Determined: A Science of Life without Free Will

by Robert M. Sapolsky

Roughly half the people incarcerated for violent antisocial criminality have a history of TBI, versus about 8 percent of the general population; having had a TBI increases the likelihood of recidivism in prison populations. Moreover, neuroimaging studies reveal elevated rates of structural and functional abnormalities in the PFC among prisoners with a history of violent, antisocial criminality.[*27]

To summarize this section, when you try to do the harder thing that’s better, the PFC you’re working with is going to be displaying the consequences of whatever the previous years have handed you.

Chapter 3 provided the basic facts: (a) when you’re an adolescent, your PFC still has a ton of construction ahead of it; (b) in contrast, the dopamine system, crucial to reward, anticipation, and motivation, is already going full blast, so the PFC hasn’t a prayer of effectively reining in thrill seeking, impulsivity, craving of novelty, meaning that adolescents behave in adolescent ways; (c) if the adolescent PFC is still a construction site, this time of your life is the last period that environment and experience will have a major role in influencing your adult PFC;[*28]

Thus, adolescent social experience, for example, will alter how the PFC regulates social behavior in adults. How? Round up all the usual suspects. Lots of glucocorticoids, lots of stress (physical, psychological, social) during adolescence, and your PFC won’t be its best self in adulthood.

changes in how PFC neurons respond to the excitatory neurotransmitter glutamate

The adult PFC will be less effective in inhibiting the amygdala, making it harder to unlearn conditioned fear and less effective at inhibiting the autonomic nervous system from overreacting to being startled. Impaired impulse control, impaired PFC-dependent cognitive tasks. The usual.[40]

an enriched environment during adolescence causes permanent changes in gene regulation in the PFC, producing higher adult levels of neuronal growth factors like BDNF.

So if you want to be better at doing the harder thing as an adult, make sure you pick the right adolescence.[41]

the sort of childhood you had shapes the construction of the PFC at the time and the sort of PFC you’ll have in adulthood.[*29]

childhood abuse produces kids with a smaller PFC, with less gray matter and with changes in circuitry: less communication among different subregions of the PFC, less coupling between the vmPFC and the amygdala (and the bigger the effect, the more prone the child is to anxiety).

Many of these effects occur in the first half decade or so of life.

Childhood abuse produces an adult PFC that is smaller, thinner, and with less gray matter, altered PFC activity in response to emotional stimuli,

weakened coupling between both the PFC and dopaminergic “reward” regions (predicting increased depression risk), and weakened coupling with the amygdala as well, predicting more of a tendency to respond to frustration with anger

at one month of age, PFC circuitry is already different in children whose mothers were abused in childhood.[44]

No surprise, the socioeconomic status of a child’s family predicts the size, volume, and gray matter content of the PFC in kindergarteners. Same thing in toddlers. In six-month-olds. In four-week-olds. You want to scream at how unfair life can be.[45]

It predicts more responsiveness of the amygdala to threat, a stronger activation signal carrying this emotional response to the PFC via the vmPFC.

By age six, low status is already predicting elevated glucocorticoid levels; the higher the levels, the less activity in the PFC on average.[*30] Moreover, glucocorticoid levels in kids are influenced not only by the socioeconomic status of the family but by that of the neighborhood as well.[*31]

by age three, your average high-socioeconomic status kid has heard—depending on the study—anywhere from four to thirty million more words at home than a poor kid, and in one study, the relationship between socioeconomic status and the activity of a child’s PFC was partially mediated by the complexity of language use at home.[47]

Childhood status (independent of the status achieved in adulthood) is a significant predictor of glucocorticoid levels, the size of the orbitofrontal cortex,

Miseries like childhood poverty and childhood abuse are incorporated in someone’s Adverse Childhood Experiences (ACE) score.

With each increase in someone’s ACE score, there’s an increased likelihood of a hyperreactive amygdala that has expanded in size and a sluggish PFC that never fully developed.[49]

Low socioeconomic status for a pregnant woman or her living in a high-crime neighborhood both predict less cortical development at the time of the baby’s birth. Even back when the child was still in utero.[*32]

It takes a certain kind of audacity and indifference to look at findings like these and still insist that how readily someone does the harder things in life justifies blame, punishment, praise, or reward.

growth factors, enzymes that generate or break down neurotransmitters, receptors for neurotransmitters and hormones, etc., etc., are all made of protein, meaning that they are coded for by genes.

the frontal cortex (like the rest of the cortex) consists of six layers of neurons

particular gene can come in different flavors, with these variants differing from one person to the next.

