HbA1c, Insulin Resistance, and β-Cell Function in Relation to Cognitive Function in Type 2 Diabetes: The CAROLINA Cognition Substudy

Abstract

Cognitive dysfunction is increasingly recognized as a complication of type 2 diabetes. There is a growing evidence for etiologic roles of glycemia and insulin resistance, although important questions remain (1,2). Elevated levels of glycosylated hemoglobin (HbA1c) appear to be related to worse cognition, but there are indications that the same holds true for lower HbA1c levels, possibly because intensive glycemic control increases the risk of hypoglycemia (1). Previous studies relating HbA1c to cognition did not sufficiently address this possible nonlinear relationship. Regarding insulin resistance, it has been postulated that disturbances in cerebral insulin signaling might negatively affect cognition (2). Indeed, in individuals without type 2 diabetes, both hyperinsulinemia and insulin resistance have been related to poorer cognitive performance and dementia (2). However, a comprehensive understanding of the interrelationship between markers of insulin homeostasis and cognition in type 2 diabetes is still lacking (1). Finally, there may be interindividual differences in susceptibility for developing cognitive dysfunction, where factors such as age and sex could modify the relations between glycemia, insulin resistance, and cognition. We therefore investigated, in a large cohort of patients with type 2 diabetes, how HbA1c and indices of insulin resistance and b-cell function relate to cognitive function, specifically addressing potential nonlinear associations and the influence of age and sex.

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Citation
Janssen J, van den Berg E, Zinman B, et al. Diabetes Care 2019;42:e1–3.