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Celiac.com 10/02/2008 - Whole grains are good sources of B-Vitamins and minerals such as calcium, iron, magnesium, and selenium, but one of their most important nutritional benefits is the fiber they bring to our diets. Whole grains such as wheat, brown rice, and oats include both soluble and insoluble fiber. Soluble fiber is easy to remember – it is water soluble, and as such can be assimilated into the body, where it plays an important role in blood sugar regulation and cholesterol balance. Soluble fiber also helps provide a sense of fullness or satiety. Insoluble fiber is - you guessed it - insoluble in water, and is not assimilated into the body, but passes through the digestive tract and is eliminated. That does not mean insoluble fiber has a less important nutritional role to play. Insoluble fiber is very important in keeping our digestive and elimination systems regular. Fiber aids the transit of toxic substances out of the body, and in doing so, helps to reduce the incidence of colon and rectal cancers. In eliminating gluten grains from your diet, have you wondered what you are missing nutritionally? Are you able to get adequate replacements for the nutrients in wheat, barley, rye, and oats, from the other nutritional components of your diet? The answer is a qualified yes. We know this on several levels. For tens of thousands of years, entire cultures have thrived without growing or consuming any of the gluten grains. We also know, from looking at what nutrients gluten grains provide, that there are more than adequate sources of these nutrients in alternative grains, and from vegetable sources. Fiber is something we do need to be aware of, though. Studies have shown that standard gluten-free diets are low in fiber, especially when baking with the “white” alternative products like white or sweet rice flour, tapioca starch, and potato starch. We can remedy this by eating alternative grains in whole, unprocessed states, and by including nuts, seeds, and other sources of fiber such as dried coconut and legumes in our diets. Wheat is an excellent source of Vitamin E, so those on gluten-free diets might want to supplement with a good brand of Vitamin E. Some commercial gluten-free flour blends seek to duplicate white flour, and are made primarily of white rice flour, tapioca starch, and potato starch (see the nutrition comparisons on the next page). These products are nearly devoid of nutrition and contain almost no fiber. Using these types of products result in baked goods that are the nutritional equivalent of wonder-bread. If you didn’t eat wonder-bread before going gluten-free, why should you attempt to duplicate it now? When making your flour blends, coming up with new recipes, and altering traditional wheat-flour recipes, try to include alternative grain products (and sometimes nut flours) that contain substantial amounts of fiber, protein, calcium, and iron, all nutrients found in whole grains, but in much smaller amounts in highly processed grains. Quinoa, sorghum, teff, amaranth, brown rice and millet flour are all good products to try. See the chart attached to this article (the link to it is in the "Attachments" section below) for the nutrient content of the many gluten-free alternative grains, starches, and nut flours. The highest levels of nutrients in each category are noted, and you can see what nutritional powerhouses grains like teff, quinoa, sorghum, and amaranth are compared to white rice flour, tapioca starch, and potato starch.

