Gastric bacterial overgrowth increases the risk of systemic infec- tion. Gastric bacteria convert dietary nitrates to nitrites and nitro- samines; hence, the increased risk of gastric cancer in individuals with hypochlorhydria( 15) . Some bacterial infections of the small bowel increase passive intestinal permeability(16).

Carbohydrate intolerance may be the only symptom of bacterial overgrowth, making it indistinguishable from intestinal candidosis; in either case dietary sugars can be fermented to produce endogenous ethanol(17,18). Chronic exposure of the small bowel to ethanol may itself impair intestinal permeability(19). Another product of bacterial fermentation of sugar is D-lactic acid. Although D-lactic acidosis is usually a complication of short-bowel syndrome or of jejuno-ileal by- pass surgery (colonic bacteria being the source of acidosis), elevated levels of D-lactate were found in blood samples of 1.12% of randomly selected hospitalized patients with no history of gastro-intestinal sur- gery or disease(20). Small bowel fermentation is a likely cause of D-lactic acidosis in these patients. British physicians working with the gut-fermentation syndrome as described by Hunisett et al(18) have tentatively concluded, based on treatment results, that the ma- jority of cases are due to yeast overgrowth and about 20% are bacte- rial in origin. The symptoms include abdominal distension, carbohy- drate intolerance, fatigue and impaired cognitive function.

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 re- duced. Low fecal short chain fatty acids provide presumptive evi- dence. This condition has been described in patients with irritable bowel syndrome and food intolerance (see below). Deficiency and pu- trefaction dysbiosis are complementary conditions which often occur together and have the same treatment.

Sensitization
Aggravation of abnormal immune responses to components of the normal indigenous intestinal microflora may contribute to the patho- genesis of inflammatory bowel disease, spondyloarthropathies, other connective tissue disease and skin disorders like psoriasis or acne. The responsible bacterial components include endotoxins, which can activate the alternative complement pathway and antigens, some of which may cross react with mammalian antigens. Treatment studies in ankylosing spondylitis and inflammatory bowel disease suggest that sensitization may complement fermentation excess and that sim- ilar treatments may benefit both conditions.

Clinical research has implicated bacterial dysbiosis in a number of diseases of inflammation within the bowel or involving skin or con- nective tissue. The published associations are reviewed below:

Atopic Eczema
Ionescu and his colleagues have studied fecal and duodenal flora in patients with atopic eczema and found evidence of small bowel dys- biosis and subtle malabsorption phenomena in the majority(21,22). Treatment with antibiotics or with a natural antibiotic derived from grapefruit seeds, produced major improvement in the gastro-intesti- nal symptoms of eczema patients and moderate improvement in se- verity of eczema(23). One advantage in the use of grapefruit seed ex- tract over conventional antibiotics lies in its anti-fungal activity. This agent adds a second therapeutic dimension and eliminates the possi- bility of secondary candidosis. The minimum effective dose of grape- fruit seed extract for bacterial dysbiosis is 600 mg a day.