It’s High Time for Rethinking Depression Models
If you routinely work with clients who are medicated with antidepressants as I do, I’d bet that you’ve heard this all too familiar refrain: “My antidepressant isn’t working the way it used to, can you tell me why?”
Such a question puts us on the spot, because depression is associated with multiple dynamics and there are myriad influences affecting the actions of antidepressants in any given client. Thus, what has historically been referred to as the monoamine hypothesis – which postulates that depression is linked to alterations in serotonin-related physiology and stress hormones – is becoming increasingly more questionable for this reason: The vast majority of antidepressant users experience at best a partial or incomplete response to these drugs, and for some, the effect is immeasurable. And to complicate matters even more, there are scores of patients who present to treatment with a number of complaints such as aches, pains, tiredness, a pleasureless life, cognitive fog and gastrointestinal distress. All of these symptoms are beyond the scope of what antidepressants are able to effectively treat. But in spite of the increasingly obvious flaws in the altered neurotransmitter hypothesis, these drugs continue to be called upon to perform at way beyond their pay grade.
The real problem here is that the diverse presentations of depressive illness suggest that our current models for defining depression are archaic or downright wrong. This will require a change in thinking regarding causes of depression that just might direct us to more effective treatment of affected individuals.
I have long contended that depression is primarily a physical disorder or illness with medical, psychological, cognitive and behavioral manifestations. What I’m saying here is that we’ve long been treating symptoms which I believe aren’t this disorder’s primary cause.
Enter the inflammation model – a new perspective on chronic depression. Although first introduced in the early 1990s, the depression-inflammation connection hadn’t blossomed into something of significance until recently. New clinical thinking is that an inflammatory process is situated “upstream” in the body of a susceptible individual, and that inflammatory “waste” traveling downstream acts as a contaminant which influences the emergence of symptoms we typically ascribe to depression.
The inflammatory model is implicated in conditions such as cardiovascular and autoimmune disorders, diabetes and cancer, so approaching depression as an inflammatory syndrome may open the door to more effective pharmacological interventions capable of delivering results that outshine the paltry track record of antidepressants.
Celebrex (celecoxib), an anti-inflammatory, has been found in randomized, placebo-controlled trials to be superior to placebo as an augmenting agent to antidepressants.
The etiology of depression has long been veiled in uncertainty and the likelihood that it is a multifaceted clinical entity with many tentacles attached is becoming more and more plausible. The inflammatory theory may very well prove to be a viable launching pad for the further exploration of more effective treatments for depression; and together with diet modification, exercise and psychotherapy, anti-inflammatory drugs may reveal themselves to be just the right medicine for targeting depression at its “headwaters.”
Joe Wegmann is a licensed pharmacist & clinical social worker has presented psychopharmacology seminars to over 10,000 healthcare professionals in 46 states, and maintains an active psychotherapy practice specializing in the treatment of depression and anxiety. He is the author of Psychopharmacology: Straight Talk on Mental Health Medications, published by PESI, Inc.