Determined, page 12
The Legacy of the Time of Pimples
Take the previous paragraph, replace the previous years with adolescence, underline the entire section, and you’re all set. 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;[*] (d) delayed frontocortical maturation has to have evolved precisely so that adolescence has this influence—how else are we going to master discrepancies between the letter and the spirit of laws of sociality?
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. There will be fewer synapses and less complex dendritic branching in the mPFC and orbitofrontal cortex, along with permanent changes in how PFC neurons respond to the excitatory neurotransmitter glutamate (due to persistent changes in the structure of one of the main glutamate receptors). 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]
Conversely, an enriched, stimulating environment during adolescence has great effects on the resulting adult PFC and can reverse some of the effects of childhood adversity. For example, an enriched environment during adolescence causes permanent changes in gene regulation in the PFC, producing higher adult levels of neuronal growth factors like BDNF. Furthermore, while prenatal stress causes reductions in BDNF levels in the adult PFC (stay tuned), adolescent enrichment can reverse this effect. All changes that impair the PFC’s ability for impulse control and gratification postponement. So if you want to be better at doing the harder thing as an adult, make sure you pick the right adolescence.[41]
Further Back
Now go back to the paragraph you underlined, discussing “whatever adolescence has handed you,” replace adolescence with childhood, and underline the paragraph eighteen more times. Whaddaya know, 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.[*]
For example, no surprise, 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). Synapses in the brain are less excitable; there are changes in the numbers of receptors for various neurotransmitters and changes in gene expression and patterns of epigenetic marking of genes—along with impaired executive function and impulse control in the child. Many of these effects occur in the first half decade or so of life. One might raise a cart-and-horse issue—the assumption in this section is that abuse causes these changes in the brain. What about the possibility that kids who already have these differences behave in ways that make them more likely to be abused? This is highly unlikely—the abuse typically precedes the behavioral changes.[42]
Unsurprising as well is that these changes in the PFC in childhood can persist into adulthood. Childhood abuse produces an adult PFC that is smaller, thinner, and with less gray matter, altered PFC activity in response to emotional stimuli, altered levels of receptors for various neurotransmitters, 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 (“trait anger”). And once again, all of these changes are associated with an adult PFC that isn’t at its best.[43]
Thus, childhood abuse produces a different adult PFC. And grimly, having been abused as a child produces an adult with an increased likelihood of abusing their own child; at one month of age, PFC circuitry is already different in children whose mothers were abused in childhood.[44]
These findings concern two groups of people—abused in childhood or not. What about looking at the full spectrum of luck? How about the effects of childhood socioeconomic status on our realm of supposed grit?
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]
All the individual pieces of these findings flow from that. Socioeconomic status predicts how much a young child’s dlPFC activates and recruits other brain regions during an executive task. It predicts more responsiveness of the amygdala to physical or social threat, a stronger activation signal carrying this emotional response to the PFC via the vmPFC. And such status predicts every possible measure of frontal executive function in kids; naturally, lower socioeconomic status predicts worse PFC development.[46]
There are hints as to the mediators. By age six, low status is already predicting elevated glucocorticoid levels; the higher the levels, the less activity in the PFC on average.[*] Moreover, glucocorticoid levels in kids are influenced not only by the socioeconomic status of the family but by that of the neighborhood as well.[*] Increased amounts of stress mediate the relationship between low status and less PFC activation in kids. As a related theme, lower socioeconomic status predicts a less stimulating environment for a child—all those enriching extracurricular activities that can’t be afforded, the world of single mothers working multiple jobs who are too exhausted to read to their child. As one shocking manifestation of this, by age three, your average high-socioeconomic status kid has heard about 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]
