* As an important point, this is indeed a case of acculturation, rather than a reflection of populational genetic differences—East Asian Americans show the typical American pattern.
* This is no surprise to fans of the history of eunuchs, who were a mainstay of the military of Imperial China, prized as fierce soldiers.
* One exception: Texas, where they still use a knife.
* Where, as with all these studies, neither the subjects nor the scientist observing them know whether the volunteers received testosterone or placebo, and where the testosterone levels produced are always within the normal range.
* This is a rich literature showing the subtleties of the human psyche. The winning effect on testosterone is lessened in circumstances where people feel like they won by luck or where, despite winning, they feel like they underperformed. In contast, the effect is enhanced among people who went into the competition having the strongest psychological motives for domination. Finally, testosterone levels can rise robustly in “losers” who nonetheless performed far better than they anticipated. Thus one might see testosterone levels rise after a marathon in a guy who came in at the back of the pack but is triumphant because he was sure he was going to drop dead halfway through, and may decline in the guy who comes in third but was expected to win. We all belong to numerous hierarchies, but some of the most powerful are the ones in our heads based on our internal standards.
* All these circumstances of testosterone levels rising raises a question: why not just produce higher levels all the time and save the effort? For one thing, all those androgens are lousy for the cardiovascular system. But more important, they’d get in the way of various prosocial behaviors. For example, among monogamous birds and rodents, if testosterone levels don’t drop around the time the female gives birth, the males won’t act paternally. And some similar patterns seem to apply to humans: Fathers have lower testosterone levels than age-matched, married men without children, and more involved fathers have lower levels than less involved ones. Moreover, evoking nurturing behavior in men lowers testosterone levels, as does the birth of a man’s child. And when compared with high-testosterone fathers, those with lower average testosterone levels are rated as better parents by their partners and have more activation of their reward-related ventral tegmentum when seeing a picture of their child.
* In studies like these, this is typically accomplished either with the administration of a drug that blocks oxytocin receptors or with genetic engineering techniques to eliminate the gene for oxytocin or for the oxytocin receptor.
* In other words, a familiar theme: vasopressin doesn’t cause paternal behavior; it facilitates it in species that are already predisposed to it.
* This turned out to be due to a genetic difference between the two species. Interestingly, it is not a difference in the DNA sequence that constitutes the gene for the vasopressin receptor. It is a difference in the sequence that constitutes the on/off switch for the gene. More on this in chapter 8.
* This generated all sorts of caustic discussions at conferences as to whether this constituted a case of “gene transfer” (i.e., the value-neutral process of transferring a novel gene into an individual in order to alter a function) or “gene therapy” (i.e., transferring a gene in order to cure those montane males of the disease of infidelity). It strikes me that if that research had been carried out instead at Berkeley during the Summer of Love in 1967, the gene-therapy goal would have been to make prairie voles transcend their Middle American bourgeois genetics and become polygamous. The times, they are a changin’ to quote a recent Nobel Laureate.
* Note that the entire romantic coupling literature I just discussed solely concerns heterosexual couples. As far as I know, very little has been studied in this realm with gay or lesbian subjects.
* Discriminating online shoppers can now buy “Liquid Trust,” touted as “the world’s first oxytocin pheromone product.” Perhaps worse, perfectly straitlaced scientific publications have referred to oxytocin as the “love drug” or the “cuddle drug.” The “cuddle” part is puzzling, since the literature is about oxytocin-laden prairie voles huddling, not cuddling, and the former doesn’t evoke images of luv-fests as much as of tubercular huddled masses yearning to breathe free.
* For the truly interested, the gene codes for a protein called CD38, which facilitates oxytocin secretion from neurons.
* In the Prisoner’s Dilemma each of the two players must decide whether to cooperate. If they both cooperate, they each get, say, two units of reward. If they both backstab, they each get one unit. If one cooperates and the other backstabs, the cheater gets three units and the stooge gets none.
* The IAT will be described in detail in a later chapter—briefly, the test takes advantage of the fact that it takes us milliseconds longer to process pairings of information that seem discordant than pairings that make sense; thus if you’re prejudiced against group X, it takes you longer to process a pairing of group X with a positive term—for example, “wonderful”—than with a negative term—“dangerous.”
* Maternal aggression involves the amygdala; no surprise there. But (harking back to chapter 1 and its discussion of the heterogeneity of types of aggression) it is also uniquely and crucially dependent on a tiny brain region that hasn’t been mentioned before, the ventral premammillary nucleus of the hypothalamus.
* The next two paragraphs can be skipped if you already have enough complications in your life.
* Called allopregnanolone.
* Hyenas have a terrible reputation, thanks to outdated zoology that characterizes them, sneeringly, as “scavengers” (snarkiness that makes little sense, given that most of us just scavenge dead stuff in the supermarket). Rather than living off the scraps of lions’ kills, they are highly effective hunters. Most often, it is scavenging lions trying to drive hyenas off a kill, rather than the other way around. And real hyenas don’t sing inane songs like in The Lion King.
