Leaky Gut Documented in Fibromyalgia

Published: August 6, 2012
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For decades, holistic physicians have known that "leaky gut" is a significant problem in fibromyalgia and CFS. Many allopathic physicians have laughed at this concept of increased intestinal permeability (the food getting absorbed into the blood before it is completely digested), stating that it was nonsense. This new study proves the presence of increased intestinal permeability ("leaky gut") in fibromyalgia patients.

The issue of leaky gut is a problem for a number of reasons. Two of the key problems caused by leaky gut are:

  1. Increased food allergies. Proteins are supposed to be digested all the way down to their component building blocks (amino acids). This is like breaking down words into their component letters, which are meaningless but can be used to build other words. When large chunks of proteins are absorbed into your blood before they are fully digested, it triggers allergic reactions to those proteins. This is one reason why food allergies are so common in CFS and fibromyalgia and why using digestive enzymes which break down the proteins before they are absorbed can be so helpful.
  2. Immune exhaustion. When undigested protein fragments are absorbed into the blood, it becomes your immune system's job to finish the digestive process. Compared to the total weight of a severe viral or even bacterial infection, the weight of incompletely digested food we eat each day can be massive. After an extended period, this can overwhelm and exhaust our immune systems.

Fortunately, the therapies we use also help eliminate the leaky gut. These helpful therapies include:

  1. Eliminate intestinal infections (especially yeast and parasites).
  2. Supply nutritional support to the bowel (especially glutamine, which is also present in a good multivitamin powder).
  3. Restore healthy bacterial function in the gut with probiotics such as probiotic pearls or yogurt with live bacterial cultures, and
  4. Optimize thyroid function (even if labs are normal) to prevent SIBO (Small Intestinal Bacterial Overgrowth).

Altered Intestinal Permeability in Patients with Primary Fibromyalgia and in Patients with Complex Regional Pain Syndrome

Rheumatology Advance Access published online on June 7, 2008 Rheumatology, doi:10.1093/rheumatology/ken140

A. Goebel,1 S. Buhner,2 R. Schedel,1 H. Lochs2 and G. Sprotte1

1Pain Management Centre, University Hospital Wuerzburg, Wuerzburg and 2Department for Gastroenterology, Hepatology and Endocrinology, Charité Universitätsmedizin, Berlin, Germany.

Correspondence to: A. Goebel, The Walton Centre NHS Trust, Lower Lane, Fazakerley, Liverpool L9 7LJ, UK. E-mail: andreasgoebel@rocketmail.com

Abstract

Objectives

The pain intensity of patients with FM has recently been reported to be correlated with the degree of small intestinal bacterial overgrowth (SIBO). SIBO is often associated with an increased intestinal permeability (IP). Increased IP, if shown in FM, may have pathogenetic relevance because it leads to the exposure of immune cells to luminal antigens and consequent immune modulation. It is currently unknown whether IP is altered in FM. We therefore examined the IP in a group of patients with primary FM and in two control groups, healthy volunteers and patients with an unrelated chronic pain syndrome, complex regional pain syndrome (CRPS). We hypothesized that patients with FM, but not volunteers or those patients with CRPS, would have altered IP.

Methods

Both gastroduodenal and small IP were assessed using an established three-sugar test, where urinary disaccharide excretion reflecting intestinal uptake was measured using HPLC.

Results

Forty patients with primary FM, 57 age- and sex-matched volunteers and 17 patients with CRPS were enrolled in this study. In the FM group, 13 patients had raised gastroduodenal permeability and 15 patients had raised small intestinal permeability, but only one volunteer had increased gastroduodenal permeability (P < 0.0001, chi-square test for the three groups). The IP values were significantly increased in the patient groups (P < 0.0003 for all comparisons, one-way analysis of variance).

Conclusions

The IPs in primary FM and, unexpectedly, CRPS are increased. This study should stimulate further research to determine the implication of altered IP in the disease pathophysiology of FM and CRPS.

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