obscures the genes; testosterone parts the veil and allows the female to see directly into the genes.6

This theory is known as the immunocompetence handicap and S T R E S S 159

it depends upon the immune-suppressive effects of testosterone being unavoidable. A male cannot get round the handicap by raising his testosterone levels and not suppressing his immune system. If such a male existed, he would surely be a great success and would leave many offspring behind, because he could grow a long tail with (literally) immunity. Hence, the theory implies that the link between steroids and immune suppression is as fixed, inevitable and important as any in biology.

But this is even more puzzling. Nobody has a good explanation for the link in the first place, let alone its inevitability. Why should bodies be designed so that their immune systems are depressed by steroid hormones? It means that whenever you are stressed by a life event, you become more vulnerable to infection, cancer and heart disease. That is kicking you when you are down. It means that whenever an animal raises its testosterone level to fight its rivals for mates or to enhance its display, it becomes more vulnerable to infection, cancer and heart disease. Why?

Various scientists have struggled with this conundrum, but to little effect. Paul Martin, in his book on psychoneuroimmunology called The sickening mind, discusses two possible explanations and rejects them both. First is the notion that it is all a mistake, and that the links between the immune system and the stress response are accidental by-products of the way some other systems have to be designed. As Martin points out, this is a deeply unsatisfactory explanation for a system full of complex neural and chemical links.

Very, very few parts of the body are accidental, vestigial or func¬

tionless, especially not complex parts. Natural selection would ruthlessly cull links that suppress the immune response if they had no function.

The second explanation, that modern life produces prolonged and unnatural stresses and that in an ancient environment such stresses would have been much shorter-lived, is equally disappointing. Baboons and peacocks live in a state of nature, yet they too - and virtually every other bird and mammal on the planet -

suffer from immune suppression by steroids.

l6o G E N O M E

Martin admits to bafflement. He cannot explain the fact that stress inevitably depresses the immune system. Nor can I. Perhaps, as Michael Davies has suggested, the depression is designed to save energy in times of semi- starvation, a common form of stress before the modern era. Or perhaps the response to Cortisol is a side-effect of the response to testosterone (they are very similar chemicals) and the response to testosterone is deliberately engineered into males by the genes of females the better to sort the fitter — that is more disease resistant - males from the less fit. In other words, the link may be the product of a kind of sexual antagonism like the one discussed in the chapter on chromosomes X and Y. I don't find this explanation convincing, so I challenge you to find a better one.

C H R O M O S O M E 1 1

P e r s o n a l i t y

A man's character is his fate.

Heraditus

The tension between universal characteristics of the human race and particular features of individuals is what the genome is all about.

Somehow the genome is responsible for both the things we share with other people and the things we experience uniquely in ourselves.

We all experience stress; we all experience the elevated Cortisol that goes with it; we all suffer from the immune-suppressive effects thereof. We all have genes switched on and off by external events in this way. But each of us is unique, too. Some people are phlegmatic, some highly strung. Some are anxious, others risk-seeking. Some are confident, others shy. Some are quiet, others loquacious. We call these differences personality, a word that means more than just character.

It means the innate and individual element in character.

To seek out the genes that influence personality, it is time to move from the hormones of the body to the chemicals of the mind

- though the distinction is by no means a hard-and-fast one. On the short arm of chromosome 11, there lies a gene called D4DR.

1 6 2 G E N O M E

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.

Its job is to stick out of the membrane of a neuron at the junction with another neuron (known as a synapse), ready to latch on to a small chemical called dopamine. Dopamine is a neurotransmitter, released from the tips of other neurons by an electrical signal. When the dopamine receptor encounters dopamine, it causes its own neuron to discharge an electrical signal of its own. That is the way the brain works: electrical signals that cause chemical signals that cause electrical signals. By using at least fifty different chemical signals, the brain can carry on many different conversations at once: each neurotransmitter stimulates a different set of cells or alters their sensitivity to different chemical messengers. It is misleading to think of a brain as a computer for many reasons, but one of the most obvious is that an electrical switch in a computer is just an electrical switch. A synapse in a brain is an electrical switch embedded in a chemical reactor of great sensitivity.

The presence of an active D4DR gene in a neuron immediately identifies that neuron as a member of one of the brain's dopamine¬

mediated pathways. Dopamine pathways do many things, including controlling the flow of blood through the brain. A shortage of dopamine in the brain causes an indecisive and frozen personality, unable to initiate even the body's own movement. In the extreme form, this is known as Parkinson's disease. Mice with the genes for making dopamine knocked out will starve to death from sheer immobility. If a chemical that closely resembles dopamine (a dopamine agonist, in the jargon) is injected into their brains, they recover their natural arousal. An excess of dopamine in the brain, by contrast, makes a mouse highly exploratory and adventurous. In human beings, excessive dopamine may be the immediate cause of schizophrenia; and some hallucinogenic drugs work by stimulating the dopamine system. A mouse addicted to cocaine so badly that it prefers the drug to food is experiencing the release of dopamine in a part of the brain known as the nucleus acumbens. A rat in which this 'pleasure centre' is stimulated whenever it presses a lever will P E R S O N A L I T Y 163

learn to return to press the lever again and again. But if a dopamine¬

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