Celiac.com 04/22/2023 - Celiac disease is an autoimmune disorder that may occur in genetically susceptible individuals. It is initiated by ingestion of gluten present in cereals, primarily wheat and to a much lesser extent other cereal proteins such as prolamines of barley and rye. Celiac disease is characterized by malabsorption resulting from inflammatory injury to the small intestinal mucosa. The classical symptoms of celiac disease include diarrhea, weight loss and malnutrition, however, only a small percentage of patients with celiac disease present with classical symptoms. Such patients represent the tip of the iceberg of gluten sensitivity. Many patients with celiac disease may present with short stature, iron and folate deficiency, anemia, bone loss, aphthous stomatitis, arthralgia, and dental enamel defects. Because of the varying and mild clinical presentations, celiac disease is often diagnosed when the patient has grown to adulthood rather than as a child. Adults may present with iron deficiency, anemia, macrocytic anemia and hypocalcemia.

Diagnosis based solely on clinical criteria can be misleading and may lead to improper diagnosis and treatment as a result of the variety of clinical presentations often seen in other conditions. Problems with diagnosis has a serious impact on the patient. Delays in diagnosis commonly extend 10-13 years from the first presentation of clinical symptoms, leaving the patient subject to chronic symptoms while searching for proper diagnosis. Failure to diagnose this condition in the short term may predispose an individual to long term complications such as splenic atrophy and intestinal lymphoma. On the other hand, attempts to diagnosis a patient based primarily on clinical criteria may unnecessarily place the individuals on life long gluten-free diet as several transient conditions may mimic celiac disease clinically.

(Howelle PD, Is Coeliac Disease a Pre-Malignant Condition? Gastrointestinal Immunology and Gluten-Sensitive Disease, 1994. p.185)

The true prevalence of celiac disease is difficult to ascertain. However, with the advent of serum antibody methods, incidences as high as one in 300 have been described in the general population, both in Western Europe and in the U.S. celiac disease is prevalent worldwide, but may be rare in individuals of Chinese and Japanese descent.

Guandalini S & Gupta P Clin appl Immun Rev 2:293-305, 2002

Historically, the diagnosis of celiac disease was based primarily on histological studies of the Jejunal biopsy characterized by villous atrophy, crypt hyperplasia, and lymphocytic and plasma cell infiltrate in the lamina propria. Histological examination of the small intestinal biopsy remains the gold standard for diagnosing celiac disease, but has its limitations. Many patients with celiac disease are small children and histological studies may be viewed by many, especially a child’s parents, to be a great discomfort. There may also be problems with accuracy. Occasionally, a biopsy with abnormally high density of intraepithelial lymphocytes with a normal villous architecture may be reported as normal. It has also been reported that some patients with latent or even active celiac disease show normal histopathology (Gastroenterlogy 104:1263-72, 1993). Celiac disease might also be confused with other disorders when diagnosed histologically. Parasitic infections (giardia lamblia) and malabsorption syndrome, for example, may mimic celiac disease histology.

As these limitations have been recognized, serum antibody tests have gained acceptance in screening for celiac disease and in follow-up of patients with celiac disease to determine their compliance to a gluten-free diet. The various serological tests employed in the work-up of patients suspected to have celiac disease include anti-gliadin antibody (AGA), anti-endomysial antibody (EMA), anti-reticulin antibody (ARA) and anti-tissue transglutaminase (tTG) antibody tests. Antibodies to gliadin and tTG are detected by ELISA, whereas endomysium and reticulin antibodies are detected by indirect immunofluorescence. Of the serum antibody tests, EMA and tTG antibody primarily detects antibodies of IgA immunoglobulin isotype, whereas the AGA test detects both IgG and IgA isotypes. No IgM class antibodies to these antigens are detected in patients with celiac disease, hence there is no need to test for IgM class antibodies in the work-up of patients with celiac disease.

Of these tests, AGA was the first to be described in the literature and has been evaluated most extensively. AGA of IgG are more sensitive but less specific then IgA-AGA. The major utility of IgGAGA is in celiac disease patients who are IgA deficient. In a study conducted recently in our laboratory, all of the 15 IgA-deficient celiac disease patients were found positive for IgG-AGA and negative for IgA-AGA and other autoantibodies (Celiac Disease and IgA deficiency: How effective are the serological methods of diagnosis? Clinical diagnostic lab Immunology 9:1295-1300, 2002).

EMA and ARA are very specific indicators of celiac disease. These assays are immuno-histochemical methods and require experience in reading immunofluorescence reactions. Some investigators suggest that they are less sensitive. However, in all the studies conducted since our laboratory first described EMA back in 1983, we find the EMA assay to be 100% specific and sensitive for celiac disease. Other investigators may find EMA to be less sensitive due to the selection of the substrate, fixation of tissue sections, specificity of conjugate employed or serum screening dilution. Internally, we find that testing for EMA at dilutions of 1:2.5 or 1:5 yield 5% of patients positive for EMA yet negative at 1:10 or 1: 20. It could be that some of the investigators who have reported low sensitivity might be screening the patients at high serum dilutions.

Since the identification of tTG as the endomyisal antigen, ELISA methods have been described for detecting antibodies in the sera of patients with celiac disease. The advantage of the anti-tTG antibody assay is that it is an automatable assay that is less subjective than EMA and it is more sensitive and specific than AGA. For these reasons, many laboratories have opted to use the tTG antibody method as the screening method. In these laboratories, it may be the only assay used for detection of celiac disease cases. In the majority of studies of the tTG antibody method, the specificity and sensitivity were found to be between 90-95%. Table 4 on page 15 summarizes the specificity of the AGA, EMA and tTG antibody methods most commonly employed by laboratories performing tests for celiac disease.

If the prevalence of undiagnosed celiac disease is 4.8 per thousand as reported by Lagerqvist et al (J Intern Med 250:241-48, 2001) then of all the serological methods, EMA is the only method that provides 100% positive and negative predictive value for celiac disease. This raises the question of the optimum method of screening for celiac disease. The answer will vary according to the likelihood of celiac disease in the population studied and upon the experience of the laboratory performing the test. Some investigators may use the AGA or tTG antibody methods for screening and, if positive, confirm using the EMA test. We recommend this approach as it also helps to identify all celiac disease patients, whether IgA-deficient or not.

