Determined, page 7
So the frontal cortex—with its roles in executive function, long-term planning, gratification postponement, impulse control, and emotion regulation—isn’t fully functional in adolescents. Hmm, what do you suppose that explains? Just about everything in adolescence, especially when adding the tsunamis of estrogen, progesterone, and testosterone flooding the brain then. A juggernaut of appetites and activation, constrained by the flimsiest of frontal cortical brakes.[30]
For our purposes, the main point about delayed frontal maturation isn’t that it produces kids who got really bad tattoos but the fact that adolescence and early adulthood involve a massive construction project in the brain’s most interesting part. The implications are obvious. 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.
A fascinating implication of the delayed maturation is important to remember when we get to the section on genes. 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. This raises the question of why the frontal cortex matures so slowly. Is it intrinsically a tougher building project than the rest of the cortex? Are there specialized neurons, neurotransmitters unique to the region that are tough to synthesize, distinctive synapses that are so fancy that they require thick construction manuals? No, virtually nothing unique like that.[*],[31]
Thus, delayed maturation isn’t inevitable, given the complexity of frontal construction, where the frontal cortex would develop faster, if only it could. Instead, the delay actively evolved, was selected for. If this is the brain region central to doing the right thing when it’s the harder thing to do, no genes can specify what counts as the right thing. It has to be learned the long, hard way, by experience. This is true for any primate, navigating social complexities as to whether you hassle or kowtow to someone, align with them or stab them in the back.
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. Reflecting that, while frontocortical maturation finally tops out around puberty in other primates, we need another dozen years. This suggests something remarkable—the genetic program of the human brain evolved to free the frontal cortex from genes as much as possible. Much more to come about the frontal cortex in the next chapter.
Next turtle.[32]
And Childhood
So adolescence is the final phase of frontal cortical construction, with the process heavily shaped by environment and experience. Moving further back into childhood, there are massive amounts of construction of everything in the brain,[*] a process of a smooth increase in the complexity or neuron neuronal circuitry and of myelination. Naturally, this is paralleled by growing behavioral complexity. There’s maturation of reasoning skills and of cognition and affect relevant to moral decision-making (e.g., transitioning from obeying laws to avoid punishment to obeying because where would society be without people obeying them?). There’s maturation of empathy (with growing capacities to empathize with someone’s emotional rather than physical state, about abstract pain, about pains you’ve never experienced, about pain for people totally different from you). Impulse control is also maturing (from successfully restraining yourself for a few minutes from eating a marshmallow in order to then be rewarded with two marshmallows, to staying focused on your eighty-year project to get into the nursing home of your choice).
In other words, simpler things precede more complicated things. Child-development researchers have typically framed these trajectories of maturation as coming in “stages” (for example, Harvard psychologist Lawrence Kohlberg’s canonical stages of moral development). Predictably, there are huge differences as to what particular maturational stage different kids are at, the speed of stage transitions, and the stage carried stably into adulthood.[*],[33]
Speaking to our interests, you have to ask where individual differences in maturation come from, how much control we have over that process, and how it helps generate the you that is you, contemplating the buttons. What sorts of influences effect maturation? An overlapping list of the most usual suspects, with incredibly brief summaries:
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. As we’ll see in the next chapter, parental socioeconomic status (SES) is also enormously important; for example, low familial SES predicts stunted maturation of the frontal cortex in kindergarteners.[34]
Peer socialization, with different peers modeling different behaviors with varying allure. The importance of peers has often been underappreciated by developmental psychologists but is no surprise to any primatologists. Humans invented a novel way to transmit information across generations, where an adult expert intentionally directs information at young’uns—i.e., a teacher. In contrast, the usual among primates is kids learning by watching their somewhat older peers.[35]
Environmental influences. Is the neighborhood park safe? Are there more bookstores or liquor stores? Is it easy to buy healthy food? What’s the crime rate? All the usual.
Cultural beliefs and values, which influence these other categories. As we’ll see, culture dramatically influences parenting style, the behaviors modeled by peers, the sorts of physical and social communities that are constructed. Cultural variability in overt and covert rites of passage, the brands of places of worship, whether kids aspire to earn lots of merit badges versus getting skilled at harassing out-group members.
A pretty straightforward list. And, of course, there are loads of individual differences in childhood patterns of hormone exposure, nutrition, pathogen load, and so on. All converging to produce a brain that, as we’ll see in chapter 5, has to be unique.
