Key result
Cigarette smoking contributed to atherosclerosis through gender-differential intermediate pathways, with central obesity common to both sexes, dyslipidemia unique to women, and elevated LDL and inflammation unique to men.
Why the study?
Does cigarette smoking increase carotid intima-medial thickness and what are the gender-specific mediating atherogenic pathways in middle-aged adults?
Cohort (n=573)
Does cigarette smoking increase carotid intima-medial thickness and what are the gender-specific mediating atherogenic pathways in middle-aged adults?
Cigarette smoking accelerates subclinical atherosclerosis through gender-specific intermediate pathways, with central obesity being common to both, dyslipidemia unique to women, and elevated LDL, sympathetic overactivity, and inflammation unique to men.
Gender-specific pathways may refine smoking risk assessment; hypothesis-generating and should not yet change practice.
Objective: This study investigates mediating atherogenic pathways caused by cigarette smoking (anthropometric, metabolic, hemodynamic, inflammatory factors) among middle-aged adults and whether there are gender differences in these pathways.
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Fan et al. (2009) conducted a cohort in Healthy adults (n=573). Cigarette smoking vs. Never smoking was evaluated on Common carotid arterial intima-medial thickness (CCA-IMT). Cigarette smoking contributed to atherosclerosis through gender-differential intermediate pathways, with central obesity common to both sexes, dyslipidemia unique to women, and elevated LDL and inflammation unique to men.
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