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Celiac disease is an autoimmune inflammatory disease of the intestines that affects an estimated 1 percent of the population of the United States and western Europe. It ranges from mild to life threatening. In the most severe cases, damage to the intraepithelial lymphocytes leads to lymphoma, with a 5-year survival rate of only 20 percent.
A recent article in the journal Immunogenetics describes how a series of unfortunate events causes celiac disease to develop and progress. First, approximately 25 percent of the Caucasian population is genetically susceptible. Second, most of us eat a lot of wheat products, which contain the protein mixture called gluten. These proteins are rich in the amino acids glutamine (30 percent) and proline (15 percent). They are resistant to complete digestion, so that large peptides can reach the intestinal mucosal surface. The immune system produces antibodies against gluten peptides. Many healthy people have measurable levels of these antibodies.
Third, viral infections of the intestines are believed to be part of a self-amplifying process that produces inflammation and tissue damage. Approximately 4 percent of the individuals who are genetically susceptible to celiac disease actually develop the illness. Young children are diagnosed after they experience diarrhea, abdominal distention, and failure to thrive. Adults may have similar symptoms, but also experience anemia, osteoporosis, or neurological symptoms. Reference 2 reports that celiac disease is often undiagnosed in Americans over age 50. These individuals experience reduced bone health, but have no increase in mortality.
A gluten free diet is sufficient to treat 97 percent of celiac disease patients. The remaining 3 percent have continued inflammation even with a perfectly gluten free diet. These patients are diagnosed with refractory celiac disease, RCD. There are two types, RCD I and RCD II. In patients with RCD II, the intraepithelial lymphocytes develop into lymphoma cells. Approximately 50 percent of RCD II patients are diagnosed with lymphoma within five years.
When I first heard about gluten sensitivity, I thought it was unbelievable that humans could have a genetic problem with such an important staple food. Why grow it if it makes people sick? However, gluten has excellent elastic properties for making bread. I expect farmers selectively cultivated wheat with higher and higher gluten content over the millennia. Thus, our ancestors may have been exposed to significantly smaller quantities of gluten. The question comes to my mind, can susceptible individuals reduce their risk of developing celiac disease by eating less gluten? I have not yet found a research study to answer this question, but I'm keeping my eyes open.
References:
1. Tjon JML et al, “Celiac disease: how complicated can it get?” Immunogenetics 2010; 62: 641-51.
2. Godfrey JD et al, “Morbidity and mortality among older individuals with undiagnosed celiac disease”, Gastroenterology. 2010 Sep; 139(3): 763-9.
Linda Fugate is a scientist and writer in Austin, Texas. She has a Ph.D. in Physics and an M.S. in Macromolecular Science and Engineering. Her background includes academic and industrial research in materials science. She currently writes song lyrics and health articles.
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Celiac disease appears to be hereditary but the gene breakdown does not necessarily mean that if you have the disease that you will pass it on to your children.
March 3, 2011 - 2:22amWhat is Celiac Disease
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