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Ebenezer T Oni1, Vincent Figueredo2, Ehimen Aneni3, Emir Veladar4, John W McEvoy5, Michael J Blaha56, Roger S Blumenthal5, Raquel D Conceicao7, Jose A M Carvalho7, Raul D Santos78, Khurram Nasir9
Author information
1Cardiology Division, Heart and Vascular Institute, Einstein Medical Center, Philadelphia, PA, USA.
2St. Mary Medical Center, 1203 Langhorne-Newtown Road, Suite 320, Langhorne, PA 19047, USA.
3Section of Cardiovascular Medicine, Department of Medicine, Yale University School of Medicine.
4Center of Advanced Analytics, Baptist Health South Florida, 8900 North Kendall Drive, Miami, FL 33176, USA.
5The Johns Hopkins Ciccarone Center for the Prevention of Heart Disease, Baltimore, MD, USA.
6Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.
7Preventive Medicine Center Hospital Israelita Albert Einstein, Sao Paulo, Brazil.
8Lipid Clinic-Heart Institute (InCor) University of Sao Paulo Medical School Hospital, Sao Paulo, Brazil.
9Houston Methodist, Debakey Heart and Vascualr Institute, Houston, TX, USA.
Abstract
Background: Serum gamma-glutamyl transferase (GGT) is a marker of oxidative stress, associated with increased cardiovascular (CV) risk. The impact of smoking on oxidative stress may be aggravated in individuals with non-alcoholic fatty liver disease (NAFLD). We aimed to ascertain the association of smoking on GGT levels in the presence or absence of NAFLD.
Methods: We evaluated 6,354 healthy subjects (43 ± 10 years, 79% males) without clinical cardiovascular disease (CVD) undergoing an employer-sponsored physical between December 2008 and December 2010. NAFLD was diagnosed by ultrasound and participants were categorized as current or non-smokers by self report. A multivariate linear regression of the cross-sectional association between smoking and GGT was conducted based on NAFLD status.
Results: The prevalence of NAFLD was 36% (n = 2,299) and 564 (9%) were current smokers. Smokers had significantly higher GGT levels in the presence of NAFLD (P < 0.001). After multivariable adjustment, current smoking was associated with 4.65 IU/L higher GGT level, P < 0.001, compared to non-smokers. When stratified by NAFLD, the magnitude of this association was higher in subjects with NAFLD (β-coefficient: 11.12; 95% confidence interval (CI): 5.76 - 16.48; P < 0.001); however, no such relationship was observed in those without NAFLD (β: -0.02; 95% CI: -3.59, 3.56; P = 0.992). Overall the interaction of NAFLD and smoking with GGT levels as markers of oxidative stress was statistically significant.
Conclusions: Smoking is independently associated with significantly increased oxidative stress as measured by GGT level. This association demonstrates effect modification by NAFLD status, suggesting that smoking may intensify CV risk in individuals with NAFLD.