Determined: A Science of Life without Free Will

by Robert M. Sapolsky

So, it seems that William James was giving a lecture about the nature of life and the universe. Afterward, an old woman came up and said, “Professor James, you have it all wrong.” To which James asked, “How so, madam?” “Things aren’t at all like you said,” she replied. “The world is on the back of a gigantic turtle.” “Hmm.” said James, bemused. “That may be so, but where does that turtle stand?” “On the back of another turtle,” she answered. “But madam,” said James indulgently, “where does that turtle stand?” To which the old woman responded triumphantly: “It’s no use, Professor James. It’s turtles all the way down!”[*]

If you believe that turtles can float in the air, the answer is that it just happened, that there was no cause besides that person having simply decided to create that behavior.

The answer is that the behavior happened because something that preceded it caused it to happen. And why did that prior circumstance occur? Because something that preceded it caused it to happen. It’s antecedent causes all the way down, not a floating turtle or causeless cause to be found.

To reiterate, when you behave in a particular way, which is to say when your brain has generated a particular behavior, it is because of the determinism that came just before, which was caused by the determinism just before that, and before that, all the way down.

And when people claim that there are causeless causes of your behavior that they call “free will,” they have (a) failed to recognize or not learned about the determinism lurking beneath the surface and/or (b) erroneously concluded that the rarefied aspects of the universe that do work indeterministically can explain your character, morals, and behavior.

we are nothing more or less than the cumulative biological and environmental luck, over which we had no control, that has brought us to any moment.

We can all agree on that; however, we’re heading into very different terrain, one that I suspect most readers will not agree with, which is deciding that we have no free will at all. Here would be some of the logical implications of that being the case: That there can be no such thing as blame, and that punishment as retribution is indefensible—sure, keep dangerous people from damaging others, but do so as straightforwardly and nonjudgmentally as keeping a car with faulty brakes off the road.

And that it makes as little sense to hate someone as to hate a tornado because it supposedly decided to level your house, or to love a lilac because it supposedly decided to make a wonderful fragrance.

This book has two goals. The first is to convince you that there is no free will,[*] or at least that there is much less free will than generally assumed when it really matters.

Why? Crucially, if you focus on any single field like these—neuroscience, endocrinology, behavioral economics, genetics, criminology, ecology, child development, or evolutionary biology—you are left with plenty of wiggle room for deciding that biology and free will can coexist.

put all the scientific results together, from all the relevant scientific disciplines, and there’s no room for free will.[*]

obstinate,

vacillating,”

Suppose that a man pulls the trigger of a gun. Mechanistically, the muscles in his index finger contracted because they were stimulated by a neuron having an action potential (i.e., being in a particularly excited state). That neuron in turn had its action potential because it was stimulated by the neuron just upstream. Which had its own action potential because of the next neuron upstream. And so on. Here’s the challenge to a free willer: Find me the neuron that started this process in this man’s brain, the neuron that had an action potential for no reason, where no neuron spoke to it just before. Then show me that this neuron’s actions were not influenced by whether the man was tired, hungry, stressed, or in pain at the time. That nothing about this neuron’s function was altered by the sights, sounds, smells, and so on, experienced by the man in the previous minutes, nor by the levels of any hormones marinating his brain in the previous hours to days, nor whether he had experienced a life-changing event in recent months or years. And show me that this neuron’s supposedly freely willed functioning wasn’t affected by the man’s genes, or by the lifelong changes in regulation of those genes caused by experiences during his childhood. Nor by levels of hormones he was exposed to as a fetus, when that brain was being constructed. Nor by the centuries of history and ecology that shaped the invention of the culture in which he was raised.

Show me a neuron (or brain) whose generation of a behavior is independent of the sum of its biological past, and for the purposes of this book, you’ve demonstrated free will. The point of the first half of this book is to establish that this can’t be shown.

Ask someone to name their favorite detergent, and if you have unconsciously cued them earlier with the word ocean, they become more likely to answer, “Tide.”

And where did that intent come from in the first place? This is so important because, as we will see, while it sure may seem at times that we are free do as we intend, we are never free to intend what we intend.

