Behave: The Biology of Humans at Our Best and Worst

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Behave: The Biology of Humans at Our Best and Worst Page 61

by Robert M. Sapolsky


  Brave and correct. And then Cantor does a stunning mitigated-free-will long jump. Does any of that biology lessen the condemnation and punishment that Sandusky deserved? No. “One cannot choose to not be a pedophile, but one can choose to not be a child molester.”

  This establishes a dichotomy of what things are supposedly made of:

  Biological stuff

  Homuncular grit

  Destructive sexual urges

  Resisting acting upon them

  Delusionally hearing voices

  Resisting their destructive commands

  Proclivity toward alcoholism

  Not drinking

  Having epileptic seizures

  Not driving if you didn’t take your meds

  Not all that bright

  Getting going when the going gets tough

  Not the loveliest of faces

  Resisting getting that huge, hideous nose ring

  Here are just a few of the things we’ve seen in this book that can influence the column on the right: blood glucose levels; the socioeconomic status of your family of birth; a concussive head injury; sleep quality and quantity; prenatal environment; stress and glucocorticoid levels; whether you’re in pain; if you have Parkinson’s disease and which medication you’ve been prescribed; perinatal hypoxia; your dopamine D4 receptor gene variant; if you have had a stroke in your frontal cortex; if you suffered childhood abuse; how much of a cognitive load you’ve borne in the last few minutes; your MAO-A gene variant; if you’re infected with a particular parasite; if you have the gene for Huntington’s disease; lead levels in your tap water when you were a kid; if you live in an individualist or a collectivist culture; if you’re a heterosexual male and there’s an attractive woman around; if you’ve been smelling the sweat of someone who is frightened. On and on. Of all the stances of mitigated free will, the one that assigns aptitude to biology and effort to free will, or impulse to biology and resisting it to free will, is the most permeating and destructive. “You must have worked so hard” is as much a property of the physical universe and the biology that emerged from it as is “You must be so smart.” And yes, being a child molester is as much a product of biology as is being a pedophile. To think otherwise is little more than folk psychology.

  BUT DOES ANYTHING USEFUL ACTUALLY COME OF THIS?

  As I noted, the most formidable skeptic of the relevance of neuroscience to the legal system is Stephen Morse, who has written extensively and effectively about the subject.22 He is the definitive advocate of free will being compatible with a deterministic world. He’s fine with M’Naghten and recognizes that there can be sufficient brain damage to compromise the notion of responsibility—“Various causes can produce genuine excusing conditions, such as lack of rational or control capacity.” But beyond those rare instances, he believes, neuroscience offers little that should challenge the notion of responsibility. As he has quipped, “Brains don’t kill people. People kill people.”

  Morse epitomizes the skepticism about bringing neuroscience into the courtroom. For one thing, he viscerally cringes at how much of a fad “neurolaw” and “neurocriminology” have become. A wonderfully sardonic writer,* he has announced the discovery of the disorder “brain overclaim syndrome,” whose sufferers have gotten carried away with the importance of neuroscience because they’ve been “infected and inflamed by stunning advances in our understanding of the brain,” causing them to “make moral and legal claims that the new neuroscience does not entail and cannot sustain.”

  One absolutely valid criticism of his is a narrow, practical one. This is the worry, aired earlier, that juries will give undue weight to neuroimaging data just because of how impressive the images are. Apropos of that, Morse has called neuroscience “determinism du jour, grabbing the attention previously given to psychological or genetic determinism. . . . The only thing different about neuroscience is that we have prettier pictures and it appears more scientific.”

  Another valid criticism concerns findings in neuroscience usually merely being descriptive (e.g., “Brain region A projects to brain region Q”) or correlative (e.g., “Elevated levels of neurotransmitter X and of behavior Z tend to go together”). Data such as those don’t disprove free will. In the words of philosopher Hilary Bok, “The claim that a person chose her action does not conflict with the claim that some neural processes or states caused it; it simply redescribes it.”23

  This is a point I’ve made throughout the book, namely that description and correlation are nice, but actual causal data are the gold standard (e.g., “When you raise the levels of neurotransmitter X, behavior Z happens more often”). That is the source of some of our most powerful demonstrations of the material bases of our more complex behaviors—for example, transcranial magnetic stimulation techniques that transiently activate or inactivate a part of the cortex can change someone’s moral decision making, decisions about punishment, or levels of generosity and empathy. That’s causality.

