The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (26 page)

   There were much earlier hints. “For most of the past century,” says Penn State geneticist Gerald E. McClearn, “the evidence has been clear that a more collaborative model of coaction and interaction of genetic and environmental agencies is more appropriate. Even in the pell-mell pursuit of Mendelian phenomena in the post-rediscovery enthusiasm at the beginning of the last century, examples of the interdependence of genetic and environmental influences surfaced. One well-known early example is that of Krafka [1920], who showed that the effect of the bar-eyed genotype (now known to be a duplication) on eye facet number of
Drosophila
is strikingly dependent on the temperature at which the flies are maintained.” (McClearn, “Nature and nurture,” p. 124.)

    
heights of Japanese children
:
Greulich, “A comparison of the physical growth and development of American-born and native Japanese children,” p. 304.

    
Greulich didn’t realize this at the time, but it was a perfect illustration of how genes really work
:
not dictating any predetermined forms or figures, but interacting vigorously with the outside world to produce an improvised, unique result.

   Two excellent summaries from two of the top figures in the field of gene-environment interaction:

A key feature of gene expression is that it can be altered in a reversible way by extra-cellular signals and by environmental influences. Although DNA starts off the causal chain, what really matters is the expression of the genes (in terms of messenger RNA). There are no genetic effects without this expression. (Rutter, Moffitt, and Caspi, “Gene-environment interplay and psychopathology,” p. 229.)

Individual genes and their environments interact to initiate a complex developmental process that determines adult personality. Most characteristic of this process is its interactivity: Subsequent environments to which the organism is exposed depend on earlier states, and each new environment changes the developmental trajectory, which affects future expression of genes, and so forth. Everything is interactive, in the sense that no arrows proceed uninterrupted from cause to effect; any individual gene or environmental event produces an effect only by interacting with other genes and environments. (Turkheimer, “Three laws of behavior genetics and what they mean,” p. 161.)

    
in truth human height has fluctuated dramatically over time
.

This from height anthropologist Richard Steckel: “We have 1200 years of adult male height trends in Northern Europe that show that height was greatest in the early middle ages, when there was a warmer climate, and reached a minimum in the Little Ice Age of the 17th and 18th centuries.” (Steckel, “Height, Health, and Living Standards Conference Summary,” p. 13.)

Also: American and British teenagers were six inches taller, on average, than their predecessors a century earlier. (Ceci, Rosenblum, DeBruyn, and Lee, “A Bio-Ecological Model of Intellectual Development.”)

    
The
New Yorker
’s Burkhard Bilger
:
Bilger, “The Height Gap.”

A few more excerpts from Bilger’s piece:

Though climate still shapes musk oxen and giraffes—and a willowy Inuit is hard to find—its effect on industrialized people has almost disappeared.
Swedes ought to be short and stocky, yet they’ve had good clothing and shelter for so long that they’re some of the tallest people in the world. Mexicans ought to be tall and slender. Yet they’re so often stunted by poor diet and diseases that we assume they were born to be small.

  Biologists say that we achieve our stature in three spurts: the first in infancy, the second between the ages of six and eight, the last in adolescence. Any decent diet can send us sprouting at these ages, but take away any one of forty-five or fifty essential nutrients and the body stops growing. (“Iodine deficiency alone can knock off ten centimetres and fifteen I.Q. points,” one nutritionist told me.)

  Steckel, after his work on slaves, went on to Union soldiers and Native Americans. (The men of the northern Cheyenne, he found, were the tallest people in the world in the late nineteenth century: well nourished on bison and berries, and wandering clear of disease on the high plains, they averaged nearly five feet ten.) Then he enlisted anthropologists to gather bone measurements dating back ten thousand years. In both Europe and the Americas, he discovered, humans grew shorter as their cities grew larger. The more people clustered together, the more pest-ridden and poorly fed they became. Heights also fell in synch with global temperatures, which reached a nadir during the Little Ice Age of the seventeenth century.

