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Dysbiosis (also called dysbacteriosis) refers to a condition with microbial imbalances on or inside the body. Dysbiosis is most prominent in the digestive tract or on the skin, but can also occur on any exposed surface or mucous membrane such as the vagina, lungs, mouth, nose, sinuses, ears, nails, or eyes. It has been associated with different illnesses, such as inflammatory bowel disease, as imbalances in the intestinal microbiome may be associated with bowel inflammation.[1][2][3] and chronic fatigue syndrome.[4]

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.[5] They also protect the body from the penetration of pathogenic microbes. These beneficial microbial colonies compete with each other for space and resources.

When this balance is disturbed, by such diverse things as repeated and inappropriate antibiotic exposure[6] or alcohol misuse,[7][8] these colonies exhibit a decreased ability to check each others' growth. This can lead to an overgrowth of one or more of the disturbed colonies which then may damage some of the other smaller beneficial ones.

This type of situation often instigates 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.

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  1. ^ 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. 
  2. ^ Marteau, Philippe (2009). "Bacterial Flora in Inflammatory Bowel Disease". Digestive Diseases 27: 99–103. doi:10.1159/000268128. PMID 20203504. 
  3. ^ 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. 
  4. ^ Lakhan, Shaheen E; Kirchgessner, Annette (2010). "Gut inflammation in chronic fatigue syndrome". Nutrition & Metabolism 7: 79. doi:10.1186/1743-7075-7-79. PMC 2964729. PMID 20939923. 
  5. ^ 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 3298082. PMID 21677749. 
  6. ^ Hawrelak, Jason A.; Myers, Stephen P. (2004). "The causes of intestinal dysbiosis: a review". Alternative medicine review 9 (2): 180–97. PMID 15253677. 
  7. ^ 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 3059122. PMID 21254165. 
  8. ^ 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. 

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