Celiac disease patients are prescribed a gluten free diet for life. Serological tests are useful in monitoring a patient’s response and adherence to the gluten free diet. The levels of the various antibodies (AGA, EMA, ARA and tTG) decrease and eventually disappear in the majority of the patients on a complete gluten free diet. Similarly, these antibodies either appear or rise in level when the patient is on a gluten containing diet. Serological methods, therefore, play a significant role in both diagnosis and follow-up of celiac disease patients.

Celiac disease has been associated with many other autoimmune disorders such as type 1 diabetes, thyroid autoimmunity and other autoimmune disorders. Approximately five percent of patients with type 1 diabetes have celiac disease. Similarly, approximately the same percentage of patients with celiac disease have type 1 diabetes. It has been proposed that early detection of celiac disease may be beneficial in such cases as it is believed that adherence to a gluten-free diet may delay the onset of diabetes. If true, this further emphasizes the utility of and need for serum antibody tests in the screening of population genetically susceptible for celiac disease.

In conclusion, clinical symptoms of celiac disease are variable and often mild, resulting in significant delays in diagnosis. The use of serological tests has improved the ease of detection, monitoring, and hence— the continuing care of celiac disease patients.

Celiac.com 04/01/2023 - I confess. I’m a chocoholic! My favorite dessert is anything chocolate, but when I need a good, quick chocolate “fi x”, I often turn to this recipe. I’ve been making it for about 20 years now and, although it’s gone through many evolutions, it never fails to please.

My fondness for chocolate dates back to my childhood when almost all of our desserts were chocolate. We enjoyed chocolate cakes, chocolate pies, chocolate puddings, and chocolate cookies––but one of my favorites was chocolate brownies. I’ve recreated that recipe for you here—with a few wickedly decadent embellishments. Luckily, my husband is fond of chocolate too and will look for any excuse to eat it. Upon learning that chocolate comes from the cocoa bean––which is actually a legume–– he announced that he would increase his vegetable consumption by eating more chocolate! Whatever your excuse, Americans apparently LOVE chocolate––on average, we consume about 10-12 pounds of it each year.

But before you head to the kitchen, here are a few tips to assure success:

1. Use the best quality cocoa possible. I’m particularly fond of Ghirardelli unsweetened natural cocoa. Look for it at your local health food store. I also like Scharffen Berger natural cocoa, which can be found at kitchen or gourmet food stores. If you can’t fi nd these brands, I recommend Hershey’s natural cocoa which is available at grocery stores.
2. Be sure to use natural cocoa, not Dutch-processed or European-style cocoa. I get many questions on this topic so here’s the explanation: Natural cocoa is always acidic. Dutch processed cocoa is treated to make it alkaline instead of acidic. The baking powder in this particular recipe is designed to balance the acid in the natural cocoa. If you use Dutch processed cocoa, the PH level is “unbalanced” and the recipe won’t work.

Carol Fenster’s Gluten-Free Chocolate Brownies

Preheat oven to 350˚. Grease 8-inch square nonstick pan. Stir dry ingredients together (fl our to xanthan gum). Set aside. In large mixing bowl, beat butter, sugars, vanilla, and egg with electric mixer on medium speed until well combined. With mixer on low speed, add dry ingredients and hot water. Mix until just blended. Mixture will be somewhat thick. Stir in nuts and additional ingredients, if using (see options below). Spread batter in prepared pan with wet spatula. Bake 20 minutes. Cool brownies completely before cutting. Serves 12.

Double Chocolate Brownies: Add 1⁄2 cup gluten-free, dairy-free chocolate chips or finely chopped dark chocolate to batter. Bake as directed.

Chocolate Mint Brownies: Prepare batter as directed. Place half of the batter in greased 8 x 8-inch pan. Add a layer of your favorite gluten-free mints such as Junior Mint patties, taking care not to cut the patties. Top with the remaining layer of batter. Bake as directed.

Rocky Road Brownies: Prepare batter as directed. Stir in 1⁄2 cup gluten-free, dairy-free chocolate chips, 1⁄4 cup chopped walnuts, 1⁄2 cup dried cranberries, and 1⁄2 cup Jet-Puff® miniature marshmallows. Because of the additional ingredients, you will need to increase pan size to 11 x 7 or 13 x 9-inch pan. Bake as directed, extending baking time by 5 to 10 minutes, or until thoroughly baked. Cool completely before cutting.

Ingredients:

• 1 cup Flour Blend*
• 1⁄2 cup unsweetened cocoa (not Dutch) 
• 1⁄2 teaspoon baking powder
• 1⁄2 teaspoon salt
• 1⁄2 teaspoon xanthan gum 
• 1⁄4 cup melted butter or margarine 
• 1⁄2 cup brown sugar, packed 
• 1⁄2 cup granulated sugar
• 2 teaspoons vanilla extract
• 1 large egg
• 1⁄4 cup hot water (110º)
• 1⁄4 cup chopped walnuts (optional

*Flour Blend:

• 1 1⁄2 cups sorghum flour
• 1⁄2 cup corn flour
• 1 1⁄2 cups potato starch
• 1 cup tapioca.

Makes 4.5 cups. (To make corn flour, grind cornmeal in small coffee grinder until consistency of flour.)

Celiac.com 03/25/2023 - Researchers reported last month that they have discovered the cause of celiac disease: A small fragment of the gluten protein fails to break down and triggers the immune systems into action. In addition to discovering the key fragment that makes gluten so poisonous to celiacs, Dr. Chaitan Khosla, researcher and founder of the Celiac Sprue Research Foundation (CSRF), reports that he has also found a bacterial enzyme that breaks down the toxic peptide and appears to make gluten digestible and safe. The enzyme could well become the key to an oral medication for celiac disease.

The CSRF is a science-driven public charity that seeks to improve the quality of life of celiac patients by promoting research and development, and by enhancing awareness of the disease among scientists, healthcare professionals, consumer product manufacturers and the general public. Its primary goal is to translate emerging knowledge about celiac disease into a comprehensive plan for developing a therapeutic alternative to a gluten-free diet. Once the Foundation’s initial drug development strategy has been launched, it will use available resources to promote basic research that might lead to fundamentally new insights into the disease, and to improve technologies for detecting new patients of this seriously under-diagnosed disease.

It is anticipated that each of the therapeutic possibilities being researched by the CSRF will require 1-3 years of pre-clinical research before a suitable Investigational New Drug (IND) candidate can be identified for further clinical studies. Once an IND application has been successfully filed with the U.S. FDA or its European equivalent, extensive human clinical studies must be performed to thoroughly assess both the safety and efficacy of the drug candidate. These clinical trials can be expected to last 5-8 years before a prescription drug emerges in the marketplace. Until such studies are successfully completed, no candidate therapeutic agent can be considered suitable for use by celiac sprue patients.

