“Autoimmune diseases are the third leading cause of morbidity and mortality in the industrialized world, surpassed only by cancer and heart disease.”1
“While many individual autoimmune diseases are rare, collectively they are thought to affect approximately 8 percent of the United States population – 24 million persons.”
“To provide a context to evaluate the impact of autoimmune diseases, cancer affected approximately 9 million people and heart disease affected approximately 22 million people in the United States.” 2
One of the things that is happening here in the U.S. is the rates of autoimmune (AI) disease continue to go up for all AI diseases. There is an explosion of AI disease happening now like never before.
Autoimmune disease occurs when the immune system begins targeting self-tissue of the body causing destruction of that tissue or organ. The type of tissue that is destroyed in this process determines the type of autoimmune disease. There are many different AI diseases that have been identified, such as rheumatoid arthritis (RA), multiple sclerosis (MS), lupus (SLE), Hashimoto’s thyroiditis, Crohn’s disease, ulcerative colitis (UC), type I diabetes, Sjogren’s syndrome, scleroderma and celiac disease (CD). Autoimmune disease can affect any tissue in the body.
“Autoimmune diseases can affect virtually every site in the body. At least 15 diseases are known to be the direct result of an autoimmune response, and circumstantial evidence links more than 80 conditions to autoimmunity.”3
There is no solution for most AI diseases. AI patients generally suffer more and more symptoms of tissue destruction over time. Conventional approach is focused on suppressing the immune response and controlling symptoms but little is offered to the patient in regards to modulating the autoimmunity and avoiding triggers that cause flare-ups of the autoimmune response. As a result, AI conditions tend to cause more and more tissue destruction over time, eventually leading to severe tissue destruction and organ failure in many cases.
Most AI disease remains undiagnosed
“Collectively autoimmune diseases have been identified in about 24 million people in the U.S., and only 1/3 are diagnosed. That means about 72 million people have an AI disease. It’s not looked for. Our system waits until the signs and symptoms are severe enough with organ failure and irreversible damage before we identify it.”4
Another thing we know about AI disease is that when people have antibodies against one known tissue type, there is likely other antibodies against other tissue as well. In other words, when a person is diagnosed with AI disease, they are at high risk of developing other autoimmune diseases during their lifetime. It is very rare that only one tissue type is targeted by the immune system. When we look at people with AI disease, they may have multiple types of tissue being targeted that have not yet been identified. For example, the literature shows people with thyroid autoimmune disease have over a 50% chance of being affected by another autoimmune disease.5
Conventional management of AI Disease: Steroids and other Immune-suppressing medication
People with AI reactions usually don’t get diagnosed and don’t get any management or support until they get diagnosed with AI disease in conventional medicine. Once patients suffer sufficient tissue destruction to be diagnosed with AI disease, what does conventional healthcare have to offer? The standard of care is steroids and other immune-suppressing drugs for many AI conditions. Steroids are usually not used in the initial stages because the adverse and damaging effects on the body make it not worth the risks. Some of the side effects of steroids include: immune suppression, bone loss, neurodegeneration, insulin-related issues and blood sugar dysregulation, epithelial thinning, catabolic states, etc. So patients aren’t given steroids until their condition has become severe and progressed. If the tissue destruction is severe enough, doctors may use a bone marrow-suppressing drug to shut down the immune system completely or they may take out the thymus in some of the more severe conditions such as myasthenia gravis.
There really is little hope in the conventional model of healthcare for patients with autoimmunity since the focus is on suppression of the immune system which is costly. These immuno-suppressive agents come with significant adverse effects, including risk of various infections and inability to fight infection when needed.
Functional Medicine: A Better Option for AI Disease
Autoimmune Regulation as a Therapeutic Approach
When you look at the dysregulation of the immune system that occurs in autoimmunity, we know that there are different systems involved in the targeting of tissue for destruction. Autoimmunity is a multi-variant process and the goal should be to calm down the autoimmunity, specifically the immune response against self-tissue. There are several innate regulating systems of immune function that begin to dysregulate in autoimmunity. In functional medicine, we attempt to modulate the autoimmunity by regulating these various systems through diet, lifestyle and nutritional supplements.
When we consider autoimmunity, there are 4 things we focus on:
- Identifying the triggers of autoimmune responses and avoid them
- Modulating the autoimmunity and decrease the tissue destruction
- Enhancing and supporting their recovery from these flare-ups
- Addressing associated conditions that promote autoimmune responses
1. Avoiding Triggers: Gluten/Gliadin
We know that gluten sensitivity has major impacts on health. One of the most extreme cases of gluten sensitivity results in an autoimmune disease called Celiac disease. In Celiac disease, the immune system’s response to gluten exposure results in chronic inflammation and destruction of the gastrointestinal (GI) tract.
However, there are many forms of gluten sensitivity that are unrelated to Celiac disease. Gluten sensitivity is defined by having an immune response to gluten. Non-celiac gluten sensitivity has now been associated with several different autoimmune diseases unrelated to Celiac disease, including type I diabetes and Hashimoto’s hypothyroidism. 6,7
The mistake that many doctors make is they associate gluten sensitivity with disease of the intestinal tract. Most medical doctors are still fixated on the celiac-disease model which is focused on intestinal manifestation of gluten sensitivity. However, 2/3 of people with gluten sensitivity do not have gastrointestinal problems. What other organs does it affect? Once a person has gluten sensitivity, it can destroy any tissue or organ. The most vulnerable tissue is the brain. In fact, most gluten sensitivity affects the central nervous system, not the GI tract.
