Mary Carmichael has a great video (and associated post) about the rise of genetic denialism–ridiculous arguments that ‘genes don’t cause disease.’* Carmichael offers two reasons why the argument is flawed; I’ll offer a third in a bit, but I do want to note one minor point of disagreement with Carmichael.
If you go to roughly the ten minute mark, Carmichael has a summary slide that lists several phenomena that could account for the ‘missing heritability’–the observation that currently identified genomic variation can’t account for much the expected heritability as determined by various studies, such as twin studies or parent-offspring studies (hertability measures how much of the variance in a quantitative** trait (e.g., height) is associated with genetic differences in a population with a certain distribution of genotypes and environments). One thing she lists is gene-environment interactions. That’s actually not entirely correct. Gene-environment interactions (“genotype by environment”), where some genetic variation behaves differently in certain environments, lowers heritability estimates; that is, we underestimate heritability.
What can lead to the overestimation of heritability is genotype-environment correlation. For example, high IQ parents might create a more stimulatory environment for their children (i.e., a ‘high IQ’ environment). This is not a trivial problem, especially since many human studies are not like animal or plant breeding experiments which occur in highly controlled environments. In the comments of one post about this whole issue (which I can’t dig up), someone mentioned how extensive experience with lab models has convinced him to think genotype plays a large role, at which point any evolutionary ecologist–which I was in days of yore–bangs his or her head against the wall***. A little humility about environmental confounding, especially when applied to methods originally designed for controlled breeding experiments would be helpful, along with multiple confirmatory studies using different approaches and cohorts.
Having said that, if heritabilities for some traits are overestimated, this means that the missing heritability problem isn’t as serious as currently thought: genomics has been more successful. Anyway, just a minor point, because what I really want to get to is why I think genetic denialism could become popular.
Carmichael lists two logical fallacies that lead to genetic denialism:
1. It assumes that absence of evidence is evidence of absence, concluding that because common diseases aren’t caused by a handful of genes with strong effects, they aren’t influenced by genes at all. This is clearly a silly position, but it’s a handy one if you are, say, a group that wants to raise the profile of biomedical research into non-genetic factors such as pollution, and if you’re concerned about money being poured into genetic research at your expense. (For the record, I agree that research into environmental factors is important. Maybe the essay’s authors and geneticists should be lobbying together against pending cuts to the NIH? To borrow a malapropism from someone with whom I disagree on almost every other point: shouldn’t we make the pie higher?)
2. It mistakenly portrays science as a monologue, and a dull one at that. First, it lists some of the potential hiding places for heritability that remain in the genome. Then it notes that a few scientists think some of them are less likely candidates than others and that there’s no consensus that one of them will explain everything. This is presented as evidence that almost all of human genetics is in crisis. But the data has just begun to be generated, and of course it’s unlikely that one type of factor will explain everything. Life, in biology as elsewhere, is complicated. (As geneticists freely point out: take it from David Altshuler, Leonid Kruglyak, and a bunch of other people who would know.) We’ve seen this line of “minor disagreement = major crisis” argument before, from creationists who conscripted Stephen Jay Gould and punctuated equilibrium as “evidence” that natural selection wasn’t a widely accepted principle. It was just as absurd — and effective — a rhetorical tactic then as it is now.
I think there’s a third reason, and, while it too is a logical fallacy, it’s far more understandable: a highly heritable trait can be largely environmentally determined. There have been a lot of changes in human health over the last fifty years, such as a real increase in breast cancer rates or the rise in obesity. Even when these changes have a high heritability, such as is potentially the case with obesity, the idea that this is largely response to selection of ‘obese’ genes is absurd. There’s an environmental component. People get this (except for Megan McArdle).
One thing we’ll have to be careful about, and I’m not sure how to do this, is to explain what high heritability means–it doesn’t mean that a trait is ‘genetic’, only that the variation in that trait under a set of certain environmental conditions is largely genetic.
This won’t be easy.
*We can legitimately disagree about the extent of heritability of certain diseases (and other traits). But to argue that there isn’t a genetic component is silly and factually unfounded.
**There are methods to do this with discrete traits too.
***Another issue with genome wide association studies (GWAS) is that the genotype is often much more rigorously specified than the environment. Consequently, “E”, the environmental component becomes a ‘left-over’ term, conflating error and temporal variation with environmental variation. As the Three Toed Sloth noted a while back, we can also run into the same problem were we to overspecify the environment, and then treat the left-over variation as the genetic component.