The CSRF has ambitious and achievable goals if it can gain the immediate support of the celiac community. The CSRF is actively raising funds to help support the above research and development efforts.

Celiac.com 03/18/2023 - It can be very confusing to person newly diagnosed with gluten intolerance to sort through all the information that abounds about celiac disease and the gluten-free diet. The information is inconsistent—support groups are not saying the same things— why is there a difference? No wonder celiacs are confused.

Fundamentally, all the national support groups in the U.S. have missions that are similar—to serve and support persons with gluten intolerance. The five national groups: Celiac Disease Foundation (CDF), Gluten Intolerance Group® (GIG®), Raising Our Celiac Kids (R.O.C.K.), Celiac Sprue Association, Inc. (CSA/USA), and American Celiac Society all list this as their primary objective. So, what is the difference between them? Very little. All five have a network of support groups throughout the country—Chapters, Connections, and Partners. All provide local and national literature and support. All are 501c3 nonprofit organizations. Some groups are larger than others, but size alone does not determine the quality or value of the work that each does. Unfortunately, there will always be disagreements between similar organizations, and what constitutes a gluten-free diet seems to be where U.S. national groups disagree. Three groups follow the American Dietetic Association gluten-free guidelines, while the others do not.

The controversy surrounding the gluten-free diet began about 25- 30 years ago when the first gluten intolerance support groups began to form. At that time medical experts on celiac disease and the gluten-free diet were few and far between, and support groups were forced to develop their own gluten-free dietary guidelines. Some of the recommendations were based on the meager scientific information available at that time, and other recommendations were based on speculation, assumption, antidotal evidence or hearsay. Over the years the field of nutrition has seen fad diets come and go. If a disease treatment includes a diet, the thinking has often been ‘if some restriction is good, more is better.’ There have been some very restrictive diets developed over the years that most people fail to maintain. One example of this is the dramatic change in recommendations for the diabetic diet. Somewhere along the way, the gluten-free diet became one of those diets where it got more and more restrictive— without sound scientific evidence and reasoning for it.

In the last ten years, medical professionals—researchers, medical practitioners, dietitians and pharmacists have become more interested in and aware of celiac disease. Research data collected during this time has changed the face of celiac disease and the gluten-free diet. Health care professionals have developed expertise in all areas related to gluten intolerance diseases. Some dietitian experts now spend their time working solely in the area of gluten intolerance. These people have the ability to make sound recommendations about the diagnosis, care and treatment of celiac patients, including recommendations about the gluten-free diet.

Several years ago dietitians with expertise in gluten intolerance and the gluten-free diet began scrutinizing the original diet recommendations, and investigating the rationale and science behind those recommendations. They soon began to question the validity of the original recommendations. Their exhaustive research has helped to reshape the gluten-free diet into what became the revised 2000 American Dietetic Association Gluten-Free Diet recommendations. These dietary revisions were the result of joint work and partnerships among many researchers in the U.S. and Canada whose work has modernized the gluten-free diet.

The gluten-free diet has changed over the years, just as nearly every aspect of what we know about celiac disease has changed. Do today’s support groups still have the role of dictating what the gluten-free diet is—even when experts in the field have made new recommendations? As more and more celiac centers are created, support groups are finding that their roles are also changing. They no longer have to make decisions about what constitutes a gluten-free diet, but instead only have to disseminate information that has been prepared by experts. Change is difficult, but resistance to change can cause confusion, discontentment, lack of respect for support groups and professionals, anger and sometimes—outright hostility.

Some have questioned the American Dietetic Association’s gluten-free dietary recommendations, and have suggested that their science was weak or flawed. In response to this, and in response to the outcry by support group members and the medical community for a single, standard gluten-free diet, the National Gluten-Free Diet Project (NGFDP) has been created. The NGFDP will be the work of dietitians in Dietitians in Gluten Intolerance Diseases (DIGID) and a multi-disciplinary professional team. The final product will address areas of controversy and make recommendations based on sound science and well-documented research. Research information will be evaluated according to standards used for rating all research in the medical community. Will the NGFDP end the controversy? Not if people are not willing to accept science, but it will clearly provide a diet accepted by celiac professionals. To facilitate an agreement for the diet all national support groups will be invited to have input into the process.

DIGID dietitians are a highly energetic group of dietitians with expertise in the glutenfree diet. Soon they will have a published referral list for support group members, a speaker’s bureau and other exciting products and information.

Celiac.com 03/09/2023 - After nearly a year on a gluten-free diet, I now look back at my recovery to evaluate its success—the severe joint pain, muscle weakness, bone pain, fatigue, abdominal bloating, steatorrhea, and weight loss plagued me until my treatment commenced in earnest. Much of the extra-intestinal symptoms resolved within the first few months. However, the intestinal and stomach symptoms have taken much longer, and my weight loss recovery is ongoing. The road to recovery has been long and arduous. Many of us experience an array of residual and persistent symptoms even with the complete removal of gluten from our diets.

Intestinal Absorption

Traditionally, response to a gluten-free diet has been assessed by blood antibody tests and biopsies. It has long been known that the intestinal villi, seen in biopsy samples, do not always revert back to normal even after a prolonged gluten-free diet (1) . A recent study by Cummins et al. found that area of the villi improved significantly by three months on a gluten-free diet, but improved only slightly more during the six to 24 month period (2) . After two years on a gluten-free diet, the villi area increased to about four times that at diagnosis of CD, but was still only about half of normal. Similarly, Wahab et al. found that at two years of follow-up on a gluten-free diet, 37% of the celiac patients still had varying degrees of villous atrophy (3) . After five years, 12% of the adult patients had villous atrophy, of which half still had total villous atrophy. All children in the study recovered completely and recovered faster than the adults in long term follow-up.

Besides intestinal biopsy, assessment of serum IgA class endomysial antibody (EmA) has been evaluated as a predictor of intestinal mucosal recovery4 . However, EmA conversion from positive to negative status was not found to be a reliable predictor of complete mucosal recovery. Intestinal mucosal recovery was incomplete in 47% of patients who had become EmA negative after 12 months on a gluten-free diet, and EmA sensivitivity for total villous atrophy and partial villous atrophy was only 33% and 9%, respectively. Likewise, Cummins et al. found that even after two years on a gluten-free diet, patients who tested positive or negative for anti-endomysial antibodies showed no difference in villous atrophy (2).

