Altered microbial ecology in the gut may produce disease and dysfunction because of the intense metabolic activity and the antigenic nature of bacterial flora. Bacterial enzymes can degrade pancreatic enzymes, damage the intestinal absorptive surface, release toxins that had previously been bound by conjugation and alter the intestinal milieu in numerous ways, some of which can be easily measured in a properly collected sample of stool.
Bacterial antigens may elicit dysfunctional immune responses which contribute to autoimmune diseases of the bowel and of connective tissue. Effective treatment of dysbiosis with diet, antimicrobial substances and bacterial replacement or support must distinguish among patterns of dysbiosis. The failure of common approaches utilizing fiber and Lactobacilli alone is a strong indication of small bowel bacterial overgrowth, a challenging disorder which demands a radically different approach from a dysbiosis of the large intestine. Stool examination generally reflects large bowel bacterial colonization. Other testing means are required for uncovering bacterial overgrowth in the small intestine.
Based on available research and clinical data, there are four general causes of intestinal dysbiosis: putrefaction, fermentation, deficiency and sensitization.
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Putrefaction
Putrefaction dysbiosis results from diets high in fat and animal flesh and low in insoluble fiber. This type of diet produces an increased concentration of Bacteroides (sp.) species and a decreased concentration of Bifidobacteria sp. in the stool. It increases bile flow and induces bacterial urease activity. Putrefaction dysbiosis is corrected by decreasing dietary fat and flesh, increasing fiber consumption and feeding Bifidobacteria and Lactobacillus preparations.
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Fermentation
This is a condition of carbohydrate intolerance induced by overgrowth of bacteria in the stomach, small intestine and beginning of the large intestine. Bacterial overgrowth here is promoted by hypochlorhydria, by stasis due to abnormal motility, physical/surgical abnormalities, by immune deficiency or by malnutrition. Gastric bacterial overgrowth increases the risk of systemic infection.
Carbohydrate intolerance may be the only symptom of bacterial overgrowth, making it indistinguishable from intestinal candidiasis; in either case dietary sugars can be fermented to produce endogenous ethanol. Chronic exposure of the small bowel to ethanol may itself impair intestinal permeability. British physicians working with the gut-fermentation syndrome have tentatively concluded, based on treatment results, that the majority of cases are due to yeast overgrowth and about 20% are bacterial in origin. The symptoms include abdominal distension, carbohydrate intolerance, fatigue and impaired mental function.
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Deficiency
Exposure to antibiotics or a diet depleted of soluble fiber may create an absolute deficiency of normal fecal flora, including Bifidobacteria, Lactobacillus and E. Coli. Direct evidence of this condition is seen on stool culture when concentrations of Lactobacillus or E. Coli are reduced. This condition has been described in patients with irritable bowel syndrome and food intolerance. Deficiency and putrefaction dysbiosis are complementary conditions which often occur at the same time and call for the same treatment regime.
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Sensitization
Aggravation of abnormal immune responses to components of the normal intestinal microflora may contribute to the development of inflammatory bowel disease, spinal arthritis, other connective tissue disease and skin disorders such as psoriasis or acne. The responsible bacterial components include toxins which can cross-react with human tissues.
Treatment
Putrefaction dysbiosis is usually managed with a diet high in both soluble and insoluble fiber and low in saturated fat and animal protein. These dietary changes work to lower the concentrations of Bacteroides and increase concentrations of lactic acid-producing bacteria (Bifidobacteria, Lactobacillus and lactic acid streptococci) in the colon.
Supplementing the diet with defined sources of fiber can have variable effects on colonic dysbiosis. Insoluble fiber decreases bacterial concentration and microbial enzyme activity. Soluble fiber, on the other hand, tends to elevate bacterial concentration and enzyme activity, at the same time raising the levels of beneficial short chain fatty acids. This disparity may explain the superior effect of insoluble fiber in the prevention of colon cancer.
Dairy products have a variable effect and fermented dairy foods such as fresh yogurt are occasionally helpful. Experimentation and careful observation of symptoms may be required to determine whether these foods will help or harm.
Fermentation dysbiosis, conversely, can cause starch and soluble fiber to exacerbate the abnormal gut ecology. When the upper small bowel is involved, simple sugars are also contraindicated. A diet free of cereal grains and added sugar is generally the most helpful. Fruit, fat and starchy vegetables are tolerated to variable degree in different cases. Oligosaccharides found in some vegetables, carrots in particular, inhibit the binding of enterobacteria to the intestinal mucosa.