Here, it seems, is at least a partial explanation for what the Oxford scholar Robert Burton had observed back in 1621 in The Anatomy of Melancholy: “For that which is but a flea-biting to one, causeth insufferable torment to another.”
Would finding out that I have the warrior version of the COMT gene be a relief because it would mean that I am not, after all, genetically doomed to high levels of “neuroticism” and “harm avoidance”? Or would discovering that I have, say, the long/long version of the SERT gene make me feel even worse than I already do: to be blessed with the genes for easygoingness and resilience and yet to feel so anxious and neurotic—how pathetic would that be? I’d be learning that I had somehow managed to squander a generous genetic inheritance.
In her 1937 book, The Neurotic Personality of Our Time, Karen Horney, a disciple of Freud, writes about how a standard behavioral tic of the neurotic is to reduce himself to nothing—I am such a loser, he says to himself, look at all the obstacles that impede me and the handicaps that confine me; it’s a wonder that I can function at all—in order to relieve the pressure to accomplish anything. The neurotic secretly (sometimes without even knowing it) nurtures a powerful ambition to achieve as a means of compensating for a weak sense of self-worth. But the fear of failing to accomplish, or of having his poor self-worth confirmed by manifest lack of achievement despite a sincere effort to succeed, is too unbearable to abide. So as a psychological self-defense tactic, the neurotic plays up the infirmities that ostensibly make achieving success difficult. Once these handicaps and disadvantages are established, the pressure is off: anything a neurotic accomplishes merits extra credit. And if the neurotic fails? Well, that’s what playing up all these deficits has aimed to prepare for: How could you expect anything but failure given the barriers stacked against him? Thus to discover that I have the neurotic version of the COMT gene or the anxious-depressive SERT gene might at some level prove to be a relief. See, I could say, here’s proof that my anxiety is “real.” It’s right there in my genes. How can anyone expect me—how can I expect myself—to do anything much more than muddle anxiously along? It’s a wonder I’ve been able to accomplish anything given my disordered constellation of genes! Now let me huddle under the covers and watch soothing television shows.
Late one night, the report on my COMT gene arrived.c I am heterozygous (val/met), which means, based on the limited data so far, I am neither warrior nor worrier but something in between. (A 2005 study at San Diego State University did find that people—mainly women—with the val/met variant tended to be more introverted and neurotic.) Some time later, I received the results from the genotyping of my SERT gene: I’m short/short—meaning I’ve got the variant that many studies have found is predictive of anxiety disorders and depression when coupled with life stress. If current genetic research is to be believed, I should—based on my genotype—be anxious and harm avoidant, inordinately susceptible to suffering and pain.
Shouldn’t this be liberating? If being anxious is genetically encoded, a medical disease, and not a failure of character or will, how can I be blamed or shamed or stigmatized for it?
But ceding responsibility for your temperament and personality and baseline level of anxiety to hereditary bad luck—however well based in genetic science this may be—quickly bleeds into vexing philosophical territory. The same building blocks of nucleotides, genes, neurons, and neurotransmitters that make up my anxiety also make up the rest of my personality. To the extent that genes encode my anxiety, they also encode my self. Do I really want to attribute the “me-ness” of me to genetic factors completely beyond my control?
The enigmatic phobias of early childhood deserve mention once again.… Certain of them—the fear of being alone, of the dark, of strangers—we can understand as reactions to the danger of object loss; with regard to others—fear of small animals, thunderstorms, etc.—there is the possibility that they represent the atrophied remnants of an innate preparedness against reality dangers as is so well developed in other animals.
—SIGMUND FREUD, The Problem of Anxiety (1926)
How could something as idiosyncratic as a specific phobia have gotten passed from my mother to me to my daughter? Can a simple phobia be genetic?
Recall that Freud, late in his career, observed that certain common phobias—fear of the dark, fear of being alone, fear of small animals, fear of thunderstorms—seem to have evolutionarily adaptive roots, representing “the atrophied remnants of an innate preparedness against reality dangers such as is so well developed in other animals.” By this logic, certain phobias are so common because they arise from instinctive fears that have been evolutionarily selected for.