It began with Benjamin Libet, a neuroscientist at the University of California at San Francisco, in a 1983 study so provocative that at least one philosopher refers to it as “infamous,” there are conferences held about it, and scientists are described as doing “Libet-style studies.”[*],[2] We know the experimental setup. Here’s a button. Push it whenever you want. Don’t think about it beforehand; look at this fancy clock that makes it easy to detect fractions of a second and tell us when you decided to push the button, that moment of conscious awareness when you freely made your decision.[*] Meanwhile, we’ll be collecting EEG data from you and monitoring exactly when your finger starts moving. Out of this came the basic findings: people reported that they decided to push the button about two hundred milliseconds—two tenths of a second—before their finger started moving. There was also a distinctive EEG pattern, called a readiness potential, when people prepared to move; this emanated from a part of the brain called the SMA (supplementary motor area), which sends projections down the spine, stimulating muscle movement. But here’s the crazy thing: the readiness potential, the evidence that the brain had committed to pushing the button, occurred about three hundred milliseconds before people believed they had decided to push the button. That sense of freely choosing is just a post hoc illusion, a false sense of agency.

With fMRI, Haynes was able to spot the which-button decision even farther up in the brain’s chain of command, in the prefrontal cortex (PFC). This made sense, as the PFC is where executive decisions are made.

One neurological disorder reinforces these findings. Stroke damage to part of the SMA produces “anarchic hand syndrome,” where the hand controlled by that side of the SMA[*] acts against the person’s will (e.g., grabbing food from someone else’s plate); sufferers even restrain their anarchic hand with their other one.[*] This suggests that the SMA keeps volition on task, binding “intention to action,” all before the person believes they’ve formed that intention.[9]

Libetian literature, starting with Libet, show?

The Libetian literature is built around people spontaneously deciding to do something.

As it turns out, predictability isn’t all that great. The original Libet study was done in such a way that it wasn’t possible to generate a number for this. However, in the Haynes studies, fMRI images predicted which behavior occurred with only about 60 percent accuracy, almost at the chance level. For Mele, a “60-percent accuracy rate in predicting which button a participant will press next doesn’t seem to be much of a threat to free will.”

The alternative conclusion is that free won’t is just as suspect as free will, and for the same reasons. Inhibiting a behavior doesn’t have fancier neurobiological properties than activating a behavior, and brain circuitry even uses their components interchangeably. For example, sometimes brains do something by activating neuron X, sometimes by inhibiting the neuron that is inhibiting neuron X. Calling the former “free will” and calling the latter “free won’t” are equally untenable.

Having now reviewed these debates, what can we conclude? For Libetians, these studies show that our brains decide to carry out a behavior before we think that we’ve freely and consciously done so. But given the criticisms that have been raised, I think all that can be concluded is that in some fairly artificial circumstances, certain measures of brain function are moderately predictive of a subsequent behavior. Free will, I believe, survives Libetianism. And yet I think that is irrelevant.

hubbub

Then there’s a fun study where subjects were either made uncomfortable (by placing their hand in ice water) or disgusted (by placing their thinly gloved hand in imitation vomit).[*] Subjects then recommended punishment for norm violations that were purity related (e.g., “John rubbed someone’s toothbrush on the floor of a public restroom” or the supremely distinctive “John pushed someone into a dumpster which was swarming with cockroaches”) or violations unrelated to purity (e.g., “John scratched someone’s car with a key”). Being disgusted by fake puke, but not being icily uncomfortable, made subjects more selectively punitive about purity violations.[3] How can a disgusting smell or tactile sensation change unrelated moral assessments? The phenomenon involves a brain region called the insula (aka the insular cortex). In mammals, it is activated by the smell or taste of rancid food, automatically triggering spitting out the food and the species’s version of barfing. Thus, the insula mediates olfactory and gustatory disgust and protects from food poisoning, an evolutionarily useful thing. But the versatile human insula also responds to stimuli we deem morally disgusting. The insula’s “this food’s gone bad” function in mammals is probably a hundred million years old. Then, a few tens of thousands of years ago, humans invented constructs like morality and disgust at moral norm violations. That’s way too little time to have evolved a new brain region to “do” moral disgust.