Preface: The following information was supplied originally in 1991 in the form of a letter to Phyllis Brogden, Chairperson of the Greater Philadelphia Celiac Sprue Support Group, by Donald D. Kasarda, who was a Research Chemist with the US Department of Agriculture at that time. Copies were sent to four other major celiac patient groups in the US. Dr. Kasarda retired from the USDA in 1999, but updated the information in February of 2000. Dr. Kasarda wishes to add the following disclaimer to the information: These are my opinions based on quite a few years of research in the area of proteins as they relate to celiac disease. They do not necessarily represent those of the Agricultural Research Service, U. S. Department of Agriculture. The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are those from wheat, rye, and barley (and the man-made wheat-rye cross called triticale). Although oats had generally been considered harmful until 1996, several high quality studies published since then indicate that oats are not harmful either in celiac disease or dermatitis herpetiformis. Some physicians choose not to accept these findings or else point out that there is some potential problem of contamination of oats by wheat. The contamination question has not yet been adequately researched, but may be overemphasized. The three harmful species are members of the grass family and are quite closely related to one another according to various schemes of plant classification (taxonomy). However, not all members of the grass family damage the intestines of celiac patients. Rice and corn, for example, are apparently harmless. Many other grains have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oats, rice, and corn in relation to celiac disease. In fact, only wheat and oats have been extensively studied in controlled experiments with the most up-to-date methods. If we accept corn and rice as safe, however, and this seems reasonable to me, then members of the grass family that are more closely related to these species (on the basis of taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Jobs tears, which appear to be reasonably closely related to corn. In some cases, there are protein studies in support of this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide a better answer. However, such studies are not likely to be carried out in the next few years because of high costs and the difficulty of obtaining patient participation (such studies would likely involve intestinal biopsy). In lieu of feeding studies, further studies of protein (and DNA) would provide the next best way to evaluate my suggestion that millet, sorghum, teff, ragi, and Jobs tears are not likely to be toxic in celiac disease, although even such studies are hampered at present by a lack of knowledge of which sequences in the wheat gluten proteins are harmful. There is evidence that a few sequences are harmful, but not all possibilities have yet been tested. The scientific name for bread wheat is Triticum aestivum var. aestivum--the first part of the name defines the genus (Triticum) and the second part, the species (aestivum). Species falling in the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins of these species include the various types characteristic of the gluten proteins found in bread wheats (including the alpha-gliadins) that cause damage to the small intestine in celiac disease. Durum wheats (Triticum turgidum var. durum) used for pasta are also harmful to celiac patients. Some Triticum species of current concern include Triticum aestivum var. spelta (common names include spelt or spelta), Triticum turgidum var. polonicum (common names include Polish wheat, and, recently, Kamut), and Triticum monococcum var. monococcum (common names include einkorn and small spelt). I recommend that celiac patients avoid grain from these species. Also, given their very close relationship to bread and durum wheats, I think it is unlikely that these grains would be safe for those with classical allergic responses to wheat. Rye (Secale cereale) and barley (Hordeum vulgare) are toxic in celiac disease even though these two species are less closely related to bread wheat than spelta and Kamut. They belong to different genera, Secale and Hordeum, respectively, and lack alpha-gliadins, which may be an especially toxic fraction. There have been anecdotal reports suggesting a lack of toxicity in celiac disease for spelta and Kamut, along with anecdotal reports of the opposite, at least in the case of spelt-celiac patients who have been harmed by eating it. Controlled tests would be necessary to draw a firm conclusion, although they hardly seem necessary insofar as spelt and Kamut should be considered forms of wheat. The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of reasonably rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are diagnosed in this way without rigorous testing may not actually have celiac disease. Claims that particular foods cause this latter group no problems in relation to their celiac disease could cause confusion. Furthermore, celiac patients who report no problems in the short run with spelt or Kamut might experience relapse later. There is now adequate evidence that when celiac patients on a gluten-free diet (that is, a diet free of any proteins or peptides from wheat, rye, and barley) have wheat reintroduced to their diets, times-to-relapse vary enormously among individuals, ranging from hours to months, or even years. And this is for wheat, presumably the most toxic of all cereal grains to celiac patients. Additionally, the relapse may not be accompanied by obvious symptoms, but be recognized only by physicians through observation of characteristic changes in the small