Awful. Given the start of constructing the frontal cortex during this period, it wouldn’t be crazy to predict that childhood socioeconomic status predicts things in adults. Childhood status (independent of the status achieved in adulthood) is a significant predictor of glucocorticoid levels, the size of the orbitofrontal cortex, and performance of PFC-dependent tasks in adulthood. Not to mention incarceration rates.[48]
Miseries like childhood poverty and childhood abuse are incorporated in someone’s Adverse Childhood Experiences (ACE) score. As we saw in the last chapter, it queries whether someone experienced or witnessed physical, emotional, or sexual childhood abuse, physical or emotional neglect, or household dysfunction, including divorce, spousal abuse, or a family member mentally ill, incarcerated, or struggling with substance abuse. 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]
Let’s push the bad news one step further, into chapter 3’s realm of prenatal environmental effects. 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.[*] And naturally, high levels of maternal stress during pregnancy (e.g., loss of a spouse, natural disasters, or maternal medical problems that necessitate treatment with lots of synthetic glucocorticoids) predict cognitive impairment across a wide range of measures, poorer executive function, decreased gray matter volume in the dlPFC, a hyperreactive amygdala, and a hyperreactive glucocorticoid stress response when those fetuses become adults.[*],[50]
An ACE score, a fetal adversity score, last chapter’s Ridiculously Lucky Childhood Experience score—they all tell the same thing. 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. Just ask those fetuses in the womb of a low-socioeconomic-status woman, already paying a neurobiological price.
The Legacy of the Genes You Were Handed, and Their Evolution
Genes have something to do with the sort of PFC you have. Big shocker—as described in the last chapter, the 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 notion that genes have something to do with all this can be totally superficial and uninteresting. Differences between the type of genes possessed by particular species help explain why a frontal cortex occurs in humans but not in barnacles in the sea or heather on the hill. The types of genes possessed by humans help explain why the frontal cortex (like the rest of the cortex) consists of six layers of neurons and isn’t bigger than your skull. However, the sort of genetics that interests us when “genes” come into the picture concerns the fact that that particular gene can come in different flavors, with these variants differing from one person to the next. Thus, in this section, we’re not interested in genes that help form a frontal cortex in humans but don’t exist in fungi. 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.[*] 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]
Nicely, the field has progressed to the point of understanding how variants of specific genes relate to frontal function. A bunch of them relate to the neurotransmitter serotonin; for example, 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 a gene related to the breakdown of serotonin in the synapse helps predict people’s performance on PFC-dependent reversal tasks. Variation in the gene for one of the serotonin receptors (there are a lot) helps predict how good people are at impulse control.[*] Those are just about the genetics of serotonin signaling. In a study of the genomes of thirteen thousand people, a complex cluster of gene variants predicted an increased likelihood of impulsive, risky behavior; the more of those variants someone had, the smaller their dlPFC.[52]
A crucial point about genes related to brain function (well, pretty much all genes) is that 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 in which it has been studied. And as a great example of this, in variants in the gene for one type of serotonin receptor helps explain impulsivity in women . . . but only if they have an eating disorder.[53]
The section on adolescence considered why dramatic delayed maturation of the PFC evolved in humans and how that makes that region’s construction so subject to environmental influences. How do genes code for freedom from genes? In at least two ways. The first, straightforward, way involves the genes that influence how rapidly PFC maturation occurs.[*] The second way is subtler and elegant—genes relevant to how sensitive the PFC will be to different environments. 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. In other words, the two variants produce dramatic differences in sensitivity to peer pressure.
Let’s frame this sort of difference more mechanically. Suppose you have an electrical cord that plugs into a socket; when it’s plugged in, you don’t steal. The socket is made of an imaginary protein that comes in two variants, which determine how wide the slots are that the plug plugs into. In a silent, hermetically sealed room, a plug remains in the socket, regardless of variant. But if a group of taunting, peer-pressuring elephants thunders past, the plug is ten times more likely to vibrate out of the loose-slot socket than the tight one.
