Posted by Larry Hoover on November 28, 2002, at 9:11:30
In reply to Re: Is depression damaging my brain? » catmint, posted by Pfinstegg on November 26, 2002, at 22:44:18
> So, there is much to be hopeful about-depression is a potentially reversible disorder, physically. As treatments become more focussed on regulating the abnormalities in stress hormones, it is going to be much easier for people to attain really good remissions. Specifically, these would be cortisol-lowering drugs such as mifepristone, and a bit more in the future, CRH (corticotrophin-releasing hormone) antagonists. There are others, too, but they all have in common the goal of restoring HPA (hypo-pituitary-adrenal) axis regulation, and, by doing so, preventing various hormone excesses (in chronic fatigue syndrome and atypical depression, there may be brief bursts of excess hormones, followed by too little, but in bipolar and unipolar depression, there is chronic overproduction). Regulating these various hormones will, in turn, allow the hippocampal and pre-frontal neurons to regain normal volumes and dendrites, which should allow the various neurotransmitters- serotonin, dopamine and nor-epinephrine, plus others-to be released and taken up in a normal fashion.Just wanted to focus on this bit, and the stages of glandular exhaustion.
In crude terms, chronic stimulation of the HPA can cause the system to get stuck in hyper mode. In time, the adrenal glands start to "sputter", giving oscillations of hormonal response to the continuous onslaught of ACTH. Finally, glandular exhaustion arrives, and hypo symptoms set in.
That's one theoretical model of adrenal fatigue.
Proc Assoc Am Physicians 1999 Jan-Feb;111(1):22-34
The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences.Gold PW, Chrousos GP.
National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892-1284, USA.
The cardinal clinical manifestations of major depression with melancholic features include sustained anxiety and dread for the future as well as evidence of physiological hyperarousal (e.g., sustained hyperactivity of the two principal effectors of the stress response, the corticotropin-releasing-hormone, or CRH, system, and the locus ceruleus-norepinephrine, or LC-NE, system). Sustained stress system activation in melancholic depression is thought to confer both behavioral arousal as well as the hypercortisolism, sympathetic nervous system activation, and inhibition of programs for growth and reproduction that consistently occur in this disorder. Data also suggest that activation of the CRH and LC systems in melancholia are involved in the long-term medical consequences of depression such as premature coronary artery disease and osteoporosis, the two-three-fold preponderance of females in the incidence of major depression, and the mechanism of action of antidepressant drugs. In addition, recent data reveal important bidirectional interactions between stress-system hormonal factors in depression and neural substrates implicated in many discrete behavioral alterations in depression (e.g., the medial prefrontal cortex, important in shifting affect based on internal and external cues, the mesolimbic dopaminergic reward system, and the amygdala fear system). We have also advanced data indicating that the hypersomnia, hyperphagia, lethargy, fatigue, and relative apathy of the syndrome of atypical depression are associated with concomitant hypofunctioning of the CRH and LC-NE systems. These data indicate the need for an entirely different therapeutic strategy than that used in melancholia for the treatment of atypical depression, and they suggest that this subtype of major depression will be associated with its own unique repertoire of long-term medical consequences.
poster:Larry Hoover
thread:129341
URL: http://www.dr-bob.org/babble/20021127/msgs/129725.html