ME/CFS Society of WA: Normalization of leaky gut in ME/CFS
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01 January 2009

Normalization of leaky gut in chronic fatigue syndrome (CFS) is 

accompanied by a clinical improvement: effects of age, duration of 

illness and the translocation of LPS from gram-negative bacteria.


Journal: Neuro Endocrinol Lett. 2008 Dec 29;29(6). [Epub ahead of print]


Authors: Maes M, Leunis JC.


Affiliation: M-Care4U Outpatient Clinics, and the Clinical Research 

Center for Mental Health, Belgium.


NLM Citation: PMID: 19112401



BACKGROUND: There is now evidence that an increased translocation of 

LPS from gram negative bacteria with subsequent gut-derived 

inflammation, i.e. induction of systemic inflammation and oxidative & 

nitrosative stress (IO&NS), is a new pathway in chronic fatigue 

syndrome (CFS).


METHODS: The present study examines the serum concentrations of IgA 

and IgM to LPS of gram-negative enterobacteria, i.e. Hafnia Alvei; 

Pseudomonas Aeruginosa, Morganella Morganii, Pseudomonas Putida, 

Citrobacter Koseri, and Klebsielle Pneumoniae in CFS patients both 

before and after intake of natural anti-inflammatory and 

anti-oxidative substances (NAIOSs), such as glutamine, N-acetyl 

cysteine and zinc, in conjunction with a leaky gut diet during 10-14 

months. We measured the above immune variables as well as the 

Fibromyalgia and Chronic Fatigue Syndrome Rating Scale in 41 patients 

with CFS before and 10-14 months after intake of NAIOSs.


RESULTS: Subchronic intake of those NAIOSs significantly attenuates 

the initially increased IgA and IgM responses to LPS of gram negative 

bacteria. Up to 24 patients showed a significant clinical improvement 

or remission 10-14 months after intake of NAIOSs. A good clinical 

response is significantly predicted by attenuated IgA and IgM 

responses to LPS, the younger age of the patients, and a shorter 

duration of illness (< 5 years).


DISCUSSION: The results show that normalization of the IgA and IgM 

responses to translocated LPS may predict clinical outcome in CFS. 

The results support the view that a weakened tight junction barrier 

with subsequent gut-derived inflammation is a novel pathway in CFS 

and that it is a new target for drug development in CFS. Meanwhile, 

CFS patients with leaky gut can be treated with specific NAIOSs and a 

leaky gut diet.


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