Smoking Cessation Intervention to Increase Plasma HDL Concentration
The majority of smoking cessation studies are small, and most, but not all, have been shown to result in a rise in HDL concentration. A meta-analysis of 27 studies incorporating over 6,000 subjects indicated that HDL-C increased by 0.10 mmol/L after smoking cessation, whilst plasma total cholesterol, LDL-C and TAG did not change (Maeda et al. 2003).
A number of lifestyle changes may also occur when smokers cease smoking, and at least one study has shown that the rise in HDL after smoking cessation is not independent of the change in diet (Quensel et al. 1989b). However, refuting this, a recent large randomised, double-blind controlled trial was carried out in over 1,500 smokers smoking an average of 21 cigarettes per day (Gepner et al. 2011). Patients were randomised to one of six treatments: nicotine lozenge, nicotine patch, sustained-release bupropion, nicotine patch plus nicotine lozenge, sustained-release bupropion plus nicotine lozenge, or placebo. Of the 923 participants who returned after 1 year intervention, 36 % who had stopped smoking showed a signiﬁcantly greater rise in HDL-C than those who did not, despite gaining an average of 4 kg more weight than those who continued to smoke. The effects of smoking cessation in this study were particularly evident in women.
Transdermal nicotine replacement therapy is a commonly used approach to support smoking cessation. A small study was carried out to compare the effects of transdermal nicotine patches, used as part of a smoking cessation intervention, on plasma HDL-C levels (Moffatt et al. 2000). Subjects who used transdermal nicotine patches over 35 days showed no improvement in HDL-C concentration. However, if the use of patches was then stopped, HDL-C concentrations rose to normal, non-smoking levels over the next 42 days. Others have observed contrasting effects in a larger study where smoking cessation, accompanied by the use of higher-dose nicotine transdermal patches, resulted in an immediate increase in HDL, whereas in contrast, low-dose nicotine did not (Allen et al. 1994). These latter ﬁndings are somewhat contradictory to data indicating that nicotine administration to non-smokers, via chewing gum, does not affect HDL-C levels (Quensel et al. 1989a). The potential effects of nicotine patches during smoking cessation on plasma HDL have yet to be clariﬁed.
In summary, smoking leads to a reduction in plasma HDL-C, HDL2-C, apo A-I and probably apoA-II concentrations. The effects of smoking on HDL are dose dependent and reversed upon smoking cessation. Much of the effect of smoking may be TAG dependent where increased plasma TAG concentration leads to remodelling of HDL to a smaller particle size which is more rapidly cleared from the circulation. TAG-independent effects have not yet been thoroughly investigated but include modiﬁcation of apoA-I, reductions in HDL antioxidant enzyme activity and reduced ability of HDL to promote cholesterol efﬂux. The effect of nicotine aids, used to support smoking cessation interventions, on HDL-C concentration and function is unclear.