Treating Dysbiosis.docx

Treating DysbiosisBy Dr. Natasha Wolf, BScH NDThe GI System and Microbiome InteractionThe entire gastrointestinal (GI) system plays a massive role in human health, including nutrient absorption, waste elimination, protection against harmful microbes, and providing a host environment for symbiotic bacteria. In turn, the composition of the GI system microflora is an important factor in the maintenance of normal GI system function and overall health. Consisting of 1014bacteria1and typically weighing around three pounds, the GI system microbiome can be viewed as an important metabolic organ. When functioning optimally, a healthy microbiome supports production of certain B-vitamins and vitamin K2,3, enhances the immune system4, improves gastrointestinal motility and transit time5, increases nutrient absorption6, inhibits pathogenic organisms3, is involved in hormone7and drug metabolism8, and helps to support the normal function of intestinal epithelial cells.DysbiosisAccording to probiotic researcher Dr. Nigel Plummer, the normal human microbiota is the “commensal microbial population which resides within the humanwhich is both persistent and stable, and which does not elicit an acute immune response”. Alterations to the normal composition of the microbiome are known as “dysbiosis”9. Dysbiosis typically involves decreased populations of commensal bacteria and an overgrowth of pathogenic bacteria10. This results in impaired intestinal function, and increased inflammation and immune sensitization10,11.Dysbiosis is associated with numerous chronic health conditions including:GI System Disorders Irritable bowel disease (IBS) Inflammatory bowel disease (IBD)Inflammatory Skin Conditions Eczema Psoriasis AcneThe Effects of DysbiosisWhen dysbiosis occurs, the normal tight junctions in healthy mucosal lining become leaky and inflamed. Dysbiosis is therefore one of the causes of food sensitivities and GI inflammation, also called leaky gut. Leaky gut syndrome occurs when bacteria and dietary antigens leak through the mucosal barrier, causing inflammation in the lamina propria and increased intestinal permeability. Dysbiosis triggers an abnormal immune response and results in an imbalance of the cell-mediated (Th1) and antibody-mediated (Th2) immune responses12. The Th1 immune response is pro-inflammatory, and when dominant, has been shown to contribute towards auto-immune conditions such as psoriasis and celiac disease13. Research has also shown that food intolerances14and leaky gut may be what triggers the Th1 dominant pro-inflammatory cascade, initiating the auto-immune response.Inflammation in the GI tract can also cause systemic inflammatory conditions: dysbiosis has been linked to several types of atopic (allergic) disorders including allergies, hives, and eczema. Other inflammatory skin conditions such as acne, psoriasis and rosacea are believed to be linked to dysbiosis.Drug-Dependent Microflora Disruption Some of the most significant contributors to dysbiosis are antibiotics and other drugs, such as proton pump inhibitors (PPIs) and non-steroidal anti-inflammatory drugs (NSAIDs). Antibiotics eliminate probiotic bacteria residing in the mouth, stomach, intestines, vaginal canal and skin. PPIs reduce production of stomach acid (HCl), which increases risk of pathogenic bacterial invasion15. Stress and aging can also reduce HCl production. Long-term NSAID usage is associated with an increase in intestinal permeability16. Drug therapies that lower stomach acid allow for pathogenic bacterial invasion into the small intestine, causing a specific form of dysbiosis called small intestinal bacterial overgrowth (SIBO).Dietary-Dependent Microflora DisruptionThe intestinal microbiome is responsible for fermenting soluble dietary fibers into short chain fatty acids (SCFA)17. The SCFA butyrate is an anti-inflammatory18product of bacterial fermentation that acts as a primary fuel for large intestine epithelial cells17. A diet that is low in fiber and high in simple carbohydrates further contributes to inflammation and dysbiosis. Certain types of dietary fiber are more readily fermented into SCFAs, including soluble fibers such as fructooligosaccharides( FOS), inulin, guar gum, fruit pectins, and legume and vegetable fibers19.When fiber and butyrate