GENTECH archive


Can short genes make you shy?

Can short genes make you shy?

Scientists are about to publish the book of life - a complete draft of human
DNA. In the final part of our exclusive extracts from his new book about this
autobiography of mankind, Matt Ridley looks at the role genes play in
influencing behaviour

GENES are what make us all so similar. Human genes build our bodies to look
like other human bodies and not like oak trees or flies. But genes are also
what make us all so different. The genes for blue eyes versus brown, or for
blonde hair versus dark, and for many other such little differences, grant us
our individuality.

What is true of appearance is also partly true of behaviour. Some people are
phlegmatic, some highly strung. Some are anxious; others risk-seeking. Some are
confident; others shy. Some are quiet; others loquacious. These differences are
determined partly by experience; but they are also determined partly by genes.

The role that genes play in influencing our behaviour is well known to the
person in the street - we accept that people have innate personalities, quite
apart from the effects of their upbringing. But to many intellectuals, this is
dangerous territory; genetic determinism is too fatalist and it denies us the
chance to change ourselves. To go further and look for personality genes in the
genome is positively suspicious. It might lead to a new wave of eugenics in
which people abort "shy foetuses" or other undesirable traits. Is this fair?

On the short arm of human chromosome 11, there lies a gene called D4DR. It is
the recipe for a protein called a dopamine receptor, and it is switched on in
cells of certain parts of the brain but not in others. We all have it. Dopamine
is, roughly speaking, 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. D4DR has a variable
repeat sequence in the middle, a DNA phrase 48 letters in length repeated
between two and 11 times. Most of us have four copies of the sequence or seven,
but some people have 2, 3, 5, 6, 8, 9, 10 or 11. 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.

Dean Hamer and his colleagues wanted to know if people with the long gene had
different personalities from people with the short gene. He measured the
novelty-seeking character of 124 people on a series of set personality tests
and then examined their genes.

Of the subjects Hamer tested - admittedly not a huge sample - people with
either one or two long copies of the gene (there are two copies of each
chromosome in the adult body, one from each parent) were distinctly more
novelty-seeking than people with two short copies of the gene. "Long" genes
were 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 commoner 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.

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

Hamer went on to demonstrate a striking example of what it means to be a novelt
y seeker. Among heterosexual men, those with the long 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.

We all know people who will try anything, and conversely people 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 40 per cent heritable, and that there are about 10
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.

Hamer is famous for having suggested in 1993 that a gene for homosexuality lies
on the X chromosome. It now looks from subsequent studies that he was wrong,
although a fairly high heritability of homosexuality is not in doubt. The jury
is still out on his personality gene, but even supposing he is right, 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? 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 results emerging from genetics,
have switched from trying to treat their clients' shyness to trying to make
them content with whatever their innate predispositions were. They have found
that it works: telling them they were naturally shy helped them overcome that

Marriage counsellors, too, report good results from encouraging their clients
to accept that they cannot change their partners' irritating habits - because
they are probably innate - but must find ways to live with them. The parents of
a homosexual are generally more accepting when they believe that homosexuality
is an immutable part of nature rather than a result of some aspect of their
parenting. Far from being a sentence, the realisation of innate personality is
often a release.

Most of us are happy to accept that genes play a part in personality. But we
find it much harder to believe that they are relevant to the everyday changes
in mood we all experience. Consider stress, for example. Many of the symptoms
of stress are caused by the steroid hormone cortisol. When you have a lot of
cortisol coursing through your veins, you are - by definition - under stress.

Stress is caused by the outside world, by an impending exam, a recent
bereavement, or the unrewarding exhaustion of caring for a person with
Alzheimer's disease. One of cortisol's most surprising effects is that it
suppresses the working of the immune system.

It is a remarkable fact that people who have been preparing for an important
exam, and have shown the symptoms of stress, are more likely to catch colds and
other infections, because one of the effects of cortisol is to reduce the
activity, number and lifetime of white blood cells. Quite why this happens -
what purpose it served in the Stone Age, for example - remains unknown.

Cortisol does all this by switching genes on. It only switches on genes in
cells that have cortisol receptors in them, which have in turn been switched on
by some other triggers. The genes that it switches on mostly switch on other
genes in turn, and sometimes the genes that they switch on will then switch on
other genes and so on. The secondary effects of cortisol can involve tens, or
maybe even hundreds of genes.

The arguments for and against "genetic determinism" presuppose that the
involvement of the genome places it above and beyond the body. But it is the
body that switches on genes when it needs them, often in response to a more or
less cerebral, or even conscious reaction to external events. You can raise
your cortisol levels just by thinking about stressful eventualities - even
fictional ones.

We instinctively assume that bodily biochemistry is cause whereas behaviour is
effect, an assumption we have taken to a ridiculous extent in considering the
impact of genes upon our lives. If genes are involved in behaviour then it is
they that are the cause and they that are deemed immutable. This is a mistake
made not just by genetic determinists, but by their vociferous opponents, the
people who say behaviour is "not in the genes"; the people who deplore the
fatalism and predestination implied, they say, by behaviour genetics.

They give too much ground to their opponents by allowing this assumption to
stand, for they tacitly admit that if genes are involved at all, then they are
at the top of the hierarchy.

They forget that genes need to be switched on, and external events - or
free-willed behaviour - can switch on genes. Far from us lying at the mercy of
our omnipotent genes, it is often our genes that lie at the mercy of "us".