Perspective

Grains in Relation to Celiac Disease¹

Donald D. Kasarda²

  The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are wheat, rye, and barley (and the wheat-rye cross triticale). Although oats were generally considered harmful until 1996, several excellent studies published since then indicate that oats are not harmful to those with either celiac disease or dermatitis herpetiformis. Some physicians do not accept these findings or point out that there is the potential problem of contamination of oats by wheat. The question of contamination has not yet been adequately researched in the United States. The three harmful species (wheat, rye, and barley) are members of the grass family and are quite closely related to one another according to various plant classification schemes (taxonomy). However, not all members of the grass family damage the intestines of celiac patients. Rice and corn, for example, are apparently harmless.

Many types of grain have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oat, rice, and corn in relation to celiac disease. In fact, only wheat and oat have been extensively studied in controlled experiments using 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 (based on taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Job’s tears, which appear to be reasonably closely related to corn. There are protein studies that support this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide better answers. 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 Job’s tears are not likely to be toxic in those with celiac disease, although such studies are hampered currently by a lack of knowledge about 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 defines the species (aestivum). Species within the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins found in these species include the various types characteristic of the gluten proteins found in bread wheats (including the -gliadins) that cause damage to the small intestine of celiac patients. Durum wheats (T. turgidum var. durum) used for pasta are also harmful to celiac patients. Some Triticum species causing concern include T. aestivum var. spelta (common names include spelt or spelta), T. turgidum var. polonicum (common names include Polish wheat, and, recently, Kamut®, although Kamut® might be properly classified a durum wheat), and T. 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 classic allergic responses to wheat.

Rye (Secale cereale) and barley (Hordeum vulgare) are toxic in celiac patients, 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 a-gliadins, which may be an especially toxic fraction.

There have been anecdotal reports suggesting a lack of toxicity for spelta and Kamut® in celiac patients, as well as anecdotal reports of the opposite (in the case of spelta, there have been reports of 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 spelta and Kamut® should be considered forms of wheat.

The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are “diagnosed” without rigorous testing may not actually have celiac disease. As a result, 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 spelta or Kamut® might experience relapse later. There is now adequate evidence that when celiac patients on a gluten-free diet (i.e., a diet free of any proteins or peptides from wheat, rye, and barley) have wheat reintroduced into their diets, time to relapse varies 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, relapse may not be accompanied by obvious symptoms and may be recognized only by physicians through observation, obtained by biopsy, of characteristic changes in the small intestinal tissues. The reasons for the enormous variability of response times are not known. It may be speculated that variability is related to the degree of recovery of the lining of the small intestine due to a gluten-free diet, the degree of stress that the patient has 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 Monocotyledoneae or monocots. The only other grouping at the subclass level is that of Dicotyledoneae or dicots. Some species about which celiac patients have questions are actually dicots, which have a very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. Rapeseed is not eaten, but an oil pressed from the seeds is commonly used in cooking and is marketed as canola oil. Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that these dicots 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. If such concerns were carried to a logical conclusion, however, 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 advisable 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 to almost any protein may occur, 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 may cause 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 that approach 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, and amaranth eaten in moderation apparently do not cause problems. (Buckwheat is sometimes found in mixtures 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 about celiac disease, including knowledge about the proteins that cause the problem and the grains that contain these proteins, is incomplete and is still being acquired. 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 Job’s tears, are close enough in their genetic relationship to corn to make it likely that they are safe for celiac patients to eat. However, significant scientific studies have not been carried out on these grains.

There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat, including 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 stating 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.

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Kasarda, D. D. 2000. Celiac disease. In The Cambridge World History of Food. Vol. 1. K. F. Kiple and C. Ormelas, eds. Cambridge University Press, Cambridge, UK, pp. 1008-1022.

Kasarda, D. D., and R. D’Ovidio.1999. Amino acid sequence of an alpha-gliadin gene from spelt wheat (Spelta) includes sequences active in celiac disease. Cereal Chem. 76:548-551.. 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., N. Leonard, E. Jones, D.D. Kasarda, D.G. Weir, C. O'Farrelly, and C. Feighery. 1996. Absence of oats toxicity in coeliac disease. British Medical Journal 313:1300-1301.

Tatham, A. S., R.J. Fido, C.M. Moore, D.D. Kasarda, D.D. Kuzmicky, J.N. Keen, and P.R. Shewry. 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. O’Farrelly, Oak Tree Press, Dublin, pp. 203-220.

Shewry, P. R., A.S. Tatham, and D.D. Kasarda. 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., S. Auricchio, H.W. Jones, E. J.-L.Lew, J.E. Bernardin, and D.D. Kasarda. 1988. In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease. Gastroenterology 94:41-49. .

Kagnoff, M. F., Y.J. Patterson, P.J. Kumar, D.D. Kasarda, F.R.Carbone, D.J. Unsworth, and R.K. Austin. 1987. Evidence for the role of a human intestinal adenovirus in the pathogenesis of celiac disease. Gut 28:995-1001.

Levenson, S. D., R.K. Austin, M.D. Dietler, D.D. Kasarda, and M.F. Kagnoff. 1985. Specificity of antigliadin antibody in celiac disease. Gastroenterology 89: 1-5.

Kagnoff, M. F., R.K. Austin, J.J. Hubert, J.E. Bernardin, and D.D. Kasarda. 1984. Possible role for a human adenovirus in the pathogenesis of celiac disease. J. Exp. Med. 160: 1544-1557.

Kagnoff, M. F., R.K. Austin, H.C.L. Johnson, J.E. Bernardin, M.D.Dietler, and D.D. Kasarda. 1982. Celiac sprue: correlation with murine T cell responses to wheat gliadin components. J. Immunology 82: 1296-2693.

Kasarda, D. D. 1981 Toxic proteins and peptides in celiac disease: relations to cereal genetics, In Food, Nutrition, and Evolution: Food as an Environmental Factor in the Genesis of Human Variability. Edited by D. Walcher and N. Kretchmer, Masson Publishing, USA, NY, pp 201-216.

Falchuk, S. M., D.L. Nelson, A.J. Katz, J.E. Bernardin, D.D. Kasarda, and W. Strober. 1980. Gluten-sensitive enteropathy: influence of histocompatibility type on gluten sensitivity in vitro. J. Clin. Invest. 66: 227-233.

Kasarda, D. D. 1978. The relationship of wheat proteins to celiac disease. Cereal Foods World 23: 240-244, 262. 1978.

Kasarda, D. D., C.O. Qualset, D.K. Mecham, D.M. Goodenberger, and W. Strober. 1978. A test of the toxicity of bread made from wheat lacking a-gliadins coded for the 6A chromosome. In Perspectives in Coeliac Disease--Proc. 3rd Int. Symposium on Coeliac Disease. Edited by B. McNicholl, C. F. McCarthy, and P. F. Fottrell, MTP Press Ltd.,Lancaster, U. K./University Park, Press, Baltimore, MD, USA, pp. 55-61.

Bernardin, J. E., R.M. Saunders, and D.D. Kasarda. 1976. Absence of carbohydrate in celiac-toxic A-gliadin. Cereal Chem. 53: 612-614.

Kasarda, D. D. 1975. Celiac disease. In: Protein Nutritional Quality of Foods and Feeds, Part 2. Friedman, M. (ed.), Marcel Dekker, New York, pp. 565-593.

Kasarda, D. D., C.C. Nimmo, and J.E. Bernardin. 1974. Structural aspects and genetic relationships of gliadins, . In Coelic Disease: Proc. 2nd Int. Conference, edited by W. Th. J. M. Hekkens, and A. S. Pena, A. S., Stenfert Kroese, Leiden, pp. 25-36.

Kasarda, D. D. 1972. Celiac disease: malabsorption of nutrients induced by a toxic factor in gluten. Baker's Digest 46(6): 25-31.

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¹The following information was originally supplied by the author in 1991 in the form of a letter to Phyllis Brogden, chair of the Greater Philadelphia Celiac Sprue Support Group. Copies were sent to four other major celiac patient groups in the United States.

²USDA-ARS, Albany, CA. The author retired from the USDA in 1999 but updated the information in February of 2000. He wishes to add the following disclaimer: “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.”

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