CONTENTS

Cover

About the Author

Also by Robert M. Sapolsky

Dedication

Title Page

Author’s Note

PART I:
Genes and Who We Are

Introduction

Nature or Nurture? “The 50 Most Beautiful People in the World” Assess the Source of Their Good Looks (Discover, 2000)

A Gene for Nothing (Discover, 1997)

Genetic Hyping (The Sciences, 2000)

The Genetic War Between Men and Women (Discover, 1999)

Of Mice and (Hu)Men Genes (Natural History, 2004)

Antlers of Clay (Natural History, 2001)

PART II:
Our Bodies and Who We Are

Introduction

Why Are Dreams Dreamlike? (Discover, 2001)

Anatomy of a Bad Mood (Men’s Health, 2003)

The Pleasure (and Pain) of “Maybe” (Natural History)

Stress and Your Shrinking Brain (Discover, 1999)

Bugs in the Brain (Scientific American, 2003)

Nursery Crimes (The Sciences, 1999)

PART III:
Society and Who We Are

Introduction

How the Other Half Heals (Discover, 1998)

The Cultural Desert (Discover, 2005)

Monkeyluv (The Sciences, 1998)

Revenge Served Warm (Natural History, 2002)

Why We Want Their Bodies Back (Discover, 2002)

Open Season (The New Yorker, 1998)

Acknowledgments

Copyright

ABOUT THE AUTHOR

Robert M. Sapolsky is Professor of Biology and Neurology at Stanford University and a Research Associate with the Institute of Primate Research, National Museums of Kenya. He is the author of The Trouble with Testosterone, Why Zebras Don’t Get Ulcers (both finalists for the LA Times Book Award) and A Primate’s Memoir. He lives in San Francisco.

ALSO BY ROBERT M. SAPOLSKY
A Primate’s Memoir: Love, Death and
Baboons in East Africa

The Trouble with Testosterone and Other Essays
on the Biology of the Human Predicament

Why Zebras Don’t Get Ulcers: A Guide to Stress,
Stress-Related Diseases, and Coping

Stress, the Aging Brain, and the Mechanisms of
Neuron Death
To
l.l., k.q.
f.s.
ROBERT M. SAPOLSKY
Monkeyluv
And Other Essays on
Our Lives as Animals
AUTHOR’S NOTE

The articles included in this volume appeared in various magazines, as noted in the table of contents. In some cases, articles appear here in slightly different form than originally published, and, in all cases, the text has been supplemented with “Notes and Further Reading.”

PART I
Genes and Who We Are
Introduction

IF YOUR CAR breaks down, we all know the best way to fix it—you don’t find someone skilled at doing an exorcism rite over the engine. Instead, you find someone knowledgeable who can take the engine apart, find the tiny piece that is the problem, fix or replace it, and put the whole thing back together.

If a violent crime occurs, with the perpetrator a mystery, we all know a good way to figure out what happened—you don’t take a suspect, set fire to him at the stake, and if he burns to a crisp, conclude that that’s a sign he was guilty. Instead, you take the mysterious event apart, find a witness who observed steps A through C, another who saw C through E, and so on, to piece together the whole picture of what happened.

And if your body breaks down, we know the drill as well—you don’t sacrifice a cow to appease the spirit of the cousin who died while you owed her money. You get an expert who takes the illness apart and finds the tiny piece that is out of whack—the virus or bacteria, for example—and then fixes it.

The “solve a big problem by finding the itty-bitty thing that’s buggered and fix it” approach is called reductionism—if you want to understand a complex system, break it into its component parts. Reductive thinking has dominated Western science for centuries, helped drag the West out of the quagmire of the Middle Ages.

