† According to Freud’s theory of the Oedipus complex, a boy’s greatest anxiety is that his father will castrate him as punishment for sexually desiring his mother, and a girl’s greatest anxiety is generated by her envy of the penis she lacks. This was largely derived from Freud’s own recollection of, as he wrote Fliess, “being in love with my mother and jealous of my father.”
‡ James Strachey, a British psychoanalyst and translator of Freud’s works, speculated that Freud’s linking of childbirth and anxiety dated to the early 1880s, when, while working as a physician, he heard secondhand about a midwife who had declared that there is a lifelong connection between birth and being frightened.
§ Rank believed the birth trauma explained everything—from territorial conquests like Alexander the Great’s (motivated by an “attempt to gain sole possession of the mother” from the father) to revolutions like the French (an attempt to overthrow “masculine dominance” and return to the mother) to phobia of animals (“a rationalization … of the wish—through the desire to be eaten—to get back again into the mother’s womb”) to the apostles’ dedication to Jesus Christ (“they could see in him one who had overcome the birth trauma”). Some of Freud’s later disciples would denounce Rank, not without reason, as insane.
‖ Most animals emerge from the uterus or the egg dependent to some extent on parental care for their survival, but the majority of them are relatively less dependent than humans are at birth.
a Freud did retain for psychoanalysis some interpretative élan by positing that childhood phobias become overly severe or persist into adulthood only when they become the outer fears (of rats or heights or darkness or thunder or open spaces—or mayonnaise, a noted phobia in the literature) onto which inner psychic conflicts get projected. Phobias, in this view, are the outward symbolic representations of the threats that the id (with its wanton impulses that must be repressed) and the superego (with its strict demands of conscience and morality) place on the ego.
b Robert Karen observes that almost everything Bowlby wrote about the needs of young children throughout his long career “could be seen as an indictment of the type of upbringing to which he’d been subjected.”
c Born in Vienna and trained as a nursery school teacher, Klein would go on, after the end of an unhappy marriage, to be psychoanalyzed by two of Freud’s closest disciples, Sándor Ferenczi and Karl Abraham, and then herself to become one of Freud’s most important followers and interpreters. In 1926, Klein, forty-four years old, moved to London, where she was exalted by Ernest Jones, the head of the British Psychoanalytic Society and the most ardent protector of Freud’s legacy. Klein’s arrival in London—and in particular her disagreements with Freud’s daughter Anna Freud over the analysis and treatment of children—precipitated a rift in the society between the Kleinians and the (Anna) Freudians that would last through World War II.
d In his initial work on hysteria, in the early 1890s, Freud had argued that adult neuroses were the product of actual early childhood traumas, mostly of a sexual nature—but by 1897 he had revised his view to support his emerging notion of the Oedipus complex, arguing now that adult neuroses were the result of repressed childhood fantasies about having sex with the opposite-sex parent and murdering the same-sex parent. Adults without neuroses were those who had successfully worked through their Oedipus complexes; adults with neuroses were those who hadn’t.
e Adult romantic relationships among those with ambivalent attachment styles tend to be characterized by clinginess and fear of abandonment.
f Adult avoidants tend to shun close relationships and are often workaholics; just as they preferred their toys to their mothers as children, they prefer work to family as adults. (Though those with avoidant attachment styles appear to be less anxious than those with ambivalent attachment styles, Bowlby came to believe that was not the case; a series of studies beginning in the 1970s have demonstrated that during separations the avoidant children exhibited increased levels of physiological arousal—elevated heart rates, increased excretion of stress hormones in the bloodstream, and so forth—of the sort associated with anxiety. The child seems to be feeling a physically manifested distress, but he is able—adaptively, or not—to suppress visible expression of the emotion.)
g As a result of Bowlby and Ainsworth’s influence, by the 1980s the psychology departments of American universities were thickly populated with attachment scholars.