Naturally, there is the flip side to the sensory disgust phenomenon—sugary (versus salty) snacks make subjects rate themselves as more agreeable and helpful individuals and rate faces and artwork as more attractive.[5] Ask a subject, Hey, in last week’s questionnaire you were fine with behavior A, but now (in this smelly room) you’re not. Why? They won’t explain how a smell confused their insula and made them less of a moral relativist. They’ll claim some recent insight caused them, bogus free will and conscious intent ablaze, to decide that behavior A isn’t okay after all.

Next, want to make someone more likely to choose to clean their hands? Have them describe something crummy and unethical they’ve done.

Particularly interesting findings regarding interoception concern hunger. One much-noted study suggested that hunger makes us less forgiving. Specifically, across more than a thousand judicial decisions, the longer it had been since judges had eaten, the less likely they were to grant a prisoner parole. Other studies also show that hunger changes prosocial behavior.

In other words, as we sit there, deciding which button to push with supposed freely chosen intent, we are being influenced by our sensory environment—a foul smell, a beautiful face, the feel of vomit goulash, a gurgling stomach, a racing heart. Does this disprove free will? Nah—the effects are typically mild and only occur in the average subject, with plenty of individuals who are exceptions. This is just the first step in understanding where intentions come from.[10]

The choice you’d seemingly freely make about the life-or-death button-pressing task can also be powerfully influenced by events in the preceding minutes to days.

scads of

For starters, T rarely generates new patterns of aggression; instead, it makes preexisting patterns more likely to happen. Boost a monkey’s T levels, and he becomes more aggressive to monkeys already lower-ranking than him in the dominance hierarchy, while brown-nosing his social betters as per usual. Testosterone makes the amygdala more reactive, but only if neurons there are already being stimulated by looking at, say, the face of a stranger. Moreover, T lowers the threshold for aggression most dramatically in individuals already prone toward aggression.[11] The hormone also distorts judgment, making you more likely to interpret a neutral facial expression as threatening. Boosting your T levels makes you more likely to be overly confident in an economic game, resulting in being less cooperative—who needs anyone else when you’re convinced you’re fine on your own?[*] Moreover, T tilts you toward more risk-taking and impulsivity by strengthening the ability of the amygdala to directly activate behavior (and weakening the ability of the frontal cortex to rein it in—stay tuned for the next chapter).[*] Finally, T makes you less generous and more self-centered in, for example, economic games, as well as less empathic toward and trusting of strangers.[12]

What factors determine whether T has strong effects in your brain? Time of day matters, as T levels are nearly twice as high during the daily circadian peak as during the trough. Whether you’re sick, are injured, just had a fight, or just had sex all influence T secretion. It also depends on how high your average T levels are; they can vary fivefold among healthy individuals of the same sex, even more so in adolescents.

Testosterone is not the only hormone that can influence your button-pressing intentions. There’s oxytocin, acclaimed for having prosocial effects among mammals. Oxytocin enhances mother-infant bonding in mammals (and enhances human-dog bonding). The related hormone vasopressin makes males more paternal in the rare species where males help parent. These species also tend to form monogamous pair bonds; oxytocin and vasopressin strengthen the bond in females and males, respectively.

Monogamous species are genetically prone toward higher concentrations of vasopressin receptors in the dopaminergic “reward” part of the brain (the nucleus accumbens). The hormone is released during sex, the experience with that female feels really really pleasurable because of the higher receptor number, and the male sticks around.

Oxytocin and vasopressin have effects that are the polar opposite of T’s. They decrease excitability in the amygdala, making rodents less aggressive and people calmer. Boost your oxytocin levels experimentally, and you’re more likely to be charitable and trusting in a competitive game. And showing how this is the endocrinology of sociality, you wouldn’t have the response to oxytocin if you thought you were playing against a computer.[15]

As an immensely cool wrinkle, oxytocin doesn’t make us warm and fuzzy and prosocial to everyone. Only to in-group members, people who count as an Us.

