I get chills whenever I hear Macbeth’s immortal soliloquy from Act 5, Scene 5:
Out, out, brief candle!
Life’s but a walking shadow, a poor player
That struts and frets his hour upon the stage,
And then is heard no more. It is a tale
Told by an idiot, full of sound and fury,
Signifying nothing.
Nothing he says is literal. He is not actually talking about candles or stagecraft or idiots. If taken literally, these lines really would be the ravings of an idiot. And yet these words are one of the most profound and deeply moving remarks about life that anyone has ever made!
Puns, on the other hand, are based on superficial associations. Schizophrenics, who have miswired brains, are terrible at interpreting metaphors and proverbs. Yet according to clinical folklore, they are very good at puns. This seems paradoxical because, after all, both metaphors and puns involve linking seemingly unrelated concepts. So why should schizophrenics be bad at the former but good with the latter? The answer is that even though the two appear similar, puns are actually the opposite of metaphor. A metaphor exploits a surface-level similarity to reveal a deep hidden connection. A pun is a surface-level similarity that masquerades as a deep one—hence its comic appeal. (“What fun do monks have on Christmas?” Answer: “Nun.”) Perhaps a preoccupation with “easy” surface similarities erases or deflects attention from deeper connections. When I asked a schizophrenic what an elephant had in common with a man, he answered “They both carry a trunk” alluding maybe to the man’s penis (or maybe to an actual trunk used for storage).
Leaving puns aside, if my ideas about the link between synesthesia and metaphor are correct, then why isn’t every synesthete highly gifted or every great artist or poet a synesthete? The reason may be that synesthesia might merely predispose you to be creative, but this does not mean other factors (both genetic and environmental) aren’t involved in the full flowering of creativity. Even so, I would suggest that similar—though not identical—brain mechanisms might be involved in both phenomena, and so understanding one might help us understand the other.
An analogy might be helpful. A rare blood disorder called sickle cell anemia is caused by a defective recessive gene that causes red blood cells to assume an abnormal “sickle” shape, making them unable to transport oxygen. This can be fatal. If you happen to inherit two copies of this gene (in the unlikely event that both your parents had either the trait or the disease itself), then you develop the full-blown disease. However, if you inherit just one copy of this gene, you do not come down with the disease, though you can still pass it on to your children. Now it turns out that, although sickle-cell anemia is extremely rare in most parts of the world, where natural selection has effectively weeded it out, its incidence is ten times higher in certain parts of Africa. Why should this be? The surprising answer is that the sickle-cell trait actually seems to protect the affected individual from malaria, a disease caused by a mosquito-borne parasite that infects and destroys blood cells. This protection conferred on the population as a whole from malaria outweighs the reproductive disadvantage caused by the occasional rare appearance of an individual with double copies of the sickle-cell gene. Thus the apparently maladaptive gene has actually been selected for by evolution, but only in geographic locations where malaria is endemic.
A similar argument has been proposed for the relatively high incidence of schizophrenia and bipolar disorder in humans. The reason these disorders have not been weeded out may be because having some of the genes that lead to the full-blown disorder are advantageous—perhaps boosting creativity, intelligence, or subtle social-emotional faculties. Thus humanity as a whole benefits from keeping these genes in its gene pool, but the unfortunate side effect is a sizable minority who get bad combinations of them.
Carrying this logic forward, the same could well be true for synesthesia. We have seen how, by dint of anatomy, genes that lead to enhanced cross-activation between brain areas could have been highly advantageous by making us creative as a species. Certain uncommon variants or combinations of these genes might have the benign side effect of producing synesthesia. I hasten to emphasize the part about benign: Synesthesia is not deleterious like sickle-cell disease and mental illness, and in fact most synesthetes seem to really enjoy their abilities and would not opt to have them “cured” even if they could. This is only to say that the general mechanism might be the same. This idea is important because it makes clear that synesthesia and metaphor are not synonymous, and yet they share a deep connection that might give us deep insights into our marvelous uniqueness.6
Thus synesthesia is best thought of as an example of subpathological cross-modal interactions that could be a signature or marker for creativity. (A modality is a sensory faculty, such as smell, touch, or hearing. “Cross-modal” refers to sharing information between senses, as when your vision and hearing together tell you that you’re watching a badly dubbed foreign film.) But as often happens in science, it got me thinking about the fact that even in those of us who are nonsynesthetes a great deal of what goes on in our mind depends on entirely normal cross-modal interactions that are not arbitrary. So there is a sense in which at some level we are all “synesthetes.” For example, look at the two shapes in Figure 3.7. The one on the left looks like a paint splat. The one on the right resembles a jagged piece of shattered glass. Now let me ask you, if you had to guess, which of these is a “bouba” and which is a “kiki”? There is no right answer, but odds are you picked the splat as “bouba” and the glass as “kiki.” I tried this in a large classroom recently, and 98 percent of the students made this choice. Now you might think this has something to do with the blob resembling the physical form of the letter B (for “bouba”) and the jagged thing resembling a K (as in “kiki”). But if you try the experiment on non-English-speaking people in India or China, where the writing systems are completely different, you find exactly the same thing.
Why does this happen? The reason is that the gentle curves and undulations of contour on the amoeba-like figure metaphorically (one might say) mimic the gentle undulations of the sound bouba, as represented in the hearing centers in the brain and in the smooth rounding and relaxing of the lips for producing the curved booo-baaa sound. On the other hand, the sharp wave forms of the sound kee-kee and the sharp inflection of the tongue on the palate mimic the sudden changes in the jagged visual shape. We will return to this demonstration in Chapter 6 and see how it might hold the key to understanding many of the most mysterious aspects of our minds, such as the evolution of metaphor, language, and abstract thought.7
FIGURE 3.7 Which of these shapes is “bouba” and which is “kiki”? Such stimuli were originally used by Heinz Werner to explore interactions between hearing and vision.
I HAVE ARGUED so far that synesthesia, and in particular the existence of “higher” forms of synesthesia (involving abstract concepts rather than concrete sensory qualities) can provide clues to understanding some of the high-level thought processes that humans alone are capable of.8 Can we apply these ideas to what is arguably the loftiest of our mental traits, mathematics? Mathematicians often speak of seeing numbers laid out in space, roaming this abstract realm to discover hidden relationships that others might have missed, such as Fermat’s Last Theorem or Goldbach’s conjecture. Numbers and space? Are they being metaphorical?