Steven Pinker gets his genome tested …


… and discovers he has the Bald Gene.

In a long article in the New York Times Magazine, “My Genome, My Self,” the author of The Blank Slate recounts all that he has learned about himself from having his genome sampled, which turns out to be unsurprisingly modest.

 

The most prominent finding of behavioral genetics has been summarized by the psychologist Eric Turkheimer: “The nature-nurture debate is over. . . . All human behavioral traits are heritable.” By this he meant that a substantial fraction of the variation among individuals within a culture can be linked to variation in their genes. Whether you measure intelligence or personality, religiosity or political orientation, television watching or cigarette smoking, the outcome is the same. Identical twins (who share all their genes) are more similar than fraternal twins (who share half their genes that vary among people). Biological siblings (who share half those genes too) are more similar than adopted siblings (who share no more genes than do strangers). And identical twins separated at birth and raised in different adoptive homes (who share their genes but not their environments) are uncannily similar.

Behavioral geneticists like Turkheimer are quick to add that many of the differences among people cannot be attributed to their genes.

Identical twins raised apart tend to be almost as similar as identical twins raised together, although part of the reason is that identical twins raised alone don`t feel the need to distinguish themselves from their twin by developing something unique about themselves. Horace Grant, the skinny power forward on Michael Jordan`s first three championship teams, would probably have become a quick forward if he hadn`t grown up playing on youth teams alongside his identical twin Harvey Grant, who became an NBA All-Star shooting forward, while Horace was given the role of rebounding forward.

I know two pairs of adult identical twins, the Brimelows and the Woodhills, and the personal affects vary mildly among the Brimelows and moderately among the Woodhills.

But not all variation in nature arises from balancing selection. The other reason that genetic variation can persist is that rust never sleeps: new mutations creep into the genome faster than natural selection can weed them out. At any given moment, the population is laden with a portfolio of recent mutations, each of whose days are numbered. This Sisyphean struggle between selection and mutation is common with traits that depend on many genes, because there are so many things that can go wrong.

Penke, Denissen and Miller argue that a mutation-selection standoff is the explanation for why we differ in intelligence. Unlike personality, where it takes all kinds to make a world, with intelligence, smarter is simply better, so balancing selection is unlikely.

Is smarter simply better? If it takes, say, bigger brains, the answer isn`t terribly clear. Analogously, Intel assumed that faster clockspeed computer CPU chips were simply better for about 15 years. But the struggle to break the 4.0 gigahertz barrier proved overwhelming and so Intel has given up and gone in different directions in recent years, when most chips sold seem to be between 2.0 and 3.0 gigahertz, although performance keeps improving.

Keep in mind that Intel has big advantages over natural selection in getting from one performance peak to another. For example, if Intel decides that its strategy of single chips with ever faster clockspeeds is heading toward a deadend, it can simultaneously start working on an R&D project for double core and quad-core chips with moderate clockspeeds. At first, the new type of CPUs won`t be as good as the old type, but it doesn`t have to sell the beta versions of the changed design. It can keep making them and throwing them away until the new style chips are as good as the competition`s old style chips.

In contrast, natural selection doesn`t provide you much of a laboratory in which to putter around while you`re working the kinks out of your next model while your factory keeps churning out the satisfactory current model.

Similarly, bigger brains require more food. They make you more likely to tip over and hurt yourself. They require your mother to have a wider pelvis so she won`t die in childbirth, which makes her a slower runner.

 

But intelligence depends on a large network of brain areas, and it thrives in a body that is properly nourished and free of diseases and defects. Many genes are engaged in keeping this system going, and so there are many genes that, when mutated, can make us a little bit stupider.

At the same time there aren’t many mutations that can make us a whole lot smarter. Mutations in general are far more likely to be harmful than helpful, and the large, helpful ones were low-hanging fruit that were picked long ago in our evolutionary history and entrenched in the species. One reason for this can be explained with an analogy inspired by the mathematician Ronald Fisher. A large twist of a focusing knob has some chance of bringing a microscope into better focus when it is far from the best setting. But as the barrel gets closer to the target, smaller and smaller tweaks are needed to bring any further improvement.

The Penke/Denissen/Miller theory, which attributes variation in personality and intelligence to different evolutionary processes, is consistent with what we have learned so far about the genes for those two kinds of traits. The search for I.Q. genes calls to mind the cartoon in which a scientist with a smoldering test tube asks a colleague, “What’s the opposite of Eureka?” Though we know that genes for intelligence must exist, each is likely to be small in effect, found in only a few people, or both. In a recent study of 6,000 children, the gene with the biggest effect accounted for less than one-quarter of an I.Q. point. The quest for genes that underlie major disorders of cognition, likeautism and schizophrenia, has been almost as frustrating. Both conditions are highly heritable, yet no one has identified genes that cause either condition across a wide range of people. Perhaps this is what we should expect for a high-maintenance trait like human cognition, which is vulnerable to many mutations.

The hunt for personality genes, though not yet Nobel-worthy, has had better fortunes. Several associations have been found between personality traits and genes that govern the breakdown, recycling or detection of neurotransmitters (the molecules that seep from neuron to neuron) in the brain systems underlying mood and motivation….

But it seems even less plausible to say that more or less of any major psychological trait is “simply better.” We may have our subjective preferences, but the major personality traits are likely to be ones on which normal variation doesn`t much change average Darwinian fitness over the generations.

 

Even if personal genomics someday delivers a detailed printout of psychological traits, it will probably not change everything, or even most things. It will give us deeper insight about the biological causes of individuality, and it may narrow the guesswork in assessing individual cases. But the issues about self and society that it brings into focus have always been with us. We have always known that people are liable, to varying degrees, to antisocial temptations and weakness of the will. We have always known that people should be encouraged to develop the parts of themselves that they can (“a man’s reach should exceed his grasp”) but that it’s foolish to expect that anyone can accomplish anything (“a man has got to know his limitations”). And we know that holding people responsible for their behavior will make it more likely that they behave responsibly. “My genes made me do it” is no better an excuse than “We’re depraved on account of we’re deprived.”

Many of the dystopian fears raised by personal genomics are simply out of touch with the complex and probabilistic nature of genes. Forget about the hyperparents who want to implant math genes in their unborn children, the “Gattaca” corporations that scan people’s DNA to assign them to castes, the employers or suitors who hack into your genome to find out what kind of worker or spouse you’d make. Let them try; they’d be wasting their time.

The real-life examples are almost as futile. When the connection between the ACTN3 gene and muscle type was discovered, parents and coaches started swabbing the cheeks of children so they could steer the ones with the fast-twitch variant into sprinting and football. Carl Foster, one of the scientists who uncovered the association, had a better idea: “Just line them up with their classmates for a race and see which ones are the fastest.” Good advice. The test for a gene can identify one of the contributors to a trait. A measurement of the trait itself will identify all of them: the other genes (many or few, discovered or undiscovered, understood or not understood), the way they interact, the effects of the environment and the child’s unique history of developmental quirks.

Well said.

On the other hand, as futile as individual genomics is likely to prove to be relative to current expectations., the Law of Large Numbers suggests that racial genomics is likely to prove more fertile.