In one study in the Netherlands, subjects had to decide if it was okay to kill one person to save five; oxytocin had no effects when the potential victim had a Dutch name but made subjects more likely to sacrifice someone with a German or Middle Eastern name (two groups that evoke negative conno...

In another study, while oxytocin made team members more cooperative in a competitive game, as expected, it made them more preemptively aggressive to opponents. The hormone even enhances gloating over strangers’ bad luck.[16] Thus, the hormone makes us nicer, more generous, empathic, trusting, loving . . . to people who count as an Us. But if it is a The...

Thus, the decisions you supposedly make freely in moments that test your character—generosity, empathy, honesty—are influenced by the levels of these hormones in your bloodstream and the levels and variants of their receptors in your brain.

Some of this neuroplasticity is immensely cool but tangential to free-will squabbles. If someone goes blind and learns to read braille, her brain remaps—i.e., the distribution and excitability of synapses to particular brain regions change. Result? Reading braille with her fingertips, a tactile experience, stimulates neurons in the visual cortex, as if she were reading printed text. Blindfold a volunteer for a week and his auditory projections start colonizing the snoozing visual cortex, enhancing his hearing. Learn a musical instrument and the auditory cortex remaps to devote more space to the instrument’s sound. Persuade some wildly invested volunteers to practice a five-finger exercise on the piano two hours a day for weeks, and their motor cortex remaps to devote more space to controlling finger movements in that hand; get this—the same thing happens if the volunteer spends that time imagining the finger exercise.[23]

Moreover, experience-induced changes aren’t limited to the brain. Chronic stress expands the adrenal glands, which then pump out more glucocorticoids, even when you’re not stressed. Becoming a father reduces testosterone levels; the more nurturing you are, the bigger the drop.[26]

By early adolescence, the brain is a fairly close approximation of the adult version, with adult densities of neurons and synapses, and the process of myelinating the brain already achieved. Except for one brain region which, amazingly, won’t fully mature for another decade. The region? The frontal cortex, of course. Maturation of this region lags way behind the rest of the cortex—to some degree in all mammals, and dramatically so in primates.[29]

At the start of adolescence, the frontal cortex has more synapses than in the adult. Adolescence and early adulthood consist of the frontal cortex pruning synapses that turn out to be superfluous, poky, or plain wrong, as the region gets progressively leaner and meaner. As a great demonstration of this, while a thirteen-year-old and a twenty-year-old may perform equally on some test of frontal function, the former needs to mobilize more of the region to accomplish this.

If you’re an adult, your adolescent experiences of trauma, stimulation, love, failure, rejection, happiness, despair, acne—the whole shebang—will have played an outsize role in constructing the frontal cortex you’re working with as you contemplate those buttons. Of course, the enormous varieties of adolescence experiences will help produce enormously varied frontal cortexes in adulthood.

By definition, if the frontal cortex is the last part of the brain to develop, it is the brain region least shaped by genes and most shaped by environment.

If that’s the case for some baboon, just imagine humans. We have to learn our culture’s rationalizations and hypocrisies—thou shalt not kill, unless it’s one of them, in which case here’s a medal. Don’t lie, except if there’s a huge payoff, or it’s a profoundly good act (“Nope, no refugees hiding in my attic, no siree”). Laws to be followed strictly, laws to be ignored, laws to be resisted. Reconciling acting as if each day is your last with today being the first day of the rest of your life. On and on.

Parenting, of course. Differences in parenting styles were the focus of highly influential work originating with Berkeley psychologist Diana Baumrind. There’s authoritative parenting, where high levels of demands and expectation are placed on the child, coupled with lots of flexibility in responding to the child’s needs; this is usually the style aspired to by neurotic middle-class parents. Then there’s authoritarian parenting (high demand, low responsiveness—“Do this because I said so”), permissive parenting (low demand, high responsiveness), and negligent parenting (low demand, low responsiveness). And each tends to produce a different sort of adult.