How the “Brain Defect” Theory of Depression Stigmatizes Depression Sufferers
by Bruce Levine
Viewing depression as a “brain defect” rather than a “character defect” is supposed to reduce the stigma of depression, according to the American Psychiatric Association, the National Alliance for the Mentally Ill, and the rest of the mental health establishment. But any defect can be stigmatizing. What if depression is the result of neither a brain defect nor a character defect?
At one time in U.S. history, Americans actually elected a known depression sufferer as president. In Lincoln’s Melancholy, Joshua Wolf Shenk reports that Abraham Lincoln’s long-time law partner William Herndon observed about Lincoln that “gloom and sadness were his predominant state.” And Shenk reports that Lincoln experienced two major depressive breakdowns which included suicidal statements that frightened friends enough to form a suicide watch. However, in Lincoln’s era, when depression was seen as neither a character defect nor a brain defect, Lincoln’s depression actually helped him politically more than it hurt him. Lincoln’s depression gained him sympathy and compassion, and drew people toward him, as it “seemed not a matter of shame but an intriguing aspect of his character, and indeed an aspect of his grand nature,” according to Shenk.
Today, when we treat depression as a brain defect, it appears unlikely that anyone with Lincoln’s temperament would receive a U.S. presidential or vice presidential nomination. In 1972, George McGovern’s vice presidential running mate Thomas Eagleton was shoved off the ticket because of his history of depression and medical treatment for it. And today, it would seem near impossible for a candidate who had received electroshock for depression to be elected president.
Lincoln’s words, humor, and face revealed a man who suffered from deep pains. This is also true for Winston Churchill, William Tecumseh Sherman, and other critically thinking leaders who have suffered from depression. Lincoln, Churchill, and Sherman visibly experienced pain but inspired people because of, in part, their capacity to overcome their pain. Today, we reject leaders who visibly suffer from pain.
While Lincoln, Churchill, and Sherman were certainly not without flaws, so too are the “compulsively upbeat”— the “bright-sided,” to use Barbara Ehrenreich’s term. The U.S. political preference for the compulsively upbeat became clear with the ascent of Ronald Reagan. Reagan’s reputation as a “great” and a “transformative” president has been cemented not only by the corporate media and Republicans but by Democrats such as Bill Clinton and Barack Obama. All this despite Reagan’s committing one of the most heinous offenses in U.S. presidential history—selling arms to Iran in violation of an embargo so as to illegally fund the Nicaraguan Contras. Reagan’s offenses have been largely ignored by present America; but not ignored, especially by modern American politicians, is the fact that Reagan’s sunny disposition defeated his more downbeat political rivals and helped create the Reagan legacy.
Americans have been increasingly socialized to be terrified of the overwhelming pain that can fuel depression, and they have been taught to distrust their own and other’s ability to overcome it. This terror, like any terror, inhibits critical thinking. Without critical thinking, it is difficult to accurately assess the legitimacy of authorities. And Americans have become easy prey for mental health authorities’ proclamation that depression is a result of a brain defect. But what does science actually say about the brain defect theory of depression?
Science and the Brain Defect Theory of Depression
The reality is there is as no scientific proof that depression is caused by either a character defect or a brain defect.
Medical conditions such as hypothyroidism and anemia can cause depression, but the American Psychiatric Association’s diagnostic manual, the Diagnostic and Statistical Manual of Mental Disorders (DSM), states that a patient should not be diagnosed with the psychiatric disorder of depression when the symptoms of depression are due to a general medical condition. The mental health establishment is committed to the idea that depression is a separate brain disorder, and it has declared several biological-chemical-electrical theories for it.
For nearly a generation, doctors and the general public have been told that depression is caused by an imbalance of neurotransmitters, most notably serotonin. However, in the 1990s, this theory was disproved, but the National Institute of Mental Health made no serious effort to communicate this to the general public until 2007, and even today today, the National Alliance for the Mentally Ill, an influential U.S. institution that disseminates mental health information, keeps this truth buried. Here’s the details of this history.
