The Many Faces of GLUTEN…Masquerader of Disease and Symptoms

Copyright, 2011, Dr. Michael Wald – 2010 (914-552-1442) What is gluten?

Gluten is an insoluble protein found in grains such as barley, rye, oats, triticale and wheat. Riceand corn have a different kind of gluten and only need to be avoided if a person is found to be specifically allergic to them (see allergy testing below). In wheat flower, gluten acts to bind the mixture together when added to water. Gluten traps air bubbles created by a leavening agent allowing the bread to rise. Gluten-free flowers or flowers with little gluten do not trap bubbles and will either not rise or rise well – they are generally heavy, soggy and flat.

Why should you care about gluten?

It has been determined that gluten can cause a wide-variety of symptoms and diseases. Many of these symptoms and disease states go unidentified by most medical specialists. The health care providers of Integrated Medicine & Nutrition, P.C. believe that gluten intolerance is often missed as it can appear as vague symptoms and specific disease states. Extensive testing has been performed on hundreds of patients that have demonstrated that the prevalence of gluten intolerance is far greater than previously suspected. In fact, our clinical suspicions have been studied and confirmed by other researchers and scientists. This paper includes many references to the scientific literature supporting our major assertion; namely, that the protein gluten can trigger the immune system to initiate an inflammatory-autoimmune (self-directed) reaction that can cause cellular and tissue destruction of virtually any tissue of the body. Most importantly, the autoimmune destruction can go unrecognized as caused by gluten intolerance by most medical professionals. The main reason for the lack of recognition of gluten as the cause of destructive immune reactions against one’s tissues is because the symptoms produced look like the characteristic disease that has been diagnosed. For example, a sub-type of multiple sclerosis, some seizures and even cerebella ataxia can all be caused initially by an adverse autoimmune reaction provoked by gluten. The immune system, in its attempt to deal with the undesirable protein (namely gluten) inadvertently causes destruction of tissues; in the three examples given above the tissues include the white matter of the central nervous system (multiple sclerosis), neurologic and neurotransmitters of the brain (seizures) and the cerebellum (hindbrain). Allopathic physicians are divided among various medical specialties, some of which are outlined below. The medical profession has traditionally chosen to compartmentalize (separate) the enormous amount of educational materials that is available regarding health and disease into the various branches of medicine. There is little doubt that expert knowledge in a particular area of medical study is necessary on many occasions. This approach also has inherent limitations often preventing a given medical specialist from appreciating the large number of disease states and symptoms that can be caused by a single trigger

(i.e. gluten).

Here are some real examples:

A young man who complains of frequent seizures over the course of several years and dozens of visits to neurologists find little relief with anti-convulsive medications. Gluten antibodies were found to be high and the patient learned that he could produce seizures after eating pizza (bread has gluten in it). Removal of gluten resulted in far fewer and less severe seizures. Inherent problem: neurologists are seemingly unaware of the evidence demonstrating that some people suffering from seizures will improve upon its elimination from the diet. A study in a major medical journal actually proved that gluten given to persons previously diagnosed with multiple sclerosis produced plaques on MRI testing. Removal of gluten caused the plaques to disappear.

A middle-aged man suffering from progressive shrinkage of his cerebellum resulting in dizziness, ocular palsies, fatigue and loss of muscle coordination receive no help from neurologists. The medical literature demonstrates that this condition can be caused in some sufferers from gluten – the condition is actually called gluten ataxia.

In order for a health care provider to fully appreciate implications of gluten intolerance he or she would need training spanning several specialties. Furthermore, a holistic-mindedness would be required to piece it all together into a coherent picture – a way of thinking and clinical practice that is found only by complementary health care providers.

Here’s why:

  1. Gluten is a food – requiring training in clinical nutritional studies
  2. Gluten provokes the immune system (i.e., rheumatoid arthritis, lupus) – requiring immunologic training.
  3. Gluten may damage the small intestines (i.e., Celiac disease, gluten intolerance) –      requiring training in gastroenterology.
  4. Gluten may affect the hormonal system (i.e., thyroid) – requiring endocrinology training.
  5. Gluten may affect the nervous system (i.e., multiple sclerosis – requiring training in neurology.
  6. Gluten may ultimately affect the joints, bones and soft tissues (i.e., osteoarthritis, osteopenia, osteoporosis) – requiring training in rheumatology.
  7. Gluten may cause depression – requiring training in psychology
  8. Gluten may predispose to infections – requiring training in infectious disease
  9. Gluten characteristically causes malabsorption – causing iron and B-vitamin and protein anemia’s and resulting fatigue and impaired physiology – requiring training in family practice, internal medicine and hematology.

Table of various medical specialties:

  • Internal medicine
  • Family practice
  • Infectious disease
  • Dietetics
  • Gynecology
  • Endocrinology
  • Cardiology
  • Neurology
  • Rheumatology
  • Psychology
  • Pathology
  • Hematology
  • Oncology
  • Orthopedics

Table of symptoms and associated health specialists

  • Diarrhea, gas, bloating, cramping
  • Pelvic and back pain, dysmenorrhea
  • Joint and muscle pain
  • Rheumatoid arthritis, osteoarthritis
  • Lupus, cerebellar ataxia
  • Unsteady gait, migraines, neuropathy
  • High blood sugar, hyperthyroidism, Addision’s
  • Sleep disturbances
  • Osteoporosis
  • Memory disturbances, general fatigue
  • Malnutrition, failure to thrive
  • Depression
  • Dermatitis herpetiformis, psoriasis
  • Lymphoma
  • Medical or Health Specialists
  • Gastroenterologist
  • Gynecologist
  • Chiropractor, Orthopedist
  • Rheumatologist
  • Immunologist
  • Neurologist
  • Endocrinologists
  • Sleep specialist
  • Internist
  • Family practitioner
  • Pediatrician, Pediatric endocrinologist
  • Psychiatrist, psychologist
  • Dermatologist, Gastroenterologist
  • Oncologist

Note: This list was compiled through research conducted on Medline – a medical reference library on-line

For example, a 39 year old women visited our office complaining that since the birth of her recent daughter, she experienced atypical migraine headaches, intestinal cramping and diarrhea, esophageal reflux and eczema. Her Internist and OBGYN prescribed powerful migraine medications and referred her to a Gastroenterologist. The visit to the GI doctor resulted in a prescription for a protein-pump inhibitor (anti-acid medication). The overall results – none of her well-intentioned and qualified healthcare practitioners attempted to look deeper for the cause of her seemingly varied health problems. At Integrative Medicine and Nutrition we hypothesize the following: Many women experience autoimmune problems after the stress of pregnancy (i.e., MS, lupus, migraines, etc.). We believe that this woman’s immune system was stressed by her pregnancy producing her migraines, GI complaints and eczema. All of these problems could have resulted from gluten intolerance – even though these were all new symptoms since the pregnancy. We checked for gluten intolerance and – “bingo” she was highly positive and all of her symptoms responded immediately to gluten withdrawal and specific nutritional interventions.

