Steven Pinker has a very lucid and engaging summary of personal genomics in the latest Times Magazine. Pinker got his exons sequenced and is optimistic that large-scale genetic testing will soon reveal the snippets of DNA underlying our preferences, predilections and peccadillos:
Dopamine is the molecular currency in several brain circuits associated with wanting, getting satisfaction and paying attention. The gene for one kind of dopamine receptor, DRD4, comes in several versions. Some of the variants (like the one I have) have been associated with “approach related” personality traits like novelty seeking, sensation seeking and extraversion.
A gene for another kind of receptor, DRD2, comes in a version that makes its dopamine system function less effectively. It has been associated with impulsivity, obesity and substance abuse. Still another gene, COMT, produces an enzyme that breaks down dopamine in the prefrontal cortex, the home of higher cognitive functions like reasoning and planning. If your version of the gene produces less COMT, you may have better concentration but might also be more neurotic and jittery.
I have no doubt that science will continue to find interesting correlations between dopaminergic receptors and risk tolerance, or kinase enzymes in the hippocampus and long-term memory. But I’m a little less optimistic that the age of genomics is going to suddenly unravel the knot of human nature.
Why? Because the brain is really, really complicated. After all, let’s not forget that we’ve barely been able to dent the genetics of autism spectrum disorder, which is extremely heritable (somewhere in the neighborhood of 80 percent). We have no idea what genes (and there are probably dozens and dozens of them) trigger schizophrenia, or psychopathy, or make someone more vulnerable to manic depression. Compared to the ephemeral elements of personality, which are constantly shifting based on mood and context, these mental illnesses should be rather easy to decipher. And yet they’ve proven to be all but impossible.
The reason, I think, gets back to something I wrote in my first book:
What makes us human, and what makes each of us our own human, is not simply the genes we have buried in our base pairs, but how our cells, in dialogue with our environment, feedback onto our DNA, changing the way we read ourselves. Life is a dialectic. For example, the code sequence GTAAGT can either be translated as instructions for the amino acids valine and serine; or it can be read as a “spacer”, a genetic pause that keeps other protein parts an appropriate distance from each other; or it can be read as a signal to cut the transcript. Our DNA is defined by its multiplicity of possible meanings; it is a code that requires context.
The best metaphor for our DNA is literature. Like all classic literary texts, our genome is defined not by the certainty of its meaning, but by its linguistic instability, its ability to encourage a multiplicity of interpretations. What makes a novel or poem immortal is, paradoxically, its complexity, the way every reader discovers in the same words a different story. For example, many readers find the ending of Middlemarch, in which Dorothea elopes with Will, to be a traditional happy ending, in which marriage triumphs over evil. On the other hand, some readers–like Virginia Woolf–see Dorothea’s inability to live alone as a turn of plot “more melancholy than tragedy.” The same book manages to inspire two completely different conclusions. But there is no right interpretation. Everyone is free to find their own meaning in the novel. Our genome works the same way. Life imitates art.