The huge question then becomes, How do different childhoods produce different adults? Sometimes, the most likely pathway seems pretty clear without having to get all neurosciencey. For example, a study examining more than a million people across China and the U.S. showed the effects of growing up in clement weather (i.e., mild fluctuations around an average of seventy degrees). Such individuals are, on the average, more individualistic, extroverted, and open to novel experience. Likely explanation: the world is a safer, easier place to explore growing up when you don’t have to spend significant chunks of each year worrying about dying of hypothermia and/or heatstroke when you go outside, where average income is higher and food stability greater. And the magnitude of the effect isn’t trivial, being equal to or greater than that of age, gender, the country’s GDP, population density, and means of production.[36]
The link between weather clemency in childhood and adult personality can be framed biologically in the most informative way—the former influences the type of brain you’re constructing that you will carry into adulthood. As is almost always the case. For example, lots of childhood stress, by way of glucocorticoids, impairs construction of the frontal cortex, producing an adult less adept at helpful things like impulse control. Lots of exposure to testosterone early in life makes for the construction of a highly reactive amygdala, producing an adult more likely to respond aggressively to provocation.
The nuts and bolts of how this happens revolves around the massively trendy field of “epigenetics,” revealing how early life experience causes long-lasting changes in gene expression in particular brain regions. Now, this is not experience changing genes themselves (i.e., changing DNA sequences), but instead changing their regulation—whether some gene is always active, never active, or active in one context but not another; a lot is known by now about how this works. As one celebrated example, if you’re a baby rat growing up with an atypically inattentive mother,[*] epigenetic changes in the regulation of one gene in your hippocampus will make it harder for you to recover from stress as an adult.[37]
Where do differences in rodential mothering style come from? Obviously, from one second, one minute, one hour, before in that rat mom’s biological history. Knowledge about epigenetic bases of this has grown at breakneck speed, showing, for example, how some epigenetic changes in the brain can have multigenerational consequences (e.g., helping to explain why being a rat, monkey, or human abused in childhood increases the odds of being an abusive parent). Just to show the scale of epigenetic complexity, differences in mothering styles in monkeys cause epigenetic changes in more than a thousand genes expressed in the offspring’s frontal cortex.[38]
If you had to compress the variability in all those facets of childhood influences into a single axis, it would be easy—how lucky was the childhood you were handed? This massively important fact has been formalized into an Adverse Childhood Experience (ACE) score. What count as adverse experiences in this measure? A logical list:
For each of these experienced, you get a point on the checklist, where the unluckiest have scores approaching an unimaginable ten and the luckiest luxuriating around zero.
This field has produced a finding that should floor anyone holding out for free will. For every step higher in one’s ACE score, there is roughly a 35 percent increase in the likelihood of adult antisocial behavior, including violence; poor frontocortical-dependent cognition; problems with impulse control; substance abuse; teen pregnancy and unsafe sex and other risky behaviors; and increased vulnerability to depression and anxiety disorders. Oh, and also poorer health and earlier death.[39]
You’d get the same story if you flipped the approach 180 degrees. As a child, did you feel loved and safe in your family? Was there good modeling about sexuality? Was your neighborhood crime-free, your family mentally healthy, your socioeconomic status reliable and good? Well then, you’d be heading toward a high RLCE score (Ridiculously Lucky Childhood Experiences), predictive of all sorts of important good outcomes.
Thus, essentially every aspect of your childhood—good, bad, or in between—factors over which you had no control, sculpted the adult brain you have while contemplating those buttons. How’s this for an example outside of someone’s control—because of the randomness of month of birth, some kids can be as much as six months older or younger than the average of their peer group. Older kindergarteners, for example, are typically more cognitively advanced. Result—they get more one-on-one attention and praise from teachers, so that by first grade their advantage is even greater, so that by second grade . . . And in the UK, which has an August 31 cutoff for kindergarten, this “relative age effect” produces a major skew in educational attainment. For example:
Luck evens out over time, my ass.[*],[40]
Does the role of childhood invalidate free will? Nope—the likes of ACE scores are about adult potential and vulnerability, not inevitable destiny, and there are plenty of people whose adulthoods are radically different from what you’d expect, given their childhoods. This is just another piece of the sequence of influences.[41]
Back to the Womb
If you couldn’t control what family you landed in at birth, you sure had no control over which womb you hung out in for nine influential months. Environmental influences begin long before birth. The biggest source of these influences is what’s in the maternal circulation, which will help determine what’s in the fetus—levels of a huge array of different hormones, immune factors, inflammatory molecules, pathogens, nutrients, environmental toxins, illicit substances, all which regulate brain function in adulthood. Not surprising, the general themes echo those of childhood. Lots of glucocorticoids from Mom marinating your fetal brain, thanks to maternal stress, and there’s increased vulnerability to depression and anxiety in your adulthood. Lots of androgens in your fetal circulation (coming from Mom; females secrete androgens, though to a lesser extent than do males) makes you more likely as an adult of either sex to show spontaneous and reactive aggression, poor emotion regulation, low empathy, alcoholism, criminality, even lousy handwriting. A shortage of nutrients for the fetus, caused by maternal starvation, and there’s increased risk of schizophrenia in adulthood, along with a variety of metabolic and cardiovascular diseases.[*],[42]
The implications of fetal environmental effects? Another route toward how lucky or unlucky you’re likely to be in the world that awaits you.[43]
Back to Your Very Beginning: Genes
Down to the next turtle. If you didn’t choose the womb you grew in, you certainly didn’t choose the unique mixture of genes you inherited from your parents. Genes have plenty to do with decision-making crossroads, and in more interesting ways than commonly believed.
