Determined: A Science of Life without Free Will

by Robert M. Sapolsky

Because there are millions of neurons involved, with gazillions of synapses, the process is subject to a lifetime of influences that are staggeringly more complex and nuanced than what goes into conditioning an eyeblink or changing how an Aplysia protects its gill. But it’s all the same mechanistic building blocks that will determine whether your views will be changed by some demagogue’s toxic attempt to form a conditioned association in you.[*13]

What is the “Do it” circuit about? The usual—the outcome of influences from one second ago to millions of years ago. You’re hungry. There was just a mysterious throbbing pain on the left side of your butt,

You’ve gone a few months without getting a decent night’s sleep. In middle school way back when, the tough kids bullied you a lot, and from that you have a vague, unspoken belief that letting someone merge in front of you on the highway equates to your being an inadequate pushover. It’s the time of day when your testosterone levels are elevated,

All of those push in the direction of “Do it.” Meanwhile, the “Don’t; slow down instead” neuron has its inputs: You like to think of yourself as a kind person. You went to Quaker meetings for a while in college. Something in the news this morning made you feel slightly less jaundiced and helpless about the idea that the incrementalism of small good acts can make the world better.

The two circuits sit there, prompting you toward opposing neurobiological outputs. At this moment, the “Don’t; slow down instead” prompt has a little more oomph than usual.

But it’s still an approximation of how the brain works—exemplars converging on nodes out of which emerge the capacity to categorize and associate. Each node being a part of multiple networks—serving as a lower-layer element in one while simultaneously serving as a higher-layer element in another, a central player in one, peripheral in another.

And where the events around us alter the strengths of various synapses—another

You learn about how experience changes the nervous system of an Aplysia, and as a result, your nervous system changes. We don’t choose to change, but it is abundantly possible for us to be changed, including for the better.

The last chapter’s point was that while change happens, we do not freely choose to change; instead, we are changed by the world around us, and in a way determined by the sort of person circumstances had made you into at that moment.

When a neuron is silent, has nothing to say, its electrical makeup is at one extreme, where the inside of the neuron is negatively charged, relative to the outside. When the neuron is triggered into an explosion of excitation called an action potential, the inside of the neuron becomes positively charged.

While the focus of the book was not remotely epilepsy, its message was clear: epilepsy was brought on by someone’s own freely chosen evil, and such demonic possession represented a danger to society and needed to be dealt with. And thus, people with some haywire potassium channels in their neurons were burned at the stake.

But prior to the early twentieth century, a person with epilepsy might experience many hundreds of seizures in their lifetime; Temkin describes one survey in the early nineteenth century documenting that chronically hospitalized people with epilepsy averaged two seizures a week for years.[2]

My lab spent decades studying how seizures can damage or kill neurons (and trying, mostly unsuccessfully, to develop gene-therapy strategies to try to protect such neurons); basically, the repeated bursts of firing deplete neurons of energy, leaving the cells without the energetic means to clean up damaging things like oxygen radicals in the aftermath.

the millions of people with epilepsy have no higher rates of violence than anyone else, and the majority of any such violence is unrelated to the disorder. Nonetheless, by the nineteenth century, there was a widespread public association of epilepsy with violence and criminality.[*7] Malleus maleficarum redux—people with this disease brought it on themselves with their moral failings and constitute a threat to society for which they must be held responsible.[5]

Which suggested that epilepsy might involve some manner of electrical problem. A giant among neurologists named Hughlings Jackson, an utter genius, introduced the idea of localization—where in the body convulsive twitching and movements at the start of a seizure could tell you where in the brain the problem was centered.

By midcentury, psychiatry heavyweights like Benedict Morel and Louis Delasiauve were more generally arguing that people with epilepsy could not be held responsible for their actions.

In the developing world, there is still a common belief that epilepsy has supernatural causes, and nearly half of the people queried would object to sharing a meal with someone with epilepsy.

So you sit at the juncture of deciding: “Should I drive without my meds or do the harder, right thing?” It’s back to chapter 4. How many neurons are there in your frontal cortex and how well do they work?

Is your frontal cortex a little light-headed and sluggish because you skipped breakfast and now your blood sugar levels are low?

What are your gonadal steroid hormone levels that morning? Has stress in the previous weeks to months neuroplastically impaired your frontal function?

Did the culture that your ancestors developed glorify following rules, or thinking of others, or taking risks? On and on. We’re back to the table on this page in chapter 4—“having seizures” and “deciding to drive even though you haven’t taken your meds” are equally biological, equally the product of a nervous system sculpted by factors over which you had no control.

if we are to live the consequences of what science is teaching us—that the brain that led someone to drive without their meds is the end product of all the things beyond their control from one second, one minute, one millennium before. And likewise if your brain has been sculpted into one that makes you kind or smart or motivated.[13]

When did most people begin to think that “Epilepsy is caused by demons” was as silly as “Hailstorms are caused by witches”? Those are the transformations that matter,

Schizophrenia is a disease of disordered thought. If you meet someone whose individual sentences sort of make sense but are juxtaposed with meandering incoherence where, after thirty seconds, you can already tell something is not right with them, there’s a good chance it’s schizophrenia

It affects 1–2 percent of the population, regardless of culture, gender, ethnicity, or socioeconomic status.

with elements of delusion, of paranoid persecution. Add to that the hallucinations. Most of them are auditory, taking the form of hearing voices—incessant, often taunting, threatening, demanding, demeaning.

