Nicholas Wade and race: building a scientific façade – Some further comments from the PoV of brain research


English: The human genome, categorized by func...
English: The human genome, categorized by function of each gene product, given both as number of genes and as percentage of all genes. (Photo credit: Wikipedia)

This is a superb and important piece by Jennifer Raff. I would make a few comments from brain science regarding this debate. There has been a very serious and large-scale effort in neuropsychiatric genetics and neurological genetics to pin down genes of relevance to conditions such as depression, schizophrenia and degenerative disorders such as Alzheimer’s. To put it mildly, these ‘in your face’ brain disorders (there’s little subtlety about these conditions) have yielded many disappointments by way of really meaningful effect sizes or gene relationships. The literature is replete with examples of disappearing effect sizes, where initial large effects disappear on replication or increased sample size (here are a few: BDNF; 5’-HTTLPR; genes for ‘alcoholism’; have a look at this Dorothy Bishop piece). Instead, the picture is very complicated with multiply-related small effects – and this is in well-controlled studies with clinical registers and disabling psychopathological conditions (see this wonderful piece on statistical genomics and schizophrenia as a good example)

The experimental transgenic literature where gene candidates have been modulated (I use the term generously to mean ko/ki or conditional) has been similarly bedevilled. The behavioural impairments in the AD mouse are small and subtle and really require a combination of insult or senescence and triple transgenes to show really reasonable effects. And in the case where pure genetic determinism would seem to be unavoidable (Huntington’s), the data in the animal models show that the condition is moderated dramatically by environmental enrichment and substantial aerobic exercise. Even in autistic spectrum disorders, ‘Family studies have shown that the risk of having ASD is 10-20 per cent if you have an affected first-degree relative’ (Gallagher and Mitchell), which is a long way from a sense of determinism. To jump from this pretty mechanist literature to genetic determinism and IQ (or intellectual function) is a stretch too far, when we know so little.

What’s my overall point? It is this: IQ data are observational data, and causal inferences about underlying neurogenetics from such observational data should only be made with extreme care. And even more so when we know from experimental data that ‘Poverty impedes cognitive function‘ by as much as a standard deviation (Science. 2013 Aug 30;341(6149):976-80; Science. 2012 Nov 2;338(6107):682-5; also this).

There’s a lot more: there have been many candidate genes to enhance cognitive function (and indeed drugs too). When you actually look at the data, there are many profound problems – such as hypoalgesia or excess neuronal excitability – or even simply inconsistent or non-replicable effects.

A final example: the human genome was fully described (to within 1% or so) 15 years ago. This lead to a massive investment in pharmacogenomics by big pharma, followed by disenchantment and finally disinvestment by most, if not virtually all, of big pharma in pharmacogenomics. Why? Because causal genotype-phenotype relationships for psychiatric disorders turns out to be horrendously complicated, even for these obvious, clinically-significant and disabling conditions. And getting druggable targets turns out to be even more difficult.


A little less myside bias in reasoning would be good in this domain.

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Violent metaphors

“…for he has no right to give names to objects which he cannot define.” –Charles Darwin

Do “races” exist as meaningful biological categories? Physical anthropologists and human biologists have been studying race (i.e., blacks vs. whites, or Europeans vs. Asians) for centuries. For most of that time, they subscribed to the perspective that race was a taxonomic category, and they sought to identify the biological characteristics (such as cranial shape or skin color) that characterized and defined these different groups. This perspective assumed that each individual was a member of a single racial category, that the differences between racial categories were biological, and that these categories were predictive of other traits (such as ancestry, temperament, intelligence, or health).

But it gradually became clear that this understanding was not scientifically sound. Groupings of people by skin color did not produce the same result as groupings of people by skull shape…

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Author: Shane O'Mara