An allergy to Gluten can trigger Celiac Disease (a confirmed Autoimmune Disorder trigger by a Food Allergy) So why couldn't a different food protein trigger a different Autoimmune Disorder? This makes sense...
Autoimmune diseases are considered to be idiopathic conditions, which is a fancy way of saying "of unknown origin". There are theories as to how and why the immune system suddenly begins attacking your own body tissues as opposed to just foreign pathogens that get in your body. But none of these have been definitively proven to be the sole cause of any autoimmune condition.
The current leading hypothesis as to the trigger(s) for these conditions is a process called Molecular Mimicry. It sounds like a very complex and difficult to understand concept, but it's actually extremely simple to understand. You can follow the steps in the diagram below.
1. Allergenic protein molecules (amino acids in unique sequences and three dimensional shapes and structures) get absorbed into the blood stream.
2. Immune system cells (T cells) recognize this protein as being foreign to the body (allergic) and bind to it.
3. The T Cells then bind to other cells called B Cells which are designed to produce antibodies which will recognize, bind to and attack anything in the body that looks like the original allergic protein.
4. Millions of antibodies designed to attack the allergic protein molecules are produced and enter the blood stream and tissues in search of anything that looks like or mimics the allergic protein.
5. Some people have natural tissue proteins in their body that look similar to (or mimic) the allergic protein. The antibodies can recognize these tissues as being allergic, and can bind to them.
6. The antibodies bound to the tissue then illicit an immunological attack against this tissue causing inflammation in the tissue (the autoimmune condition). If the tissue being attacked is the synovial tissue around a joint, that will cause rheumatoid arthritis around that joint.
If the tissue being attacked lines or covers the bowel, this can trigger crohn's or colitis.
If the tissue being attacked is the fascial covering of the muscles, this can trigger fibromyalgia.
If the tissue being attacked is the myelin sheath covering the neurons in the brain, this can trigger glial body formation and multiple sclerosis.
Pretty much any tissue can be affected by this process, and therefore any autoimmune disease can fit into this model. It just depends on which tissue in the body mimics the allergic protein that was reacted against.
The exciting part of this hypothesis is that if you can identify the original allergic protein that is mimicked in the body and remove it, you can shut down production of that particular antibody being produced. If you don't have that antibody in the system anymore, you won't have the immunological attack against the tissue. Subsequently, you won't have the inflammation or autoimmune symptoms anymore. It can be this simple.
Research into food triggers for autoimmune disease goes back into the 1980's. Some ground breaking research into Insulin Dependent Diabetes Mellitus in children was published in 1992 which showed the direct correlation between antibodies to bovine protein in the blood stream of kids with diabetes.
Epidemiological research correlates directly with the findings of the 1992 studies as well.
This all sounds very logical and makes sense. If it were this simple, how come I haven't heard of this before or why has my doctor told me about this? There are many reasons for this.
Since the concept of molecular mimicry as a potential mechanism for autoimmune disease was put forth, the vast majority of research into molecular mimicry has been done on trying to find infectious agents (bacteria, viruses, etc.) and their potential role in the molecular mimicry process. Research has showed some strong correlations with various viruses and bacteria with molecular mimicry. It has also showed some definitive correlations with some autoimmune diseases and vaccinations.
But there has been significantly less research done into food allergens as potential triggers for the molecular mimicry process in autoimmune disease. This, in spite of the fact that some of the first research ever done correlated a food (dairy) with type I diabetes in children. Why has research been so limited?
Research money comes predominately from industry (primarily the pharmaceutical industry). This industry is very adept and capable of producing anti-viral, antibacterial and anti-fungal medications. If molecular mimicry was triggered by one of these infectious agents, then medication targeting the specific infectious agent could be quite lucrative. This is what has driven much of the research in this regard. It's very difficult to create an anti-dairy, anti-gluten or anti-food drug. You can't create these drugs.
Another reason why research has been slow to prove the molecular mimicry process and it's potential association with food allergens, is how the research is done. Research design tends to be done from the condition/treatment backwards rather than from the patient forward. What do I mean by this?
Each patient with a specific autoimmune condition (we'll use rheumatoid arthritis as an example) will have potentially different food, viral, vaccination triggers for their condition. One might be a casein (dairy) allergy. Another might be a gluten allergy. Yet another could have a cross reaction between a vaccine antibody and their tissue. Each person with rheumatoid has unique DNA, therefore the tissue proteins on their joints will be completely unique from one another. Therefore it could take different antigenic proteins in the diet or environment to produce antibodies to react with the tissue proteins in these patients with rheumatoid arthritis. If you design a study with 1000 different rheumatoid arthritis patients, and take them all off the same food. Chances of this one food being the mimicking food allergen in all 1000 people are extremely low. Chances are this study will not show a positive correlation between the dairy elimination and improvements in the patients symptoms. It will in people who actually DID have a dairy cross reaction, but it won't in all the others. This study could get "thrown out" because of lack of response. This is designing the study backwards. Focusing on the treatment and all those with the same condition and working back to the individual patients symptoms.
Designing the study forward would go like this. Take each of the 1000 patients with rheumatoid, and test them individually for what allergic antibodies (to foods, viruses, vaccines, etc.) Once you identify each patients individual antibody profile, design a treatment for each individual based on their unique profiles. The study results would be significantly different. The conventional medical model for research doesn't do studies like this for many reasons. The main reason being cost of implementing this type of study design would be prohibitive.
Another reason is lack of clinical and scientific expertise in the area of clinical nutrition and autoimmune disease as it relates to nutrition. Many patients hear and read this type of information and it makes sense to them. Then they begin thinking it must be too simple and too good to be true, because otherwise their Doctors would have mentioned this to them before.
Until very recently in North America, there was no mandatory clinical nutrition training in a conventional medical degree program. It has only been recently when optional nutritional programs have been added to some of the medical degree programs. The curriculum for most medical schools are readily available online, and I encourage all to quickly review this for themselves. It's shocking in many ways.
Many physicians who treat sufferers with these autoimmune conditions have never received any training in the nutritional interventions such as those described on this site. Since they haven't studied it, it's unlikely that they will discuss these treatments with their patients.
Finally, there are some critical immune system "logistics" that must be understood and implemented properly before any nutritional intervention will be able to be helpful. You must understand how the immune system makes these cross reactive antibodies, and how long the antibodies can stay in the body. If you don't remove the potential cross reactive allergenic food properly, or for a long enough period of time, then chances of success with the nutritional program diminish significantly. Success on this program depends on understanding these small details of the immune system function.
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