Another assessment of recovery is disaccharidase activity, which can be deficient secondarily to mucosal injury from celiac disease. Disaccharides are sugars (such as lactose, sucrose, and maltose) which must be split by disaccharidases (enzymes produced by villi in the small intestine) to be absorbed properly as monosaccharides and utilized by the body. Disaccharides such as lactose and sucrose are likely to be malabsorbed in patients with villous atrophy2 . Cummins et al. found that lactase activity increased by more than double after two years on a gluten-free diet, but this was still only about 55% of normal. Similar two-year recovery patterns were seen for activity levels of sucrase (83% of normal) and maltase (79%), yet, because disaccharidase activities improve despite incomplete recovery of the surface lining, they are thought to be the main reason why clinical symptom relief comes early on in treatment. (1)

Gastrointestinal Symptoms

Fine et al. found that celiac patients initially experienced chronic diarrhea (79%), excessive flatulence (74%), abdominal bloating (68%), nausea (36%), vomiting (19%), and constipation (6%)5 . After one year on a gluten-free diet these gastrointestinal symptoms completely resolved with the exception of chronic diarrhea, although 17% of celiac patients had chronic diarrhea to a lesser extent than before starting the diet.

Anemia

Celiac patients’ anemia-related symptoms receded and resolved as normalization of hemoglobin levels correlated with intestinal mucosal improvement on a gluten-free diet, even without oral iron supplementation (6) . This finding suggested that iron absorption was inefficient due to villous atrophy, and that oral iron therapy may not be effective during the first six months of treatment. After six months on a gluten-free diet, 78% of adult celiac patients recovered from iron deficiency anemia based on an assessment of their hemoglobin levels, and only 28% were no longer iron deficient based on serum ferritin levels. From 12 to 24 months of treatment, 94% of the patients were no longer anemic; however, only 55% of the patients reversed from iron deficiency (i.e., iron absorption was greater than iron loss) after 24 months of treatment.

Bone

Osteoporosis and osteopenia are common findings in newly diagnosed and untreated celiac patients. The deficiency of serum vitamin D which results in secondary calcium malabsorption is associated with low bone mineral density at diagnosis. A five year study follow-up with of adult celiac patients on a gluten-free diet found that bone mineral density improves or may normalize over the long-term, but that nearly all of the improvement occurs in the first year (7) . Blood 25(OH) vitamin D, the active form of vitamin D, increased 14% in the first year of a gluten-free diet, and increased another 80% by the fifth year. A slight (7%) but significant increase in blood calcium was seen after the first year with a further slight increase by the fifth year. Villous atrophy changes and the adherence to a gluten-free diet did not correlate with bone mineral density improvement. Patients’ weight gain in the study was associated with an increase in their bone mineral density. In a separate one-year study, bone mineral density and bone metabolism markers significantly improved in 43 percent of CD patients despite incomplete mucosal recovery (8) . These markers improved even in postmenopausal women and patients with low serum vitamin D levels.

These studies confirm that recovery can take a long time and can often be incomplete in adults. Cummins et al. studied patients for villous atrophy up to 15 years after diagnosis, while most of the studies followed patients from one to five years after diagnosis. Indeed, more follow-up studies need to be performed to address the length of time it takes to achieve complete recovery in all aspects. To the extent that recovery is still incomplete, future studies need to identify and explain the reasons why.

Celiac.com 03/04/2023 - Being diagnosed as a celiac is always a bittersweet moment. On one hand, we are relieved to finally be able to point to the cause of our long-winded illness. On the other hand, we are inundated (or not) with information about the foods that we can no longer eat. For many of us finding out that we can no longer drink beer is quite a shock. Granted, good gluten-free bread seems to top the list of the most requested gluten-free products, and there are now satisfactory substitutes. When it comes to beer, however, there are no substitutes. Yes, we can drink wine and some other alcoholic beverages, but beer has always had a place in the hearts of the millions. Can you really drink a glass of wine while watching a ballgame or eating a pizza? We think not.

The key to brewing gluten-free beer is to understand why barley is deemed to be the perfect brewing grain and used as a base ingredient in almost every commercial beer on the world market. Since brewing beer is heavily based upon the principles of chemistry, determining alternative techniques and ingredients is very difficult, though not impossible. As diagnosed celiacs, we felt that by studying the chemical principles of malting and brewing, we could find a suitable gluten-free ingredient mix and brewing process that would result in high quality gluten-free beers. We also feel that using natural ingredients is critical to the beer’s quality, and we would not want to use any processed ingredients even if it meant lower costs. After several years of testing alternative grains and recipes, we were finally able to prove our hypothesis correct—high quality gluten free beer is not only a possibility—but is now a reality!

As part of our venture, we feel that it is also important to educate celiacs and non-celiacs about the issues of gluten and alcohol, obviously concentrating on beer. There have been claims by several companies that their beer is safe for celiacs. We have been unable to confirm or refute these claims— but we do know is this: lagers are deemed to have less gluten than ales, with the lighter lagers (such as pilsners) containing the least amount of gluten. Unfortunately, the global medical and scientific communities do not agree on a safe lower limit of gluten that people with celiac disease can ingest on a regular basis. Another area of controversy is based upon the lack of published research on the gluten sub-components known as peptides and their involvement in celiac disease. While most, though not all, gluten proteins are broken into the smaller peptides during the brewing process, it is unclear whether the remaining peptides are problematic for celiacs. More research is needed in this area before being able to recommend barley-based beers to celiacs.

After strong showings at The Gluten Free Living Conference of our Pale Ale and at the Celiac Sprue Association Conference of our Blonde Ale, we are extremely confident that commercial production will begin early in 2003. We have received a lot of e-mail inquiring about our beer and expressing the desire to get some as soon as possible. We are working as hard and fast as possible to make this a reality for all beer-drinking celiacs.

Celiac.com 02/24/2023 - Milk and milk products contain a natural sugar called lactose (see table below). People who are lactose intolerant or, more precisely, who are lactose maldigesters, lack enough of the enzyme lactase needed to completely digest the lactose into its simple sugars, glucose and galactose. Lactase is produced in the villi of the small intestine. Symptoms of lactose intolerance may include some or all of the following: cramping, bloating, nausea, headache and diarrhea. Symptoms can occur 15-30 minutes after digestion of lactose or as long as several hours later.

