So referring again to Callie Burt’s post, here, while failing to adhere to my own strictures about being brief. I see two major issues.
First, whether the BG side of the debate is being defensive in taking issue with bringing an end to “heritability studies,” or by characterizing the Burt et al stance as “anti-BG”. Burt insists that she is not anti-BG, but aside from the one strictly theoretical quote I mentioned in the last post, as far as I know there is no evidence of that in any of these articles. She says it wasn’t the point of the articles to get into the positive contributions a genetically informed point of view might make, and OK, but then it isn’t such a surprise that people take the articles the wrong way. Really, the same can be said for the BG side. Mightn’t it be a good idea to pay a little closer attention to the EEA and its consequences, not to mention a million other assumptions that twin studies make? rGE, random mating, the list goes on and on. I think if you go back to classic papers in the seventies and eighties by people like Eaves, Martin, Heath, Loehlin, etc, they worried about these things a lot, all the time. It’s just good modeling practice, really.
Both sides of the debate are accusing the other of a scorched earth strategy, and I hope it doesn’t make me sound too kum-bye-a to say that finding a way to concede that your opponent might have a point about something is a pretty good way to move forward. Criminology has ignored the possibility of genetic pathways for years; BG sometimes conducts twin studies without putting a hell of a lot of thought into exactly why we are doing it, what the assumptions are, or what the results mean.
Second is the “heritability studies” question. Burt claims that the studies she was criticizing were strictly h2-equals studies. So I read all the studies in the Table. (By the way, what is it with people whose names begin with B in the BG of criminality? Barnes, Beaver, Boutwell, Boisvert. And now Burt! Attn Tim Bates, Tom Bouchard, and Chris Beam). And, drum roll…. the studies in question are not strictly heritability studies, in fact none of them are, although a couple come close. They are bivariate twin studies, so let me say a few words about that.
Let’s say a sociologist observes that children who are held back a grade in elementary school are more likely to get arrested in high school. Now of course that is just a correlation, it doesn’t mean that getting held back causes delinquency. Randomly assigning kids to getting held back is out of the question. What can be done? So it occurs to the sociologist to find sibling pairs who are discordant for getting held back. Within pairs, it turns out that the one who was held back is no more likely to get arrested than his sibling who was not held back.
What do we conclude from this? Presumably it would decrease our impression that holding-back causes arrest, because if that were true why wouldn’t it happen within pairs as well as between them? We might further conclude that the original observed correlation must have been the result of something else that sibling pairs share, eg families and everything that goes along with them. On the other hand, it might turn out that the held-back sibling is more likely to get arrested than the co-sib. Does this prove causation? No, but it strengthens our confidence in a causal hypothesis, as it survived a fairly rigorous test. In the absence of randomization, this may be the best we can do.
My main point is that this sociologist is doing “behavior genetics.” Among the familial things that siblings share, of course is half their genes. The other is their family environment. OK, you say, but it isn’t a “heritability study”. But it is. If you drew sibling pairs at random from the population rather than selecting them for being discordant for held-back, you could partition the held-back variance into a Between and a Within pair component, and B/(B+W) would be the intraclass correlation for sibling pair. The design is not yet genetically informative, so the correlation would be the “familiality” of being held back. If you wanted, you could report this quantity, and include a latent variable for it (like an ACE latent variable) when you analyzed the data.
The key to doing a bivariate twin study clearly, in my view, is recognizing that (a) The variance components (the h2-equal part) are not the main point, (b) The within-pair effects (the genetically informed quasi-experimental regression part) are the main point, and (c) The correct way to analyze the within pair effects is to ensure that they are invariant against changes in the variance components, that is ensuring that (a) doesn’t interfere with (b). This is what the Turkheimer and Harden chapter is about.
DZ twins are just siblings, of course, and if you throw in MZ twins and all the assumptions that Burt et al don’t like it turns into a bivariate twin study, but the basic logic doesn’t change. Held-back and arrest are related between and within pairs, now in MZ and DZ twins. Zygosity and the twin assumptions, if you are so inclined, allow you to divide the “familiality” thing from the sibling study into A and C, and I think it is often interesting to think about whether the confounds of the purported causal effect appear to be genetic or family environmental. However, it remains absolutely true that the magnitude of these components is not the main point– the within pair relationship between held-back and arrest is the main point, and the data should ideally be analyzed in a way that keeps this relationship invariant to changes in the decomposition of the predictor.
The bivariate criminology twin studies that I read, in my opinion, don’t do a great job of keeping the “heritability” issues separate from the within pair regression issues. I would analyze and report the results differently. Burt et al, in the same way, see the MZ and DZ twins and the reported heritabilities, and conclude that they must be “heritability studies” even though they are, at least potentially, more than that. And the great irony is that in most of them, the within pair relationships between X and Y survive the test of having their common genetic background controlled. So in Boutwell et al, for example, there is a significant within-pair relationship between low self-control and victimization. This means that in pairs of identical twins, the twin with lower self-control is more likely than the co-twin to be a victim, controlling for whatever genes and family background identical twins have in common. This is a victory for environmental– better to say phenotypic– causation, but it gets lost in both the original report and the objections, because everyone is hung up on worrying about what might have turned out to be heritable.
Well as usual this has turned into more tooting my own horn than resolving this particular debate. My conclusion is that behavior genetics has an important role to play in criminology, not because criminal behavior has in any important sense turned out to be “genetic” or “biological,” but instead because criminology is almost always stuck with inferring causal processes from correlational data, and careful use of twins can help rule out important classes of confounds of those causal hypotheses. This is less attention grabbing than concluding that “criminality lurks in the genes” like they said in that infidelity study, but ultimately much more useful scientifically