Thank you for thee excellent post. I had erred on the side of oversimplification regarding serotonergic systems in my post, and I agree with many of your points. I would just add that we all operate on the basis of assumptions regarding which dynamics create which symptom clusters that are not 'proven.' For example, one can state that standard SSRI's affect appetite on the basis of impacting depressive or OC variables, but since the precise role of serotonin systems in appetite/satiation/obesity is not really understood, we cannot be sure that it is via this mood-state modulation as opposed to some other satiety mechanism putatively modulated by the 'fens'. After all, the initial hypothesis pursued by the Wurtmans was that obese individuals were self-medicating against a serotonin-deficient dysphoric mood state via food intake, and they pursued this via dexfenfluramine. Ultimately, the mechanisms are not so well defined that the question is irrelevant. The lack of broadminded inquiry is more apparent in the neurotoxicity argument, which is one reason that the Phase IV study being initiated at Columbia will include an arm of patients on Prozac. I have no quarrel with the need to explore this, but I do believe that there are internal contradictions in the arguments that pertain to base rates, peripheral serotonin levels, and an underlying bias regarding obesity ('if you lazy obese people would just cut back on eating and exercise more, instead of looking for a quick fix').
So far as the diet mills are concerned, we agree, I simply believe that the NEJM definition of what is cosmetic vs noncosmetic weight reduction is overstated, this is not to excuse those prescribing these drugs to all comers.
I look forward to future comments. NeuroInvestment |
