Matt Ridley

most such pidgins, the language lacked consistent grammatical rules and remained both laboriously complex in the way it had to express things and relatively simple in what it could express. But all that changed when for the first time a generation of children learnt the language in their youth.

The pidgin acquired rules of inflection, word order and grammar that made it a far more efficient and effective language - a creole.

In short, as Bickerton concluded, pidgins become Creoles only after they are learnt by a generation of children, who bring instinct to bear on their transformation.

Bickerton's hypothesis has received remarkable support from the study of sign language. In one case, in Nicaragua, special schools for the deaf, established for the first time in the 1980s, led to the invention, de novo, of a whole new language. The schools taught lip-reading with little success, but in the playground the children brought together the various hand signs they used at home and established a crude pidgin language. Within a few years, as younger children learnt this pidgin, it was transformed into a true sign language with all the complexity, economy, efficiency and grammar of a spoken language. Once again, it was children who made the language, a fact that seems to suggest that the language instinct is one that is switched off as the child reaches adulthood. This accounts for our difficulty in learning new languages, or even new accents, as adults. We no longer have the instinct. (It also explains why it is so much harder, even for a child, to learn French in a classroom than on holiday in France: the instinct works on speech that it hears, not rules that it memorises.) A sensitive period during which something can be learnt, and outside which it cannot, is a feature of many animals' instincts. For instance, a chaffinch will only learn the true song of its species if exposed to examples between certain ages. That the same is true of human beings was proved in a brutal way by the true story of Genie, a girl discovered in a Los Angeles apartment aged thirteen. She had been kept in a single sparsely furnished room all her life and deprived of almost all human contact.

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She had learnt two words, 'Stopit' and 'Nomore'. After her release from this hell she rapidly acquired a larger vocabulary, but she never learnt to handle grammar - she had passed the sensitive period when the instinct is expressed.

Yet even bad ideas take a lot of killing, and the notion that language is a form of culture that can shape the brain, rather than vice versa, has been an inordinate time a-dying. Even though the canonical case histories, like the lack of a concept of time in the Hopi language and hence in Hopi thought, have been exposed as simple frauds, the notion that language is a cause rather than consequence of the human brain's wiring survives in many social sciences. It would be absurd to argue that only Germans can understand the concept of taking pleasure at another's misfortune; and that the rest of us, not having a word for Schadenfreude, find the concept entirely foreign.2

Further evidence for the language instinct comes from many sources, not least from detailed studies of the ways in which children develop language in their second year of life. Irrespective of how much they are spoken to directly, or coached in the use of words, children develop language skills in a predictable order and pattern.

And the tendency to develop language late has been demonstrated by twin studies to be highly heritable. Yet for many people the most persuasive evidence for the language instinct comes from the hard sciences: neurology and genetics. It is hard 'to argue with stroke victims and real genes. The same part of the brain is consistently used for language processing (in most people, on the left side of the brain), even the deaf who 'speak' with their hands, though sign language also uses part of the right hemisphere.3

If a particular one of these parts of the brain is damaged, the effect is known as Broca's aphasia, an inability to use or understand all but the simplest grammar, even though the ability to understand sense remains unaffected. For instance, a Broca's aphasic can easily answer questions such as 'Do you use a hammer for cutting?' but has great difficulty with: 'The lion was killed by the tiger. Which one is dead?' The second question requires sensitivity to the grammar I N S T I N C T 9 7

encoded in word order, which is known by just this one part of the brain. Damage to another area, Wernicke's area, has almost the opposite effect - people with such damage produce a rich but senseless stream of words. It appears as if Broca's area generates speech and Wernicke's area instructs Broca's area what speech to generate. This is not the whole story, for there are other areas active in language processing, notably the insula (which may be the region that malfunctions in dyslexia).4

There are two genetic conditions that affect linguistic ability. One is Williams syndrome, caused by a change in a gene on chromosome 11, in which affected children are very low in general intelligence, but have a vivid, rich and loquacious addiction to using language.

They chatter on, using long words, long sentences and elaborate syntax. If asked to refer to an animal, they are as likely to choose something bizarre like an aardvark as a cat or a dog. They have a heightened ability to learn language but at the expense of sense: they are severely mentally retarded. Their existence seems to undermine the notion, which most of us have at one time or another considered, that reason is a form of silent language.

The other genetic condition has the opposite effect: it lowers linguistic ability without apparently affecting intelligence, or at least not consistently. Known as specific language impairment (SLI), this condition is at the centre of a fierce scientific fight. It is a battleground between the new science of evolutionary psychology and the old social sciences, between genetic explanations of behaviour and environmental ones. And the gene is here on chromosome 7.

That the gene exists is not at issue. Careful analysis of twin studies unambiguously points to a strong heritability for specific language impairment. The condition is not associated with neurological damage during birth, is not associated with linguistically impoverished upbringings, and is not caused by general mental retardation. According to some tests — and depending on how it is defined — the heritability approaches one hundred per cent. That is, identical twins are roughly twice as likely to share the condition as fraternal twins.

That the gene in question is on chromosome 7 is also not in much 9 8 G E N O M E

doubt. In 1997 a team of Oxford-based scientists pinned down a genetic marker on the long arm of chromosome 7, one form of which co-occurs with the condition of S L I . The evidence, though based only on one large English family, was strong and unambiguous.6

So why the battleground? The argument rages about what SLI is. To some it is merely a general problem with the brain that affects many aspects of language-producing ability, including principally the ability to articulate words in the mouth and to hear sounds correctly in the ear. The difficulty the subjects experience with language follow from these sensory problems, according to this theory. To others, this is highly misleading. The sensory and voice problems exist, to be sure, in many victims of the condition, but so does something altogether more intriguing: a genuine problem understanding and using grammar that is quite independent of any sensory deficits. The only thing both sides can agree upon is that it is thoroughly disgrace-ful, simplistic and sensationalist of the media to portray this gene, as they have done, as a 'grammar gene'.

The story centres on a large English family known as the Ks.

There are three generations. A woman with the condition married an unaffected man and had four daughters