Non-pharmacological modification of cardiac risk factors: part 3. Smoking cessation and alcohol consumption

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Abstract
Smoking cessation (SC) is probably the single most important risk factor modification for both primary and secondary prevention of cardiovascular disease. Interventions to stop smoking are highly cost effective. SC produces reductions in mortality and morbidity that generally outweigh any increase in risk due to weight gain, unless the gain is so great that it is accompanied by adverse changes in blood pressure, lipid profile or glucose tolerance. There is clear evidence that SC improves the lipid profile, decreases thrombotic tendency, reduces vascular endothelial damage and improves insulin sensitivity. Epidemiological studies consistently demonstrate a reduced risk of developing coronary heart disease (CHD) with moderate alcohol consumption (showing protection at < or = 2 drinks per day), but an increased risk at higher alcohol consumption levels. Potential mediators of these cardioprotective effects include an increase in high-density cholesterol (HDL-C), decreased clotting propensity, enhanced insulin sensitivity and glucose tolerance, and a possible lowering of blood pressure at low consumption levels in women. Alcohol consumption may not, however, compensate for the large increase in risk produced by smoking. Whereas moderate alcohol consumption slightly reduces the risk of death between the ages of 35 and 69 years, cigarette smoking approximately doubles the risk.