Posted by Tomatheus on June 19, 2008, at 1:34:27
In reply to Re: Clomipramine vs. Nardil » SLS, posted by Phoenix1 on June 18, 2008, at 11:12:18
> What, neurochemically speaking, would explain such a positive response to an MAOI, but negative responses to all other classes? Does this suggest some sort of trace amine deficiency that the other AD's don't touch?
High-activity variants of the MAO-A gene have been shown to be positively correlated with depressed suicide, major depressive disorder, and sleep disturbance in males (Du et al., 2002; Du et al., 2004). More recently, high levels of the MAO-A enzyme itself have been shown to be elevated in depressive patients (Meyer et al., 2006).
Theoretically, individuals with high levels of either MAO-A or MAO-B might respond uniquely to the nonselective MAOIs Nardil, Parnate, and Marplan. Given the evidence for an association between high levels of MAO-A and depression, it could be the case that individuals like yourself who respond most favorably to MAOIs might be doing so because MAOIs are the only medications that truly address the problem of having abnormally high levels of MAO-A. Despite increasing monoamine neurotransmission, antidepressants such as the TCAs, SSRIs, and SNRIs might not be adequate treatments for those who respond uniquely to MAOIs (a group of patients who could conceivably include those with high levels of MAO-A) because such antidepressants do not reduce the levels of monoamine-oxidization byproducts such as ammonia and hydrogen peroxide.
Having said this, there is no way for me to conclusively say that you (or anybody else) has high MAO-A levels *and* will only be responsive to MAOIs. Individuals with high levels of MAO-A might conceivably respond well to medications other than MAOIs, so even if you are one of these individuals, the only way to determine what your response to various meds will be is through trial and error. Hopefully, the practice of psychiatry will one day involve less guesswork, but unfortunately, that day is not here yet.
Tomatheus
==
Du, L., Faludi, G., Palkovits, M., Sotonyi, P., Bakish, D., & Hrdina, P.D. (2002). High activity-related allele of MAO-A gene associated with depressed suicide in males. Genetics of Nervous System Disease, 13, 1195-1198. Abstract: http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-200207020-00025.htm;jsessionid=LZ4Q1CmvwgypvLj7tFy5fJgpNtRGVXBX1lXH8R7KFTTWQxhL22cn!-74786611!181195628!8091!-1
Du, L., Bakish, D., Ravindran, A., & Hrdina, P.D. (2004). MAO-A gene polymorphisms are associated with major depression and sleep disturbance in males. Molecular Neuroscience, 15, 2097-2101. Abstract: http://www.neuroreport.com/pt/re/neuroreport/abstract.00001756-200409150-00020.htm;jsessionid=LZ4G0fYwQlgTyNGcZCzGYvXqPrJGx9BszWth1TGCJCpqldsPMYNX!-74786611!181195628!8091!-1
Meyer, J.H., Ginovart, N., Boovariwala, A., Sagrati, S., Hussey, D., Garcia, A., et al. (2006). Elevated monoamine oxidase A levels in the brain: An explanation for the monoamine imbalance of major depression. Archives of General Psychiatry, 63, 1209-1216. Abstract: http://archpsyc.ama-assn.org/cgi/content/abstract/63/11/1209
poster:Tomatheus
thread:835192
URL: http://www.dr-bob.org/babble/20080617/msgs/835402.html