Posted by jedi on January 25, 2006, at 3:02:49
In reply to Tired-all the time? advice?, posted by Paulbwell on January 18, 2006, at 22:31:49
> I have been apathetic lately and tired, all i wanna do is sleep, and leave the world alone.
>Hi,
The gold standard for treatment resistant atypical depression is the MAOI phenelzine(Nardil). When nothing else works, there is a very good chance that this will. I have been on and off Nardil for ten years. It is the only thing that has brought me out of three major atypical depressions.
Atypical depression is actually quite typical. Probably the most common type of depression.
Take care,
Jedi
Link:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15564336&query_hl=9&itool=pubmed_docsum
Endocrinology. 2005 Mar;146(3):1338-47. Epub 2004 Nov 24. Related
Chronic treatment with the monoamine oxidase inhibitor phenelzine increases hypothalamic-pituitary-adrenocortical activity in male C57BL/6 mice: relevance to atypical depression.Kier A, Han J, Jacobson L.
Center for Neuropharmacology and Neuroscience, MS 501E, Albany Medical College, Mail Code 136, Albany, New York 12208, USA.
Atypical depression has been linked to low hypothalamic-pituitary-adrenocortical axis activity and exhibits physical and affective symptoms resembling those of glucocorticoid deficiency. Because atypical depression has also been defined by preferential responsiveness to monoamine oxidase inhibitors (MAO-I), we hypothesized that MAO-I reverse these abnormalities by interfering with glucocorticoid feedback and increasing hypothalamic-pituitary-adrenocortical activity. To test this hypothesis, we measured plasma hormones and ACTH secretagogue gene expression in male C57BL/6 mice treated chronically with saline vehicle or phenelzine, a representative MAO-I. Changes in glucocorticoid feedback were evaluated using adrenalectomized (ADX) mice with and without corticosterone replacement. Antidepressant efficacy was confirmed by decreased immobility during forced swim testing. Phenelzine significantly increased circadian nadir and postrestraint plasma corticosterone levels in sham-operated mice, an effect that correlated with increased adrenocortical sensitivity to ACTH. Phenelzine increased circadian nadir, but not poststress ACTH in ADX mice, suggesting that phenelzine augmented corticosterone secretion in sham-operated mice by increasing stimulation and decreasing feedback inhibition of hypothalamic-pituitary activity. Consistent with the latter possibility, phenelzine significantly increased plasma ACTH and paraventricular hypothalamus CRH mRNA in ADX, corticosterone-replaced mice. Phenelzine did not increase paraventricular hypothalamus CRH or vasopressin mRNA in ADX mice lacking corticosterone replacement. We conclude that chronic phenelzine treatment induces sustained increases in glucocorticoids by impairing glucocorticoid feedback, increasing adrenocortical responsiveness to ACTH, and increasing glucocorticoid-independent stimulation of hypothalamic-pituitary activity. The resulting drive for adrenocortical activity could account for the ability of MAO-I to reverse endocrine and psychiatric symptoms of glucocorticoid deficiency in atypical depression.
PMID: 15564336 [PubMed - indexed for MEDLINE]
poster:jedi
thread:600569
URL: http://www.dr-bob.org/babble/20060122/msgs/602568.html