Posted by jerrympls on March 16, 2006, at 3:02:43
In reply to Re: Vicodin questions............ » fairywings, posted by TylerJ on March 15, 2006, at 8:47:49
>
> Great for pain, but for clinical depression it is a dead-end!
>
> TylerI'll have to disagree with you Tyler. My doctor has me on hydrocodone 5mg 4x daily along with my other meds for depression. There ARE studies out there supporting the use of opiates in treatment-resistant cases. I've been on hydrocodone (the opiate part of Vicodin) for 18 months now. No tolerance. No abuse. No change in dosage. This is actually a typical response from those on opiates w/ treatment-resistant depressions.
Take a look at this:
http://opioids.com/naloxone/depcrf.html
----------------------------
The effect of naloxone on adrenocorticotropin and cortisol release: evidence for a reduced response in depression
by
Burnett FE, Scott LV, Weaver MG, Medbak SH, Dinan TG
Department of Psychological Medicine,
The Medical Colleges of St. Bartholomew's
and the Royal London Hospitals,
West Smithfield, UK.
J Affect Disord 1999 Jun; 53(3):263-8ABSTRACT
BACKGROUND: Endogenous opioid peptides inhibit the hypothalamic-pituitary-adrenal (HPA) axis by influencing the release of hypothalamic corticotropin releasing factors. This study examines whether increased activity of the HPA axis in major depression is associated with reduced opioid tone. METHODS: We measured the adrenocorticotropin (ACTH) and cortisol responses to an intravenous bolus of naloxone 0.125 microg/kg in 13 depressed outpatients and 13 healthy volunteers. RESULTS: The mean cortisol response was significantly reduced (P<0.05), and the ACTH response was also non-significantly reduced in the depressed subjects. CONCLUSIONS: These findings imply that the degree of inhibitory endogenous opioid tone is reduced in depression. Various mechanisms for the finding are discussed, including possible alteration in the function of alpha-adrenergic pathways. CLINICAL IMPLICATIONS: Reduced endogenous opioid tone may explain why some depressed individuals self-medicate with opiates, and depression is associated with opiate withdrawal. Opioid pathways may have a role in the mechanism of action of antidepressant drugs, and may be of relevance in the development of novel antidepressants. LIMITATIONS OF THE STUDY: The sample size was small, leading to a failure of the difference of the basal cortisol levels and also the delta ACTH between the groups to reach statistical significance.
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Now don't misunderstand me -I'm not advocating opiate therapy as a first-line therapy by ANY means. However, one cannot generalize that all "addicitive" medications will ultimately briing out the "addicit" in all of us - no matter what. This is not true. Not all people who drink alcohol are alcoholics - correct?
I believe that "fairywing's" positive antidepressant repsonse to Vicodin is an important clue that points to other models of depressive response that do NOT include the basic - overused and over-simplfied model of "serotonin-imbalance." These "other" models include imbalnces in the HPA axis/cortisol levels/hormonal balances, etc.
I believe we have to accept that an imbalance in serotonin most likely is the RESULT of imblances within other neural-hormonal systems within the brain.
I don't mean to negate anything you are saying - or disrepect you - or preach - I just wanted to post my experiences.
Thanks
Jerry
poster:jerrympls
thread:620477
URL: http://www.dr-bob.org/babble/20060315/msgs/620852.html