Whilst the interplay between type 2 diabetes and cardiovascular disease (CVD) has been recognised for many years, recent analyses of existing studies have helped refine several aspects of this relationship with relevance to clinical practice. First, recent data demonstrate that fasting glucose is not linearly related to CVD risk in those without diabetes; rather, risk levels escalate (modestly at first) only beyond specific glucose thresholds. Consequently, glucose-based measures may not necessarily enhance CVD risk prediction in those without diabetes. Second, other data confirm that new-onset diabetes is not a post-myocardial infarction ‘risk equivalent’ state and that, on average, several years of diabetes duration is needed to attain this level of risk. Third, meta-analyses and systemic reviews have confirmed that diabetes increases CVD risk by around twofold on average and this risk is subject to wide variation, being lowest in those newly diagnosed and highest in those with existing vascular disease, proteinuria or renal disease. Fourth, meta-analyses of major glucose-lowering trials suggest that, whilst glucose-lowering lessens vascular risk, risk reduction arising from statins and blood pressure-lowering is greater. Fifth, statins increase diabetes risk, albeit modestly, adding to the emerging concept that some agents that primarily target CVD risk may be diabetogenic, and vice versa. Finally, arising in part from the latter observation, as well as an understanding that CVD and diabetes risk overlap in some individuals but not others, the case for combined CVD/diabetes risk screening (generally using non-fasting lipids and HbA 1c ), has gained strength.