Leaky Gut Syndrome - English Version

Pain from Inside-Out: Leaky Gut Syndrome - English Version

The large intestine (a.k.a. colon) is a dumpsite, and an important barrier that contain germs and toxin from remaining part of the body. The collapse of the structure’s integrity causes contamination of human body. {Schneeman, 2002}

The wall of colon are made up of columnal epithelia tightly bind with each other. When the binding force weaken, waste substances, toxin, and germs invade the blood vessels in the surrounding, and carried to entire body.


Leaky gut syndrome could arise from many causes, briefly grouped as pathogens (e.g. Vibrio cholerae, and Salmonella enterica), toxins (e.g. zonulin), allergens (e.g. gluten), drugs (e.g. aspirin, and ibuprofen), pro-inflammatory cytokines (e.g. TNFα, and IL-13), missing probiotics, and genetic diseases (e.g. celiac disease, and type 1 diabetes).

People who have constipation are most likely to suffer leaky gut syndrome because of the accumulation of these diverse harmful substances. The incubation of fecal bacteria in the gut amplifies the damage to the colon.

{El Asmar et al., 2002; van der Walle et al., 2011; Fasano, 2012; Hollon, 2015; Odenwald and Turner, 2013; Weber at al., 2010}

Pathology and Symptoms

As the bloodstream around the colon is constantly contaminated with fecal materials and carried throughout the body. These bad substances trigger immune response, recurring inflammations that occur for no apparent reason, anytime and any part of body. This is called autoimmune disease. {Fasano, 2012}

Leaky gut syndrome may have multiple and random symptomatic outcomes, depending on the site where the immune responses (a.k.a. white blood cell attack) concentrate. Common symptoms are joint pain (potentially rheumatoid arthritis), attention deficit hyperactive disorder (ADHD), eczema, psoriasis, chronic fatigue, frequent cold, sinusitis and bad breath. To a heavier extent, organ failuresmultiple sclerosis, and systemic lupus erythematosus (SLE) may also develop.

Inflammation → malnutrition → bacterial dysbiosis → hepatic stress

Patients of this syndrome commonly suffer malnutrition. Somatic cells are resistant against nutrients that are carried together with ‘dirty’ blood. Loads of toxin and unaccepted nutrients end up in liver, thus increasing the risk of hepatitis.

{Abdelhamid and Luo, 2018}


1.Fibre: Dietary fibres improve intestinal integrity while also prevent accumulation of feces in the colon. {Shiau and Chang, 1986}

2.Liver and Kidney Tonic: Liver and kidneys share the toxin load with the diseased colon. Protection and nourishment to these organs are especially important. Vitamin A, B complexes, lecithin, milk thistle, dandelion, turmeric, and virgin coconut oils are widely used. {Cody, 1988}

3.Protein: Threonine, glycine, and glutamine are important elements of intestinal mucosa to keep the colon intact, prevent bacteria and toxin to escape from colon. {Van Der Hulst et al., 1993}

4.Antioxidant: Glutathione (GSH) reduce toxic metabolites in the guts and toxic xenobiotics in the liver. {Deitch, 1990}

5.Probiotics: Lactobacillus sp. and Bifidobacterium sp.maintain a good ecosystem in the guts, assist some nutrient absorption, and reduce the likehood of bad bacteria invasion.

6.Essential Fatty Acid: EFAs such as γ-linolenic acid (GLA) promotes E-series prostaglandins, restore epithelial stability, repair mucosa lining. {Vanderhoof et al., 1991; Kapoor and Huang, 2006}

7.Reduce Allergic Food

8.Good Quality Sleep


Abdelhamid, L. and Luo, X.M., 2018. Retinoic acid, leaky gut, and autoimmune diseases. Nutrients, 10(8), p.1016.

Deitch, E.A., 1990. The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Archives of Surgery, 125(3), pp.403-404.

El Asmar, R., Panigrahi, P., Bamford, P., Berti, I., Not, T., Coppa, G.V., Catassi, C. and Fasano, A., 2002. Host-dependent zonulin secretion causes the impairment of the small intestine barrier function after bacterial exposure. Gastroenterology, 123(5), pp.1607-1615.

Fasano, A., 2012. Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences, 1258(1), p.25.

Hollon, J., Puppa, E., Greenwald, B., Goldberg, E., Guerrerio, A. and Fasano, A., 2015. Effect of gliadin on permeability of intestinal biopsy explants from celiac disease patients and patients with non-celiac gluten sensitivity. Nutrients, 7(3), pp.1565-1576.

Kapoor, R. and Huang, Y.S., 2006. Gamma linolenic acid: an antiinflammatory omega-6 fatty acid. Current pharmaceutical biotechnology, 7(6), pp.531-534.

Odenwald, M.A. and Turner, J.R., 2013. Intestinal permeability defects: is it time to treat?. Clinical Gastroenterology and hepatology, 11(9), pp.1075-1083.

Schneeman, B.O., 2002. Gastrointestinal physiology and functions. British journal of nutrition, 88(S2), pp.S159-S163.

Shiau, S.Y. and Chang, G.W., 1986. Effects of certain dietary fibers on apparent permeability of the rat intestine. The Journal of nutrition, 116(2), pp.223-232.

Vanderhoof, J.A., Blackwood, D.J., Mohammadpour, H. and Park, J.H., 1991. Effect of dietary menhaden oil on normal growth and development and on ameliorating mucosal injury in rats. The American journal of clinical nutrition, 54(2), pp.346-350.

Van Der Hulst, R.R., Von Meyenfeldt, M.F., Deutz, N.E.P., Soeters, P.B., Brummer, R.J.M., von Kreel, B.K. and Arends, J.W., 1993. Glutamine and the preservation of gut integrity. The Lancet, 341(8857), pp.1363-1365.

Van Der Walle, C.F. and Schmidt, E., 2011. Modulation of the intestinal tight junctions using bacterial enterotoxins. In Peptide and Protein Delivery (pp. 195-219). Academic Press.

Weber, C.R., Raleigh, D.R., Su, L., Shen, L., Sullivan, E.A., Wang, Y. and Turner, J.R., 2010. Epithelial myosin light chain kinase activation induces mucosal interleukin-13 expression to alter tight junction ion selectivity. Journal of Biological Chemistry, 285(16), pp.12037-12046.

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