5.3. Nicotine and Lipids.
Nicotine, by release of catecholamines, induces lipolysis and releases plasma free fatty acids. There is evidence that these free fatty acids are primarily taken up by the liver, which might be expected to increase the synthesis of VLDL, consistent with changes described in cigarette smokers ([93]).
Results of studies of the effects of nicotine on lipids in animals are conflicting. Injection of nicotine or feeding of nicotine has been reported ([83, 84, 88]) to increase total cholesterol in rabbits and monkeys receiving a high cholesterol diet. Nicotine feeding in squirrel monkeys for 2 years has been shown ([94]) to increase plasma levels of LDL. The mechanism in monkeys included both accelerated synthesis of LDL
through lipolysis of HDL and VLDL and impaired clearance of LDL. Of importance in interpreting these animal studies is that high doses of nicotine have been administered, often by an oral route, and without measurement of blood levels of nicotine to determine exposure adequately.
Most studies in humans given nicotine preparations suggest that nicotine delivered in these forms does not have an adverse effect on lipid profiles. In one study ([95]), nicotine chewing gum (2 mg eight times a day) was given to healthy nonsmokers for 2 weeks. No changes in plasma concentrations of triglycerides; total, HDL or LDL cholesterol; or apolipoprotein A1 or B were noted. In another study ([96]), 20 nonsmokers with ulcerative colitis received transdermal nicotine (15 mg/day) for 12 weeks. No changes in plasma lipids were found. Also, there were no changes in white cell count or platelet activation (assessed by platelet volume and expression of P-selectin), and no evidence of endothelial damage (assessed by plasma Von Willebrand factor antigen levels) was detected.
Data from smokers who stop smoking and use transdermal nicotine indicate that lipids change toward normal while taking nicotine ([97]).
