Society Logo
ME/CFS Australia Ltd
Please click here to donate ME/CFS Australia (SA) Inc
 
 
Facebook
 
ME/CFS SOUTH AUSTRALIA INC

Registered Charity 3104

Email:
sacfs@sacfs.asn.au

Mailing address:

PO Box 322,
Modbury,
South Australia 5092

Phone:
1300 128 339

Office Hours:
Monday - Friday,
10am - 4pm
(phone)

ME/CFS South Australia 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.

Disclaimer

ME/CFS South Australia 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.

Unless otherwise stated, the views expressed on this Web site are not necessarily the official views of the Society or its Committee and are not simply an endorsement of products or services.

Become a Member
DOCX Application Form (PDF, 156KB)
Why become a member?

ME/CFS: How Could The Illness Develop?

Friday 15 February 2019

 

From the medical journal Metabolic Brain Disease:

 

Stethoscope puzzle
 

Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

By Gerwyn Morris, Michael Maes, Michael Berk, Basant K. Puri
First Online: 13 February 2019
© 2018 Springer Nature Switzerland AG. Part of Springer Nature.

Abstract

A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals.

The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities.

Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation.

The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next.

Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

Keywords

Chronic fatigue syndrome
Myalgic encephalomyelitis
Endotoxin tolerance
Inflammation
Mitochondria
Oxidative and nitrosative stress

 

Full article…

 

 


 

blog comments powered by Disqus
Previous Previous Page