Lactose Intolerance and Celiac Disease

Many people with celiac disease, especially those who are newly diagnosed, may also develop secondary lactose intolerance. This is a temporary condition in which the level of lactase has fallen as a result of injury to the gastrointestinal tract. Once on a gluten-free diet, the villi begin to heal and the level of lactase increases back to normal levels. This process may take several weeks to months. For some, a temporary lactose-free diet may also be necessary, in addition to a life-long gluten-free diet, to control symptoms. There are a variety of products specially developed to help in the management of lactose intolerance:

1. Lactose-Reduced Milk and Ice Cream. The lactase enzyme has been added to regular milk and 99% of the naturally occurring lactose has been converted to simple, easily digested sugars. This milk tastes slightly sweeter than regular milk, but has the same nutritional value. Ice cream made with lactose-reduced milk is also available.
2. Lactase Enzyme Drops. These contain the lactase enzyme that can be added to liquid dairy products making them more easily digestible. Approximately 70-99% of the lactose is broken down based on the number of drops used.
3. Lactase Enzyme Tablet and Caplets. They are available in regular strength, extra-strength and ultra-strength and should be taken just before a meal or snack that contains lactose.
4. Non-Dairy Beverages. There are a variety of soy, rice, nut or potato-based beverages that can be substituted for regular milk. Be aware that some products may contain barley malt extract/fl avoring so read labels carefully. Choose gluten-free beverages that are enriched with calcium and vitamin D.

Table 1 *

Lactose Content of Selected Dairy Foods 

Food	Serving Size	Lactose (grams per serving)
Milk (whole, 2%, 1%, skim)	1 cup (250 mL)	11
Lactose Reduced Milk	1 cup (250 mL)	0.1
Cheddar Cheese	1 oz. (30g)	1
Cottage Cheese (creamed)	1 cup (250 mL)	6
Ice Cream	1 cup (250 mL)	12
Ice Milk	1cup (250 mL)	18
Sour Cream	½ cup (125 mL)	4
Yogurt (low fat)	½ cup (125 mL)	2.5**

*From the Gluten-Free Diet: A Comprehensive Resource Guide by Shelley Case, RD, Case Nutrition Consulting

**The lactose in yogurt is digested by the lactase enzymes in the active cultures. However, lactase activity in yogurt may vary from brand to brand. Yogurts that have cultures added after pasteurization have more lactase activity. Look for brand that contains “live” or “active” cultures.

Celiac.com 02/18/2023 - Chomp, chomp, chomp, chomp....GULP. Slurp, slurp, slurp, slurp....BELCH—this is the sound of "Fido" eating his scientifically formulated, well-balanced dog food. Most people know that you get what you pay for in a pet food and that the higher grade foods come from certain recognizable manufacturers and can only be found at specialty pet supply outlets. But, is that axiom true? Does purchasing the most expensive food guarantee that your pet will be receiving the best in nutrition that the industry has to offer?

Chomp, chomp, chomp, chomp....GULP. Slurp, slurp, slurp, slurp....BELCH—this is the sound of "Fido" eating his scientifically formulated, well-balanced dog food. Most people know that you get what you pay for in a pet food and that the higher grade foods come from certain recognizable manufacturers and can only be found at specialty pet supply outlets. But, is that axiom true? Does purchasing the most expensive food guarantee that your pet will be receiving the best in nutrition that the industry has to offer?

The wake-up call comes when one realizes that once the meat source is removed from the food, the remaining ingredients are mostly unnatural for the pet. If we exclude the beef, poultry, fish, and lamb, the remaining calorie sources are mostly wheat, barley, corn, rice, and oats, all of which are man-raised crops that the dog and cat would never consume in the wild. I love to inquire of my clients "How would your pet get rice—swim to Viet Nam?" But what is the problem with these complex carbohydrates being in the diet? Humans consume these with every meal and they are doing just fine, aren't they? Ahhhh—are we? If we were, those reading this would likely be reading something else right now, wouldn't they? The problem is that the grains listed above have some universal problems among humans and pets alike, as do a couple of other foods that eclipse even the grains with regard to health issues.

To digress for just a moment, I am a recovered celiac. For over forty years, I suffered like most other celiacs from a myriad of symptoms, including allergies, heart burn and intestinal problems, depression/ chronic fatigue, memory and balance difficulties, joint pain, and even fibromyalgia. I was taking at least four drugs twice daily; caffeine addicted, and was quite frankly not having any fun anymore. I am now two and a half years gluten AND casein-free, off all drugs, symptom-free, and feeling better than I did when I was twelve. This miraculous recovery got my attention as a patient and as a doctor. How could this be? How could I be suffering from what millions of people and pets were experiencing but get well in such a short period of time? How could all of these conditions be linked together?

The readers of Celiac.com and its publications have read many a testimony like this. Many have experienced similar responses while others are still wondering when wellness is going to happen to them. Those in the latter category have been trying to faithfully adhere to the gluten-free regime but are frustrated by the fact that they are making such huge sacrifices with less than optimal responses.

Well, "Fido" is about to teach us all something. The fact is that the celiac is a "who's who" of what is wrong with human beings but the conditions that we suffer from are not limited to those who walk upright. When I read the list of conditions that we as gluten intolerants experience, my first thought was that "This is me—this describes me to a T." My second thought was "...but this describes everything that is wrong with everyone, including their dogs and cats." And it does! Suddenly, medicine through the eyes of celiac disease (and other similar food intolerances) made sense. I tell everyone that it was like someone had finally put the right program into a stalled computer and it began operating at lightning speed. All of the idiopathic conditions that are so poorly understood in medicine became "open season" for this medical headhunter.

Soon the answers did come—one after another. I launched into two years of intensive research while applying the newly unveiled principles to my patients as well as myself. Miracles started happening around me. Allergies abated, intestinal problems cleared up, older pets became less painful and more active, and yes, even their epilepsy stopped. "Wait a second! Epileptic seizures stopped?", you may be asking. Yes, 100% of my epileptics have stopped having seizures, just like many celiac children that were placed on gluten-free diets have responded. I got the idea from the celiac literature. How that occurs is totally explainable but beyond the scope of this article.

In a nutshell, after all of my research into so many of the medical problems and conditions that plague pets and mankind, I concluded that the center of our health universe lies in that "J-shaped" stretch of intestine known as your duodenum. Most celiacs are aware of the pathophysiology of their condition and are familiar with the terms malabsorption and "leaky gut syndrome". But, many just don't understand all of the fine details.

