The standard psychoanalytic account of hypochondria maintains that the behavior is an expression of repressed conflicts—unexamined grief, yearning for parental love, distress over real or imagined transgressions. Fallon has seen some patients whose hypochondria can, he believes, be explained in this way. But he has also begun to provide a far more comprehensive account of a range of influences on the development of hypochondria. These include the habit, formed in childhood, of using medical complaints as an effective tool of gaining attention from parents. “These patients don’t even realize that it’s a habit,” Fallon says. “It’s just the way they deal with stress.” Another subgroup of hypochondriacs are strongly akin to obsessive-compulsives, though they limit their fixations to illness. (People with OCD tend to dwell on transmitting a disease, not dying from one.) Yet others have a deeper affinity with depressives. Such hypochondriacs, Fallon says, are often guilt-ridden. “Not uncommonly, it’s someone who has had an affair and is afraid they’ve contracted a sexually transmitted disease. Even though they’ve been to the doctor and are told they’re fine, they can’t stop thinking about it, and it becomes a major source of self-flagellation.” Strangely, some hypochondriacs barely suffer physical complaints at all, but are simply consumed by the thought that something must be wrong with them; across the spectrum, other hypochondriacs focus less on disease than on nagging pains, from which they get no relief, regardless of how many doctors they see or how many tests they are administered. Fallon points to compelling new evidence that the elusive physical ailments with which some hypochondriacs are oppressed might be caused by abnormalities in certain proteins, called cytokines, which are produced by the immune system and help to generate an immune response to disease. Cytokines are believed to cause bodily symptoms like fatigue, pain, and cognitive problems; according to Fallon, it’s likely that a hypochondriac’s brain, beset by abnormal cytokines, could produce such symptoms in the absence of other identifiable causes.
Fallon, whose primary orientation is the overlap between psychiatric and neurological disorders, is working toward providing a description of the neurochemistry of hypochondria that may, ultimately, help to crack the mystery of the disorder. Brain scans, he says, suggest that hypochondria involves a heightening of metabolic activity in the same areas of the brain that are affected in obsessive-compulsive disorder. In OCD patients, this hyperactivity depletes the brain of the neurotransmitter serotonin, which helps to account for the success in treating OCD with serotonin-reuptake inhibitors like Prozac. Fallon was the first scientist to study the effects of such medications on hypochondriacs and has convincingly challenged the traditional notion, supported by cultural and medical prejudice, that hypochondria is untreatable and that its hapless sufferers ought, above all, to buck up. In the late eighties, during his residency at Columbia, Fallon was introduced to a 50-year-old stockbroker with an unwavering belief that he had a brain tumor. The patient had had four brain scans, each of which proved negative, and none of which appeased his fears. He had already received a great deal of psychotherapy and had taken medication for anxiety. Nothing seemed to help. Indeed, given the literature on hypochondria, Fallon himself held out little hope for the man, who was also irritable and unpleasant. As a desperation measure, Fallon’s supervisor, an OCD researcher, suggested administering fluoxetine—Prozac—which was new to the market. In short order, the patient’s worries subsided and his personality was transformed. “Suddenly, he was this gracious, grateful person.”
In 1993, Fallon drew on this success and designed a large-scale study to treat hypochondriacs with Prozac. Within twelve weeks of taking the medication, 70 percent of Fallon’s subjects were substantially relieved of their health-related fears. Given the effectiveness of Prozac for a wide variety of depressive, obsessional, and anxiety disorders, the results were, perhaps, not surprising. Fallon was startled, though, by some of his peripheral findings, which demonstrated the dazzling, and disturbed, powers of the hypochondriacal mind. To begin with, a large number of subjects given a placebo improved just as substantially as those who had been given Prozac. More peculiarly, though, one patient taking the placebo developed an extraordinarily convincing array of the side effects associated with Prozac. Yet another patient, believing she had been switched, midway through the trial, from Prozac to the placebo, underwent a classic case of withdrawal from the drug and suffered a relapse of her hypochondria. It turned out, though, that she had remained on Prozac the whole time.
To complement Fallon’s work, Barsky has demonstrated comparable success in treatments using cognitive-behavioral therapy, which attempts to train patients in techniques to dismantle or circumvent their troubled thought patterns. Brain scans have shown that such therapy has been as effective as Prozac in restoring the hypochondriac’s neurochemistry to normal function. In 2006, Fallon and Barsky decided to pursue the question of treatment further, and joined forces in the largest study ever conducted on hypochondria, a five-year project funded by a grant of more than $5 million from the National Institute of Mental Health. They plan to enroll 264 subjects, and to compare the effectiveness of various therapies and medication separately and in combination. Recruitment of subjects, however, has been slow. Hypochondriacs, being who they are, tend to seek solace in medical, not psychiatric, settings.