Who’s affected? How about you?

A large percentage of the population has a varying degree of sensitivity (allergy) to gluten protein and perhaps related proteins in non-gluten containing foods (such as dairy and soy). Gluten can be problem some as it may precipitate (trigger) an immune reaction in any number of tissues and organs. Typically it is recognized as the cause of the gastrointestinal disorder Celiac Disease (CD) and the topical (skin) form of CD called dermatitis herpetiformis. Gluten may cross- react with virtually any tissue causing impairment of cellular, tissue and organ function. The chemical structure (amino acid sequence) of gluten may appear (and may actually be) similar to various tissues in the body. The similarity between certain tissues in the body and gluten is known as molecular mimicry or homogeny. As gluten may look similar to body tissues the body’s immune system may react against the related tissues as it reacts against gluten – the perceived stressor.

How gluten causes disease:

The antibodies (AB) formed by the immune system against the gluten and other similar looking body tissues (cross-reactivity) evokes an inflammatory and degenerative cascade of biological

events. Initially this reaction is meant to be one of protecting the body against what it perceives as a foreign or unfriendly substance (initially the gluten), but may extend to other body tissues.

The tissues affected in each individual depend upon the unique genetic predisposition of the person. For example, gluten can often cross-react with the thyroid gland producing thyroiditis or Hashimoto’s Thyroiditis – forms of autoimmune thyroid disease. This health letter has summarized several dozen medical studies that describe the extent that gluten contributes to nutritional deficiency and various disease states.

Celiac Disease (CD) – a common, but far from the only, problem…

In certain individuals the gluten causes the CD, a well- recognized malabsorption disorder producing gastrointestinal signs and symptoms such as villous atrophy (degeneration) and diarrhea. CD is known as a gluten enteropathy (gut). CD is a malabsorption disorder resulting in any number of nutritional deficiencies including protein, B-vitamin, mineral (including calcium), hormonal (vitamin D – yes, “vitamin” D is not a vitamin, but a hormone) and many others. As a malabsorption disorder extensive nutritional deficiencies can result – even if you eat a balanced diet and take high doses of nutritional supplements. Remember – malabsorption literally means inadequate absorption. Malabsorption is only the “tip of the iceberg” as the cells, tissues and organs of the body may suffer from degeneration secondary to nutritional deficiencies. Without proper nutrition tissues cannot heal – it’s as simple as that. The gastroenterologist’s typical approach is to recommend that the CD patient remove gluten from the diet. This approach is usually enough for eliminating or reducing GI symptoms, but not always. The nutritional health care provider who recognizes the multitude of symptoms and diseases of gluten intolerance is most qualified to identify the extent of the associated nutritional problems associated with it.

How gluten causes disease

  1. Cross-reacts (molecular mimicry or homogeny) with body tissues causin tissue degeneration – almost always tissues are involved other than the one’s producing the obvious GI symptoms.
  2. The removal or lessening of reactive-gluten symptoms is important, but is incomplete as other tissues may not fully heal unless their nutrition is corrected.
  3. Causes malabsorption in the intestinal tract due to villous atrophy and crypt hyperplasia.
  4. Precipitating an inflammatory response that goes beyond and often includes the small intestines.
  5. Results in a higher than average need for nutrition for the correction of tissue degeneration.
  6. May precipitate many other disease conditions that will require specific nutritional and/or medical interventions.
  7. May precipitate other allergic reactions.
  8. Causes chronic symptoms that may not respond to conventional medical treatments.


Who should be tested for gluten sensitivity?

  • Persons with persistent symptoms for which no other cause(s) has been identified.
  • Persons who are eating well and/or who take nutritional supplements with limited or no success.
  • Persons with proven malabsorption disorders.
  • Persons who have been diagnosed with leaky gut syndrome.
  • Family members who have tested positive for Celiac disease and/or gluten intolerance.

Testing for Gluten Intolerance (sensitivity)

Testing for gluten intolerance is a simple matter. Blood samples are tested for three primary antibodies (AB) namely, gliadin AB, transglutaminase AB and reticulin AB. The medical literature suggests that the transglutaminase AB is the most commonly positive type detected on blood testing in those with gluten. However, extensive research on the part of the doctors of Integrated Medicine and Nutrition, P.C. seems to suggest that gliadin AB are far more commonly detected in an approximate ratio of 40:2 (gluten AB-to-Transglutaminase AB).

The scientific literature generally recommends that all three AB are measured simultaneously in each person suspected of gluten sensitivity. Testing must extend beyond the initial measurement of one or more AB. Gluten commonly cross-reacts with any number of tissues potentially resulting in multiple nutritional deficiencies directly and indirectly – possibly impairing tissue function to various extents. Studies have demonstrated that gluten intolerance directed intestinally, such as in CD, can cause malabsorpbion (lack of uptake from the gut into the cells) of calcium, protein and vitamin D. Deficiencies of these nutrients may cause a failure of normal bone remodeling and mineralization causing osteoporosis. All of the calcium supplements in the world will not correct the osteoporosis if it cannot be absorbed by the gut.

Commonly, osteoporosis medications such as Fosomax are prescribed by well-intentioned physicians in an attempt to reduce continued bone loss. Although seemingly affective, none of the medications used for osteoporosis attempt to correct the underlying malabsorption disorder.

