Tracey G Simon1, Maria Esther Perez Trejo2, Irfan Zeb3, Alexis C Frazier-Wood4, Robyn L McClelland2, Raymond T Chung1, Matthew J Budoff5. 1. Liver Center, Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, United States. 2. Department of Biostatistics, University of Washington, Seattle, WA, United States. 3. Department of Cardiology, Mount Sinai St. Luke's Roosevelt Hospital (Bronx-Lebanon Hospital Center), United States. 4. Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX, United States. 5. Los Angeles Biomedical Research Institute, Division of Cardiology, Harbor-UCLA Medical Center, Los Angeles, CA, United States. Electronic address: mbudoff@labiomed.org.
Abstract
BACKGROUND: Atherosclerosis and its clinical sequelae represent the leading cause of mortality among patients with nonalcoholic fatty liver disease (NAFLD). While epidemiologic data support the hepatoprotective benefits of coffee in NAFLD, whether coffee improves NAFLD-associated CVD risk is unknown. METHODS: We examined 3710 ethnically-diverse participants from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, without history of known liver disease, and with available coffee data from a validated 120-item food frequency questionnaire. All participants underwent baseline non-contrast cardiac CT from which NAFLD was defined by liver:spleen ratio (L:S<1.0), and subclinical CVD was defined by coronary artery calcium (CAC)>0. Major CVD events were defined by the first occurrence of myocardial infarction, cardiac arrest, angina, stroke, or CVD death. We used log-binomial regression to calculate the adjusted prevalence ratio (PR) for CAC>0 by coffee intake and NAFLD status, and events were compared between groups using frequency of events within adjusted Cox proportional hazard regression models. RESULTS: Seventeen percent (N=637) of participants met criteria for NAFLD. NAFLD participants were more likely to have elevated BMI (mean 31.1±5.5kg/m2 vs. 28.0±5.2kg/m2, p<0.0001), and diabetes (22% vs. 11%, p<0.0001), but did not differ in daily coffee consumption (p=0.97). Among NAFLD participants, coffee consumption was not associated with prevalent, baseline CAC>0 (PR=1.02 [0.98-1.07]). Over 12.8years of follow-up, 93 NAFLD and 415 non-NAFLD participants experienced a CV event. However, coffee intake was not associated with incident CVD events, in either NAFLD (HR=1.05 [0.91-1.21]) or non-NAFLD participants (HR=1.03 [0.97-1.11]). CONCLUSION: In a large, population-based cohort, coffee consumption was not associated with the prevalence of subclinical CVD, nor did coffee impact the future risk of major CVD events, regardless of underlying NAFLD status.
BACKGROUND:Atherosclerosis and its clinical sequelae represent the leading cause of mortality among patients with nonalcoholic fatty liver disease (NAFLD). While epidemiologic data support the hepatoprotective benefits of coffee in NAFLD, whether coffee improves NAFLD-associated CVD risk is unknown. METHODS: We examined 3710 ethnically-diverse participants from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort, without history of known liver disease, and with available coffee data from a validated 120-item food frequency questionnaire. All participants underwent baseline non-contrast cardiac CT from which NAFLD was defined by liver:spleen ratio (L:S<1.0), and subclinical CVD was defined by coronary artery calcium (CAC)>0. Major CVD events were defined by the first occurrence of myocardial infarction, cardiac arrest, angina, stroke, or CVD death. We used log-binomial regression to calculate the adjusted prevalence ratio (PR) for CAC>0 by coffee intake and NAFLD status, and events were compared between groups using frequency of events within adjusted Cox proportional hazard regression models. RESULTS: Seventeen percent (N=637) of participants met criteria for NAFLD. NAFLD participants were more likely to have elevated BMI (mean 31.1±5.5kg/m2 vs. 28.0±5.2kg/m2, p<0.0001), and diabetes (22% vs. 11%, p<0.0001), but did not differ in daily coffee consumption (p=0.97). Among NAFLD participants, coffee consumption was not associated with prevalent, baseline CAC>0 (PR=1.02 [0.98-1.07]). Over 12.8years of follow-up, 93 NAFLD and 415 non-NAFLD participants experienced a CV event. However, coffee intake was not associated with incident CVD events, in either NAFLD (HR=1.05 [0.91-1.21]) or non-NAFLD participants (HR=1.03 [0.97-1.11]). CONCLUSION: In a large, population-based cohort, coffee consumption was not associated with the prevalence of subclinical CVD, nor did coffee impact the future risk of major CVD events, regardless of underlying NAFLD status.
Authors: Jeffrey W Molloy; Christopher J Calcagno; Christopher D Williams; Frances J Jones; Dawn M Torres; Stephen A Harrison Journal: Hepatology Date: 2011-12-22 Impact factor: 17.425
Authors: Aaron R Folsom; Richard A Kronmal; Robert C Detrano; Daniel H O'Leary; Diane E Bild; David A Bluemke; Matthew J Budoff; Kiang Liu; Steven Shea; Moyses Szklo; Russell P Tracy; Karol E Watson; Gregory L Burke Journal: Arch Intern Med Date: 2008-06-23
Authors: Kiran Bambha; Laura A Wilson; Aynur Unalp; Rohit Loomba; Brent A Neuschwander-Tetri; Elizabeth M Brunt; Nathan M Bass Journal: Liver Int Date: 2013-11-24 Impact factor: 5.828
Authors: Diane E Bild; David A Bluemke; Gregory L Burke; Robert Detrano; Ana V Diez Roux; Aaron R Folsom; Philip Greenland; David R Jacob; Richard Kronmal; Kiang Liu; Jennifer Clark Nelson; Daniel O'Leary; Mohammed F Saad; Steven Shea; Moyses Szklo; Russell P Tracy Journal: Am J Epidemiol Date: 2002-11-01 Impact factor: 4.897