The Relationship Between Food Allergies, Leaky Gut and Autoimmune Disorders
by Dr. Eric Snow on Oct 22, 2020
Every day in our practice, we see people who are very sick but are unaware that it’s the food that makes them sick. They also sought medical treatments for their health conditions, but rarely did their doctors mention that food could contribute to their illnesses. In this article, we will discuss how food allergies contribute to autoimmune disorders and chronic inflammation.
What are food allergies?
Conventionally, food allergies refer to classic allergic reactions to food, such as hives, swelling (edema), runny nose, itchy throat, or airway closures. These reactions are typically severe and sudden but short-lived. This type of food allergies can be managed by simply avoiding the food and using allergy medicine and first-aid in case of exposure.
Another type of food allergies refers to a delayed and more prolonged inflammatory response to food, also called “food sensitivities.” There are many ways modern food components can do this.
How food components cause leaky gut
Natural pesticides in food
Plants can’t run away from their predators, so they come up with substances to harm their predators. In susceptible people, these substances can damage the gut lining and activate the immune system.
Lectins are carbohydrate-binding proteins that your cells use to recognize each other. Lectins are present in all living organisms, including humans. Some scientists hypothesize plants use lectins to protect their reproductive organs because the most harmful lectins are found in fruits and seeds. Many plant lectins can cause health problems because they can withstand digestion, get absorbed whole, and stimulate the immune system 1,2. In fact, tomato and mistletoe lectins are used to stimulate the immune system as adjuvants in vaccines 3.
Some lectins are poisonous, such as castor bean oil and mistletoe lectins. Bean lectins can cause digestive problems if eaten raw. However, many other common dietary lectins can contribute to chronic health problems, such as:
- Wheat germ agglutinin
- Legume, grain, nut, and seed lectins
- Nightshade lectins, found in tomatoes, potatoes, tomatillos, ground cherries, peppers, and chili peppers
- Insecticidal proteins in genetically engineered crops
- Gliadin, a type of gluten
Pressure cooking may break down some types of lectins, such as legume lectins, but not others, such as grain lectins.
Nightshade alkaloids are soap-like bitter substances that can disrupt the cell membrane of your gut lining. In mice with a genetic tendency to inflammatory bowel syndrome, exposure to potato alkaloids triggered the IBD4. Also, these alkaloids can withstand most cooking methods. We’ve found that many people who have an autoimmune disease or chronic inflammation tend to feel much better once they completely eliminate nightshades. Also, among these people, once they try bringing back foods to their diet, the nightshades tend to re-trigger symptoms.
Gluten is a group of sticky proteins found in wheat, rye, and barley. We now know that gluten can open the gut barrier through the zonulin pathway 5. Also, because gluten is poorly digested, incompletely digested fragments of gluten can cause inflammation. These gluten fragments may look similar to our own tissues, such as thyroid glands and joints, which can trigger autoimmunity via molecular mimicry 6,7.
Other common gut disruptors
Food texturizers also often act like soap, so they can disrupt the gut barrier function and expose the gut content to the immune system. Polysorbate 80, carboxymethylcellulose, and carrageenan are associated with inflammatory bowel disease 8.
Dairy can be a very inflammatory food, both due to lactose and casein intolerances. It is also a common food allergen. As a typical food for newborns of mammals, dairy induces both food addiction and leaky gut. Casein, a dairy protein, is hard to digest. Also, incompletely digested casein fragments, especially the A1 version that is common in American milk, can mimic the effect of opiates. Many studies have shown that A1 milk increases gut inflammation, slows gut movement, and often causes digestive problems 9. A1 milk consumption is also associated with type 1 diabetes and other autoimmune conditions 10.
Loss of immune tolerance
Neither food allergies nor food sensitivities are normal, but rather a result of our diet and lifestyle. A perfectly healthy person should be able to eat anything without suffering from symptoms. When they eat these foods, their gut may become temporarily leaky but soon re-seals itself after. Their immune system can recognize that these food allergens or irritants are safe foreign invaders, and treat them as safe accordingly.
Loss of tolerance refers to the inability of the gut to re-seal and ignore food accordingly 11. You may experience this as you start to develop food sensitivities. Often, this precedes an autoimmune or allergic diagnosis 11.
Many factors can contribute to this loss of immune tolerance, such as 12:
- Genetic tendency - Some people have genes that increase their risk of autoimmunity.
- Lacking immune training as a child - growing up on a farm or playing in the dirt at a young age can train the immune system to ignore harmless antigens (molecules that can provoke antibodies).
- Imbalanced gut bacteria, such as from C-section birth and antibiotic use
Keep in mind that it takes multiple factors to cause our immune system to stop tolerating food, so food allergies are not food problems. While eliminating the food is crucial to healing the gut, you also need to support your gut, gut bacteria, and immune system back into balance. We recommend our 30-day Eat & Be Well Gut Reset to support this process.