After all, disease is not a result of drug- deficiency, but commonly results from or is at least worsened by, nutritional deficiencies. In either case, nutritional interventions including identifying food sensitivities such as gluten and the associated nutritional problems goes a long way towards correcting the underlying mechanisms of disease. In the above case, not only must the extent of gluten involvement be tested, but other nutritional tests such as serum vitamin D levels, urinary hydroxyproline (for protein loss from bone), urinary calcium and protein levels are helpful for determining the most appropriate nutritional interventions.

Dietary, nutritional supplements and intravenous and/or intramuscular nutritional administration will correct nutritional  deficiencies and improve healing overall. Here’s an important point, the diseases reviewed in Table 3 are commonly treated through the use of medications. No matter the potential symptomatic effectiveness of the medications used for these and other health problems – this approach does not, and cannot, fix the underlying autoimmune process triggered by gluten or correct the nutritional deficiencies resulting from the malabsorption or heal the secondary tissue damage that gives rise to the various symptoms and diseases (i.e., the thyroid disease, multiple sclerosis, etc.)

Testing for potentially cross-reacting foods and food allergies:

Food allergies are commonplace in North America in children and adults. True allergies represent only one type of reaction which the body may have against specific foods. Eating the same foods day after day is one of the major contributing factors towards food allergies and intolerance. Given the opportunity food sensitivities can be resolved, or over a period of time, significantly lessened. Diligence is often required as even minimal exposure periodically can re-sensitize an individual to an offending food. Although food sensitivity and food allergy will be used interchangeably in this health letter, these terms are technically not identical. What is important to understand is that persons with gluten antibodies often have other food allergies– most of which they are completely unaware of. Allergists and their patients are fully familiar with what are known as immediate-hypersensitiy reactions also called IgE (Type 1) allergy. Allergic wheels caused by strawberries are an example of Type 1 Hypersensitiy reactions. This type of allergy is obvious as one can notice symptoms either immediately or within 12 or so hours after a food is consumed or the environmental allergen inhaled. Food allergies of a delayed type can manifest as the diseases described in this paper and of course their symptoms. Gluten often causes, or may result from, a breakdown of the intestinal immune systems (known as the Gut-Associated-Lymphoid-Tissue and the Macrophage-Associated-Lymphoid-Tissue). These conditions, and many of their symptoms, are the delayed results of gluten sensitivity directly; it’s secondary tissue effects, nutritional deficiency and other destructive secondary biologic effects.

Possible acceptable substitutions for gluten in the diet:

Buckwheat, amaranth, teff, keenwa, millet and wild rice. High complex carbohydrate vegetables and tubers are easily substituted for grains and include: yams, sweet potatoes, red and white potatoes, turnips, yucca, taro, winter squash and parsnips Note: Food allergy testing will reveal other allergic foods may need to be eliminated from the diet.

Other foods containing gluten:

The scope of this article does not allow a comprehensive exploration of all of the potential foods that contain gluten. Furthermore, many foods may cross-react with gluten that must be individually determined for each person. With the help of a trained nutritional professional, a balanced, healthy diet can be developed that can be maintained and will eliminate or substantially improve the various potential primary and extended symptoms of gluten and other food intolerances.

How gluten causes tissue damage:

Gluten is a protein that contains chains of amino acids. These amino acids are in a specific order that is unique to the gluten itself. However, although the amino acids are in a particular sequence (order) in gluten other tissues of the body may have amino acids in a similar (but not perfectly identical) order. When gluten is ingested by a person it comes in contact with the immune system located in the intestinal tract. If the intestinal-immune system of the individual who has consumed gluten reacts to it as a foreign and unfriendly protein it will mount an immune reaction. This immune reaction is complex and involves the production of antibodies (AB) against the gluten; the gluten is known as an antigen. Thus the body reacts to a foreign antigen, the gluten, producing AB that produces various chemical products. These chemical products initiate an inflammatory type of immune reaction meant to rid the body of the foreign antigen (the gluten). The problems begin when the antigen (gluten) is continuously entering the system that does not want it and the inflammatory response continues of time (chronically). This chronic, inflammatory-immune reaction, initially beginning in the gut, precipitates changes in the intestinal tract that often extent throughout the body. The gluten has evoked an inflammatory reaction in the gut. This inflammatory immune response is known as immune activation (IA). The IA, when persistent, may result in a breakdown of the integrity of the intestinal wall causing cells of the gut to separate slightly. The areas in the gut where this separation occurs are known as tight junctions. The major purpose of healthy tight junctions is to prevent certain molecules (substances) of certain sizes from readily passing through the intestinal wall from the intestinal lumen (center) into the capillaries that line the intestinal wall. If IA causes the tight junctions to separate gluten itself (or a large portion of it) can pass from the intestinal lumen into the blood stream before it is fully digested. Our immune system is on constant patrol for foreign or unwanted materials that have crossed from the gut into the blood where they do not belong. When discovered, the immune system will mount a vigorous attack against it – in this case against the gluten. Antibodies (AB) are produced against the gluten over time, as the inflammatory chemicals produced by the immune system continue to circulate and contact tissues causing damage. As damage continues against specific tissues (i.e., the gut, thyroid, brain, ovaries, etc.) the immune system creates AB against these damaged tissues – as, in their damaged state, they appear as foreign proteins. Hence, a chronically activated, inflammatory, autoimmune response perpetuates feeding upon itself. The various disease states and symptoms are the results of the cascade of reactive immune system events. Sometimes the immune system, once activated, becomes confused and cross- reacts with the gluten and other body tissues causing cellular degeneration and loss of function.

