Heritability Ratios
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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