The answer is not straightforward—or, rather, it depends on whom you ask. For Søren Kierkegaard, writing in the mid-nineteenth century, anxiety (angst in Danish) was a spiritual and philosophical problem, a vague yet inescapable uneasiness with no obvious direct cause.‡ For Karl Jaspers, the German philosopher and psychiatrist who wrote the influential 1913 textbook General Psychopathology, it was “usually linked with a strong feeling of restlessness … a feeling that one has … not finished something; or … that one has to look for something or … come into the clear about something.” Harry Stack Sullivan, one of the most prominent American psychiatrists of the first half of the twentieth century, wrote that anxiety was “that which one experiences when one’s self-esteem is threatened”; Robert Jay Lifton, one of the most influential psychiatrists of the second half of the twentieth century, similarly defines anxiety as “a sense of foreboding stemming from a threat to the vitality of the self, or, more severely, from the anticipation of fragmentation of the self.” For Reinhold Niebuhr, the Cold War–era theologian, anxiety was a religious concept—“the internal precondition of sin … the internal description of the state of temptation.” For their part, many physicians—starting with Hippocrates (in the fourth century B.C.) and Galen (in the second century A.D.)—have argued that clinical anxiety is a straightforward medical condition, an organic disease with biological causes as clear, or nearly so, as those of strep throat or diabetes.
Then there are those who say that anxiety is useless as a scientific concept—that it is an imprecise metaphor straining to describe a spectrum of human experience too broad to be captured with a single word. In 1949, at the first-ever academic conference dedicated to anxiety, the president of the American Psychopathological Association opened the proceedings by conceding that although everyone knew that anxiety was “the most pervasive psychological phenomenon of our time,” nobody could agree on exactly what it was or how to measure it. Fifteen years later, at the annual conference of the American Psychiatric Association, Theodore Sarbin, an eminent psychologist, suggested that “anxiety” should be retired from clinical use. “The mentalistic and multi-referenced term ‘anxiety’ has outlived its usefulness,” he declared. (Since then, of course, the use of the term has only proliferated.) More recently, Jerome Kagan, a psychologist at Harvard who is perhaps the world’s leading expert on anxiety as a temperamental trait, has argued that applying the same word—“anxiety”—“to feelings (the sensation of a racing heart or tense muscles before entering a crowd of strangers), semantic descriptions (a report of worry over meeting strangers), behaviors (tense facial expressions in a social situation), brain states (activation of the amygdala to angry faces), or a chronic mood of worry (general anxiety disorder) is retarding progress.”
How can we make scientific, or therapeutic, progress if we can’t agree on what anxiety is?
Even Sigmund Freud, the inventor, more or less, of the modern idea of neurosis—a man for whom anxiety was a key, if not the key, foundational concept of his theory of psychopathology—contradicted himself repeatedly over the course of his career. Early on, he said that anxiety arose from sublimated sexual impulses (repressed libido, he wrote, was transformed into anxiety “as wine to vinegar”).§ Later in his career, he argued that anxiety arose from unconscious psychic conflicts.‖ Late in his life, in The Problem of Anxiety, Freud wrote: “It is almost disgraceful that after so much labor we should still find difficulty in conceiving of the most fundamental matters.”
If Freud himself, anxiety’s patron saint, couldn’t define the concept, how am I supposed to?
Fear sharpens the senses. Anxiety paralyzes them.
—KURT GOLDSTEIN, The Organism: A Holistic Approach to Biology (1939)
Standard dictionary definitions make fear (“an unpleasant emotion caused by the belief that someone or something is dangerous, likely to cause pain, or a threat”) and anxiety (“a feeling of worry, nervousness, and unease, typically about an event or something with an uncertain outcome”) seem relatively synonymous. But for Freud, whereas fear (Furcht in German) has a concrete object—the lion that’s chasing you, the enemy sniper that’s got you pinned to your position in battle, or even your knowledge of the consequences of missing the crucial free throw you’re about to shoot in the closing moments of an important basketball game—anxiety (Angst) does not. According to this view, fear, properly occasioned, is healthy; anxiety, which is often “irrational” or “free-floating,” is not.a
“When a mother is afraid that her child will die when it has only a pimple or a slight cold we speak of anxiety; but if she is afraid when the child has a serious illness we call her reaction fear,” Karen Horney wrote in 1937. “If someone is afraid whenever he stands on a height or when he has to discuss a topic he knows well, we call his reaction anxiety; if someone is afraid when he loses his way high up in the mountains during a heavy thunderstorm we would speak of fear.” (Horney further elaborated her distinction by saying that while you always know when you are afraid, you can be anxious without knowing it.)
