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In general, the strength of the causal inference one can draw from a study increases along this continuum, with policy changes typically appropriate only when supported by solid clinical trial evidence. Nonetheless, these risk factors are important to consider in evaluating an individual patient at risk. Event rates are three to four times higher in regular smokers, with a dose-response relationship. Although much of the interindividual variability in cholesterol is genetic, dietary consumption of cholesterol, saturated fat, and trans-fatty acids (typically formed by partial hydrogenation [saturation] of unsaturated vegetable fat) increases serum cholesterol. The similarity of the amino acid sequences of Lp(a) and plasminogen suggests the possibility of a connection between atherogenesis and thrombosis. Intervention, however, is somewhat problematic, with only niacin and estrogen showing some effect in lowering Lp(a). Meta-analyses of pharmacologic treatment of mild hypertension have also shown benefit. Systolic pressure rises with age throughout life in Western populations, whereas diastolic pressure plateaus in late mid-life and decreases somewhat thereafter. Randomized trials of cardiac rehabilitation for secondary prevention also suggest benefit. Prior concerns about the possible acute risk of exercise for cardiac ischemia in susceptible persons are clearly outweighed by the benefits for most individuals; nevertheless, it is appropriate to evaluate high-risk individuals before beginning an exercise program. In type I diabetes the risks are even higher, particularly in patients with proteinuria. However, controversy persists as to whether reduction of glucose levels will improve macrovascular risk. New oral agents that lower glucose and insulin and improve insulin resistance may help resolve this issue. 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