Jay Joseph on Heritability

The latest post by Jay Joseph at Mad in America is a good rundown of heritability:  Are DSM psychiatric diseases 'Heritable'?

Even when heritability is high, or even when it is 100%, a simple environmental change or intervention can have an important preventative or curative impact. In most cases, therefore, heritability estimates tell us nothing about the potential effectiveness or non-effectiveness of an environmental intervention, or to what extent a psychological characteristic is or is not changeable.

Rutter cited flamingos as an example of gene-environment interaction. He noted that both genes and environment play a crucial role in the ability of flamingos to turn pink, and that “you could feed seagulls for ever on the same diet and they would never turn pink.” He concluded that “it would make no sense to say that flamingos’ color was 50 percent due to genes and 50 percent due to diet. It is 100 percent due to genes (which have to be present) and 100 percent due to the environmental diet (which has to be present).”

As an example of how heritability estimates do not measure the “strength” or “magnitude” of genetic influences, imagine “Country A,” where all citizens (100%) carry the gene predisposing them to favism (glucose-6-phosphate dehydrogenase deficiency), a disease marked by the development of hemolytic anemia. Favism is caused by an inherited deficiency of glucose-6-phosphate located on the X chromosome, combined with the consumption of fava (broad) beans or the inhalation of fava bean pollen. In other words, both “beans and genes” are necessary for favism to appear. Let us then imagine that 3% of the citizens of Country A, all of whom are of course genetically predisposed to develop favism, consume fava beans and are subsequently diagnosed with favism. 

In this case, because all citizens carried the gene but only some ate fava beans, all favism variation in Country A would be caused by environmental factors (fava bean exposure), and the heritability of favism therefore would be 0%. At the same time, it obviously would be mistaken to conclude that genes play no role in developing the disease in Country A, or that the genetic influence is weak or irrelevant. A genetic predisposition is, in fact, a prerequisite for developing favism.

On the other extreme, in “Country B,” 100% of the citizens eat a diet that includes fava beans, but only some citizens carry the favism gene. All favism variation in Country B therefore would be caused by genetic factors (carrying or not carrying the gene), and the heritability of favism in Country B would be 100%. As we see, heritability estimates assess variation as opposed to cause, and do not at all indicate the strength or weakness of the genetic influence—or by implication the strength or weakness of the environmental influence.In the above example, the heritability of favism is 0% in Country A, and 100% in Country B, even though the causes of favism are the same in both countries. As Moore concluded, “Because heritability statistics are about accounting for variation and not about causation, they do not actually reflect the strength of influence of genes on the development of a trait, even if it seems like they do.

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I have tried to give examples of both of the above in terms of behavioral analysis previously on this blog. Social behaviors are far messier than the fava bean example. So, when we turn to something like introverted/extroverted and start trying to understand and analyze behaviors (and I do find it best to turn such psychological trait into behavior speak), trying to tease apart what exactly genes are coding for in these examples becomes absurd. Furthermore, like the fava bean example, when we radically alter a social condition, analogous to replacing fava bean consumption with wheat consumption, we can radically alter behavioral expression. We can make it so that a “psychological trait,” or whatever genetically is structuring that psychological trait, such as introversion/extroversion, play a much different role in the life, identity, self of any individual.

On a simpler note, we have beliefs about identity, about why we are the way we are. So much of our identity becomes essentialized in the world. It becomes simply the way that “I am.” And to that all-encompassing personal gaze, it is all that it ever sees its self as. That is, having a self that has arisen in a socially contingent environment, its reflection on its own characteristics within such an environment gives us great difficulty in imagining a self, and thus behaviors, that would have arisen in our body given a vastly different environment. Similarly, parents have a difficult time understanding the contingent social factors that lead their girls to like pink, for example. Instead, they rely on a constant, consistent interaction and behavior anticipation that encourages them to see this as simply always an aspect of their child's identity. Perhaps the Rawlsian veil of ignorance is a pipe dream.

An example: You give me the right social matrix, and any set of genes will by necessity be a “wide receiver” within that social environment. That is, we may have reared apart identical twins that both bizarrely go on to be wide receivers, to exhibit “wide receiver” behaviors. They may, as well, have many other coexisting behaviors. But our inference about what exactly genes are encoding for within these two individuals is of course barren. If other complex factors go with the “wide receiver” social function, such as lack of school study and very high praise from social groups, then we may have further characteristics that are seemingly similar in these twins. Of course, the only things that were structured by the genes may have been that they would be (with certain environmental minimums) a 6'3” individual that runs very fast.

There is good reason to believe that identity and self-models complexly interact with the world they inhabit. But there are surely similar structuring factors. Thus, we can see the similarity of the identity and self models that have been internalized by our two wide receivers above. That is, there is good reason to believe that these individuals will exhibit other similar identity characteristics. This is especially true given environmental overlap, such as the fact that a certain group of 8-year-olds will be influenced by the movie Shrek at the same time and at similar developmental stages, and will thus hear the same message at a similar stage of development about how to treat ugly looking people (?). Or, better still, as budding 13-year-old star wide receivers, our twins above both internalize the public role models currently exhibiting “wide-receiver” behavior at that exact moment. Also important, all their friends and teammates also learn what it is to be a star wide receiver, and how one should “treat a star wide receiver.” This is of course some standard sociological theory from the likes of Cooley, George Herbert Mead, and Berger and Luckmann. But, the key here is that the analysis of the identity and behaviors of these two twins (including most behavioral and emotional elements) will be far better told by asking about the interplay between socially contingent structures along with genetic factors. The final stories about why any given individual shows behavior X is going to be far more parsable within such an analysis than it is by many of the behavioral claims of the geneticists, of evolutionary psychologists (see this latest Guardian article about genes for sexuality). The messiness with heritability claims as shown above is but one slice of why genetic behavioral techniques and claims are problematic.