Inflammatory and oxidative and nitrosative stress pathways underpinning chronic fatigue

Discussion in 'Fibromyalgia Main Forum' started by RadioFM, Mar 5, 2015.

  1. RadioFM

    RadioFM Active Member

    "A study performed by Michael Maes found that the functional symptoms of CFS have a genuine organic cause in the activation of peripheral and central inflammatory and oxidative and nitrosative stress pathways and gut-derived inflammation."

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

    "The aim of this paper is to review recent findings on inflammatory and oxidative and nitrosative stress (IO&NS) pathways in chronic fatigue and somatization disorder."


    "Activation of IO&NS pathways is the key phenomenon underpinning chronic fatigue syndrome (CFS): intracellular inflammation, with an increased production of nuclear factor kappa beta (NFkappabeta), cyclo-oxygenase-2 (COX-2) and inducible NO synthase (iNOS); and damage caused by O&NS to membrane fatty acids and functional proteins. These IO&NS pathways are induced by a number of trigger factors, for example psychological stress, strenuous exercise, viral infections and an increased translocation of LPS from gram-bacteria (leaky gut). The 'psychosomatic' symptoms experienced by CFS patients are caused by intracellular inflammation (aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection); damage caused by O&NS (aches and pain, muscular tension and fatigue); and gut-derived inflammation (complaints of irritable bowel). Inflammatory pathways (monocytic activation) are also detected in somatizing disorder."


    "'Functional' symptoms, as occurring in CFS and somatization, have a genuine organic cause, that is activation of peripheral and central IO&NS pathways and gut-derived inflammation. The development of new drugs, aimed at treating those disorders, should target these IO&NS pathways."

    See more here:
    Last edited: Mar 5, 2015
  2. RadioFM

    RadioFM Active Member

    Last edited: Mar 5, 2015
  3. RadioFM

    RadioFM Active Member

    Gliadin causes intestinal permeability in both celiac and non-celiac intestinal mucosa:


    "Based on our results, we concluded that gliadin activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased intestinal permeability to macromolecules."

    Abstract Source:
    Scand J Gastroenterol. 2006 Apr;41(4):408-19. PMID: 16635908

    Reactive nitrogen species (RNS) are a family of antimicrobial molecules derived from nitric oxide (·NO) and superoxide (O2·−) produced via the enzymatic activity of inducible nitric oxide synthase 2 (NOS2) and NADPH oxidase respectively. NOS2 is expressed primarily in macrophages after induction by cytokines and microbial products, notably interferon-gamma (IFN-γ) and lipopolysaccharide (LPS).[2]

    Reactive nitrogen species act together with reactive oxygen species (ROS) to damage cells, causing nitrosative stress. Therefore, these two species are often collectively referred to as ROS/RNS.

    Reactive nitrogen species are also continuously produced in plants as by-products of aerobic metabolism or in response to stress,

    See more here: Infectious Oxidative Inflammation: The Vicious Cycle Of Contributing Factors
    Last edited: Mar 5, 2015
  4. RadioFM

    RadioFM Active Member

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