Reductionism can be a great thing. Having been a kid early in the Jonas Salk era, I’m mighty glad I got a fine product of reductive science, namely his vaccine (or maybe it was Albert Sabin’s—let’s not even go there), instead of having my pediatrician do a ceremony over me with some fetish gewgaw and goat innards to please the Polio Dybbuk. Reductive medical approaches have gotten us vaccines, drugs that block the precise step in the replication of a virus, have identified the precise piece of us that is broken in a variety of diseases. Our life expectancy has been extended to remarkable extents over the last century thanks to reductionism.

So if you want to understand the biology of who we are, of our normal and abnormal behaviors, the reductive approach gives you a pretty clear game plan. Understand the individuals who make up a society. Understand the organs that make up those individuals. Understand the cells that make up those organs. And way down at the foundations of the whole edifice, understand the genes that instruct those cells what to do. This approach gave rise to an orgy of reductive optimism in the form of the most expensive research project in the history of the life sciences, namely the sequencing of the human genome.

So genes seem to be pretty fundamental reductive building blocks of biology, including the biology of behavior. What does it mean to most people to say that a behavior “is genetic”?

That the behavior is innate, instinctual.

That the behavior is going to happen no matter what you do.

That (if you’re operating in a public policy realm) you shouldn’t bother wasting resources trying to prevent that behavior, because it’s inevitable.

That (if you’re a bit outdated about what evolution is about) the behavior is somehow adaptive, has some reason why it is actually a good and useful thing, reflects some sort of wisdom of nature, how an “is” is actually a “should be.”

The first third of this book considers what genes have to do with behavior, with who we are. And you might already see where I’m heading, which is to debunk the ideas just listed, to show how little genes often have to do with the biology of who we are.

In the first essay, I consider what genes might have to do with one of the most important issues facing our troubled planet—explaining who gets into People magazine’s special issue on the fifty most beautiful people in the world. As will be seen, there is a tragic paucity of good research in this area; I’ll consider this book to have served its purpose if the first essay inspires even a single young scientist to tackle this daunting question.

The second essay, “A Gene for Nothing,” introduces the reader to what genes actually do. As will be seen, you can’t begin to understand the functions of genes without appreciating how the environment regulates those genes. Essay three, “Genetic Hyping,” takes this theme in a different direction. One of the most important concepts in all of biology is that you can’t really ever state what the effect is of a particular gene, or what the effect is of a particular environment. You can only consider how a particular gene and particular environment interact. “Gene/environment” interactions are so important that you can’t be taught the biologist secret handshake until you use the phrase in conversation at least once a day. And like any concept that is that ubiquitous and foundational, it winds up getting ignored in all sorts of settings. Essay three tries to counter this, reviewing a study showing that imperceptibly subtle differences in environment can utterly change the effects of genes on behavior. Essay five, “Of Mice and (Hu)Men Genes,” considers gene/environment interactions in fetal and early postnatal life and how they affect adult behavior, including in humans.

Amid all this gene-bashing, essay four, “The Genetic War between Men and Women,” reviews a realm in which genes have some major effects on the development of brains, bodies, and behavior. In this case, the main point is that these genes are some of the weirdest ever uncovered, ones that violate all sorts of cherished beliefs in genetics. What is strangest is that they make perfect sense as soon as one recognizes that throughout evolution, there has been a genetic war going on between females and males, including human females and males. Warning: this essay does not make pleasant wedding-night reading.

Finally, essay six, “Antlers of Clay,” returns to the foibles of relationships between the sexes. In species in which males and females go their separate ways after mating, all a female gets from a male are the genes contained in his sperm. The essay reviews how in many of these species males have evolved ways to advertise to females that they’d be great to mate with because of what terrific genes they have. And what females have evolved are ways to figure out if the guy is actually telling the truth. As we’ll see, amid these intersexual battles over truth in advertising, genes may be getting a lot more credit than they deserve.

