ME/CFS AUSTRALIA (SA) INC
Registered Charity 698
PO Box 28,
South Australia 5007
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19 North Terrace,
Hackney, SA, 5069
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(reopened 1 February 2017)
ME/CFS Australia (SA) Inc supports the needs of sufferers of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and related illnesses. We do this by providing services and information to members.
ME/CFS Australia (SA) Inc aims to keep members informed of various research projects, diets, medications, therapies, news items, etc. All communication, both verbal and written, is merely to disseminate information and not to make recommendations or directives.
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Could mitochondrial dysfunction be a marker to distinguish FM from ME/CFS?
Monday 29 April 2013
Editor's comment: Mitochondria are the energy producers of the cells. The mitochondria supply this energy in the form of adenosine triphosphate (ATP), the molecule upon which all cellular functions in the body depend. Coenzyme Q10 acts as the catalyst that makes it possible for the mitochondria to produce ATP. Previous research has demonstrated that mitochondrial dysfunction is present in both fibromyalgia and ME/CFS (chronic fatigue syndrome). However, this is the first study to suggest that the type of mitochondrial dysfunction may serve as a marker that is able to differentiate FM from ME/CFS. For more information about mitochondrial dysfunction in FM, see “Dr. Myhill on Fibromyalgia and Mitochondrial Dysfunction.”
Could mitochondrial dysfunction be a differentiating marker between Chronic Fatigue Syndrome and Fibromyalgia?
By J. Castro-Marrero, et al.
Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM) are complex and serious illnesses. It is estimated to affects up to 2.5% and 5% of the general population worldwide, respectively. The aetiology is unknown; however, recent studies suggest that mitochondrial dysfunction has been involved in the pathophysiology of both conditions.
We have investigated the possible association between mitochondrial biogenesis and oxidative stress in patients with CFS and FM. We studied 23 CFS patients, 20 FM patients and 15 healthy controls.
These data lead to the hypothesis that mitochondrial dysfunction-dependent events could be a marker of differentiation between CFS and FM indicating the mitochondria as a new potential therapeutic target for these conditions.
Source: Antioxidants & Redox Signaling, April 22, 2013. By J. Castro-Marrero, M.D. Cordero, N. Saez-Francas, C. Jimenez-Gutiérrez, F.J. Aguilar-Montilla, L. Aliste, and J. Alegre-Martin. Vall de Hebron Univ Hospital Research Institute, CFS Unit, BARCELONA, Barcelona, Spain; email@example.com.
The above, with comments, originally appeared here.
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