Introduction

For most of the 20th century, diabetes mellitus was recognised as a condition characterised by the presence of hyperglycaemia with a crippling burden of both microvascular and macrovascular disease. This association led to a view that the morbidity and mortality seen in diabetes were a consequence of hyperglycaemia which could be prevented by rigorous glycaemic control. This glucocentric view of diabetes has stood the test of time in relation to microvascular disease affecting the eyes, nerves and kidneys. However, the relationship between glycaemia and the development of macrovascular disease is much less clear. In 1971, the disappointing results from the University Group Diabetes Program (UDGP) trial had led Goldner to comment “…UDGP has given little hope that the degenerative complications of diabetes were preventable by simple control of blood sugar…”.1 In the next 25 years, several important developments started the process whereby the battle against complications began to swing in favour of the patient rather than the disease. In the late 1970s, it became possible to measure glycated haemoglobin which provided an indication of glycaemic control over a period of weeks as opposed to minutes seen with glucose estimation. Epidemiological evidence reported a reduction in stroke and myocardial infarction (MI) associated with improvements in care; however, the prevalence of chronic kidney disease was unaltered.2 Two landmark trials were reported, Diabetes Control and Complications Trial (DCCT) in type 1 diabetes3 and United Kingdom Prospective Diabetes Study (UKPDS) in type 2 diabetes.4 Both described a reduction in microvascular disease in patients with improved glycaemic control and both indicated that …