Gluten-sensitivity (GS) is a very controversial subject, but new research has been performed which will answer this very question. Before I explore whether or not gluten-sensitivity is real, I would first like to explore “gluten-sensitivity,” itself, as well as “gluten-intolerance” and “celiac disease” in order to provide a better understanding of the research.
Celiac Disease Defined
Most people have heard of celiac disease. It is where an individual cannot consume gluten (a protein found in wheat, rye, barley and sometimes oats) without activating specific antibodies (a blood protein which is produced in response to a toxin or other foreign substance in the body): anti-endomysium (EMA) and anti-tissue transglutaminase (ATA), in their blood stream which in turn attacks their intestinal tract. When antibodies attack ones own body it is referred to as an autoimmune disease. The symptoms of celiac disease vary from patient to patient, but it is not uncommon for them to experience nutritional deficiencies, loss of intestinal villi (hair-like folicles that carry the food through the intestines and help absorb nutrients), and a host of other symptoms and conditions, some
of which are secondary to celiac itself. However, some with celiac disease do not have any symptoms at all. In celiac disease, the most common nutrients that the body usually does not absorb are fat, protein and carbohydrates. It is the lack of fat absorption that causes most of the digestive symptoms: gas, bloating, diarrhea, floating stool, and tan or grey stool. Celiac disease is also associated with intestinal permeability (leaky gut); and other auto-immune diseases, as are most auto-immune diseases. Many studies have confirmed that the toxicity of the cells are mainly caused by gliadin, a component of gluten. Antigliadin antibodies (AGA) are produced in response to gliadin.
Celiac disease is not diagnosed by testing for ATA and EMA antibodies alone. If one’s antibody tests are positive, then a biopsy is performed by obtaining tiny pieces of tissue from the small intestine to check for damage to the villi. However, much damage needs to be found for the test to result in a positive. Testing for specific genes, HLA genes (DO2 and DO8) can also be performed, but are usually used to rule out celiac disease. If you test positive for one of these genes it does not result in diagnosis of celiac disease. The patients symptoms, nutritional deficiencies, etc. are also taken into account.
Those with Type 1 Diabetes, Hashimoto’s Thyroiditis and autoimmune liver conditions may have a deficiency in IgA. In those patients, testing for IgG-tTG may be necessary for diagnosis. With the above said, if one continues to present symptoms they should seek further evaluation for celiac disease or other conditions. To learn more about testing visit UC Hospitals “Antibody Blood Tests“.
In the U.S., 1 in 133 people have celiac disease (CD), but some studies show as much as 97% are undiagnosed.
The term “gluten-intolerance” is used differently by various individuals. Because many people use the word intolerance in reference to someone who may be dairy-intolerant one may think of a gluten-intolerance as something which produces mild symptoms. Many people think that someone with a gluten-intolerance may just get an upset stomach or experience other mild digestive issues. However, the word “intolerance” is defined as incapable to bear or endure. In regards to food, it is defined as an abnormal sensitivity or allergy. If one cannot tolerate a particular food, it means that they cannot consume that food without an adverse reaction. Medical professionals may use this term in regards to those who are and are not diagnosed with celiac disease. When used in either of these conditions, they are referring to someone who really cannot tolerate gluten.
If one has a gluten-sensitivity, they have some type of reaction to gluten, but it may not be as severe as someone with a gluten-intolerance or celiac disease. They may experience temporary headaches, digestive issues, etc., but no immediate or permanent harm is noticeable. However, there are doctors who use the term gluten-sensitivity in regards to someone who has the symptoms of celiac disease, but are not diagnosed, even when some of the test results are positive.
In a University of Maryland article, the broad sphere of gluten issues are further explained by Dr. Fasano, the Director of the Center for Celiac Research.
“Imagine gluten ingestion on a spectrum, says Dr. Fasano. “At one end, you have people with celiac disease, who cannot tolerate one crumb of gluten in their diet. At the other end, you have the lucky people who can eat pizza, beer, pasta and cookies — and have no ill effects whatsoever. In the middle, there is this murky area of gluten reactions, including gluten sensitivity. This is where we are looking for answers about how to best diagnose and treat this recently identified group of gluten-sensitive individuals,” says Dr. Fasano.”
With so much attention on celiac disease, gluten sensitivity research has also spiked. Interestingly, 2 years ago the medical community considered gluten-sensitivity (GS) to be in the patients mind. We’ve come a long way!
Between four laboratories in Italy and the U.S., clinical studies were performed to separate celiac disease and gluten sensitivity. The results provided the first affirmation, to date, of genes and other avenues possibly involved in the development of gluten-sensitivity.
The study included 26 patients with gluten-sensitivity, 42 with celiac disease, and 39 control subjects (non-treated individuals in a study who serves as a reference) undergoing upper endoscopy (uses a lighted tube with a camera to help get a better look at your upper digestive tract) for indigestion. All control subjects had no underlying inflammation, verified through urinalysis.
