Intestinal permeability

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The "leaky gut" syndrome or increased intestinal permeability or chronic increase of intestinal permeability hypothesis states that certain stressors increase intestinal mucosal paracellular permeability, which allows harmful bacteria and bacterial toxins to cross through the lining of intestines (gut) into circulation in the body, which is then proposed causes widespread inflammation and triggers a variety of diseases.[1][2] In a healthy digestive tract, the intestinal walls provide a tight, selective barrier to allow the absorption of nutrients but prevent the entry of bacteria or pathogens.[2]

The leaky gut hypothesis has been linked to irritable bowel syndrome (IBS), Alzheimer's disease, asthma, type 2 diabetes, numerous gastrointestinal diseases, and many others illnesses, although evidence supporting this is largely limited or lacking.[1]

Possible causes[edit | edit source]

The physiologic stressors proposed to cause intestinal permeability are anxiety, intense exercise, or components in food (such as emulsifiers), short chain fatty acids and lipopolysaccharides (LPS), and others.[1][2]

Theory[edit | edit source]

Evidence[edit | edit source]

Prevalence[edit | edit source]

Symptom recognition[edit | edit source]

Potential treatments[edit | edit source]

Notable studies[edit | edit source]

  • 2007, Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome[3](Full text)
  • 2007, Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syn- drome (CFS): indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability[4](Full text)
  • 2013, High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients[5](Full text)
  • 2015, Increased expression of activation antigens on CD8+ T lymphocytes in Myalgic Encephalomyelitis/chronic fatigue syndrome: inverse associations with lowered CD19+ expression and CD4+/CD8+ ratio, but no associations with (auto) immune, leaky gut, oxidative and nitrosative stress biomarkers[6](Abstract)
  • 2015, Changes in gut and plasma microbiome following exercise challenge in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)[7](Full text)
  • 2016, The role of microbiota and intestinal permeability in the pathophysiology of autoimmune and neuroimmune processes with an emphasis on inflammatory bowel disease type 1 diabetes and chronic fatigue syndrome[8](Full text)
  • 2016, A role for the intestinal microbiota and virome in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)[9](Full text)
  • 2018, The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications[10](Full text)
  • 2018, A role for a leaky gut and the intestinal microbiota in the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)[11](Thesis - Full text)
  • 2020, The “Leaky Gut”: Tight Junctions but Loose Associations?[1](Full text)
  • 2020, Mitochondria and immunity in chronic fatigue syndrome[12](Full text)
  • 2021, The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications[13](Full text)
  • 2021, Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome[14](Full text)