In Freud’s later writings, he replaced his distinction between fear and anxiety with a distinction instead between “normal anxiety” (defined as anxiety about a legitimate threat, which can be productive) and “neurotic anxiety” (anxiety produced by unresolved sexual issues or internal psychic conflicts, which is pathological and counterproductive).
So am I, with my phobias and worries and general twitchiness, “neurotically” anxious? Or just “normally” so? What’s the difference between “normal” anxiety and anxiety as a clinical problem? What differentiates the appropriate and even helpful nervousness that, say, a law student feels before taking the bar exam or that a Little Leaguer feels before stepping into the batters’ box from the distressing cognitive and physical symptoms that attend the official anxiety disorders as defined by modern psychiatry since 1980: panic disorder, post-traumatic stress disorder (PTSD), specific phobia, obsessive-compulsive disorder (OCD), social anxiety disorder, agoraphobia, and generalized anxiety disorder?
To distinguish the “normal” from the “clinical,” and the different clinical syndromes from one another, pretty much everyone in the entire wide-ranging field of mental health care relies on the American Psychiatric Association’s Diagnostic and Statistical Manual (now in its just-published fifth edition, DSM-V). The DSM defines hundreds of mental disorders, classifies them by type, and lists, in levels of detail that can seem both absurdly precise and completely random, the symptoms (how many, how often, and with what severity) a patient must display in order to receive a given psychiatric diagnosis. All of which lends the appearance of scientific validity to the diagnosing of an anxiety disorder. But the reality is that there is a large quotient of subjectivity here (both on the part of patients, in describing their symptoms, and of clinicians, in interpreting them). Studies of the DSM-II found that when two psychiatrists consulted the same patient, they gave the same DSM diagnosis only between 32 and 42 percent of the time. Rates of consistency have improved since then, but the diagnosis of many mental disorders remains, despite pretensions to the contrary, more art than science.b
Consider the relationship between clinical anxiety and clinical depression. The physiological similarities between certain forms of clinical anxiety (especially generalized anxiety disorder) and clinical depression are substantial: both depression and anxiety are associated with elevated levels of the stress hormone cortisol, and they share some neuroanatomical features, including shrinkage of the hippocampus and other parts of the brain. They share genetic roots, most notably in the genes associated with the production of certain neurotransmitters, such as serotonin and dopamine. (Some geneticists say they can find no distinction between major depression and generalized anxiety disorder.) Anxiety and depression also have a shared basis in a feeling of a lack of self-esteem or self-efficacy. (Feeling like you have no control over your life is a common route to both anxiety and depression.) Moreover, reams of studies show that stress�
��ranging from job worries to divorce to bereavement to combat trauma—is a huge contributor to rates of both anxiety disorders and depression, as well as to hypertension, diabetes, and other medical conditions.
If anxiety disorders and depression are so similar, why do we distinguish between them? Actually, for a few thousand years, we didn’t: doctors tended to group anxiety and depression together under the umbrella terms “melancholia” or “hysteria.”c The symptoms that Hippocrates attributed to melaina chole in the fourth century B.C. included those we would today associate with both depression (“sadness,” “moral dejection,” and “tendency to suicide”) and anxiety (“prolonged fear”). In 1621, in The Anatomy of Melancholy, Robert Burton wrote, with a clinical accuracy that modern research supports, that anxiety was to sorrow “a sister, fidus Achates [trusty squire], and continual companion, an assistant and a principal agent in the procuring of this mischief; a cause and symptom as the other.”d It is a fact—I say this from experience—that being severely anxious is depressing. Anxiety can impede your relationships, impair your performance, constrict your life, and limit your possibilities.
