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March 7, 1966

Gluten and the Small Intestine in Rheumatoid Arthritis

Author Affiliations

From the Department of Internal Medicine, Yale University School of Medicine, and the Yale—New Haven Hospital, New Haven, Conn. Dr. Binder is a Special Fellow of the National Institutes of Arthritis and Metabolic Diseases.

JAMA. 1966;195(10):857-858. doi:10.1001/jama.1966.03100100109033

An entirely new concept of the pathogenesis of rheumatoid arthritis and other connective-tissue diseases, a theory in which a genetically determined abnormality of the small imtestine is the basic defect, has been proposed. Shatin's hypothesis1 is that patients with rheumatoid arthritis are heterozygous for nontropical sprue (adult celiac disease). Although they have no intestinal complaints, the intestinal mucosa is abnormal and important metabolites essential to connective tissue are not absorbed. The clinical expression of this heterozygotic condition is rheumatoid arthritis. He further states that the worldwide distribution of rheumatoid arthritis corresponds to the distribution of wheat ingestion, lending indirect support for his hypothesis. The validity of this theory is strengthened by Shatin's report that 18 out of 18 patients with rheumatoid arthritis improved on a gluten-free diet, often within two weeks after the beginning of the dietary restriction of cereal grains.2

Although many arguments could be marshaled against

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