Photo by Tijana Drinic @tijana94 of wheat flour as dough, a food ingredient that contains gluten

Gluten is one of the prime issues discussed when exploring holistic health, and it’s become a marketing trend to proudly display “gluten-free” on health-conscious brands, raising awareness and “representation”. Conversely, there has been much ridicule and dismissal of gluten intolerance as a “rich person’s illness”, likening it to a spoiled, hypochondriac, sheltered lifestyle, or some kind of character weakness. Disney aired a sitcom featuring that very caricature, a hysterical gluten-free child, and after backlash from real, sick, effected celiac individuals, Disney apologized and pulled the episode from syndication (CBS News).

Not only does gluten harm those with celiac disease (~2% of the population, with ~80% sufferers undiagnosed) and non-celiac gluten sensitivity (~13% of the population), but there is evidence that gluten consumption increases intestinal permeability (“leaky gut”) in all individuals; that is, an increase in systemic inflammation, endotoxin exposure, and essentially all disease (Hollon, et al., 2015). In cell cultures, gluten is directly toxic to cells (Elli, et al., 2015).

Oftentimes, sufferers may not know they’re intolerant, as adverse reactions are delayed, and the immediate reaction to eating wheat can appear positive, as it contains exorphins, which have an opiate-like effect, producing a mild, euphoric, perhaps sedating “high”. It would then follow that removing exorphigenic foods from the diet may cause a withdrawal (I experienced psychedelic nightmares after removing it in 2016), which could further obfuscate what’s actually going on, and discourage the sufferer from quitting gluten (Pruimboom & Punder, 2015).

Glutinous grains, like wheat, barley, and rye, contain their protein component (prolamins) in a storage form; wheat’s prolamin, for example, is gliadin. Molecularly, gliadin resembles the enzyme transglutaminase, found abundantly in the thyroid. Whenever gluten is eaten and gliadin enters the bloodstream, the immune system mounts an attack on both gliadin and transglutaminase. This is the mechanism by which gluten can cause thyroid disease in susceptible individuals (Wong, 2017).

Wheat and gluten are implicated in Type 2 Diabetes, and can directly cause Type 1 Diabetes (Kizilgul, et al., 2017). Removal of dietary gluten can delay or completely prevent the development of diabetes in mice bred specifically to develop Type 1 Diabetes (Funda, et al., 1999).

Celiac disease and gluten intolerance can cause or contribute to fatigue, depression, anxiety, malabsorption, anemia, psoriasis, fibromyalgia, numbness, insomnia, brain fog, indigestion, diarrhea, constipation, dementia, Alzheimer’s, schizophrenia, attention-deficit disorder, autism, Tourette’s, OCD, epilepsy, migraine, heart disease, and cancer (Dimitrova et al., 2013Ergün, et al., 2018; Gajulapalli, et al., 2017; Rodrigo et al., 2018; Tio, et al., 2012).

Autoimmunity from gluten exposure can cause antibodies to destroy the glutamic acid decarboxylase enzyme, which is what normally converts glutamate into GABA. This lack of inhibitory GABA, with a continuous pooling of excitatory glutamate, combined with systemic inflammation and nutrient malabsorption, is enough to explain the myriad of psychiatric and degenerative symptoms that arise.

Depressive celiacs have aberrant serotonergic function, and experience improvement or remission from mood symptoms simply by avoiding gluten. Celiac disease rates in schizophrenics are doubled compared to the general population, and some schizophrenics experience remission on a gluten-free diet (Jackson, et al., 2013). 60-82% of gluten-intolerant people are known to experience abnormal amounts of fatigue (Zipser, et al., 2003), and the malabsorption from gluten’s destructive effects on the intestine can cause deficiency syndromes of any vital nutrients, so fatigue can manifest from several different pathways, with one root cause.

Celiac patients who discontinue gluten, but continue to take NSAIDs, proton-pump inhibitors, or SSRIs, show persistent intestinal villi atrophy (Mahadev, et al., 2017). There are clear mechanisms whereby all of these could continually irritate the intestine, and additionally, it was recently found that 93% of all oral medications contain at least 1 potential allergenic additive, so even benign compounds can have toxic fillers, or industrial contaminants that inhibit intestinal healing (Voelker, 2019).

As for repairing the gut, the offensive substances must be avoided, and in my experience, no amount of supplementary compensation will protect from continuous indulgence; the body will progressively and insidiously break down in every which way.

Vitamin A helps cultivate healthy gut bacteria and strengthen gut barrier function even in the absence of any probiotic bacteria (Abdelhamid & Luo, 2018).