  It is when we get to the issue of causality that Morse distinguishes between causation and compulsion. He writes, “Causation is neither an excuse per se nor the equivalent of compulsion, which is an excusing condition.” Morse describes himself as a “thoroughgoing materialist” and states, “We live in a causal universe, which includes human action.” But try as I might, I cannot see any way of making this distinction that does not tacitly require a homunculus that is outside the causal universe, a homunculus that can be overwhelmed by “compulsion” but that can and should handle “causation.” In the words of philosopher Shaun Nichols, “It seems like something has to give, either our commitment to free will or our commitment to the idea that every event is completely caused by the preceding events.”24

  Despite these criticisms of his criticisms, my stance has a major problem, one that causes Morse to conclude that the contributions of neuroscience to the legal system “are modest at best and neuroscience poses no genuine, radical challenges to concepts of personhood, responsibility, and competence.”25 The problem can be summarized in a hypothetical exchange:

  Prosecutor: So, professor, you’ve told us about the extensive damage that the defendant sustained to his frontal cortex when he was a child. Has every person who has sustained such damage become a multiple murderer, like the defendant?

  Neuroscientist testifying for the defense: No.

  Prosecutor: Has every such person at least engaged in some sort of serious criminal behavior?

  Neuroscientist: No.

  Prosecutor: Can brain science explain why the same amount of damage produced murderous behavior in the defendant?

  Neuroscientist: No.

  The problem is that, even amid all these biological insights that allow us to be snitty about those silly homunculi, we still can’t predict much about behavior. Perhaps at the statistical level of groups, but not when it comes to individuals.

  Explaining Lots and Predicting Little

  If a person’s leg is fractured, how predictable is it that they will have trouble walking? I think it would be safe to predict something close to 100 percent. If they have serious inflammatory lung disease, how predictable is it that their breathing will be labored at times and that they will tire easily? Again, around 100 percent. Same for the effects of significant blockage of blood flow to the legs or extensive cirrhosis of the liver.

  Let’s switch to the brain and neurological dysfunction. What if someone has had a brain injury, and the neurons around the resulting scar tissue rewire so that they stimulate both themselves and one another—how predictable is it that the person will have a seizure? How about if they have congenital weaknesses in the walls of the blood vessels throu
ghout the brain—how likely is a cerebral aneurysm at some point? How about if they have a mutation in the gene that causes Huntington’s disease—how likely are they to have a neuromuscular disorder by age sixty? Really high in all cases; probably approaching 100 percent.

  Let’s incorporate behavior. If someone has extensive frontocortical damage, how predictable is it that you’d note something odd about them, behaviorally, after a five-minute conversation? Something like 75 percent.

  Now let’s consider a broader range of behaviors. How predictable is it that this person with the frontal damage will do something horrifically violent at some point? Or that someone who was abused repeatedly as a child will become an abusive adult? That a soldier who went through a battle that killed his buddies will develop PTSD? That a person with the “montane vole” polygamous version of the vasopressin receptor gene promoter will have numerous failed marriages? That a person with a particular array of glutamate receptor subtypes throughout their cortex and hippocampus will have an IQ above 140? That someone raised with extensive childhood adversity and loss will have a major depressive disorder? All under 50 percent, often way under.

  So how do a fractured leg inevitably impairing locomotion and the noninevitabilities of the previous paragraph differ? Do the latter somehow involve “less” biology? Is the point that the brain contains a nonbiological homunculus but that leg bones do not?

  Hopefully, after this many pages, the start of an answer is apparent. It’s not that there’s “less” biology in those circumstances related to social behavior. It’s that it’s qualitatively different biology.

  When a bone shatters, there’s a relatively straight line of steps leading to inflammation and pain that will impair the person’s gait (should he try to walk an hour later). That straight line of biology won’t be altered by conventional variation in his genome, his prenatal hormone exposure, the culture he was raised in, or when he ate lunch. But as we’ve seen, all of those variables can influence social behaviors that shape our best and worst moments.

  The biology of the behaviors that interest us is, in all cases, multifactorial—that is the thesis of this book.

  Let’s see what “multifactorial” means in a practical sense. Consider someone with frequent depression who is visiting a friend today, pouring her heart out about her problems. How much could you have predicted the global depression and today’s behavior by knowing about her biology?

  Suppose “knowing about her biology” consisted only of knowing what version of the serotonin transporter gene she has. How much predictive power does that give you? As we saw in chapter 8, not much—say, 10 percent. What if “knowing about her biology” consists of knowing the status of that gene plus knowing if one of her parents died when she was a child? More, maybe 25 percent. How knowing her serotonin transporter gene status + childhood adversity status + whether she is living alone in poverty? Maybe up to 40 percent. Add knowledge of the average level of glucocorticoids in her bloodstream today. Maybe a bit more. Toss in knowing if she’s living in an individualist or a collectivist culture. Some more predictability.* Know if she is menstruating (which typically exacerbates symptoms in seriously depressed women, making it more likely that they’ll be socially withdrawn rather than reaching out to someone). Some more predictability. Maybe even above the 50 percent mark by now. Add enough factors, many of which, possibly most of which, have not yet been discovered, and eventually your multifactorial biological knowledge will give you the same predictive power as in the fractured-bone scenario. Not different amounts of biological causation; different types of causation.

