Cognitive Impairment Mediates Workplace Impairment in Adults With Type 2 Diabetes Mellitus: Results From the Motivaction Study.

Abstract

Type 2 diabetes mellitus (DM) is associated with substantial impairments in workplace function; however, the mediators of workplace performance in DM are not well characterized. Herein, we investigate depressive symptomatology and cognitive dysfunction as mediators of workplace productivity and hypothesize that workplace impairment is mediated principally by cognitive dysfunction in DM. The Motivaction study screened individuals employed across Canada for diabetes. Subjects with impairments in glucose regulation indicative of risk for (i.e. glycated hemoglobin [A1C] levels 5.5% to 5.9%) or the presence of (i.e. A1C≥6.0%) DM were assessed on measures of depressive symptom severity [Patient Health Questionnaire, 9-item (PHQ-9)], self-rated cognitive impairment [Perceived Deficits Questionnaire, 5-item (PDQ-5)], and workplace impairment [Endicott Work Productivity Scale (EWPS)]. Multivariate regression and mediational analyses assessed for correlations between PHQ-9, PDQ-5 and EWPS total scores and the mediational role of self-reported cognitive dysfunction on the effect of depressive symptom severity on workplace impairment, respectively. A total of 3627 individuals were screened, 1738 met eligibility criteria and 724 consented to the Motivaction study; 205 subjects with impaired glucose regulation were included in the analysis. Self-rated depressive and cognitive symptoms were positively correlated with workplace impairment among subjects with or at risk for DM. The deleterious effects of depressive symptomatology on workplace effectiveness was mediated principally by cognitive dysfunction in subjects with impaired glucose tolerance. Among employed Canadians, impaired glucose tolerance is highly associated with impaired workplace performance. We report a novel finding insofar as the association between depressive symptoms and workplace impairment in individuals with impaired glucose regulation is mediated principally by self-rated cognitive dysfunction.