Epidemiology of the Metabolic Syndrome 2

Insulin resistance—an essential component of the metabolic syndrome—has been known for nearly 70 years. Himsworth [1] suggested the existence of two different types of diabetes: one characterised by high levels of insulin sensitivity (what we now know as type 1 diabetes, characterised by beta-cell destruction) and another characterised by insulin insensitivity (what we now know as type 2 diabetes, characterised by insulin resistance). Detailed, explanatory studies in this field were impossible until the introduction of the radioimmunoassay for insulin in 1960 [2]. This technology opened the door for larger studies of the role of insulin resistance in relation to diabetes as well as to cardiovascular disease (CVD). Throughout the following 25 years the association between hypertension, dyslipidaemia, glucose intolerance and hyperinsulinaemia was established through first smaller case–control studies and subsequently through large, population-based studies [3–6]. In 1988 Reaven reviewed the existing knowledge around the association between insulin resistance and a variety of metabolic risk factors for diabetes and CVD in his paper “Role of insulin resistance in human disease” [7]. Reaven had a background in physiology, and he concludes his review by elegantly proposing a hypothesis offering the suggestion that insulin resistance could be the common denominator underlying a syndromic clustering of metabolic risk factors explaining the clustering of CVD risk factors in selected groups. By doing so, he offered a pathophysiological model that could be tested, confirmed or rejected. The scientific community rather uncritically accepted his suggestion of a new “syndrome”, and rather than designing studies that could test his hypothesis, a plethora of studies confirming the basic associations or proposing new markers that were also