Inflammation and central adiposity as mediators of depression and uncontrolled diabetes in the study on global AGEing and adult health (SAGE).

Abstract

Diabetes and depression are commonly present in the same individuals, suggesting the possibility of underlying shared physiological processes. Inflammation, as assessed with the biomarker C-reactive protein (CRP), has not consistently explained the observed relationship between diabetes and depression, although both are associated with inflammation and share proposed inflammatory mechanisms. Central adiposity has also been associated with both conditions, potentially by causing increased inflammation. This study uses the World Health Organization's Study on global AGEing and adult health (SAGE) Mexico Wave 1 biomarker data (n = 1831) to evaluate if inflammation and central adiposity mediate the relationship between depression and diabetes. Depression was estimated using a behavior-based diagnostic algorithm, inflammation using venous dried blood spot (DBS) CRP, central adiposity using waist-to-height ratio (WHtR), and uncontrolled diabetes using venous DBS-glycated hemoglobin (HbA1c). The association between depression and uncontrolled diabetes was partially mediated by CRP before but not after WHtR was considered. When WHtR was added to the model, it partially mediated the relationship between diabetes and depression while fully mediating the relationship between depression and CRP. These findings suggest that central adiposity may be a more significant mediator between diabetes and depression than inflammation and account for the relationship between these disorders and inflammation. Depression may cause an increase in central adiposity, which then may lead to diabetes, but the increase in known systemic inflammatory pathways caused by central adiposity may not be the key pathological mechanism.