Determined, page 6
Our judgments, decisions, and intentions are also shaped by sensory information coming from our bodies (i.e., interoceptive sensation). Consider one study concerning the insula confusing moral and visceral disgust. If you’re ever on a ship in rough waters and are heaving over the rail, it’s guaranteed that someone will sidle over and smugly tell you that they’re feeling great because they ate some ginger, which settles the stomach. In the study, subjects judged the wrongness of norm violations (e.g., a morgue worker touching the eye of a corpse when no one is looking; drinking out of a new toilet); consuming ginger beforehand lessened disapproval. Interpretation? First, hearing about that illicit eyeball touching pushes your stomach toward lurching, thanks to your weird human insula. Your brain then decides your feelings about that behavior based in part on lurching severity—less lurching, thanks to ginger, and funeral home shenanigans don’t seem as bad.[*],[8]
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. “Changes”—decreasing prosociality, as with the judges, or increasing it? It depends. Hunger seems to have different effects on how charitable subjects say they are going to be, versus how charitable they actually are,[*] or where subjects have either only one or multiple chances to be naughty or nice in an economic game. But as the key point, people don’t cite blood glucose levels when explaining why, say, they were nice just now and not earlier.[9]
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]
Minutes to Days Before
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. As one of the most important routes, consider the scads of different types of hormones in our circulation—each secreted at a different rate and effecting the brain in varied ways from one individual to the next, all without our control or awareness. Let’s start with one of the usual suspects when it comes to hormones altering behavior, namely testosterone.
How does testosterone (T) in the preceding minutes to days play a role in determining whether you kill that person? Well, testosterone causes aggression, so the higher the T level, the more likely you’ll be to make the more aggressive decision.[*] Simple. But as a first complication, T doesn’t actually cause aggression.
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]
A pretty crummy picture. Back to your deciding which button to press. If T is having particularly strong effects in your brain at the time, you become more likely to perceive threat, real or otherwise, less caring about others’ pain, and more likely to fall into aggressive tendencies that you already have.
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. Moreover, the brain’s sensitivity to T also varies, with T receptor numbers in some brain regions varying up to tenfold among individuals. And why do individuals differ in how much T their gonads make or how many receptors there are in particular brain regions? Genes and fetal and postnatal environment matter. And why do individuals differ in the extent of their preexisting tendencies toward aggression (i.e., how the amygdala, frontal cortex, and so on differ)? Above all, because of how much life has taught them at a young age that the world is a menacing place.[*],[13]
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. What’s the nuts-and-bolts biology of why males in some rodent species are monogamous and others not? 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. Amazingly, boost vasopressin receptor levels in that part of the brain in males from polygamous rodent species, and they become monogamous (wham, bam, thank . . . weird, I don’t know what just came over me, but I’m going to spend the rest of my life helping this female raise our kids).[14]
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 connotations among the Dutch) and increased implicit bias against those two groups. 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 Them, who looks, speaks, eats, prays, loves differently than we do, forget singing “Kumbaya.”[*]
On to individual differences related to oxytocin. The hormone’s levels vary manyfold among different individuals, as do levels of receptors for oxytocin in the brain. Those differences arise from the effects of everything from genes and fetal environment to whether you woke up this morning next to someone who makes you feel safe and loved. Moreover, oxytocin receptors and vasopressin receptors each come in different versions in different people. Which flavor you were handed at conception influences parenting style, stability of romantic relationships, aggressiveness, sensitivity to threat, and charitableness.[17]
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.
One last class of hormones. When an organism is stressed, whether mammal, fish, bird, reptile, or amphibian, it secretes from the adrenal gland hormones called glucocorticoids, which do roughly the same things to the body in all these cases.[*] They mobilize energy from storage sites in the body, like the liver or fat cells, to fuel exercising muscle—very helpful if you are stressed because, say, a lion is trying to eat you, or if you’re that lion and will starve unless you predate something. Following the same logic, glucocorticoids increase blood pressure and heart rate, delivering oxygen and energy to those life-saving muscles that much faster. They suppress reproductive physiology—don’t waste energy, say, ovulating, if you’re running for your life.[18]
As might be expected, during stress, glucocorticoids alter the brain. Amygdala neurons become more excitable, more potently activating the basal ganglia and disrupting the frontal cortex—all making for fast, habitual responses with low accuracy in assessing what’s happening. Meanwhile, as we’ll see in the next chapter, frontal cortical neurons become less excitable, limiting their ability to make the amygdala act sensibly.[19]
Based on these particular effects in the brain, glucocorticoids have predictable effects on behavior during stress. Your judgments become more impulsive. If you’re reactively aggressive, you become more so, if anxious, more so, if depressive, ditto. You become less empathic, more egoistic, more selfish in moral decision-making.[20]
The workings of every bit of this endocrine system will reflect whether you’ve been stressed recently by, say, a mean boss, a miserable morning’s commute, or surviving your village being pillaged. Your gene variants will influence the production and degradation of glucocorticoids, as well as the number and function of glucocorticoid receptors in different parts of your brain. And the system would have developed differently in you depending on things like the amount of inflammation you experienced as a fetus, your parents’ socioeconomic status, and your mother’s parenting style.[*]
Thus, three different classes of hormones work over the course of minutes to hours to alter the decision you make. This just scratches the surface; Google “list of human hormones,” and you’ll find more than seventy-five, most effecting behavior. All rumbling below the surface, influencing your brain without your awareness. Do these endocrine effects over the course of minutes to hours disprove free will? Certainly not on their own, because they typically alter the likelihood of certain behaviors, rather than cause them. On to our next turtle heading all the way down.[21]
Weeks to Years Before
So hormones can change the brain over the course of minutes to hours. In those cases, “change the brain” isn’t some abstraction. As a result of a hormone’s actions, neurons might release packets of neurotransmitter when they otherwise wouldn’t; particular ion channels might open or close; the number of receptors for some messenger might change in a specific brain region. The brain is structurally and functionally malleable, and your pattern of hormone exposure this morning will have altered your brain now, as you contemplate the two buttons.