Nature or Nurture? “The 50 Most Beautiful People in the World” Assess the Source of Their Good Looks

AS A SCIENTIST doing scads of important research, I am busy, very busy. What with all those midnight experiments in the lab, all that eureka-ing, I hardly have any time to read the journals. Nonetheless, I stopped everything to thoroughly study the May 10, 1999, issue of People magazine, the special double issue, “The 50 Most Beautiful People in the World.” It was fabulous. In addition to the full-color spreads and helpful grooming tips, the editors of People have gone after one of the central, pressing issues of our time. “Nature or nurture?” they ask on the opening page, as in, What gets you in our special issue? “About beauty, the arguments can be endless” (P. Mag. [1999] 51, 81). Best of all, the write-ups on each of the fifty contain some thoughts from the Chosen Ones or from members of their entourage (significant other, mom, hairdresser …) as to whether their celebrated states are a product of genes or environment.

Now, one should hardly be surprised at the range of answers that would come from a group that includes both a seventeen-year-old singer named Britney Spears and Tom Brokaw. What was striking, though, and, frankly, disappointing to this reporter was that our Fifty Most Beautiful and their inner circles harbor some rather militant ideologues in the realm of the nature/nurture debate.

Consider first the extreme environmentalists, who reject the notion of anything being biologically fixed, with everything, instead, infinitely malleable with the right environmental intervention. There’s Ben Affleck, newly arrived on the movie scene in the last few years, who discusses the impact of his pumping iron and getting his teeth capped. “Oh my God, you are a movie star!” one of his advisers is reported to have gushed in response to the dentistry (P. Mag. [1999] 51, 105). Mr. Affleck is clearly a disciple of John Watson, famous for the behaviorist/environmentalist credo, “Give me a child and let me control the total environment in which he is raised, and I will turn him into whatever I wish.” It is unclear whether Mr. Watson’s environmentalist hegemony included turning people into the Fifty Most with cosmetic dentistry, but a torch appears to have been passed to young Mr. Affleck. Thus, it hardly becomes surprising that Mr. Affleck’s much celebrated affair with Gwyneth Paltrow, clearly of the genetic determinist school (see below), was so short-lived.

A strongly environmentalist viewpoint is also advanced by one Jenna Elfman, apparently a successful television star, who attributes her beauty to drinking one hundred ounces of water a day, following the teachings of a book that prescribes diets based on your blood type, and religiously making use of a moisturizer that costs $1,000 a pound. However, even a neophyte in the studies of human developmental biology and anatomy could quickly note that no amount of said moisturizer would result in the inclusion on People’s list of Walter Matthau or, say, me.

Then there is Jaclyn Smith, having moved into the stage of life where People mostly exclaims over the extent to which she still looks like the Charlie’s Angel that she once was, explaining how her beauty has been preserved with good habits—not smoking, drinking, or doing drugs. This seems reasonable, until one reflects that that salutary nurturing of her self couldn’t quite be the whole story, since no similarly ascetic Amish appears on the list of fifty. (A close friend of Ms. Smith’s countered that her beauty is, in fact, maintained by her “humor, honesty, and unpretentiousness” [P. Mag. (1999) 51, 98], which left this reporter sincerely confused as to whether that should count as nature, nurture, or what.)

Perhaps the most extreme stance of this band is advanced by the actress Sandra Bullock, claiming that her beauty is all “smoke and mirrors” (P. Mag. [1999] 51, 81), a viewpoint that aligns her squarely with the Lysenkoism of the Soviet wheat experiments of the 1930s. One need merely to examine her work—for example, the scene in which she first takes the wheel of the bus in Speed—to detect the undercurrents of this radicalism in her oeuvre.

Naturally, similarly fringe opinions are coming from the opposing ideological faction, namely the genetic determinists among the Most Beautiful. Perhaps the brashest of this school is Josh Brolin, an actor whose statement would seem inflammatory to middle-of-the-roaders, but which could readily serve as a manifesto at the barricades for his cadre—“I was given my dad’s good genes” (P. Mag. [1999] 51, 171). Similar sentiments come from the grandfather of the aforementioned Paltrow—“She was beautiful from the beginning” (P. Mag. [1999] 51, 169). Ah, young Brolin and Paltrow, an environmentalist adversary might counter, but what if your genetic destiny had encountered a good case of rickets or cowpox along the way, what magazine would you now be gracing?

