The Tell-Tale Brain: A Neuroscientist's Quest for What Makes Us Human

The late biologist Peter Medawar provides a compelling analogy to illustrate the fallacy. An inherited disorder called phenylketonuria (PKU) is caused by a rarely occurring abnormal gene that results in a failure to metabolize the amino acid phenylalanine in the body. As the amino acid starts accumulating in the child’s brain, he becomes profoundly retarded. The cure is simple. If you diagnose it early enough, all you do is withhold phenylalanine-containing foods from the diet and the child grows up with an entirely normal IQ.

Now imagine two boundary conditions. Assume there is a planet where the gene is uncommon and phenylalanine is everywhere, like oxygen or water, and is indispensable for life. On this planet, retardation caused by PKU, and therefore variance in IQ in the population, would be entirely attributable to the PKU gene. Here you would be justified in saying that retardation was a genetic disorder or that IQ was inherited. Now consider another planet in which the converse is true: Everyone has the PKU gene but phenylalanine is rare. On this planet you would say that PKU is an environmental disorder caused by a poison called phenylalanine, and most of the variance in IQ is caused by the environment. This example shows that when the interaction between two variables is labyrinthine it is meaningless to ascribe percentage values to the contribution made by either. And if this is true for just one gene interacting with one environmental variable, the argument must hold with even greater force for something as complex and multifactorial as human intelligence, since genes interact not only with the environment but with each other.

Ironically, the IQ evangelists (such as Arthur Jensen, William Shockley, Richard Herrnstein, and Charles Murray) use the heritability of IQ itself (sometimes called “general intelligence” or “little g”) to argue that intelligence is a single measurable trait. This would be roughly analogous to saying that general health is one thing just because life span has a strong heritable component that can be expressed as a single number—age! No medical student who believed in “general health” as a monolithic entity would get very far in medical school or be allowed to become a physician—and rightly so—and yet whole careers in psychology and political movements have been built on the equally absurd belief in single measurable general intelligence. Their contributions have little more than shock value.

Returning to language, it should now be obvious which side of the fence I am on: neither. I straddle it proudly. Hence this chapter is not really about how language evolved—though I have been using that phrasing as shorthand—but how language competence, or the ability to acquire language so quickly, evolved. This competence is controlled by genes that were selected for by the evolutionary process. Our questions in the rest of this chapter are, Why were these genes selected, and how did this highly sophisticated competence evolve? Is it modular? How did it all get started? And how did we make the evolutionary transition from the grunts and howls of our apelike ancestors to the transcendent lyricism of Shakespeare?

RECALL THE SIMPLE bouba-kiki experiment. Could it hold the key to understanding how the first words evolved among a band of ancestral hominins in the African savanna between one and two hundred thousand years ago? Since words for the same object are often utterly different in different languages, one is tempted to think that the words chosen for particular objects are entirely arbitrary. This in fact is the standard view among linguists. Now, maybe one night the first band of ancestral hominins just sat around the tribal fire and said,

“Okay, let’s all call this thing a bird. Now let’s all say it together, biiirrrrddddd. Okay let’s repeat again, birrrrrrrdddddd.”