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When, and Why, Did Everyone Stop Eating Gluten?

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Celiac disease is an autoimmune disease in which the ingestion of gluten induces enteropathy, or inflammation of the gut, in genetically susceptible individuals. This destruction of the gut means that nutrients cannot be absorbed, leading to a variety of clinical symptoms: anemia due to the lack of iron, atherosclerosis due to the lack of calcium, failure to thrive in children, and GI stress, among others.  

Gluten is the primary protein component of wheat – it is what gives breads their delicious chewy texture. The only known cure for celiac disease is complete elimination of gluten from the diet – so no pizza, bagels, pasta, pancakes, waffles, doughnuts, cookies, soy sauce (it has wheat in it), licorice (ditto) … you get the idea. Even communion wafers are verboten.  

Although this is obviously extremely onerous on many levels, unlike any drug regimen it is 100 percent effective and free of side effects. Ingestion of gluten puts celiacs at risk for developing other autoimmune diseases and lymphomas.

Celiac disease was first described in A.D. 100 by the Greek doctor Aretaeus. When his extant works were first published in Latin in 1552 the Greek word for abdominal, koiliaki, was transcribed to celiac.1

But it was not until the Dutch famine of 1944 that wheat was positively identified as the factor instigating the enteropathy. An observant pediatrician, Willem Dicke, noticed that the celiac patients on his ward improved with the strict rationing of flour.   When the first supplies of precious bread were generously given to these sick children they relapsed, proving that wheat was in fact the culprit2.  

The scarcity of celiac diagnoses in this country had been a self fulfilling prophecy for many years: medical students were taught that celiac was so rare they would probably never encounter it, so they never bothered looking. The variable clinical presentations compounded this idea. When doctors started looking for it, they found it in roughly the same rates as it is found in Europe: 1 in 133 people3.     

Although many autoimmune diseases are thought to result from an interplay of genetic and environmental components, celiac is the only one for which the environmental trigger is actually known. It is gluten, as well as hordein and secalin, the homologous protein components of barley and rye.   So no beer or malt vinegar for celiacs either. For the sake of convenience, foods labeled “gluten free” are free of these proteins as well.   But foods labeled “wheat free” may still contain them, so these foods are not necessarily gluten free.  

Celiac disease is hardly the beginning and end of this story. Dermatitis herpetiformis is a rash that results when gluten induces an autoimmune response in the skin rather than the gut, and there is evidence that gluten can provoke a similar autoimmune response in the brain as well1.  

Gluten sensitivity or intolerance – a somewhat vague claim by people who definitely do not have celiac that they feel better when they eliminate gluten – was belittled by the scientific and medical establishment for a long time because it had no discernable cause or explanation, but now they are starting to come around and believe that it might be real4. It might be mediated by the innate, rather than the adaptive, immune system, meaning that T and B cells are not involved5.  

All this is completely separate from wheat allergies, which are mediated by a completely separate adaptive immune response (allergies are mediated by IgE class antibodies, and celiac antibodies are IgA).   People with wheat allergies can safely eat spelt as well as barley and rye, while those with celiac cannot.   And allergies can be outgrown, whereas celiac is forever.

So whether it is due to an actual increase in occurrence or merely an increase in diagnosis, there are certainly more celiacs around than there used to be. Wheat has been cultivated by humans for some 10,000 years, but as is the case with so many popular crops, the number of varieties we used to grow and consume has been reduced to those few that are commercially viable.6  

The soft white winter wheat that was traditionally grown in the mid-Atlantic states is low in gluten, so it is great for pastry and cake flour but not so much for bread. Now, most wheat used in this country is hard wheat grown in the Midwest, and it is bred to yield flour that is consistent in taste and texture. Hard wheat contains twice as much gluten as soft wheat does, so it produces chewy loaves of bread with crunchy crusts rather than flaky pie crusts.

As of now, FDA labeling laws do not require that the presence of gluten in foods be disclosed. These laws require only that the presence of eight major allergens be declared on food labels. Wheat is one of these allergens, but gluten is not. Manufacturers may label foods as gluten free, but such labeling is voluntary. For the millions of Americans with celiac disease, dermatitis herpetiformis, and gluten intolerance who must ensure that they are not consuming any gluten, this translates to A LOT of time spent reading labels in supermarket aisles.

References:

1. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, and Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol 2010; 9: 318–30

2. van Berge-Henegouwen GP, and Mulder CJ. Pioneer in the gluten free diet: Willem-Karel Dicke 1905-1962, over 50 years of gluten free diet. Gut. 1993 34(11): 1473–1475.

3. Roberts AG. Gluten Free Baking Classics. Surry Books, Chicago, 2006.

4. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, Shepherd SJ, Muir JG, and Gibson PR. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol. 2011 106(3):508-14.

5. Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, Stefanile R, Mazzarella G, Tolone C, Russo MI, Esposito P, Ferraraccio F, Cartenì M, Riegler G, de Magistris L, and Fasano A. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011; 9: 23.

6. Indrani Sen. Flour that has the flavor of home. The New York Times Sept. 10, 2008.

About The Author: Diana Gitig received her Ph.D. in Cell Biology and Genetics from Cornell University's Graduate School of Medical Sciences in 2001. Since then she is a freelance science writer. Diana is based in New York.

The views expressed are those of the author and are not necessarily those of Scientific American.

The views expressed are those of the author and are not necessarily those of Scientific American.

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