The epitome of the natalist program, in which genetics is seen to form an imperative trajectory that is impervious to environmental manipulation, festers in the case of TV host Meredith Vieira. One is first told of various disasters that have befallen her—shoddy makeup application, an impetuous and unfortunate peroxide job on her hair—and yet, and yet, it doesn’t matter; at each juncture, she is still beautiful because of her “phenomenal genes” (P. Mag. [1999] 51, 158). This reader, for one, blanched at the boldness of this analysis.

Finally, we consider Andrea Casiraghi, he of the Grimaldis of Monaco, grandson of Grace Kelly. Amid the wonderment at his lovely complexion and classically sculpted cheekbones, the word comes out—“thoroughbred.” Thoroughbred. Oh, could it be so long before his advocates are pushing the eugenics programs that darkened our past? One searches the pages for a middle ground, for the interdisciplinary synthesist who would perceive the contributions of nature and nurture. Hope emerges with seventeen-year-old Jessica Biel, an actress celebrated for her skin, judiciously attributing it to her Choctaw blood plus getting regular facials with Oil of Olay.

And at last, one encounters one of the Chosen whose camp incorporates the most modern, most sophisticated and integrative insights concerning the nature/nurture conundrum, namely the idea that there is an interaction between genes and environment. For this, we consider a singer named Monica, who, despite lacking a last name, is not only one of the Most Beautiful People in the World, but apparently also one of the most important, because of the fame of an album of hers entitled The Boy Is Mine (a work unfamiliar to this reporter, whose association with popular culture ended somewhere around Janis Joplin). We are first informed about her wondrous skill at applying makeup and its role in gaining her acceptance into the Chambers of the Fifty. This, at first, seems like just more environmentalist agitprop. But then one asks, And where does she get this cosmetic aptitude from? Her mother supplies the answer: with Monica, “it’s something that’s inborn” (P. Mag. [1999] 51, 146).

One’s breath is taken away at this incisive wisdom: a genetic influence on how one interacts with the environment. Too bad a few more people can’t think this way when figuring out what genes have to do with, say, intelligence, or substance abuse, or violence.

At the end of each piece, I’ll bring the reader up-to-date on any recent developments in the subject, reference the contents, and point to further readings.

This article, naturally, has become dreadfully obsolete, as is and should be the case with any such piece of investigative reporting by People magazine. Since that time, the fortunes of The Fifty Select have shifted. Ms. Elfman, I’ve dimly noted, seems to have appeared in a number of movies that tanked badly. Meanwhile, Mr. Affleck managed to spend at least two fifteen-minute blocks of fame as one-half of the world’s most incandescently important couple, one so important that it even prompted the coining of a new word to describe it. Sadly, as a measure of his eclipse, current news (6/10/04) has been dominated by the revelation that J. Lo, at least this week, is married to someone else. And Ms. Spears, who only a few short years ago still had to be identified as “a singer,” no longer needs an introduction for most readers; however, just around the time of career where most personal handlers would be convincing her that it’s time for an image-burnishing trip to a Sudanese refugee camp as a special UN envoy, she is instead neurobiology’s greatest teaching tool for demonstrating that the frontal cortex of the brain does not fully come online until around age thirty. As for what’s happening with most of the rest of the Legion of the Select, I haven’t a clue, not having had any idea who they were in the first place.

Lysenkoism—for those who haven’t specialized in the “Embarrassing Chapter of Science” category of Jeopardy!—was a movement that dominated Soviet genetics for some decades. Named for the marginal geneticist Lysenko, it was an extreme environmentalist viewpoint in which organisms can inherit acquired traits (for example, be Caucasian and spend enough time in the tropics to get darkly tanned skin, and your offspring will be born with the same dark skin). This thinking was very much in line with Soviet environmental optimism, but didn’t have the slightest shred of science supporting it, having been discredited before Darwin’s time. This didn’t prevent Lysenko from gaining vast influence over Stalin and agricultural planning. A bizarre episode in science that would just leave one shaking one’s head in bemusement if Lysenkoism hadn’t played a role in the death by starvation of vast numbers of Soviet citizens.