We start with an unbelievably superficial primer on genes, to position us to appreciate things when we get to genes and free will.
First, what are genes, and what do they do? Our bodies are filled with thousands of different types of proteins doing dizzyingly varied jobs. Some are “cytoskeletal” proteins that give different cell types their distinctive shapes. Some are messengers—many neurotransmitters, hormones, and immune messengers are proteins. It’s proteins that make up enzymes that construct those messengers and that tear them apart when they’re obsolete; virtually all receptors for messengers throughout the body are made of protein.
Where does all this proteinaceous versatility come from? Each type of protein is constructed from a distinctive sequence of different types of amino acid building blocks; the sequence determines the shape of the protein; the shape determines function. A “gene” is the stretch of DNA that specifies the sequence/shape/function of a particular protein. Each of our approximately twenty thousand genes codes for the production of a unique protein.[*]
How does a gene “decide” when to initiate the construction of the protein it codes for, and whether there will be one or ten thousand copies made? Implicit in this question is the popular view of genes as the be-all and end-all, the code of codes in regulating what goes on in your body. As it turns out, genes decide nothing, are out at sea. Saying that a gene decides when to generate its associated protein is like saying that the recipe decides when to bake the cake that it codes for.
Instead, genes are turned on and off by environment. What is meant here by environment? It can be the environment within a single cell—a cell is running low on energy, which generates a messenger molecule that activates the genes that code for proteins that boost energy production. Environment can encompass the entire body—a hormone is secreted and is carried in the circulation to target cells at the other end of the body, where it binds to its distinctive receptors; as a result, particular genes are turned on or off. Or environment can take the form of our everyday usage, namely events happening in the world around us. These different versions of environment are linked. For example, living in a stressful, dangerous city will produce chronically elevated levels of glucocorticoids secreted by your adrenal glands, which will activate particular genes in neurons in the amygdala, making those cells more excitable.[*]
How do different environmentally activated messengers turn on different genes? Not every stretch of DNA contributes to the code in a gene; instead, long stretches don’t code for anything. Instead, they are the on/off switches for activating nearby genes. Now for a wild fact—only about 5 percent of DNA constitutes genes. The remaining 95 percent? The dizzyingly complex on/off switches, the means by which various environmental influences regulate unique networks of genes, with multiple types of switches on a single gene and multiple genes being regulated by the same type of switch. In other words, most DNA is devoted to gene regulation rather than to genes themselves. Moreover, evolutionary changes in DNA are usually more consequential when they alter on/off switches rather than the gene. As another measure of the importance of the regulation, the more complex the organism, the greater the percentage of its DNA is devoted to gene regulation.[*]
Where have we gotten in this primer? Genes code for workhorse proteins; genes don’t decide when they are active but are, instead, regulated by environmental signals; the evolution of DNA is disproportionately about gene regulation rather than about genes.
So environmental signals have activated some gene, leading to the production of its protein; the newly made proteins then do their usual thing. As a next key point, the same protein can work differently in different environments. Such “gene/environment interactions” are less important in species that inhabit only one type of environment. But they’re plenty relevant in species that inhabit multiple types of environments—species like, say, us. We can live in tundra, desert, or rain forest; in an urban megalopolis of millions or in small hunter-gatherer bands; in capitalist or socialist societies, polygamous or monogamous cultures. When it comes to humans, it can be silly to ask what a particular gene does—only what it does in a particular environment.