The point of this section is that such “neuroplasticity” is small potatoes compared with how the brain can change in response to experience over longer periods. Synapses might permanently become more excitable, more likely to send a message from one neuron to the next. Pairs of neurons can form entirely new synapses, or disconnect existing ones. Branchings of dendrites and axons might expand or contract. Neurons can die; others are born.[*] Particular brain regions might expand or atrophy so dramatically that you can see the changes on a brain scan.[22]
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]
But then there’s neuroplasticity relevant to free will–lessness. Developing post-traumatic stress disorder after trauma transforms the amygdala. Synapse number increases along with the extent of the circuitry by which the amygdala influences the rest of the brain. The overall size of the amygdala increases, and it becomes more excitable, with a lower threshold for triggering fear, anxiety, and aggression.[24]
Then there’s the hippocampus, a brain region central to learning and memory. Suffer from major depression for decades and the hippocampus shrinks, disrupting learning and memory. In contrast, experience two weeks of rising estrogen levels (i.e., be in the follicular stage of your ovulatory cycle), and the hippocampus beefs up. Likewise, if you enjoy exercising regularly or are stimulated by an enriching environment.[25]
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]
How’s this for how unlikely the subterranean biological forces on your behavior can be over weeks to months—your gut is filled with bacteria, most of which help you digest your food. “Filled with” is an understatement—there are more bacteria in your gut than cells in your own body,[*] of hundreds of different types, collectively weighing more than your brain. As a burgeoning new field, the makeup of the different species of bacteria in your gut over the previous weeks will influence things like appetite and food cravings . . . and gene expression patterns in your neurons . . . and proclivity toward anxiety and the ferocity with which some neurological diseases spread through your brain. Clear out all of a mammal’s gut bacteria (with antibiotics) and transfer in the bacteria from another individual, and you’ll have transferred those behavioral effects. These are mostly subtle effects, but who would have thought that bacteria in your gut were influencing what you mistake for free agency?
The implications of all these findings are obvious. How will your brain function as you contemplate the two buttons? It depends in part on events during previous weeks to years. Have you been barely managing to pay the rent each month? Experiencing the emotional swell of finding love or of parenting? Suffering from deadening depression? Working successfully at a stimulating job? Rebuilding yourself after combat trauma or sexual assault? Having had a dramatic change in diet? All will change your brain and behavior, beyond your control, often beyond your awareness. Moreover, there will be a metalevel of differences outside your control, in that your genes and childhood will have regulated how easily your brain changes in response to particular adult experiences—there is plasticity as to how much and what kind of neuroplasticity each person’s brain can manage.[27]
Does neuroplasticity show that free will is a myth? Not by itself. Next turtle.[28]
Back to Adolescence
As will be familiar to any reader who is, was, or will be an adolescent, this is one complex time of life. Emotional gyrations, impulsive risk-taking and sensation seeking, the peak time of life for extremes of both pro- and antisocial behavior, for individuated creativity and for peer-driven conformity; behaviorally, it is a beast unto itself.
Neurobiologically as well. Most research examines why adolescents behave in adolescent ways; in contrast, our purpose is to understand how features of the adolescent brain help explain button-pushing intentions in adulthood. Conveniently, the same hugely interesting bit of neurobiology is relevant to both. 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]
Some of that delayed maturation is straightforward. Starting with fetal brain building, there’s a steady increase in myelination up to adult levels, including in the frontal cortex, just with a huge delay. But the picture is majorly different when it comes to neurons and synapses. 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.