Further reading: the issue of People magazine cited above, of course, and as long as we’re at it, the entire collection of People magazines. And for the best read on the science of this piece, see Matt Ridley’s Nature via Nurture: Genes, Experience, & What Makes Us Human (New York: HarperCollins, 2003).

A Gene for Nothing

REMEMBER DOLLY THE Sheep, the first mammal cloned from adult cells, in 1996? She was lovely, really an inspiration. She endured endless state dinners at the White House, all grace and cordiality. Then there was her triumphant ticker-tape parade down Broadway that won over even the most hardened New Yorker. Her appearances in those ubiquitous billboard ads for Guess? jeans (jeans, genes—get it? Those advertising guys are just awesome sometimes). Roller-blading at Disneyland for charity with the cast from Friends. Throughout the media circus, she was poised, patient, even-tempered, the epitome of what we look for in a celebrity and role model.

And despite that charm, people kept saying mean things about Dolly. Heads of state, religious leaders, editorialists, fell over themselves shortly after her debut to call her an aberration of nature, an insult to the sacred biological wonder of reproduction, something that should never remotely be considered in a human.

What was everyone so upset about? Some possibilities come to mind: (a) The Dolly Sheep/Dolly Parton connection unsettled everyone in a way that they just couldn’t quite put their finger on. (b) Because the cloning technology that gave rise to Dolly could be extended to humans, we face the potential of droves of clones of someone running around, all with the exact same liver function. (c) Thanks to that technology, we might wind up with a bunch of clones who have the same brain.

Sure, the first two possibilities are creepy. But the dis-ease prompted by Dolly was overwhelmingly, remains overwhelmingly, about the third option. The same brain, the same neurons, the same genes directing those neurons, one multibodied consciousness among the clones, a mind meld, an army of photocopies of the same soul.

In actuality, people have known that this is not really the case ever since scientists discovered identical twins. Such individuals constitute genetic clones, just like Dolly and her mother (what was her name? Why does she get shortchanged in the media?), from whom that original cell was taken. Despite all those breathless stories about identical twins separated at birth who share all sorts of traits, like flushing the toilet before using it, twins do not have mind melds, do not behave identically. As one important example, if an identical twin is schizophrenic, the sibling, with the identical “schizophrenia gene(s),” has only about a 50 percent chance of having the disease. A similar finding comes from a fascinating experiment by Dan Weinberger of the National Institute of Mental Health. Give identical twins a puzzle to solve, and they might come up with answers that are more similar than one would expect from a pair of strangers. Hook those individuals up during the puzzle-solving to a brain-imaging instrument that visualizes metabolic demands in different regions of the brain, and the pattern of activation in the pair can differ dramatically, despite the same solution. Or get yourself some brains from identical twins. I don’t mean pictures from a brain scanner. Get the real, squishy stuff, postmortem brains. Slice ’em, dice ’em, examine them with every kind of microscope, and every obsessive measure—the numbers of neurons in particular brain regions, the complexity of the branching cables coming out of those neurons, the numbers of connections among those neurons—and they all differ. Same genes, different brains.