For quite some time, unknown to most of the general public and even many doctors, researchers have used a variety of methods to test the serotonin (and other neurotransmitter) imbalance theory of depression. Research methods included comparing serotonin metabolites in depressed and nondepressed people, and depleting serotonin levels through a variety of means and then observing whether this caused depression. The results? Elliot Valenstein, professor emeritus of psychology and neuroscience at the University of Michigan, in Blaming the Brain, reported in 1998 that it is just as likely for people with normal serotonin levels to feel depressed as it is for people with abnormal serotonin levels, and that it is just as likely for people with abnormally high serotonin levels to feel depressed as it is for people with abnormally low serotonin levels. Valenstein concluded, “Furthermore, there is no convincing evidence that depressed people have a serotonin or norepinephrine deficiency.”
In 1999 the journal International Clinical Psychopharmacology ( in “Antidepressants and the Brain”) reported on serotonin, norepinephrine, and dopamine depletion studies, and stated that “depletion in unmedicated patients with depression did not worsen the depressive symptoms, neither did [depletion] cause depression in healthy subjects with no history of mental illness.”
In 1996 Pharmacopsychiatry (in “The Revised Monoamine Theory of Depression: A Modulatory Role fo Monamines, Based on New Findings from Monamine Depletion Experiments in Humans”) reported that nonmedicated subjects—whether depressed or nondepressed —do not suffer depression deterioration in response to depletion of serotonin, dopamine, or norepineprhine. Ironically, subjects previously medicated with antidepressants do suffer depression deterioration in response to depletion of these neurotransmitters. In other words, a person’s naturally occurring level of serotonin (and other neurotransmitters) is unrelated to depression but, as psychiatrist Grace Jackson writes in 2005 in Rethinking Psychiatric Drugs, “The available evidence suggests that antidepressants may induce persistent sensitivities in the brain which increase a patient’s vulnerability to recurrent depression beyond that which would occur naturally.”
Thus, by the 1990s, it was known in the scientific community that the serotonin (and other neurotransmitters) imbalance theory of depression had been disproved. Yet, as detailed in Society in 2008 (“The Media and the Chemical Imbalance Theory of Depression”), the general public continued to hear—through antidepressant commercials, the mainstream media, and some mental health authorities—about the neurotransmitter imbalance theory of depression. Even today, the National Alliance for the Mentally Ill states on its Web site, “Scientists believe that if there is a chemical imbalance in these neurotransmitters [norepinephrine, serotonin and dopamine], then clinical states of depression result.”
So, many Americans are surprised to discover that by 2007 the National Institute of Mental Health had moved on to another theory. Newsweek, in its February 26, 2007 cover story, reported that:
For decades, scientists believed the main cause of depression was low levels of the neurotransmitters serotonin and norepinephrine. Newer research, however, focuses [on something else]. . . . A depressed brain is not necessarily underproducing something, says Dr. Thomas Insel, head of the National Institute of Mental Health—it’s doing too much. . . . Instead of focusing on boosting neurotransmitters. . . scientists are developing medications that block the production of excess stress chemicals.
Stress can stimulate the release of cortisol, which can negatively affect both body and mind. And many other medical conditions can also result in symptoms of depression. However, as noted, the DSM states that a patient should not be diagnosed with the psychiatric disorder depression when the symptoms of depression are due to the “direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., hypothyroidism).” If hypothyroidism is considered a medical condition, it’s unclear why the overproduction of cortisol would not also be considered a medical condition.
Thus, rather than a specific psychiatric brain disorder causing depression, we are simply talking about the uncontroversial reality that certain physical, familial, and societal pains can trigger depression.
While individuals vary in their belief about the benefits and costs of continuing to view depression as a psychiatric disorder caused by a brain defect, as long as depression is considered a psychiatric disorder caused by a brain defect, Americans are unlikely to ever elect another pained depressive such as Abraham Lincoln as president. I can’t help but wonder what American political leadership would be like if Americans had been led to believe that it’s actually the insipidly upbeat who have a brain defect.