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PostPosted: Mon Mar 11, 2013 7:21 am 
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A new study suggests that treatment with adrenocorticotropic hormone (ACTH) may be helpful for people whose multiple sclerosis (MS) is not well-controlled through their regular treatment. The study was released today and will be presented at the American Academy of Neurology's 65th Annual Meeting in San Diego, March 16 to 23, 2013.

The study involved 23 people with MS who were taking beta-interferon treatment and had at least one relapse or brain scan showing new disease activity within the previous year. They were considered to have "breakthrough" MS, which means that their treatment that had been working previously stopped being effective, leading to worsening disability and more frequent relapses, as well as increased evidence of disease activity on brain scans.... Read More - http://www.ms-uk.org/index.cfm/hormones

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PostPosted: Mon Mar 11, 2013 8:29 am 
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Very interesting! I'm going to have to poke around this idea. I experienced improvements while suppressing ACTH. I wonder if the DMDs don't suppress it as well...maybe too far???


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PostPosted: Mon Mar 11, 2013 9:45 am 
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Beta-interferon actually stimulates ACTH release. But after a while, it fails to do so. I wonder if it doesn't cause adrenal exhaustion (can only find so-so evidence of this so far). If our relapses/progression are due to electrolyte imbalances, that exhaustion would work for us to a point. And then we would relapse because of a different electrolyte imbalance, which might be temporarily corrected by exogenous administration of ACTH.

http://www.ncbi.nlm.nih.gov/pubmed/15947464
Quote:
Effects of interferon-beta 1a on the hypothalamic-pituitary-adrenal axis, leukocyte distribution and mood states in multiple sclerosis patients: results of a 1-year follow-up study.
Goebel MU, Czolbe F, Becker H, Janssen OE, Schedlowski M, Limmroth V.
Source
Department of Medical Psychology, Medical Faculty, Division of Endocrinology, University of Duisburg-Essen, Duisburg-Essen, Germany.
Abstract
Acute interferon-beta (IFN-beta) administration transiently activates the hypothalamic-pituitary-adrenal (HPA) axis, increases granulocytes, and reduces lymphocytes in peripheral blood. To test whether these effects are still present after long-term treatment, 13 patients with relapsing-remitting multiple sclerosis were analyzed at baseline, and 1, 2, 4, and 8 h after IFN-beta 1a injection at two occasions: at the initial administration and after 1 year of continuous treatment. Long-term treatment reduced the responsiveness of the HPA axis to the injection, and abolished the distributional changes in leukocyte numbers. One-year treatment with IFN-beta 1a did not induce mood alterations as assessed by the Profile of Mood States. These results suggest that long-term IFN-beta therapy has a profound impact on leukocyte distribution and the neuroendocrine response to the drug.


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