coldhearted scientist وداد

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.

That’s why.

Axé.