The results from our study indicate that W could influence diabetes risk through insulin resistance rather than β-cell function—though insulin resistance and β-cell dysfunction often interact in the development of diabetes,45 and it is possible that the measurement methods for HOMA-β were less accurate (especially for participants on insulin medication).46 More generally, W can be pro-inflammatory,47 and inflammation can lead to endothelial dysfunction and insulin resistance.48 This could partially explain the association between W and diabetes incidence as well as between W and HOMA-IR. Here, INS is linked to diabetes mellitus.