In the 1970s, Martin Seligman, a psychologist at the University of Pennsylvania, elaborated this notion into what he called preparedness theory: certain phobias are common because evolution has selected for brains primed to have exaggerated fear responses to dangerous things. Cro-Magnons who innately feared—and who therefore avoided—falling off cliffs or getting bitten by poisonous snakes or bugs or being exposed to predators in open fields were more likely to survive.
If the human brain is predisposed to develop fears of certain things, that casts one of the most famous experiments in the history of psychology in a new light. What if John Watson misinterpreted the Little Albert experiment that I discussed in chapter 2? What if the real reason Albert developed such a profound phobia of rats, and so readily generalized it to other furry creatures, was not that behavioral conditioning is so powerful but that the human brain has a natural predisposition to fear small furry things? Rodents, after all, can carry lethal diseases. Early humans who acquired a prudent fear of rats would have had an evolutionary advantage that made them more likely to survive. So it may be that neither the outward projections of inner psychic conflict (as the early Freud would have it) nor the power of behavioral conditioning (as Watson had it) is the primary reason so many people today develop rodent phobias; rather, it may be the connection of such fears to an atavistic response that is readily triggered.
For a long time, primatologists believed monkeys emerged from the womb with an innate fear of snakes. When researchers would observe a monkey encounter a snake (or even a snakelike object), the monkey would react fearfully—seemingly a clear instance of purely innate preparedness, of an inborn fear somehow handed down through the genes. But Susan Mineka, a psychologist at Northwestern University, discovered that monkeys who have been separated from their mothers and raised in captivity display no fear when they first encounter a snake. Only after infant monkeys have observed their mothers reacting fearfully to a snake—or after they have watched a video of another monkey reacting fearfully to a snake—do they later exhibit fearful behavior when exposed to a snake themselves. This suggests young monkeys learn to be afraid of snakes from watching their mothers—which in turn would seem to be strong evidence that the phobia is acquired by environmental learning rather than through the genes. But Mineka discovered another wrinkle: she found that monkeys could not easily acquire fears of things that were not intrinsically dangerous. Young monkeys who were shown videos of other monkeys reacting fearfully to a snake subsequently developed the fear of snakes—but monkeys shown (artfully spliced) videos of other monkeys reacting fearfully to flowers or rabbits did not develop fears of flowers or rabbits. Evidently, a combination of social observation and intrinsic danger is necessary to produce phobic-like behavior in monkeys.
Arne Öhman, the Swedish psychologist whose work on social anxiety I mentioned in chapter 4, points out that while all humans are evolutionarily primed to acquire certain adaptive fears, most people do not develop phobias. This is evidence, Öhman argues, that there is genetic variation in how sensitive our brains are to even those stimuli we are evolutionarily primed to fear. Some people—like my mother, my daughter, my son, and me—have a genetically encoded propensity to acquire fears and to have them be more intense than average.d
In support of Seligman’s preparedness theory, Öhma
n found that those phobias—including acrophobia (fear of heights), claustrophobia (enclosed spaces), arachnophobia (spiders), murophobia (rodents), and ophidiophobia (snakes)—that would have had clear adaptive relevance in our early evolutionary history were much harder to extinguish with exposure therapy than phobias of objects like horses or trains that were not historically “fear relevant.” Furthermore, Öhman found that even phobias of guns and knives—which are clearly “fear relevant” today but would not have been for Neanderthals and other evolutionary forebears—were much easier to extinguish than fears of snakes and rats, suggesting that the fears we are most readily primed for, and least easily rid of, were inscribed in our genes relatively early in primate evolution.
But what, if anything, is evolutionarily useful about emetophobia? Vomiting is adaptive; it can rid us of toxins that could kill us. What would account for a genotype for such a phobia?