* Think about this: Among typical mammals, when males are terrified, they lose erections. Among hyenas, that’s when they get one (and when some moth-eaten male has the chance to mate, he’s probably terrified out of his mind). This implies some very different wiring of the autonomic nervous system, whereby stress promotes rather than inhibits erections.
* More than two thousand years ago Aristotle, for reasons obscure to even the most learned, dissected some dead hyenas, discussing them in his treatise Historia Animalium, VI, XXX. He drew the incorrect conclusion that these animals were hermaphrodites, possessing all the machinery of both sexes.
* This leads us to another great factoid from the hyena world. If a low-ranking female is being menaced by a high-ranking one, the subordinate gets a clitoral erection—“Please don’t hurt me; look, I’m just like one of those bedraggled, innocuous males.”
* This is due to an obscure hormone called DHEA (dehydroepiandrosterone) that is converted to an androgen within only certain neurons, and, even stranger, some of those neurons even synthesize their own androgens.
* Many people more properly think of PMS as perimenstrual syndrome, in that the symptoms occur typically not just before the onset of menses, but for a few days after as well.
* Mead has been savaged by later generations of Oceanic anthropologists for having painted a grossly inaccurate picture of Samoa as the Garden of Eden, in part because of her ideological desire to see Samoa that way, and in part because the Samoans had a grand time making things up and then gleefully watching the starry-eyed white lady fall for it hook, line, and sinker.
* This literature also has produced sentences like “Such a symbolic analysis is consistent with the hermeneutic, meaning-centered focus of the ‘new cross-cultural psychiatry.’” I haven’t a clue what in hell that means.
* For example, the “fusiform face area” is more responsive to faces in ovulating women than in those menstru
ating. Similarly, the “emotional” vmPFC is more responsive to men’s faces when women are approaching ovulation than when they are approaching menses; the higher the ratio of estrogen to progesterone in the bloodstream during that preovulatory phase, the more vmPFC responsiveness. Finally, women find faces of men judged to look “aggressive” to be more attractive when they are ovulating.
* The broad question of what this book’s avalanche of information says about criminal justice will be considered in chapter 16. I thank Dylan Alegria, a research assistant of mine, for superb assistance in reviewing the PMS/criminality literature.
* For real aficionados: In recent years “homeostasis” has been expanded and fancified into the new, elegant concept of “allostasis.” Most basically, it incorporates the fact that an ideal homeostatic set point in the body varies dramatically depending on the circumstance.
* More info for aficionados: The suppression of immunity and inflammation during chronic stress is caused by glucocorticoids. This is the reason why glucocorticoids are used to suppress the immune system in people with an overactive immune system (i.e., an autoimmune disease), to prevent rejection of a transplanted organ, or to suppress an overactive inflammatory response. This is what happens when people are put on immunosuppressive/anti-inflammatory “steroids” like cortisone or prednisone (two synthetic glucocorticoids).
* How does the brain pull off an inverted U, where a moderate rise in glucocorticoid levels enhances memory (for example), while a bigger rise does the opposite? One solution that the brain has evolved is to have two receptor systems for glucocorticoids. One (the “MR”) is responsive to small increases in glucocorticoid levels above baseline and mediates the stimulatory effects. The other (“GR”) receptors respond only to big, prolonged increases and mediate the adverse effects. Predictably, levels of the two types of receptors vary by brain region, person, and circumstance.
* As just stated, stress increases overall excitability in the amygdala. This involves the inhibition of particular neurons—namely the inhibitory GABA interneurons. Inhibiting the inhibitors in the circuit causes the activity of the big, excitatory glutamate-releasing neurons to increase.
* Plus, more obscurely, via the sympathetic nervous system indirectly activating the amygdala by way of that norepinephrine-releasing projection into it from the locus coeruleus (the brain-stem region that was mentioned briefly in chapter 2—its activation leads to arousal throughout the brain).
* And the underlying neurobiology is probably similar to what is going on in those other realms of poor decision making during stress, e.g., eating or drinking more.
* The test is a standard in the field called the Trier Social Stress Test, which is a fifteen-minute combination of a mock job interview and a mental arithmetic task, both carried out in front of a panel of stone-faced evaluators.
* Note that these are studies about what people say they would do, not what they actually do. The difference between the two will be considered in chapter 13, when considering moral reasoning versus moral action.
* Okay, that was a juvenile cheap shot thrown in merely to increase the number of moose buying copies of this book.
* Although nothing was known about NMDA and non-NMDA receptors at the time.