Depending upon the cells, tissue or organs that the immune system reacts against (autoimmune reaction) various symptoms can develop. Any number of seemingly unrelated symptoms could develop in a single individual that may have a common precipitator – namely gluten. By the process of cross-reactivity, the immune system has directed an autoimmune response against the gluten and the body – with potentially devastating results. Can a person develop a gluten sensitivity if he/she never had one? Yes. People with various autoimmune conditions such as thyroiditis, hepatitis C, allergies, multiple sclerosis and other immune problems are at a higher risk for developing aberrant immune responses against gluten and related proteins in the diet. The reason for this is because the immune system is already hyper-responsive as a result of the virus (in the case of Hepatitis C and possibly MS). Interestingly, the immune system activation seen in gluten sensitivity (gluten enteropathy) is similar to the immune systems reactions in a variety of different immune diseases. In short, the immune system can respond to perceived threats in just so many ways. Far from completely understood, the immune system commonly responds by producing AB and inflammatory chemicals (i.e.,cytokines). It is known that aging in general is associated in an increased production of AB against various tissues and organ systems. Contrary to popular belief, many of the aging and elderly population suffer disease as a result from a heightened immune response rather than a blunted (lowered) one. The doctors of Integrated Medicine and Nutrition, P.C. speculate that aging in general, and its associated decline in stomach acid (HCL) and pancreatic enzyme secretions, could cause malabsorption. The GI tract as a whole and its immune system would have an increased inflammatory immune response to many foods including gluten simply because it cannot digest specific foods well enough. If foods are only partially digested because of inefficient (or absent) HCL and/or pancreatic enzymes then the intestinal lining becomes “leaky” – this is called leady gut syndrome (LGS). LGS allows partially undigested food products to make their way into the general blood circulation. Once in the circulation, where food particles should not be in a partially undigested state, an inflammatory immune response is evoked against food remnants. The foods could be of literally any type including gluten, dairy (casein) soy or virtually any other. The immune response can cause further damage of the intestinal lining. An important point to remember is that the immune response, initially directed against specific food remnants, can become generalized and affect any other body tissue. In some persons food reactions of this type can cause chronic fatigue, in others thyroid disease and even brain shrinkage (i.e., cerebellar atrophy or gluten ataxia). In summary, in genetically susceptible persons the aging gut could serve as a conduit allowing for the establishment of autoimmune disease, cancer or milder forms of malabsorption.

Case Studies

Osteoporosis and digestive problems

A 37 year old woman presents with weight loss, fatigue, intestinal cramping, intestinal gas and osteoporosis. He had visited a gastroenterologist and several nutritionists and holistic medical doctors.

She was put on a vegetarian diet and a huge list of nutritional supplements. The diet and supplements did not help. Gluten intolerance was suspected as the young woman consumed gluten foods often, she noticed they worsened her gas. Most importantly, it is highly unusual for a 37 year old woman to have bone-density confirmed osteoporosis without a true malabsorption disorder. Gluten foods and other food allergies were identified and removed from the diet.

Various other tests and evaluations were performed to determine the extent of her nutritional and metabolic problems. The appropriate supportive nutritional interventions were recommended. She no longer suffers from her symptoms. The osteoporosis is expected to regress significantly.

Removing the Gluten:

Removing the gluten once it has been identified as a problem will almost always result in dramatic improvement of symptoms – particularly those relating to the digestive tract directly such as diarrhea, gas and bloating and cramping. As we have stated throughout this paper, the symptoms of gluten intolerance expressed by many other cells, tissues and organ symptoms may not respond so readily to dietary manipulations. The primary reasons for a lack or sluggish response to gluten removal from the diet are summarized above.

Nutritional deficiencies may have resulted over an extended period of time and will take adequate time to be corrected – even after gluten removal. Removal of gluten may remove the major cause (trigger) of malapsorption and cellular damage, but it may not be the only cause. Dairy products may also cross-react with gluten in some persons. Simply removing the gluten may not cause healing to occur to an adequate level until other allergens are identified and eliminated. Proper nutrition can then be prescribed for healing to occur. Even if gluten, dairy or other related and reactive foods are identified and removed, nutritional deficiencies may have adversely affected the function of one or more tissues and organ systems (secondary effects). These secondary effects of gluten or related food sensitivities may be extensive and will require additional nutritional and medical attention to correct – extensive time may also be required. As each individual responds differently to gluten healing time and response to therapy will vary widely based on these and other considerations: age of the individual; general state of health; intake of prescription and non-prescription medications, stress levels; and other lifestyle factors. Correction of the diet without paying the proper attention to the quality of the nutritional interventions often results in incomplete or failed nutritional therapies.

For example, even if the correct nutritional factors are identified (i.e., protein and B-12 deficiency), and given orally once gluten and gluten-related foods are removed, they still may not be fully absorbed. Intramuscular and/or intravenous administration of nutrition may be required to bypass faulty intestinal absorption until the gut itself is healed.

Potential Disease Conditions Caused and/or Precipitated by

Gluten Intolerance (sensitivity).

Table 1:

  1. Celiac Disease (CD)
  2. Rheumatoid Arthritis (RA)
  3. Psoriasis
  4. Neurologic Disorders in children
  5. Dermatotis herpetiformis
  6. Autism
  7. Diabetes
  8. Oral lesions (sores)
  9. Osteoporosis
  10. Lymphoma
  11. Nephropathy (kidney disease)
  12. Anemia (iron, B-vitamin, protein)
  13. Chronic uticaria
  14. Multiple sclerosis
  15. Cerebellar atrophy (brain shrinkage)
  16. Hyperthyroidism
  17. Weight loss (muscle and fat)
  18. Addison’s disease
  19. Sjogren’s syndrome
  20. Malabsorption disease
  21. Dysmenorrhea
  22. Pelvic pain
  23. Chromosomal diseases: Down’s syndrome, Turner’s syndrome and William’s Disease

Note: this least is probably far from complete. These conditions are not necessarily caused by gluten, but may be exacerbated by gluten. In either case, gluten removal and appropriate nutritional-healing attempts are essential.


Table 2: A limited list of foods containing gluten

Barley (flours, rolls, bread), rye, oats, wheat, kamut, spelt
All commercial bread mixes
Pancakes, muffins, biscuits, waffles, crackers
Commercial ice creams
Cookies, doughnuts, pies, pastries
Breaded meat, poultry, fish, patties, croquettes and loaves with bread crumbs
Dishes with cold cuts and frankfurters (unless guaranteed pure meat)
Creamed sauces, gravies, cheese spreads
Instant coffee (if wheat flour is added)
Spaghetti, noodles, macaroni, dumplings


Table 3: Some conditions that can be worsened by the malabsorption of specific nutrition

Malabsorbed nutrient
Essential fatty acids (omega 3 and 6)
Calcium and protein
Allergies (dairy and gluten)
Chromium, protein, antibodies
Antibody production
Iron, B-vitamins, protein
Antibody production


Table 4: Condition that may be caused or worsened by gluten intolerance

Multiple sclerosis, lupus, eczema,
Autoimmune thyroid disease
Failure to thrive, increased susceptibility to infection
Autism (may generate gluteomorphins and caseomorphins)
Kidney disease
Cerebellar atrophy

Summary of MedLine research pertaining to gluten and disease

A French article found a high prevalence of antigliadin antibodies (IgA) in those with rheumatic arthritis. RA was positive in as many as 60% of those with positive Abs.

