Smoking and smoking cessation -- the relationship between cardiovascular disease and lipoprotein metabolism: a review

Atherosclerosis. 2008 Dec;201(2):225-35. doi: 10.1016/j.atherosclerosis.2008.04.046. Epub 2008 May 13.


Cigarette smoking is generally accepted as the most preventable cause of death in the United States today. Individuals who smoke experience a wide range of physiologic side effects that increase the risk of cardiovascular disease (CVD), including insulin resistance, elevated catecholamine levels which contribute to an elevated heart rate and blood pressure, and hypercholesterolemia. The link between hypercholesterolemia and cardiovascular disease has been extensively researched and is undeniable. What is more, this link is strengthened in smokers as cigarette smoking is known to increase total cholesterol (TC), triglycerides (TG), and low-density lipoprotein (LDL), while acting to decrease the cardio-protective high-density lipoprotein (HDL). Alterations in the enzymes that control lipid transport may be a key underlying mechanism contributing to these health destroying effects. This review examines the current literature related to: (1) smoking, lipoproteins, and lipid-related enzymes; (2) the impact of nicotine, carbon monoxide and free radicals on physiologic parameters related to health; and (3) metabolic issues involving smoking cessation and nicotine replacement therapy.

Publication types

  • Review

MeSH terms

  • Carbon Monoxide / chemistry
  • Cardiovascular Diseases / blood*
  • Cardiovascular Diseases / etiology
  • Cardiovascular Diseases / prevention & control*
  • Dose-Response Relationship, Drug
  • Female
  • Humans
  • Lipids / chemistry
  • Lipoproteins / metabolism*
  • Male
  • Nicotine / metabolism
  • Risk Factors
  • Smoking / adverse effects*
  • Smoking Cessation / methods*


  • Lipids
  • Lipoproteins
  • Nicotine
  • Carbon Monoxide