The majority of adults have overweight or obesity.1,2 Prior research demonstrates associations between body mass index (BMI) and chronic inflammation and body mass index with new-onset type-2-diabetes.3,4 Increased interleukin-6 production from the white adipose tissue, particularly visceral fat, in patients with obesity is a component of chronic low-level inflammation that includes interleukin-6.4, 5, 6 Further, visceral fat is associated with new-onset type-2-diabetes.5 Societal pressures and the concept of “health at every size” promote a treatment paradigm where obesity is not medically treated.7 The objective of this study was to develop a greater understanding of how obesity is related inflammation and how inflammation impacts new-onset chronic disease. Therefore, we planned a mediation analysis to assess to what degree interleukin-6, an inflammatory cytokine, mediates the diabetogenic effect of increasing BMI.8 The rationale for this study is that by further clarifying why obesity is linked with type-2-diabetes clinicians will be better able to communicate the health risks of obesity to their patients.