h Despite what Freud wrote late in his life about the evolutionary roots of phobic anxiety, his conversion to this line of thinking came too late to influence his followers, who were now spreading the gospel of psychoanalysis around the globe. Through at least World War II, psychoanalytic theorists still viewed castration fears, the repressive superego, and the sublimated death instincts as the “cornerstones”—in Bowlby’s word—of anxiety. (Bowlby believed that if Freud had had a fuller understanding of Darwin’s work, psychoanalysis would have more convincingly incorporated biological principles into its corpus.)
i When Bowlby made a series of presentations, “The Nature of the Child’s Tie to His Mother,” to his colleagues in the British Psychoanalytic Society in the late 1950s, he tried to place himself and his work squarely within the Freudian tradition. The reactions against him were harsh. “What’s the use to psychoanalyze a goose?” the psychoanalyst Hanna Segal would later ask (channeling Ogden Nash), mocking Bowlby’s resort to ethology. “An infant can’t follow its mother; it isn’t a duckling,” another analyst said dismissively.
j There were other parallels between the monkeys’ behavior and what Bowlby had observed in human babies. When Harlow introduced a new object into their cages, the monkeys would rush to the cloth mother in agitation and rub up against it until they felt soothed; after they calmed down, they would begin to investigate and play with the object, using the cloth mother as—to invoke the phrase that Bowlby and Ainsworth would soon be using—“a secure base.”
k As so often seems to be the case across the history of psychology, Harlow was unable to apply to his own life what he learned from his research on parent-child relationships: he died alcoholic and depressed, estranged from his children.
l Related research on rodents finds the same thing: the amount of licking and grooming that a mother rat lavishes on her pups has a powerful effect on the pups’ tolerance for stress throughout their lifetimes—the more licking and grooming a rat receives as a pup, the more resistant to stress it will be as an adult. The rats who receive extra maternal licking display reduced autonomic nervous system activity—a diminished level of activity in the hypothalamic-pituitary-adrenal axis—and a concomitant increased tolerance for stress. These well-licked rats have what researchers call an “augmented ‘off’ switch” for the stress response; after just four days of extra maternal licking, they show reduced activity in the amygdala. In contrast, those rats that receive low levels of maternal grooming exhibit an exaggerated stress response.
These effects can be adaptive even when they might seem to be negative. Rats who as pups received low levels of grooming and licking are more fearful and quicker to learn to avoid frightening environments—a useful adaptation in a harsh or dangerous environment. In fact, that dangerous environment may, in the state of nature, have been what produced the low levels of licking and grooming in the first place, as the mothers were focused on finding food or avoiding external threats rather than on lavishing affection on their children. Rats who receive high levels of maternal affection are less fearful, more adventurous, and slower to learn to avoid threats—useful adaptations in a stable environment but liabilities in a dangerous one.
m Neuroscience research has begun to find suggestive evidence for the specific mechanisms by which early life stress generates later psychopathology. In essence, elevated levels of stress hormones in childhood correlate with adverse effects on the brain’s serotonin and dopamine systems, which are strongly implicated in clinical anxiety and depression. Neuroimaging studies also show that protracted childhood stress tend
s to have what scientists call neuropathological consequences: for instance, the hippocampus, a part of the brain crucial to creating new memories, shrinks.
n The exception was specific animal phobias, which Bowlby, like Freud, believed came from evolutionary adaptations gone awry.
CHAPTER 9
Worriers and Warriors: The Genetics of Anxiety
The manner and conditions of mind are transmitted to the children through the seed.
—HIPPOCRATES (FOURTH CENTURY B.C.)
Such as the temperature of the father is, such is the son’s, and look what disease the father had when he begot him, his son will have after him. I need not therefore make any doubt of melancholy, but that it is an hereditary disease.
—ROBERT BURTON, The Anatomy of Melancholy (1621)
Daddy, I’m nervous.
—MY DAUGHTER, AT AGE EIGHT
I could blithely blame my anxiety on the behavior of my parents—my father’s drinking, my mother’s overprotectiveness and phobias, their unhappy marriage and eventual divorce—were it not for, among other reasons, this inconvenient fact: my children, now nine and six, have recently developed anxiety that, to a distressing degree, parallels my own.
