| If genetic factors are to be included in the models of development of traits, there are good methodological reasons for not categorizing individuals according to racial group membership [e.g. no measurable genetic factor admits a clean subdivision between whites and African-Americans (Nisbett, 1998, pp. 89–90; see also Taylor, 2006a)]. On the other hand, racial group membership continues to bring disadvantages to African-American individuals and, reciprocally, to bring benefits to white individuals (Flynn, 2000, 142ff)—moderated somewhat, but in a decreasing set of circumstances, by affirmative action policies for African-Americans... Can researchers shift the focus from group membership to heterogeneous pathways without bolstering the fiction that racial group membership no longer brings social benefits and costs. Conversely, can researchers continue to examine differences between averages for racial groups without bolstering the ubiquitous stereotyping that employs group membership when deciding how to treat an individual? In short, a paradox that applies to the use of IQ test scores in US society seems to be that researchers and policy-makers who want to move beyond explanations and policies based on racial group membership need to take into account the disadvantages and benefits individuals experience because of their group membership... |
| The conflation of family and population might help explain why the Nature versus Nurture formulation persists This book is by no means the first to assert that Nature versus Nurture or genes versus environment is an ill-framed formulation. Yet, this formulation continues to be the default in popular discussion. This final section suggests that it is the conflation of family and population helps explain why that formulation persists. We know that both genes and environment are involved even in the cases in which there is a single gene with a major and direct effect, such as phenylketonuria (PKU). Recall that in PKU the development of individuals having two copies of a non-functioning allele for the enzyme phenylalanine hydroxylase (PAH) is extremely impaired by the level of phenylalanine present in normal diets, but much much less impaired if a special diet is maintained. OK, but we might say that genes are primary here: Without the genetic condition, we do not need to worry about the diet (the environment). Knowing the genetics, or at least, knowing the biochemistry associated with the genetic condition, points to the appropriate environment to alter. In fact, all kinds of changes in upbringing of individuals with the genetic condition would have no effect. In short, nature interacts with nurture, but it is most important to know about the genetics and biochemistry. And, if that is the case for PKU, we might well suspect that there are many other genes, perhaps of smaller and less direct effect, for which the same primacy would hold. And, why decide in advance that certain traits, such as IQ test scores, are not amenable to genetic study? We might say all that. The response sketched in this item, however, suggests that the issue is more than the (possible) primacy of genes (as just sketched above); there is a conflation of family and population involved in the persistence of the Nature vs. Nurture formulation. Starting within a family, it is very easy for someone to see that children physically resemble their (birth) parents, where resemble means more than look like their parents. It means look more like their parents than any two people randomly picked from the population. In most cases parents pass onto their offspring environment as well as genes, so we might well ask how important is each? That is hard to say when parents pass on both so you imagine identical twins raised apart from birth and ask: Does the one raised at home resemble the parents more than the one raised away? But, of course, no offspring resembles both parents well—(generally) a child is male or female and lots of characteristics (e.g., height, hips) go along with that. So, perhaps we should look at resemblance between offspring and the same-sex parent for physical traits and between offspring and the average of the parents for other traits (e.g., IQ test score). But that does not quite work for sexual characteristicsqq. Conversely, the average of the parents might also capture resemblance for physical traits such as height. We simply expect there to be variation around that average, e.g., female offspring end up on the shorter side of the average and male offspring end up on the taller side. Once we start talking about variation and averages, and stop expecting a clean picture of resemblance in any one family, we can shift our sense of resemblance from the family to averages over many offspring-parent pairs. Going back to the identical twins, if we imagine many such pairs of twins, on average does the one raised at home resemble the parents more than the one raised away? We could also ask, if we have many sets of same-sex non-identical twins raised together and many sets of same-sex identical twins raised together, on average does one identical twin resemble the other twin more than one non-identical twin resemble the other? (Shifting to same-sex twins means that we do not have the complication of differences between an offspring and its other-sex parent. And shifting to twins raised together means we do not have to search for the rare cases of twins separated and raised in truly independent families.) If the answer in the twin-resemblance study is yes, it seems reasonable to conclude that the identical twins are on average more similar because they share all their genes whereas the non-identical twins share fewer of their genes. However, that conclusion does not say that it is the same nature—the same genes—or the same nurture that brings about the resemblance from one pair of twins to the next. (this qq the possibility of underlying heterogeneity.) So then where are we? We might take the results of the multiple twins study and transfer them back into thinking about your family. Suppose that the non-identical twins are very much less similar so that sharing fewer genes makes a big difference (skipping here the technicalities of getting the number, “heritability,” that quantifies that result). If that is so, we might say: “There is nothing I could do as a parent to change the outcome for my offspring (for whatever trait we are thinking about, e.g., IQ test score). I’m not to blame for the outcome (other than having passed on my genes). If that seems justified, we might then reason that the same is true for every other family, and thus society as a whole should not try to change what it is doing for it will not make a difference. Now flip that scenario. Suppose that the non-identical twins are just as similar so that sharing fewer genes makes little difference. What can we do as a parent? Or, if our offspring are grown, what could we have done? What then can we advise others for the future, or society at large? In this scenario, we have to face the possibility of underlying heterogeneity. Our study of twins has not shown us what environmental factors have had an effect so we do not know what to change. And, if we cannot expect the factors to be the same from one family to the next, we might just give up on trying to identify those factors. Notice an asymmetry in these scenarios. The possibility of underlying heterogeneity did not lead us to give up on looking for the genetic factors because our reasoning did not lead us to look for them at all. We simply concluded that we were not to blame for the outcome in our family and, by extrapolation, society should not try to change what it is doing. This asymmetry should make us suspect that there is a problem in the reasoning that says, because sharing fewer genes makes a big difference, there is nothing a parent can do to make a difference. qqsegueAny set of