Posted by ed_uk on June 2, 2005, at 15:30:51
In reply to Re: Gymnemna Sylvestre (sp?) » Chairman_MAO, posted by Ktemene on June 2, 2005, at 11:09:45
Med Hypotheses. 1994 Oct;43(4):247-52.
Enhancing central and peripheral insulin activity as a strategy for the treatment of endogenous depression--an adjuvant role for chromium picolinate?
McCarty MF.
Nutrition 21, San Diego, California 92109.
Depression is often associated with insulin resistance, owing to cortisol overproduction; conversely, many studies suggest that diabetics are at increased risk for depression. Recent evidence indicates that insulin is transported through the blood-brain barrier and influences brain function via widely distributed insulin receptors on neurons. These receptors are particularly dense on catecholaminergic synaptic terminals, and, while effects are variable dependent on brain region, several studies indicate that insulin promotes central catecholaminergic activity, perhaps by inhibiting synaptic re-uptake of norepinephrine. Additionally, it is well known that insulin enhances serotonergic activity in increasing blood-brain barrier transport of tryptophan. Since impaired monoaminergic activity in key brain pathways is believed to play an etiological role in depression, techniques which promote effective insulin activity, both centrally and peripherally, may be therapeutically beneficial in this disorder. This may rationalize anecdotal reports of improved mood in clinical depressives and diabetics receiving the insulin-sensitizing nutrient chromium picolinate. This nutrient, perhaps in conjunction with other insulin-sensitizing measures such as low-fat diet and aerobic exercise training (already shown to be beneficial in depression), should be tested as an adjuvant for the treatment and secondary prevention of depression.
J Clin Psychiatry. 1999 Apr;60(4):237-40.Chromium potentiation of antidepressant pharmacotherapy for dysthymic disorder in 5 patients.
McLeod MN, Gaynes BN, Golden RN.
Department of Psychiatry, University of North Carolina School of Medicine, Chapel Hill 27599-7160, USA.
BACKGROUND: Dysthymic disorder is a relatively common illness that is often treated with antidepressants. Compared with the study of major depression, there has been little systematic study of potentiation strategies for antidepressant-refractory dysthymic disorder. METHOD: Following a patient's report of dramatic response to the addition of chromium supplementation to sertraline pharmacotherapy for dysthymic disorder (DSM-IV), the authors initiated a series of single-blind and open-label trials of chromium picolinate or chromium polynicotinate in the treatment of antidepressant-refractory dysthymic disorder. RESULTS: In a series of 5 patients, chromium supplementation led to remission of dysthymic symptoms. Single-blind substitution of other dietary supplements in each of the patients demonstrated specificity of response to chromium supplementation. CONCLUSION: Preliminary observations suggest that chromium may potentiate antidepressant pharmacotherapy for dysthymic disorder. Controlled studies are indicated to test the validity of these initial observations.
Biol Psychiatry. 2003 Feb 1;53(3):261-4.
Effectiveness of chromium in atypical depression: a placebo-controlled trial.Davidson JR, Abraham K, Connor KM, McLeod MN.
Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina 27710, USA.
BACKGROUND: Chromium picolinate (CP) has been reported to benefit patients with symptoms of atypical depression. METHODS: A placebo-controlled, double-blind, pilot study of CP was conducted in 15 patients with DSM-IV major depressive disorder, atypical type. Patients received 600 micro g of CP or matching placebo (PBO) for 8 weeks. RESULTS: Seven (70%) CP and zero (0%) PBO patients met responder criteria (p =.02). Other outcomes were consistent with greater effect of CP. Three patients on CP failed to show any improvement. Chromium picolinate was well tolerated. CONCLUSIONS: Chromium picolinate shows promising antidepressant effects in atypical depression. Its mechanism of action may relate to 5HT2A downregulation, increased insulin sensitivity, or to other effects.
poster:ed_uk
thread:506832
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