A few years ago I wrote that uncertainty is inevitable in psychiatry. We literally don’t know the pathogenesis of any psychiatric disorder. Historically, when the etiology of abnormal behavior became known, the disease was no longer considered psychiatric. Thus, neurosyphilis and myxedema went to internal medicine; seizures, multiple sclerosis, Parkinson’s, and many other formerly psychiatric conditions went to neurology; brain tumors and hemorrhages went to neurosurgery; and so forth.
This leaves psychiatry with the remainder: all the behavioral conditions of unknown etiology. Looking to the future, my fervent hope that researchers will soon discover causes and definitive cures for schizophrenia, bipolar disorder, and other psychiatric disorders comes with the expectation that these conditions will then leave psychiatry for other specialties. We will always deal with what is left. At minimum we psychiatrists should accept this reality about our chosen field. After all, there appears to be no alternative. Some of us go beyond this to embrace uncertainty as intellectually attractive. We like that the field is unsettled, in flux, alive.
Yet many of us clutch at illusory certainty. Decades ago, psychoanalysis purportedly held the keys to unlock the mysteries of the mind. It later lost favor when many conditions, particularly the most severe, were unaffected by this lengthy, expensive treatment. Now the buzzword is that psychiatric disorders are “neurobiological.” This is said in a tone that implies we know more than we do, that we understand psychiatric etiology. It’s a bluff.
Patients are told they suffer a “chemical imbalance” in the brain, when none has ever been shown. Rapid advances in brain imaging and genetics have yielded an avalanche of findings that may well bring us closer to understanding the causes of mental disorders. But they haven’t done so yet — a sad fact obscured by popular and professional rhetoric. In particular, functional brain imaging (e.g., fMRI) fascinates brain scientists and the public alike. We can now see, in dramatic three-dimensional colorful computer graphics, how different regions of the living brain “light up,” that is, vary in metabolic activity. Population studies reveal systematic differences in patients with specific psychiatric disorders as compared to normals. Don’t such images prove that psychiatric disorders are neurobiological brain diseases?
Not quite. Readers of these exciting reports often overlook two crucial facts. First, these metabolic differences only appear in group studies and cannot be used to diagnose individual patients. As of this writing there is no lab test or brain scan to diagnose any psychiatric disorder. Attempting to do so would be like diagnosing malnutrition based on height. While malnourished people are shorter than the well-nourished on average, there is wide overlap and height is not diagnostic. Second, etiology — the cause of these differences in brain function — remains unknown. Differences in brain function (and structure) are not necessarily inborn. Brain anatomy can change as a result of life experience, and metabolic activity (function) from experimental manipulation of cognitive effort, induced mood, guided imagery, etc. Just as multiple factors affect a subject’s height, multiple biological and psychological factors affect brain findings as well. Thus, learning that patients with borderline personality show decreased metabolism in the frontal lobes (hypofrontality) is neither surprising nor indicative of a neurobiological etiology. We already know the frontal lobes inhibit impulsive activity, and we already know borderline personality is characterized by impulsivity. What else would we expect?
Genetic studies consistently show both heritable and environmental factors at play in psychiatric disorders. Since the 1960s, psychiatry has called this combination the diathesis-stress model: an inborn predisposition meets an environmental stress, leading to an overt disorder. The model helped shift the field from “nature versus nurture” to “nature and nurture” — and no research discovery or neurobiological rhetoric so far has shifted it back. Patients and their doctors still contend with diathesis and stress: recreational drug use tips one patient into psychosis, sudden abandonment tips another into borderline rage. Indeed, clinicians remain much more able to influence stress than diathesis. A dispassionate assessment of what we currently know should lead to humble agnosticism about psychiatric etiology. Genetics, biology, and environment all play a role, but beyond that there isn’t much we can say. This is why all current psychiatric medications treat symptoms and are not curative.
In this light, the popularity and zeal of neurobiological language is startling. The American Psychiatric Association (APA) subtly changed the wording in its new Diagnostic and Statistical Manual, DSM-5, to imply that all psychiatric conditions are biological in nature. The National Institute of Mental Health (NIMH) assumes that “Mental disorders are biological disorders …” The National Alliance on Mental Illness (NAMI) says, “A mental illness is a medical condition …”
A more ground-level version is expressed by editor-in-chief Henry A. Nasrallah, MD in the latest edition of Current Psychiatry. In an editorial not-so-subtly titled, “Borderline personality disorder (BPD) is a heritable brain disease,” Dr. Nasrallah proclaims BPD a “neurobiological illness” and “a serious, disabling brain disorder, not simply an aberration of personality” — as though these were distinct alternatives rather than two terms for the same thing. After citing a number of biological findings which fail to prove etiology (e.g., the hypofrontality mentioned above) and which show partial heritability, Dr. Nasrallah concludes that “the neuropsychiatric basis of BPD must guide treatment.”
Of course, it already does. We already treat borderline personality disorder the best we know how, with psychotherapy (shown by functional imaging to modify brain metabolism, by the way) and often with adjunctive medication to treat symptoms. What more do breathless declarations of brain disease buy us, other than reduced credibility? It’s not as though any of us currently withhold neurobiological treatment as a result of outmoded ideology.
On the contrary, the moment the FDA approves a cure for borderline personality disorder based on an established neurobiological etiology, I will gladly refer my patients to the neurologist, virologist, or genetic counselor who would thereafter treat such patients.
Steven Reidbord is a psychiatrist who blogs at Reidbord’s Reflections.