Since the publication of the UK Prospective Diabetes Study (UKPDS),1 much of the discourse around the management of type 2 diabetes has been dominated by an emphasis on reduction in levels of glycated haemoglobin (HbA1c). This emphasis is ubiquitous in clinical guidelines, in quality measures for healthcare organisations, and in metrics for reimbursement. Yet, recent evidence suggests the need for a shift in this paradigm. This is particularly the case in terms of the ability of lowering HbA1c to predict cardiovascular benefit, but we argue that it also applies to the persistent faith in glycated haemoglobin reduction as a marker of microvascular complication risk. We have previously argued that because HbA1c is a poor surrogate disease marker for cardiovascular disease (CVD), it is important to engage patients with diabetes in decision making based on discussion of the risks and benefits of treatment on outcomes that have clinical meaning to them.2 While recent guidelines now call for its use as a treatment measure to be tailored to the individual patient,3 we argue now that there remains a reluctance to apply this in practice. We argue that the reasons for this reluctance are several, and include an overconfidence in the impact of HbA1c reduction on the early markers of diabetic microvascular disease, which we term ‘soft endpoints’. We outline the paucity of trial data on the impact of HbA1c reduction on the clinically relevant ‘hard endpoints’ of vision loss and renal failure,2 and of clinical trial data in younger patients or demographically diverse populations.

Successive reductions in diagnostic thresholds for type 2 diabetes4 mean that at any given time, many people have a condition that is arguably less an asymptomatic disease than a risk factor for future disease. This is even more so for the growing numbers …