Dysbiosis

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Dysbiosis (also called dysbacteriosis) is a term for a microbial imbalance or maladaptation on or inside the body,[1][2] such as an impaired microbiota. For example, in the human microbiota, including the skin flora, gut flora, and vaginal flora, can become deranged, with normally dominating species underrepresented and normally outcompeted or contained species increasing to fill the void. Dysbiosis is most commonly reported as a condition in the gastrointestinal tract,[2] particularly during small intestinal bacterial overgrowth (SIBO) or small intestinal fungal overgrowth (SIFO).[3][4] It has been reported to be associated with illnesses, such as periodontal disease, inflammatory bowel disease[6],[7][8] chronic fatigue syndrome,[9] obesity,[10][11] cancer,[12][13] bacterial vaginosis,[14] and colitis.[15]

Typical microbial colonies found on or in the body are normally benign or beneficial. These beneficial and appropriately sized microbial colonies carry out a series of helpful and necessary functions, such as aiding in digestion.[16] They also help protect the body from the penetration of pathogenic microbes. These beneficial microbial colonies compete with each other for space and resources and outnumber human cells by a factor 10:1.[17]

Causes[edit]

Dysbiosis may be caused by such diverse things as repeated and inappropriate antibiotic exposure,[18][19] alcohol misuse,[20][21] or inappropriate diet.[22]

Effects[edit]

When this balance is disturbed, these colonies exhibit a decreased ability to check each other's growth, which can then lead to overgrowth of one or more of the disturbed colonies which may further damage some of the other smaller beneficial ones in a vicious cycle. As more beneficial colonies are damaged, making the imbalance more pronounced, more overgrowth issues occur because the damaged colonies are less able to check the growth of the overgrowing ones. If this goes unchecked long enough, a pervasive and chronic imbalance between colonies will set in, which ultimately minimizes the beneficial nature of these colonies as a whole.

Microbial colonies also excrete many different types of waste byproducts. Using different waste removal mechanisms, under normal circumstances the body effectively manages these byproducts with little or no trouble. Unfortunately, oversized and inappropriately large colonies, due to their increased numbers, excrete increased amounts of these byproducts. As the amount of microbial byproducts increases, the higher waste byproducts levels can overburden the body's waste removal mechanisms.

It is the combination of these two negative outcomes that causes many of the negative health symptoms observed when dysbiosis is present.

See also[edit]

Notes and references[edit]

