Genome: The Autobiography of a Species in 23 Chapters. Matt Ridley
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Название: Genome: The Autobiography of a Species in 23 Chapters
Автор: Matt Ridley
Издательство: HarperCollins
Жанр: Прочая образовательная литература
isbn: 9780007381845
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Gender differences are just as pronounced as racial ones. According to research by the American Lung Association, whereas ozone from petrol-burning cars triggers asthma in men, particulates from diesel engines are more likely to trigger asthma in women. As a rule, males seem to have an early bout of allergy and to outgrow it, while females develop allergies in their mid or late twenties and do not outgrow them (though rules have exceptions, of course, including the rule that rules have exceptions). This could explain something peculiar about asthma inheritance: people often appear to inherit it from allergic mothers, but rarely from their fathers. This could just mean that the father’s asthma was long ago in his youth and has been largely forgotten.
The trouble seems to be that there are so many ways of altering the sensitivity of the body to asthma triggers, all along the chain of reactions that leads to the symptoms, that all sorts of genes can be ‘asthma genes’, yet no single one can explain more than a handful of cases. ADRB2, for example, lies on the long arm of chromosome 5. It is the recipe for a protein called the beta-2-adrenergic receptor, which controls bronchodilation and bronchoconstriction – the actual, direct symptom of asthma in the tightening of the windpipe. The commonest anti-asthma drugs work by attacking this receptor. So surely a mutation in ADRB2 would be a prime ‘asthma gene’? The gene was pinned down first in cells derived from the Chinese hamster: a fairly routine 1,239-letter long recipe of DNA. Sure enough a promising spelling difference between some severe nocturnal asthmatics and some non-nocturnal asthmatics soon emerged: letter number 46 was G instead of A. But the result was far from conclusive. Approximately eighty per cent of the nocturnal asthmatics had a G, while fifty-two per cent of the non-nocturnal asthmatics had G. The scientists suggested that this difference was sufficient to prevent the damping down of the allergic system that usually occurs at night.4
But nocturnal asthmatics are a small minority. To muddy the waters still further, the very same spelling difference has since been linked to a different asthmatic problem: resistance to asthma drugs. Those with the letter G at the same forty-sixth position in the same gene on both copies of chromosome 5 are more likely to find that their asthma drugs, such as formoterol, gradually become ineffective over a period of weeks or months than those with a letter A on both copies.
‘More likely’…‘probably’…‘in some of’: this is hardly the language of determinism I used for Huntington’s disease on chromosome 4. The A to G change at position 46 on the ADRB2 gene plainly has something to do with asthma susceptibility, but it cannot be called the ‘asthma gene’, nor used to explain why asthma strikes some people and not others. It is at best a tiny part of the tale, applicable in a small minority or having a small influence easily overridden by other factors. You had better get used to such indeterminacy. The more we delve into the genome the less fatalistic it will seem. Grey indeterminacy, variable causality and vague predisposition are the hallmarks of the system. This is not because what I said in previous chapters about simple, particulate inheritance is wrong, but because simplicity piled upon simplicity creates complexity. The genome is as complicated and indeterminate as ordinary life, because it is ordinary life. This should come as a relief. Simple determinism, whether of the genetic or environmental kind, is a depressing prospect for those with a fondness for free will.
The hereditarian fallacy is not the simple claim that IQ is to some degree ‘heritable’ [but] the equation of ‘heritable’ with ‘inevitable’.
Stephen Jay Gould
I have been misleading you, and breaking my own rule into the bargain. I ought to write it out a hundred times as punishment: GENES ARE NOT THERE TO CAUSE DISEASES. Even if a gene causes a disease by being ‘broken’, most genes are not ‘broken’ in any of us, they just come in different flavours. The blue-eyed gene is not a broken version of the brown-eyed gene, or the red-haired gene a broken version of the brown-haired gene. They are, in the jargon, different alleles – alternative versions of the same genetic ‘paragraph’, all equally fit, valid and legitimate. They are all normal; there is no single definition of normality.
Time to stop beating about the bush. Time to plunge headlong into the most tangled briar of the lot, the roughest, scratchiest, most impenetrable and least easy of all the brambles in the genetic forest: the inheritance of intelligence.
Chromosome 6 is the best place to find such a thicket. It was on chromosome 6, towards the end of 1997, that a brave or perhaps foolhardy scientist first announced to the world that he had found a gene ‘for intelligence’. Brave, indeed, for however good his evidence, there are plenty of people out there who refuse to admit that such things could exist, let alone do. Their grounds for scepticism are not only a weary suspicion, bred by politically tainted research over many decades, of anybody who even touches the subject of hereditary intelligence, but also a hefty dose of common sense. Mother Nature has plainly not entrusted the determination of our intellectual capacities to the blind fate of a gene or genes; she gave us parents, learning, language, culture and education to program ourselves with.
Yet this is what Robert Plomin announced that he and his colleagues had discovered. A group of especially gifted teenage children, chosen from all over America because they are close to genius in their capacity for schoolwork, are brought together every summer in Iowa. They are twelve- to fourteen-year-olds who have taken exams five years early and come in the top one per cent. They have an IQ of about 160. Plomin’s team, reasoning that such children must have the best versions of just about every gene that might influence intelligence, took a blood sample from each of them and went fishing in their blood with little bits of DNA from human chromosome 6. (He chose chromosome 6 because he had a hunch based on some earlier work.) By and by, he found a bit on the long arm of chromosome 6 of the brainboxes which was frequently different from the sequence in other people. Other people had a certain sequence just there, but the clever kids had a slightly different one: not always, but often enough to catch the eye. The sequence lies in the middle of the gene called IGF2R.1
The history of IQ is not uplifting. Few debates in the history of science have been conducted with such stupidity as the one about intelligence. Many of us, myself included, come to the subject with a mistrustful bias. I do not know what my IQ is. I took a test at school, but was never told the result. Because I did not realise the test was against the clock, I finished little of it and presumably scored low. But then not realising that the test is against the clock does not especially suggest brilliance in itself. The experience left me with little respect for the crudity of measuring people’s intelligence with a single number. To be able to measure such a slippery thing in half an hour seems absurd.
Indeed, the early measurement of intelligence was crudely prejudiced in motivation. Francis Galton, who pioneered the study of twins to tease apart innate and acquired talents, made no bones about why he did so:2
My general object has been to take note of the varied hereditary faculties of different men, and of the great differences in different families and races, to learn how far history may have shown the practicability of supplanting inefficient human stock by better strains, and to consider whether it might not be our duty to do so by such efforts as may be reasonable, thus exerting ourselves to further the ends of evolution more rapidly and with less distress than if events were left to their own course.
In other words he wanted to selectively cull and breed people as if they were cattle.
But it was in America СКАЧАТЬ