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Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences

Discussion in 'The Gut: De Meirleir & Maes; H2S; Leaky Gut' started by nanonug, Jun 26, 2012.

  1. nanonug

    nanonug Senior Member

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    Virginia, USA
  2. Sherlock

    Sherlock tart cherry etc. for joints, insomnia

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    Czechosherlockia, USA
    "Endotoxin initiates liver injury via activation of hepatic Kupffer cells...Endotoxin after binding with LPS-binding protein
    activates Kupffer cells through two types of receptors, CD-14 and Toll-like receptors-4 (TLR-4)... The finding that alcoholic liver injury is blocked in both CD-14 (Yin et al., 2000) and TLR-4 deficient mice (Uesugi et al., 2001) suggests that both of these receptors are required to initiate liver injury caused by alcohol."

    That makes me wonder if the macrophage activators being used would result in more liver injury in those with Gramm(-) overgrowth, even without alcohol consumption but resulting from alcohol and/or acetaldehyde produced in the gut.
     
  3. Sherlock

    Sherlock tart cherry etc. for joints, insomnia

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    Czechosherlockia, USA
    ...and in keeping with my currently favorite topic of histamine:
    "Histamine Affects Alcohol-Related Behavior"
    http://www.sciencedaily.com/releases/2009/06/090616080147.htm

    i.e., if a person chronically consumed alcohol, then they might wonder if they are naturally high in histamine, which has its own CFS related effects and also shares the acetaldehyde dehydrogenase enyzmes for degrading both alcohol and histamine.

    Also, a person who never consumes alcohol can still have alcohol in their gut lumen from production by yeast. The fact that humans do have the alcohol dehydrogenase enzyme probably probably isn't accounted for by cavemen brewing berries but probably existed very long before that because of intestinal yeast.
     

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