The careful editorialists pointed this out about Dolly (and instead, some of the most disturbing issues about cloning raised by Dolly center on the possibilities of generating life simply for the purpose of banking away transplant-compatible tissues). Nonetheless, that business about identical genes supposedly producing identical brains tugs at a lot of people. And other gene/behavior stories keep getting propelled to the front pages of newspapers. One popped up shortly before Dolly with the report, headed by a Stanford team, of a single gene, called fru, that determines the sexual behavior of male fruit flies. Courtship, opening lines, foreplay, whom they come on to—the works. Mutate that gene and, get this, you can even change the sexual orientation of the fly. And that wasn’t front-page news because of our insatiable fly voyeurism. “Could our sexual behaviors be determined by a single gene as well?” every article asked. And a bit earlier, there was the hubbub about the isolation of a gene related to anxiety, and before that, one for risk-taking behavior, and a while before that, the splash about another gene, whose mutation in one family was associated with their violent antisocial behavior, and then before that …

Why do these command attention? For many, genes and the DNA that comprises genes represent the holy grail of biology, the code of codes (two phrases often used in lay-public discussions of genetics). The worship at the altar of the gene rests on two assumptions. The first concerns the autonomy of genetic regulation. This is a notion that biological information begins with genes and flows outward and upward. DNA as the alpha, the initiator, the commander, the epicenter from which biology emanates. Nobody tells a gene what to do. It’s always the other way around. The second assumption is that when genes give a command, biological systems listen. In that view, genes instruct your cells as to their structure and function. And when those cells are neurons, those functions include thought and feelings and behavior. And thus we are finally identifying the biological factors, so this thinking goes, that make us do what we do.

This view was put forward in a lead piece in the The New Yorker by a literature professor named Louis Menand. Mr. Menand ruminated on those anxiety genes, when “one little gene is firing off a signal to bite your fingernails” (the first assumption about the autonomy of genes, firing off whenever some notion pops into their head). He considers what this does to our explanatory systems. How do we reconcile societal, economic, psychological explanations of behavior with those ironclad genes? “The view that behavior is determined by an inherited genetic package”—the second assumption, genes as irresistible commanders—“is not easily reconciled with the view that behavior is determined by the kinds of movies a person watches.” And what is the solution? “It is like having the Greek gods and the Inca gods occupying the same pantheon. Somebody’s got to go.”

In other words, if you buy into genes firing off and determining our behaviors, such modern scientific findings are simply incompatible with the environment having an influence. Sumpin’s gotta go.

Now, I’m not quite sure what sort of genetics they teach in Mr. Menand’s English department, but the sumpin’s-gotta-go loggerhead is what most behavioral biologists have been trying to unteach for decades. Apparently with only limited success. Which is why it’s worth another try.

Okay. You’ve got nature—neurons, brain chemicals, hormones, and, of course, at the bottom of the cereal box, genes. And then there’s nurture, all those environmental breezes gusting about. And the biggest cliché in this field is how it is meaningless to talk about nature or nurture, only about their interaction. And somehow, that truism rarely sticks. Instead, somebody’s got to go, and when a new gene is trotted out that when “firing off,” “determines” a behavior, environmental influences are inevitably seen as something irrelevant that have to go. And soon, poor sweet Dolly became a menace to our autonomy as individuals, and there are perceived to be genes that control whom you go to bed with and whether you feel anxious about it.

Let’s try to undo the notion of genes as neurobiological and behavioral destiny by examining those two assumptions. Let’s begin with the second one, the notion that genes equal inevitability, generate commands that drive the function of cells, including those in our head. What exactly do genes do? A gene, a stretch of DNA, does not produce a behavior. Or an emotion, or even a fleeting thought. It produces a protein, where a specific DNA sequence that constitutes a gene codes for a specific type of protein. Now, some of these proteins certainly have lots to do with behavior and feelings and thoughts. Proteins include some hormones and neurotransmitters (chemical messengers between neurons), the receptors that receive hormonal and neurotransmitter messages, the enzymes that synthesize and degrade those messengers, many of the intracellular messengers triggered by those hormones, and so on. All vital for a brain to do its business. But the key is that it is extremely rare that things like hormones and neurotransmitters cause a behavior. Instead, they produce tendencies to respond to the environment in certain ways.

