Effect of smoking cessation on lipoprotein A-I and lipoprotein A-I:A-II levels

Abstract

Cigarette smoking is associated with low plasma high-density lipoprotein cholesterol (HDL-C) and apolipoprotein (apo) A-I levels, which may explain, in part, its deleterious effects on coronary heart disease (CHD). In a group of ex-smokers, we assessed the influence of smoking cessation on apo A-I particle levels. Plasma lipid, apolipoprotein, and lipoparticle concentrations of 58 subjects who had completely stopped smoking (ex-smokers) were compared with those of 37 subjects who had continued smoking (smokers) before and after a smoking cessation counseling program. Nutritional intake was recorded before and after the program to adjust for potential interaction with plasma lipid variables. Smokers and ex-smokers were similar in gender distribution, age, body mass index (BMI), social status, and nutrient intake. There were significantly greater increases in total cholesterol (P < .04), HDL-C (P < .005), HDL2-C (P < .008), and lipoprotein (Lp) A-I:A-II (P < .04) in ex-smokers than in smokers. After smoking cessation, ex-smokers consumed more vegetable protein (P < .02) and polysaccharides (P < .04) and had higher plasma levels of HDL-C (P < .0004), apo A-I (P < .001), Lp A-I (P < .007), and Lp A-I:A-II (P < .01) than smokers. Adjustments on nutritional variables did not show any additional difference between ex-smokers and smokers, suggesting that smoking per se effects Lp A-I and Lp A-I:A-II levels. In conclusion, HDL particles including Lp A-I and Lp A-I:A-II are higher in ex-smokers than in smokers.