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Twin Studies

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Above is the Ngram result for paradigm shift, a ubiquitous descriptive concept which can be quite slippery when applied to contemporary science. For example, every few years there is always a new “revolution” which is going to overturn “Darwinism.” Be it punctuated equilibrium, symbiogenesis, or epigenetics. But over time revolutionary fervor abates, and the orthodoxy remains standing, albeit with modifications and alterations, making it all the more robust.

I thought of this when I saw Andrea Cantor’s comment below in relation to twin studies:

Twin studies underestimate heritability only if you subscribe to the crude notion that the effect of genes is additive, i.e., keeping “environments” the same, the more similar two people are genetically the more alike they will be. This ignores everything we now know about the way genes work.

Genes are not self-activating: they do not turn themselves on and produce traits. Genes do not, in fact, produce anything. Genes are turned on and off by the epigenome in response to environmental inputs. If you are inclined to doubt this, then consider: If all the cells in our body are supposed to contain identical DNA, how do you account for the existence of different tissues and cells types (answer: the epigenome). Twins have been shown to have significantly different epigenomes in the womb. Does this show that twin studies underestimate heritability? Of course not. It shows, rather, that these studies are out of touch with advances in molecular genetics.

You are all committed to a crude, 19th century conception of the relationship between genotype and phenotype. Twin studies are based upon a scientific paradigm that has remained unchanged since the time of Galton. Problem is, recent advances in molecular genetics are bringing about a paradigm shift in the science of genetics.

Twin studies make it seem all so easy: All you need is a large data set that has zygosity status and statistical software and any undergraduate can unravel the biomolecular basis of human behavior.
Would that it were so easy.

I get comments like this frequently. Often I don’t publish them (in fact, I usually ban the commenter). These contributions to the discussion exhibit internal coherency, and thankfully they’re not personal attacks (though they do tend to stink of condescension). But they don’t really further the discussion, and are liable to just confuse people. I let this comment through because I thought it might be interesting to respond to it, to clarify a few points.

I highlighted some buzzwords and tendencies which unify a broad range of commenters/opinionators on science, from Creationists to quasi-Blank Slaters. There are general terms such as “paradigm shift.” There are almost always references to how dated the science that you are alluding to is. You are “out of touch” (or being perverse). Then there are the weird “what does that even mean?” assertions which often litter this class of comments. This is probably the main reason I often don’t let these comments through: they waste your time because they require a lot of interpretation. I honestly don’t know what it means to assert that anyone would think that twin studies can unravel the “biomolecular basis of human behavior.” I’d like to meet the person who thinks this. Finally, there are the specific buzzwords. Here you have epigenome. A reference to the mysterious connection between genotype and phenotype usually helps to impress as well.

But it turns out that I didn’t even need to respond. Luke Jostins is at it again, defending the honor of the twin study! Here’s his comment:

@Andrea Cantor

The relationship between biological interaction and genetic addativity on the variance component scale is more complex than I think you realise, and the common terms between the two (additivity, interaction, etc) seem to have thrown off your intuition. The fact is that virtually all the assumptions of twin studies have been extensively tested, and they have all been found to be relatively good approximations (statistically) the behaviour of genetic risk in populations, in certain relatively well characterised circumstances. This doesn’t mean that biological systems aren’t full of interaction, or that epigenetic effects are not important, or that genetic effects are stationary over time, or that interactions between genes and environment do not exist. It just means that your intuitive feel that these effects result in statistical non-additivity on the genetic risk scale is wrong.

In other words, Andrea Cantor doesn’t know what she’s talking about. That’s fine. But using her comment as a prototype, I hope it will help us navigate the turbulent waters of the scientific discourse.

• Category: Science • Tags: Behavior Genetics, Twin Studies 
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I’m still scratching my head over the rather atrocious Brian Palmer piece in Slate, Double Inanity: Twin studies are pretty much useless. It’s of a quality which would make it appropriate for WorldNetDaily. Here are the responses of Jason Collins, Daniel MacArthur, and Alex Tabarrok. The comments at Slate were rather scathing too. I observed over at Genomes Unzipped that many of the assertions in the piece were in the “not even wrong/what does that even mean?” class. Palmer is apparently a freelancer at Slate, and they’re doing a bunch of stories on twins this week. I wonder if they just sent him the assignment with instructions on the slant, and he took it a little too far. Even if it was a polemic it was a shoddy and embarrassing one. My main concern is that many people perceive Slate to be an organ which publishes “smart” and well researched pieces, and they’ll take Palmer’s screed at face value.