are lacking, colon cells have been shown to atrophy in as little as five days, resulting in a compromise of the mucosal barrier function and an increase in intestinal permeability. Simple carbs and sugar increase inflammation and act as food forCandidaand other pathogenic species. Food intolerances, if not removed from the diet, contribute to inflammation and damage to the intestinal wall. Malabsorption of nutrients and immune system reactions will also perpetuate dysbiosis.Preventing DysbiosisSo how can we prevent the cycle of dysbiosis from starting? Avoid unnecessary antibiotic usage. Take a daily probiotic that has been clinically proven to be safe and effective Eating a high fiber diet, especially one thats high in soluble fiber Eliminate refined sugar and avoiding other simple carbohydratesTreating DysbiosisDysbiosis and leaky gut can be treated and healed by first identifying and eliminating harmful pathogens, replenishing the digestive tract with human-sourced probiotics, using nutrients to heal the intestinal barrier, and supporting the immune system. The first step is to use antimicrobials to rid the body of harmful pathogens. Allicin extract from garlic has been shown to have broad-spectrum antimicrobial activity against bacteria (includingH. Pylori),Candidaand parasites20. Cinnamon (Cinnamomumverum) oil extracts also have powerful antimicrobial effects against pathogenic bacteria andCandida21-23. When used together, allicin and cinnamon oil can be effective in killing off pathogenic organisms creating dysbiosis in the GI tract.Re-populating the digestive tract with clinically proven, human-sourced probiotic strains is essential for treating dysbiosis and leaky gut. Probiotics can give symptomatic relief of abdominal pain, gas and bloating, while at the same time re-establishing the intestinal barrier function. With sufficient amounts of probiotics, this barrier will prevent further adherence of pathogenic candida, bacteria and parasites.References:1. Shim JO. Gut Microbiota in Inflammatory Bowel Disease. Pediatric Gastroenterology, Hepatology & Nutrition. 2013; 16: 17-212. LeBlanc JG, Laio JE, del Valle MJ, Vannini V, van Sinderen D et al. B-group vitamin production by lactic acid bacteriacurrent knowledge and potential applications. Journal of Applied Microbiolology. 2011; 111(6): 1297-3093. Weber T and Polanco I. 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Hong SN and Rhee PL. Unraveling the ties between irritable bowel syndrome and intestinal microbiota. World Journal of Gastroenterology. 2014; 20(10): 2470-248110. Hold G, Smith M, Grange C, Watt ER, El-Omar EM and Mukhopadhya I. Role of the gut microbiota in inflammatory bowel disease pathogenesis: What have we learnt in the past 10 years? World Journal of Gastroenterology 2014; 20(5): 1192-121011. Basso PJ, Fonseca MTC, Bonf G, Alves VBF, Sales-Campos H et al. Association among genetic predisposition, gut microbiota, and host immune response in the etiopathogenesis of inflammatory bowel disease. Brazilian Journal of Medical and Biological Research. 2014;47(9): 727-73712. Kramer MF and Heath MD. Probiotics in the treatment of chronic rhinoconjunctivitis and chronic rhinosinusitis. Journal of Allergy. 2014; Article ID 983635: 7 pages13. Sjberg V, Sandstrm O, Hedberg M, Hammarstrm S, Hernell O, and Hammarstrm ML. Intestinal T-cell Responses in Celiac Disease Impact of Celiac Disease Associated Bacteria.PLoS One. 2013; 8(1): e5341414. Tomici S, Flth-Magnusson K, Bttcher MF. Dysregulated Th1 and Th2 responses in food-allergic childrendoes elimination diet contribute to the dysregulation? Pediatric Allergy and Immunology. 2010; 21: 649-65515. Biswal S. Proton pump inhibitors and risk for Clostridium difficile associated diarrhea. Biomed Journal. 2014; 37(4): 178-8316. Bjarnason I and Takeuchi K. Intestinal permeability in the pathogenesis of NSAID-induced enteropathy. Journal of Gastroenterology 2009; 44Suppl XIX: 232917. Hamer HM, Jonkers D, Venema K, Vanhoutvin S, Troost FJ, and Brummer RJ. Review article: the role of butyrate on colonic function. Alimentary Pharmacology and Therapeutics. 2008; 27(2):104-1918. Furusawa Y, Obata Y, Fukuda S, Endo TA, Nakato G, Takahashi D, et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. 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