My daughter, Maren, has always had, like me, an inhibited temperament—shy and withdrawing in unfamiliar situations, risk averse in her approach to the world, and highly reactive to stress or any kind of novelty. More strikingly, when she was in first grade she developed an obsessive phobia of vomiting. When a classmate of hers threw up during math, she couldn’t get the image out of her head. “I can’t stop thinking bad thoughts,” she said, and my heart broke.
Have I—despite my decades of therapy, my hard-won personal and scholarly knowledge of anxiety, my wife’s and my informed efforts at inoculating our children against it—bequeathed to Maren my disorder, as my mother bequeathed it to me?
Unlike my mother, I never revealed my emetophobia to my daughter before she developed it herself. I have tried not to betray evidence of my anxiety to Maren, knowing that to do so might be to pass it on to her through what psychologists call modeling behavior. My wife is not an anxious person; she has none of the nervously overprotective tendencies that, expressed for so many years by my mother, I had thought reduced my sister and me to such states of neurotic dependency. And we are both, my wife and I, loving and nurturing, and we strive to be emotionally present for our kids in ways that my parents sometimes were not.
Or so we like to think.
And yet here is my daughter exhibiting symptoms very similar to mine and at almost the same age I first developed them. Somehow, despite our best efforts at providing emotional prophylaxis, Maren seems to have inherited my nervous temperament—and, remarkably, the exact same phobic preoccupation. Which happens to be, moreover, a preoccupation I share with my mother.
Is it possible, my wife asks, that so idiosyncratic a phobia can be genetically transmitted?
One would think not. And yet we have here the evidence of three generations on my mother’s side with the same phobia. And unless Maren has picked up on subtle or unconscious cues (which, I concede, is possible), she cannot have “learned” the phobia from me through some kind of behavioral conditioning, as I thought I might have learned mine from my mother.
While observers since Hippocrates have noted that temperaments are heritable, and while the modern field of behavioral genetics is revealing with increasing precision—down to the individual nucleotide—the relationship between the molecules we inherit and the emotions we’re predisposed to, no one has yet identified a gene, or even a set of genes, for emetophobia. Nor, for that matter, has anyone reduced anxiety—or any behavioral trait—to pure genetics. But in recent years, thousands of studies have pointed to various genetic bases for clinical anxiety in its different forms.
Some of the earliest research on the genetics of anxiety studied twins. In the most basic studies, researchers compared rates of anxiety disorder between sets of identical and fraternal twins. If, say, panic disorder were completely genetic, that would mean in a set of identical twins—genetic copies—you would never find just one with the disease. But that’s not the case. When one twin has the disorder, the other is much more likely than a randomly selected person from the population to have the disease—but not guaranteed to have it. This suggests that while panic disorder—like height or eye color—has a powerful genetic component, the disease is not completely genetic.
In 2001, Kenneth Kendler, a psychiatrist at Virginia Commonwealth University, compared the rates of phobic disorders among twelve hundred sets of fraternal and identical twins, determining that genes account for about 30 percent of the individual differences in vulnerability to anxiety disorders. Subsequent studies have tended to roughly support Kendler’s findings. Meta-analyses of genetic studies conclude that if you don’t have any close relatives with generalized anxiety disorder, your odds of having it yourself are less than one in twenty-five—but having a single close relative with the disorder boosts your odds of developing it to one in five.
Wait, you might object, this doesn’t prove a genetic basis for anxiety. Couldn’t the high probability of the same mental illness occurring in members of the same family be a result of their sharing what researchers call a pathogenic environment, one that is predictive of anxiety or depression? If twins share a traumatic upbringing, mightn’t that engender in both of them a higher susceptibility to mental illness?
Certainly. While genes may predispose a person to schizophrenia or alcoholism or anxiety, there is almost always some environmental contribution to the disease. Still, the number of studies on the heritability of anxiety is climbing into the tens of thousands, and the overwhelming conclusion of almost all of them is that your susceptibility to anxiety—both as a temperamental tendency and as a clinical disorder—is strongly determined by your genes.