A study in the, American Journey of Kidney Disease examined the correlation between increased levels of immunoglobulins A against gluten in persons with IgA nephropathy. Study suggests a common pathogenic pathway for CD and IgA nephropathy and concluded that persons with this type of kidney disease should be screened for gluten and a gluten free diet attempted.

Table 5: Laboratory tests to consider in addition to antibodies

Gliadin AB (IgA, IgA)
Reticulin AB
Thyroglobulin AB
Nutritional Considerations
Thyroid panel
Transglutaminase AB
Thyroid peroxidase AB
Methylmalonic acid
Serum B12
Serum folic acid
RBC folic acid


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Some scientific journal summaries

American Journal of Clinical Dermatology 2003:4(1):13-20 Recognition and management of the cutaneous manifestations of celiac disease: A guide for Dermatologist.

Collin P, Reunala T

Department of Medicine and Dermatology, Tampere University Hospital and Medical School, University of Tampere, Tampere, Finland In celiac disease consumption of gluten-containing cereal such as rye, barley, and wheat result in mucosal inflammation of the small bowel along with crypt hyperplasia and villous atrophy. The persistence of this condition is as high as 1% in the adult population. Various extraintestinal manifestation may also result, the best known of which is dermatitis herpetiformis. It was originally thought that dermatitis herpetiformis was a skin condition that occurred concomitantly with celiac disease. However, present knowledge recognizes that it is a cutaneous manifestation of celiac affecting approximately 25% of patients with CD. Both conditions are 1:31 known to HLA class II locus on chromosome 6; 90% have HLA-DQ2 and almost all the remainder HLA-DQ8. All of those with dermatitis herpetiformis have some degree of mucosal inflammation or lesions consistent with CD. The tissue transglutaminase seems to be the most prominent autoantigen in both the skin and intestines. Serum antibodies against tissue transglutaminase are used as a serological followup screening marker. A gluten- free diet is essential treatment for both conditions. Alopecia areata, vitiligo, and oral mucosal lesions probably occur more frequently in those with DH than in the general population.

Semin Gastrointestinal Diseases 2002: October; 13(4):232-44 celiac sprue. Cardenas A, Kelly CP

Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

CD is a malabsorption disorder of the small intestines due to ingestion of gluten in susceptible individuals. CD has a high prevalence in Western Europe and North America where its is estimated to affect 1:120 to 1:300 individuals. The pathogenesis of CD is related to inappropriate intestinal T-cell activation in HLA- DQ2 positive individuals triggered by the antigenic peptides in wheat gluten or prolamins from rye and barley. Previously thought to be a disease of childhood onset. Its diagnosis is increasingly made in adults. It occurs as a wide variety of presentations ranging from the asymptomatic to severe diarrhea, nutritional deficiencies, and weight loss. Extraintestinal manifestations include neurological disorders, osteopenia, and anemia along with hypothyroidism and diabetes. Treatment consists of lifelong avoidance of gluten.

Journal Biological Chemistry 2002 October 29;

A type I diabetes-related protein from wheat (Triticum aestivum): cDNA clone of a wheat storage globulin, G1b1, linked to islet damage.

MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. Molecular Medicine, Ottawa Health Research Institute, Ottawa, Ontario K1H 8L6

The development of autoimmune type I diabetes involves complex interactions among several genes and environmental agents. Type I diabetes shows an unusually high frequency in wheat gluten-sensitive enteropathy. T-cell response to wheat gluten proteins is increased in some patients and high concentrations of wheat autoantibodies have been reported. There is an association between pancreatic islet inflammation and damage in gliadin sensitive individuals. The WP5212 putative protein has high amino acid sequence homology with a wheat storage globulin G1b1. This study raises the possibility that in some individuals type I diabetes maybe induced by wheat proteins.

Current Opinions Neurology 2002 October;15(5): 519-23

The neurology of gluten sensitivity: Separating the wheat from the chaff.

Wills AJ, Unsworth DJ. Department of Neurology, Queens Medical Center, Nottingham, UK

Clinical pathological features in gluten-sensitive individuals heal on a gluten-free diet and relapse when gluten is reintroduced. Therefore, an immunopathology is suspected. Various neurological symptoms maybe associated with celiac disease, but it is unclear whether they are indirectly or directly related. It is suspected that idiopathic ataxias and central nervous system white matter diseases are gluten-sensitive syndromes. This is an exciting possibility as gluten elimination and possibility of symptom improvement is possible.

Vet Clin North AM Food Animal Practices 2002 July; 18(2:215-31) Annuals New York Academy of Science 2002 April; 958:232-4

10-20% of CD patients also have IDDM. Mainly the study was to estimate the prevalence of tissue transglutaminase antibodies in MMDM. In summary, the study noted it is important to look for subclinical celiac disease in differential diagnosis of MMDM.

Allergy Immunology (Paris) 2002 March; 34(3):100-2

Celiac Disease: Clinical and Subclinical Forms Morali A Hospital d’Enfants, CHU Nancy-Brabois, Allee du Morvan, 54500, Vandoeuvre- Les-Nancy CD classically produces chronic diarrhea with a picture of malabsorption with villous atrophy. Atypical forms involve delayed isolated stature, constipation.

The conclusion was allergy to wheat flour merits individualization in the framework of celiac disease.

Neurologic Sciences 2001 November: 22 SUPPL 2:S117-22

Neurological manifestations of gastrointestinal disorders, with particular reference to the differential diagnosis of multiple sclerosis.

