Published in Nutritional Perspectives Journal April 2013
By. Dr. Michael Jurgelewicz

Most physicians are trained to look only in specific places for the answers, using the same familiar labs or diagnostic tests. Yet, many causes of chronic illness cannot be found in these places. The usual tests do not look for food sensitivities, hidden infections, environmental toxins, mold exposures, heavy metal toxicities, nutritional deficiencies and metabolic imbalances.

Patients with autoimmune diseases such as, IDDM (Insulin-Dependent Diabetes Mellitus), Hashimoto’s thyroiditis or Graves’ disease, and connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus, or Sjogren’s disease) are given protocol driven treatments with limited success because an acute care model is given to a chronic problem and the underlying cause is never investigated.

The problem is that everyone has their own biochemical individuality. Each person’s biochemical individuality exerts a major influence on his or her health. The level of nutrient intake that maintains the best possible health is highly variable from person to person. Lifestyle choices and environmental exposures filtered through genetic predisposition are fundamental factors in the expression of disease, and a successful treatment approach must include investigation into these factors.

Patients with similar symptoms can have totally different test results. In addition, patients with similar test results can have totally different symptoms. There is endless research on intestinal permeability aka intestinal epithelial hyperpermeability aka Leaky Gut. This is a common problem with almost all autoimmune diseases. The gastrointestinal tract is 80% of our immune system. Whenever you have inflammation present, the tight junctions and intestinal mucosa can become damaged causing gaps or “pores” in the lining of the GI tract. Then toxic byproducts in the digestive tract can be absorbed into the bloodstream and transported on to the liver. The molecules of food and toxins are “leaked” through the GI lining and then eventually they affect systems throughout the body causing inflammation in our joints, expressing toxins in skin disorders, autoimmune conditions, and food sensitivities.
If you have an autoimmune disease, there are some tests to consider. There have been great strides in advancement in technology and what labs can test today. There are labs that assess a patient’s salivary hormones, urine organic acids, food sensitivities, and stool testing.

Combining salivary IgA with evaluation of cortisol and DHEA may be beneficial in the overall assessment of the stress response and the management of leaky gut, food allergy, inflammatory arthritis, immunogenic thyroiditis, autoimmunity and other chronic disease.1

Organic acids are products of metabolism that can sensitively identify nutrient deficiencies that lead to metabolic roadblocks. When specific cellular functions are blocked due to impairment or a lack of cofactors, such as nutrients, organic acids will spill into urine. Increased nutrients can help to push and sustain appropriate enzyme activity. Individuals with faulty enzyme binding can have increased nutrient needs that will not be revealed by measures of vitamin concentrations in blood.

Abnormal concentrations of organic acids in the urine can provide a functional marker for metabolic effects of nutrient deficiencies, genetic errors in metabolism, impaired enzyme function, toxic exposure, neuroendocrine activity, and intestinal bacterial overgrowth.2

Patients with autoimmune diseases often have an association between food intake and their disease severity. Food Sensitivity testing measures reactions to specific foods, which can cause inflammatory reactions at various sites in the body, including the large and small intestines, kidneys, skin, sinuses, head, joints, and lungs. Delayed food sensitivities can take up to three days to appear. This type of reaction is IgG and IgA mediated and is different from the immediate IgE testing traditional allergists perform. Since these are a delayed response, there does not have to be an obvious association between a particular food and an adverse reaction.

Gluten sensitivity/intolerance is a major cause and contributor to autoimmune diseases. Most doctors dismiss gluten as a problem unless a person develops celiac disease. Because of this, millions suffer needlessly with a multitude of health problems.

Rheumatoid Arthritis has been shown to improve, and occasionally remit entirely, with gluten removal.3 In a recent study of this immunological link between gut immunity and RA, food IgG, IgA and IgM antibodies were measured. In the intestinal fluid of many RA patients, all three immunoglobulin classes showed increased food specific activities, including gliadin antibodies.

Traditional diagnostic testing has focused on blood antibody tests and or intestinal biopsies. Unfortunately traditional tests for gluten sensitivity are often incorrect.

In the digestive process, if you are gluten sensitive, your body produces antibodies to gluten. The gold standard for confirming a diagnosis of celiac disease is a positive blood test for antigliadin IgA antibodies, anti-tissue transglutaminase, and anti-endomysial antibodies. Blood tests are inadequate to detect gluten sensitivity for several reasons: They only measure a fraction of how a person’s immune system can react to gluten. Blood tests only measure the gluten found in wheat (gliadin). The other problem is that people react to gluten in different ways. In addition, partial atrophy is ignored. You can only be guaranteed to test positive if total villous atrophy has occurred, meaning the villi are completely flattened. If you have partial or infiltrating villous atrophy, you may not test positive. The atrophy and inflammation of the villi may not be severe enough to allow all these antibodies to easily pass through the intestinal barrier. Unfortunately, by the time that total villous atrophy occurs, you are pretty sick with many symptoms. Blood tests are also incomplete because they do not identify all the antibodies in the blood. The most common antibody that a gluten-sensitive produces is antigliadin. The agent labs use for this antibody is wheat mixed into a water solution. The problem is gliadin does not dissolve in water. As a result, more than 30 gliadin peptides are not evaluated by this test. Your body may be reacting to gliadin peptides that are not picked up by these blood tests. 5

Some doctors are not satisfied with blood test. If blood tests come back negative but you still have symptoms, they do a biopsy. Unless significant structural damage has occurred to the villi of the small intestine, physicians rule out celiac disease and gluten sensitivity. Without total villous atrophy, doctors consider a biopsy negative even if early inflammatory changes are seen. Research has shown that the brunt of the immune reaction to gluten can affect the functions of the intestines and cause symptoms without structural damage.