We’re interested in the variation in versions of genes that helps explain variation in the volume of the frontal cortex, its level of activity (as detected with EEG), and performance on PFC-dependent tasks.[*34] In other words, we’re interested in the variants of those genes that help explain why two people differ in their likelihood of stealing a cookie.[51]

there’s a gene that codes for a protein that removes serotonin from the synapse, and which version of that gene you have influences the tightness of coupling between the PFC and amygdala.

Variation in the gene for one of the serotonin receptors (there are a lot) helps predict how good people are at impulse control.[*35]

the same gene variant will work differently, sometimes even dramatically differently, in different environments. This interaction between gene variant and variation in environment means that, ultimately, you can’t say what a gene “does,” only what it does in each particular environment

Consider an (imaginary) gene, coming in two variants, that influences how prone someone is to stealing. A person, on their own, has the same low likelihood, regardless of variant. However, if there’s a peer group egging the person on, one variant results in a 5 percent increase in likelihood of succumbing, the other 50 percent. Thus, the two variants differ dramatically in sensitivity to peer pressure.

different sorts of ecosystems generate different sorts of cultures, which affects a child’s upbringing from virtually the moment of birth, tilting the brain construction toward ways that make it easier for them to fit into the culture.

Of course, cultural differences majorly influence the PFC. Essentially all the studies done concern comparisons between Southeast Asian collectivist cultures valuing harmony, interdependence, and conformity, and North American individualist ones emphasizing autonomy, individual rights, and personal achievement.

children are raised differently in collectivist versus individualist cultures, with implications for how the brain is constructed.

Collectivist and individualist cultures differ significantly in the incidence of gene variants related to dopamine and norepinephrine processing,

In other words, there’s coevolution of gene frequencies, cultural values, child development practices, reinforcing each other over the generations, shaping what your PFC is going to be like.

But the reality is that whether you display admirable gumption, squander opportunity in a murk of self-indulgence, majestically stare down temptation or belly flop into it, these are all the outcome of the functioning of the PFC and the brain regions it connects to. And that PFC functioning is the outcome of the second before, minutes before, millennia before.

talk about the evolution of the PFC, and you’re also talking about the genes that evolved, the proteins they code for in the brain, and how childhood altered the regulation of those genes and proteins.

The takeaway from chapters 2 and 3 is that it’s impossible to successfully wish what you’re going to wish for. This chapter’s punchline is that it’s impossible to successfully will yourself to have more willpower.

the sciences of chaos theory, emergent complexity, and quantum indeterminacy.

This and the next chapter focus on chaos theory, the field that can make studying the component parts of complex things useless.

This is reductionism, the idea that to understand something complicated, break it down into its component parts, study them, add your insights about each component part together, and you will understand the complicated whole.

a reductive approach has long been the gold standard for scientifically exploring a complex topic. And then, starting in the early 1960s, a scientific revolution emerged that came to be called chaoticism, or chaos theory. And its central idea is that really interesting, complicated things are often not best understood, cannot be understood, on a reductive level.

If Lorenz’s original program had contained only two weather variables, instead of the twelve he was using, the familiar reductiveness would have held—after a slightly wrong number was fed into the computer, the output would have been precisely as wrong at every step for the rest of time. Predictably so.

When you have a nonlinear system, tiny differences in a starting state from one time to the next can cause them to diverge from each other enormously, even exponentially,[*6]

So a tiny difference in a starting state can magnify unpredictably over time.

Thus was born the symbol of the chaos theory revolution, the butterfly effect.[*8]

The rule we’ve been following (if and only if one box of the trio above is filled…) is called rule 22 in the cellular automata universe, which consists of 256 rules.[*12]

Very few generate complex, dynamic patterns. And of the few that do, rule 22 is one of the favorites.

What is chaotic about rule 22? We’ve now seen that, depending on the starting state, by applying rule 22 you can get one of three mature patterns: (a) nothing, because it went extinct; (b) a crystallized, boring, inorganic periodic pattern; (c) a pattern that grows and writhes and changes,