In NEJM editorial, Harlan and Lee comment on study connecting infant diet to diabetes

A study that makes a connection between infant diet and the onset of type 1 diabetes is intriguing and should be pursued further, according to an editorial in the New England Journal of Medicine (NEJM) by UMass Medical School diabetes experts David Harlan, MD, the William and Doris Krupp Professor of Medicine, and Mary Lee, MD, professor of pediatrics and cell biology. 

Diabetes occurs when pancreatic islet cells fail to produce sufficient insulin, the hormone needed for cells to convert the sugar in food to energy that cells can use. Unlike type 2 or “adult onset” diabetes, type 1 diabetes is an autoimmune disease, where the body's own immune system destroys the islet cells as though they are foreign, like an infection.

One of the enduring mysteries of type 1 diabetes is what causes the immune system to start attacking the body’s insulin-producing cells. Some evidence suggests that environmental factors, such as infant feeding practices or infections, may start this immune destruction of insulin-producing cells in people who are genetically susceptible. Because diabetes is such a devastating, expensive and difficult-to-control disease, researchers are aggressively seeking to identify factors that may trigger type 1 diabetes, especially if such factors can be eliminated.

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An intriguing possible connection between breastfeeding and lower rates of type 1 diabetes was first observed more than three decades ago, when researchers studied the role of cow’s milk in the diet of infants as a possible precursor to the onset of diabetes. If early consumption of cow’s milk somehow triggered the immune response against the insulin producing cells, then it might be feasible to alter cow’s milk to reduce that response–and the onset of diabetes. 

In the current issue of NEJM, a long-term research study from Finland sought to carefully compare the onset of diabetes in infants fed breast milk, cow’s milk-based infant formula, or hydrolyzed formula, where the milk proteins are broken down into components too small to cause an immune response. The study, “Dietary intervention in infancy and later signs of beta-cell autoimmunity,” is the subject of an editorial in the same issue by Dr. Harlan, the director of the UMass Memorial Diabetes Center of Excellence, and Dr. Lee, the director of pediatric diabetes at the Center for Excellence.

In the editorial, Harlan and Lee seek to painstakingly parse the findings of the Finnish study, which randomized infants — all of whom had a family history of diabetes — who were weaned from breast milk to a diet of either standard infant formula or hydrolyzed formula. The results were subtle, but intriguing: autoimmune antibodies occurred less frequently in the hydrolyzed formula group. The results hint at a possible immunoprotective effect from hydrolyzed infant formula.

“Families are devastated when a child receives a diagnosis of type 1 diabetes,” Harlan and Lee wrote. “Although tremendous strides in treatment . . . have contributed to remarkable improvements in the prognosis of the disease, the proper management of type 1 diabetes is expensive and time consuming . . . Thus, one of the ‘Holy Grails’ of modern medicine has been that an understanding of the pathogenesis underlying type 1 diabetes would lead to a cure or prevention.”

Harlan and Lee also noted that larger ongoing trials should be able to more definitively address the putative association between early dietary constituents and type 1 diabetes.