Gluten sensitivity and celiac disease can be evaluated with genetic testing. Genetic testing is done by swabbing the inside of your mouth. If the mucosa tests positive, there is a high probability that you have a gluten sensitivity and may develop celiac disease. In addition, stool and salivary testing is more conclusive, however, if your total secretory IgA is suppressed, you can get a false negative.5

In addition, a comprehensive stool profile is essential for anyone suffering from an autoimmune condition. The intestinal flora is a complex ecosystem consisting of over 400 bacterial species that greatly outnumber the total number of cells making up the entire human body.6 Dysregulation in this system can lead to a change in homeostasis and increase disease states. Gastrointestional imbalances have been identified as involved in the pathogenesis of rheumatoid arthritis.7 Stool testing performed by PCR (Polymerase Chain Reaction), which is a DNA template, is the gold standard as well as a huge leap forward. It eliminates errors due to overgrowth in transport from culture testing and requires only 1 to 5 bacterial cells present for identification vs. 1,000 to 5,000 necessary for culture.8
There is also testing that can confirm intestinal permeability. Through the serum they are able to detect antibodies to LPS, Occludin/Zonulin and the Actomyosin Network to identify breakdown of a healthy intestinal barrier. Lipopolysaccharides (LPS) are large molecules found in gram-negative bacteria. They are endotoxins, and if absorbed, elicit a strong immune response.9 The detection of antibodies against LPS reveals macromolecule-sized endotoxin infiltration through the intestinal barrier into the systemic circulation. Occludin is part of the main component of proteins holding together tight junctions. The detection of antibodies to occludin indicates that the tight junctions are breaking down. This is a measure of an autoimmune mechanism damaging the intestinal barrier membrane. Zonulin is a protein that regulates the permeability of the intestine.10 The detection of these antibodies indicates that the normal regulation of tight junctions is compromised. This confirms a presence of an ongoing autoimmune mechanism damaging the intestinal barrier. The Actomyosin network is a protein complex regulating intestinal barrier function by maintaining the plasticity of the tight junctions.11 These antibodies are biomarkers of intestinal barrier dysregulation.

It is also very important to get your vitamin D levels checked since it plays a large role in inflammatory and autoimmune processes. Low vitamin D levels are associated with increased inflammation and with increased incidence of numerous diseases.12

Once these underlying areas your health are explored, nutritional and lifestyle support would be used to address any dysfunctions, deficiencies, toxicities, etc.

References
1Ansaldi N, Palmas T, Corrias A, et al. Autoimmune thyroid disease and celiac disease in children. J Pediatric Gastroenterol Nutr 2003;37(1):63-66.

2Lord R, Bralley J. Alexander. Laboratory Evaluations for Integrative and Functional Medicine. 2nd Edition. Chapter 6: Organic Acids. p. 324.

3Hafstrom I, Ringertz B, Spangberg A et al. A vegan diet free of gluten improves the signs and symptoms of rheumatoid arthritis: the effects on arthritis correlate with a reduction in antibodies to food antigens. Rheumatology (Oxford) 2001 Oct; 40(10):1175-9.

4 A. Vojdani, T. O’Bryan and G.H. Kellermann. The Immunology of gluten sensitivity beyond the intestinal tract. European Journal of Inflammation: :Vol. 6, no. 2, 0-0 (2008) p.2

5 The Gluten Connection: How gluten sensitivity may be sabotaging your health. Shari Lieberman, PhD, CNS, FACN. p. 94-101.

6Finegold SM, Attebery HR, Sutter VL. Effect of diet on human fecal flora: comparison of Japanese and American diets. Am J Clin Nutr. 1974;27(12):1456-1469.

7Fasano A. Surprises from celiac disease. Sci Am 2009;301:54-61.

8Forbes BA, Sahm DF, Weissfeld AS, et al. Bailey & Scott’s Diagnostic Microbiology. 10th ed. St. Louis: Mosby; 1998.

9Maes M, Mihaylova I, Leunis, J. “Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability.” Journal of Affective Disorders, 2006.

10Thomas K, Sapone A, Fasano A, Vogel S. “Gliadin stimulation of murine macrophage inflammatory gene expression and intestinal permeability are MYD88-dependent: role of the innate immune system in Celiac Disease.”

11Kong J, Zhang Z, Musch M, Ning G, Sun J, Hart J, Bissonnette M, Chun Li Y. “Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier.” Am J Physiol Gastrointest Liver Physiol 294: G000-G000, 2008

12Holick MF. Vitamin D deficiency. N Engl J Med 2007; 357: 266-281.

Sharing is caring!