This would not have surprised Hippocrates or Robert Burton or Charles Darwin or any number of observers who long predate the era of molecular genetics. Once a family tree has one or two individuals with anxiety disorder or depression, then you will likely find the rest of the tree stippled with anxiety and depression. Researchers call this phenomenon “familial aggregation due to genetic risk.”*
Does “familial aggregation” mean that my daughter, like my mother and me, is biologically predestined to be anxious, perhaps genetically fated to develop nervous illness? On my mother’s side of the family alone, there is, in addition to my mother and my daughter and me, my son, Nathaniel, now six, who has separation anxiety that threatens to become as bad as mine ever was; my sister, who has struggled since age twelve with anxiety and has tried as many drug treatments as I have; another blood relative who has similarly wrestled his whole life with anxiety and depression and a nervous stomach and who has been medicated off and on for decades; that relative’s older brother, who was diagnosed with clinical depression in the early 1980s, at the tender age of eight, and who vomited from anxiety before school nearly every day for a year; and my mother’s father, ninety-two years old, who today takes a variety of antianxiety and antidepressant medications. Looking further back into my ancestry, I have discovered that my mother’s father’s grandfather was painfully reserved and hated dealing with people, dropping out of Cornell to start a “quiet life” cultivating fruit orchards (“The outdoor life saved him,” his daughter-in-law would say later), and that my grandfather’s aunt suffered from severe anxiety, depression, and a famously nervous stomach.
And then there is my grandfather’s father Chester Hanford, whose anxiety and depression were severe enough that he had to be institutionalized multiple times, leaving him frequently incapacitated during the last thirty years of his life.
I suspect that most, but not all, of the large number of human temperaments are the result of genetic factors that contribute to the profiles of molecules and receptor densities that influence brain function.
—JEROME KAGAN, What Is Emotion? (2007)
It frequently happens
that hysteria in the mother frequently begets hysteria in the son.
—JEAN-MARTIN CHARCOT, Lectures on Diseases of the Nervous System, VOLUME 3 (1885)
Jerome Kagan, a developmental psychologist at Harvard, has spent sixty years studying the effect of heredity on human personality. In longitudinal studies extending across decades, he has consistently found that about 10 to 20 percent of infants are, from the time they are a few weeks old, demonstrably more timid than other infants. These infants are fussier, sleep more poorly, and have faster heart rates, more muscle tension, and higher levels of cortisol in their blood and of norepinephrine in their urine. They exhibit faster startle reflexes (meaning that in response to a sudden noise they twitch nanoseconds faster and show greater increases in pupil dilation). In fMRI scans, the fear circuits of their brains—namely, the amygdala and the anterior cingulate—show higher-than-normal neuronal activity. These physiological measures remain consistently higher for these children than for other children throughout their lifetimes. Whether they are tested at six weeks, seven years, fourteen years, twenty-one years, or older, they continue to have higher heart rates, faster startle reflexes, and more stress hormones than their low-reactive peers.
Kagan has labeled as inhibited the temperament of these children with high-reactive physiology. “We believe that most of the children we refer to as ‘inhibited’ belong to a qualitatively distinct category of infants who were born with a lower threshold for arousal to unexpected changes in the environment or novel events,” Kagan says. “For these children, the prepared reaction to novelty that is characteristic of all children is exaggerated.”
A few years ago, Kagan and his colleagues took brain scans of a group of twenty-one-year-olds they had been studying for nineteen years. In 1984, when Kagan had first observed these subjects as two-year-olds, he had described thirteen of them as inhibited and the other nine as uninhibited. Two decades later, when Kagan showed pictures of unfamiliar faces to all twenty-two test subjects, now young adults, the thirteen who had been identified as inhibited displayed significantly more amygdala response than the nine who had been identified as uninhibited. Kagan believes that your genes determine the reactivity of your amygdala—and we know from other research that the reactivity of your amygdala, in turn, helps determine how you will react to stress.
My Age of Anxiety: Fear, Hope, Dread, and the Search for Peace of Mind Page 32