The Gut of Autoimmune Diseases

The digestive system and autoimmune disease have an important relationship.

The Connection between The Digestive Tract and Autoimmune Disease

The manifestation of autoimmunity and the occurrence of digestive dysfunction is a two way street. Having an autoimmune disease will create problems in your digestive system and having a poorly working gut can lead to autoimmunity, or make it worse. Inflammation is the main culprit here. A genetic predisposition, poor diet, gut microbiome, stress, drugs and/or a preexisting condition can bring about inflammation. Inflammation involves certain white blood cells that go into your cells to clean up debris from damage or outside invaders and then those same white blood cells aren’t rid of in time and die. These dead white blood cells become necrotic and create an inflammatory response by accumulating in your cells. How this comes about varies by which factor mentioned above is in play.

The autoimmune condition Systemic Lupus Erythematosus (SLE) is usually represented with a butterfly. This is due to the butterfly rash that appears on the face of some SLE patients. And the flower, Echinacea, is a common contraindication for autoimmune conditions.
Photo: Taken by Kris Kuciel at The Winnipeg Zoo.

An overgrowth of bad bacteria in the intestines, a stress related response, antibiotics killing off good bacteria, eating junk food high in trans fats are all ways your digestive system can be aggravated or manifest autoimmunity. Then the resulting autoimmunity can create an overreaction of your immune system in the gut causing more disease. It is a constant cycle. The gut needs to remain hyposensitive to food coming in and the bacteria living there while also being able to mount effective defense to outside invaders and not the body itself.

The Big Three

Autoimmune diseases have been on the rise since the mid 1940s and is only becoming more and more prevalent with “unknown pathogenesis” being the main descriptor for them. We may not know what exactly is going on with a lot of autoimmune diseases yet but we know what has been influencing their prevalence and making symptoms worse. Environmental factors, genetics and gut dysbiosis have been the main triad for disorders of autoimmunity. As broad as those categories are let’s go into some detail.

Environmental Factors

The largest category of factors but probably the most important here. Diet (yes, food is an environmental factor, but more on that in the gut microbe section), heavy metals, toxins, viruses, bacteria, emotional stress, lifestyle and drugs all influence your immune response. This is a category that creates each and everyone of us to have a unique health profile. Some things can’t be controlled while others can be. And some have a possibility to reverse their long term effects on your system. Aggravating environmental factors that have been researched are ones you probably wouldn’t think of, from breast implants to sun exposure (1,2). This topic has endless books on it and is always changing.

Genetics

The genes scripted into our DNA do a lot. Actually, pretty much everything in the body. These genes are translated to make enzymes and proteins that cause many functions in the body while also have the instructions to replicate cells and make structures. These genes are predictors of many diseases that you may be more susceptible to than others. An example of this is a gene that makes the protein tyrosine phosphatase called PTPN22. An allele (variant in this gene) that involves a tryptophan (amino acid) instead of arginine (another amino acid) is found more commonly in those with autoimmune diseases such as type 1 diabetes, Addisons, systemic lupus erythematous (SLE), rheumatoid arthritis and thyroiditis (3,4). There are still ethical reasons around testing for these genes widely. With the study of epigenetics (the change in the expression of said genes) it is seen that a gene showing that you will be susceptible to a disease doesn’t always mean that it will translate to that. Our environment has influence on what genes will be expressed. And as we are all very unique in our DNA we are also unique in its expression, dependant on a lot of factors. To say shortly, it’s complicated.

Gut Microbes

Astonishing enough, scientific research and study on the bacteria living inside of us (mainly in the digestive system) is only a handful of decades old. Yet, it’s influence on our health has now been seen in all systems of our body, from not only digestion but mental health to immunity. As much as it is important to our health it is also easily put off balance and destroyed. Smoking, poor nutrition, drugs, alcohol and much more influence our gut microbes. Which in turn affects your health. Just like ourselves, when it comes to our microbiome, you are what you eat, do AND think. And with that, the organisms in our gut and our intestinal lining influence and are composed of 70% of our immune system (5). A disruption in this bacterial environment creates an impaired ability to fight off infection, increasing the chances of a take-over of ‘bad bacteria’ while also allowing outside invaders to come penetrate our system. Which now leads me to talk about something called leaky gut.