The “negative” symptoms of the disease, the things that are absent, include strong or appropriate emotions, expression of affect, and social connections.

A strikingly consistent feature of schizophrenia is that the onset is typically in late adolescence or early adulthood.

Individuals destined for a schizophrenia diagnosis have higher rates of “soft neurological” signs in early life, such as late standing and walking, delayed toilet training, sustained problems with bed-wetting.

in one study, trained observers who watched home movies were able to identify children de...

It was called “schizophrenogenic” mothering, and it had become the dominant explanation for the disease, rooted in Freudian thinking.

By 1940, the chair of every major American medical school’s psychiatry department was a Freudian psychoanalyst, a stranglehold that was to last many decades. In the words of the influential psychiatrist E. Fuller Torrey, “The transformation of Freud’s theory from an exotic New York plant to an American cultural kudzu is one of the strangest events in the history of ideas.”[*20]

In a classic gene/environment interaction, getting the disease basically requires a combination of the genetic vulnerability plus a stressful environment. What sort of stress? During fetal life, disease risk many years later is raised by prenatal malnutrition

exposure to any of a number of viruses by way of maternal infection, placental bleeding, maternal diabetes,

Later during development, the risk is raised by psychosocial stressors such as loss of a parent to death, parental separation, early adolescent trauma, migration, and urban living.[20]

The most dramatic and reliable one involves an excess of the neurotransmitter dopamine. This chemical messenger plays a role, particularly in the frontal cortex, in marking the salience of an event.

Dopamine is the mediator of the message “Pay attention; this is important.”[21]

The best evidence is that not only are dopamine levels elevated in schizophrenia but this is due to random bursts of its release. Producing random bursts of salience. For example, if you have schizophrenia and a pointless dump of dopamine just happens to occur when you are noting someone glancing at you, then, heavy with this faux feeling of significance in the glance, you conclude that they are monitoring you, reading your mind. Schizophrenia is a thought disorder of, as it’s termed, “aberrant salience.”[22]

Most people have an internal voice in our heads, narrating events, reminding us of things, intruding with unrelated thoughts. Have a random burst of dopamine along with one of those, and it becomes marked with so much salience, so much presence, that you perceive it, respond to it as an actual voice. Most schizophrenic hallucinations are auditory, reflecting how much of our thinking is verbal.

once it was possible to identify those genetically at risk and follow them from childhood, seeing who would develop the disease and who not, it became clear that some of the brain changes were happening well before the most serious symptoms were emerging.[24] So these brain changes preceded and predicted the disease. The most dramatic change is that the cortex is abnormally thin, compressed

the cortical changes are most dramatic in the frontal cortex. The thinning turns out not to be due to loss of neurons. Instead, there’s loss of the complex cables—the axons and dendrites—that allow neurons to communicate with each other.[*27]

functional brain imaging shows that the thinned-out, impoverished frontal cortex in someone with schizophrenia has to work harder to pull off the same degree of efficacy at tasks than the frontal cortex of a control subject.[26]

In schizophrenia, an array of gene variants constitute a risk for the disease, and certain times of major stress early in life regulate those genes in such a way that things divert onto the road leading to schizophrenia. These manifestations then include an excess of dopamine and sparse neuron- to-neuron connections in the frontal cortex. Why the late-adolescent/ early-adult onset typical of the disease? Because that’s when the frontal cortex is having its final burst of maturational growth

it’s a biological problem. It’s the world of people in lab coats with test tubes, rather than Viennese psychoanalysts whose modus operandi would be to tell the mother that she sucks at mothering.

When dopamine is released by a neuron intent on sending a “dopaminergic” message to the next neuron in line, it works only if that next neuron has receptors that bind and respond to dopamine. Basic neurotransmitter signaling. And the first effective drugs were ones that blocked dopamine receptors. These were termed “neuroleptics” or “antipsychotics,”

And if people with the disease start acting less schizophrenic at that point, you have to logically conclude that the problem was too much dopamine on the scene in the first place.[*29]

Torrey, emphasizing how schizophrenia was a biological disease. It has “nothing to do with what your mother did to you. Just like multiple sclerosis. Like diabetes.” Not because of an unloved childhood. He showed the brain scans of a pair of twins, one with the disease and one without. The enlarged ventricles jumped out in a powerful demonstration of a picture being worth at least a thousand words.

advocating for medical schools to change their curriculum about schizophrenia and to shift psychiatry departments away from psychoanalysis and toward biological psychiatry,[*35] funding the next generation of young researchers in the field.

Moreover, many with milder versions of autism (what used to be called Asperger’s syndrome and is now labeled something like “high-functioning autism spectrum disorder” [ASD])

the anti-vaxxer movement, which insists, in the face of every possible scientific refutation, that autism can be caused by vaccinations gone awry. Amid these often well-educated and privileged medieval witch-hunters being responsible for decreased vaccination rates, a resurgence of measles, and the deaths of children, I note what is often a secondary theme. There is, of course, the primary conspiracy theory of some sort of medico-pharmaceutical willingness to shower autistic hell down on the innocent for the sake of vaccine profits.