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Authors: Daniel J. Fairbanks

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Few scientists dispute that both genetic and environmental effects interact to influence variation for most characteristics, including human intelligence (in whatever way it is measured). What is disputed is whether differences between racially defined groups—such as the fifteen-point difference for average IQ scores between “American blacks and whites,” as stated by Herrnstein and Murray—is influenced by innate genetic differences between these groups.

As simple as it seems to be, heritability is unfortunately one of biology's most misunderstood and misapplied concepts. And most of this misunderstanding and misapplication boils down to three main points: First, heritability is a measure of
variation
, not magnitude. It tells us nothing about the degree of a trait, only what proportion of its variation can be attributed to genetic variation. Second, because it deals entirely with variation among individuals, it never applies to any single individual. Rather, it applies to each defined population in which it is measured. Third, heritability is not a permanently fixed value that can be measured in one population, then applied to another. It may vary among populations, and even over time in the same population, because environmental variation may change over time. Thus, strictly speaking, any measurement of heritability applies only to the population in which it is measured and at the time it is measured.

An often-used analogy, presented in various iterations by different authors, illustrates how heritability may be misapplied when attempting to explain racial-group differences in IQ. Perhaps the most cited version is by Harvard geneticist Richard Lewontin in a 1970 article titled “Race and Intelligence,”
35
which was a critical response to Jensen's 1969 article “How Much Can We Boost IQ and School Achievement?” Lewontin asks us to imagine taking two handfuls of seeds from the same bag of genetically diverse seed corn, such that the genetic diversity of seeds in each handful is equivalent. One handful is planted and raised in a highly uniform environment with a fertilizer solution containing all the mineral nutrients the corn plants need for optimal growth (like the liquid fertilizers for houseplants sold in department and home improvement stores). The other is planted and grown in exactly the same environment but with a suboptimal fertilizer solution that has only half the nitrogen (a major nutrient needed by plants in relatively large amounts),
and half the zinc (a minor nutrient needed in trace amounts). Over time, the corn plants grown in the environment with the optimal nutrient solution vary in height due solely to their genetic differences. The same is true for the plants grown with the solution that lacks optimal amounts of nitrogen and zinc. But the
average
height of plants grown in the optimal environment is greater than the average height of plants grown in the suboptimal environment because of the difference in nutrient supply. In both cases, heritability is 100 percent for each group because all variation
within
each group is due to genetic differences. The difference
between
the averages of the two environments, however, is entirely environmental because the genetic diversity of plants in the two environments is the same. Lewontin's point is that high heritability
within
a group provides no evidence whatsoever that differences
between
groups are genetic.

He then further extends the analogy, asking us to presume that the lack of nutrients in the suboptimal environment is due to a careless laboratory worker who failed to add the proper amounts of nitrogen and zinc. A chemist is called in to diagnose the cause of the difference between the two groups and determines that one solution lacks sufficient nitrogen. The nitrogen is added, the experiment is repeated, and the difference is narrowed but not eliminated because the chemist did not test for differences in the trace quantities of zinc required for optimal growth. Lewontin's point here is that identifying some environmental causes and correcting them may not completely erase group differences until
all
environmental causes have been identified and corrected. Thus, failure to erase a gap through environmental intervention does not necessarily offer evidence of a genetic cause for that gap.

Lewontin's analogy with corn plants is a good visual representation of heritability, and it also represents the concept's origin. Heritability and methods for measuring it arose from plant and animal breeding, where its utility is very powerful. When heritability is high, plant and animal breeders can rapidly improve inherited characteristics through artificial selection because they are able to select individuals that are genetically most predisposed to inherit genes conferring the traits they wish to improve. When heritability is low, however, progress from artificial selection is slow and unproductive because environmental differences mask genetic differences. Therefore, much of modern plant and animal breeding is aimed at implementing measures
to maximize heritability, usually through reducing environmental variation, such as planting experimental plants in environments that are as uniform as possible or providing experimental animals with adequate food in exactly the same rations for each individual. Plant- and animal-breeding experiments designed to measure heritability are usually highly controlled, with elaborate statistical and experimental designs to ensure accurate results.

By contrast, measuring heritability in humans is notoriously challenging. Researchers, for obvious ethical reasons, must not subject humans to highly controlled environments as they do for experimental plants and animals. And even if they were to do so, the results would have little meaning because heritability in the real world is dependent on actual environments, not experimental conditions. As Nisbett and his colleagues put it in their 2012 review:

The concept of heritability has its origins in animal [and plant] breeding, where variation in the genotype and environment is under the control of the experimenter, and under these conditions the concept has some real-world applications. In free-ranging humans, however, variability is uncontrolled, there is no “true” degree of variation to estimate, and heritability can take practically any value for any trait depending on the relative variability of genetic endowment and environment in the population being studied.
36

Some of the most common estimates of heritability in humans are based on studies of identical twins who were separated at birth and raised apart. The idea here is that identical twins are
genetically
identical. Therefore, any differences between them are assumed to be entirely environmental (in other words, heritability is zero for identical-twin pairs). Measurement of how much two twins differ for any characteristic, therefore, offers an estimate of purely environmental variation between them. By combining these differences among multiple pairs of identical twins reared apart, researchers can derive an average estimate of environmental variation for the environments of these twin pairs without the confounding effects of genetic variation. If they then apply these estimates of environmental variations to people who
do
differ genetically but are raised in similar environments to the twins, they can derive estimates of heritability for the people who are genetically different. The assumption—which is key—is that any variation greater than that observed between twins
must be genetic. In some cases, identical twin pairs are compared to fraternal twin pairs, who differ genetically as much as full siblings but have the comparative advantage of having shared the same womb and been born on the same day, like identical twins. Alternatively, researchers can compare variation among relatives with different degrees of genetic similarity—such as full siblings, half siblings, and cousins—who are raised in similar environments as a means of statistically estimating heritability.

