World Digestive Health Day WDHD – May 29, 2016 the increased intestinal epithelial permeability induced by gliadin.8 The vast majority of research describes differences in the composition, structure, and diversity of the fecal and small intestinal microbiota in patients with CD based on age, disease status, and associated signs and symptoms. Associated metabolic activity, as measured by patterns of short chain fatty acids (SCFA) in the stool, is altered in patients with active CD and linked to the described dysbiosis. However, differences in specimen collection, analysis techniques, age of the study population, and disease status make it difficult to compare studies. IRRITABLE BOWEL SYNDROME Several studies suggest that gut microbiota is altered in IBS, with different composition and decreased complexity in microbiota of IBS patients compared to healthy controls as well as within the subgroups of IBS patients.9 Although these microbiota signatures are a meaningful step towards a better understanding of a link between gut dysbiosis and IBS, it must be taken into consideration that these results are obtained from relatively small sample populations. Considering that IBS is a multifactorial syndrome with many possible causes and different clinical presentations, it is possible to predict that results derived from these studies will explain the role of specific microbiota composition in subgroups of patients rather than explaining the pathogenesis of the IBS population as a whole.9 CONCLUSIONS AND FUTURE DIRECTIONS The major limitation of current studies linking gut microbiome with clinical outcomes is their descriptive nature. To link gut microbiome composition with disease pathogenesis, it is necessary to generate solid mechanistic evidence of disease onset and progression in relation to dynamic changes of abnormal microbiome causing host epigenetic modifications controlling gut barrier, immune functions, and, ultimately, loss of tolerance. Currently there are limited effective strategies for the treatment or prevention of these chronic diseases. The advent of genomics, proteomics, and now advanced microbiome analysis raised the expectation of therapeutic solutions that have yet to materialize. It is now becoming clear that these diseases are final destinations, but that the paths to disease development vary from patient to patient. To date, a myriad of cross sectional studies have described alterations in the gut microbiota composition in a variety of disease states, after the disease has already presented. THE HUMAN GUT MICROBIOME, continued It now appears clear that to understand and study these microbiome shifts, prospective cohort design is required to capture changes that precede or coincide with disease and symptom onset. Additionally, prospective studies integrating microbiome, metagenomic, metatranscriptomic, and metabolomic data with comprehensive clinical and environmental data are necessary to build a systems-level model of interactions between the host and the development of disease.10 The creation of novel network models is essential to providing a mechanistic approach to exploring the development of disease. As the field expands exponentially in the wake of non-culture-based technologies to study the microbiome, a multi-omic research approach has the potential to revolutionize our understanding of most common diseases affecting humankind. This knowledge will provide personalized therapeutic (precision medicine) and preventive (primary prevention) targets for microbiome manipulation using prebiotics, probiotics, and/or symbyotics (See Figure 1). REFERENCES 1. Aagaard K, Ma J, Antony KM, Ganu R, Petrosino J, Versalovic J. The placenta harbors a unique microbiome. Sci Transl Med. 2014 May 21;6(237):237ra65–5. 2. Koren O, Goodrich JK, Cullender TC, Spor A, Laitinen K, Bäckhed HK, et al. Host remodeling of the gut microbiome and metabolic changes during pregnancy. Cell. 2012 Aug 3;150(3):470–80. 3. Yatsunenko T, Rey FE, Manary MJ, Trehan I, Dominguez- Bello MG, Contreras M, et al. Human gut microbiome viewed across age and geography. Nature. 2012 Jun 14;486(7402):222–7. 4. Greenwood BM. Autoimmune disease and parasitic infections in Nigerians. Lancet. 1968 Aug 17;2(7564):380–2. 5. Shreiner A, Huffnagle GB, Noverr MC. The “Microflora Hypothesis” of allergic disease. Adv Exp Med Biol. New York, NY: Springer New York; 2008;635(Chapter 10):113–34. 6. Manichanh C, Borruel N, Casellas F, Guarner F. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012 Oct;9(10):599–608. 7. Fasano A, Catassi C. Clinical practice: Celiac disease. N Engl J Med. 2012 Dec 20;367(25):2419-26. 52 WGO Handbook on DIET AND THE GUT World Digestive Health Day WDHD May 29, 2016
WGO Handbook on Diet and the Gut_2016_Final
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