One speculative possibility is that emetophobia is genetically derived from an impulse that is evolutionarily adaptive: avoiding other people who are vomiting. Instinctively running away from regurgitating peers might have saved those early hominids from being exposed to ambient toxins that could have poisoned them. Another possibility is that an array of genetically conferred temperamental traits and behavioral and cognitive predispositions, plus a high innate level of physiological reactivity, combined to enhance a vulnerability to phobic anxiety—and maybe especially, somehow, to this particular phobic anxiety. My mother, my daughter, and I all have high-reactive physiologies, with jittery amygdalae and bodies always on DEFCON 4 alert, which make us constantly hypervigilant about danger. My mother—like my daughter and like me—is a high-octane worrier; at times, she emits a nervous thrum that is practically audible. Our physiological reactivity and inhibited temperaments make all three of us more generally nervous, and more likely to experience intense negative emotion when exposed to a frightening stimulus, than someone with a low-reactive, uninhibited temperament.
Here’s a conversation I had with my daughter the night before a trip to Florida not long after she turned six.
“I’m afraid of the plane ride tomorrow.”
“There’s nothing to be afraid of,” I say, trying to project calm. “What is it about the plane that makes you scared?”
“The safety instructions.”
“The safety instructions? What about the safety instructions?”
“The part where they talk about crashing.”
“Oh, planes are very safe. The plane’s not going to crash.”
“Then why do they have the instructions telling you what to do if it does crash?”
“That’s just because there’s special rules that say flight attendants have to give us the instructions in order to keep us extra safe. But flying is much safer than driving in a car.”
“Then how come we don’t have to listen to safety instructions when we get in the car?”
“Susanna,” I yell down the stairs, “can you come talk to Maren about something?”
Maren seems to have come by her fear of flying without any overt instruction from me. She was already temperamentally equipped to worry about things, to scan the environment for potential threats; the natural cast of her mind—like mine, like my mother’s, like those of typical patients with generalized anxiety disorder—is such that she seeks out and worries (in the original sense of “playing with it,” turning it over in her mind to consider it from every angle) every worst-case scenario. Her dawning awareness of the safety instructions, with their references to water landings and crash positions, stimulated her anxiety.
Both my children share my gift for catastrophizing—for always imagining, and worrying about, the worst-case scenario, even if that scenario is not statistically likely. If I detect a small bump on my face while shaving, I immediately worry that it is not (as is most likely) a burgeoning pimple but rather a malignant and possibly fatal tumor. If I feel a twinge in my side, I instantly worry that it is not a strained muscle or a digestive blip but rather the onset of acute appendicitis or liver cancer. If, while driving into the sunlight, I feel a bit of dizziness, I am convinced that it is not a trick of the flickering light but rather an early sign of a stroke or a brain tumor.
Some time later, we were once again preparing to fly off for a family vacation. Maren clutched the armrests on the plane before takeoff, keenly attentive to every clank and whir from the aircraft’s innards, asking after each one if the noise meant that the plane was broken.
“No, it doesn’t,” my wife said.
“But how do you know?”
“Maren, would we ever put you somewhere that was dangerous?”
Another noise from the engine: Clank! “But what about that noise,” Maren says, tears in her eyes. “Does that noise mean the plane is broken?”
Sigh. The apple has fallen all too close to the tree.e
And that which is more to be wondered at, [melancholy] skips in some families the father, and goes to the son, “or takes every other, and sometimes every third in a lineal descent, and doth not always produce the same, but some like, and a symbolizing disease.”
—ROBERT BURTON, The Anatomy of Melancholy (1621)
The patient has been shown to be a perfectionist, ambitious to succeed though not in an egocentric way, and sensitive to small degrees of failure. Whether such psychodynamic explanations give the cause of the depression is not known. Anxiety seems the larger feature.
