reference to this one gene. He estimates that novelty seeking is about forty per cent heritable, and that there are about ten equally important genes whose variation matches the variation in personality. That is just one element in personality, but there are many others, perhaps a dozen. Making the wild assumption that they all involve similar numbers of genes leads to the conclusion that there may be 500

genes that vary in tune with human personalities. These are just the ones that vary. There may be many others that do not normally vary, but if they did would affect personality.

This is the reality of genes for behaviour. Do you see now how unthreatening it is to talk of genetic influences over behaviour? How ridiculous to get carried away by one 'personality gene' among 500?

How absurd to think that, even in a future brave new world, somebody might abort a foetus because one of its personality genes is not up to scratch — and take the risk that on the next conception she would produce a foetus in which two or three other genes were of a kind she does not desire? Do you see now how futile it would be to practise eugenic selection for certain genetic personalities, even if somebody had the power to do so? You would have to check each of 500 genes one by one, deciding in each case to reject those with the 'wrong' gene. At the end you would be left with nobody, not even if you started with a million candidates. We are all of us mutants. The best defence against designer babies is to find more genes and swamp people in too much knowledge.

Meanwhile, the discovery that personality has a strong genetic component can be used in some very non- genetic therapy. When naturally shy baby monkeys are fostered to confident monkey mothers, they quickly outgrow their shyness. It is almost certainly the same with people - the right kind of parenting can alter an innate personality. Curiously, understanding that it is innate seems to help to cure it. One trio of therapists, reading about the new 166 G E N O M E

results emerging from genetics, switched from trying to treat their clients' shyness to trying to make them content with whatever their innate predispositions were. They found that it worked. The clients felt relieved to be told that their personality was a real, innate part of them and not just a bad habit they had got into. 'Paradoxically, depathologising people's fundamental inclinations and giving group members permission to be the way they are seemed to constitute the best insurance that their self-esteem and interpersonal effectiveness would improve.' In other words, telling them they were naturally shy helped them overcome that shyness. Marriage counsellors, too,