Love Your Guts By Millie H. Abplanalp

Hippocrates, a Greek physician in 400 B.C., has often been called the Father of Modern Medicine because of his advanced philosophies on disease and the body’s natural power to re-balance and heal itself. His famous quotes, “death sits in the bowels,” and “bad digestion is the root of all evil,” (Sekirov, Russell, Antunes, & Finlay, 2010) are still being recited and researched today.


Gut function is not only connected to nutrient processing and absorption but directly communicates with bacteria supporting digestion and their enzymatic activities (Bischoff, 2011).

Bacteria supporting digestion through enzymatic activity regulate epithelial and immune functions, reporting to the brain through the vagus nerve pathway and hormones (Bischoff, 2011). The microbiota directly affects GI function as well as behavior and neurochemical changes in the brain (Bischoff, 2011).

The microbiome directly influences over 75% of the immune system, protecting the body from infection and regulating the metabolism (Kresser, n.d.).

The complexities of two functional entities of the gut, the microbiome, and GI barrier or wall are the key to achieving and maintaining gut health (Bischolff, 2011). The intestinal wall has two important functions; to allow essential nutrients and fluids into the blood stream and to also act as a barrier against pathogens causing infections (Axe, 2016a). The intestinal wall has four layers, serous, muscular, submucosa, and the mucosa. The serous layer is the outermost layer consisting of connective tissue while the muscular layer moves food through the digestive tract (Axe, 2016a). The mucosa and submucosa are the innermost layers and together make up the mucosal barrier (Axe, 2016a).

The Beginning of Gut Flora

Colonization of the microbiota is thought to begin at birth as the baby passes through the vaginal canal (Sekirov et al., 2010) and sucks from the mother's breast. Vaginally delivered infants show similar intestinal microbiota of their mother (Sekirov et al., 2010). Researchers at Ohio State University are beginning to suspect the microbiota of the mother may have an influence on the fetus, even before birth.

Infants delivered by cesarean section have a different microbial composition than infants who were delivered vaginally (Sekirov et al., 2010). In the first year of life, the microbiota composition is simple but may vary widely between individuals (Sekirov et al., 2010).

Diet is directly related to the diversity and composition of the microbiome.

Diet influences the microbiome. The decline of fiber in the diet, especially Westernized societies, has been shown to increase inflammatory diseases.
Diets high in fiber from fruits and vegetables provide energy for the beneficial microbes and gut cells.
The Hygiene Hypothesis

Antibacterial soaps, sprays, pasteurized and sterilization of milk and other food products, as well as decontamination of the water supply and childhood vaccinations, have decreased disease. This decrease in the infectious burden is also associated with a rise in allergic and autoimmune diseases (Okada, Kuhn, Feillet, & Bach, 2010).

The "hygiene hypothesis" maintains any disturbance of balance between the microbiome and mucosal immune system will lead to impairment of the GI barrier, increase the risk to gut health and subsequently develops into GI disease (Bischoff, 2011). The hygiene hypothesis could explain the increase of autoimmune diseases.

Diseases Causes By Dysbiosis

Dysbiosis of the microbiotal population has also been shown to be associated with weaknesses in gut barrier function and innate and systemic immune dysregulation (Jones, 2016). Many diseases, such as inflammatory bowel disease, Celiac disease, type 1 diabetes, and irritable bowel syndrome, are characterized by altered GI microbiota, which suggests a link between gut barrier function and microbiota composition (Bischoff, 2011; Serena, Camhi, Sturgeon, Yan, & Fasano, 2015).

The Leaky Gut

When shifts in the microflora occur, small intestinal bacterial overgrowth develops altering the tight junctions and causing gut permeability, respectively (Dai & Wang, 2015). Permeability begins when a molecular substance can cross through the intestinal epithelium by simple diffusion, which is caused by a disruption of the intercellular tight junctions (Dai & Wang, 2015). A decrease in cellular ATP results in the breakdown of tight junction complexes causing barrier dysfunction (Groschwitz & Hogan, 2009).

The barrier becomes “leaky” when the tight junctions in the gut wall become permeable. There are many pathological and physiological reasons for the gut to become leaky. Stresses on the body, such as injury, infection, or an unhealthy diet, can cause a disruption in the intestinal mucosal barrier, resulting in “leaky gut,” allowing bacteria and pathogens into other parts of the body (Sekirov et al., 2010).

Wheat and Zonulin

Zonulin triggers the opening of the tight junctions when exposed to bacterial infections and gliadin, the main protein in gluten. Gliadin up-regulates a receptor on the intestinal epithelial which releases zonulin, causing the tight junctions to remain open and increasing intestinal permeability.

Zonulin production is increased in type 1 diabetics. Research suggests diabetics have a combination of predisposed genetics and a dysregulated intestinal barrier function with increased exposures to antigens trigger an autoimmune response (Groschwitz & Hogan, 2009).

Heal Thy Guts

Eat Fermentable Foods

Fibers and Starches
Kombucha and Kefir
Sauerkraut and Kimchi
Bone Broths
Take Probiotics


Chronic Stress
Antibiotics and NSAIDS
Foods High in Refined Carbohydrates and Sugar


Mindful Eating

Yoga and Mediation


Herbs and Supplements


Axe, J. (2016a). Eat Dirt. New York, NY: HarperCollins Publishers.

Bischoff, S, C. (2011). ‘Gut health’: a new objective in medicine? BMC Medicine, 9(24). Retrieved from

Dai, X., & Wang, B. (2015). Role of gut barrier function in the pathogenesis of nonalcoholic fatty liver disease. Gastroenterology Research and Practice, 2015. doi: 10.1155/2015/287348.

Groschwitz, K, R., & Hogan, S, P. (2009, July). Intestinal barrier function: Molecular regulation and disease pathogenesis. Journal of Allergy and Clinical Immunology, 124(1). 3-22. doi: 10.1016/j.jaci.2009.05.038.

Jones, R, M. (2016). The influence of the gut microbiota on host physiology: In pursuit of mechanisms. Yale Journal of Biology and Medicine, 89. 285-297. Retrieved from

Kresser, C. (2016). Gut Health. Chris Kresser. Retrieved from­‐health/.

Okada, H., Kuhn, C., Feillet, H., & Bach, J, F. (2010, January 21). The ‘hygiene hypothesis’ for autoimmune disease and allergic diseases: an update. Clinical & Experimental Immunology, 160. 1 – 9. doi: 10.111/J.1365.2249.2010.04139.x.

Sekirov, I., Russell, S, L., Antunes, C, M., & Finlay, B, B. (2010, July). Gut microbiota in health and disease. American Physiological Society, 90. 859-904. doi: 10.1152/physrev.00045.2009.

Serena, G., Camhi, S., Sturgeon, C., Yan, S., & Fasano, A. (2015, August). The role of gluten in celiac disease and type 1 diabetes. Nutrients, 7. 7143-7162. doi: 10.3390/nu7095329.

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Millie Abplanalp

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