Commentary: Lifelong prevention of atherosclerosis: the critical importance of major risk factor exposures

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Abstract
More than 40 years ago, a model that expressed then-prevailing concepts about atherogenesis1 proposed that atherosclerosis begins relatively early in life (ages 10–20 years) with deposition of the fatty streak, progresses (ages 20–30 years) to the fibrous plaque, and further advances from ages 30–50 years by the action of traditional risk factors such as cigarette smoking, unfavourable blood lipid and blood pressure levels, overweight and insulin resistance (or glucose intolerance related factors) and eventually results in occlusive plaques and clinical manifestations of the atherosclerotic diseases from approximately age 50 onward. In this issue of the International Journal of Epidemiology, Beaglehole and Magnus2 remind us that ‘traditional’ risk factors explain perhaps as much as 85% or more of the world’s experience with atherosclerosis. They state that research on further refinements of this model cannot add much to epidemiological knowledge of this disease, and they argue that more energy should be expended in lowering the prevalence of tobacco use, unfavourable cholesterol levels, dyslipidaemia, physical inactivity, and the obesity/insulin resistance syndrome.