The dividing line between the set of disorders the American Psychiatric Association lumps under “depression” and the set of disorders it lumps under “anxiety disorders”—and, for that matter, the line between mental health and mental illness—seems to be an artifact as much of politics and culture (and marketing) as of science. Every time the scope of a given psychiatric disorder grows or shrinks in the DSM’s definition, it has powerfully ramifying effects on everything from insurance reimbursements to drug company profits to the career prospects of therapists in different fields and subspecialties. Quite a few psychiatrists and drug industry critics will tell you that anxiety disorders do not exist in nature but rather were invented by the pharmaceutical-industrial complex in order to extract money from patients and insurance companies. Diagnoses such as social anxiety disorder or general anxiety disorder, these critics say, turn normal human emotions into pathologies, diseases for which medication can be profitably dispensed. “Don’t allow the sum total of your life to be reduced to phrases like clinical depression, bipolar disorder, or anxiety disorder,” says Peter Breggin, a Harvard-trained psychiatrist who has become a fierce antagonist of the pharmaceutical industry.
As someone who has been diagnosed with some of these disorders, I can tell you the distress they cause is not invented; my anxiety, which can at times be debilitating, is real. But are my nervous symptoms necessarily constitutive of an illness, of a psychiatric disorder, as the DSM and the pharmaceutical companies would have it? Mightn’t my anxiety be just a normal human emotional response to life, even if the response is perhaps somewhat more severe for me than for others? How do you draw the distinction between “normal” and “clinical”?
You might expect that recent scientific advances would make the distinction between normal and clinical anxiety more precise and objective—and certainly in some ways they have. Neuroscientists, working with functional magnetic resonance imaging (fMRI) technology that enables them to observe mental activity in real time by measuring oxygenated blood flow to different regions of the brain, have produced hundreds of studies demonstrating associations between specific subjectively experienced emotions and specific kinds of physiological activity that can be seen on a brain scan. For instance, acute anxiety generally appears on fMRI scans as hyperactivity in the amygdala, that tiny almond-shaped structure located deep in the medial temporal lobes near the base of the skull. Reductions in anxiety are associated with diminished activity in the amygdala and with heightened activity in the frontal cortex.e
All of which makes it sound like you should be able to identify anxiety, and gauge its intensity, on the basis of something akin to an X-ray—that you could differentiate between normal and clinical anxiety in the way X-rays can differentiate between a broken ankle and a sprained one.
Except you can’t. There are people who exhibit telltale physiological signs of anxiety on a brain scan (their amygdalae light up colorfully in response to stress-inducing stimuli) but who will tell you they are not feeling anxious. Moreover, the brain of a research subject who is sexually aroused by a pornographic movie will light up on an MRI scan in much the same way it does in response to a fear-inducing event; the same interconnected brain components—the amygdala, the insular cortex, and the anterior cingulate—will be activated in both cases. A researcher looking at the two brain scans without knowing their context might be unable to determine which image is a response to fear and which is to sexual arousal.
When an X-ray shows a fractured femur but the patient reports no pain, the medical diagnosis is still a broken leg. When an fMRI exhibits intense activity in the amygdala and basal ganglia and the patient reports no anxiety, the diagnosis is … nothing.
When it comes to detecting and responding to danger, the [vertebrate] brain just hasn’t changed much. In some ways we are emotional lizards.
