Abstract
Currently, a psychologically based model is widely held to be the basis for the aetiology and treatment of chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME)/systemic exertion intolerance disease (SEID). However, an alternative, molecular neurobiological approach is possible and in this paper evidence demonstrating a biological aetiology for CFS/ME/SEID is adduced from a study of the history of the disease and a consideration of the role of the following in this disease: nitric oxide and peroxynitrite, oxidative and nitrosative stress, the blood–brain barrier and intestinal permeability, cytokines and infections, metabolism, structural and chemical brain changes, neurophysiological changes and calcium ion mobilisation. Evidence is also detailed for biologically based potential therapeutic options, including: nutritional supplementation, for example in order to downregulate the nitric oxide-peroxynitrite cycle to prevent its perpetuation; antiviral therapy; and monoclonal antibody treatment. It is concluded that there is strong evidence of a molecular neurobiological aetiology, and so it is suggested that biologically based therapeutic interventions should constitute a focus for future research into CFS/ME/SEID.
Highlights
The disorder variously known inter alia as chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME) and systemic exertion intolerance disease (SEID) has a phenotype of unknown aetiology, whilst there is considerable controversy over the most appropriate treatment approach(es)
After briefly discussing the history and definition of this disorder, we consider a wide variety of molecular neurobiological factors and we describe an evidence-based approach to the treatment of CFS/ME/SEID
In 2003, Smirnova and Pall reported that the serum protein carbonyl levels are elevated in CFS patients compared with controls, while there is no significant difference in total protein levels [26]
Summary
The disorder variously known inter alia as chronic fatigue syndrome (CFS), myalgic encephalomyelitis (ME) and systemic exertion intolerance disease (SEID) has a phenotype of unknown aetiology, whilst there is considerable controversy over the most appropriate treatment approach(es). In this in-depth review, we bring together the results of research into the molecular neurobiological mechanisms which underpin CFS/ME/SEID, thereby providing helping to inform an evidence-based approach to its treatment. After briefly discussing the history and definition of this disorder, we consider a wide variety of molecular neurobiological factors and we describe an evidence-based approach to the treatment of CFS/ME/SEID
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