twins, call it set i, is raised together in family i—each nature i has a nurture i. There are lots of i's. There is nothing in the average over many sets of nature i – nurture i pairs that says there cannot be a nurture j or k or l in which nature i in nurture j or k or l would not be different in interesting ways. Perhaps if we found that identical twins raised apart were just as similar on average as identical twins raised together, we would doubt that such a nurture j or k or l could be found. We would doubt, but not be sure. We could be surprised. Japanese offspring after World War II grew taller on average than their parents, but a comparison of twins in the previous generation would have shown that sharing fewer genes makes a big difference (i.e., heritability for height was high). Once we entertain the possibility that nature i varies across nurture i, j, k, l, … we can ask about what genetic factors and what environmental factors are involved and how they act together. Now there is symmetry in how difficult it is to identify those factors if you cannot expect them to be common across families. One response to the difficulty is, putting aside the search for common genetic factors, to look for rare variants that have a large effect on some biomedical or behavioral condition (McClellan and King 2010). This approach can be justified in two ways: a. For those individuals carrying the rare variant—or for relatives among whom the variant is common—knowing about the genetics could lead to genetic counseling (about having children), screening and selective abortion of fetuses carrying the variant, screening of newborns and other relatives, or investigation of biochemical pathways that might eventually be modified by pharmaceutical treatment; and b. Investigation of biochemical pathways related to the rare variant might suggest mechanisms and pharmaceutical treatments to explore that might help others who have the condition but lack the particular variant. For the second possibility, notice that we have slipped from family (i.e., sets of close relatives) to a wider population. This time the slip depends on a hope that the biology is amenable to investigation, intervention, and extrapolation or generalization. Perhaps that will turn out sometimes to be the case. If so, the resulting biomedical interventions or treatments will not be based on screening for who has the original genetic variant, but for signs of the biochemical or related conditions that turned out to be amenable to intervention. That kind of screening, of course, dominates Western medicine already. There is nothing especially genomic about that. If we return to the family-based justification for searching for rare variants of large effect (#a above), we can envisage, because it already happens, parents whose children possess rare genetic variants of large effect agitating for more research on the mechanisms and possible treatments. Biomedical researchers have joined forces with such families in part because the hope of a treatment is important to people who they get to know personally. In part, also, because researchers benefit from such cases to the extent that they fuel the claim that genomics will lead to a revolution in biomedicine. More recently, this has mutated into the claim that genomics opens up a realm of personalized medicine in which knowledge of one's particular and not-necessarily-common genetic profile allows for customized and thus more effective therapies. There is no denying the emotional power of addressing the needs of families whose children suffer from conditions related to rare variants with a large effect. Notice, however, that addressing these needs is a retreat from the idea of a genomic biomedical revolution where, because all conditions would be linked back to their genetic basis, diseases could be better treated for everyone—for the population. That research on rare genetic variants affecting some members of some families could fuel genomics speaks again to the conflation of family and population. The more recent tactical regrouping of genomics around the ideal of personalized medicine (qqref) does not, however, come with clear distinction between the levels of family and population. The realm of personalized medicine is supposed to be one in which knowledge of one's particular and not-necessarily-common genetic profile allows for customized and thus more effective therapies. However, as discussed in Item I.qq, genomics-based pharmaceutical research will generally depend on there being an advantage on average in some given population of a treatment—perhaps prophylatic—related to the effect of a genetic variant. At the same time, there will be variation of effects and responses to drug treatment around that average for the group or subpopulation who have the genetic variant. Given this variation, pressure may emerge to find ways to subdivide the group who has the genetic variant into smaller subcategories so that the treatment can be made to fit each person better. Pharmaceutical companies will not, however, have an incentive to trim the potential market unless the side-effects of treatment for some people so outweigh the benefits or the treatment fails to help them and these people push back strongly. In that case, negative publicity on those side-effects or failures could erode adoption of the drug even among those who might have benefited. In short, from the point of view of the pharmaceutical company, the pathway to personalized medicine goes through a phase in which carriers of the genetic variant are treated according to the group they belong to. The company may or may not be driven to move beyond that phase to a place where variation within the group or subpopulation are taken into account. This item casts doubt on the idea that there are genes for most traits and that genetics or genomics will be able to identify those genes. Of course, genetic and environmental factors are involved in the development of traits, but heterogeneity means that these factors need not be the same across all families within a population. Yet claims that researchers are now finding, or can be expected to find, genes for X and Y abound without reference made to the problem that heterogeneity poses for their claims. This problem is one that should be understandable without any technical specialization. My argument in this section has been that the blindspot about finding genes for traits comes from a persistent conflation of family and population. Let me put forward a conjecture: The conflation of family and population derives from people being readily able to envisage family-level care and support, but not so readily able to envisage relying on social-level support. People can see that social institutions do not care well for everyone; some are left out. Sometimes it seems that institutions “care more about” (i.e., operate so as to ensure) their own perpetuation than they do about individuals. People have a stronger sense that being cared for at a family level is a norm, even if their own family falls short of their ideal. The challenge that follows from this conjecture is not only to expose the limitations of gene-for-X thinking and research, but also to contribute to a sense that social institutions can be supportive and caring for all. Moreover, to contribute to a sense that social institutions can care in ways beyond treating each individual simply as a member of a population, all subject to the same measure, say, fluoridation of water supply, seat belt laws, and so on. To meet this challenge is to address the different and overlapping pathways, each consisting of heterogeneous factors, which lead to any outcome in the world, from our heights to our income, health, and happiness. Somehow a caring society has to support each of us in all our heterogeneous developments. How we, individually and collectively, move towards that goal is..qq. |