This is critical. Let’s consider anxiety. When an organism is confronted with some sort of threat, it typically becomes vigilant, searches to gain information about the nature of the threat, struggles to find an effective coping response. And once a signal indicates safety—the lion has been evaded, the traffic cop buys the explanation and doesn’t issue a ticket—the organism can relax. But this is not what occurs in an anxious individual. Instead, there is a frantic skittering among coping responses—abruptly shifting from one to another without checking whether anything has worked, an agitated attempt to cover all the bases and attempt a variety of responses simultaneously. Or there is an inability to detect when the safety signal occurs, and the restless vigilance keeps going. By definition, anxiety makes little sense outside the context of what the environment is doing to an individual. In that framework, the brain chemicals and, ultimately, the genes relevant to anxiety don’t make you anxious. They make you more responsive to anxiety-provoking situations, make it harder to detect safety signals in the environment.

The same theme continues in other realms of our behaviors as well. The exciting (made-of-protein) receptor that seems to have something to do with novelty-seeking behavior doesn’t actually make you seek novelty. It makes you more excitable in response to a novel environment than the folks without that receptor variant. And those (genetically influenced) neurochemical abnormalities of depression don’t make you depressed. They make you more vulnerable to stressors in the environment, to deciding that you are helpless in circumstances where you are not (this particular point will be returned to in detail in essay five). Over and over it’s the same theme.

One may retort that, in the long run, we are all exposed to anxiety-provoking circumstances, all exposed to the depressing world around us. If we are all exposed to those same environmental factors, yet it is only the people who are genetically prone toward, say, depression who get depressed, that is a pretty powerful vote for genes. In that scenario, the “genes don’t cause things, they just make you more sensitive to the environment” becomes empty and semantic.

The problems there, however, are twofold. First, not everyone who has a genetic legacy of depression gets depressed (only about 50 percent—the same punch line as for individuals with a genetic legacy of schizophrenia), and not everyone who has a major depression has a genetic legacy for it. Genetic status is not all that predictive, in and of itself.

Second, only on a superficial level do we share the same environments. For example, the incidence of the genes related to depression is probably roughly equal throughout the world. However, geriatric depression is epidemic in our society and virtually nonexistent in traditional societies in the developing world. Why? Remarkably different environments in different societies, in which old age can mean being a powerful village elder or an infantilized has-been put out to a shuffleboard pasture. Or the environmental differences can be more subtle. Periods of psychological stress involving loss of control and predictability during childhood are recognized to predispose toward adult depression. Two children may have had similar childhood lessons in “there’s bad things out there that I can’t control”—both may have seen their parents divorce, lost a grandparent, tearfully buried a pet in the backyard, experienced a bully who got away with endlessly menacing them. Yet the temporal patterning of their two experiences is unlikely to be identical, and the child who experiences all those stressors over one year instead of over six years is far more likely to come with the cognitive distortion “There’re bad things out there that I can’t control, and in fact, I can’t control anything” that sets you up for depression. The biological factors coded for by genes in the nervous system don’t typically determine behavior. Instead, they influence the way you respond to the environment, and those environmental influences can be extremely subtle. Genetic vulnerabilities, tendencies, predispositions, biases. … but rarely genetic inevitabilities.

It’s also important to realize the inaccuracy of the first assumption about behavioral genetics, the notion of genes as autonomous initiators of commands, as having minds of their own. To see the fallacy of this, it’s time to look at two startling facts about the structure of genes, because they blow that assumption out of the water and bring environmentalism back into this arena big-time.

A chromosome is made of DNA, a vastly long string of it, a long sequence of letters coding for genetic information. People used to think that the first eleventy letters of the DNA message would comprise Gene 1. A special letter sequence signaled the end of that gene, and then the next eleventy and a half letters coded for Gene 2, and so on, through tens of thousands of genes. And in the pancreas, Gene 1 might specify the construction of insulin, and in your eyes, Gene 2 might specify protein pigments that give eyes their color, and Gene 3, active in neurons, might make you aggressive. Ah, caught you: might make you more sensitive to aggression-provoking stimuli in the environment. Different people would have different versions of Genes 1, 2, 3, and some versions worked better than others, were more evolutionarily adaptive. The final broad feature was that an army of biochemicals would do the scut work, transcribing the genes, reading the DNA sequences, and thus following the instructions as to how, eventually, to construct the appropriate proteins. Sure, we would torture our students with an entire year’s worth of trivial details about that transcription process, but the basic picture suffices.