* Where do more copies of the receptors come from? Miles away from that dendritic spine, in the center of that neuron, is the nucleus, containing the DNA, which includes genes coding for glutamate receptors. Somehow the nucleus needs to hear that a calcium wave occurred in one dendritic spine in the boondocks. The nucleus then directs the synthesis of more copies of the receptor, which are then shipped to that specific spine, out of the neuron’s ten thousand. That’s insanely hard. Typically, instead, there are extra glutamate receptors mothballed inside dendritic spines, and the calcium tidal wave is the signal that pulls them onto the spine’s membrane.
* For aficionados, the non-NMDA receptors are “phosphorylated,” which causes their sodium channels to stay open longer.
* Actually, LTP in the spinal cord has more to do with “neuropathic” pain, syndromes where a severe injury causes all sorts of nonnoxious stimuli to start hurting chronically—in effect, your spine has “learned” to always feel pain. Interestingly, such LTP arises in part from the inflammation that accompanies the initial injury.
* The mechanisms underlying LTP elsewhere in the nervous system often differ from those of hippocampal LTP—some involve a third class of glutamate receptors; some may not even involve glutamate. The LTP old guard has generally coped with the indignity of LTP outside the hippocampus by viewing the hippocampal kind as classical, canonical, textbook, divine, etc., and the rest as chintzy knockoffs.
* Equally remarkably, over the course of the menstrual cycle in humans, the amount of myelin in the corpus callosum, the massive bundle of axons that connects the two hemispheres, fluctuates as well.
* Not all remapping is logical; some is just plain weird. A few years back, during an extremely stressed period, I developed a tic—when I’d be acutely upset about something, the second and third fingers on my left hand would rhythmically contract for a few seconds. What the hell was that about? No idea, but I marvel at the randomness of the remapping, at how unpleasant tumult in limbic circuitry somehow tapped into this motor circuit.
* Nottebohm, interviewed in an excellent New Yorker piece recounting this history, said, “Pasko has taken on the role of hard-nosed defender of standards. And that’s fine—it’s even warranted. . . . [But] as much as I hate to say this, I think Pasko Rakic single-handedly held the field of neurogenesis back by at least a decade.”
* The fact that brain injury, such as a stroke, triggers neurogenesis created huge excitement—wow, the brain has a means to try to repair itself after an injury, how cool is that? What was obvious from the start is that whatever compensatory neurogenesis there is, there isn’t a ton, since so many neurological insults leave the nervous system an irreparable mess afterward. But to add insult to injury, work in that area began to show that sometimes the new neurons actually made things worse, migrating where they shouldn’t, integrating into circuits the wrong way, making those circuits seizure prone. To metaphorically appropriate a concept from chapter 1, this seems a case of neuronal pathological altruism—beware when freshly minted neurons that may not yet know feces from Shinola want to lend a helping hand.
* Listing these various factors that “enhance” or “inhibit” neurogenesis glosses over lots of detail. The number of new neurons that are integrated into circuits reflects (a) the number of new cells that are formed from stem cells in the brain; (b) the percentage of new cells that differentiate into neurons (as opposed to glial cells); and (c) the rate at which new neurons survive and form functional synapses. Each of these manipulations—learning, exercise, stress, etc.—targets different steps. Complicating things further is the fact that not all stressors are equal. If a rodent secretes glucocorticoids because it thinks there is a predator around and the fight-or-flight sirens are going off, neurogenesis is inhibited. But if it secretes glucocorticoids while voluntarily running in a running wheel, it enhances neurogenesis (in other words, the contrast between “bad” and “good” stress).
* As one additional, grim piece of this picture of neural plasticity, extremes of chronic stress and glucocorticoid overexposure can also kill hippocampal neurons. While this is probably pertinent to nightmare extremes of stress, it is unclear how relevant it might be to more garden-variety sustained stress.
* For example, the phenomenon where experience can turn the on/off switch on a gene in a particular direction used to be considered permanent; that is turning out not to be the case. Similarly, the hippocampal atrophy in Cushing’s syndrome appears to reverse within a year or so after the tumor is removed. As one disturbing exception to this theme, most studies suggest that the atrophy of the hippocampus with long-term major depression persists after th
e depression is successfully treated. Moreover, the reversibility of some of these effects (for example, of stress-induced retraction of dendritic processes) decreases with age.
* The delayed attainment of legal adulthood in the West also sometimes reflected something as mundane as muscle mass. In thirteenth-century England the age of legal majority was raised from fifteen to twenty-one years—protective armor was getting heavier, and it wasn’t until the older age that males were typically strong enough to comport themselves in armor on the battlefield. There is no mention as to whether the age of majority of the horses carrying these heavier weights was raised as well. But sometimes technological advancements have made it possible for younger adolescents to join the ranks of adult occupations—it has been pointed out that the development of lightweight automatic weapons has been a boon for the usefulness of the estimated 300,000 child soldiers on earth.
Behave: The Biology of Humans at Our Best and Worst Page 97
