Leaky gut syndrome


  • Disordered intestinal permeability
  • Increased intestinal permeability
  • Compromised intestinal lining

Nature

Leaky gut syndromes are clinical disorders associated with increased intestinal permeability. They include inflammatory and infectious bowel disease, chronic inflammatory arthritide, cryptogenic skin conditions like acne, psoriasis and dermatitis herpetiformis, many diseases triggered by food allergy or specific food intolerance, including eczema, urticaria, irritable bowel syndrome, AIDS, chronic fatigue syndrome, chronic hepatitis, chronic pancreatitis, cystic fibrosis and pancreatic carcinoma.

When undigested proteins end up in the bloodstream, they are considered as “foreign” by the immune system. The resulting immune response is similar to what happens when the body mobilizes its defenses (i.e. T cells, B cells and antibodies) to eradicate a viral or bacterial infection. This type of immune response against proteins we eat contributes to food allergies. A similar mechanism that is not fully understood predisposes people with a leaky gut to develop more serious autoimmune disorders such as lupus, rheumatoid arthritis, type 1 diabetes, Graves disease, and inflammatory bowel disorders like Crohn’s and ulcerative colitis.

Background

Leaky gut syndromes are usually provoked by exposure to substances which damage the integrity of the intestinal mucosa. The commonest causes of damage are infectious agents (viral, bacterial and protozoan), ethanol, and non-steroidal anti-inflammatory drugs. Hypoxia of the bowel (occurring as a consequence of open-heart surgery or of shock), elevated levels of reactive oxygen metabolites (biliary, food-borne or produced by inflammatory cells), and cytotoxic drugs also increase para-cellular permeability. Some practitioners refer to both small bowel bacterial overgrowth and candida-related complex collectively as "dysbiosis". Both conditions are initiated by a disruption of the normal gastrointestinal microflora.

Claim

  1. Increased intestinal permeability to food antigens can be thought of as a generic explanation of systemic food allergy. The association of Crohn's GIT disease, for example, with psoriasis, arthropathies, sacroiliitis and ankylosing spondyliltis suggests that increased uptake of food antigens may be a pathogenic mechanism of systemic inflammatory disease. The absorption of antigenic molecules that originate from food and/or gut microbes may initiate and then maintain inflammation in target organs.


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