OBJECTIVEDiabetes is a risk factor for an accelerated rate of cognitive decline and dementia. However, the relationship between cognitive function and the subsequent development of diabetes is unclear.
RESEARCH DESIGN AND METHODSWe conducted a historical-prospective cohort study merging data collected at premilitary recruitment assessment with information collected at the Staff Periodic Examination Center of the Israeli Army Medical Corps. Included were men aged 25 years or older without a history of diabetes at the beginning of follow-up with available data regarding their general intelligence score (GIS), a comprehensive measure of cognitive function, at age 17 years.
RESULTSAmong 35,500 men followed for a median of 5.5 years, 770 new cases of diabetes were diagnosed. After adjustment for age, participants in the lowest GIS category had a 2.6-fold greater risk for developing diabetes compared with those in the highest GIS category. In multivariable analysis adjusted for age, BMI, fasting plasma glucose, sociogenetic variables, and lifestyle risk factors, those in the lowest GIS category had a twofold greater risk for incident diabetes when compared with the highest GIS category (hazard ratio 2.1 [95% CI 1.5-3.1]; P < 0.001). Additionally, participants in the lowest GIS category developed diabetes at a mean age of 39.5 6 4.7 years and those in the highest GIS group at a mean age of 41.5 6 5.1 years (P for comparison 0.042).
CONCLUSIONSThis study demonstrates that in addition to a potential causal link between diabetes and enhanced cognitive decline, lower cognitive function at late adolescence is independently associated with an elevated risk for future diabetes.Evidence from the last several years suggests that dysglycemia accelerates the rate of cognitive decline and increases the risk for dementia. Indeed, people with diabetes are about 1.5-fold more likely to experience an accelerated rate of cognitive decline and are twice as likely to develop dementia (1-4). It also has been shown that dysglycemia per se is associated with an increased risk for dementia (5). This relationship is partially explained by cardiovascular risk factors, education, socioeconomic status (SES), and lifestyle factors. However, common mechanistic pathways such as inflammation, microvascular disease, and the effects of insulin sensitivity on the brain and in the periphery have also been hypothesized as an explanation for this relationship.