Holistic Treatment For Autoimmune Disease

Abstract

There are many theories regarding stress, trauma and hormones being triggers of autoimmunity; however, although they are part of the landscape that sets the stage for autoimmunity, they are not the mechanisms in which loss of self-tolerance occurs.  There are countless studies proving links between infections, chemicals, and food sensitivities as the mechanisms in which we develop autoantibodies. These autoantibodies are produced because of infections, chemicals and food proteins ability to cross-react and or bind with human tissue. I plan to show the link between food sensitivities, infections and chemicals as the main three leading mechanisms of autoimmunity.

Understanding Autoimmunity

Autoimmunity is a disorder in which an overzealous immune system attacks and breaks down its own tissue. Another term for the process of autoimmunity is “loss of self -tolerance.” Rates of autoimmunity have exploded in the last few decades. According to the American Related Disease Autoimmune Association, it is estimated that 50 million Americans suffer from an autoimmune disorder, costing over $100 billion annually in healthcare costs. To put this in perspective, cancer costs approximately $45 billion annually. It is the most popular health topic requested by people who call the National Women’s Health Information Center; however, we only spend $591 million on autoimmunity research, compared to $6.1 billion on cancer research (AARDA 2019).

Although there is a myriad of underlying factors that set the foundation for autoimmunity – stress, trauma, diet and lifestyle, for example – I propose we start differentiating the actual mechanisms that trigger loss of self-tolerance with the other sources that help ‘set the stage’ but are not the mechanisms that activate the immune system to identify tissues as “foreign articles.”  The importance of categorizing these mechanisms is not for us to ignore the whole picture, but rather to identify the components that can, and will often, cause further autoimmune disorders. There are three categories of mechanisms that have been thoroughly researched that initiate loss of self-tolerance: infections, chemicals and foods.

The Mechanisms Behind Autoimmunity

FIRST MECHANISM OF AUTOIMMUNITY: CROSS-REACTIVITY:

Cross-reactivity stems from molecular mimicry, defined as when two different objects share a similar amino acid sequence (Cusick et al. 2012). The theory was first identified in 1942 in a study which found patients who had pollen allergens also developed reactions to certain fruits (Tuft et al. 1942). Further studies identified proteins in food also shared similar sequences with human tissue. Amino acids are the building blocks that make up proteins, like links in a long chain. You can have two different chains that are very different looking yet contain within them two identical patterns.

For example: A bacteria and brain tissue are two completely different things; however, they can still contain identical amino acid sequences. The problem arises when the immune system becomes under stress. When under stress, the immune system looks for ways to protect the body and can confuse a viral sequence with a similar sequence found in the body, triggering an attack on the tissue its erroneously identified as the virus. The concept of cross-reactivity can be applied to varying types of infections, foods, allergens, chemicals, heavy metals, and even medications.

SECOND MECHANISM BEHIND AUTOIMMUNITY: MOLECULAR BINDING.

Molecular binding is another mechanism where one can lose self-tolerance. Chemicals, lectins, bacterial infections, fungi, mycotoxins, and parasites are all potential foreign objects to the body that can bind to human tissues. This is especially a concern for chemicals as research has proven the binding of BPA to human proteins will lead to new protein epitopes that can activate autoimmunity (Kharrazian 2014).

Three Categories of Triggers

1. INFECTIONS

Ample evidence has suggested that viruses play a part in the development of chronic diseases, especially autoimmunity. Through diagnostic testing many autoimmune patients find they host multiple infections from viruses, bacteria, parasites or fungi. It is important to note that not everyone who is exposed to a certain virus or bacteria develops an autoimmune condition. Logically, a variety of factors must usually be present to set the stage for an infection to result in an autoimmune disease. Typically, this includes, to name a few:

• Stress
• Lack of sleep
• Emotional trauma
• Regular consumption of genetically modified, and or processed foods
• Environmental toxins
• Heavy metal exposure
• Heightened intestinal permeability
• Genetic predisposition
• Food allergies and sensitivities

Infections can lead to autoimmunity by either one of the mechanisms discussed: through either cross reactivity or by binding to tissue proteins creating a new “compound.”  Unfortunately, even when a viral load is reduced, or a parasite is completely eradicated, the immune system may have already identified the similar sequence of the protein the infection bound to, resulting in the continued attack on that tissue. Once the immune system has tagged the human tissue that originally combined with the infection, it creates an antibody, just like it would with a virus. The patient is then at the whims of common daily triggers such as stress, food sensitivities, or hormone imbalances triggering autoimmune flair ups.

