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How ME/CFS Progresses: The Natural History Of ME/CFS

Friday 4 September 2020


From Frontiers in Neurology:


Frontiers in Neurology

How Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) Progresses: The Natural History of ME/CFS


Front. Neurol., 11 August 2020 |

Luis Nacul1,2, Shennae O'Boyle1*, Luigi Palla3,4, Flavio E. Nacul5, Kathleen Mudie1, Caroline C. Kingdon1, Jacqueline M. Cliff6, Taane G. Clark6, Hazel M. Dockrell6 and Eliana M. Lacerda1

1Department of Clinical Research, Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom
2B.C. Women's Hospital and Health Centre, Vancouver, BC, Canada
3Department of Medical Statistics, Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom
4Department of Global Health, School of Tropical Medicine and Global Health, Nagasaki University, Nagasaki, Japan
5Pro-Cardiaco Hospital and Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
6Department of Infection Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom

Copyright © 2020 Nacul, O'Boyle, Palla, Nacul, Mudie, Kingdon, Cliff, Clark, Dockrell and Lacerda. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY).

We propose a framework for understanding and interpreting the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) that considers wider determinants of health and long-term temporal variation in pathophysiological features and disease phenotype throughout the natural history of the disease.

As in other chronic diseases, ME/CFS evolves through different stages, from asymptomatic predisposition, progressing to a prodromal stage, and then to symptomatic disease.

Disease incidence depends on genetic makeup and environment factors, the exposure to singular or repeated insults, and the nature of the host response.

In people who develop ME/CFS, normal homeostatic processes in response to adverse insults may be replaced by aberrant responses leading to dysfunctional states.

Thus, the predominantly neuro-immune manifestations, underlined by a hyper-metabolic state, that characterize early disease, may be followed by various processes leading to multi-systemic abnormalities and related symptoms.

This abnormal state and the effects of a range of mediators such as products of oxidative and nitrosamine stress, may lead to progressive cell and metabolic dysfunction culminating in a hypometabolic state with low energy production.

These processes do not seem to happen uniformly; although a spiraling of progressive inter-related and self-sustaining abnormalities may ensue, reversion to states of milder abnormalities is possible if the host is able to restate responses to improve homeostatic equilibrium.

With time variation in disease presentation, no single ME/CFS case description, set of diagnostic criteria, or molecular feature is currently representative of all patients at different disease stages.

While acknowledging its limitations due to the incomplete research evidence, we suggest the proposed framework may support future research design and health care interventions for people with ME/CFS.


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