  The artificial intelligence pioneer Marvin Minsky once defined free will as “internal forces I do not understand.”26 People intuitively believe in free will, not just because we have this terrible human need for agency but also because most people know next to nothing about those internal forces. And even the neuroscientist on the witness stand can’t accurately predict which individual with extensive frontal damage will become the serial murderer, because science as a whole still knows about only a handful of those internal forces. Shattered bone → inflammation → constricted movement is easy. Neurotransmitters + hormones + childhood + ____ + ____ + isn’t.*27

  Another factor comes into play. When I go to the Web of Science, a search engine for scanning databases of papers published in science and medical journals. Under search terms I put in “oxytocin” and “trust”—just to pick an example of the umpteen links between biology and social behavior that we’ve covered. And up comes the news that 193 papers have been published on the subject. Consider the following figure, showing that most of those papers have been published in the last few years.

  Same with the next figure, a search for “oxytocin” and “social behavior” or, after that, “transcranial magnetic stimulation” and “decision-making,” and then “brain” and “aggression.”

  Visit bit.ly/2nyi5Ip for a larger version of these graphs.

  And just to give a sense of some more of these:

  Visit bit.ly/2neYFVP for a larger version of this table.

  Our behaviors are constantly shaped by an array of subterranean forces. What these figures and the table show is that most of these forces involve biology that, not that long ago, we didn’t know existed.

  So what do we do with Minsky’s definition of free will needing to be amended to “internal forces I do not understand yet”?

  HOW THEY WILL VIEW US

  If you still think there is mitigated free will, there are three possible routes to take at this juncture.

  To appreciate the first, let’s briefly consider epilepsy. Scientists understand a lot about the neurological bases of seizures and how they involve firing with abnormally high frequency and synchrony. But not that long ago, say, a century ago, epilepsy was viewed as a type of mental illness. And before that it was thought by many to be a communicable infectious disease. And at other times and places, it was thought to be caused by menstruation, or excessive sex, or excessive masturbation. But in 1487 two German scholars uncovered a cause of epilepsy that really seemed to hit the nail on the head.

  The two Dominican friars, Heinrich Kramer and Jakob Sprenger, published Malleus Maleficarum (Latin for “Hammer of the Witches”), the definitive treatise about why someone becomes a witch, how to identify them, and what to do with them. What was one of the surest ways to identify a witch? If they are seized by Satan, if they convulse from the malign power of the devil within them.

  Their guideline was the Gospel according to Mark, 9:14–29. A man brings his son to Jesus, saying there is something wrong with him and asking Jesus to cure him—a spirit comes and seizes him, making him mute, and then that spirit throws him to the ground, where he foams at the mouth and grinds his teeth and becomes rigid. The man presents his son, who is promptly seized by that spirit and falls to the ground, convulsing and foaming. Jesus perceives that the boy is infested with an unclean spirit and commands that vile spirit to come out and be gone. The seizing ceases.

  Thus seizures were a sign of demonic possession, a certain marker of a witch. Malleus Maleficarum arrived in time to take advantage of mass production through the recently invented printing press. In the words of historian Jeffrey Russell, “The swift propagation of the witch hysteria by the press was the first evidence that Gutenberg had not liberated man from original sin.” The book was widely read and went through more than thirty editions over the subsequent century. Estimates are that from 100,000 to a million people were persecuted, tortured, or killed as witches in the aftermath.*28

  I don’t think much of Kramer and Sprenger. My assumption is that they were sadistic monsters, but that could reflect my being influenced too much by the likes of The Name of the Rose or The Da Vinci Code. Maybe they were opportunists who reasoned that the book would make their careers. Maybe they were utterly sincere.

  Instead I imagine a scenario of an evening
during the late fifteenth century. A church inquisitor comes home from work weary, burdened. His wife coaxes him to talk—“It was a usual day of condemning witches, but this one case bothered me. Everyone testified about this woman who falls and gnashes and convulses—a witch, without a doubt. I don’t feel sorry for her—no one told her to open wide for Satan. But she had these two beautiful kids—you should have seen them, just so confused as to why their mother was being taken away. Distraught husband also. So that part was hard, seeing them suffer. But it is what it is—we burned her, of course.” Burnings and killings and centuries were to pass until we in the West would have learned enough to say, “It’s not her; it’s her disease.”*

  We’re only a first few baby steps into understanding any of this, so few that it leaves huge, unexplained gaps that perfectly smart people fill in with a homunculus. Nevertheless, even the staunchest believers in free will must admit that it is hemmed into tighter spaces than in the past. It’s less than two centuries since science first taught us that the frontal cortex has something to do with appropriate behavior. Less than seventy years since we learned that schizophrenia is a biochemical disorder. Perhaps fifty years since we learned that reading problems of a type that we now call dyslexia aren’t due to laziness but instead involve microscopic cortical malformations. Twenty-five since we learned that epigenetics alters behavior. The influential philosopher Daniel Dennett has written about the free will that is “worth wanting.” If there really is free will, it’s getting consigned to domains too mundane to be worth the effort to want—do I want briefs or boxer shorts today?29

 

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