Insulin resistance and compensatory hyperinsulinemia: the key player between cigarette smoking and cardiovascular disease?
Hyperinsulinemia, dyslipidemia, and endothelial dysfunction are characteristic findings in insulin-resistant individuals, and all of these abnormalities have been identified as increasing cardiovascular disease (CVD) risk. Smokers tend to be relatively insulin resistant, hyperinsulinemic, and dyslipidemic, with evidence of endothelial dysfunction, as compared with nonsmokers, and recent epidemiologic data have suggested that CVD in smokers is primarily seen in those individuals who also have the characteristic findings of insulin resistance. Based on these observations, it is argued that insulin resistance and its consequences represent a major mechanistic link between cigarette smoking and CVD. It is also postulated that the enhanced CVD risk in smokers, resulting from hyperinsulinemia, abnormalities of lipoprotein metabolism, and endothelial dysfunction, will primarily be present in those smokers who are insulin resistant. As a corollary, it is suggested that CVD risk in individuals who cannot, or will not, stop smoking can be reduced by therapeutic efforts aimed at attenuating the adverse effects of insulin resistance and its consequences.
Reaven
Gerald
G
Division of Cardiovascular Medicine, Falk CVRC, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305, USA. greaven@cvmed.stanford.edu
Tsao
Philip S
PS
D002318:Cardiovascular Diseases / Q000209:etiology* / Q000503:physiopathology*; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications* / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology*; D012907:Smoking / Q000009:adverse effects* / Q000503:physiopathology*