Abstract
Association of obesity and cigarette smoking with markers of inflammation and thrombosis Background: The association between obesity with inflammation and thrombosis has been understudied. The combined association of obesity and cigarette smoking with inflammation and thrombosis also has not been systematically investigated in a well characterized cohort. Methods: We investigated 2549 participants from the Genetic Epidemiology Network of Arteriopathy (GENOA) study (mean age 61±10 years, 64% women, 51% African American). Participants were classified by body mass index (BMI) as normal BMI (n=371), overweight (n= 864), or obese (n= 1314). Obese participants were further classified by self-reported smoking status as having never smoked (n= 747), smoked in the past (n= 454), and currently smoking (n= 113). We compared adjusted associations among these groups with 18 biomarkers of inflammation and 8 biomarkers of thrombosis using generalized estimating equations. Results: After adjusting for potential confounders, individuals who were obese but had never smoked had higher levels of high sensitivity CRP, serum amyloid A, TNFR1 and TNFR2, IL-6, fibrinogen, and VWF compared to participants with normal BMI that were had never smoked (all p<0.05). However, individuals with obesity currently smoking had higher levels of these biomarkers compared to those who never smokers, particularly within the domains of systemic inflammation and cytokines (Table). Compared with participants without obesity who never smoked, the odds of hsCRP >10 milligram/liter in individuals with obesity was 3.6 times for those who currently smoked, and 2.7 times for those who never smoked. Conclusions: In adjusted analyses, obesity is associated with several proinflammatory biomarkers; but when combined with cigarette smoking, this relationship becomes stronger. These findings underscore the need to recommend smoking cessation and weight loss in patients with both of these important risk factors.
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