Gluten sensitivity may manifest in a number of neurological deficits, depending on what part of the brain or nervous system is affected, including numbness and tingling, ataxia (balance problems), migraines, attention-deficit problems or ADHD, “brain fog”, and cognitive deficits. Gluten sensitivity is now being found to be involved in the pathological processes of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, supranuclear palsy, and Huntington’s disease. 8,9,10,11
There are a number of nutritional compounds that have been shown to a powerful effect on the modulation of the physiologic systems involved in the immune response and decreasing attacks on self tissue. In the functional medicine model, we use these compounds which have been shown in the literature to modulate these systems and decrease immune responses to self-tissue.
We are not talking about curing these AI conditions because we don’t know how to do that. But we can make it so a person has more good days than bad days. Identifying the triggers of autoimmunity and modulating the immune response can have powerful long-term positive effects on slowing or stopping tissue destruction and improving quality of life.
- Balance TH1 and TH2 systems
- Enhance the TH3 regulatory system
- Decrease the TH-17 response
3. Enhancing and Supporting Recovery
In autoimmune disease, there are always periods of aggravation of the autoimmunity (“flare-ups”) and periods of minimal aggravation (“calming”, “quiet” or dormant” periods). In addition to minimizing flare-ups, one of the goals in managing autoimmunity is supporting a faster recovery from the flare-ups. There are a number of natural compounds, which have been shown to help support a faster recovery by breaking down offending triggers (ie: digestive enzymes to breakdown gluten), increasing blood flow to target tissue, or dampening the immune response. These are some of the ways in which we can support recovery of flare-ups in the autoimmune patient.
Intestinal permeability promotes autoimmunity
Paper after paper in the literature is showing that intestinal permeability breach promotes autoimmune reactions, flare-ups and overzealousness of the immune system
“It is now apparent that tight junctions are dynamic structures that are involved in developmental, physiological, and pathological processes. As a result, particular attention is being placed on the role of tight junction dysfunction in the pathogenesis of several diseases, particularly autoimmune diseases”12
“In all cases, increased permeability appears to precede disease and causes an abnormality in antigen delivery that triggers the multiorgan process leading to the autoimmune response” 13
“There is growing evidence that increased intestinal permeability plays a pathogenic role in various autoimmune diseases Therefore, we hypothesize that loss of intestinal barrier function is necessary to develop autoimmunity”14
Identifying the existence and assessing the severity of conditions such as intestinal permeability and addressing these conditions when necessary, in conjunction with the immune response, leads to a more comprehensive and satisfactory outcome in the autoimmune patient.
Content provided by Datis Kharrazian, D.C., Autoimmune Regulation of the Nitric Oxide and Glutathione Systems, 11/4/10
Below, you will find a series of articles on autoimmune disease and related topics and how these conditions are managed in the functional medicine model.
What role do chronic bacterial and viral infections play in autoimmunity? What role do environmental toxins play? The role of the glutathione and nitric oxide synthase (NOS) systems and development of autoimmunity.
What is the Functional Medicine approach to AI disease? The importance of supporting the glutathione and nitric oxide systems. The importance of addressing intestinal permeability and the GI tract. The role of vitamin D.
What is intestinal permeability or “leaky gut”? Why haven’t I heard of this? Intestinal permeability causes systemic inflammation. Intestinal permeability as a precondition for the development of autoimmune disease
Intestinal permeability: mechanisms and causes that lead to leaky gut. Diet, medication, infections, stress, hormonal imbalances, neurologic and metabolic issues and autoimmunity can all promote leaky gut.
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2. NIH. Autoimmune Diseases Coordinating Comm. Autoimmune Diseases Research Plan. 2006
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4. Jeffrey S. Bland, Ph.D.; Metagenics Educational Programs. 2006
5. ACTA BIO MEDICA 2003; 74; 9-33
6. Elimination of dietary gluten and development of type 1 diabetes in high-risk subjects. Rev Diabet. Stud. 2004 Spring;1(1):39-41
7. Thyroid disorders in Brazilian patients with CD. J Clin Gastroenterol. 2006 Jan;40(1):33-6
8. Transglutaminase-catalyzed post translational modifications of proteins in the nervous system and their possible involvement in neurodegenerative diseases. CNS Neurol Disord Drug Targets. 2008 Oct; 7(4):370-5.
9. Psychic disturbances in CD. II. Psychological findings. Scand J Gastroenterol. 1982 Jan;17(1):21-4
10. Migraine may also be a symptom of mild CD Migraine, CD and cerebral calcifications: a new case. Headache. 2005 Oct;45(9):1263-7
11. A preliminary investigation of ADHD symptoms in persons with CD. J Atten Disord. 2006 Nov;10(2):200-4
12. NAT CLIN PRAC GASTRO & HEP SEPT 2005 VOL 2 NO 9
13. DIABETES, VOL. 55, MAY 2006
14. Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms Ann N Y Acad Sci. 2009 May;1165:195-205