There are various conditions that practitioners would be surprised to know are linked to infections. For instance, a common oral pathogen streptococcus mutans is now linked to autoimmune cardiovascular disorders and psoriasis (Ferretti et al. 1980), (Valdimarsson et al. 1995).  Another great example of common infections not commonly known to trigger autoimmunity is a bacterial infection called Helicobacter Pylori, thought only to cause stomach symptoms, and in some cases ulcers. Helicobacter Pylori is now connected to heart autoimmunity, parietal cell autoimmunity, rheumatic diseases, lupus, and even pancreatic autoimmune disorders. Furthermore, Helicobacter Pylori has been linked with Hashimoto’s disease by way of cross-reacting with thyroid peroxidase, an enzyme used by the body to make thyroid hormones (Zekry and Abd Elwahid 2013).

There are countless infections humans are exposed to, many that scientists have not even identified or categorized. Additional research is necessary to link what other infections are linked to autoimmune disorders; however, there is enough substantial evidence proving various infections are the major mechanism to autoimmunity.

2. FOODS

First, we should differentiate allergies with delayed reactions to food such as a food sensitivity. Allergies elicit a IgE mediated response within a short time frame, typically within 15 minutes; whereas, food sensitivities elicit a IgG and or IgA response anywhere from one hour to three days after initial exposure. In most of the research linking foods as a mechanism to autoimmunity, the focus has been on food sensitivities, not allergies. These subtle reactions to foods not only can cause autoimmune flare ups, but more importantly are often the initial mechanism in which we lose self-tolerance in the first place.

Recent studies have identified various foods that cross-react with thyroid tissue and even thyroid hormones, further dispelling the notion that we do not need to adjust our diet once diagnosed with an autoimmune disorder.  More importantly, this groundbreaking research identifies mechanisms in which autoimmunity is ignited in the first place. Dr. Datis Kharrazian’s recent study identified cross-reactivity between thyroid hormones T4 and T3, the enzyme that is needed to convert T4 to T3 – DIO2, thyroglobulin which is used by the thyroid to produce thyroid hormones, and numerous food proteins. Kharrazian states that “specific monoclonal and polyclonal antibodies binding to purified proteins suggests the potential for immunological cross reactivity in a subset of susceptible individuals (Kharrazian et al. 2017).”

Even what we assume to be healthy foods such as tomatoes and spinach may be the mechanism of autoimmune expression in some patients. Kharrazian states that in patients with relapsing remitting multiple sclerosis (RRMS) they measured human aquaporins potential to cross-react with plant aquaporins. Aquaporins are water filtering systems found in soy, corn, tomatoes, tobacco and spinach, but are also found in various parts of the body, especially the brain. Compared to controls there was a high correlation between plant aquaporins and brain antigens. They concluded that patients with RRMS often will react to both. More importantly, they felt this information will help patients with these neurological disorders develop more customized dietary modifications (Vojdani et al. 2015).

Examples of foods cross-reacting with human tissue is abundant, with other studies identifying corn, baker’s yeast, brewer’s yeast, and shrimp being linked to inflammatory bowel disease such as Crohn’s as a result of cross reacting with human colon tissue and cytoskeletal proteins found in the gastrointestinal tract (Davidson et al. 1979), (Oshitani et al. 2003), (Das et al. 1993).

Consumers have been bombarded with dietary advice with trends of autoimmune paleo, Eat Right for Your Blood Type, GAPS, the Specific Carbohydrate Diet and many others. Although these are good starting points, practitioners should take a closer look at how we can customize someone’s diet to have biggest clinical impact. If we do not, and the patient is sensitive to a food that cross-reacts with various tissues, it is typically a matter of time before they develop their second or third autoimmunity.

3.CHEMICALS

The EPA has over 85,000 chemicals listed on its chemical substance inventory. New chemicals are being introduced into the environment every year. Living a chemical free life is impossible and a constant never-ending battle, like we are swimming upstream! Our ability to detoxify chemicals is complex, with various bodily systems playing roles. Most of our ability to detoxify chemicals however is governed by our genetics. We have all seen examples of people who can smother themselves in chemicals without any repercussion indicating that some patients can tolerate more toxic exposure than others.

Regarding autoimmunity, the mechanism in which a chemical triggers loss of self-tolerance is produced when a chemical is not transformed and detoxified out of the body effectively; as a result, the chemical binds to tissue creating a new compound the immune system identifies as a foreign article. Once the immune system has identified this, in a similar way it would a virus, upon the next exposure the immune system reacts to the toxin as if it was a food sensitivity. Take for example Bisphenol A (BPA) a common plastic found throughout the environment, especially all over grocery store receipts. Troublingly BPA is proven to be destructive to the lining of nerves. Autoimmune nerve breakdown is linked to Parkinson’s, multiple sclerosis, and even autistic spectrum disorders (Kharrazian 2014). The next time you are in the grocery store, consider all the employees who are susceptible to autoimmune disorders handling countless receipts covered in this toxic chemical!