And that turns out to be something like a genetic basis for being freer from genes. Work by Benjamin de Bivort at Harvard concerns a gene coding for a protein called teneurin-A, which is involved in synapse formation between neurons. The gene comes in two variants that influence how tightly a cable from one neuron plugs into a teneurin-A socket on the other (to simplify enormously). Have the loose-socket variant, and the result will be more variability in synaptic connectiveness. Or stated our way, the loose-socket variant codes for neurons that are more sensitive to environmental influences during synapse formation. It’s not known yet if teneurins work this way in our brains (these were studies of flies—yes, environmental influences even affect synapse formation in flies), but things conceptually similar to this have to be occurring in umpteen dimensions in our brains.[54]
The Cultural Legacy Bequeathed to Your PFC by Your Ancestors
As we saw in the previous chapter’s overview, 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. And thus pass its values on to the next generation . . .
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. And their findings make sense.[*]
Here’s one you couldn’t make up—in Westerners, the vmPFC activates in response to seeing a picture of your own face but not your mother’s; in East Asians, the vmPFC activates equally for both; these differences become even more extreme if you prime subjects beforehand to think about their cultural values. Study bicultural individuals (i.e., with one collectivist culture parent, one individualist); prime them to think about one culture or the other, and they then show that culture’s typical profile of vmPFC activation.[55]
Other studies show differences in PFC and emotion regulation. A meta-analysis of thirty-five studies neuroimaging subjects during social-processing tasks showed that East Asians average higher activity in the dlPFC than Westerners (along with activation of a brain region called the temporoparietal junction, which is central to theory of mind); this is basically a brain more actively working on emotion regulation and understanding other people’s perspectives. In contrast, Westerners present a picture of more emotional intensity, self-reference, capacity for strongly emotional disgust or empathy—higher levels of activity in the vmPFC, insula, and anterior cingulate. And these neuroimaging differences are greatest in subjects who most strongly espouse their cultural values.[56]
There are also PFC differences in cognitive style. In general, collectivist-culture individuals prefer and excel at context-dependent cognitive tasks, while it’s context-independent tasks for individualistic-culture folks. And in both populations, the PFC must work harder when subjects struggle with the type of task less favored by their culture.
Where do these differences come from on a big-picture level?[*] As discussed in the last chapter, East Asian collectivism is generally thought to arise from the communal work demands of floodplain rice farming. Recent Chinese immigrants to the United States already show the Western distinction between activating your vmPFC when thinking about yourself and activating it when thinking about your mother. This suggests that people back home who were more individualistic were the ones more likely to choose to emigrate, a mechanism of self-selection for these traits.[57]
Where do these differences come from on a smaller-picture level? As covered in the last chapter, children are raised differently in collectivist versus individualist cultures, with implications for how the brain is constructed.
But in addition, there are probably genetic influences. People who are spectacularly successful at expressing their culture’s values tend to leave copies of their genes. In contrast, fail to show up with the rest of the village during rice-harvesting day because you decided to go snowboarding, or disrupt the Super Bowl by trying to persuade the teams to cooperate rather than compete—well, such cultural malcontents, contrarians, and weirdos are less likely to pass on their genes. And if these traits are influenced at all by genes (which they are, as seen in the previous section), this can produce cultural differences in gene frequencies. Collectivist and individualist cultures differ in the incidence of gene variants related to dopamine and norepinephrine processing, variants of the gene coding for the pump that removes serotonin from the synapse, and variants of the gene coding for the receptor in the brain for oxytocin.[58]
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.
The Death of the Myth of Freely Chosen Grit
We’re pretty good at recognizing that we have no control over the attributes that life has gifted or cursed us with. But what we do with those attributes at right/wrong crossroads powerfully, toxically invites us to conclude, with the strongest of intuitions, that we are seeing free will in action. 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. The same punch line as in the previous chapter concerning the entire brain. And invoking the same critical word—seamless. As we’ve seen, 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. A seamless arc of influences bringing your PFC to this moment, without a crevice for free will to lodge in.
