Incognito (32 page)

And don’t forget that the long list of influences on your mental life stretches far beyond chemicals—it includes the details of circuitry, as well. Consider
epilepsy. If an epileptic seizure is focused in a particular sweet spot in the temporal lobe, a person won’t have motor seizures, but instead something more subtle. The effect is something like a cognitive seizure, marked by changes of personality, hyperreligiosity (an obsession with religion and a feeling of religious certainty), hypergraphia (extensive writing on a subject, usually about religion), the false sense of an external presence, and, often, the hearing of voices that are attributed to a god.
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Some fraction of history’s prophets, martyrs, and leaders appear to have had temporal lobe epilepsy.
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Consider
Joan of Arc, the sixteen-year-old-girl who managed to turn the tide of the Hundred Years War because she believed (and convinced the French soldiers) that she was hearing voices from Saint Michael the archangel, Saint Catherine of Alexandria, Saint Margaret, and Saint Gabriel. As she described her experience, “When I was thirteen, I had a voice from God to help me to govern myself. The first time, I was terrified. The voice came to me about noon: it was summer, and I was in my father’s garden.” Later she reported, “Since God had commanded me to go, I must do it. And since God had commanded it, had I had a hundred fathers and a hundred mothers, and had I been a king’s daughter, I would have gone.” Although it’s impossible to retrospectively diagnose with certainty, her typical reports, increasing religiosity, and ongoing voices are certainly consistent with temporal lobe epilepsy. When brain activity is kindled in the right spot, people hear voices. If a physician prescribes an
anti-epileptic medication, the seizures go away and the voices disappear. Our reality depends on what our biology is up to.

Influences on your cognitive life also include tiny nonhuman creatures: microorganisms such as
viruses and
bacteria hold sway over behavior in extremely specific ways, waging invisible battles inside us. Here’s my favorite example of a microscopically small organism taking over the behavior of a giant machine: the rabies virus. After a bite from one mammal to another, this tiny bullet-shaped virus climbs its way up the nerves and into the temporal lobe of the brain. There it ingratiates itself into the local neurons, and by changing the local patterns of activity it induces the infected host to aggression, rage, and a propensity to bite. The virus also moves into the salivary glands, and in this way it is passed on through the bite to the next host. By steering the behavior of the animal, the virus ensures its spread to other hosts. Just think about that: the virus, a measly seventy-five billionths of a meter in diameter, survives by commandeering the massive body of an animal twenty-five million times larger than it. It would be like you finding a creature 28,000 miles tall and doing something very clever to bend its will to yours.
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The critical take-home lesson is that invisibly small changes inside the brain can cause massive changes to behavior. Our choices are inseparably married to the tiniest details of our machinery.
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As a final example of our dependence on our biology, note that tiny mutations in single genes also determine and change behavior. Consider
Huntington’s disease, in which creeping damage in the frontal cortex leads to changes in personality, such as aggressiveness, hypersexuality, impulsive behavior, and disregard for social norms—all happening years before the more recognizable symptom of spastic limb movement appears.
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The point to appreciate is that Huntington’s is caused by a mutation in a single gene. As
Robert Sapolsky summarizes it, “Alter one gene among tens of thousands and, approximately halfway through one’s life, there occurs a dramatic transformation of personality.”
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In the face of such examples, can we conclude anything other than a dependence
of our essence on the details of our biology? Could you tell a person with Huntington’s to use his “free will” to quit acting so strangely?

So we see that the invisibly small molecules we call narcotics, neurotransmitters,
hormones,
viruses, and genes can place their little hands on the steering wheel of our behavior. As soon as your drink is spiked, your sandwich is sneezed upon, or your genome picks up a mutation, your ship moves in a different direction. Try as you might to make it otherwise, the changes in your machinery lead to changes in you. Given these facts on the ground, it is far from clear that we hold the option of “choosing” who we would like to be. As the neuroethicist
Martha Farah puts it, if an antidepressant pill “can help us take everyday problems in stride, and if a stimulant can help us meet our deadlines and keep our commitments at work, then must not unflabbable temperaments and conscientious characters also be features of people’s bodies? And if so, is there anything about people that is
not
a feature of their bodies?”
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Who you turn out to be depends on such a vast network of factors that it will presumably remain impossible to make a one-to-one mapping between molecules and behavior (more on that in the moment). Nonetheless, despite the complexity, your world is directly tied to your biology. If there’s something like a soul, it is at minimum tangled irreversibly with the microscopic details. Whatever else may be going on with our mysterious existence, our connection to our biology is beyond doubt. From this point of view, you can see why biological reductionism has a strong foothold in modern brain science. But reductionism isn’t the whole story.

Most people have heard of the
Human Genome Project, in which our species successfully decoded the billions-of-letters-long sequence
in our own genetic codebook. The project was a landmark achievement, hailed with the proper fanfare.