Ghezzi A, Zaffaroni M. Centro Studi Sclerosi Multipla, Ospedale di Gallarate, Universita di Milano, Gallarate, Varese, Italy

Neurological manifestations of GI disorders are described that resemble multiple sclerosis on clinical MRI grounds. Patients with CD can present with cerebellar ataxia, progressive myoclonic ataxia, cerebral, peripheral nerve, and brainstem involvement, and myelopathy. Antigliadin antibodies can be found in subjects with neurological dysfunction of unknown cause, particularly in those with cerebellar or gluten ataxia. Those with Whipple’s disease can develop mental and psychiatric changes supranuclear gaze palsy, upper motor neuron signs, hypothalamic dysfunction, seizures, ataxia, myorhythmia, and sensory defects along with nerve abnormalities. Neurologic manifestations can complicate inflammatory bowel disease such as ulcerative colitis and Crohn’s disease. Possible connections between chronic inflammatory polyneuropathy, epilepsy, muscle involvement, and myasthenia gravis are also reported. The CNS can be affected in patients with hepatitis C virus because of vasculitis associated with HCV-related cryoglobulinemia. Neurologic manifestations can be the consequence of nicotinamide, B1, vitamin D, B12, or vitamin E and from nutritional deficiency states following gastric surgery.

Epilepsia 2001 September; 42(9):1153-5

Silent celiac disease in patients with childhood localization-related epilepsies. Labate A, Gambardella A, Messina D, Tammaro S, Le Piane E, Pirritano D, Cosco C, Doldo P, Mazzei R, Oliveri RL, Bosco D, Zappia M, Valentino P, Aguglia U, Quattrone A. Institute of Neurology, University Magna Græcia, Catanzaro, Italy

The problems of those with childhood localization-related epilepsies was compared against silent celiac disease to determine whether or not investigation of CD should be restricted in those patients with childhood partial epilepsy with occipital paroxysms (CPEO) or should be extended to all patients with childhood epilepsy regardless of seizure type and electroencephalographic paroxysms. The study concluded that CD screening should be performed routinely only on patients with CPEO.

Journal of Internal Medicine 2001 October; 250(4):361-6

Problems of undiagnosed celiac syndrome in osteoporotic women Nuti R, Martini G, Valenti R, Giovani S, Salvadori S, Avanzati A. Institute of Internal Medicine, Metabolic Disease Unit, University of Siena, Siena, Italy. The study was to quantify the prevalence of asymptomatic CD in a cohort of osteoporotic females. They looked at 255 women with primary osteoporosis based upon WHO diagnostic criteria. Serum IgG antigliadin antibodies were measured in 53 women showed a positive test. In IgG-AG positive patients a statistically significant inverse correlation was found between 25(OH)D serum levels and log-transformed TG-ab values. The conclusion supported the hypothesis that patients with undiagnosed celiac disease develop high remodelling processes related to calcium malabsorption, secondary hyperparathyroidism, and unavailability of vitamin D with a consequent more marked bone loss.

Review of gastroenterology Mex 2000 April-June; 65(2)85-8

Hypochromic microcytic anemia as the only manifestation of celiac disease. Solana-de lope J, Diaz-Reyna A, Perez-Manauta J Medico Adscrito al Servicio de Gastroenterologia, Hospital De Mexico.

Extraintestinal manifestations and signs may be the only manifestation of celiac sprue. This study looked at a case of a patient with hypochromic microcytic anemia as the only expression of the disease. The result showed that the patient was asymptomatic with pallor at physical examination and laboratory showed only hypochromic microcytic anemia due to iron deficiency. She was previously treated twice with oral iron without achieving good results. The colonoscopy and the small intestinal bowel absorption contrast study were normal. Antiendomysial and antireticulin antibodies were negative. IgA antigliadin antibodies was positive (1:120). After four months of treatment, hemoglobin and iron serum levels were normal and at six months, the small bowel biopsy showed striking improvement. Conclusions: Familiarity with the diverse extraintestinal manifestation of celiac sprue with a high index of suspicion for those with subtle presentations.

Journal of Endocrinology Investigation 2001 May; 24(5):298-302

Prevalence of celiac disease in patients with autoimmune thyroiditis from Northern Sardinia. Meloni GF, Tomasi PA, Bertoncelli A, Fanciulli G, Delitala G, Meloni T Pediatric Clinic A. Filia, University of Sassari, Italy

CD is frequently associated with other autoimmune diseases such as type I diabetes, Addison’s disease, and autoimmune thyroiditis. Patients with autoimmune thyroiditis should be followed up as being at high risk of CD and should be screened routinely for it. If negative, screening test should be repeated at regular intervals.

Clin Chem Lab Med 202 May; 40(5):485-92 Tissue transglutaminase-serology markers for celiac disease Kocna P, Vanickova, Z; Perusicova J; Dvorak M. Institute of Clinical Biochemistry, First Faculty of Medicine and General Faculty Hospital, Charles University, Prague, Czech Republic

Various testing procedures including serological markers for CD including antigliadin antibodies type A and G along with purified alpha-gliadin, antiendomysium, IgA antibodies, and anti-tissue transglutaminase antibodies were reviewed. The study concluded that ELISA determination of atTG with human antigen could increase the specificity, especially in patients with other autoimmune diseases.

An ESP PEDIATR 2002 October; 57(4)321-6 Silent celiac disease: Exploring the iceberg in the school-age population Cilleruelo Pascual

The study demonstrated a high prevalence of silent CD among an unselected pediatric population. The most frequent symptom is iron deficiency followed by recurrent aphthous stomatitis and mild malnutrition. The conclusion of the article is that greater awareness of the minor symptoms of CD would reduce the number of patients with undiagnosed CD.

Neurology 2002 April 23; 58(8):1221-6 The humoral response in the pathogenesis of the gluten ataxia. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM Department of Clinical Neurology, The Royal Hallamshire Hospital, Sheffield, UK.

This article investigated what is known as the humoral response (immune response) to the cerebellum in patients with gluten ataxia. Gluten ataxia is a common neurological manifestation of gluten sensitivity. The conclusion of the article is that patients with gluten ataxia have antibodies against Purkinje cells. Antigliadin antibodies cross-react with epitopes on Purkinje cells.

Child nervous system 1994 September; 10(7):450-4 Celiac disease and epilepsy in pediatric patients. Fois A, Vascotto M, Di-Bartolo RM, Di-Marco V. Institute of Clinical Pediatrics, University of Siena, Italy.

