Since controlling BP and using an angiotensin enzyme inhibitor or angiotensin receptor blocker is only partially effective at regressing LVH, additional ways of regressing LVH are now required. Insulin resistance is another mediator of LVH. The literature is awash with observational studies linking insulin resistance to LVH. Pub Med identifies 67 such papers, 5 of which are inconclusive. In the remaining 62 papers, 46 identify a significant relationship between LVH and some measure of insulin resistance while 16 found no such relationship. The large studies are mostly positive which includes Framingham, the Whitehall trial, the Strong Heart trial and the Women's Health Initiative trial while the Hypertension Genetic Epidemiology Network (HyperGEN) trial is the one large negative trial. There are a multitude of mechanisms whereby hyperinsulinaemia should produce LVH e.g. through signalling pathways such as Akt, transforming growth factor and peroxisome proliferator-activated receptors, through increased myocardial free fatty acid oxidation and through RAS activation causing sodium retention and thus increased cardiac preload. Therefore, it is likely that glycaemia contributes to LVH. However, reducing glycaemia per se appears to be insufficient to reduce CV events and key ancillary properties of each anti-glycaemic drug will be necessary to deliver the CV benefits we so badly need in diabetes.