Issue: July 2016
June 15, 2016
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Life stress increases islet autoimmunity risk in genetically at-risk children

Issue: July 2016

NEW ORLEANS — Life stress in children with the HLA-DR3/4 genotype increases the risk for development of islet autoimmunity and diabetes, according to a presenter here.

Suzanne B. Johnson, PhD, distinguished research professor at Florida State University College of Medicine, and colleagues evaluated data on children aged up to 6 years from The Environmental Determinants of Diabetes in the Young (TEDDY) study to determine the link between negative life events and islet autoimmunity.

The TEDDY study follows 8,676 genetically at-risk children from age 3 months to 15 years for development of islet autoimmunity and type 1 diabetes. Researchers made a distinction between negative life events affecting the parents and negative life events affecting the child. Negative life events were divided into three categories: early negative life events occurring during the first year after enrollment, recent negative life events occurring in the year preceding islet autoimmunity and cumulative negative life events.

Suzanne B. Johnson

In any given year, approximately 25% of children experience a negative life event and 10% of children experience consistently high rates of negative life events year after year. Cumulative negative life events in children were independently linked to increased risk for islet autoimmunity among the children with HLA-DR3/4 (P < .003); this risk was not apparent in children with other HLA risks (P < .009 for interaction).

“We now know stress is important for the development of type 1 diabetes in some genetically at-risk children, but we do not yet know how stress leads to antibody positivity in these children,” Johnson told Endocrine Today. “We do know that stress effects the immune function, but how this translates into an autoimmune attack on the pancreatic beta cell is not known. It is also possible that stress increases the risk of other illnesses — like respiratory infections — which, in turn, lead to antibody positivity. Although we do not know the answers, this study provides an important direction for further research.” – by Amber Cox

Reference:

Johnson SB, et al. 374-OR. Presented at: American Diabetes Association’s Scientific Sessions; June 10-14, 2016; New Orleans.

Disclosure: Johnson reports financial ties with NIH.