Berberine protects from endotoxin and inflammation by structural modification of gut bacteria, and also has a tightening, restorative effect on intestinal tight junctions, the gut barrier (Gu, et al., 2011; Li, et al., 2010; Xu, et al., 2012).

N-acetyl-glucosamine can tighten the intestinal cell junctions, reducing permeability and inflammation. It is derived from shellfish, which some people are reactant to.

Zinc enhances intestinal mucosal repair (Roy, et al., 1992) and enhances epithelial barrier function, reducing the leaky state of intestinal tight junctions (Cario, et al., 2000; Wang, et al., 2013).

I think it’s important for anyone to know the extent to which such common dietary substances can wreak such havoc and illness on unsuspecting people, so they can then identify it happening in themselves or others. It can save lives and massively reduce unnecessary suffering to be able to troubleshoot causes of supposedly genetic or idiopathic diseases, and fix them with simple, easy, and free dietary and lifestyle changes.

Further reading:

Works Cited

Cario, et al. “Effects of Exogenous Zinc Supplementation on Intestinal Epithelial Repair in Vitro.” European Journal of Clinical Investigation, vol. 30, no. 5, 2000, pp. 419–428., doi:10.1046/j.1365-2362.2000.00618.x.

Castillo, Michelle. “Disney Pulls ‘Jessie’ Episode That Makes Fun of Gluten-Free Child.” CBS News, CBS Interactive, 20 May 2013, http://www.cbsnews.com/news/disney-pulls-jessie-episode-that-makes-fun-of-gluten-free-child/.

Dimitrova, Alexandra K., et al. “Prevalence of Migraine in Patients With Celiac Disease and Inflammatory Bowel Disease.” Headache: The Journal of Head and Face Pain, vol. 53, no. 2, 2012, pp. 344–355., doi:10.1111/j.1526-4610.2012.02260.x.

Elli, Luca. “Non-Celiac Gluten Sensitivity: Time for Sifting the Grain.” World Journal of Gastroenterology, vol. 21, no. 27, 2015, p. 8221., doi:10.3748/wjg.v21.i27.8221.

Funda, David P., et al. “Gluten‐Free Diet Prevents Diabetes in NOD Mice.” Diabetes/Metabolism Research and Reviews, vol. 15, no. 5, 1999, pp. 323–327., doi:10.1002/(sici)1520-7560(199909/10)15:5<323::aid-dmrr53>3.3.co;2-g.

Gajulapalli, Rama D, and Deepak J Pattanshetty. “Risk of Coronary Artery Disease in Celiac Disease Population.” Saudi Journal of Gastroenterology : Official Journal of the Saudi Gastroenterology Association, Medknow Publications &amp; Media Pvt Ltd, 2017, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5539680/.

Gu, Lili, et al. “Berberine Ameliorates Intestinal Epithelial Tight-Junction Damage and Down-Regulates Myosin Light Chain Kinase Pathways in a Mouse Model of Endotoxinemia.” The Journal of Infectious Diseases, vol. 203, no. 11, 2011, pp. 1602–1612., doi:10.1093/infdis/jir147.

Hadjivassiliou, M., et al. “Headache and CNS White Matter Abnormalities Associated with Gluten Sensitivity.” Neurology, vol. 56, no. 3, 2001, pp. 385–388., doi:10.1212/wnl.56.3.385.

Hollon, Justin, et al. “Effect of Gliadin on Permeability of Intestinal Biopsy Explants from Celiac Disease Patients and Patients with Non-Celiac Gluten Sensitivity.” Nutrients, vol. 7, no. 3, 2015, pp. 1565–1576., doi:10.3390/nu7031565.

Jackson, Jessica R., et al. “Neurologic and Psychiatric Manifestations of Celiac Disease and Gluten Sensitivity.” Psychiatric Quarterly, vol. 83, no. 1, 2011, pp. 91–102., doi:10.1007/s11126-011-9186-y.

Kizilgul, Muhammed, et al. “Screening for Celiac Disease in Poorly Controlled Type 2 Diabetes Mellitus: Worth It or Not?” BMC Endocrine Disorders, vol. 17, no. 1, 2017, doi:10.1186/s12902-017-0212-4.

Li, Ning, et al. “Berberine Attenuates pro-Inflammatory Cytokine-Induced Tight Junction Disruption in an in Vitro Model of Intestinal Epithelial Cells.” European Journal of Pharmaceutical Sciences, vol. 40, no. 1, 2010, pp. 1–8., doi:10.1016/j.ejps.2010.02.001.

