One Comment

  1. YoungProfessorD

    Okay, this too may be an exhausting read, and I am aware of the fact that my personal bias (being an addict) may very well influence my insight or opinion on the matter, but less so than the original commentor (edie)…
    Very good entry. I’m happy to see some objective input on this notion which has been speculated about for a while; and not surprisingly, many of those who do get carried away with this theory and preach it as a ‘major breakthrough’ happen to be those with a history of opioid dependence/addiction. On the one hand, I think the idea of “EDS” for some serves as a convenient rationalization for narcotic use, or at least offers them a sense of comfort in ‘understanding’ a very intricate something about themselves which before they were unable to grasp. It’s human nature to take comfort in knowing the unknown, even if our understanding is false.
    BUT On the other hand; I believe that the somewhat exclusive embracement by the medical and pharmaeutical establishment of the monoamine hypothesis for depression has severely handicapped our current understanding of depressive disorders in a sense that one specific theory has been applied to a wide spectrum of illnesses which could be manifestations of MANY different components; hormonal, neurological, neurochemical/protein, physiological/somatic. I also believe that much of the stigma surrounding opioids has led to a reluctance of the medical and research establishment to even consider the theory of an opioidergic role in certain subtypes of depression-anxiety spectrum disorders. If the medical establishment is to embrace the idea of a mesolymbic role involving-dopamine in depressive disorders, than I would think it would be reasonable to at least (open mindedly) explore a role in the opioidergic systems – It’s my understanding that the opioid & dopamine systems are closely linked in many ways, opioidergic neurons terminate in the VTA, inhibiting GABA’s ‘braking’ role and allowing increased dopaminergic firing into the nucleus accumbens; while conversely, increased dopamine activity promotes increases in beta-endorphin.. I believe slow acting serotonergic and noradrenergic targeted pharmacotherapy indeed has its place in many cases; even with modest response rates, it may be better than the alternative (i.e. nothing), but I also believe that more research targeting the mesolymbic reward circuits (and its primary component dopamine), as well as our natural ‘pain modulators’, would be beneficial as well. With advances in research and new drug developments, better targeted, site specific opioids could possibly offer symtomatic improvement with reduced adverse effects including rapid progression of tolerance & respiratory depression (I personally don’t consider the ‘euphoric’ effect to be evil in itself, but when combined with the aforementioned can lead to destructive results)… Selective mu-1 agonists, kappa antagonists, enkephalinase reuptake inhibitors, selective delta agonists, ORL-1 antagonists, perhaps even supplemented with SRI/NRI-type drugs when ACTUALLY necessary, along with non-drug approaches the possibilities are vast… I do believe it should be explored; or at least not neglected to the degree it is currently.. Which I believe is all due to the socially taboo status of opioids and “fast acting” relief.. What better is a slower acting, non rewarding tricyclic, maoi, or ssri? It’s still a temporary, exogenous solution; only not frowned upon why, because it’s slower acting and doesn’t make one so happy (or “high” as they call it)?

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