The scientific problems with the article are legion. But still: how does something like this get published in a relatively high-end publication? Brian Palmer has editors presumably. If the copy was an undergraduate paper the prose would be relatively polished, but the overall structure of the argument and the naked guilt by association are marks of hurried sloppiness. The attempt to smear twin studies by association with Francis Galton was pathetic and childish. What next, turn against the concept of statistical correlation because Galton introduced it? There has to be more to this story than what we know. Or perhaps the people at Slate just don’t know anything about science.

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A few friends have pinged me on this piece in Slate, Double Inanity: Twin studies are pretty much useless. The headline is bold, but the piece is just a sloppy mishmash. It’s really something amenable for a major “fisking,” but I generally don’t like doing that sort of thing, because it doesn’t seem a optimal allocation of time (though I have to note that the author seems to be implicitly using a colloquial form of the concept of heritability, which I think is going to confuse an already naive audience). A lot of the article is taken up with criticisms of political scientist John Alford’s behavior genetic findings on the heritability of ideology. I’ve had personal communication with other researchers in this area who actually are broadly critical of Alford’s methodology, but they’re still strongly invested in using genomics and behavior genetics to explore this issue. In other words, rejecting Alford’s conclusions does not entail that you just reject twin studies, as such.

Of course there’s a lot more to twin studies than behavior genetics. Luke Jostins at Genomes Unzipped had a long post up defending the methodology, with caveats, in estimating heritability. But what I find perplexing is that in many ways we are right now confirming the broad results of twin studies using genomic methods. I blogged a paper on the heritability of I.Q. a few weeks ago, but here’s a paper from 2006, Assumption-Free Estimation of Heritability from Genome-Wide Identity-by-Descent Sharing between Full Siblings:

…. Following the classic paper by R. A. Fisher in 1918, the estimation of additive and dominance genetic variance and heritability in populations is based upon the expected proportion of genes shared between different types of relatives, and explicit, often controversial and untestable models of genetic and non-genetic causes of family resemblance. With genome-wide coverage of genetic markers it is now possible to estimate such parameters solely within families using the actual degree of identity-by-descent sharing between relatives. Using genome scans on 4,401 quasi-independent sib pairs of which 3,375 pairs had phenotypes, we estimated the heritability of height from empirical genome-wide identity-by-descent sharing, which varied from 0.374 to 0.617 (mean 0.498, standard deviation 0.036). The variance in identity-by-descent sharing per chromosome and per genome was consistent with theory. The maximum likelihood estimate of the heritability for height was 0.80 with no evidence for non-genetic causes of sib resemblance, consistent with results from independent twin and family studies but using an entirely separate source of information. Our application shows that it is feasible to estimate genetic variance solely from within-family segregation and provides an independent validation of previously untestable assumptions….

The point is that before modern genomics one had to assume relatedness, and from these assumptions derived various estimates as to the heritability of a trait when taking into account patterns of genetic relatedness and phenotypic similarity. Today genetic relatedness can be pinned down on an individual basis with much greater precision. Two of my siblings for example have a relatedness of 0.42, instead of 0.50. This does not mean that all of the criticisms in the Slate piece are invalid, but there was a slapdash throw-the-kitchen-sink feel to it all.

Finally, I want to point out that just because a trait is not substantially heritable, it does not mean it is not substantially biological. This is the possible case with male homosexuality. I think as a scientific matter this is a huge issue, but when it comes to public policy it is much less important because the relevance of the genetic origin of a trait is that that necessarily means that it is biologically specified. If the biological specification is through random developmental processes or infection with pathogens, it means that it isn’t heritable and genetic, but it doesn’t mean that once the trait has fixed it is any less plastic.

Razib Khan
About Razib Khan

"I have degrees in biology and biochemistry, a passion for genetics, history, and philosophy, and shrimp is my favorite food. If you want to know more, see the links at"