Genetic arguments and social policy

This is drawn from arguments posted on the Radical Statistics mailing list.

Genes are not a blueprint for the way we live. Biologists distinguish between genotype – the underlying pattern – and phenotype, the observable outcomes stemming from the interaction of genes, environment and the combined process of development. The argument has been made that environmental factors can make genes more important. For example, myopia, a condition rooted in genetic makeup, has been exacerbated by the development of reading. Variation in height, which is clearly governed by genotype, is nevertheless largely produced by environmental factors (which is why height has increased in succeeding modern generations). To illustrate the point, we know that two centuries ago, even if they were drawn from the same genetic pool, people were much smaller and lighter than we are now. One French study records that 79% of male recruits in 1792-9 were below 1.5 metres tall. The difference between that range and the range of heights in contemporary society is large enough to move people with a similar genetic endowment from a relatively low position to a relatively high one, depending on the developmental environment (primarily, in the case of height, on nutrition). A similar comment can be made about obesity. Estimates for the heritability of obesity vary between 40% and 70%.  That does not mean it is genetically caused; it means only that it runs in families.  Anyone who imagines that recent increases in obesity are due to changes in genetics isn’t living in the real world.

Despite nearly 150 years of trying, no-one has produced any good evidence that genes affect developed social behaviour in humans. With about 42,000 genes, it is easy to find statistical associations – at the conventional level where p<.05, there will probably be 2100 genes associated with any given character trait – but that does not demonstrate any causal link. Beyond that, however, most studies making claims about genetic origins of behaviour do not even try to show that there is a general association between the gene and the behaviour. They have simply relied on the occurrence of behaviour in specific families (1), and families have shared environments as well as shared genes. To the best of my knowledge, no study has ever shown that any social competence, personality trait or pattern of behaviour, of any kind, is shared by people with a common genotype or combination of genes while it is not present in others without that genotype. This is the minimum data that would be required to show that genes determine such issues.

Many studies rely, instead, on twin studies, in the belief that the similarity between identical twins must be genetic. This has three obvious problems. Firstly, any similarities within families may well reflect similar environmental factors. Second, identical twins generally have social environments which are very similar, and certainly more similar than fraternal twins. That’s why past studies tried to concentrate on identical twins reared apart – the problem being that (a) not enough twins are reared apart to make for a valid study, and (b) that even when twins are reared apart, social services agencies try to match their environments to the greatest possible extent. Third, identical twins are only relevant if one begins from the proposition that their genetic endowment is crucial. In other words, the studies assume the phenomenon they set out to prove.

The argument is not just bad science, It was used at the end of the 19th Century to justify the isolation of “degenerates” from the rest of the community. It was the basis for eugenics. It was closely associated with fascism, because it is an argument that was made by fascists for political reasons and offered in justification of the extermination of inferior humans. (2) The argument is sinister, and it deserves to be treated with deep scepticism.

Update, 24th November 2012. New Scientist reports this week about Mendelian randomisation, and that serves as a reminder to me that this criticism is beginning to be dated. The genetic linkage studies that were just being developed when I wrote this (e.g. Lancet, 2005 Sep 17-23;366(9490):1036-44) have started to bear fruit. A new epidemiology, described in Palmer et al’s Introduction to genetic epidemiology, has moved away from the old fallacy that behaviour is simply determined by genes; it begins, instead, with the proposition that different environments affect people with different genetic endowments differently. That makes it possible to distinguish the circumstances of people with certain genetic patterns from others – which is just what I was complaining here that studies hadn’t done to date.

Further update, 21st June 2020  The kind of work I was discussing here has, in all seriousness,  just saved my life.  A condition that would have been considered terminal five years ago has been distinctly identified through genomics and is now known to respond to a specific remedy.  This is a real and major development – and, as far as anyone can tell, heredity has nothing to do with it.

Note 1. S Jones, 1993, The language of the genes, London: Flamingo, ch 12.
Note 2. See R Lerner, Final solutions, Pennsylvania State University Press 1992.

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