Further studies at the University of Alberta comparing 25,000 women with breast implants to 100,000 without them, confirmed that one in four implant recipients is at risk for developing autoimmune disorders such as Sjögren’s, an autoimmune disorder affecting the lubricating ducts, systemic sclerosis often resulting in connective tissue issues, and even sarcoidosis which typically impacts the lungs. Ultimately, they found the risk for women with breast implants developing an autoimmune disease is 45 percent higher than for those without implants. Furthermore, other types of implants such as ones used for hernias, are also linked to a higher incidence of rheumatoid arthritis and lupus (Watad et al. 2018).

Obviously, there are endless amounts of chemicals in our environment and not enough funding, scientists or even the motivation to find out how they are linked to autoimmunity. If future studies show results like the one regarding BPA, the future doesn’t look good and we can expect the rates of autoimmune disorders to continue to surge.

Risking multiple autoimmunity

As practitioners, every detail in a case is important and must be managed for clinical success. Hormone imbalances, lifestyle stressors and emotionally traumatic events are common findings in an autoimmune patient’s history, but if we do not seek out the initial mechanism that causes loss of self-tolerance, the risk of the patient developing another autoimmunity increases substantially. It is well understood patients with one autoimmune disorder have a higher risk of developing another. Considering the two suggested mechanisms to the development of autoimmunity, it would be logical to assume if left untreated, a spirochetal infection, mycotoxin, lectin or chemical could ultimately trigger multiple systemic autoimmunity.

Examples of these instances are infections such as Porphyromonas gingivalis, which can trigger both rheumatoid arthritis and cardiovascular autoimmunity (Kharlamova et al. 2015), autoimmunity in two different anatomical areas that can be traced back to exposure from one infection. Similarly, in Candida infections “the potential to ignite autoimmunity is high due to the homology between the fungus and multiple human tissues (Vojdani et al. 1996).” Cytomegalovirus can increase the risk of Type 1 diabetes, lupus and arthritis; in addition to, “its potential for cross-reactivity with heart myosin and nervous system myelin (Rider et al. 1997).” Patients at risk for coronary disorders and/or demyelinating disorders, should be screened and treated for CMV antibodies (Wink and Schmitz 1980), (Lunardi et al. 2006).”  Simply put, the mechanism to losing self-tolerance must be addressed considering the likelihood it may cross-react or bind to various tissues.

Conclusion

With more and more autoimmune disorders being diagnosed every year, our focus as practitioners needs to be on finding the true mechanisms for our patient’s loss of tolerance. Finding the triggering mechanisms within the long list of varying factors playing a role in their cases is not easy; however, these mechanisms need to be found to not only manage their current condition, but more importantly, to help prevent the potential of the patient developing multiple autoimmune conditions.

References

Autoimmune Disease Statistics (n.d.). Retrieved January 25th, 2019, from www.aarda.org  https://%20www.aarda.org/NEWS-INFORMATION/STATISTICS/

Corouge, M., Loridant, S., Fradin, C., Salleron, J., Damiens, S., Moragues, M.D., Souplet, V., Jouault, T., Robert, R., Dubucquoi, S., Sendid, B., Colombel, J.F. and Poulain, D. 2015. Humoral immunity links Candida albicans infection and celiac disease. Plos One 10(3), p. e0121776.

Cusick, M.F., Libbey, J.E. and Fujinami, R.S. 2012. Molecular mimicry as a mechanism of autoimmune disease. Clinical Reviews in Allergy & Immunology 42(1), pp. 102–111.

Das, K.M., Dasgupta, A., Mandal, A. and Geng, X. 1993. Autoimmunity to cytoskeletal protein tropomyosin. A clue to the pathogenetic mechanism for ulcerative colitis. Journal of Immunology 150(6), pp. 2487–2493.

Davidson, I.W., Lloyd, R.S., Whorwell, P.J. and Wright, R. 1979. Antibodies to maize in patients with Crohn’s disease, ulcerative colitis and coeliac disease. Clinical and Experimental Immunology 35(1), pp. 147–148.

Ferretti, J.J., Shea, C. and Humphrey, M.W. 1980. Cross-reactivity of Streptococcus mutans antigens and human heart tissue. Infection and Immunity 30(1), pp. 69–73.

Kharlamova, N., Jiang, X., Sherina, N., Potempa, B., Israelsson, L., Quirke, A.-M., Eriksson, K., Yucel-Lindberg, T., Venables, P.J., Potempa, J., Alfredsson, L. and Lundberg, K. 2016. Antibodies to Porphyromonas gingivalis Indicate Interaction Between Oral Infection, Smoking, and Risk Genes in Rheumatoid Arthritis Etiology. Arthritis & rheumatology (Hoboken, N.J.) 68(3), pp. 604–613.

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