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. 1.01.11.21.31.4 Hollander, Daniel; Kaunitz, Jonathan D. (May 2020). "The "Leaky Gut": Tight Junctions but Loose Associations?". Digestive diseases and sciences. 65 (5): 1277–1287. doi:10.1007/s10620-019-05777-2. ISSN 0163-2116. PMC 7193723. PMID 31471860.
  2. 2.02.12.2 Usuda, Haruki; Okamoto, Takayuki; Wada, Koichiro (July 16, 2021). "Leaky Gut: Effect of Dietary Fiber and Fats on Microbiome and Intestinal Barrier". International Journal of Molecular Sciences. 22 (14): 7613. doi:10.3390/ijms22147613. ISSN 1422-0067. PMC 8305009. PMID 34299233.
  3. Maes, Michael; Coucke, Francis; Leunis, Jean-Claude (December 2007). "Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome". Neuro Endocrinology Letters. 28 (6): 739–744. ISSN 0172-780X. PMID 18063928.
  4. Maes, Michael; Mihaylova, Ivana; Leunis, Jean-Claude (April 1, 2007). "Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): Indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut–intestinal permeability". Journal of Affective Disorders. 99 (1): 237–240. doi:10.1016/j.jad.2006.08.021. ISSN 0165-0327.
  5. Frémont, Marc; Coomans, Danny; Massart, Sebastien; De Meirleir, Kenny (August 1, 2013). "High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients". Anaerobe. 22: 50–56. doi:10.1016/j.anaerobe.2013.06.002. ISSN 1075-9964.
  6. Maes, Michael; Bosmans, Eugene; Kubera, Marta (2015). "Increased expression of activation antigens on CD8+ T lymphocytes in Myalgic Encephalomyelitis/chronic fatigue syndrome: inverse associations with lowered CD19+ expression and CD4+/CD8+ ratio, but no associations with (auto)immune, leaky gut, oxidative and nitrosative stress biomarkers". Neuro Endocrinology Letters. 36 (5): 439–446. ISSN 0172-780X. PMID 26707044.
  7. Shukla, Sanjay K.; Cook, Dane; Meyer, Jacob; Vernon, Suzanne D.; Le, Thao; Clevidence, Derek; Robertson, Charles E.; Schrodi, Steven J.; Yale, Steven; Frank, Daniel N. (December 18, 2015). "Changes in Gut and Plasma Microbiome following Exercise Challenge in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)". PLOS ONE. 10 (12): e0145453. doi:10.1371/journal.pone.0145453. ISSN 1932-6203. PMC 4684203. PMID 26683192.
  8. Morris, Gerwyn; Berk, Michael; Carvalho, André F.; Caso, Javier R.; Sanz, Yolanda; Maes, Michael (2016). "The Role of Microbiota and Intestinal Permeability in the Pathophysiology of Autoimmune and Neuroimmune Processes with an Emphasis on Inflammatory Bowel Disease Type 1 Diabetes and Chronic Fatigue Syndrome". Current Pharmaceutical Design. 22 (40): 6058–6075. doi:10.2174/1381612822666160914182822. ISSN 1873-4286. PMID 27634186.
  9. Morris, Gerwyn; Berk, Michael; Carvalho, André F.; Caso, Javier R.; Sanz, Yolanda; Maes, Michael (2016). "The Role of Microbiota and Intestinal Permeability in the Pathophysiology of Autoimmune and Neuroimmune Processes with an Emphasis on Inflammatory Bowel Disease Type 1 Diabetes and Chronic Fatigue Syndrome". Current Pharmaceutical Design. 22 (40): 6058–6075. doi:10.2174/1381612822666160914182822. ISSN 1873-4286. PMID 27634186.
  10. Varesi, Angelica; Deumer, Undine-Sophie; Ananth, Sanjana; Ricevuti, Giovanni (October 29, 2021). "The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications". Journal of Clinical Medicine. 10 (21): 5077. doi:10.3390/jcm10215077. ISSN 2077-0383. PMC 8584653. PMID 34768601.
  11. Vipond, Daniel (2018). "A role for a leaky gut and the intestinal microbiota in the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)". University of East Anglia.
  12. Anderson, G.; Maes, M. (December 20, 2020). "Mitochondria and immunity in chronic fatigue syndrome". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 103: 109976. doi:10.1016/j.pnpbp.2020.109976. ISSN 0278-5846.
  13. Varesi, Angelica; Deumer, Undine-Sophie; Ananth, Sanjana; Ricevuti, Giovanni (October 29, 2021). "The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications". Journal of Clinical Medicine. 10 (21): 5077. doi:10.3390/jcm10215077. ISSN 2077-0383. PMC 8584653. PMID 34768601.
  14. Simonato, Manuela; Dall’Acqua, Stefano; Zilli, Caterina; Sut, Stefania; Tenconi, Romano; Gallo, Nicoletta; Sfriso, Paolo; Sartori, Leonardo; Cavallin, Francesco; Fiocco, Ugo; Cogo, Paola (November 19, 2021). "Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome". Biomedicines. 9 (11): 1724. doi:10.3390/biomedicines9111724. ISSN 2227-9059. PMC 8615774. PMID 34829952.

serum The clear yellowish fluid that remains from blood plasma after clotting factors have been removed by clot formation. (Blood plasma is simply blood that has had its blood cells removed.)

etiology The cause of origin, especially of a disease.

microbiome The full collection of microscopic organisms (especially bacteria and fungi) which are present in a particular environment, particularly inside the human body.

T cell A type of white blood cell which is mostly produced or matured in the thymus gland (hence T-cell) and is involved in the adaptive immune response on a cellular level. Also known as a T lymphocyte. (Learn more: www.youtube.com)

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.

microbiome The full collection of microscopic organisms (especially bacteria and fungi) which are present in a particular environment, particularly inside the human body.

virome The human virome is the collection of all viruses that are found in or on humans.

mitochondria Important parts of the biological cell, with each mitochondrion encased within a mitochondrial membrane. Mitochondria are best known for their role in energy production, earning them the nickname "the powerhouse of the cell". Mitochondria also participate in the detection of threats and the response to these threats. One of the responses to threats orchestrated by mitochondria is apoptosis, a cell suicide program used by cells when the threat can not be eliminated.

metabolite A chemical compound produced by, or involved in, metabolism. The term is often used to refer to the degradation products of drugs in the body.

cytokine any class of immunoregulatory proteins secreted by cells, especially immune cells. Cytokines are small proteins important in cell signaling that modulate the immune system. (Learn more: me-pedia.org)

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From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history.