The Anatomy of
Depression: Part I
GOAL: The person with depression is in a complex homeostatic state, albeit a disturbed, negative, painful one. The task of the clinician is to develop an understanding of the homeostatic processes (social, biological, etc) involved, and the nodal points that require intervention. The clinician must then intervene at as many of these points as possible, at the same time, to re-establish a new more functional equilibrium.
THE PARADIGM: Neurotransmitters are built from a number of essential nutrients. The process, not too different from making a ‘big mac with special sauce', requires that certain ingredients (e.g., tryptophan, tyrosine, B vitamins, folic acid, B12, magnesium, etc.) be available in adequate supply. High demand (i.e., stress, certain medications such as stimulants and prilosec) requires a greater supply of the essential ingredients. If any of these is in short supply production and maintenance of a steady state is impaired. In addition, the breakdown and or recirculating of the neurotransmitters requires other nutrient dependent processes (e.g.folic acid, methionine). The task of the clinician is to assess the adequacy of diet, nutritional value of the food sources, digestion, and absorption of the key ingredients used to make the neurotransmitters.
BEN'S STORY: In June of 1985, Benjamin sat in the corner seat of my waiting room, feeling distraught and humiliated. Recently released after three weeks on "the psych ward" at McLean Hospital, this rejection-sensitive young man was still highly anxious, experiencing panic, hopelessness and suicidal ideation. His pain was poorly disguised by a thin veneer of quick humor. Using a combination of individual and group therapies, and phenelzine (an MAO inhibitor), gradually, over 5 years, he came to live a full life, and his visits to me were reduced to a biannual event, when I would catch up with his life, and enjoy some of his excellent sense of humor. In 1989, I switched Benjamin over to fluoxetine (Prozac) which lacked the risk of a hypertensive crisis. Benjamin did quite well, and eventually, he married and had three children. His wife, stressed by the maternal role which her own mother had abdicated, developed fibromyalgia. Benjamin's parent's health and finances deteriorated. As the breadwinner of his own family, and only child to his parents, his stress level rose significantly. In August of 1999, Benjamin came for an early visit. Fourteen years after his first panic and depression, he was now having a recurrence of the panic attacks. He was terrified that he would end up back in the hospital. He was convinced that he needed to change his medication to Zoloft. "I think it's ‘Prozac Poop out', he said.
THE PARADIGM: In general, when one is depressed regardless of the causes (i.e. metabolic, nutritional, social) distortions in one's thinking become part and parcel of the depression. Selective attention to these distorted thoughts (usually catastrophic thinking, all or nothing, etc-for a full description of this read Aaron Beck's Cognitive Therapy of Depression or "Feeling Good" by David Burns) is the norm for depressed patients. One aspect of the treatment of the depressed person is identifying these thoughts, the nature of the distortion, testing the logic behind the ‘automatic assumption'.
BEN'S STORY: I asked Benjamin what basis he had for thinking this, and explored his logic. I asked him if there were any other ways of looking at the situation. Finally I reassured him that hospitalization would not happen, and explained the reasons why (e.g., panic could easily be treated with a short acting benzodiazepine while we were searching for the cause, we could increase the frequency of contact as needed rather than use the hospital, he had a relationship with a psychiatrist he trusted, and who cared about him, whereas that was not the case 15 years earlier), knowing that it was important to deal directly with this negative thought and preoccupation.
THE PARADIGM: Untended, this "catastrophic fear" was causing anticipatory anxiety (activating his dorsal raphe nucleus), priming his limbic system for panic (locus coeruleus), and feeding-forward via the amygdala and locus coeruleus into full fledged panic, and the ‘hypothalamic-pituitary-adrenal gland (HPA) axis-activation-positive-feedback' loop. It would become a self-fulfilling prophecy.
Having addressed this thought, I explained to Benjamin that ‘Prozac poop-out', (the commonly held idea that the antidepressants often stop working after a while) was not a concept that makes sense. If a person with unipolar depression is fully responding to an antidepressant in an essentially stable manner for several months or more, and then relapses, it is incumbent on the practitioner to search for other factors that are now over-riding the medication (assuming adherence to the medication), such as psychosocial changes and stressors, as well as any aspect of metabolism.
At this point I decided that in order to approach the situation with ‘fresh eyes', I would evaluate Benjamin as if he were a new patient. I would do my best to leave no stone unturned, no assumption of mine unchallenged.
Tomorrow, I will detail the surprising domino-like events that nearly brought Ben to his knees.
