Friendly bacteria are critically important for the health of our digestive and immune systems, for their detoxification and hormone-regulating capabilities, and for nutrient formation and absorption.
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.
Based on available research and clinical data, there are four general causes of intestinal dysbiosis: putrefaction, fermentation, deficiency and sensitization.
Fermentation / Small Bowel Bacterial Overgrowth (SBBO). 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 bowel motility, physical/surgical abnormalities, by immune deficiency or by malnutrition. Gastric bacterial overgrowth increases the risk of systemic infection and the sufferer develops an intolerance to carbohydrate. Any carbohydrate ingested is fermented by the bacteria and results in production of toxic waste products.
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.
The risk factors for SBBO include those for yeast overgrowth and also: Insufficient stomach acid; Abnormal stool motility; Strictures; Surgery; Immune deficiency; Malnutrition. SBBO has been implicated in gastric cancer and can cause acidosis (where the body becomes too acidic) due to increased production of lactic acid.
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.
In cases of Putrefaction Dysbiosis, the alterations in bacterial population dynamics which result from this diet are measured by an increase in stool pH (partly caused by elevated ammonia production) and in bile or urobilinogen and possibly by a decrease in short chain fatty acids, especially in butyrate.
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.
Intestinal overgrowth of an organism called Klebsiella plays a role in determining who is affected by ankylosing spondylitis and how severely. Research by doctors at King's College has uncovered a tissue similarity between this organism and the spine. In an autoimmune reaction to excessive amounts of Klebsiella, the immune system attacks the spine. Controlling this dysbiosis by diet reduces symptoms of the disease.
During the early 1980s, exaggerated immunologic responses to components of the normal fecal flora were proposed as possible mechanisms behind inflammatory bowel disease. Little progress has been made in confirming or disproving this theory, although bacterial overgrowth of the jejunum has been found in 30% of patients hospitalized for Crohn's disease, in which it contributes to diarrhea and malabsorption. The demonstration of increased intestinal permeability in patients with active Crohn's disease and in healthy first degree relatives suggests the existence of a preexisting abnormality, such as dysbiosis, that allows an exaggerated immune response to normal gut contents to occur.
Elimination diets can induce remission in Crohn's disease as effectively as prednisone. The primary bacteriologic effect of elemental diets is to lower the concentration of Lactobacilli in the stool drastically without altering levels of other bacteria.
Some bacterial infections of the small bowel increase passive intestinal permeability. IBS has been studied in patients with diarrhea, cramps and specific food intolerances. Abnormal fecal flora has been a consistent finding, with a decrease in the ratio of anaerobes to aerobes, apparently due to a deficiency of anaerobic flora. Previous exposure to antibiotics – metronidazole in particular – was associated with the development of this disorder.
Immunologic responses to gut flora have been advanced by several authors as being important causative factors of inflammatory joint diseases. It is well-known that reactive arthritis can be activated by intestinal infections with Yersinia, Salmonella and other enterobacteria. In some cases bacterial antigens have been found in synovial cells and may enter the circulation because of the increased intestinal permeability associated with the intestinal infection. Increased intestinal permeability and immune responses to bacterial debris may cause other types of inflammatory joint disease as well.
Epidemiologic and experimental data implicate putrefactive dysbiosis in the development of colon cancer and breast cancer. A putrefaction dysbiosis is accompanied by an increase in fecal concentrations of various bacterial enzymes which metabolize bile acids to tumor promoters and deconjugate excreted estrogens, raising the plasma estrogen level.
Research suggests that gastritis and ulcers are triggered by bacterial overgrowth, rather than by stomach acidity. Long-term treatment of patients with potent acid blockers (proton pump inhibitors) which produce a more alkaline environment that is unfriendly to acid-tolerant bacteria such as Helicobacter pylori, may actually allow the overgrowth of other types of bacteria in the stomach, including Lactobacillus, Enterobacter, Staphylococcus and Propionibacterium which can result in inflammation, gastritis and ulceration. [Gastroenterology, Jan 2002]
Citrus seed extract may be a desirable first line of treatment because of its broad spectrum of antibacterial, antifungal and antiprotozoan benefits. The usual dose required is 600-1600mg per day. Animal studies have shown no toxicity except for intestinal irritation producing diarrhea at very high doses. The mechanism of action is not known; there is no evidence of systemic absorption.
Larch Arabinogalactan acts as a food supply for friendly bacteria. The term used to describe this action is "prebiotic". The most well known prebiotic substance is "fructooligosaccharides" or "FOS". Larch Arabinogalactan acts in the same manner as FOS in humans. The effect is to increase good bacteria such as bifidobacteria and lactobacillus, while decreasing bad bacteria.
Bayberry leaf (or other sources of the alkaloid berberine) appears to kill enterobacteria, yeasts and amoeba. The control of dysbiotic symptoms usually requires several grams per day.
The claimed benefits of drinking Kombucha tea may be derived solely from its ability to help correct an intestinal flora imbalance.
How do the friendly bacteria keep the bad bacteria in check? Think of a crowded theater. You walk in, and there is no place to sit; all the seats are taken. So you can't stay. It is the same with bacteria. There are only a certain number of "seats" in the colon. If they're all taken by friendly bacteria, then there's no chance for the bad bacteria to set up shop and start to duplicate themselves.
According to most researchers, normal probiotics should be more numerous than the cells of the intestinal lining itself. One of the ways to help reestablish a balanced bacterial population in the GI tract is the use of probiotic supplements. There are many products on the market containing a variety of organisms and a general approach could be taken using a broad spectrum probiotic formula. However, a better method is to discover the type of imbalance by testing and then supplementing those specific bacteria that are needed. Bringing these normally-occurring bacteria into balance will help prevent the overgrowth of more pathogenic organisms.
Bifidobacteria are the predominant lactic acid bacteria of the colon with a concentration that is 1000 times higher than Lactobacilli. Administration of Bifidobacterium breve to humans and animals reduces fecal concentrations of Clostridia and Enterobacter species, ammonia, and toxin-releasing bacterial enzymes including beta-glucuronidase and tryptophanase. Bacillus laterosporus, a novel organism classified as non-pathogenic to humans, produces unique metabolites with antibiotic, antitumor and immune modulating activity. This organism is available as a food supplement in the United States. It has been found to be an effective adjunctive treatment for control of symptoms associated with small bowel dysbiosis in a number of patients.
Fructose-containing oligosaccharides (FOS), found in vegetables like onion and asparagus, have been developed as a food supplement for raising stool levels of Bifidobacteria and lowering stool pH.
Antibiotic drugs may either cause or help control dysbiosis, depending upon the drug and the nature of the disorder. Where contamination of the small bowel by anaerobes is the problem, metronidazole or tetracyclines may be beneficial. When enterobacterial overgrowth predominates, ciprofloxacin is usually the drug of choice because it tends to spare anaerobes. Herbal antibiotics may be preferred because of their greater margin of safety and the need for prolonged antimicrobial therapy in bacterial overgrowth syndromes.
A microbiological assessment of bacterial populations in the GI tract is important for determining the nature of the imbalance when dysbiosis is suspected. Repeat testing should occur after treatment to ensure that the imbalance has been corrected.
The most useful test for large intestine dysbiosis is a Comprehensive Digestive Stool Analysis (CDSA) which includes an evaluation of many different aspects of digestion as well as a report on bacterial growth.
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