Leaky Gut and probiotics

Intestinal permeability (“leaky gut”) is another leading factor in the development and progression of non-alcoholic fatty liver disease [2014], which gives us a condition to also search on.

A 2015 study found “Antitumor necrosis factor-α(TNF-α) therapy reduces mucosal inflammation and restores intestinal permeability in IBD patients. Butyrate, zinc, and some probiotics also ameliorate mucosal barrier dysfunction but their use is still limited and further studies are needed before considering permeability manipulation as a therapeutic target in IBD.” and continues with:

  • “To date the ones with proven efficacy are Escherichia coli Nissle 1917, Bifidobacterium,Lactobacillus rhamnosus GG, or the multispecies VSL#3 which contains eight different probiotics [132]”
  • Zinc is a trace element essential for cell turnover and repair systems. Inflammatory conditions and malnutrition are known risk factors for zinc deficiency and several works proved the efficacy of its supplementation during acute diarrhoea and experimental colitis [127129]”
  • “Finally, vitamin D is worth a mention because it is involved in maintaining intestinal barrier function”
  • “Furthermore, there is increasing concern about the role of industrial food additives as promoters of immune-related diseases. A recent review showed the ability of additives to increase intestinal permeability by interfering with the TJs, promoting the passage of immunogenic antigens [113].”

Wait a minute — these seem to be the same items that I recommended for CFS!


  • “A butyrate-producing probiotic (MIYAIRI 588) reduced the lipid deposition and significantly improved the triglyceride content, IR, serum endotoxin levels, and hepatic inflammatory indexes in a rat model of choline-deficient diet-induced Non-alcoholic fatty liver disease[77].” [2014] This is Miyarisan!
  • “In particular,Lactobacillus casei DN-114001[60] and VSL#3 (a mixture of pre- and probiotics)[61] seem to restore intestinal barrier function by enhancing the expression of ZO-2 and protein kinase C in TJs. … Escherichia coli strain Nissle 1917 restored mucosal permeability in the murine dextran sulfate sodium-induced colitis model by increasing ZO-1 expression[43].” [2014]
  • Bifidobacterium longum was superior in attenuating liver fat accumulation… lack of changes in intestinal permeability in treated mice” [2014]
  • “With regard to exercise-induced GI permeability problems, there is still a lack of studies with appropriate data and a gap to understand the underlying mechanisms”[2012] – this may be a significant factor for the CFS crash after exercising, increased leaky gut!
    • “..cycling resulted in increased I-FABP levels, reflecting small intestinal injury … This is the first study to reveal that ibuprofen aggravates exercise-induced small intestinal injury and induces gut barrier dysfunction in healthy individuals. We conclude that nonsteroidal anti-inflammatory drugs consumption by athletes is not harmless and should be discouraged.” [2012]
    • Exercise-induced splanchnic hypoperfusion results in quantifiable small intestinal injury. Importantly, the extent of intestinal injury correlates with transiently increased small intestinal permeability, indicating gut barrier dysfunction in healthy individuals.”[2011]

Short List of What to take

Avoid PREPARED foods, food from raw materials is strongly preferred.

An Alzheimer connection?

An Oct 2015 article “Different Brain Regions are Infected with Fungi in Alzheimer’s Disease” suggests that leaky gut may be a contributing factor for AD.

“Many investigators have also considered the idea that AD is an infectious disease, or at least that infectious agents constitute a risk factor for AD21,22,23. Accordingly, genetic material from several viruses and bacteria have been reported in brains from AD patients. In particular, herpes simplex type 1 (HSV-1) and Chlamydophila pneumoniae have been suggested as potential aetiological agents of AD. In addition, brain infection by several pathogens may induce amyloid formation24,25,26. Furthermore, Αβ peptide exhibits antimicrobial activity and shows particularly strong inhibitory activity against Candida albicans27.”

This appears to be further indicated by this earlier 2015 study “Increased concentrations of fecal calprotectin indicate a disturbed intestinal barrier function in AD patients which could be of relevance for the lowering of essential aromatic amino acids concentrations in the blood.”

Interesting that IBD and IBS are different here “Fecal calprotectin has been shown to consistently differentiate IBD from irritable bowel syndrome because it has excellent negative predictive value in ruling out IBD in undiagnosed, symptomatic patients.” [2006]

If you have IBS — you may wish to have fecal calprotectin tested to verify if it is IBD or IBS (and potentially if you have a higher Alzheimer’s Disease risk).

A light went on?

Hypoperfusion (decrease access to tissue) produces increased leaky gut. Hypocoagulation produces hypoperfusion. Hypercoagulation(aka “Thick Blood”) has been reported to occur in over 85% of CFS patients (not severe enough to cause strokes, some may have TIAs). Is hypercoagulation why there may be significant increase in leaky gut in CFS after exercise (see earlier post). That is — there was already significant hypoperfusion before exercising resulting in an amplified response with exercise?

There appear to be some studies heading in that direction….