Leaky Gut

Surprisingly our intestines are made up of just one layer of cells called the epithelial lining. Together with chemical factors secreted from these cells create a barrier that separates us from the outside environment (because technically the inside of our gut is exposed to the outside, well to whatever you put in your mouth). When someone is exposed to disease, this lining may become compromised allowing many outside invaders, antigens and toxins inside our blood stream; this is what is called ‘leaky gut.’ The epithelial lining is maintained by a mucosal barrier (6). This layer is mostly composed of mucus that is filled with immune cells and protective molecules. The single cell epithelial lining consist of many tight junctions that allow for absorption but also prevention of foreign antigens. Any changes to these different factors will lead to leaky gut which in turn creates a local and/or systemic immune response that if left for a long time becomes autoimmune (self attacking self). It’s an all doors open idea to a lot of outside invaders that will cause your body to attack and inflame itself. Some of the autoimmune diseases that come from or are made worse due to leaky gut are IBD, celiac disease, type 1 diabetes, multiple sclerosis and SLE (7-9). A leaky gut is developed through lifestyle factors/choices, environment and disease. Alcohol, diet, toxin exposure, stress and drugs all can contribute to your gut dysbiosis and permeability.

Repairing the Gut and Managing Autoimmunity

Gut inflammation and gut permeability can be reversed with some work. There are many studies using probiotics, supplements and diet modifications to greatly improve gut health and also repair leaky gut. A lot of this requires specific strains, therapeutic dosing, and detailed diet modifications to show effectiveness. As I have stated before, there is a bit of a two way street when it comes to digestive health and autoimmunity. Most times it is difficult to know which is affecting the other more without becoming a laboratory specimen. Managing autoimmunity through diet and supplementary modifications is just as important as those made to repair the gut, and most times the same treatments overlap. Which in turn, most treatments for autoimmune conditions should consider involving gut healing protocols as for the reasons stated above.

A lot of improvements in health can be made for someone living with an autoimmune disease, you just have to get to the gut of it.

Seeking Autoimmune Disease Care

Dr. Kris Kuciel, ND (me) is a licensed Naturopathic Doctor that focuses on treating autoimmune diseases by investigating all your body systems and creating a plan that is holistic in approach but specific to your condition. If you or a family member are struggling with an autoimmune condition, I provide 15 minute free consultations where we can meet, get to know one another and explain what is needed of you to create a plan to manage your condition and symptoms. Then you can decide if we are a good fit and want to start Naturopathic care. Living with an autoimmune disease doesn’t need to put a burden on your life plans and goals.

References:

1) Colaris MJL, de Boer M, van der Hulst RR, Cohen Tervaert JW. Two hundreds cases of ASIA syndrome following silicone implants: a comparative study of 30 years and a review of current literature. Immunol Res. 2017;65(1):120-128. doi:10.1007/s12026-016-8821-y

2) Munger KL, Levin LI, Hollis BW, Howard NS, Ascherio A. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006;296(23):2832–2838.

3) Burn GL, Svensson L, Sanchez-Blanco C, Saini M, Cope AP. Why is PTPN22 a good candidate susceptibility gene for autoimmune disease?. FEBS Lett. 2011;585(23):3689-3698. doi:10.1016/j.febslet.2011.04.032

4) Criswell LA, Pfeiffer KA, Lum RF, et al. Analysis of families in the multiple autoimmune disease genetics consortium (MADGC) collection: the PTPN22 620W allele associates with multiple autoimmune phenotypes. Am J Hum Genet. 2005;76(4):561-571. doi:10.1086/429096

5) Vighi G, Marcucci F, Sensi L, Di Cara G, Frati F. Allergy and the gastrointestinal system. Clin Exp Immunol. 2008;153 Suppl 1(Suppl 1):3-6. doi:10.1111/j.1365-2249.2008.03713.x

6) Peterson LW, Artis D. Intestinal epithelial cells: regulators of barrier function and immune homeostasis. Nat Rev Immunol. 2014;14(3):141-153. doi:10.1038/nri3608

7) Khaleghi S, Ju JM, Lamba A, Murray JA. The potential utility of tight junction regulation in celiac disease: focus on larazotide acetate. Therap Adv Gastroenterol. 2016;9(1):37-49. doi:10.1177/1756283X15616576

8) Fasano A, Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol. 2005;2(9):416-422. doi:10.1038/ncpgasthep0259

9) Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci. 2012;1258(1):25-33. doi:10.1111/j.1749-6632.2012.06538.x