Not everyone has heard that the project has been, in some sense, a failure. Once we sequenced the whole code, we didn’t find the hoped-for breakthrough answers about the genes that are unique to humankind; instead we discovered a massive recipe book for building the nuts and bolts of biological organisms. We found that other animals have essentially the same genome we do; this is because they are made of the same nuts and bolts, only in different configurations. The human genome is not terribly different from the frog genome, even though humans are terribly different from frogs. At least, humans and frogs
seem
quite different at first. But keep in mind that both require the recipes to build eyes, spleens, skin, bones, hearts, and so on. As a result, the two genomes are not so dissimilar. Imagine going to different factories and examining the pitches and lengths of the screws used. This would tell you little about the function of the final product—say, a toaster versus a blow dryer. Both have similar elements configured into different functions.

The fact that we didn’t learn what we thought we might is not a criticism of the Human Genome Project; it had to be done as a first step. But it
is
to acknowledge that successive levels of reduction are doomed to tell us very little about the questions important to humans.

Let’s return to the Huntington’s example, in which a single gene determines whether or not you’ll develop the disease. That sounds like a success story for reductionism. But note that Huntington’s is one of the very few examples that can be dredged up for this sort of effect. The reduction of a disease to a
single
mutation is extraordinarily rare: most diseases are polygenetic, meaning that they result from subtle contributions from tens or even hundreds of different genes. And as science develops better techniques, we are discovering that not just the coding regions of genes matter, but also the areas in between—what used to be thought of as “junk”
DNA. Most diseases seem to result from a perfect storm
of numerous minor changes that combine in dreadfully complex ways.

But the situation is far worse than just a multiple-genes problem: the contributions from the genome can really be understood only in the context of interaction with the environment. Consider
schizophrenia, a disease for which teams of researchers have been gene hunting for decades now. Have they found any genes that correlate with the disease? Sure they have. Hundreds, in fact. Does the possession of any one of these genes offer much in the way of prediction about who will develop schizophrenia as a young adult? Very little. No single gene mutation is as predictive of schizophrenia as the color of your passport.

What does your passport have to do with schizophrenia? It turns out that the social stress of being an immigrant to a new country is one of the critical factors in developing schizophrenia.
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In studies across countries,
immigrant groups who differ the most in culture and appearance from the host population carry the highest risk. In other words, a lower level of social acceptance into the majority correlates with a higher chance of a schizophrenic break. In ways not currently understood, it appears that repeated social rejection perturbs the normal functioning of the
dopamine systems. But even these generalizations don’t tell the whole story, because within a single immigrant group (say, Koreans in America), those who feel worse about their ethnic differences from the majority are more likely to become psychotic. Those who are proud and comfortable with their heritage are mentally safer.

This news comes as a surprise to many. Is schizophrenia genetic or isn’t it? The answer is that genetics play a
role
. If the genetics produce nuts and bolts that have a slightly strange shape, the whole system may run in an unusual manner when put in particular environments. In other environments, the shape of the nuts and bolts may not matter. When all is said and done, how a person turns out depends on much more than the molecular suggestions written down in the
DNA.

Remember what we said earlier about having an 828 percent
higher chance of committing a violent crime if you carry the
Y chromosome? The statement is factual, but the important question to ask is this: why aren’t
all
males criminals? That is, only 1 percent of males are incarcerated.
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What’s going on?

The answer is that knowledge of the genes alone is not sufficient to tell you much about behavior. Consider the work of
Stephen Suomi, a researcher who raises monkeys in natural environments in rural Maryland. In this setting, he is able to observe the monkeys’ social behavior from their day of birth.
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One of the first things he noticed was that monkeys begin to express different personalities from a surprisingly early age. He saw that virtually every social behavior was developed, practiced, and perfected during the course of peer play by four to six months of age. This observation would have been interesting by itself, but Suomi was able to combine the behavioral observations with regular blood testing of hormones and metabolites, as well as genetic analysis.

What he found among the baby monkeys was that 20 percent of them displayed social anxiety. They reacted to novel, mildly stressful social situations with unusually fearful and anxious behavior, and this correlated with long-lasting elevations of stress hormones in their blood.

On the other end of the social spectrum, 5 percent of the baby monkeys were overly aggressive. They showed impulsive and inappropriately belligerent behavior. These monkeys had low levels of a blood metabolite related to the breakdown on the neurotransmitter
serotonin.

Upon investigation, Suomi and his team found that there were two different “flavors” of genes (called alleles by geneticists) that one could possess for a protein involved in transporting serotonin
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—let’s call these the short and long forms. The monkeys with the short form showed poor control of violence, while those with the long form displayed normal behavioral control.

But that turned out to be only part of the story. How a monkey’s personality developed depended on its environment as well. There were two ways the monkeys could be reared: with their mothers
(good environment) or with their peers (insecure attachment relationships). The monkeys with the short form ended up as the aggressive type when they were raised with their peers, but did much better when they were raised with their mothers. For those with the long form of the gene, the rearing environment did not seem to matter much; they were well adjusted in either case.

There are at least two ways to interpret these results. The first is that the long allele is a “good gene” that confers resilience against a bad childhood environment (lower left corner of the table below). The second is that a good mothering relationship somehow gives resiliency for those monkeys who would otherwise turn out to be bad seeds (upper right corner). These two interpretations are not exclusive, and they both boil down to the same important lesson: a combination of genetics and environment matters for the final outcome.