  Around the time of the Civil War, Americans’ heights predictably decreased: Union soldiers dropped from sixty-eight to sixty-seven inches in the mid-eighteen-hundreds, and similar patterns held for West Point cadets, Amherst students, and free blacks in Maryland and Virginia. By the end of the nineteenth century, however, the country seemed set to regain its eminence. The economy was expanding at a dramatic rate, and public-hygiene campaigns were sweeping the cities clean at last: for the first time in American history, urbanites began to outgrow farmers.

In personal correspondence, Patrick Bateson warns: “[Don’t] overstate your case. Differences in genes can be correlated with a difference in behaviour or morphology. Not everyone will reach the same height if they are all given a superb diet. Pygmies, for example, produce less growth hormone or, in the case of other populations (the phenotype seems to have evolved at least five times in different parts of the world), are less receptive to growth hormone.”

    
“Maze-dull” rats, which had consistently tested poorly in those same mazes, making an average of 40 percent more mistakes
.

   This second group consistently stumbled through the same maze over and over again without remembering or learning, making an average of 40 percent more mistakes than the smarter group. They seemed obviously dumber than the Maze-bright strain, possessing an apparently inferior set of intelligence genes.

    
“a classic example of gene-environment interaction
”:
McClearn, “Genetics, Behavior and Aging,” p. 11.

    
temperature surrounding turtle and crocodile eggs determined their gender
:
Bateson, “Behavioral Development and Darwinian Evolution,” p. 52.

    
In 1972, Harvard biologist Richard Lewontin supplied a critical clarification that helped his colleagues understand GxE
.

Paolo Vineis, chair of Environmental Epidemiology, Imperial College, London, explains:

This issue was clarified in an important paper by Richard Lewontin many years ago, but it is still a matter of confusion. The main idea of Lewontin’s paper is that when we evaluate gene-environment interactions we use the “analysis of variance” paradigm, that is, we try to combine the two main effects (genes versus environment), plus their interactive term, in a linear model. Causal models presuppose a linear combination of factors as the base line, variances are then computed and the role of the two main effects (or their interaction) is apportioned accordingly. But, Lewontin argues, the analysis-of-variance approach is misleading. There is no theoretical justification for the presumption of a linear explanation (this is done for the sake of simplicity but does not correspond to any reasonable biological reason). By contrast, all the experiments done with, for example,
Arabidopsis
(a plant) or
Drosophila
(based for example on radiation-induced mutations) show that mutations cause a change in what is called the “norm of reaction,” that is, the ability of the organism to react to different environmental conditions. The way in which the mutant strain will react, say, to different temperatures, is not predictable if the environmental conditions are not specified. Usually what happens is “canalization,” that is, under “normal” conditions there is a certain norm of reaction that is the same for the wild type and the mutants, whereas in changing environments the wild type and
the mutant differ in the norm of reaction.
What this suggests is that in at least some cases a nonlinear explanation is going to be required. In practical terms, it means that all attempts to explain disease on the basis of either the environment or genes (or their interaction) are in fact doomed to fail, because two organisms with different gene variants will have exactly the same response in a normal environment, and a totally different response in an abnormal environment
. (Italics mine.) (Vineis, “Misuse of genetic data in environmental epidemiology,” pp. 164–65. The paper Vineis is referring to is Lewontin, “The analysis of variance and the analysis of causes.”)

    
“the way genes and environments interact dialectically to generate an organism’s appearance and behaviour
”:
Pigliucci, “Beyond nature and nurture,” pp. 20–22.

    
“the individual animal starts its life with the capacity to develop in a number of distinctly different ways
”:
Bateson and Martin,
Design for a Life
, pp. 102–3.

“Everything we have learned about molecular biology has shown that gene activity is regulated by the intracellular environment,” explains McGill’s Michael Meaney. He continues:

The intracellular environment is a function of the genetic make-up of the cell and the extracellular environment (e.g. hormones released by endocrine organs, cytokines from the immune system, neurotransmitters from neurons, nutrients derived from food) [which is] also influenced by the environment of the individual. Neurotransmitter and hormonal activity is profoundly influenced, for example, by social interactions, which lead to effects on gene activity. (Meaney, “Nature, nurture, and the disunity of knowledge,” p. 52.)

    
Your life is interacting with your genes
.

   If genes are merely the bricklayers, where’s the foreman? Where’s the architect?