There are three food ingredients that adhere to the villi of the duodenum and induce the change that is characteristic of celiac disease known as villous atrophy. These three substances are gluten (from the grains), casein (from cow milk products), and soy protein. What is it that links these substances together? For one, they are all used as adhesives. Yes, gluten, casein, soy and even corn are all used in industry as adhesives, some even being waterproof. Put "gluten", "casein", "soy protein adhesive" or "corn adhesive" in the search engine of any computer and read the responses. Wow!

As it turns out, the foods that are the "stickiest" are the ones that cause the most problems. For instance, casein and gluten are used for the most powerful adhesives. Therefore, it should be not be a shock that they are the number one and number two childhood food allergens according to the FDA. Number four is soy. Number three is egg (This is the first secondary allergen brought about by the damage done to the gut by the first two). Now, imagine these proteins leaving the stomach of a human or their pet. I have always used the illustration of three slices of pizza leaving our stomach. But, for the sake of this article, I will use a wheat, barley, or soy-based pet food to drive the point home. Now that you have an idea of where we are headed, you can imagine the stomach is filled with "glue"-containing food. This "glue" leaves the stomach after it has been worked on as much as possible by that organ. This, I believe, is the origin of most heartburn. As simple-stomached animals, our pets and we are not designed to eat grasses like the ruminants do and all of the grains are in that grass family. By adding extra acid, our stomach is doing its best to break down the "glue". Unfortunately it's just inadequate (Yes, my two years of acid reflux abated after just one week of being gluten-free, which should be no surprise). So, it is this remaining sticky substance that adheres to the villi of the duodenum, which are so vital for the absorption of nutrients. This coating reduces the amount of those essential ingredients absorbed.

What are those nutrients? The vital substances are calcium, iron, iodine, all B complex, vitamin C, most water-soluble vitamins, and most of our trace minerals such as zinc, boron, manganese, magnesium, etc. In other words, just about everything that is important other than our proteins, fats, and calories are absorbed by the duodenum. How well can this organ function when it is coated with "glue"? The important thing to realize here is that this happens to everyone and every pet that eats these foods. That bears repeating. This happens to everyone and every simple-stomach creature that eats these foods. We have simply focused on the "worst-of-the-worst"—the celiacs, casein intolerants, and soy intolerants—in which an immune response is mounted against the glue leading to severe villous atrophy. This immune assault also generates the warning antibodies that we call "allergies" to tell you that this process is taking place, otherwise, it would be a "stealth operation" that goes on undetected for years and years until the bottom falls out. Yes, this is all too familiar of a scenario, isn't it? It happens in pets all of the time, I'm afraid.

So, the ultimate question is whether pets suffer from celiac disease? My answer now is that it doesn't really matter. In the pet, every bite of the average commercial food has "glue" in it, whether it is of wheat, barley, soy, corn, or rice origin. Yes, there are better glues" than others and they are in line with what we see as the principle allergens in the pet, just as one would expect. Wheat and soy are the worst (now that dairy has been eliminated from pet foods) while oats and rice are the best—they happen to be the least sticky. Corn is in the middle. This is exactly what veterinarians see as the main sources of food allergies in the pet, a problem of huge importance in dogs and cats. Now people can understand why lamb and rice foods have become so popular. It does all make sense.

But celiac disease has occurred in the dog. It has been definitively identified in one breed, which is almost extinct now.... the Irish setter. This hapless breed was effectively sent the way of the buffalo when the industry added wheat, the number one dog and cat food allergen, to pet foods about 15 years ago. Thanks to the wheat-glut in this country, corn-based diets were quickly replaced with wheat and the subsequent decline in our pet's health began. Veterinarians found themselves wondering why the immune system of the dog and cat were having such problems, ranging from worsening allergies to a rapid rise in immune-mediated diseases. The answer was right before us. You don't add the number one dog and cat food allergen to the diet without having some major repercussions. The veterinary profession was just as shortsighted as the medical profession is today about the ramifications of consuming the top food allergens as the bulk of the diet. Around 60-70% of the American diet is comprised of cow milk products and wheat alone, with 40-50% being the number one food allergen—dairy products. There is a price to pay for this sort of ignorance and it is heavier than most realize.

The main cost is the disruption of duodenal function. Once the essential nutrients have been malabsorbed for a long enough time, Pandora's Box is opened. This may occur very early in life or very late, partly governed by the degree of immune-mediated component. The "worst of the worst" will experience severe problems by the time they are adolescents while the more resilient will not be affected until late in life. But, as I tell my clients, I believe that with the top three foods...wheat, dairy and soy...it is a matter of when they cause problems, not if. The "glue" will eventually affect everyone and every pet with its nutrient-blocking qualities.

Suddenly, conditions such as hip dysplasia, elbow and shoulder problems, intervertebral disc syndrome, cruciate ligament ruptures, and even heart valve failure all have better explanations. All of these problems are caused by failing cartilage and connective tissue, both of which are structured similarly and made up of calcium and collagen. Collagen is the building block of most of your skeletal support structures. The principle component of collagen is vitamin C. Therefore, when it is understood that calcium and vitamin C are absorbed by the duodenum, then it is easily seen that inadequate amounts of these in the diet or failure of their absorption will compromise the integrity of these structures—all of them.

Now, imagine that a German shepherd puppy begins eating a wheat, barley, corn, or soy-based diet from the moment it is weaned. If inadequate levels of calcium and vitamin C are absorbed, what are the chances that its hips, elbows, spine, and other cartilaginous structures are going to form properly? I would say "not good". Most people familiar with dogs know that this breed has a reputation for horrible hip dysplasia. But, they also have serious allergies and other immune-related disorders. These, we can see now, are all likely to be interrelated.

I used to be concerned that the veterinary profession had somehow missed the incidence of celiac disease in breeds other than the Irish setter. But, now that I understand the effects of the "glue" on the absorptive ability of the duodenal villi, I believe this possible oversight to be much less important. I believe the same to be true for humans. The "glues" affect all that consume them. Certainly, the "worst of the worst"— the celiacs, casein intolerants, and soy intolerants—have the most to be concerned about. But with these troubled foods, for all that consume them, it is a matter of when they will create a problem, not if.

“No Gluten” means avoiding all wheat, rye, barley, malt, kamut, spelt, triticale, graham flour, and contaminated oats.  But that won’t stop anyone who loves chocolate chip cookies from finding an alternative way to make them!  On a gluten-free diet, combinations of substitute flours are used (see Table 1).

Once you have the magic combination of gluten-free flours, add a little more flavoring, a little more leavening, and voila!  You have wonderful chocolate chip cookies!
But how do you make those cookies if you are also allergic to dairy products?  Do not despair.  There are viable alternatives to all ingredients.  Allergies to dairy products may be a reaction to the lactose in dairy products (the natural sugar in milk), to casein (milk protein), or to both.

Lactose is often used in breads, cakes, cereals, cooking mixes, prepared meats and fish, and in soups.  Tuna fish often contains sulfites and has lactose in the broth.  It is even found in some medications.  Read labels constantly for hidden lactose.  Some lactose-sensitive people may tolerate un-pasteurized yogurt because yogurt cultures produce the enzyme lactase, which breaks down lactose into a simpler, more readily-digestible form.  This also applies to buttermilk and some cheeses.

Casein is the protein found in milk.  Fortunately, cow’s milk is one of the easier ingredients to substitute in cooking; use equal amounts of soy milk, rice milk, coconut milk, water, or fruit juices.  Read labels—beware of products labeled “Dairy Free”, like Cool Whip, which often contain casein (milk protein).  Some non-dairy cheese substitutes made from soybeans and almonds may still contain casein to give them a more authentic texture.  Casein is also used as a binder in products like hot dogs, pepperoni, salami and sausage.  Milk protein increases production of mucus-aggravating conditions, such as asthma, bronchitis and sinusitis.  It acts as an irritant to our immune systems, contributing to allergies and autoimmune diseases. 

Let’s get back to our chocolate chip cookies.  What do we use instead of the butter and milk?  Here are some substitutions that I often use:

• Applesauce (may replace up to ¾ of the butter in a recipe.)
• Coconut Butter (Use ¾ cup coconut butter for each 1 cup of butter called for in a recipe.)
• Coconut Milk
• Lactaid Milk (The lactase enzyme has been added to milk to convert 99% of the lactose into an easily-digestible sugar.  While many lactose-intolerant people are able to safely consume this milk, it contains casein and is not suitable for those on a casein-free diet.)
• Milk-free Margarine (Fleischmann’s makes a milk-free, gluten-free margarine.  Milk-free margarine may burn if heated too high over direct heat.)
• Non-Dairy Yogurt
• Nut Butter
• Oil (Use ¾ cup corn, vegetable or olive oil for each cup of butter called for in a recipe.)
• Rice Milk
• Soymilk (Each brand of soymilk reacts differently.  Some will give an un-wanted color to your dish; others cannot be heated to a high temperature.  When substituting soymilk for cream, add a little vegetable oil to achieve the right consistency.  Read labels carefully, as some commercial soymilk products are not gluten-free.)
• Vegetable Shortening

When in doubt about the diary-free status of a product, the Kosher symbols found on some packages may also be used as a guide:

• UD:  Contains diary
• KD:  The product has milk protein.
• DE:  The product was produced on equipment shared with dairy products.
• Pareve  (or Parve):  The product is “neutral”, which means no animal ingredients.  The majority of Parve products are dairy-free.  However, Jewish law states that if the product has less than 1/5% dairy by volume, they may take special measures to allow for the product to be labeled Pareve.

Now we just have to search for safe chocolate chips for our cookies.  Many of the darker chocolates do not contain diary or gluten, for example, “Now” brand carob chips contain no dairy or gluten.

Eureka!  You have successfully converted your chocolate chip recipe!  Eat and enjoy!  The important thing to remember is that there are always good, viable substitutions available.  The more diet restrictions you have, the more innovative you have to be with your cooking.  There is almost nothing you cannot eat—you just have to learn to make it a little differently—enjoy!

Table 1

• Almond flour
• Amaranth flour
• Brown rice flour
• Buckwheat flour
• Chestnut flour
• Corn flour
• Fava bean flour
• Flax Seed Flour
• Garbanzo bean flour (Chickpea flour)
• Lentil flour
• Mung bean flour
• Pea flour
• Potato flour
• Potato starch flour
• Pure Cornmeal
• Sorghum flour
• Sweet potato flour
• Sweet rice flour
• Tapioca flour
• White bean flour
• White rice flour

Celiac.com 01/06/2003 - Evolution is an interactive process. Those of us who learn quickly and well are more likely to survive, thrive, and reproduce. Learning capacities then, are factors in the survival of our genes. Research is now revealing that cereal grains, along with other allergenic and highly glycemic foods, pose a serious threat to our sustained ability to learn. These foods have been shown to interfere at almost any stage of the learning process, impeding our attempts to focus our attention, observe, ponder, remember, understand, and apply that understanding. Grains can alter learning capacities in four specific ways: as sequelae of untreated celiac disease; through an immune sensitivity to gluten; through dietary displacement of other nutrients and; through the impact of grain on blood sugar/insulin levels.

There are many reports of learning problems in association with untreated celiac disease. A majority of children with celiac disease display the signs and symptoms of attention deficit disorder (ADD/ADHD)^{1, 2} a range of learning difficulties3 and developmental delays^4-6. Many of the same problems are found more frequently among those with gluten sensitivity⁷ a condition signaled by immune reactions against this most common element of the modern diet. Grain consumption can also cause specific nutrient deficiencies that are known to play an important role in learning. Grains can also cause problems with blood sugar/insulin levels resulting in reduced capacities for learning. Further, foods derived from grain are an important element in the current epidemic of hypoglycemia, obesity, and Type 2 diabetes^8-10. Our growing understanding of the biological impact of cereal grain consumption must move educators to challenge current dietary trends.

Part of our improved understanding comes from new testing protocols which are revealing that celiac sprue afflicts close to 1% of the general population, making it the most common life-long ailment among humans, with frequencies ranging from 0.5% to more than 5% of some populations^{11, 12}. It is widespread and appears to occur more frequently among populations that have experienced relatively shorter periods of exposure to these grains13. The importance of this newly recognized high frequency of celiac disease becomes obvious when we examine the impact it has on learning and behavior.

Research has identified ADHD in 66-70% of children with untreated celiac disease, which resolves on a gluten-free diet, and returns with a gluten challenge^{1, 2}. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD^13-15. Other reports have connected untreated celiac disease with similarly abnormal blood flow patterns in the brain¹⁶. One might be able to dismiss such reports if viewed in isolation, but the increased rates of learning disabilities among celiac patients³, and the increased rates of celiac disease among those with learning disabilities leave little to the imagination¹⁷. Further, there is one report of gluten-induced aphasia (a condition characterized by the loss of speech ability) that resolved after diagnosis and institution of a gluten-free diet1⁸. Still other investigations suggest a causal link between the partial digests of gluten (opioid peptides) and a variety of problems with learning, attention, and development.

Gluten sensitivity, afflicting close to 15% of the general population^{19, 20} is an immune reaction to one or more proteins in found in grains. When a persons immune system has developed antibodies against any of these proteins, undigested and partly digested food particles have been allowed entry into the bloodstream²¹. The leakage of food proteins through the intestinal wall signals a failure of the protective, mucosal lining of the gastrointestinal tract, as is consistently found in untreated celiac disease. Many of the same health and learning problems that are found in celiac disease are significantly overrepresented among those with gluten sensitivity for the very good reason that many of the same proteins are being leaked into the blood of those with gluten sensitivity.

Our cultural obeisance to grains is at odds with the remains of ancient humans. Archaeologists have long recognized that grains are a starvation food—one for which we are not well suited. Grains result in consistent signs of disease and malnourishment in every locale and epoch associated with human adoption of grain cultivation.

Grains are a poverty food. As we increase our grain consumption, we cause deficiencies in other nutrients by overwhelming the absorptive and transport mechanisms at work in our intestines. For instance, diets dominated by grains have been shown to induce iron deficiency²²—a condition that is widely recognized as causing learning disabilities^23-29. This should not be surprising since iron is the carrier used to distribute oxygen throughout our bodies, including various regions of our brains. There is little room to dispute the hazards to learning posed by reductions in oxygen supply to the brain. Iron deficiency reduces available oxygen in the brain, revealing yet another dimension of gluten grains as mediators of learning difficulties.

There is more. The impact of grain consumption on our blood sugar levels is yet another facet of its contribution to learning problems. We evolved as hunter-gatherers, eating meats, and complex carbohydrates in the form of fruits, vegetables, and seeds. Refined sugars were a rare treat wrested from bees with some difficulty. At best, it was a rare treat for our pre-historic ancestors.

Today, with unprecedented agricultural/industrial production of refined sugars along with cultivation and milling of grain flours, these products have become very cheap and available, particularly over the last fifty years. During that time, we have added enormous quantities of grain-derived starches to the overwhelming quantities of sugar we consume. The result of this escalating dietary trend may be observed in the current epidemic rates of Type 2 diabetes, hypoglycemia, obesity, and cardiovascular disease. In the classroom, we see these trends manifest in students mood swings, behavioral disorders (fluctuating between extreme lethargy and hyperactivity), chronic depression, forgetfulness, and muddled thinking—all of which reflects the inordinate, counter-evolutionary burden placed on many homeostatic systems of the body, particularly those related to blood sugar regulation.

The pancreas has many functions. One important activity of the pancreas is to stabilize blood sugar levels. When blood sugar is not well regulated, learning is impaired³⁰. The pancreas secretes carefully monitored quantities of glucagon and insulin. The pancreas responds to the presence of proteins, sugar, and starch in the digestive tract by producing insulin. It produces glucagon in response to fats. The balanced presence of both of these hormones in the bloodstream is critical to learning because they regulate the transport of nutrients into cells. Too little or too much insulin can cause blood sugar levels go out of control inducing a wide range of symptoms.

Today, when the insulin/glucagon balance goes awry, it is frequently due to insulin overproduction due to a diet dominated by sugars and starches. This overproduction is caused by chronic consumption of highly glycemic foods. The resulting elevated levels of insulin cause rapid movement of nutrients into cells, either for storage as fat, or to be burned as energy, causing increased activity levels, "hot spells", sweating, increased heart rate, etc. This energized stage requires a constant supply of sugars and starches to be maintained. Otherwise, it is soon followed by bouts of lethargy, light-headedness, tremors, and weakness, which are all signs of hypoglycemia or very low blood sugar levels.

Despite having stored much of the blood sugars as fats, there is insufficient glucagon to facilitate its use for energy. As this condition progresses, and as blood sugar levels plummet, periods of irrational anger and/or confusion often result. These moods often result from adrenaline secreted to avoid a loss of consciousness due to low blood sugar levels. The next step in the progression, in the absence of appropriate nutritional intervention, is lapsing into a coma.

In the short term, the answer to these fluctuations is more frequent consumption of sugars/starches. However, the long term result of such an approach is either a state of insulin resistance, where more and more insulin is required to do the same task, or a state of pancreatic insufficiency, where the pancreas is simply unable to keep pace with the demand for insulin. In either case, once this stage is reached, the individual may be diagnosed with type 2 diabetes. This disease has so increased among North Americans, particularly among children, that an autoimmune form of diabetes, previously called juvenile onset, had to be renamed to "Type 1 diabetes".

By now, it will not surprise the reader to learn that Type 1 diabetes has also been shown to be significantly associated with gluten. Research reveals that there is considerable overlap between celiac disease and Type 1 diabetes. About 8% of celiacs also have Type 1 diabetes^31-33, and 5-11% of Type 1 diabetics have celiac disease^34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten^39-42.

The growing reaction against gluten and other allergenic foods should not be confused with the several dietary fads of the 20th Century. The vegetarian perspective ignores the vitamin deficiencies that result from a strict vegetarian diet. The low-fat craze is another fad that has mesmerized the industrialized world for the last 30-40 years. Fortunately, this perspective has recently come under scrutiny. Despite having served as the driving force behind most physicians dietary recommendations during the last several decades, the low fat dictum is overwhelmingly being discredited by research reported in peer reviewed publications.

Recognition and avoidance of allergenic and highly glycemic foods is a whole new trend that is based on scientific research and evidence. It reflects an improved understanding of the function of the gastrointestinal tract, the endocrine system, particularly the pancreas, and the immune system. Past dietary fads are consistently deficient in important nutrients that are necessary to our good health and survival. Further, they frequently contain substances that are harmful to us, such as the phytates that are abundantly present in whole grain foods, and interfere with absorption of many minerals.

It is increasingly clear that grains, especially those that contain gluten, are contraindicated for human learning. The evidence is overwhelming. The mandate of eating to learn is learning to eat as our ancestors did.

Ron Hoggan is an author, teacher and diagnosed celiac who lives in Canada. His book "Dangerous Grains" can be Open Original Shared Link.

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• Of Relevant interest:
  Gormanous M, Hunt A, Pope J, Gerald B. Lack of knowledge of diabetes among Arkansas public elementary teachers: implications for dietitians. J Am Diet Assoc. 2002 Aug;102(8):1136-8.