A column opposed to the antagonizing of people who would prefer not to take antidepressants for their whole lives.
From the way people talk about it, you’d think the decision to stop taking antidepressants or to refuse to start taking them was like shunning power steering out of mere stubbornness. “It can help so much,” people say. “Why struggle when things can be so easy?”
The pressure is even stronger because the choice affects not just the person but everyone he or she interacts with. “Take your meds, and use your power steering,” the ethic goes, “or no one will want to be around you.” The unspoken question is, “What sort of weird combination of Luddism, stubbornness, vanity and ignorance would make you want to take out your power steering or be off of antidepressants, if they help you?”
Power steering and antidepressants were both invented in the mid-20th century and are now almost ubiquitous. Nearly all cars have power steering and we’re practically putting antidepressants in the drinking supply.
But whereas power steering generally is a good thing for widespread use, antidepressants might not be. Unlike power steering, they have many drawbacks and dangers — so many that we’d do well to support people who want to disable their power steering, as it were, and experience life without antidepressants.
Because of the say some cars are built, they’re almost un-drivable without power steering. It’s widely assumed that some people are like this, too — that certain people, for whatever reason, have a chemical imbalance that requires them to take antidepressants for life. In an essay on the phenomenon of taking medicines indefinitely, MIT anthropology professor Joseph Dumit cites a depression sufferer with the common explanation,” [T]hat I have to take some pills every day to maintain my life is no different from my friend who takes sulfa drugs daily to stave off a recurrence of colitis, or another who injects herself with insulin.”
Pharmaceutical companies are doing a good job spreading the bio-amine hypothesis of depression, exemplified in this paragraph on the Prozac Web site: “Depression is not fully understood, but a growing amount of evidence supports the view that people with depression have an imbalance of the brain’s neurotransmitters, the chemicals that allow nerve cells in the brain to communicate with each other. Many scientists believe that an imbalance in serotonin, one of these neurotransmitters, may be an important factor in the
development and severity of depression. Prozac may help to correct this imbalance by increasing the brain’s own supply of serotonin.”
The public is buying it — the medicine as well as the theory. More than 50 percent of Americans have taken a medication for depression at some point in their lives. A 2001 poll conducted by the National Mental Health Association found that 55 percent of people never diagnosed with depression “understand depression is a disease, and not a state of mind that a person can snap out of,” up from 38 percent ten years before. Of those with a diagnosis of depression, more than three-quarters believe that they will need treatment for the rest of their lives.
Much of this ease with which people are buying into antidepressants could be attributed to the bioamine hypothesis of depression, a theory supported much less by research than by drug companies. The eminent neuroscientist Elliott Valenstein challenged this theory in his book, “Blaming the Brain,” writing that no biochemical or anatomical traits have been found to reliably distinguish the brains of the depressed, and attempts to prove the chemical deficiency hypothesis of depression have been in vain. Contrary to predictions, depressed people don’t have less serotonin, and they don’t seem to have predictable imbalances of other neurotransmitters, either.
Valenstein’s conclusion about why the chemical imbalance theory persists despite decades of failures to validate it is similar to that which David Healey voices in “The Antidepressant Era,” — “It can reasonably be asked whether biological language offers more in the line of marketing copy than it offers in terms of clinical meaning.”
Dr. Jonathan Metzl writes that when a patient asks how his or her psychiatric medication is thought to work, “[t]he question, amazingly enough, often results in a disquieting pause. Sometimes, the physician will take the scientific approach. ‘What we know about their in vivo action is simply theory. There are many, many neurotransmitters in the brain. We know medications such as Prozac work on the serotonin system, thought to be involved in the mechanism of depression.’
“Sometimes, the response can sound a bit defensive. ‘Well, let’s just say they work.’ And sometimes, one can just change the subject. ‘Well, how about this weather, huh?’ But beneath these responses, or lack thereof, lies a discomforting truth: We are not entirely sure of the mechanism of action, broadly speaking, of many psychotropic medications. Moreover, while we have ample evidence attesting to these medications’ effect on brain chemistry, much remains to be said about the connection of brain chemistry and emotional well being.”
At least, people who decide to stop taking antidepressants might not be like diabetics choosing to stop using insulin. But they might not be like people disabling their power steering, either . [to be continued].
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