—FROM CHESTER HANFORD’S 1948 MCLEAN HOSPITAL REPORT
As unnerving as it has been to watch my children’s anxiety develop along lines similar to mine, it’s been equally so to discover the similarities between my great-grandfather’s neuroses and my own. If there is such behavioral similarity between my mother and me, and between me and my kids, then mightn’t the anxious genotype run all the way from my great-grandfather through my children—five generations (at least) of the hereditary taint?
Chester Hanford died the summer I turned six. I mainly recall him as a gentle, kindly presence, simultaneously distinguished and decrepit, sitting in his wheelchair in my grandparents’ living room in suburban New Jersey, or in his room at the nursing home nearby, wearing a burgundy blazer, a dark tie, and gray flannel slacks. After his death in 1975, he remained a presence in our house, gazing out with wise, sad eyes from various photos and living on in a letter to him from President Kennedy that hung on the living room wall alongside a picture of the two of them campaigning together with Jacqueline Kennedy.
When I was growing up, I knew only about Chester’s accomplishments: his long and successful deanship at Harvard; his respected academic publications on municipal government; his association with JFK over the course of several decades, from Kennedy’s undergraduate years to his time in the White House. Only when I got older did I begin to glean the dark bits: that he had suffered from anxiety and depression; that he had undergone multiple courses of electroshock therapy; that he had been institutionalized for extended periods many times between the late 1940s and the mid-1960s and had been forced into premature semiretirement (giving up his deanship) and then full retirement (leaving Harvard) as a result; and that he had spent some portion of his final decades moaning in a fetal ball in the bedroom of his home in western Massachusetts.
What was the cause of Chester’s afflictions? Was the problem primarily what we would today call an anxiety disorder or clinical depression? How closely did his anxieties resemble mine?
According to his psychiatric records from several hospitals, Chester’s general existential fears and anxieties were akin to my own. Does this mean I share—whether owing to the transmission of specific genes or to a neurotic family culture established by our ancestors—a specific psychiatric disease in common with my great-grandfather? Or merely that, in an inversion of Tolstoy, all psychoneurotics are unhappy in the same way?
Reading about my great-grandfather—especially after having learned a little bit about behavioral genetics—has kindled a sense of deep uneasiness, be
cause so much about him reminds me of myself. His nervousness. His fears of public speaking. His tendency to procrastinate.f His obsessive hand washing.g His fixation on his bowels.h His relentless self-criticism. His lack of self-esteem despite his respectable job. His ability to project a demeanor of seeming imperturbability and good cheer while roiling with internal torment.i His emotional and practical dependence on his more outgoing, more together wife.j
His first institutionalization, at age fifty-six, seems to have been precipitated by the anxiety he felt about a series of lectures he was to give to graduate students. “He had read a good deal this past fall,” his principal psychiatrist wrote after Chester was admitted to McLean Hospital in 1948, “but began to fear that he could not organize the material into lectures.” He felt that other professors were better than he was and that he was not enough of a scholar to produce satisfactory lectures. In the late spring of 1947, Chester “became very upset over his inability to organize his work and be creative. Anxiety overwhelmed him. He became quite depressed and wept at times.”
Chester’s psychotherapists tried to get him to quiet his superego. “The patient’s sense of self-criticism has been attacked as a factor in his depression, and shows itself to be more rigid and excessive than his talents and virtues warrant.” (Over the years, my own therapists have tried to do the same thing—only they generally don’t call it a superego anymore; they call it an “inner critic” or a “critical self.”) In my great-grandfather’s case, this didn’t work. Despite abundant evidence of his effectiveness as a scholar and an administrator, he couldn’t subdue his feelings of ineffectuality and inferiority. (“He is not glad to think back over his great usefulness to the college as in any way ameliorating his present plight of uselessness,” his psychiatrist wrote.) The objective evidence suggests that he was a figure who commanded considerable respect among both students and academic peers. Yet by the fall of 1947, he had come to believe himself a fraud, unequal to the task of composing lectures of sufficient interest and cogency for his students.
My Age of Anxiety: Fear, Hope, Dread, and the Search for Peace of Mind Page 34