All patients consumed gluten for four months and then went on a gluten-free diet. The researchers defined gluten-sensitivity individuals as those with (1) little or no intestinal damage after eating the gluten; (2) their symptoms improved on a gluten-free diet; and (3) tested negative for anti-endomysial (EMA), which onlyoccurs in celiac disease and dermatitis herpetiformis (DH) (the skin condition of celiac disease), and anti-transglutaminase antibodies (ATA) found in celiacs and non-celiacs.
Per the Mayo Clinic, endomysial antibodies (EMA) are not only present in 70% to 80% of patients with dermatitis herpetiformis or celiac disease, but most all individuals who have high grade gluten-sensitive enteropathy (disease of the intestinal tract) and who are not adhering to a gluten-free diet. (This was not part of the study.)
When tested for the HLA genes (DQ2 and DQ8), 43% of the gluten-sensitive patients were DQ2/DQ8 positive, which is similar to that of the general public.
The presence of anti-gliadin antibody in the blood is a common (though not definitive) phenomenon for celiac patients. In this study, only 43% of patients were antibody-positive. This implies that anti-gliadin antibody (AGA) is not a good marker for gluten-sensitivity. However, a substantial fraction (44%) of the antibody-positive patients lacked DQ2/DQ8, another difference from celiac patients.
The symptoms of the 42 celiac patients consisted of chronic diarrhea, abdominal pain, weight fluctuation, weakness, smelly fatty stools, bone or joint pain, osteoporosis, behavioral changes, tingling, leg numbness, muscle cramps, missed menstruation, infertility, recurrent miscarriage, delayed growth, thyroiditis, tooth discoloration, and unexplained anemia.
The symptoms of the 26 gluten-sensitivity patients were: diarrhea, abdominal pain, weight loss, gas, bone or joint pain, osteoporosis, leg numbness, muscle cramps, unexplained anemia and glossitis (a condition in which the tongue is swollen and changes color and there is a loss of the finger-like bumps on the surface, known as papillae).
Those patients with gluten-sensitivity experienced overlapping symptoms as those with celiac disease. However, their symptoms disappeared with a few days after implementing the gluten-free diet. In addition, they remained symptom-free for up to 4 years. None of the gluten-sensitive patients tested positive for wheat allergies. Of the 26 GS patients, 12 (46%) were anti-gliadin antibody (AGA) positive; 12 (46%) were HLA-DQ2-positive and/or HLA DQ8-positive; all (100%) were anti-tissue transglutaminase (tTG-IgA) (an enzyme normally present in the intestines) negative and EMA-IgA negative (antibodies). All of which determined that HLA-DQ2 or HLA-DQ8 genes were not associate with GS. Fifty-six percent of the anti-gliadin antibody (AGA) positive gluten-sensitive patients were HLA (genes) positive. The other 44% were HLA negative (both DQ2 and DQ8), which suggested that AGA (antibody) production was not associated with GS. This provided the differences they were searching for in GS patients.
Symptoms in gluten-sensitivity may resemble some of the gastrointestinal symptoms that are associated with celiac disease or wheat allergy, but objective diagnostic tests for this condition are still missing. Therefore, a diagnosis of gluten-sensitivity is commonly made by exclusion.
Intestinal Permeability (also known as Leaky Gut) – hole(s) in the gut
Permeability definition: The state or quality of a material or membrane that causes it to allow liquids or gases to pass through it.
Impaired permeability in the small intestines and in intestinal barrier function (mucous in the intestinal tract which carries antibodies to protect us) are regularly found in celiac patients. To determine whether or not gluten-sensitivity patients had impaired permeability in these areas, a urinary analysis was performed, (LA/MA urinary ratio). It was discovered that the levels of permeability was much higher in the celiac patients than in the gluten-sensitivity patients. Permeability also showed higher in celiac patients when compared to the control group (those with indigestion). Interestingly, permeability was lower in gluten-sensitive patients than in the control group.
The findings suggested that gluten-sensitivity is associated with a noticeable activation of an innate (natural or existing from birth) immune response, which is different compared to those with celiac disease. With gluten-sensitivity the body automatically starts attacking what it considers a foreign body (gluten). Although the cause responsible for the loss of intestinal barrier function (mucous) in celiac disease have only been portrayed in part, the factors responsible for the loss of gluten tolerance and the development of autoimmunity in this condition are still not completely understood.
Gluten-sensitivity does exist! It is not in your mind. It is immune related. Staying on a gluten-free diet relieves the symptoms.
Read the full Gluten Sensitivity Research Study
Copyright 2011 Carla Spacher Gluten Free Recipe Box. All rights reserved.