The frequency of antigliadin and antiendomysial antibodies in a large number of patients was examined. CD or antibodies to gluten are not infrequently associated with various types of seizures including complex partial seizures (CPS).

American journal of gastroenterology 1999 April; 94(4):1042-6 Celiac disease. The markers of celiac disease latency in patients with primary Sjögren’s syndrome. Iltanen S, Collin P, Korpela M, Holm K, Partanen J, Polvi A, Mäki M. Institute of Medical Technology, University of Tampere, Finland

It is known that many autoimmune diseases occur concomitantly with celiac disease. The study investigated the occurrence of CD and small bowel mucosal inflammation in patients with primary Sjögren’s syndrome. The findings of the study show a close association between Sjögren’s syndrome and CD. Even among nonceliac patients with primary Sjögren’s syndrome an ongoing inflammation is often present in the small bowel.

Scandinavian Journal of Gastroenterology 1998 September; 33(9):944-9

Small-bowel mucosal inflammation in reticulum or gliadin antibody-positive patients without villous atrophy.

Kaukinen K, Collin P, Holm K, Karvonen AL, Pikkarainen P, Mäki M. Department of Medicine and Pediatrics, Tampere University Hospital, Medical School and Institute of Medical Technology, University of Tampere, Finland.

The study investigated with the individuals with positive CD antibodies may not have small bowel villous atrophy. This study demonstrated that a large number of patients may have normal villous architecture, although they are positive for gliadin or other types of associated antibodies. Prevalence of celiac disease autoantibodies in patients with systemic lupus erythematosus.

Rensch MJ, Szyjkowski R, Shaffer RT, Fink S, Kopecky C, Grissmer L, Enzenhauer R, Kadakia S Department of Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas, USA.

Systemic lupus erythematosus has been associated with false positive autoantibodies. An increased prevalence of autoantibodies are found in CD and systemic lupus erythematosus, which share the human lymphocyte HLA-B8 and HLA-DR3 histocompatibility antigens. The conclusion of the study is that the presence of false positive autoantibodies in patients with lupus is very common.

Although this article suggested that there was not an association between CD and lupus, the office of this health letter believed that this is a misinterpretation of the facts simply because these authors had no evidence not to suggest that there is either a direct or indirect relationship between gliadin antibodies and lupus, as it is known that many immune and neurologic conditions are related to gliadin antibodies.

American journal of gastroenterology 1998 June; 93(6):976-9 Thyroid and celiac disease: Clinical, serological, and echographic study. Velluzzi F, Caradonna A, Boy MF, Pinna MA, Cabula R, Lai MA, Piras E, Corda G, Mossa P, Atzeni F, Loviselli A, Usai P, Mariotti S. Department of endocrinology, Institute of Internal Medicine, University of Cagliari, Italy.

This study sought to reevaluate the prevalence of thyroid dysfunction and autoimmunity in those with celiac disease. The conclusion of the article was that there is an elevated prevalence of clinical and subclinical autoimmunity in CD patients, particularly those displaying the DQB1 genotype. This finding could be related to a particular genetic background of the population of the study (Sardinian).

American Family Association 1998 March 1; 57(5):1023-34, 1039-41 Detecting Celiac disease in your patients. Pruessner HT. University of Texas Medical School, Houston, USA

The study reviews the known evidence that CD is a genetic and neurologically mediated small bowel enteropathy (disease that causes malabsorption). Immune inflammatory response to gluten causes damage not only to the gut but to many other tissues, and the condition is frequently undiagnosed due to its wide range of nonintestinal symptoms. The age of onset ranges from infancy to old age and may involve the skin, the blood system, the musculoskeletal system, mucosal system, dental, psychological, and neurological systems. Untreated patients have an increased incidence of osteoporosis and intestinal lymphoma.

Fortunately, excellent diagnostic screening tests are now available.

American Journal of Medical Science 1998 February; 315(2):139-6 Osteomalacia secondary to celiac disease, primary hypoparathyroidism, and Graves’ disease. Gannage MH, Abikaram G, Nasr F, Awada H. Division of Endocrinology, Hotel Dieu de France Hospital, Beirut, Lebanon

Primary hypothyroidism is seldom associated with other autoimmune diseases. The presence of normal blood calcium, however, in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency. This article emphasizes the need to rule out intestinal malabsorption in the case of normocalcemic (normal blood calcium) hyperparathyroidism.

Obstet Gynecol 2002 May; 99(5Pt 2):937-9

Celiac disease as a cause of chronic pelvic pain, dysmenorrhea, and pelvic dyspareunia.

Porpora MG, Picarelli A, Prosperi Porta R, Di Tola M, D’elia C, Cosmi EV Second Institute of Gynecology and Obstetrics, University of Rome “La Sapienza”, Rome, Italy.

CD may be subclinical and difficult to diagnose in adults. It has been associated with infertility and miscarriage. The conclusion of this article is that CD should be considered in women presenting with unexplained chronic pelvic pain, dysmenorrhea, and deep dyspareunia.

Journal of Medical Genetics 2001 November; 38(11):767-8 Celiac disease and Williams syndrome. Giannotti A, Tiberio G, Castro M, Virgilii F, Colistro F, Ferretti F, Digilio MC,Gambarara M, Dallapiccola B Servizio Di Genetica Medica, Ospedale Bambino Gesu IRCCS, Piazza S Ofrio 4, 00165 Rome, Italy.

CD has been reported in several patients affected with chromosomal disorders including Down’s syndrome and Turner’s syndrome as well as Williams syndrome. The conclusion of the study suggests that the prevalence of CD in Williams syndrome patients is higher than in the general population and is comparable to the higher levels reported in those with Down’s syndrome and Turner’s syndrome. Therefore, antibody antigliadins of the IgA type as well as endomysium antibodies are recommended in patients with Williams syndrome.