Except that that’s not really how things work. The real picture, while different, does not initially seem earth-shattering. Instead of one gene coming immediately after another and all of that vast string of DNA devoted entirely to coding for different proteins, long stretches of DNA don’t get transcribed. Sometimes those stretches even split up a gene into subsections. Nontranscribed, noncoding DNA. What’s it for? Some of it doesn’t seem to do anything. “Junk DNA,” long, repetitious sequences of meaningless gibberish. But some of that noncoding DNA does something interesting indeed. It’s the instruction manual for how and when to activate those genes. These stretches have a variety of names—regulatory elements, promoters, repressors, responsive elements. And different biochemical messengers bind to those regulatory elements and thereby alter the activity of the gene immediately “downstream”—immediately following in the string of DNA.

Aha, the death of the gene as the autonomous source of information, as having a mind of its own. Instead, other factors regulate when and how genes function. And what regulates this genetic activity? Often the environment.

A first example of how that might work. Suppose something stressful happens to some primate. There’s a drought and not much to eat, forcing the animal to forage miles each day for food. As a result, it secretes stress hormones from its adrenals called glucocorticoids. Among other things, glucocorticoid molecules enter fat cells, bind to glucocorticoid receptors. These hormone/receptor complexes then find their way to the DNA and bind to a particular regulatory stretch of DNA, one of those operating instructions. As a result, a gene downstream is activated, which produces a protein that, indirectly, inhibits that fat cell from storing fat. A logical thing to do—while that primate is starving and walking the grasslands in search of a meal, this is the time to divert energy to working muscles, not to fat cells.

This constitutes a cleverly adaptive mechanism by which the environment triggers a genetic response that modifies metabolism. This is a very different scenario for thinking about where information originates in these cascades. In effect, these regulatory elements introduce the possibility of environmentally modulated if/then clauses: if the environment is tough and you’re working hard to find food, then make use of your genes to divert energy to exercising muscle. And if a human refugee wanders miles from home with insufficient food because of civil strife, then the same is probably occurring—the behavior of one human, the sort of environment that that individual generates, can change the pattern of gene activity in another person.

Let’s get a fancier example of how these regulatory elements of DNA are controlled by environmental factors. Suppose that Gene 4037 (a gene that has a real name, but I’ll spare you the jargon), when left to its own devices, is transcriptionally active, generating the protein that it codes for. However, a regulatory element comes just before 4037 in the DNA string, and typically a particular messenger binds to the regulatory element, shutting down Gene 4037. Fine. How about the following: That inhibitory messenger is sensitive to temperature. In fact, if the cell gets hot, that messenger goes to pieces, unwinds, and comes floating off the regulatory element. What happens? Freed from the inhibitory regulation, Gene 4037 suddenly becomes active. Maybe it’s a gene that works in the kidney and codes for a protein relevant to water retention. Boring—another metabolic story, this one having to do with how a warm environment triggers a metabolic adaptation that staves off dehydration. But suppose, instead, Gene 4037 codes for an array of proteins that have something to do with sexual behavior. What have you just invented? Seasonal mating. Winter is waning, each day gets a little warmer, and in relevant cells in the brain, pituitary, or gonads, genes like 4037 are gradually becoming active. Finally, some threshold is passed, and wham, everyone starts rutting and ovulating, snorting and pawing at the ground, and generally carrying on. If it is the right time of year, then use those genes to increase the likelihood of mating. (Actually, in most seasonal maters, the environmental signal for mating is the amount of daily light exposure—the days are getting longer—rather than temperature—the days are getting warmer. But the principle is the same.)