Regarding such estimates of heritability, Herrnstein and Murray conclude that

the genetic component of IQ is unlikely to be smaller than 40 percent or higher than 80 percent. The most unambiguous direct estimates, based on identical twins raised apart, produce some of the highest estimates of heritability. For purposes of this discussion [differences between racial groups], we will adopt a middling estimate of 60 percent heritability, which, by extension, means that IQ is about 40 percent a matter of environment.
37

Critics of
The Bell Curve
rightly point to this generalization of “a middling estimate of 60 percent heritability” as a gross misapplication of the concept. According to Nisbett and colleagues' 2012 review of current research, “the heritability of intelligence test scores is apparently not constant across different races or socioeconomic classes,”
38
reinforcing the long-standing caveat that heritability should not be generalized from one population to another.

Moreover, reliance on estimates of heritability based on environmental variation measured in identical twins has also been criticized because, even when twins are reared apart, environmental similarities may be confounded with the genetic identity of twins. For example, adopted children are typically raised in more affluent homes in environments that tend to be more uniform and less representative of overall environmental variation, thus resulting in potential overestimates of heritability on the basis of twin studies.

Also, the shared uterine environment of twins (identical or fraternal), which is unrepresentative of people who are not twins, can have a confounding effect on heritability estimates, even when identical and fraternal twins are compared. Identical twins typically share the same placenta, whereas fraternal twins have separate placentas, resulting in different uterine environments.
The uterine environment is especially pertinent to measurements of IQ later in life, particularly if prenatal care is poor or if a birth mother has abused alcohol, tobacco, or illicit drugs during pregnancy because these factors can permanently affect brain development, and, in the case of twins, such factors may or may not affect the twins similarly, leading to misinterpretation about the degree of genetic influence on the brain.

Similar obstacles confront researchers who conduct nontwin studies for measuring heritability in humans. One of the most serious obstacles has been the inability to directly estimate genetic variation. Historically, researchers have estimated genetic variation by the degree of relatedness of subjects, such as comparing identical twins, full siblings (including fraternal twins), half siblings, and cousins to people who are unrelated. Such indirect measures of genetic variation are highly problematic, however. For instance, the degree of genetic variation between full siblings is not generalizable because it depends on how genetically different their lines of ancestry are. For instance, it is often said, as Herrnstein and Murray put it, that “full siblings share about 50 percent of genes.”
39
Such a statement represents a seriously naïve understanding of human genetics. In reality, full siblings share about 50 percent
of the variants that are heterozygous in each parent
and 100 percent of the variants that are homozygous in each parent. The more diverse the lines of ancestry are for an individual's parents, the greater the degree of heterozygosity in the parents and the greater the degree of genetic variation in their children. Therefore, genetic variation among full siblings varies considerably from one family to another; full siblings whose parents have similar ancestry are genetically more similar to one another than full siblings whose parents have genetically diverse ancestry. The same holds true for half siblings, cousins, and other people who are genetically related. Differing degrees of genetic diversity from one family to another result in different heritabilities among biological full siblings or other relatives, further dispelling the notion that heritabilities in humans can be generalized.

To their credit, many scientists who conduct research on heritability in humans recognize these and other limitations and clarify them when reporting research. Scientists often use complex and elaborate scientific and statistical methods to derive estimates of heritability that are as reliable as possible
despite the large margins of error that are typical of heritability measures in humans. Most of these scientists are well-trained researchers who appropriately apply scientific methods to their work. Unfortunately, not everyone is as attentive; overly simplistic generalizations of heritability for IQ in humans often lead those who advocate hereditarian models to unsubstantiated conclusions that may be based more on political ideology than on scientific evidence.

Published studies on IQ and the interaction between genetic and environmental variation often report contrary conclusions. For instance, Herrnstein and Murray determined that, according to the studies they reviewed, socioeconomic status and shared environment (the fact that children raised in the same family share many of the same environmental influences) had little effect on heritability for IQ. Rushton and Jensen arrived at similar conclusions. By contrast, other researchers offer evidence that socioeconomic status and shared environment have a considerable effect on heritability for IQ. These latter studies often, though not always, portray a positive correlation between heritability and socioeconomic status, especially when shared environment is taken into account. Heritabilities tend to be highest in families in which parents are well educated or families of high socioeconomic status, whereas heritabilities are lowest for impoverished families and when parents have attained little education.
40
However, yet other studies have led researchers to arrive at the opposite conclusion: heritabilities are highest in families of low socioeconomic status when compared to the more affluent.
41

In many of these contradictory studies, there is nothing wrong with the science or the interpretations. In fact, it is no surprise that studies on heritability of IQ may show widely differing results. They often are conducted on different populations in different places with people whose degree of genetic relatedness differs, and with subjects of different age groups and educational backgrounds. They are excellent examples of the malleability of heritability estimates in humans. By focusing on a selected subset of studies, advocates of a particular point of view can assemble what seems to be ample evidence to support their preferred models, when, in fact, the real situation is highly complex, varied, and inconclusive.

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