Mahadev, Srihari, et al. “Factors Associated with Villus Atrophy in Symptomatic Celiac Disease Patients on a Gluten-Free Diet.” Gastroenterology, vol. 152, no. 5, 2017, doi:10.1016/s0016-5085(17)30851-x.

Pruimboom, Leo, and Karin De Punder. “The Opioid Effects of Gluten Exorphins: Asymptomatic Celiac Disease.” Journal of Health, Population and Nutrition, vol. 33, no. 1, 2015, doi:10.1186/s41043-015-0032-y.

Rodrigo-Sáez, Luis, et al. “Refractory Iron-Deficiency Anemia and Gluten Intolerance: Response to Gluten-Free Diet.” Revista Española De Enfermedades Digestivas, vol. 103, no. 7, 2011, pp. 349–354., doi:10.4321/s1130-01082011000700003.

Rodrigo, Luis, et al. “Efficacy of a Gluten-Free Diet in the Gilles De La Tourette Syndrome: A Pilot Study.” Nutrients, vol. 10, no. 5, 2018, p. 573., doi:10.3390/nu10050573.

Roy, S. K., et al. “Impact of Zinc Supplementation on Intestinal Permeability in Bangladeshi Children with Acute Diarrhoea and Persistent Diarrhoea Syndrome.” Journal of Pediatric Gastroenterology and Nutrition, vol. 15, no. 3, 1992, pp. 289–296., doi:10.1097/00005176-199210000-00010.

Skrovanek, Sonja. “Zinc and Gastrointestinal Disease.” World Journal of Gastrointestinal Pathophysiology, vol. 5, no. 4, 2014, p. 496., doi:10.4291/wjgp.v5.i4.496.

Sturniolo, Giacomo Carlo, et al. “Effect of Zinc Supplementation on Intestinal Permeability in Experimental Colitis.” Journal of Laboratory and Clinical Medicine, vol. 139, no. 5, 2002, pp. 311–315., doi:10.1067/mlc.2002.123624.

Tio, M., et al. “Meta-Analysis: Coeliac Disease and the Risk of All-Cause Mortality, Any Malignancy and Lymphoid Malignancy.” Alimentary Pharmacology &amp; Therapeutics, vol. 35, no. 5, 2012, pp. 540–551., doi:10.1111/j.1365-2036.2011.04972.x.

Voelker, Rebecca. “Nearly All Medications Contain Potentially Allergenic Inactive Ingredients, Analysis Shows.” Jama, 2019, doi:10.1001/jama.2019.4667.

Volta, Umberto, et al. “An Italian Prospective Multicenter Survey on Patients Suspected of Having Non-Celiac Gluten Sensitivity.” BMC Medicine, vol. 12, no. 1, 2014, doi:10.1186/1741-7015-12-85.

Volta, Umberto, et al. “An Italian Prospective Multicenter Survey on Patients Suspected of Having Non-Celiac Gluten Sensitivity.” BMC Medicine, vol. 12, no. 1, 2014, doi:10.1186/1741-7015-12-85.

Wang, Xuexuan, et al. “Zinc Supplementation Modifies Tight Junctions and Alters Barrier Function of CACO-2 Human Intestinal Epithelial Layers.” Digestive Diseases and Sciences, vol. 58, no. 1, 2012, pp. 77–87., doi:10.1007/s10620-012-2328-8.

Wessells, K. Ryan, et al. “Associations Between Intestinal Mucosal Function and Changes in Plasma Zinc Concentration Following Zinc Supplementation.” Journal of Pediatric Gastroenterology and Nutrition, vol. 57, no. 3, 2013, pp. 348–355., doi:10.1097/mpg.0b013e31829b4e9e.

Wong, Kaufui  V. “Gluten and Thyroid Health.” Juniper Online Journal of Public Health, vol. 1, no. 3, 2017, doi:10.19080/jojph.2017.01.555563.

Zhang, Xu, et al. “Structural Changes of Gut Microbiota during Berberine-Mediated Prevention of Obesity and Insulin Resistance in High-Fat Diet-Fed Rats.” PLoS ONE, vol. 7, no. 8, 2012, doi:10.1371/journal.pone.0042529.

Zipser, Robert D., et al. Digestive Diseases and Sciences, vol. 48, no. 4, 2003, pp. 761–764., doi:10.1023/a:1022897028030.

One thought on “Delicious, Destructive: Gluten’s Toxicity & How to Heal the Gut

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