Independent Perspective News

It no longer makes any sense to talk of "nature versus nurture" or "genes versus the environment". When it comes to human development, the two are inextricably intertwined, says Matt Ridley.

When genes came along, late in the second millennium of the Christian era, they found a place already prepared for them at the table of philosophy. They were the fates of ancient myth, the entrails of oracular prediction. They were destiny and predetermination, the enemies of choice. They were constraints on human freedom. They were the gods. The very phrase "genetic determinism" has come to be synonymous with inevitability. This is a false picture. Now that we have lifted the lid on the human genome and peered inside at what genes actually do, a more liberating vision is emerging. Human nature is indeed a product of genes in every particular, but so is human nurture, because genes spend just as much of their time responding to our actions as they do causing them. Genes do not constrain human freedom, they enable it.

Take, for example, the FOXP2 gene on chromosome 7, which was recently isolated by Anthony Monaco's group at the Wellcome Trust Centre for Human Genetics in Oxford. Mutations in this gene cause specific language impairment - the gene seems to be necessary for the proper development of human speech and language. Yet nobody would dream of arguing that FOXP2 "determines" speech. Rather, it allows the human mind to absorb from its early experience the learning necessary for speaking. It allows nurture. Charles Darwin called language "an instinct to acquire an art".

Where did we get the idea that genes were implacable puppet masters immune to outside influence? In the 1890s, the German biologist August Weismann cut off the tails of 57 generations of mice and then bred from them a further generation. The babies had normal tails: ergo, he argued, Lamarck was wrong to assert that acquired characteristics alter the hereditary elements in the germline.

Translated into molecular terms, Weismann's point takes the form of Francis Crick's "central dogma" that information flows out of the gene, and not back into it. Experience does not change gene sequences, except through rare, random mutations. Crick's dogma remains largely true, even perhaps completely so. But it misses, as Crick fully admits, a way in which information does feed back to the gene. The encoded sequence is indeed immune to outside influence, but the expressed sequence is not. Genes are switched on and off by transcription factors that bind to their promoter sequences, and the actions of promoters are at the mercy of external factors. Experience may not change a gene's sequence, but it may change its expression.

An example. The 17 CREB genes are a vital part of the mechanism of learning and memory. If one of them is not working, no long-term memory can be formed. The genes' job is to alter the connections between nerves to form a new association, and they are switched on in real time when the brain lays down a new memory. Gene transcription is controlled by behaviour; the act of learning turns on genes. Here is another way in which nature and nurture work together, and again promoter sequences are at the heart of it. The vasopressin receptor gene, which lies on chromosome 12 in humans, is controlled by a promoter whose length varies between species. The expression of this gene in certain parts of the brain in rodents seems to be necessary for them to form monogamous pair bonds - to fall in love, as it were. (Vasopressin and oxytocin are small peptide hormones that stimulate bonding behaviour.)

For example, the prairie vole has a 460-base-pair insert in the gene's promoter which is lacking in its close relation the montane vole. This has the effect of causing the gene to be expressed in a part of the prairie vole's brain where it is absent in the montane vole. It makes that part of the brain sensitive to vasopressin, a molecule released into the brain by the act of sex. The consequence is that the male prairie vole becomes, let us say, "socially addicted" to females it has had sex with, whereas the montane vole is socially indifferent to its mates. According to Tom Insel and Larry Young at Emory University in Atlanta, this explains the monogamy of the first species and the polygamy of the second. The longer promoter has opened the animal to the possibility of falling in love with its sexual partners - of pair-bonding with them, if you prefer.

Now here is the interesting bit. The human vasopressin receptor gene looks not unlike the prairie vole gene in both its promoter length and its expression pattern. But it varies in length between individuals. In the first 150 people whose genes Insel looked at, he found 17 different promoter lengths. Might these differences lead to differences in the ability to hold down a pair bond? It would not be altogether surprising: the probability of divorce is highly heritable, and adopted people are more like their biological parents than their adoptive parents in this respect.

The shift of focus from the encoded to the expressed genome is going to alter the terms of debate about human nature, for both esoteric and applied science. For instance, research unveiled last year by Avshalom Caspi and his colleagues at the Institute of Psychiatry in London offers a fascinating hint of how antisocial behaviour can be affected by an interaction between genes and environment. When they examined a large cohort of New Zealanders for evidence that an abusive childhood can induce antisocial behaviour, they found that indeed it can - but far more strongly in people of one genotype.

Men who had been maltreated as children and had "low-active" genes for monoamine oxidase A on the X chromosome were much more likely to get into trouble with the law, to describe themselves as violent, and to show up as antisocial in personality tests. Those with "high-active" genes were broadly resistant to the effects of childhood maltreatment. The difference between the high-active and low-active genes lies once more in the promoter lengths: long and short promoters produce low activity, intermediate promoters produce high activity. (Women are less likely to show this effect, as they have a spare X chromosome.)

Myopia works the same way. Just as maltreatment causes antisocial behaviour only in those with susceptible genes, so reading causes short sight only in those with susceptible genes. Moreover, genes cause short sight only in those who learn to read. In societies where few people read, myopia will correlate more closely with reading than with "myopia genes". But in a society where everybody learns to read, only those with the susceptible genes become short-sighted. So the more powerful the environmental factor - in this case reading - the more, not less, the genes seem to matter. Myopia is more "heritable" in a literate than in an illiterate society, in the same way that IQ is more heritable in a well-educated than in a poorly educated society. It is, therefore, far more illuminating to think of genes as mechanisms of human nature rather than causes of it. They are cogs, not gods.

In his recent book Freedom Evolves Daniel Dennett argues that organisms can acquire, through evolution, the capacity to avoid fat (see interview with Daniel Dennett in next week's issue). The ability to move out of the way of a predator, to sense danger, to imagine the future, to ask somebody a question or to invent vaccines are all in this sense degrees of freedom from inevitability.

From this perspective, having a FOXP2 gene that allows you to learn language does not constrain your free will: it enhances it. Even science itself expands free will. Knowing that you have an instinct makes it possible that you will decide to override that instinct. The more we learn about the genome, the more freedom we will find, and the more freedom we will gain.