• Corpus ID: 5792328

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.

  title={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.},
  author={Michael Maes and J C Leunis},
  journal={Neuro endocrinology letters},
  volume={29 6},
  • M. MaesJ. Leunis
  • Published 1 December 2008
  • Medicine, Biology
  • Neuro endocrinology letters
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. [] Key Method 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.

Tables from this paper

Leaky gut in chronic fatigue syndrome: A review

Treatment for 10-14 months with specific anti- inflammatory and -oxidative substances (NAIOSs), with or without immunoglobins intravenously (IVIg), significantly attenuates the initially increased IgA and IgM responses to LPS, showing that the gut-derived inflamma- tion is attenuated and thus that the weakened tight junction barrier is partly restored.

Changes in Gut and Plasma Microbiome following Exercise Challenge in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

A role for an altered gut microbiome and increased bacterial translocation following exercise in ME/CFS patients that may account for the profound post-exertional malaise experienced by patients is suggested.

The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications

A review of genetics, infections, and other influences that may factor into the alterations seen in the GM of ME/CFS individuals are reflected, consequences arising from these changes are discussed, and the therapeutic potential of treating the gut to alleviate ME/ CFS symptoms holistically is contemplated.

Modification of Immunological Parameters, Oxidative Stress Markers, Mood Symptoms, and Well-Being Status in CFS Patients after Probiotic Intake: Observations from a Pilot Study

The results suggest that probiotics can modify the well-being status as well as inflammatory and oxidative indexes in CFS/ME patients.

Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS.

It is found that the mean age of patients with myalgic encephalomyelitis/chronic fatigue syndrome dying from heart failure is significantly lower than the age of those dying fromHeart failure in the general US population, i.e. 58.7 years, and this implicate that ME/CFS is a risk factor to cardio-vascular disorder.

Attenuation of autoimmune responses to oxidative specific epitopes, but not nitroso-adducts, is associated with a better clinical outcome in Myalgic Encephalomyelitis/chronic fatigue syndrome.

Reductions in IgM responses to oleic acid, MDA and Pi, but not in any of the NO-adducts, were associated with reductions in severity of illness, and these pathways are a new drug target in a subgroup of ME/CFS patients.

The reification of the clinical diagnosis of myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) as an immune and oxidative stress disorder: construction of a data-driven nomothethic network and exposure of ME/CFS subgroups.

This bottom-up explicit data model of ME/CFS objectivates the descriptive narratives of the ME/ cFS phenome, using causome-protectome-AOP data, whereby the abstract concept ME/ CFS is translated into pathways, thereby securing the reification of the Me/C FS phenome.

In schizophrenia, chronic fatigue syndrome- and fibromyalgia-like symptoms are driven by breakdown of the paracellular pathway with increased zonulin and immune activation-associated neurotoxicity.

FF symptoms are part of the phenome of schizophrenia and BCPS-worsening as well, and belong to a common core shared by G-CoDe, symtopmatome, and QoL phenomenome.

A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior

It is concluded that sickness behavior and ME/CFS are two different conditions, where the pathophysiology is related to activation of immunoinflammatory and oxidative pathways and autoimmune responses.



Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome.

A case of a 13 year old girl with CFS who showed very high values for serum IgM against the LPS of some enterobacteria and signs of oxidative and nitrosative stress, activation of the inflammatory response system, and IgG3 subclass deficiency is reported.

Chronic fatigue syndrome is accompanied by an IgM-related immune response directed against neopitopes formed by oxidative or nitrosative damage to lipids and proteins.

The results show that CFS is characterized by an IgM-related immune response directed against disrupted lipid membrane components, by-products of lipid peroxidation, S-farnesyl-L-cysteine, and NO-modified amino-acids, which are normally not detected by the immune system but due to oxidative and nitrosative damage have become immunogenic.

Not in the mind of neurasthenic lazybones but in the cell nucleus: patients with chronic fatigue syndrome have increased production of nuclear factor kappa beta.

The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NFkappabeta.

Not in the mind but in the cell: increased production of cyclo-oxygenase-2 and inducible NO synthase in chronic fatigue syndrome.

It is found that the production of COX-2 and iNOS was significantly higher in CFS patients than in normal controls and an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS.

Inflammatory and oxidative and nitrosative stress pathways underpinning chronic fatigue, somatization and psychosomatic symptoms

  • M. Maes
  • Medicine
    Current opinion in psychiatry
  • 2009
‘Functional’ symptoms in CFS and somatization, have a genuine organic cause, that is activation of peripheral and central IO&NS pathways and gut-derived inflammation, and the development of new drugs, aimed at treating those disorders, should target these IO& NS pathways.

Glutamine: role in gut protection in critical illness

  • P. Wischmeyer
  • Medicine
    Current opinion in clinical nutrition and metabolic care
  • 2006
Mechanistic findings, combined with a limited amount of clinical data showing benefit on gut permeability in illness and injury, indicate more formal studies need to be carried out looking the role of glutamine in gut protection and as an antiinflammatory in critical illness.

Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis

Adding GLN to standard TPN not only reduces the permeability of the colon but decreases pancreatic infections in acute necrotizing pancreatitis in the rat, confirming previous reports that GLN decreases bacterial translocation by stabilizing the intestinal mucosal barrier.

Environmental stress-induced gastrointestinal permeability is mediated by endogenous glucocorticoids in the rat.

BACKGROUND & AIMS Abnormal presentation of luminal constituents to the mucosal immune system, caused by dysfunction of the intestinal epithelial barrier, is a candidate theory for the cause of

Zinc Supplementation Tightens “Leaky Gut” in Crohn’s Disease

The findings show that zinc supplementation can resolve permeability alterations in patients with Crohn’s disease in remission and improving intestinal barrier function may contribute to reduce the risk of relapse in Crohn's disease.