Brain 2001 May; 124 (Pt 5): 1013-9. Sporadic cerebellar ataxia associated with gluten sensitivity Burks K, Bosch S, Muller CA, Melms A, Zuhlke S, Stern M, Besenthal I, Skalej M, Ruck P, Ferber S, Klockgether T, Dichgans J. Department of Neurology, University of Tubingen, Germany

A group of patients with sporadic cerebellar ataxia were tested for antigliadin and antiendomysium antibodies. The clinical neurological syndrome was dominated by progressive cerebellar ataxia with ataxia of stance and gait, dysarthria, limb ataxia, oculomotor abnormalities, spontaneous nystagmus, saccade slowing, and other symptoms are included. The study concluded that sporadic ataxia may be associated with positive antibodies against gliadin. They also recognize that the mucosal pathology does not represent an obligatory condition of ataxia with gluten sensitivity. The fact that the disease is strongly associated with same HLA haplotypes found in CD not only demonstrates celiac disease and ataxia with gluten sensitivity to be part of the same disease entity but supports the hypothesis of an immunological pathogenesis of cerebellar degeneration.

American Journal of Gastroenterology 2001 Mar; 96 (3:745-50) Vitamin B12 deficiency in untreated CD Dahele A, Ghosh S Department of Medical Sciences, University of Edinburgh, Western General Hospital, Scotland

The objective of the study was to discuss the fact that iron and folate malabsorption are common in untreated CD as the proximal small intestine is mostly affected. The conclusion of the study is contrary to what is popularly known that in fact B12 deficiency is common in untreated celiac disease and concentration should be measured routinely before hematinic replacement. Vitamin B12 concentrations normalize on a gluten-free diet alone, but  symptomatic patients may require supplementation.

American Journal of Gastroenterology 2001 January; 96 (1:138-45) Celiac Sprue; another autoimmune syndrome associated with hepatitis C. Fine KD, Ogunji F, Saloum Y, Beharry S, Crippin J, Weinstein J. The Intestinal Health Institute, Dallas, Texas, USA.

During this study, the investigator sought to test our hypothesis that hepatitis C also may predispose to CD because it can trigger autoimmune reactions. The result of the study showed that there was a statistically significantly higher prevalence of antigliadin antibodies in all groups of patients with liver disease compared with GI controls and normal controls. Because hepatitis C is much more frequently encountered than autoimmune liver disease, hepatitis C appears to be the most common hepatic diseases associated with the development of celiac sprue.

Scandinavian Journal of Immunology 2001 January; 53 (1:92-8) IgG subclass profile with serum antigliadin antibodies and antibody-dependent cell-mediated cytotoxicity in young children with CD. Saalman R, Dahlgren UI, Fallstrom SP, Hanson LA, Ahlstedt S, Wold AE. Department of Clinical Immunology, Goteborg University, Goteborg, Sweden

Sera from children with active CD were found to efficiently induce antibody- dependent cell-mediated toxicity of gliadin-coated cells. Children with untreated celiac disease had high antigliadin antibody activities of all four IgG subclasses. However, they had a particularly high proportion of IgG1 antigliadin antibodies. The results of the study suggest that gliadin-specific antibodies of predominantly the IgG1 subclass mediate tissue-damaging immune reactions like ADCC (antibody-dependent cell-mediated cytoxicity) and thus may contribute to the disease process of celiac disease.

European Journal of Neurology 2000 November; 7 (6:707-11) A high frequency of CD among children with neurological disorders. Salur L, Uibo O, Talvik I, Juscus I, Metsküla K, Talvik T, Uibo R Department of Immunology, University of Tartu, Tartu, Estonia.

The study explored antigliadin antibodies and antireticulin antibody tests as screening for CD in 206 children with neurological disorders. The conclusion of the study was that CD occurs more frequently among children with neurological disorders. In the study, they were able to demonstrate using indirect immunofluorescence testing that the weak presence of autoantibodies against the brain tissue in CD and AGA-positive patients.

Journal of Pediatric Gastroenterology and Nutrition 2001 September; 33 (3:276-82) Serologic markers of untreated CD in Libyan children: Antigliadin, antitransglutaminase, antiendomysial, and anticalreticulin antibody Ashabani A, Errabtea H, Shapan A, Tuckova L, Tlaskalova-Hogenova H, Department of Immunology and Gnotobiology Institute of Microbiology, Czech Academy of Sciences, Prague, Czech Republic

There is also the study, which looked at the incidence of CD in Libya demonstrated that clinical symptoms at presentation were weight loss in 82%, abdominal distension in 61.5%, diarrhea or steatorrhea in 59%, pallor in 41%, abdominal pain in 20.5%, constipation at 50%, vomiting at 10%, and short stature at 7.7%. Mostly symptoms disappeared after introduction of a gluten-free diet. The conclusions were that the authors stressed the importance of serologic testing not only for screening but also for conformation of CD.

 Inc J Dermatology 1998 July; 37 (7) 515-9 Etiologic aspects of chronic urticaria Liutu M, Kalimo K, Uksila J, Kalimo H Department of Dermatology, Medical Microbiology and Pathology, University of Turku, Finland

Urticaria is a common disease that is always a challenge to dermatologists due to its invasive etiology. 170 chronic urticaria patients were studied. The results of the study showed that the pathologic findings were seen in 92% of patients that were consistent with concomitant disease that suggest autoimmune reactivity in some patients. 55 of these patients had dyspeptic symptoms. H. Pylori IgG antibodies were found in 40 out of 107 patients. Active gastritis was verified by esophagogastroduodenoscopy in 30 out of 32 patients with positive H. pylori test. The conclusions of the study suggested abnormal immunological activation detected in those with chronic urticaria. Inflammation in the GI tract caused by H. pylori may have an important role in the etiology of chronic urticaria.

American Health Gastroenterology 2001 April; 96 (4:113-5) 

End of Summary.  Dr. Michael Wald can be reached by calling 914-666-2942.



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*DISCLAIMER: Dr. Michael Wald is a doctor of chiropractic with a masters degree in nutrition. He is also a Certified Dietitian Nutritionist and a Certified Nutritional Specialist and Sports Nutritionist. Dr. Wald is certified to provide acupuncture in several states, but not New York. Dr. Wald has two board certifications in nutrition. Dr. Michael Wald earned his MD diploma, but did not complete a residency and is thus not licensed to practice medicine. The information on this site is intended for educational purposes only and is not to substitute for sound medical or health advice. Information contained within this website may change at any time without prior notice. The information on this website is under copyright, 2021.