—JOSEPH LEDOUX, The Emotional Brain (1996)
Researchers since Aristotle have made frequent recourse to “animal models” of emotion, and the many thousands of animal studies conducted each year are predicated on the notion that the behaviors, genetics, and neurocircuitry of a rat or a chimpanzee are similar enough to our own that we can glean relevant insight from them. Writing in The Expression of the Emotions in Man and Animals in 1872, Charles Darwin observed that fear reactions are fairly universal across species: all mammals, including humans, exhibit readily observable fear responses. In the presence of perceived danger, rats, like people, instinctively run, freeze, or defecate.f When threatened, the congenitally “anxious” rat trembles, avoids open spaces, prefers familiar places, stops in its tracks if encountering anything potentially threatening, and emits ultrasonic distress calls. Humans don’t issue ultrasonic distress calls—but when we get nervous, we do tremble, shy away from unfamiliar situations, withdraw from social contact, and prefer to stay close to home. (Some agoraphobics never leave their houses.) Rats that have had their amygdalae removed (or whose genes have been altered so that their amygdalae are not working properly) are incapable of expressing fear; the same is true of humans whose amygdalae get damaged. (Researchers at the University of Iowa have for years been studying a woman, known in the literature as S.M., whose amygdala was destroyed by a rare disease—and who cannot, as a consequence, experience fear.) Moreover, if continuously exposed to stressful situations, animals will develop some of the same stress-related medical conditions that humans do: high blood pressure, heart disease, ulcers, and so forth.
“With all or almost all animals, even with birds,” Darwin wrote, “terror causes the body to tremble. The skin becomes pale, sweat breaks out, and hair bristles. The secretions of the alimentary canal and of the kidneys are increased, and they are involuntarily voided, owing to the relaxation of the sphincter muscles as is known to be the case with man, and as I have seen with cattle, dogs, cats, and monkeys. The breathing is hurried. The heart beats quickly, wildly, and violently.… The mental faculties are much disturbed. Utter prostration soon follows, and even fainting.”
Darwin pointed out that this automatic physical response to threat is evolutionarily adaptive. Organisms that respond to danger in this way—by being physiologically primed to fight or flee, or to faint—are more likely to survive and reproduce than organisms that don’t. In 1915, Walter Cannon, the chair of the physiology department at Harvard Medical School, coined the term “fight or flight” to describe Darwin’s idea of an “alarm reaction.” As Cannon was the first to document systematically, when the fight-or-flight response is activated, peripheral blood vessels constrict, directing blood away from the extremities to the skeletal muscles, so the animal will be better prepared to fight or run. (This streaming of blood away from the skin is what makes a frightened person appear pale.) Breathing becomes faster and deeper to keep the blood supplied with oxygen. The liver secretes an increased amount of glucose, which energizes various muscle
s and organs. The pupils of the eyes dilate and hearing becomes more acute so that the animal can better appraise the situation. Blood flows away from the alimentary canal and digestive processes stop—saliva flow decreases (causing that anxious feeling of a dry mouth), and there is often an urge to defecate, urinate, or vomit. (Expelling waste material allows the animal’s internal systems to focus on survival needs more immediate than digestion.) In his 1915 book, Bodily Changes in Pain, Hunger, Fear and Rage, Cannon provided a couple of simple early illustrations of the way the experience of emotion translates concretely into chemical changes in the body. In one experiment, he examined the urine of nine college students after they had taken a hard exam and after they had taken an easy one: after the hard exam, four of the nine students had sugar in their urine; after the easy exam, only one of them did. In the other experiment, Cannon examined the urine of the Harvard football team after “the final and most exciting contest” of 1913 and found that twelve of the twenty-five samples had positive traces of sugar.
The physiological response that produces fainting is different from the one that primes the organism for fighting or fleeing, but it can be equally adaptive: animals that respond to bleeding injuries with a sharp drop in blood pressure suffer less blood loss; also, fainting is an involuntary way for animals to feign death, which in certain circumstances might be protective.g
When the fight-or-flight reaction is activated appropriately, in response to a legitimate physical danger, it enhances an animal’s chances of survival. But what happens when the response is activated inappropriately? The result of a physiological fear response that has no legitimate object, or that is disproportionate to the size of the threat, can be pathological anxiety—an evolutionary impulse gone awry. William James, the psychologist and philosopher, surmised that the cause of severe anxiety, and of what we would today call panic attacks, might be modernity itself—specifically, the fact that our primitive fight-or-flight responses are not suited to modern civilization. “The progress from brute to man is characterized by nothing so much as by the decrease in frequency of proper occasions for fear,” James observed in 1884. “In civilized life, in particular, it has at last become possible for large numbers of people to pass from the cradle to the grave without ever having had a pang of genuine fear.”h
My Age of Anxiety: Fear, Hope, Dread, and the Search for Peace of Mind Page 5