intestinal tissues obtained by biopsy. The reasons for the enormous variability of response times are not known. It may be speculated that the variability has something to do with the degree of recovery of the lining of the small intestine on a gluten-free diet, the degree of stress that the patient had been experiencing (including infections), and individual genetic differences. As I have indicated, all known grain species that cause problems for celiac patients are members of the grass family. In plant taxonomy, the grass family belongs to the Plant Kingdom Subclass known as monocotyledonous plants (monocots). The only other grouping at the Subclass level is that of dicotyledonous plants (dicots). Some other species about which celiac patients have questions actually are dicots, which places them in very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. The seed of the last plant listed, rape, is not eaten, but an oil is pressed from the seeds that is commonly used in cooking. This oil is being marketed as canola oil. Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that these dicots will contain the same type of protein sequence found in wheat proteins that causes problems for celiac patients. Of course, some quirk of evolution could have given rise in these dicots to proteins with the toxic amino acid sequence found in wheat proteins. But if such concerns were carried to a logical conclusion, celiac patients would have to exclude all plant foods from their diets. For example, buckwheat and rhubarb belong to the same plant family (Polygonaceae). If buckwheat were suspect for celiac patients, should not rhubarb, its close relation, be suspect as well? It may be in order to caution celiac patients that they may have undesirable reactions to any of these foods--reactions that are not related to celiac disease. Allergic reactions may occur to almost any protein, including proteins found in rice, but there is a great deal of individual variation in allergic reactions. Also, buckwheat, for example, has been claimed to contain a photosensitizing agent that will cause some people who have just eaten it to develop a skin rash when they are exposed to sunlight. Quinoa and amaranth may have high oxalate contents-approaching those of spinach and these oxalate levels may cause problems for some people. Such reactions should be looked for, but for most people, buckwheat, quinoa, or amaranth eaten in moderation apparently do not cause problems. (Buckwheat is sometimes found in mixture with wheat, which of course would cause a problem for celiac patients.) It seems no more necessary for all people with celiac disease to exclude buckwheat from their diets because some celiac patients react to it than it would be for all celiac patients to exclude milk from their diets because some celiac patients have a problem with milk. In conclusion, scientific knowledge of celiac disease, including knowledge of the proteins that cause the problem, and the grains that contain these proteins, is in a continuing state of development. There is much that remains to be done. Nevertheless, steady progress has been made over the years. As far as I know, the following statements are a valid description of the state of our knowledge: Spelt or spelta and Kamut are wheats. They have proteins toxic to celiac patients and should be avoided just as bread wheat, durum wheat, rye, barley, and triticale should be avoided. Rice and corn (maize) are not toxic to celiac patients. Certain cereal grains, such as various millets, sorghum, teff, ragi, and Jobs tears are close enough in their genetic relationship to corn to make it likely that these grains are safe for celiac patients to eat. However, significant scientific studies have not been carried out for these latter grains. There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat. These include buckwheat, quinoa, amaranth, and rapeseed oil (canola). Some celiac patients might suffer allergies or other adverse reactions to these grains or foodstuffs made from them, but there is currently no scientific basis for saying that these allergies or adverse reactions have anything to do with celiac disease. A celiac patient may have an allergy to milk, but that does not mean that all celiac patients will have an adverse reaction to milk. Again, however, scientific studies are absent or minimal for these dicots. A list of my publications with pertinence to celiac disease follows. Cross-references to the literature for most of the points discussed above can be found in these publications. Kasarda, D. D., and DOvidio, R. 1999. Amino acid sequence of an alpha-gliadin gene from spelt wheat (Spelta) includes sequences active in celiac disease. Cereal Chem. 76:548-551. Kasarda, D. D. 1997. Celiac Disease. In Syllabus of the North American Society for Pediatric Gastroenterology & Nutrition, 4th Annual Postgraduate Course, Toronto, Ontario, Canada, pp. 13-21. Kasarda, D. D. 1997. Gluten and gliadin: precipitating factors in coeliac disease. In Coeliac Disease: Proceedings of the 7th International Symposium on Coeliac Disease (September 5-7, 1996), edited by M. Mäkki, P. Collin, and J. K. Visakorpi, Coeliac Disease Study Group, Institute of Medical Technology, University of Tampere,Tampere, Finland, pp. 195-212. Srinivasan, U., Leonard, N., Jones, E., Kasarda, D. D., Weir, D. G., OFarrelly, C., and Feighery, C. 1996. Absence of oats toxicity in coeliac disease. British Medical Journal 313:1300-1301. Tatham, A. S., Fido, R. J., Moore, C. M., Kasarda, D. D., Kuzmicky, D. D., Keen, J. N., and Shewry, P. R. Characterization of the major prolamins of tef (Eragrostis tef) and finger millet (Eleusine coracana). J. Cereal Sci. 24:65-71. 1996. Kasarda, D. D. 1994. Defining cereals toxicity in coeliac disease. In Gastrointestinal Immunology and Gluten-Sensitive Disease, edited by C. Feighery, and F. OFarrelly, Oak Tree Press, Dublin, pp. 203-220. Shewry, P. R., Tatham, A. S., and Kasarda, D. D. 1992. Cereal proteins and coeliac disease. In Coeliac Disease, edited by M. N. Marsh, Blackwell Scientific Publications, Oxford, U. K., pp. 305-348. De Ritis, G., Auricchio, S., Jones, H. W., Lew, E. J.-L., Bernardin, J. E. and Kasarda, D. D. 1988. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease. Gastroenterology 94:41-49. Kagnoff, M. F., Patterson, Y. J., Kumar, P. J., Kasarda, D. D., Carbone, F. R., Unsworth, D. J. and Austin, R. K. 1987. Evidence for the role of a human intestinal adenovirus in the pathogenesis of celiac disease. Gut 28:995-1001. Levenson, S. D., Austin, R. K., Dietler, M. D., Kasarda, D. D. and Kagnoff, M. F. 1985. Specificity of antigliadin antibody in celiac disease. Gastroenterology 89: 1-5. Kagnoff, M. F., Austin, R. K., Hubert, J. J., Bernardin, J. E. and Kasarda, D. D. 1984. Possible role for a human adenovirus in the pathogenesis of celiac disease. J. Exp. Med. 160: 1544-1557. Grains in Relation to Celiac (Coeliac) Disease by Donald D. Kasarda.

I am always amused by the argument that one grain or another is more likely to be contaminated than another, as I believe the real source of danger for contamination is found at mills and processing plants, and is more or less spread out equally for most gluten-free grains. Oats are often cited as having a higher chance of cross-contamination with wheat than other grains because it is often a rotational crop with wheat or barley, and kernels of these gluten-containing grains occasionally get mixed with the non-gluten grains. I do not understand why the same people who make this claim do no also include soy in this category, as it is one of the crops that is most commonly rotated with wheat. In any case, from the knowledge that I have gathered over the years about farming and processing grains, I must say that with most grains there is little likelihood of contamination due to the mixing of two different whole grains (i.e., the rotational crop hypothesis). This is due to the different sizes and shapes of different grains, and the machines which sort them after a harvest. If any grains do get mixed together the amount of actual contamination would likely be extremely low. In Trevor Pizzeys (Vice President of Operations for Can-Oat Milling) October 30, 1998 letter he expresses his belief that celiacs should avoid oats because he finds between 2.1 and 4.1 kernels of barley or wheat in every 4,000 (0.0525% and 0.1025% respectively). He says that this level can legally go up to a maximum level of 10 kernels per 4,000 (0.25%). In either of these scenarios we are talking about very low amounts. Even at these amounts the likelihood that a celiac eating these grains would eat 1 or 2 kernels of wheat or barley on a given day would be very, very low. Also, since most people who eat oatmeal tend to eat the whole oatmeal as a hot cereal, which means they can take very simple additional precautions to make their chances of eating any kernels of wheat or barley practically zero. The obvious way to do this is to look at the oats before you eat them or mill them and pull out any kernels that are of non-oat type. Now we turn to the other part of the argument to scare people away from grains that, taken by themselves, do not cause harm to people with celiac disease. This is the wheat dust in the mill (or during transport, or somewhere else) argument. There are many reasons, both health and safety, why mills take steps to keep dust levels down. Dust contamination is still possible, but I think we are also talking about even lower amounts that we were with the occasional kernel of wheat that pops up in oats, although there is no data that I know of to back this up. I think with whole oats (i.e., oatmeal) people can reduce any possible risk of wheat-dust contamination to almost zero by rinsing off their oats well with water before cooking or milling them. The famous oat study that was done in Finland and published in the NEJM used a source of non-contaminated oats to eliminate any possible factors that could ruin the results of their long and expensive study. It is possible that they could have used regular, uncontrolled Quaker oats for their study and gotten the same results, but again, the reasons for not doing so were to eliminate any possible factors that might affect the results of their study. This is the scientific process, and it is important with any study to eliminate any possible factors which could affect the outcome of the study. Last, there is a danger of contamination which comes from unclean equipment at mills, and at processing plants. This danger is present with any gluten-free grain, bean, etc., that is milled using the same equipment as is used to mill a gluten-containing grain. In other words we cannot speak of only oats with regard to this issue, as rice flour, soy flour, etc., could be contaminated equally in this way. Aside from legislation to require cleaning between milling runs, those who are worried about this need to buy flours from mills which they have researched and found to be gluten-free, or ones that adequately clean their equipment between runs. I think contamination issues are real, but need to be put in perspective with regard to other, perhaps more important issues, like labeling laws and getting agreement between the major celiac organizations in this country with regard to which grains are safe. See Also: Journal of the American Dietetic Association, Dec. 1997 v97n12p1413(4). Do oats belong in a gluten-free diet? by Tricia Thompson.

Celiac.com 08/31/2010 - In my work as an author, researcher, and gluten-free advocate, I know how challenging the gluten-free diet can be. One of the most vital and tricky parts of the diet is learning what foods have gluten and which are "naturally" gluten-free as well as learning how to read labels. Unfortunately, these aren't always enough. Just because a grain is supposed to be "naturally" gluten-free, doesn't mean that it is. In fact, a recent study tested 22 so-called "inherently" gluten-free grains and found that over thirty percent of them had gluten. Gluten is a protein found in the grains wheat, barley, and rye, and is inherently lacking in grains such as oats, buckwheat, quinoa, millet, soy, sorghum, flaxseed, rice, and amaranth seed. A study tested 22 of these "naturally" gluten-free grains, and 7 of them had a gluten amount higher than 20 ppm, which would disqualify them from being labeled as gluten-free under the proposed FDA guidelines. One type of soy flour tested had nearly 3,000 ppm of gluten, two millet flour products had an average of between 305-327 ppm, and the sorghum flour had a mean average of 234 ppm. Four of those seven products didn't have allergen advisory statements. What's the reason behind these alarming research results? Dr. Mercola, an osteopathic physician and board-certified family medicine doctor, attributes the cause to cross-contamination during the processing of these grains and also to a lack of testing of final products for gluten. Dr. Mercola, who is trained in both traditional and natural, or holistic, medicine, raises the question, however, about whether not only celiacs but people in general should even be consuming grains in the first place. According to Dr. Mercola, "Most people need to avoid grains." On his website, he states that several autoimmune disorders, not just celiac disease, can be "significantly improved by avoiding grains," and eliminating grains from your diet can also decrease your risk of heart disease, high cholesterol, Type 2 Diabetes, and cancer. This is due to the fact that, as Dr. Mercola explains, "grains and sugars are inherently pro-inflammatory and will worsen any condition that has chronic inflammation at its root – and not just inflammation in your gut, but anywhere in your body." In his experience, about 75-80% of all people benefitted from going grain-free. According to Grain Free Living, the health benefits of going grain-free have been proven "through the personal experience of hundreds of people worldwide who have experienced significant relief from symptoms of Crohn's disease (and many other illnesses of the digestive system) and also for chronic fatigue." The mainstream medical community has been critical of the "anecdotal evidence" from the testimonies of those who have reported an improvement in health. Clinical studies on the matter have yet to be carried out. A grain-free diet doesn't have to be boring. In fact, grain-free cookbooks have come out with grain-free recipes for favorite American foods such as pancakes, muffins, lasagna, cakes, and cookies. For those who have a digestive or other condition or who wish to eliminate health risks, I would recommend talking to your healthcare practitioner about a grain-free diet. For the gluten-free community who wishes to continue to eat grains, this study of the gluten content of "naturally" gluten-free grains can be startling. Look for grain products that are certified gluten-free by such organizations as the Gluten-Free Certification Organization (GFCO) or make sure to do thorough company research before you try "inherently" gluten-free grains. References: Thompson T, Lee A, Grace T. Gluten contamination of grains, seeds, and flours in the United States: A pilot study. J Am Diet Assoc. 2010;110:937-940. Abstract available at: http://www.ncbi.nlm.nih.gov/pubmed/20497786 Thompson, T. Contamination of Naturally Gluten-Free Grains. Living Gluten-Free. June 1, 2010. Available at: http://www.diet.com/dietblogs/read_blog.php?title=&blid=19524

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 delays4-6. 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 diabetes8-10. 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 populations11, 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 challenge1, 2. Several investigators have connected particular patterns of reduced blood flow to specific parts of the brain in ADHD13-15. 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 population19, 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 disabilities23-29. 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 diabetes31-33, and 5-11% of Type 1 diabetics have celiac disease34-38. Further, Scott Frazer et al. have repeatedly shown, in animal studies, a causal, dose-dependent relationship between type 1 diabetes and gluten39-42. 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. References: Kozlowska, Z: (1991). Results of investigation on children with coeliakia treated many years with glutethen free diet Psychiatria Polska. 25(2),130-134. Paul, K., Todt, J., Eysold, R. (1985) [EEG Research Findings in Children with Celiac Disease According to Dietary Variations]. Zeitschrift der Klinische Medizin. 40, 707-709. Grech, P.L., Richards, J., McLaren, S., Winkelman, J.H. (2000) Psychological sequelae and quality of life in celiac disease. Journal of Pediatric Gastroenterology and Nutrition 31(3): S4 Reichelt, K., Sagedal, E., Landmark, J., Sangvic, B., Eggen, O., Helge, S. (1990a). The Effect of Gluten-Free Diet on Urinary peptide Excretion and Clinical State in Schizophrenia. Journal of Orthomolecular Medicine. 5(4), 169-181. Reichelt, K., Ekrem, J., Scott, H. (1990b). Gluten, Milk Proteins and Autism: DIETARY INTERVENTION EFFECTS ON BEHAVIOR AND PEPTIDE SECRETION. Journal of Applied Nutrition. 42(1), 1-11. Reichelt, K., Knivsberg, A., Lind, G., Nodland, M. (1991). Probable etiology and Possible Treatment of Childhood Autism. Brain Dysfunction. 4, 308-319. Hoggan, R. (1997a). Absolutisms Hidden Message for Medical Scientism. Interchange. 28(2/3), 183-189. Caterson ID, Gill TP. Obesity: epidemiology and possible prevention. Best Pract Res Clin Endocrinol Metab. 2002 Dec;16(4):595-610. Hennessy AR, Walker JD.Silent hypoglycaemia at the diabetic clinic. Diabet Med. 2002 Mar;19(3):261. Kue Young T, Chateau D, Zhang M. Factor analysis of ethnic variation in the multiple metabolic (insulin resistance) syndrome in three Canadian populations.Am J Human Biol. 2002 Sep-Oct;14(5):649-58. Wahab PJ, Meijer JW, Dumitra D, Goerres MS, Mulder CJ. Coeliac disease: more than villous atrophy.Rom J Gastroenterol. 2002 Jun;11(2):121-7. Catassi C, Ratsch IM, Gandolfi L, Pratesi R, Fabiani E, El Asmar R, Frijia M, Bearzi I, Vizzoni L. Why is coeliac disease endemic in the people of the Sahara?Lancet. 1999 Aug 21;354(9179):647-8. Langleben DD, Acton PD, Austin G, Elman I, Krikorian G, Monterosso JR, Portnoy O, Ridlehuber HW, Strauss HW. Effects of Methylphenidate Discontinuation on Cerebral Blood Flow in Prepubescent Boys with Attention Deficit Hyperactivity Disorder.J Nucl Med. 2002 Dec;43(12):1624-1629. 2: Kim BN, Lee JS, Shin MS, Cho SC, Lee DS. Regional cerebral perfusion abnormalities in attention deficit/hyperactivity disorder Statistical parametric mapping analysis. Eur Arch Psychiatry Clin Neurosci. 2002 Oct;252(5):219-25. Lou, H., Henriksen, L., Bruhn, P. (1984). Focal cerebral hypoperfusion in children with dysphasia and/or attention deficit disorder. Archives of Neurology. 825-829. De Santis A, Addolorato G, Romito A, Caputo S, Giordano A, Gambassi G, Taranto C, Manna R, Gasbarrini G. Schizophrenic symptoms and SPECT abnormalities in a coeliac patient: regression after a gluten-free diet. J Intern Med. 1997 Nov;242(5):421-3. Knivsberg AM. Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia.Pediatr Rehabil. 1997 Jan-Mar;1(1):25-33. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia.N Engl J Med. 1988 Oct 27;319(17):1139-48. Hadjivassiliou M, Boscolo S, Davies-Jones GA, Grunewald RA, Not T, Sanders DS, Simpson JE, Tongiorgi E, Williamson CA, Woodroofe NM. The humoral response in the pathogenesis of gluten ataxia. Neurology. 2002 Apr 23;58(8):1221-6. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness.J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. Review. Husby, V., Jensenius, C., Svehag, S.(1985). Passage of Undegraded DietaryAntigen into the Blood of Healthy Adults. Scandinavian Journal of Immunology. 22, 83-92. Ma A, Chen X, Zheng M, Wang Y, Xu R, Li J. Iron status and dietary intake of Chinese pregnant women with anemia in the third trimester. Asia Pac J Clin Nutr. 2002;11(3):171-5. Kapil U, Bhavna A. Adverse effects of poor micronutrient status during childhood and adolescence. Nutr Rev. 2002 May;60(5 Pt 2):S84-90. Review. Youdim MB, Yehuda S. The neurochemical basis of cognitive deficits induced by brain iron deficiency: involvement of dopamine-opiate system. Cell Mol Biol (Noisy-le-grand). 2000 May;46(3):491-500. Otero GA, Aguirre DM, Porcayo R, Fernandez T. Psychological and electroencephalographic study in school children with iron deficiency. Int J Neurosci. 1999 Aug;99(1-4):113-21. Guesry P. The role of nutrition in brain development. Prev Med. 1998 Mar-Apr;27(2):189-94. Review. Bruner AB, Joffe A, Duggan AK, Casella JF, Brandt J. Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls. Lancet. 1996 Oct 12;348(9033):992-6. Soewondo S. The effect of iron deficiency and mental stimulation on Indonesian childrens cognitive performance and development. Kobe J Med Sci. 1995 Apr;41(1-2):1-17. McCarthy AM, Lindgren S, Mengeling MA, Tsalikian E, Engvall JC. Effects of diabetes on learning in children. Pediatrics. 2002 Jan;109(1):E9. Bertini M, Sbarbati A, Valletta E, Pinelli L, Tato L. Incomplete gastric metaplasia in children with insulin-dependent diabetes mellitus and celiac disease. An ultrastructural study.BMC Clin Pathol. 2001;1(1):2. Schuppan D, Hahn EG. Celiac disease and its link to type 1 diabetes mellitus.J Pediatr Endocrinol Metab. 2001;14 Suppl 1:597-605. Holmes GK. Coeliac disease and Type 1 diabetes mellitus - the case for screening.Diabet Med. 2001 Mar;18(3):169-77. x Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E. Coeliac disease in children and adolescents with type 1 diabetes: a study of growth, glycaemic control, and experiences of families.Acta Paediatr. 2002;91(3):297-302. Spiekerkoetter U, Seissler J, Wendel U. General Screening for Celiac Disease is Advisable in Children with Type 1 Diabetes.Horm Metab Res. 2002 Apr;34(4):192-5. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori G, Meschi F, Bianchi C, Chiumello G. Occurrence of celiac disease after onset of type 1 diabetes: a 6-year prospective longitudinal study.Pediatrics. 2002 May;109(5):833-8. Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, Hegedu LS, Jacobsen BB, Husby S. High prevalence of coeliac disease in Danish children with type I diabetes mellitus.Acta Paediatr. 2001 Nov;90(11):1238-43. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt DT, Werlin SL. The prevalence and clinical characteristics of celiac disease in juvenile diabetes in Wisconsin.J Pediatr Gastroenterol Nutr. 2001 Oct;33(4):462-5. MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW. A type 1 diabetes-related protein from wheat (triticum aestivum): cDNA clone of a wheat storage globulin, Glb1, linked to islet damage.J Biol Chem. 2002 Oct 29. Scott FW, Rowsell P, Wang GS, Burghardt K, Kolb H, Flohe S. Oral exposure to diabetes-promoting food or immunomodulators in neonates alters gut cytokines and diabetes.Diabetes. 2002 Jan;51(1):73-8. Scott FW, Cloutier HE, Kleemann R, Woerz-Pagenstert U, Rowsell P, Modler HW, Kolb H. Potential mechanisms by which certain foods promote or inhibit the development of spontaneous diabetes in BB rats: dose, timing, early effect on islet area, and switch in infiltrate from Th1 to Th2 cells.Diabetes. 1997 Apr;46(4):589-98. Scott FW. Food-induced type 1 diabetes in the BB rat.Diabetes Metab Rev. 1996 Dec;12(4):341-59. 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.

Celiac.com 10/26/2009 - With the ever-increasing awareness of celiac disease comes an expanding market of gluten-free options. The days of lengthy supermarket trips spent pouring over labels has given way to the tiny oasis of the “gluten-free” section is many grocery stores. While this section is still limited in many respects, the food production industry as a whole has become aware of the need to cater to the expanding gluten-free community. Gluten-free snacks, prepackaged meals, and baking supplies are no longer elusive, and the variety is continually expanding. While rice, potato, and corn flours are common strongholds in a Celiac’s kitchen, there is now a new wave of flavorful flours from Peru making their way into the United States. Many Peruvian heritage grains, dating back to pre-Incan times, have been found to be naturally gluten-free and incredibly nutritious. The first wave of these grains and flours to hit the U.S. market come to us from Zocalo Gourmet. Marching to shelves are kaniwa, mesquite, purple corn, and sweet potato flours. Each has a distinct flavor and “personality” that is sure to delight any gluten-free baker and reinvigorate their favorite recipes. Kaniwa is a species of goosefoot, closely related to quinoa. This tiny grain is packed with protein and has an Earthy taste that lends itself well to breads, pancakes, and muffins. Mesquite is also protein rich and imparts a warm, sweet, slightly smoky taste on foods while enhancing the flavors of cinnamon, chocolate, caramel, and coffee. Adding mesquite flour to your favorite recipes will transform their flavor and put a completely new spin on your old favorites. Purple Corn can be used in any recipe calling for traditional corn meal or flour while providing an antioxidant boost. Although similar in nutrition to yellow corn, purple corn contains substantial amounts of phenolics and anthocyanins, among other phytochemicals, which gives the corn its vibrant color. Its main colorant is cianidin-3-b-glucosa which is a known antioxidant. The high anthocianin content does not degrade with heat exposure. Sweet Potato is a velvety flour that holds moisture well, imparts a subtle sweetness on baked goods, and is incredibly versatile. With these flours come more complete flavor and nutritional profiles for the gluten intolerant. To learn more about these flours and how they can be used check out: http://www.zocalogourmet.com/products/floursgrains2.html and http://zocalogourmet.blogspot.com/

The following was written by Donald D. Kasarda who is a research chemist in the Crop Improvement and Utilization Research Unit of the United States Department of Agriculture. If you have any questions or comments regarding the piece, you can address them to Don at: kasarda@pw.usda.gov. Most sprouted wheat still has gluten or gluten peptides remaining. Although the sprouting begins enzymatic action that starts to break down the gluten (a storage protein for the plant) into peptides and even amino acids. Generally this is not a complete process for sprouts used in foods so some active peptides (active in celiac disease) remain.