Genes are overrated
This is hardly news, but this Guardian article reminded me of it—genes are really overrated, both among unwashed masses, and also here on Less Wrong.
I don’t want to repeat things which have been said by so many before me, so I’ll just link a lot.
Summary of evidence against genes being important:
Almost no genes correlating with anything interesting been found. This is totally crushing evidence. If genes were important, Bayesian surprise of this lack of results would be in the land of impossible.
Massive very fast changes of various supposedly highly hereditary characteristic with time in same populations. To name a few—Flynn effect, changes in people’s height, obesity epidemic.
Plenty of evidence of very large very reliable associations of various environmental factors with various important outcomes. For example unlike with genes and cancer where we get just noise, we know very well how much smoking increases chance of lung cancer.
Summary of evidence for genes being important:
Some twin and adoption studies—which rely on very tiny highly atypical samples and a lot of statistical manipulation to get results they want. To make matters worse, results they got were wildly inconsistent.
And there’s nothing more. Decades ago, before we had direct evidence of lack of correlation between genes and outcomes, it was excusable to believe genes matter a lot, even if it was never the best interpretation of data. Now it’s just going against bulk of the evidence.
And in case you’re wondering how could twin studies show high heredity when everything else says otherwise, I have two examples for you.
This one from a critique of twin studies by Kamin and Goldberger:
“A case in point is provided by the recent study of regular tobacco use among SATSA’s twins (24). Heritability was estimated as 60% for men, only 20% for women. Separate analyses were then performed for three distinct age cohorts. For men, the heritability estimates were nearly identical for each cohort. But for women, heritability increased from zero for those born between 1910 and 1924, to 21% for those in the 1925-39 birth cohort, to 64% for the 1940-58 cohort. The authors suggested that the most plausible explanation for this finding was that “a reduction in the social restrictions on smoking in women in Sweden as the 20th century progressed permitted genetic factors increasing the risk for regular tobacco use to express themselves.” If purportedly genetic factors can be so readily suppressed by social restrictions, one must ask the question, “For what conceivable purpose is the phenotypic variance being allocated?” This question is not addressed seriously by MISTRA or SATSA. The numbers, and the associated modeling, appear to be ends in themselves.”
As the final nail in the coffin of heredity studies:
The Body-Mass Index of Twins Who Have Been Reared Apart
We conclude that genetic influences on body-mass index are substantial, whereas the childhood environment has little or no influence. These findings corroborate and extend the results of earlier studies of twins and adoptees. (N Engl J Med 1990; 322:1483–7.)
Or as paraphrased by a certain commenter on Marginal Revolution:
IOWs, the reason why white kids of today are much fatter than white kids of the 50s and 60s is due to genetic influences and environment has little or no influence
To summarize—heredity studies are pretty much totally worthless data manipulation. Once we accept that, all other evidence points for environment being extremely important, and genes mattering very little. We should accept that already.
I am only an amateur in all the relevant areas of expertise, but I have invested quite a bit of effort trying to make sense of these controversies. I have to say that your post is very confused, and you seem to lack familiarity with many important facts that would have to be considered before pronouncing such a sweeping judgment.
The lack of obvious correlations between genes and phenotypes implies only that the phenotypes in question are not determined by the genotype in a simple way. If they are determined by complex interactions between genes, then straightforward association studies won’t detect this connection. To make an imperfect but relevant analogy, if you took the machine code of various computer programs and did a statistical association study between these codes and the resulting behavior of the computer, while being ignorant of the way the instructions are actually decoded and executed—as we are still largely ignorant of the relevant biochemistry, which is also far more complicated—you could easily end up with no observable correlations.
Similarly, if some trait can be influenced by environmental factors strongly and rapidly, it is still a total fallacy to conclude that it is therefore determined purely by environmental factors. To take a trivial example, nobody disputes that hair color is highly heritable, but the development of cheap and convenient hair dyes has changed the average hair colors in the population dramatically. The behavior of computer programs is highly dependent on what you give them as input, but it doesn’t mean that the program code is irrelevant.
As for heritability studies, you are certainly right that there is a lot of shoddy work, and by necessity they make a whole lot of wildly simplifying assumptions. If there existed only a handful of such studies, one would be well advised not to take them very seriously. However, the amount of data that has been gathered in recent decades is just too overwhelming to dismiss, especially taking into account that often there have been considerable ideological incentives to support the opposite conclusions.
On the whole, you are making a wholly unsubstantiated sweeping conclusion.
This is like saying “atoms are overrated”.
This is simply untrue. Even leaving aside the fact that there is a single gene that causes Huntington’s disease with 100% probability, there are many cases in which there is a well understood chain of causality from the molecular genetic level to the behavioral level. I have a whole textbook devoted to behavioral genetics you may want to read.
Off the top of my head, there is the Dutch “crime gene” which is mutation found in some Dutch populations, that causes extreme aggression (rape and arson especially common) in males. The mutation causes low levels of Monoamine Oxidase A. When mice were created with the mutation, they exhibited similar “fearless-aggressive” behavior. An environmental trigger (child abuse) was necessary before the effects manifested themselves.
But this in no way contradicts studies purporting to show that (e.g.) height and IQ are significantly heritable, because (I am given to understand) heritability in this context isn’t a judgment of the overall “geneticness” of a trait (whatever that would mean)---rather, it is a technical term referring to the amount of variance in phenotypes that can be ascribed to variance in geneotypes. Changes in (say) a population’s food supply could have rapid impact on the population’s average height or weight, even as the variation in height or weight could be largely explained by variation in genes.
Also, IQ height and weight are distributed on bell curves, suggesting that they are controlled by many small factors.
I thought IQ was distributed on a bell curve by the design of the metric?
I hadn’t thought of that! Is there any independent reason to believe that intelligence is “naturally” distributed this way?
To answer that question, you first have to specify how the number that serves as the measure of intelligence is obtained. Unlike with height, there is no obvious simple way to come up with a number, and elaborate methods can always be engineered so as to change the resulting distribution.
In fact, at the time when I delved into the IQ research literature to try and make some sense out of these controversies, one of my major frustrations was that nobody, to my knowledge, asks the following question. Once a test has been normed to produce a normal distribution for a given population, what exact patterns of deviation from normal distribution do we see when we try to apply it to different populations (or to various non-representative subpopulations)? It seems to me that a whole lot of insight about the Flynn effect and other mysterious phenomena could be gained this way, and yet as far as I know, nobody has done it.
I think Vladimir has the right of it—it’s neither clear how best to measure ‘intelligence’ nor how what-is-measured-by-IQ is ‘naturally’ distributed.
As I understand it, we see what seems to be higher levels of separation between, say, IQs of 100 and 110 than between 160 and 170. This suggests to me that the scale is ‘stretched’ at the high end (though not at the low end?).
It’s an interesting question!
I’m not an expert, but no, I don’t think so. I think IQ tests are normalized, (set so they have the same mean and standard deviation), but the distribution could still be non-normal. Of course, the tests are controlled by many small factors (questions) which perhaps gives another reason for why the observed distribution would be normal.
In a Natural History of Ashkenazi Intelligence Greg Cochran and two other authors provide strong evidence that the genes which cause the diseases that disproportionately strike Ashkenazi Jews significantly contribute to this groups’ high average IQs and intellectual achievements.
From 23andMe: (no non-members’ link)
“Studies have shown that the odds of developing AD [Alzheimer’s Disease] increases with each copy of the ε4 variant of APOE. One copy is associated with about two times increased odds of developing AD and two copies is associated with about 11 times increased odds in populations of European ancestry, compared to average.”
20.3% of Europeans have just one ε4 variant and 1.7% have two of this variant.
23andMe rates the study as four stars meaning that ” At least two studies examined more than 750 people with the trait or condition and/or the associations are widely accepted in the scientific community.”
23andMe posted these results just a few days ago.
It seems that you are operating under an overly-simplistic consideration of how genes work. There is an entire field called epigenetics which studies gene expression. Having “the gene for something” does not necessarily mean one will have that trait, because the expression of that gene can be altered in a variety of ways. However, that does not imply that the gene is not an important factor in the existence of the trait in those who do display it.
How much work is “interesting” doing in “anything interesting”? They haven’t found genes for breast cancer but they have found them for skin color.
BRCA1 and BRCA2 are both genes where certain forms of them result in breast cancer being more likely, and we have a somewhat well understood mechanism for how they do this.
Actually, they have: see the BRCA genes. (These are also related to the Ashkenazi intelligence theory posted below.)
Takedown of the Guardian article you lead with:
Bioscience Resource Project critique of modern genomics: a missed opportunity—Daniel MacArthur, “Genetic Future”, Wired.com, December 15, 2010. “Edit 18/04/11: Depressingly, one of the authors of the BRP piece criticised here now has an opinion piece over at the Guardian recycling the same fallacious message.”
Surely any characteristic that has been created or optimized by natural selection must be highly heritable. How would, say, human intelligence have evolved otherwise?
The rate of evolutionary change in humans has accelerated since the development of civilization (2007 study). To me that can only mean that, for the past 20,000 years, fitness-relevant human traits have been highly heritable. There’s no reason to expect that to have changed since the development of genetic testing.
That’s not true. On the contrary, heritability is defined as the part of the observed variation in a trait that is due to genetic differences, and if there has been intense natural selection on some trait, it may be that only those organisms with the same favorable genes for that trait have survived it, so that now there is almost no genetic variation at all.
Note that saying that a trait is heritable and that it’s determined genetically in some general sense are two very different things. A trait can be under almost exclusive control of genes, with next to zero environmental influences, but if all the organisms of the species have the same relevant genes, its heritability will be zero. For example, humans are clearly genetically predisposed to develop two arms, but the variation in the number of arms is almost wholly environmental—people lose arms in accidents, wars, etc. much more often than they get born armless due to genetic causes. So if you calculated the heritability of this trait (the number of arms), it would be near zero, and yet it’s clearly absurd to say that the number of your arms is not genetically determined.
We seem to care most about fitness related traits, and fitness related traits usually have a decent genetic component. However, what makes a trait a good indicator of genetic quality is that it has a large mutational target size, hence most traits we would care for to know which genes affect them are highly polygenic and not under the straightforward influence of only a few genes.
This seems to be the general finding of recent genetic association studies. They find many genes of low effect, but no single ones which could serve as the target for identification or intervention or even designer babies. This seems to be where a lot of disappointment in genetics is coming from.
This doesn’t apply to non-fitness related traits of course, though they could be highly polygenic for other reasons.
In the specific case of height increases it is possible that heterosis played a role; genes correlated with greater height are more often dominant than recessive, and as modern transport led to people mating further afield rather than mainly marrying others within their village average homozygosity decreased.
Well, then explain sexual attraction.
“Genes influence everything but determine almost nothing on their own.”—David Shenk, “The Truth About IQ.” A somewhat related article.
That’s a pretty awful article. It cherry-picks the literature for convenient soundbites, and then proceeds to put even more spin on top of them. It also misinterprets various findings that demonstrate nothing except the restriction of range effect, etc., etc.
Trusting science reporters in the popular press is generally a bad idea, and when it comes to especially charged topics such as this one, they are probably less than worthless on average.
Edit: Just as one example, the authors of that 1987 German study about chess and intelligence themselves explain the result as a restriction of range effect. (“Dieses Ergebnis wird auf die Homogenität der Spielstärke der Bundesligaspieler zurückgeführt.”—“The result is explained by the homogeneity of the skill level of Bundesliga players.”)
And if the author of the Atlantic article had spent a few more minutes googling for newer results, he would have found this 2006 study stating that: