Celiac.com 02/05/2022 - Since my diagnosis of celiac disease a year ago, I have found it very difficult to dine out or travel without significant anxiety. All things considered, going anywhere had become an ordeal involving planning all meals in advance. Whether calling restaurants ahead of time to talk with a manager about a diet restriction that he hasn’t even heard of, or bringing any and all food that I plan to eat in a day—it is time consuming and demanding. As you can imagine, when it came time to plan a vacation there was some debate over a safe location. Where would I possibly eat for five days? Without question, I am glad that I chose Walt Disney World.

The first step was booking the hotel and flight reservations, and purchasing Disney theme park tickets. Then, I sat down and planned out the order we would visit parks to narrow the list of restaurants for each day. By signing up for the Disney dining plan ($35 per day for a counter service lunch with a dessert and a 3 course sit down dinner), I had a pre-selected restaurant list and was on my way to doing some research. The Unofficial Disney Guide had ratings for each restaurant on the list and some examples of meals on the menu which proved to be very helpful.

Next, I planned out what restaurant I was going to eat at each day for lunch and dinner. I called 407-WDW DINE about a month before I was scheduled to leave. Through Disney’s central dining hub, I was able to make reservations with my gluten intolerance noted in their database for each restaurant that I chose. The person whom I spoke with gave me the phone numbers for the head chefs of each restaurant. It was also suggested that I call each restaurant about a week ahead of time to ensure that they could accommodate my dietary restrictions. I assumed that the sit-down restaurants would be able to assist me, but I was a little more concerned with the counter service restaurants. I anticipated lunch being a busy time and wondered if it would be possible for everything to be prepared without any contamination. In addition to calling the establishments ahead of time, I made sure to bring some cereal, bread, my own toaster (I was told that the hotel would be unable to provide an unopened one), and lots of gluten-free rice bars.

Once I arrived at Disney World and set out to eat my first meal, I was pleasantly surprised. Not only were the chefs able to assure me that there would be no risk of contamination, but the counter service managers were also able to promise the same. They only asked that I tried to arrive either before noon or after 2 PM to avoid their busiest times. For counter service restaurants, I would recommend the Tusker House in the Animal Kingdom, although every establishment that I went to for lunch was exceptional. The managers made my food themselves to ensure there would be no contamination and even baked the French fries in the oven rather than deep frying them.

At each restaurant that I went to for dinner, the head chef came out to speak with me prior to my ordering. I could ask them directly any questions about the food and they were able to alleviate any of my concerns. In the Magic Kingdom I was able to have a character breakfast at the Crystal Palace with gluten-free pancakes, and dinner at Tony’s Town Square with gluten-free rolls. Spoodles in Disney’s Boardwalk was also delicious with a Mediterranean twist to a great chicken dish. The only location that I was disappointed with was Les Chefs du France in Epcot. Despite calling ahead of time, the chef did not return my call. Once I was there and spoke with the waiter about my dietary restrictions, he informed me that there were no gluten-free starches for me to pick from. Needless to say, I left Epcot fairly hungry.

I set out planning for this vacation with a lot of reservations and apprehension. This was the first time I was going to put myself into a situation where I had to dine out for every meal since my diagnosis with celiac disease. I am proud to say that I not only left Disney World with mouse ears on my head, but a huge smile of my face. Actually, this was one of the best vacations that I have ever taken. The employees at Disney World are truly there to make your stay unforgettable. To them, it may have been any other week of their lives. To me, it was a milestone. This trip proved that I can continue to live a normal and happy life without always worrying about food. Disney World truly is the happiest place on Earth!

Celiac.com 01/28/2022 - When you purchase a gluten-free cookbook, the author— hopefully—has spent time in the kitchen experimenting with the recipe until the final version is tasty, light, and worthy of being included in the book. However, we all have recipes at home that were handed down through the family, or ones that we found in a magazine, which we would like to convert to be gluten-free. Believe it or not it is possible to do this without sacrificing taste or texture—simply by making a few adjustments to the ingredients.

Consider the issue of “taste.” How often have you taken a fork full of a scrumptious-looking gluten-free dessert or slice of gluten-free bread only to be sadly disappointed in the dry taste, its aftertaste, or NO taste at all? Alternative flours do not have the same taste as wheat flour. To cover up this deficiency, you have to add more flavoring to your recipe, and the ways to do this are almost limitless. With a little imagination, you can create desserts and bread products that are so tasty that no one will know they are gluten-free!

Consider substituting half of the gluten-free flour mixture (traditionally made of rice, potato starch and tapioca flours) with more flavorful flours, such as cornmeal, almond, or sweet potato flour. Whether you are making sweet bread, muffins or cake, look at the ingredients listed and start to brainstorm about what you can add for extra flavor. Assuming you are not allergic to nuts, this is a good starting point. If you traditionally add chopped walnuts, vary this by substituting peanuts, pecans, hazelnuts, black walnuts, pistachios, cashews, pine nuts or even candied chestnuts. Spread dry nuts in a pan and bake them (watch them closely so they don’t burn)—toasting the nuts will bring out the natural oils and increase their flavor. For added taste, toss the nuts with a tiny bit of oil and seasonings (cinnamon, nutmeg, ginger, or ground cloves) before toasting. Coconut is another candidate for toasting. While shredded coconut adds flavor, toasted coconut has a far more vibrant taste.

Other flavorful ‘add-ins’ include marshmallows (miniature or melted), caramels (melted), dark chocolate (chips, chunks, shaved, or melted), instant coffee granules for a mocha taste, or orange, lemon or lime zest. For breads and muffins consider folding in seeds like sesame, poppy, caraway or sunflower for added flavor—or chopped dried fruits such as cranberries, raisins, apricots, prunes, dates, figs, and/or glazed fruits.

Canned and fresh fruits and fruit juices will not only add flavor, but moisture as well. For chocolate cakes, open a can of sweet, dark pitted cherries or thawed frozen raspberries. Use the juice from the can (or frozen package) as part of your liquid measurement, and then fold in the chopped cherries or raspberries into the batter. For a white cake, use crushed pineapple and the pineapple juice. Open a can of sliced peaches and put both peaches and their juice into a blender—use this as the liquid when making coffeecake. Blueberries, shredded apples or pears, or mashed bananas are also great to add to baked products, but so are more unusual selections. Think out of the box. Add mashed mangos, kiwi or papayas, chopped maraschino cherries, shredded rhubarb, or canned, whole cranberry sauce to muffins—add pomegranate seeds to coffeecakes. In place of all or part of the liquid called for in the recipe, substitute apple cider, apricot nectar, cranberry juice, orange juice, grape juice, lemonade, or limeade. Add tomato juice mixed with a little cinnamon to crumb cakes (yes, tomatoes are a fruit). Experiment by using jars of strained baby fruits for part of the liquid amount.

Don’t overlook the power of vegetables to add flavor. Shredded zucchini, carrots, or onions have long been staples when baking breads. Carrot juice may be used for part of the liquid in many muffin mixes. Mashed sweet potatoes or winter squash make excellent, flavorful additions to baked goods. Even rinsed sauerkraut may be used!

In place of some of the liquid listed in the recipe, use Kahlúa, wine, sherry, rum or brandy. Melted jellies, jams and preserves work well, too. Other substitutes for the liquid listed include (gluten-free) eggnog, brewed coffee, maple syrup, molasses, canned pumpkin, flavored yogurts, cottage cheese, peanut butter, apple butter, applesauce, and even gluten-free beer. Canned pie filling may be used in place of two thirds of the liquid called for in the recipe.

Instead of white sugar, measure out an equal amount of brown sugar or 3⁄4 the amount of honey (both of which have more flavor than white sugar). Increase the amount of flavoring called for in the recipe, plus think about adding an additional gluten-free extract: almond, butternut, mint, anise, lemon, rum butter, or caramel flavoring. Cinnamon may be added to most any dessert recipe, along with nutmeg and a hint of ground cloves.

When baking yeast breads, popular ‘add ins’ include fruits (fresh, dried, or canned), nuts, coconut, mashed sweet potatoes, bacon bits, olive slices, chopped sun-dried tomatoes, or grated cheeses, and even a sprinkling of Lea & Perrins Worcestershire sauce. Even with a plain white bread, some kind of flavoring will enhance the finished product. Try adding rosemary, dill, thyme, chopped parsley, oregano, basil, garlic powder, Italian seasoning, ginger, mint, cinnamon or chopped preserved ginger in syrup. And don’t be afraid to add a little vanilla flavoring—it will help improve the taste. A hint of balsamic vinegar added to yeast breads will liven up the flavor and help the bread to rise!

Are you willing to be even a little more experimental? Substitute some of the gluten-free flour mixture with a package of gluten-free instant pudding dry mix. Use gluten-free cream cheese in place of some of the shortening. In a blender, whip corn relish into a puree and add to yeast breads. Try brushing cornbread with a jalapeno-honey glaze.

Yes—your gluten-free baked products will taste scrumptious just by adding a little more flavoring—happy eating!

Gluten-Free Cinnamon Popovers

This recipe may be found in the “Recipes for Special Diets” cookbook by Connie Sarros. It recipe is approved for diabetics, low-sodium diets, and vegetarians. It is nut-free and yeast-free. For corn-free diets, use baking soda plus 1⁄2 tsp. cream of tartar in place of the baking and omit cornstarch and xanthan gum from gluten-free flour mixture. For dairy-free diets, substitute soymilk for the whole milk.

Note: To help insure that the popovers rise, spoon dough into warmed pans.

Ingredients:

• 3 eggs
• 3⁄4 cup gluten-free flour mixture
• 1⁄4 teaspoon salt
• 2 1⁄4 teaspoons gluten-free baking powder
• 2 teaspoons sugar
• 1⁄2 teaspoon cinnamon
• 1 cup whole milk

Directions:

Preheat oven to 400F. In a medium bowl, whisk eggs till light. Sift together dry ingredients. Add flour mixture to eggs alternately with milk, stirring with a whisk just until blended. Do not over beat! Fill greased popover pans or deep custard cups 1⁄2 full with batter. Bake for 10 minutes; lower heat to 325F and continue baking for 20 minutes or until popovers are golden brown. Serve immediately. Makes 6 large popovers or 12 muffin-size.

Calories (for 12 muffin-size popovers): 52; Total fat: 1.5g; Saturated fat: 0.4g; Cholesterol: 53mg; Sodium: 79mg; Carbohydrates: 6.7g; Fiber: 0.2g; Sugar: 1.2g; Protein: 2.9g

Celiac.com 01/21/2022 - Less than a decade ago in Chicago, there was a time when thousands of residents would have claimed that the best basketball team of all time was right here, right now. In the 1990’s, the combined magic of Michael Jordan, Scottie Pippen and the rest of that stellar Bulls team was, to a basketball fan, like nothing ever experienced in the past.

But then, there are those who would argue that a different team of the past (perhaps Larry Bird and the Boston Celtics, or Magic Johnson & Kareem Abdul Jabar of the Los Angeles Lakers) was the best ever. And, there are statistics, personal experience and memories of games played to validate each position—everyone was right within their own world of experience.

For an individual with celiac disease (often incorrectly referred to as “an allergy to wheat and gluten products”), there are several factors to consider in determining if oats is a safe food. The questions which are commonly asked by patients with known wheat or gluten sensitivity include:

• Oats are not a wheat product. Are oats safe for me to eat?
• Can oats have gluten?
• My Doctor says that oats are Ok, but I’ve read conflicting reports that say oats are to be avoided. Which is true?

As with ‘the greatest basketball team of all time’, the answer depends on your point of view. You can easily find doctors and researchers who will offer evidence on both sides of these questions. Here’s the latest information to help you in answering these questions for yourself.

There are three factors to be addressed:

1. Is there gluten in oats?
2. Can oats trigger a gluten-type sensitivity reaction?
3. Is there anything else in oats that can be offensive?

Let’s consider these factors one at a time. First, is there gluten in oats? The clear and uncontested answer is no, there is no gluten in oats— and, yes, there is gluten in oats.

Confused? Here’s why: gluten is the offensive prolamin (simple protein found in seeds) protein found in wheat. It is known to be one of the triggers to the symptoms of celiac disease. Avenin is the prolamin protein of oats. It has a different chemical structure than gluten and avenins have been predicted to contain only a few glutamines that can be deaminated by tissue transglutaminase, presumably making avenins less immunogenic thus substantially less offensive to the lining of the intestines than gluten(15,16). The offensive protein in oats is not gluten. So, no, there is no gluten in oats.

And now to the yes answer regarding the gluten content of oats. In a recent study entitled ‘Gluten Contamination of Commercial Oat Products in the United States’, the author purchased 12 containers of rolled or steel-cut oats representing four different lots of each of three different brands between October 2003 and March 2004(14). The three brands were Quaker (processed in Chicago—selected because it is a popular brand of oatmeal in the U.S.), Country Choice (Eden Prairie, Minnesota—because it is certified to be organic) and McCann’s (Odlum Group, Nass, Ireland, because it is processed in an oats-only facility).

Following the Codex limit for naturally occurring gluten-free foods, oat samples were considered gluten-free if they contained 20 parts per million (20 ppm) or less of gluten17. The results were startling. All three brands of oats had gluten contamination above 20 ppm in at least two of the four samples tested. Ranges of gluten in the four samples from the 3 different companies ranged from:

• McCann’s, none to 725 ppm;
• Country Choice, none to 210 ppm; and
• Quaker, 338 to 1807 ppm.

Even the best of the three (Country Choice) was 10 times above the safe limit of gluten contamination, and the worst was 90 times above the limit. So, even though oats are not composed of gluten, it appears that oats contain gluten more than half the time—and the amount of gluten present is often dangerously high for someone with Celiac Disease. So, you are asking: Where does the gluten in oats come from? The author of the study wrote:

“Celiac organizations across the United States continue to advise against the consumption of oats because of concerns that commercial oat products may be contaminated with wheat, barley, or rye during harvesting, transporting, milling and processing.”(18)

Can Oats Trigger a Gluten-type Sensitivity Reaction?

Once again, there are two answers. On one hand, if oats are contaminated with gluten at dangerously high levels more than half the time, the answer would have to be ‘yes, oats can trigger a gluten-type sensitivity reaction.

Basically if you are following a strict gluten-free diet, doing very well at food selections, AND eating oats (‘because there is no gluten in oats’), you could still develop celiac disease complications.

We know that celiac disease is a chronic inflammatory immune response in the intestines and other tissues due to gluten exposure(1) . Is it safe to eat oats on a gluten-free diet? Given the above information, it is likely not safe for celiac patients to eat oats or oat products.

Can oats trigger a gluten-type sensitivity reaction? The second answer has to do with the composition of oats. Due to the protein in oats (avenin) having such a different chemical structure, it has been predicted to be much less offensive to the immune system making oats less immunogenic (immune system stimulating)(2,3). There have also been a number of studies that have suggested oats do not trigger the same type of immune response as gluten(4-11).

However, there have been studies on the other side of the coin that identify an immune response of some type. A recent study of 39 Finnish patients randomized to eat a gluten-free diet with 50 grams of oats daily or a standard gluten-free diet for one year reported more intestinal symptoms and more gut inflammation in the group of patients eating oats(13).

The researchers wanted to find out why this was happening to some celiac patients. When searching for the mechanism that was causing an oat-sensitivity reaction for some celiacs they discovered a similar-to-gluten type of immune system response in the intestines. They described this as:

“We established oats-avenin-specific and - reactive intestinal T-cell lines from these three patients, as well as from two other patients who appeared to tolerate oats. The avenin-reactive T-cell lines recognized avenin peptides in the context of HLA-DQ2. These peptides have sequences rich in proline and glutamine residues closely resembling wheat gluten epitopes. Deamidation (glutamine/glutamic acid conversion) by tissue transglutaminase was involved in the avenin epitope formation.”

We conclude that some celiac disease patients have avenin-reactive mucosal T-cells that can cause mucosal inflammation. Oat intolerance may be a reason for villous atrophy and inflammation in patients with celiac disease who are eating oats but otherwise are adhering to a strict gluten-free diet. Clinical follow-up of celiac disease patients eating oats is advisable.” (12)

Summary

Although technically there is no gluten in oats, and celiac disease is associated with gluten exposure, it is a roll of the dice for celiac patients to eat oats for two reasons:

1. Given the frequency of contamination of oats with gluten, it is impossible to be assured of a gluten-free oat product.
2. Some celiac patients (and as of yet it is impossible to know which ones), appear to have an immune system sensitivity reaction to oats similar to gluten.

Thus the safest approach at this point may be to include elimination of oats to a gluten-free diet, allow the intestines to heal (and have that documented with a recheck endoscopic exam), then do an oat-challenge diet and regularly recheck via endoscope for any signs of intestinal damage. This is a timely process (and a nuisance for the patient), but if one wants to eat oats this may be the only way to do it safely.

References:

1. Sollid LM (2002) Coeliac disease: Dissecting a complex inflammatory disorder. Nat Rev Immunol 2: 647–655.
2. Vader LW, de Ru A, van Der WY, Kooy YM, Benckhuijsen W, et al. (2002), Specificity of tissue transglutaminase explains cereal toxicity in celiac disease. J Exp Med 195: 643–649.
3. Piper JL, Gray GM, Khosla C (2002) High selectivity of human tissue transglutaminase for immunoactive gliadin peptides: Implications for celiac sprue. Biochemistry 41: 386–393.
4. Janatuinen EK, Pikkarainen PH, Kemppainen TA, Kosma VM, Jarvinen RM, et al. (1995) A comparison of diets with and without oats in adults with celiac disease. N Engl J Med 333: 1033–1037.
5. Srinivasan U, Leonard N, Jones E, Kasarda DD, Weir DG, et al. (1996) Absence of oats toxicity in adult coeliac disease. BMJ 313: 1300–1301.
6. Hardman CM, Garioch JJ, Leonard JN, Thomas HJ, Walker MM, et al. (1997) Absence of toxicity of oats in patients with dermatitis herpetiformis. N Engl J Med 337: 1884–1887.
7. Reunala T, Collin P, Holm K, Pikkarainen P, Miettinen A, et al. (1998) Tolerance to oats in dermatitis herpetiformis. Gut 43: 490–493.
8. Hoffenberg EJ, Haas J, Drescher A, Barnhurst R, Osberg I, et al. (2000) A trial of oats in children with newly diagnosed celiac disease. J Pediatr 137: 361–366.
9. Janatuinen EK, Kemppainen TA, Julkunen RJ, Kosma VM, Maki M, et al.(2002) No harm from five year ingestion of oats in coeliac disease. Gut 50:332–335.
10. Størsrud S, Olsson M, Arvidsson LR, Nilsson LA, Nilsson O, et al. (2003),Adult coeliac patients do tolerate large amounts of oats. Eur J Clin Nutr 57:163–169.
11. Ho¨ gberg L, Laurin P, Fa¨ lth-Magnusson K, Grant C, Grodzinsky E, et al.(2004) Oats to children with newly diagnosed coeliac disease: A randomized double blind study. Gut 53: 649–654.
12. Helene Arentz-Hansen1, Burkhard Fleckenstein1,2, Øyvind Molberg1, Helge Scott3, Frits Koning4, Gunther Jung5, Peter Roepstorff2, Knut E. A. Lundin1,6, Ludvig M. Sollid1*, The Molecular Basis for Oat Intolerance in Patients with Celiac Disease, PLoS Medicine, http://www.plosmedicine.org, October 2004, Volume 1, Issue.
13. Pera¨ aho M, Kaukinen K, Mustalahti K, Vuolteenaho N, Ma¨ ki M, et al. (2004) Effect of an oats-containing gluten-free diet on symptoms and quality of life in coeliac disease. A randomized study. Scand J Gastroenterol 39: 27–31.
14. Thompson,T., Gluten Contamination of Commercial Oat Products in the United States, NEJM,Nov.4,2004,2021-22.
15. Vader LW, de Ru A, van Der WY, Kooy YM, Benckhuijsen W, et al. (2002) Specificity of tissue transglutaminase explains cereal toxicity in celiac disease. J Exp Med 195: 643–649.
16. Piper JL, Gray GM, Khosla C (2002) High selectivity of human tissue transglutaminase for immunoactive gliadin peptides: Implications for celiac sprue. Biochemistry 41: 386–393.
17. Joint FAO/WHO Food Standards Program, Codex Committee on Nutrition and Foods for Special Dietary Uses. Draft revised standard for gluten-free foods. CX/NFSDU 98/4 July 1998: 1-4, http://intlspectrum.diabetesjournals.o rg/cgi/content/full/15/3/197.
18. Thompson,T. Oats and the Gluten-Free Diet, J Am Diet Assoc. 2003;103,876-9.

Celiac.com 01/08/2022 - Celiac disease is a chronic inflammatory disease of the gut occurring in genetically susceptible individuals after ingestion of gluten. It is characterized by a flattened mucosa, villous atrophy and crypt hyperplasia in the small intestine and by the classic malabsorption syndrome (diarrhea, steatorrhea, and weight-loss) or by minor apparently unrelated symptoms such as iron-deficiency anaemia, osteopenic bone disease, amenorrhea and infertility(1).

The diagnostic algorithm of this disease demand a screening approach based on anti-endomysium (EmA) and anti-tissue transglutaminase (anti-tTG) and, in case of antibodies-positivity, patients should undergo intestinal biopsy to confirm the presence of small bowel lesions according to celiac disease.

Unfortunately, this approach is rarely effective in clinical practice, especially in patients with mild to moderate histological lesions. In fact several recent studies have shown that 5-10% of patients affected by mild to moderate lesions of the small bowel typically seen in celiac disease actually lack EmA and anti-tTG antibodies(2-5). In light of these scientific results, should all patients who are suspected to have, or who are at risk for celiac disease—including first degree relatives of celiacs, those with Down’s syndrome or autoimmune thyroid disease, patients whose stories indicate celiac disease, etc.—undergo intestinal biopsy? This does not seem like a very reliable approach—perhaps other more non-invasive tests should be done in conjunction with serological testing to help determine which patients should undergo a biopsy. The sorbitol H2 -breath test (H2 -BT) could be exactly what is needed.

Sorbitol is a hexahydroxy alcohol that is present in many fruits such as peaches6 . It is used as a sugar substitute in dietetic foods and as a drug vehicle. At low doses (5 grams/day) sorbitol is completely absorbed by the small bowel, and low dose ingestion does not typically produce any symptoms. However, we know that celiac disease patients often experience sugar malabsorption (as lactose malabsorption)(7), which prompted us to hypothesize that the same may be true for sorbitol. In general terms, sugar malabsorption could be primary— congenital enzymatic/ carrier deficiency, or acquired—developing after intestinal damage caused by acute gastroenteritis, medications, Crohn’s disease, celiac disease, etc.(8) In the normal individual, gut bacteria are primarily located in the colon and in the distal small intestine. When sugar malabsorption is present, unabsorbed sugars in excess are available in the distal small bowel and colon for bacterial fermentation, with air excretion of H2 and CH4 9 . This mechanism occurs for all sugars— lactose, fructose, glucose, sorbitol—and H2 lactose, fructose and sorbitol breath tests are commonly used to detect specific sugar malabsorption issues.

Sorbitol H2-BT Methods

This is a simple, non invasive, repeatable, and cheap test. To minimize basal hydrogen excretion, subjects are asked to have a carbohydrate-restricted dinner on the day before the test (for example, a meal of rice and meat) and are studied after an overnight fasting for at least 12 hours. On the testing days, patients do a mouthwash with 20 ml of chlorhexidine 0.05%; smoking and physical exercise are not allowed for 30 minutes before and during the test. End expiratory samples are collected before the patients drink the test solution— 5g of sorbitol in 150/200 ml of tap water—and every 30 minutes for 4 hours using a two-bag system. The two-bag system is a device consisting of a mouthpiece, a T-valve and two collapsible bags, for collection of dead space and alveolar air. From this system, the breath sample is aspirated into a 20 ml plastic syringe. Samples are generally evaluated for H2 using a model DP Quintron Gas Cromatograph (Quintron Instrument Company, Milwakee, WI). It is also possible to measure the hydrogen concentration in each collected sample by a portable breath-hydrogen analyzer (for example, EC60 Gastrolyzer Breath Hydrogen Monitor, Bedfont Scientific Ltd, Upchurch – Kent, England [U.K.]). An increase in H2 concentration of at least 20 ppm over fasting baseline is considered positive for sorbitol malabsorption. The cut-off for calculating the validity of the test is shifted every 30 minutes, and a Response Operating Characteristics (ROC) curve is plotted on the basis of the obtained results. Results are expressed as parts per million (ppm).

Sorbitol H2-BT and Celiac Disease

The first study assessing the effectiveness of sorbitol in detecting intestinal damage in celiac disease was performed by Corazza, et al. in 1988. They showed for the first time that low dose concentrations of sorbitol (5 grams at 2%) are malabsorbed in almost all celiac disease patients(10), and these results were confirmed in a more recent study(11). These provocative results led to the idea that it could be used as a screening tool in celiac disease, in addition to serological tests. However, these results have not been completely considered by investigators, and using sorbitol H2 -BT to screen for celiac disease was not investigated further for another four years.

In the 2001 we published a paper about the low-prevalence of anti-gliadin and anti-endomysium antibodies in a sub-clinical/silent form of celiac disease. We found that 5-20% of celiac disease patients affected by this form of the disease lack these antibodies according to histological damage4 , and we found the same results using anti-tTG12. Based on this research it was apparent that there was a risk of not properly diagnosing a very high percentage of celiac disease patients if their screening is based solely on serological tests. At this point we tried to use the sorbitol H2 -BT as screening tool to obtain more information on patients’ intestinal absorption, and to help select patients who should undergo intestinal biopsy.

Sorbitol H2-BT in Detecting the Sub-clinical/Silent Form of Celiac Disease

Sub-clinical celiac disease is defined by the presence of a gluten sensitive enteropathy with extra-intestinal symptoms (iron-deficiency anemia, alopecia, recurrent abortion, Breath Test, continued “there was a risk of not properly diagnosing a very high percentage of celiac disease patients if their screening is based solely on serological tests” etc.) but without gastrointestinal symptoms, whereas silent celiac disease is defined by the presence of a gluten-sensitive enteropathy not accompanied by any symptoms, but identified during the course of screening of high-risk groups such as first-degree relatives of celiac patients, patients with insulin-dependent diabetes, Down’s syndrome, IgA deficiency and thyroid disorders.

In detecting silent celiac disease sorbitol H2 -BT seems to be better than serological tests. We found that EmA were positive in 77/96 (80.80%) and sorbitol H2 -BT was positive in 94/96 (97.91%) of patients with sub-clinical celiac disease, whereas EmA were positive in 17/27 (62.96%) and sorbitol H2 -BT was positive in 26/ 27 (96.29%) of patients with silent celiac disease (p<0.001 in both forms of celiac disease). The best cut-off value in ppm and minutes in both forms of celiac disease are higher and shorter in the severe form rather than in the mild form of intestinal damage respectively (p<0.001 in both forms)13. Therefore sorbitol excretion seems to be closely correlated with the severity of histological lesions.

Sorbitol H2-BT as Screening Test in Relatives of Celiac Disease Patients

The prevalence of celiac disease among first-degree relatives has been reported to be about 10- 20%, and approximately 50% of the newly diagnosed cases are asymptomatic(14,15). It is known that lymphoma and cancer deaths(16,17) occur more frequently in first-degree relatives of celiac disease patients, and it is also known that gluten withdrawal has a protective role in the complications associated with the disease(18). However, up to 50% of celiac disease relatives show mild histological damage without evident mucosal atrophy(19-21). Since several recent studies showed that serological tests are ineffective in detecting celiac disease in patients with mild histological damage, there is a concrete risk that a significant proportion of celiacs among relatives may be missed. Since a routine intestinal biopsy in all family members is, however, unfeasible—asymptomatic individuals would rarely accept such an approach—it is very important to identify an optimal non-invasive method of screening first-degree relatives. In this regard sorbitol H2 -BT screening seems to be better than serological tests.

In my experience, sorbitol H2 -BT is extremely effective at detecting histological damage in relatives of those with celiac disease. We found that AGA, EmA and anti-tTG showed strong positivity only when there was severe intestinal damage (Marsh IIIb-c lesions—but overall positivity was 36.73%, 38.78%, and 44.89% for AGA, EmA and anti-tTG respectively), whereas sorbitol H2 -BT showed a strong positivity in patients with only mild histological damage (Marsh I - IIIa—overall positivity was 83.67%). A significant proportion of celiac disease patients will be missed if relatives of those with celiac disease are screened only via serology(22).

Sorbitol H2-BT in Assessing Histological Recovery after a Gluten-free Diet

Currently the only effective therapeutic approach to celiac disease is the gluten-free diet, and the result of a proper gluten-free diet is clinical and histological improvement. In particular, the gluten-free diet plays a key role in preventing nutritional deficiency, especially of micronutrients, and in reducing the risk of the development of intestinal malignancies. There is great demand for highly sensitive, non-invasive tests that can be done to determine histological recovery in patients after the start of a gluten-free diet—with the ultimate goal of reducing or eliminating the need of follow-up endoscopies and biopsies.

If we consider EMA an indicator of small bowel damage, it would be expected to persist until histological recovery occurs. However, several recent studies failed to show a positive relationship between EMA and histological improvement after a gluten-free diet(23-26). Our study confirmed these experiences, since microscopic damage persists at histological examination during the follow-up despite EMA negativity. It is difficult to explain the poor predictor value of EMA in assessing histological recovery. EMA positivity seems to be related not only to the length of intestinal involvement but also to the grade of histologic damage(4) . Thus, when histological damage improves we can note a false EMA negativity, since histological lesions improve more slowly than EMA seroconversion. Moreover, EMA are a marker of the immunological activity related to the gluten sensitivity, it is therefore hypothesized that after a period of gluten restriction the immunological process can be quite inactive and thus EMA will subside.

Similarly, anti-tTG do not seem effective to assess histological recovery in the follow-up of celiac patients after they have started a gluten-free diet due to its poor correlation with histological damage. Anti-tTG is generated in genetically predisposed individuals by complexes formed between anti-tTG and gluten(27). So, it is hypothesize that anti-tTG should disappear soon after gluten withdrawal, and these findings have been frequently recognized in our clinical practice, for example we sometimes see a quick subsiding of anti-tTG values soon after patients begin a gluten-free diet—in some cases within few weeks.

In my experience, sorbitol H2-BT seems to be very effective even in assessing histological recovery after gluten-free diet. We found a strict correlation between cut-off values (in ppm and minutes) of H2 excretion and the patients’ histological lesions. In particular, maximal cut-off values (in ppm and in minutes) correlate statistically with a more severe degree of intestinal damage—patients with more severe histological lesions had higher cut-off value H2 levels and earlier peaks (in minutes). Likewise, we found that progressive histological recovery correlated significantly with decrease of maximal cut-off values (in ppm) and with the later appearance of the peak (in minutes). This is a very important finding, since it permits us to observe and to monitor the progressive improvement of the histological damage of small bowel after a gluten-free diet—without any small bowel biopsy(28, 29).

Sorbitol H2 -BT in Borderline Entheropathy

A clinical problem arises when patients present with symptoms suggestive of gluten sensitivity (diarrhea, weight loss, unresponsive iron-deficiency anemia, etc.) but small intestinal biopsies reveal only minor abnormalities, particularly lymphocytosis with or without crypt hyperplasia (Marsh I-II lesions). It is hypothesized that some of these patients have borderline celiac disease. A gluten challenge may be a good choice in these patients, as it may provoke a significant worsening of the mucosal lesions, which could lead to a correct diagnosis. This approach, however, may not be necessary if we have a sensitive non-invasive method to detect such mild intestinal lesions. Serological tests are insufficient in this area. We recently found that AGA, EmA and anti-tTG were positive in 0-20% of patients showing Marsh I-II lesions, whereas sorbitol H2 -BT was positive in 18- 41% of such cases(30). Clearly this data shows that it makes sense to use Sorbitol H2 -BT to detect cases of borderline entheropathy.

Factors Affecting Sorbitol H2-BT in Clinical Practice

Unfortunately, several factors may affect the results of sorbitol H2 -BT. First of all, sorbitol H2 -BT shows high sensitivity but low specificity. Several small bowel disorders, including Crohn’s disease, are associated with excessive rates of H2 breath excretion and then with sorbitol H2 -BT positivity(31). Moreover, the breath tests will be positive in the setting of not only small bowel mucosal injury, but also in cases of rapid intestinal transit and small bowel bacterial overgrowth(32). Finally, despite its low cost, the breath test is quite cumbersome, since it requires an overnight fast followed by at least 4 hours of the patient’s time for testing.

Conclusion

Sorbitol H2 -BT is a simple, feasible, repeatable, cheap, non-invasive test that can accurately assess intestinal absorption. Unfortunately low specificity may affect the results and may make it difficult for us to distinguish the different causes of malabsorption using only the sorbitol H2 -BT results. On the other hand, sorbitol H2 -BT may be very helpful and seems to be very promising in the following areas:

• Identifying patients suspected of having celiac disease with mild intestinal damage, who are serologically negative for celiac disease;
• Screening relatives of patients with celiac disease;
• Monitoring dietary compliance to the gluten-free diet

Although intestinal biopsies will remain the “gold standard” for assessing the state of small bowel, sorbitol H2 -BT is a very interesting and non-invasive test that has the potential to reveal just how large the current “black hole” in celiac disease diagnosis is. At the very least it can help diagnose patients whose complaints cause us to suspect celiac disease but who have negative blood tests, and it is an excellent method to monitor the recovery of patients who are on a gluten-free diet. It is a key part of my medical practice in the treatment of celiac disease.

References:

1. Martucci S, Biagi F, Di Sabatino A, Corazza GR. Coeliac disease. Dig Liver Dis 2002; 34(suppl. 2): S150-3.
2. Rostami K, Kerckhaert J, Tiemessen R, von Blomberg ME, Meijer JWR, Mulder CJJ. Sensitivity of antiendomysium and antigliadin antibodies in untreated celiac disease: disappointing in clinical practice. Am J Gastroenterol 1999;94: 888-94.
3. Dickey W, Hughes DF, McMillan SA. Reliance on serum endomysial antibody testing underestimates the true prevalence of coeliac disease by one fifth. Scand J Gastroenterol 2000;35: 181-3.
4. Tursi A, Brandimarte G, Giorgetti GM, Gigliobianco G, Lombardi D, Gasbarrini G. Low prevalence of antigliadin (AGA) and anti-endomysium (EMA) antibodies in subclinical/silent celiac disease. Am J Gastroenterol 2001;96: 1507-10.
5. Abrams JA, Diamone B, Rotterdam H, Green PHR. Seronegative celiac disease: increased prevalence with lesser degrees of villous atrophy. Dig Dis Sci 2004;49: 546-50.
6. Washüttl J, Reiderer P, Baucher E. A qualitative and quantitativestudy of sugar-alcohols in several foods. J Food Sci 1973;38: 1262-3.
7. Ojetti V, Nucera G, Migneco A et al. High prevalence of celiac disease in patients with lactose intolerance. Digestion 2005;71: 106-10.
8. wagerty DL Jr, Walling AD, Klein RM. Lactose intolerance. Am Fam Physician 2002;65: 1845-50.
9. Strocchi A, Ellis C, Levitt MD. Reproducibility of measurement of trace gas concentrations in expired air. Gastroenterology 1991;101: 175-9.
10. Corazza GR, Strocchi A, Rossi R, Sirola D, Gasbarrini G. Sorbitol malabsorption in normal volunteers and in patients with coeliac disease. Gut 1988;29: 44-8.
11. Pelli MA, Capodicasa E, De Angelis V, Morelli A, Bassotti G. Sorbitol H2-breath test in celiac disease. Importance of early positivity. Gastroenterol Int 1998;11: 65-8.
12. Tursi A, Brandimarte G, Giorgetti G. Prevalence of anti-tissue transglutaminase antibodies in different degrees of intestinal damage in celiac disease. J Clin Gastroenterol 2003; 36(3): 219-221.
13. Tursi A, Brandimarte G, Giorgetti GM. Sorbitol H2- breath test versus anti-endomysium antibodies for the diagnosis of subclinical/ silent coeliac disease. Scand J Gastroenterol 2001;36: 1170-2.
14. Marsh MN. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunologic approach to the spectrum of gluten sensitivity (celiac sprue). Gastroenterology 1992;102: 330-54.
15. Auricchio S, Mazzacca G, Tosi R, Visakorpi J, Maki M, Polanco I. Coeliac disease as familial condition: identification of asymptomatic patients within family groups. Gastroenterol Int 1988;1: 25-31.
16. Barry RE, Morris JS, Kenwright S, Read AE. Coeliac disease and malignancy. The possible importance of familial involvement. Scand J Gastroenterol 1971;6: 205-207.
17. Stokes PL, Prior P, Sorahan TM, McWalter RJ, Waterhouse JA, Cooke WT. Malignancy in relatives of patients with coeliac disease. Br J Prev Soc Med 1976;30: 27-21.
18. Holmes GKT, Prior P, Lane MR, Pope D, Allan RN. Malignancy in coeliac disease – effect of gluted free diet. Gut 1989;30: 333-8.
19. Corazza GR, Valentini RA, Frisoni M ETAL. Gliadin immune reactivity is associated with overt and latent enteropathy in relatives of celiac patients. Gastroenterology 1992; 103: 1517-22.
20. Maki M, Holm K, Lipsaen V, Hallstrom O, Viander M, Collin P et al. Serological markers and HLA genes among healthy first-degree relatives of patients with coeliac disease. Lancet 1991;338: 1350-3.
21. Vazquez H, Cabanne A, Sugai E, Fiorini A, Pedreira S, Maurino E et al. Serological markers identify latent coeliac disease among first-degree relatives. Eur J Gastroenterol Hepatol 1996;8: 15-21.
22. A. Tursi, G. Brandimarte, G.M. Giorgetti, C.D. Inchingolo. Effectiveness of sorbitol H2 breath test in detecting histological damage among relatives of coeliacs. Scand J Gastroenterol 2003;38: 727-31.
23. Bardella MT, Trovato C, Cesana BM, Pagliari C, Gebbia C, Peracchi M. Serological markers of celiac disease: is it time to change? Digest Liver Dis 2001;33: 426-31.
24. Valentini RA, Andreani ML, Corazza GR, Gasbarrini G. IgA endomysium antibody. A valuable tool in the screening of coeliac disease but not its follow-up. Ital J Gastroenterol 1994;26: 279-82.
25. Sategna-Guidetti C, Grosso SB, Bruno M, Grosso S. Is human umbilical cord the most suitable substrate for the detection of endomysium antibodies in the screening and follow-up of coeliac disease? Eur J Gastroenterol Hepatol 1997;9: 657-60.
26. Dickey W, Hughes DF, McMillan SA. Disappearance of endomysial antibodies in treated celiac disease does not indicate histological recovery. Am J Gastroenterol 2001;95: 712-4.
27.  Dieterich W, Ehnis T, Bauer M et al. Identification of tissue transglutaminase as the autoantigen of celiac disease. Nat Med 1997;3: 797-801.
28. Tursi A, Brandimarte G, Giorgetti GM. Sorbitol H2- breath test versus antiendomysium (EMA) antibodies to assess histological recovery after gluten-free diet in coeliac disease. Dig Liver Dis 2002;34: 846-50.
29. Tursi A, Brandimarte G, Giorgetti GM. Lack of effectiveness of anti-transglutaminase antibodies in assessing histological recovery after gluten-free diet in celiac disease. J Clin Gastroenterol 2003;37: 381-5.
30. Tursi A, Brandimarte G. The symptomatic and histological response to a gluten-free diet in patients with borderline enteropathy. J Clin Gastroenterol 2003;36: 13-7.
31. Tursi A, Giorgetti GM, Brandimarte G, Elisei W. High prevalence of celiac disease among patients affected by Crohn’s disease. Inflamm Bowel Dis 2005;11: 662-6.
32. Nucera G, Gabrielli M, Lupascu A et al. Abnormal breath test to lactose, fructose and sorbitol in irritable bowel syndrome may be explained by small intestinal bacterial overgrowth. Aliment Pharmacol Ther 2005;21: 1391-5.

Celiac.com 10/06/2005 - You’ve all heard the joke proclaiming that “denial is not a river in Egypt.”  No, it’s not.  What it is, though, is a very real issue for many, if not most people who have been diagnosed with celiac disease or gluten sensitivity.  There are a couple of types of denial—the first type affects us—while the other type affects those around us.

When We’re in Denial
Many people who are diagnosed—or when their kids are—go through some type of denial.  It usually occurs at a few key times after diagnosis—and for a few different reasons, here are some examples:

1. Immediate denial—the diagnosis isn’t right.  Nope.  Couldn’t be.  I don’t know anyone who has that.  I don’t even know what gluten is.  I’ve never heard of celiac disease.  I don’t have symptoms…my symptoms are mild.  It’s just lactose intolerance, I’m sure.  I don’t have diarrhea, so I couldn’t have that.  I’m overweight, and all celiacs are skinny.  My results were inconclusive.  Someone must have made a mistake.  All of these thoughts can be symptoms of denial.
2. A few weeks into the diet—I don’t think that diagnosis was right.  This is when the reality of doing this for the rest of your life sets in.  One angel (the good one, of course) sits on one shoulder whispering, “You know you need to stay gluten-free—keep it up—you can do it! Mmmm, yummy cheese on this gluten-free toast.  The other shoulder is home to the Devil-in-Denial: “No way are you going to another happy hour and order wine and celery sticks while all the other guys are drinkin’ beer and deep-fried stuff.  You don’t have no stinkin’ intolerance.  Come on—just one beer...and one piece of pizza.  It won’t hurtcha.  No stinkin’ intolerance…”  This is really just a period of ambivalence, hoping beyond hope that you don’t really have this condition, choosing to lean toward believing you don’t.
3. Danger zone:  I never had that.  The most dangerous type of denial occurs several months into the diet, when all of a sudden you realize you feel so good that you don’t even remember the last time you felt bad.  That’s when people often think, “I knew I just needed a little bit of time to get over that bug I had!  I feel great.  I’ll bet I never even had anything wrong with me.”

When Others are in Denial
Then there’s the type of denial that our family members and loved ones express.  Ask anyone who is gluten intolerant or has been diagnosed with celiac disease if they have relatives who won’t be tested, and chances are, you’ll get a surprised look as though you just guessed what color of underwear they’re wearing, and a “yeah, how did you know?”  Because we all have them.  Well, most of us do.  Why is it so hard for our relatives to believe they might have this?  It is, after all, one of the most common genetic diseases one can have—and it does run in the family.  Yet we’ve all heard comments like:

• No, I don’t have that (blunt, bold, and full-on denial).
• I don’t think I need to be tested (oh, really, and that would be because….?!?)
• I was tested once, and the tests were negative (remember, once-negative does not mean always negative—also remember there are false negatives).
• I was tested, and my results were inconclusive, so I don’t think I have it (inconclusive may be a euphemism for mildly positive).
• I don’t have any symptoms (oh, really?  There are about 250 symptoms, and you have NONE?)
• My symptoms really aren’t that severe; I can live with them (so you’ll just wait till you’re really sick and doing long-term damage to start trying to improve your health?).
• I couldn’t do the diet anyway, so I’m not going to bother being tested (now there’s a rational argument for you).

Bottom line is they don’t want to have celiac disease, or they don’t want to give up gluten.  Some of your relatives may even refuse to believe you have it.  I’ve met many people with celiac disease who have been accused of being hypochondriacs or neurotic.

The problem with denial is that it justifies eating gluten.  When you have this epiphany “realizing” that you don’t have celiac disease or don’t need to be gluten-free, it’s tempting to run, not walk, to the nearest Krispy Kreme outlet.

Resist the temptation.  If you’ve been on the diet for awhile, then yes, you feel great, but it’s because you’re not eating wheat or gluten, not in spite of it.  The danger in testing the waters is that you may not have any reaction when you do, and then you’re likely to jump to the obvious (by which I mean “desired”) conclusion and confirmation that you never needed to eliminate wheat or gluten in the first place.

If you still wonder whether or not you have a medical reason for cutting gluten from your diet, here are a few things you can do to help solidify things in your mind:

• Get properly tested.
• Get a second (or third) opinion.
• Talk to other people who have been diagnosed with the same condition about your symptoms and your feelings of denial (chances are they’ll grin and say, “Yep, I felt that way at one point, too”).
• Write it down: List your symptoms, the symptoms of the condition, and how you feel if you’ve been following the diet.  Sometimes seeing it in writing is the just the proof you need.

Denial, by the way, is one of the most compelling arguments in support of proper testing and diagnosis.  If you’ve been confirmed with a diagnosis, you may be tempted to fall into a state of denial, but it’s going to seem pretty silly, even to you.

But also keep in mind that if you’ve been tested and your results were inconclusive or negative, you may need to consider re-testing or other alternatives.  The tests have changed over the years, and maybe your tests were done long ago.  There are also false negatives; and you can be triggered at any point in your life, so just because you were negative once doesn’t mean you’ll be negative again.  And finally, there are people who are negative on all of the tests, yet their health improves dramatically on a gluten-free diet.  Go figure.

Remember, if it looks like a duck, walks like a duck, and quacks like a duck, it’s most likely a duck, even if you wish it were a pigeon.

Celiac.com 01/11/2006 - There is an abundance of stories about people who begin a gluten-free diet, find that they feel better then decide they want a firm diagnosis of celiac disease. They are facing several problems. First, they may be gluten sensitive without the intestinal lesion of celiac disease. This is very likely since about twelve percent of the population is gluten sensitive, but only a little more than one percent of the general population has celiac disease. Another problem faced by gluten-free individuals who want a diagnosis is that it can take more than five years after returning to a regular gluten-containing diet before the characteristic damage of celiac disease can be seen on a biopsy¹. Simply put, after beginning a gluten-free diet, only a positive biopsy is meaningful. A negative biopsy does not rule out celiac disease.

A variety of opinions have been offered regarding how much gluten, for how long, should result in a definitive biopsy. The reality is that no such recommendation is consistent with the medical literature^1-4. Some people with celiac disease will experience a return of intestinal damage within a few weeks of consuming relatively small amounts of gluten. Such brief challenges are valuable for these individuals. However, many people with celiac disease or dermatitis herpetiformis will require much larger doses of gluten, over much longer periods, to induce characteristic lesions on the intestinal wall. Unfortunately for these latter individuals, a negative biopsy after a brief gluten challenge can, and often is, misinterpreted as having ruled out celiac disease. Blood tests can compound this problem. If, as seems likely, celiac patients who are slow to relapse are also the ones who develop milder intestinal lesions, they are the very celiac patients for whom blood tests are very unreliable⁵. Claims to have ruled out celiac disease based on brief challenges with small quantities of gluten is a mistake that could lead to serious, even deadly, consequences.

We may forget that gluten consumption by a person with celiac disease can lead to deadly cancers and a variety of debilitating autoimmune diseases. Any recommendation of a gluten challenge should be accompanied by a clear warning that the process may overlook many cases of celiac disease. The absence of such warnings is inexcusable.

And what about non-celiac gluten sensitivity? The absence of an intestinal lesion does not rule out gluten induced damage to other tissues, organs, and systems. Evidence and research-based information in this area is sadly lacking but we do know that undigested or partly digested gliadin can damage a wide range of human cells⁶. Thus, one need only be consuming gluten and experience increased intestinal permeability for gluten-induced damage to be a factor in an almost infinite number of ailments.

There are several partial answers to this problem. One, which Ive raised before, is to employ Dr. Michael N. Marshs rectal challenge for the diagnosis of celiac disease, particularly when the individual has already begun a gluten-free diet. This test permits a definitive diagnosis of celiac disease for up to six months after beginning a gluten-free diet. That would catch a great number of celiac patients who have found relief through a gluten-free diet and now want a diagnosis. Another piece of this puzzle is to test for IgG anti-gliadin antibodies. Although these antibodies are considered "non-specific," they inarguably identify an immune response to one of the most common foods in a regular North American diet. Although these individuals may experience improved wellness on a gluten-free diet, we just dont know enough about non-celiac gluten sensitivity to do more than recommend that they continue on this diet since it makes them feel better.

Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be ordered at Celiac.com. Rons Web page is: www.DangerousGrains.com.

References: