Abstract

Insulin-Dependent Diabetes (IDD) results from an autoimmune destruction of the insulin secreting pancreatic beta cells. The immunological mechanisms underlying the development of IDD as well as the role of environmental agents (e.g., diet, viruses, stress) in the pathogenesis of the disease are the subject of considerable research efforts. Significant attention has recently been directed to a hypothesis that consumption of cows' milk in infancy may trigger the autoimmune process underlying IDD. Early evidence supporting this “cows' milk hypothesis” included case-control studies surveying infant nutrition practices (i.e., breast feeding versus consumption of infant formula) and the subsequent development of IDD. However, intense media interest surrounding a report indicating anti-bovine serum albumin (BSA) immunity as the cause of IDD has lead to heightened public awareness of the issue, and, together with the epidemiological data, prompted The American Academy of Pediatrics to modify its guidelines for infant feeding practices. However, less public and scientific attention has been given toward the observations that many of these case-control studies were retrospective in design and subject to recall bias, narrow in scope in terms of collecting dietary information, and that similar results have not been duplicated in other more recent (and better designed) investigations. Furthermore, the immunological report implicating anti-BSA immunity with the disease has become controversial due to difficulties in conforming the findings, and experiments in animal models closely resembling human IDD have not uniformly supported a role for anti-BSA immunity in the pathogenesis of IDD. Given the significant morbidity and mortality associated with IDD, an improved understanding of the cause of this disorder as well as identifying possible methods for its prevention are essential. However, without additional supporting information, modification of the cows' milk/BSA composition of diets in order to avoid the disease may be premature. Further studies are needed to clearly establish a role for diet in the pathogenesis of IDD.

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