  1. ^ Tamboli, CP; Neut, C; Desreumaux, P; Colombel, JF (2004). "Dysbiosis in inflammatory bowel disease". Gut. 53 (1): 1–4. doi:10.1136/gut.53.1.1. PMC 1773911free to read. PMID 14684564. 
  2. ^ a b Moos WH, Faller DV, Harpp DN, Kanara I, Pernokas J, Powers WR, Steliou K (2016). "Microbiota and Neurological Disorders: A Gut Feeling". Biores Open Access. 5 (1): 137–45. doi:10.1089/biores.2016.0010. PMC 4892191free to read. PMID 27274912. As reviewed in this report, synthetic biology shows potential in developing microorganisms for correcting pathogenic dysbiosis (gut microbiota-host maladaptation), although this has yet to be proven. 
  3. ^ Fujimori S (2015). "What are the effects of proton pump inhibitors on the small intestine?". World J. Gastroenterol. 21 (22): 6817–9. doi:10.3748/wjg.v21.i22.6817. PMC 4462721free to read. PMID 26078557. Several meta-analyses and systematic reviews have reported that patients treated with PPIs, as well as post-gastrectomy patients, have a higher frequency of small intestinal bacterial overgrowth (SIBO) compared to patients who lack the aforementioned conditions. Furthermore, there is insufficient evidence that these conditions induce Clostridium difficile infection. At this time, PPI-induced dysbiosis is considered a type of SIBO. 
  4. ^ Erdogan A, Rao SS (April 2015). "Small intestinal fungal overgrowth". Curr Gastroenterol Rep. 17 (4): 16. doi:10.1007/s11894-015-0436-2. PMID 25786900. Small intestinal fungal overgrowth (SIFO) is characterized by the presence of excessive number of fungal organisms in the small intestine associated with gastrointestinal (GI) symptoms. Candidiasis is known to cause GI symptoms particularly in immunocompromised patients or those receiving steroids or antibiotics. However, only recently, there is emerging literature that an overgrowth of fungus in the small intestine of non-immunocompromised subjects may cause unexplained GI symptoms. Two recent studies showed that 26 % (24/94) and 25.3 % (38/150) of a series of patients with unexplained GI symptoms had SIFO. The most common symptoms observed in these patients were belching, bloating, indigestion, nausea, diarrhea, and gas. The underlying mechanism(s) that predisposes to SIFO is unclear but small intestinal dysmotility and use of proton pump inhibitors has been implicated. However, further studies are needed; both to confirm these observations and to examine the clinical relevance of fungal overgrowth, both in healthy subjects and in patients with otherwise unexplained GI symptoms. 
  5. ^ Seksik, P. (2010). "Gut microbiota and IBD". Gastroentérologie Clinique et Biologique. 34 (Suppl 1): S44–51. doi:10.1016/S0399-8320(10)70020-8. PMID 20889004. 
  6. ^ Imbalance in the intestinal microbiome may be associated with bowel inflammation.[5]
  7. ^ Marteau, Philippe (2009). "Bacterial Flora in Inflammatory Bowel Disease". Digestive Diseases. 27: 99–103. doi:10.1159/000268128. PMID 20203504. 
  8. ^ Lepage, P.; Leclerc, M. C.; Joossens, M.; Mondot, S.; Blottiere, H. M.; Raes, J.; Ehrlich, D.; Dore, J. (23 April 2012). "A metagenomic insight into our gut's microbiome". Gut. 62 (1): 146–58. doi:10.1136/gutjnl-2011-301805. PMID 22525886. 
  9. ^ Lakhan, Shaheen E; Kirchgessner, Annette (2010). "Gut inflammation in chronic fatigue syndrome". Nutrition & Metabolism. 7: 79. doi:10.1186/1743-7075-7-79. PMC 2964729free to read. PMID 20939923. 
  10. ^ Turnbaugh, Peter J; Ruth E Ley; Michael A Mahowald; Vincent Magrini; Elaine R Mardis; Jeffrey I Gordon (2006-12-21). "An obesity-associated gut microbiome with increased capacity for energy harvest". Nature. 444 (7122): 1027–1031. doi:10.1038/nature05414. ISSN 1476-4687. PMID 17183312. 
  11. ^ Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI (2009-01-22). "A core gut microbiome in obese and lean twins". Nature. 457 (7228): 480–484. doi:10.1038/nature07540. ISSN 0028-0836. PMC 2677729free to read. PMID 19043404. 
  12. ^ Castellarin M, Warren RL, Freeman JD, Dreolini L, Krzywinski M, Strauss J, Barnes R, Watson P, Allen-Vercoe E, Moore RA, Holt RA (2012). "Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma". Genome Research. 22 (2): 299–306. doi:10.1101/gr.126516.111. ISSN 1549-5469. PMC 3266037free to read. PMID 22009989. 
  13. ^ Kostic AD, Gevers D, Pedamallu CS, Michaud M, Duke F, Earl AM, Ojesina AI, Jung J, Bass AJ, Tabernero J, Baselga J, Liu C, Shivdasani RA, Ogino S, Birren BW, Huttenhower C, Garrett WS, Meyerson M (2012). "Genomic analysis identifies association of Fusobacterium with colorectal carcinoma". Genome Research. 22 (2): 292–298. doi:10.1101/gr.126573.111. ISSN 1549-5469. PMC 3266036free to read. PMID 22009990. 
  14. ^ Africa, Charlene; Nel, Janske; Stemmet, Megan (2014). "Anaerobes and Bacterial Vaginosis in Pregnancy: Virulence Factors Contributing to Vaginal Colonisation". International Journal of Environmental Research and Public Health. 11 (7): 6979–7000. doi:10.3390/ijerph110706979. ISSN 1660-4601. PMC 4113856free to read. PMID 25014248. 
  15. ^ Mazmanian, Sarkis K (2008). "Capsular polysaccharides of symbiotic bacteria modulate immune responses during experimental colitis". Journal of pediatric gastroenterology and nutrition. 46 Suppl 1: –11–12. doi:10.1097/01.mpg.0000313824.70971.a7. ISSN 1536-4801. PMID 18354314. 
  16. ^ Kau, Andrew L.; Ahern, Philip P.; Griffin, Nicholas W.; Goodman, Andrew L.; Gordon, Jeffrey I. (15 June 2011). "Human nutrition, the gut microbiome and the immune system". Nature. 474 (7351): 327–336. doi:10.1038/nature10213. PMC 3298082free to read. PMID 21677749. 
  17. ^ Xuan, Caiyun; Jaime M. Shamonki; Alice Chung; Maggie L. DiNome; Maureen Chung; Peter A. Sieling; Delphine J. Lee (2014-01-08). "Microbial Dysbiosis Is Associated with Human Breast Cancer". PLoS ONE. 9 (1): e83744. doi:10.1371/journal.pone.0083744. ISSN 1932-6203. PMC 3885448free to read. PMID 24421902. 
  18. ^ Hawrelak, Jason A.; Myers, Stephen P. (2004). "The causes of intestinal dysbiosis: a review" (PDF). Alternative medicine review. 9 (2): 180–97. PMID 15253677. 
  19. ^ Dowson, David, Dr. "Dysbiosis by Dr David Dowson". 
  20. ^ Yan, Arthur W.; E. Fouts, Derrick; Brandl, Johannes; Stärkel, Peter; Torralba, Manolito; Schott, Eckart; Tsukamoto, Hide; E. Nelson, Karen; et al. (2011). "Enteric dysbiosis associated with a mouse model of alcoholic liver disease". Hepatology. 53 (1): 96–105. doi:10.1002/hep.24018. PMC 3059122free to read. PMID 21254165. 
  21. ^ Mutlu, Ece; Keshavarzian, Ali; Engen, Phillip; Forsyth, Christopher B.; Sikaroodi, Masoumeh; Gillevet, Patrick (2009). "Intestinal Dysbiosis: A Possible Mechanism of Alcohol-Induced Endotoxemia and Alcoholic Steatohepatitis in Rats". Alcoholism: Clinical and Experimental Research. 33 (10): 1836–46. doi:10.1111/j.1530-0277.2009.01022.x. 
  22. ^ Chan, Yee Kwan; Estaki, Mehrbod; Gibson, Deanna L. (2013). "Clinical consequences of diet-induced dysbiosis". Ann. Nutr. Metab. 63 (suppl2): 28–40. doi:10.1159/000354902. PMID 24217034. 

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