Dr. Alessio Fasano, the doctor who discovered how gluten can open up the gut barrier, explains that there are three factors that cause autoimmunity. These include a genetic tendency, a leaky gut, and an environmental trigger. Often, when people already have the genes and leaky gut, an infection or food allergy can be the final trigger through molecular mimicry 5.
Molecular mimicry happens when an antigen is so similar to your own protein that it can cause your immune system to attack your own protein. For example, some proteins from infectious bacteria and viruses are very similar to our own, which may trigger autoimmunity 13. Food antigens, such as gluten and lectins, can also trigger self-attacking immune responses 14.
Changing the gut bacteria towards a more pro-autoimmunity composition
Food allergies can also breed the wrong bacteria in your gut. For example, lectins promote the autoimmune-associated gut bacteria 14. In addition, gut inflammation can promote dysbiosis because it makes the gut less hospitable to friendly bacteria 15.
Can food cause autoimmunity?
The simple answer is that it depends on your genetic and epigenetic (upbringing that influences your genes) makeup. More susceptible people may develop full-on autoimmune diseases, while others suffer from other symptoms of chronic inflammation. These symptoms could include pain, brain fog, fatigue, inability to focus, or even depression.
Interestingly, some who are not susceptible or otherwise very immunologically balanced may be able to consume these foods just fine with no symptoms. For them, these foods are more like what doesn’t kill them makes them stronger. Also, some people with food sensitivities may be able to eat these foods once in a while after they heal their gut, re-balance their immune system, or get rid of their stressors. However, not everyone can completely restore their immune balance to the same extent.
The easy way to tell whether food could be causing your health problems is to listen to your body. If you have symptoms, it is likely the food. Identifying food sensitivities and working to heal the gut can often put chronic inflammation and autoimmunity into remission. Our 30-day Eat & Be Well Challenge will guide you through this process, and provide supplements that support the gut to heal and re-balance.
- Tchernychev, B. & Wilchek, M. Natural human antibodies to dietary lectins. FEBS Lett. 397, 139–142 (1996).
- Patrick G. Brady, M.D., Ann M. Vannier, John G. Banwell. IDENTIFICATION OF THE DIETARY LECTIN, WHEAT GERM AGGLUTININ, IN HUMAN INTESTINAL CONTENTS. GASTROENTEROLOGY by the American Gastroenterological Association (1978).
- Lavelle, E. C., Grant, G., Pusztai, A., Pfüller, U. & O’Hagan, D. T. The identification of plant lectins with mucosal adjuvant activity. Immunology 102, 77–86 (2001).
- Patel, B. et al. Potato glycoalkaloids adversely affect intestinal permeability and aggravate inflammatory bowel disease. Inflamm. Bowel Dis. 8, 340–346 (2002).
- Fasano, A. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann. N. Y. Acad. Sci. 1258, 25–33 (2012).
- Lerner, A., Jeremias, P. & Matthias, T. Gut-thyroid axis and celiac disease. Endocr Connect 6, R52–R58 (2017).
- Hvatum, M., Kanerud, L., Hällgren, R. & Brandtzaeg, P. The gut-joint axis: cross reactive food antibodies in rheumatoid arthritis. Gut 55, 1240–1247 (2006).
- Marion-Letellier, R., Amamou, A., Savoye, G. & Ghosh, S. Inflammatory Bowel Diseases and Food Additives: To Add Fuel on the Flames! Nutrients 11, (2019).
- Brooke-Taylor, S., Dwyer, K., Woodford, K. & Kost, N. Systematic Review of the Gastrointestinal Effects of A1 Compared with A2 β-Casein. Adv. Nutr. 8, 739–748 (2017).
- Birgisdottir, B. E., Hill, J. P., Thorsson, A. V. & Thorsdottir, I. Lower consumption of cow milk protein A1 beta-casein at 2 years of age, rather than consumption among 11- to 14-year-old adolescents, may explain the lower incidence of type 1 diabetes in Iceland than in Scandinavia. Ann. Nutr. Metab. 50, 177–183 (2006).
- Mackay, I. R. Topics in Review: Tolerance and autoimmunity. West. J. Med. 174, 118 (2001).
- Janeway, C. A., Jr, Travers, P., Walport, M. & Shlomchik, M. J. The mucosal immune system. (Garland Science, 2001).
- Oldstone, M. B. Molecular mimicry and autoimmune disease. Cell 50, 819–820 (1987).
- Cordain, L., Toohey, L., Smith, M. J. & Hickey, M. S. Modulation of immune function by dietary lectins in rheumatoid arthritis. Br. J. Nutr. 83, 207–217 (2000).
- Zeng, M. Y., Inohara, N. & Nuñez, G. Mechanisms of inflammation-driven bacterial dysbiosis in the gut. Mucosal Immunol. 10, 18–26 (2017).