Clearly, then, the role of genetic factors in shaping intelligence depends on the circum-stances. In some settings, genes play a large role; in other settings, they do not. This invites a new question: Is there some way to measure the contribution of genetics so that we can ask, in a particular setting, how much of the data pattern can be understood in genetic terms?
To address this question, investigators often rely on a measure. For any trait, this measure involves a comparison of two numbers. First, what is the total phenotypic variability—that is, how much do individuals differ from each other in their actual characteristics? Second, how much of this variability can be understood in genetic terms? Heritability is then calculated as the ratio between these two numbers—and so tells us, roughly, what percentage of the total variation can be attributed to genetics.
Let’s be clear, though, that heritability is a measure that describes a group, because to calculate heritability, we need to ask how much variation occurs within that group, from one individual to the next. Thus, it makes no sense to apply measures of heritability to single individuals, and it would be a mistake (for example) to read a heritability esti-mate as implying that a certain percentage of a person’s IQ (say) came from her genes, and the remainder from her environment. Instead, as we’ve emphasized throughout, the influence of genes and environment is, for any individual, fully intertwined—with both factors shaping all aspects of whatever the person becomes.
Overall, researchers estimate that the heritability for IQ is, in most environments, between .40 and .70; often, a figure of .50 or .60 is quoted (Neisser et al., 1996). This can be understood as the assertion that, of the variability we observe in IQ , half or a lit-tle more is attributable to variations in genetic material. (And, since the other 50% is attributable to factors other than genetics, this means that genes and environment have roughly equal weight in determining IQ.)
Let’s be very clear, though, that these estimates are always calculated with reference to a particular group—and, in fact, we’ve already seen an example of how this matters: If we draw our data from low-SES groups, we find that the heritability of IQ is much lower—and may even be zero (Turkheimer et al., 2003). Likewise, we mentioned earlier that the genetic influence on IQ becomes more visible as people move from childhood into adulthood; this, too, is reflected in heritability estimates: Overall, the heritability for IQ in middle-class children is estimated as around .50; the heritability of middle-class adults, in contrast, may be as high as .80 (Plomin & Spinath, 2004).
The linkage between heritability and a particular set of circumstances was also evident when we discussed the medical condition known phenyl-ketonuria, or PKU (Widaman, 2009). This condition is caused by a problem with asingle gene that ordinarily governs the production of an enzyme needed to digest phenylalanine, an amino acid that’s commonly part of our diet. A defect in this gene derails production of the required enzyme, with the result that phenylalanine is instead converted into a toxic agent. If an infant is born with PKU, the toxin accu-mulates in her bloodstream and damages her developing nervous system, leading to profound mental retardation.
PKU is unmistakably of genetic origin; and for many years, we had no way to remedy this condition. As a result, the heritability was extremely high. The pheno-typic variation (whether someone did or did not have this type of retardation) was almost entirely attributable to whether or not he had the relevant genetic pattern. But we now know that a simple environmental manipulation can minimize the impact of PKU: All we need to do is ensure that the infant (and, later, the child) gets a special diet that contains very little phenylalanine (Figure 11.20). If this diet is introduced at an early enough age, retardation can be minimized or—far better— avoided altogether. As a result, the heritability estimate for PKU is, in most countries, currently quite low. Whether retardation is observed depends largely on the individ-ual’s diet, and so most of the phenotypic variation we observe is due to this environ-mental factor, not to genes.
Notice that the case of PKU offers us many lessons. First, the case reminds us once again that genetic effects don’t unfold in a vacuum; instead, genetic effects interact with environmental influences—sometimes with good effect, sometimes with bad. Second (and related), the example of PKU makes it clear that patterns that are powerfully shaped by genes can still be dramatically altered. Indeed, PKU is a case in which having a particular genotype can (with a carefully controlled diet) end up having no impact at all on the phenotype! Be aware, therefore, that genetic factors are important but do not set someone’s destiny (Figure 11.21).
Third, keeping the case of PKU in mind will be helpful when you think about heritability ratios. These ratios are a powerful—and often useful—data summary that allows us to capture complex patterns in a single number. But the case of PKU reminds us that this number reflects only a particular set of circumstances for a particular group of individuals, and the heritability ratio can change if the circumstances change. In addition, heritability ratios tell us nothing about the future. Even if a trait’s heritability ratio is near 1.00 (as it used to be, for PKU), we may be able to alter the trait enormously once a suitable intervention is found.
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