Kamil F Faridi1, Di Zhao2, Seth S Martin3, Joshua R Lupton3, Steven R Jones3, Eliseo Guallar2, Christie M Ballantyne4, Pamela L Lutsey5, Erin D Michos6. 1. Division of Cardiology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA; Ciccarone Center for Prevention of Heart Disease, Johns Hopkins University, Baltimore, Maryland, USA. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. 3. Ciccarone Center for Prevention of Heart Disease, Johns Hopkins University, Baltimore, Maryland, USA. 4. Section of Cardiovascular Research, Baylor College of Medicine, Houston, Texas, USA. 5. Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA. 6. Ciccarone Center for Prevention of Heart Disease, Johns Hopkins University, Baltimore, Maryland, USA; Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. Electronic address: edonnell@jhmi.edu.
Abstract
OBJECTIVES: Deficiency of 25-hydroxyvitamin D (25[OH]D) is associated with increased risk for cardiovascular disease, perhaps mediated through dyslipidemia. Deficient 25(OH)D is cross-sectionally associated with dyslipidemia, but little is known about longitudinal lipid changes. The aim of this study was to determine the relationship of 25(OH)D deficiency to longitudinal lipid changes and risk for incident dyslipidemia. METHODS: This was a longitudinal community-based study of 13 039 participants from the ARIC (Atherosclerosis Risk in Communities) study who had 25(OH)D and lipids measured at baseline (1990-1992) and lipids remeasured in 1993 to 1994 and 1996 to 1998. Mixed-effect models were used to assess the association of 25(OH)D and lipid trends after adjusting for clinical characteristics and for baseline or incident use of lipid-lowering therapy. Risk for incident dyslipidemia was determined for those without baseline dyslipidemia. RESULTS: Baseline mean ± SD age was 57 ± 6 y and 25(OH)D was 24 ± 9 ng/mL. Participants were 57% women, 24% black. Over a mean follow-up of 5.2 y, the fully adjusted average differences (95% confidence interval [CI]) comparing deficient (<20 ng/mL) to optimal (≥30 ng/mL) 25(OH)D were: total cholesterol (TC) -2.40 mg/dL (-4.21 to -0.60), high-density lipoprotein cholesterol (HDL-C) -3.02 mg/dL (-3.73 to -2.32) and the ratio of TC to HDL-C 0.18 (0.11-0.26). Those with deficient compared with optimal 25(OH)D had modestly increased risk for incident dyslipidemia in demographic-adjusted models (relative risk [RR], 1.19; 95% CI, 1.02-1.39), which was attenuated in fully adjusted models (RR, 1.12; 95% CI, 0.95-1.32). CONCLUSIONS: Deficient 25(OH)D was prospectively associated with lower TC and HDL-C and a greater ratio of TC to HDL-C after considering factors such as diabetes and adiposity. Further work including randomized controlled trials is needed to better assess how 25(OH)D may affect lipids and cardiovascular risk.
OBJECTIVES: Deficiency of 25-hydroxyvitamin D (25[OH]D) is associated with increased risk for cardiovascular disease, perhaps mediated through dyslipidemia. Deficient 25(OH)D is cross-sectionally associated with dyslipidemia, but little is known about longitudinal lipid changes. The aim of this study was to determine the relationship of 25(OH)D deficiency to longitudinal lipid changes and risk for incident dyslipidemia. METHODS: This was a longitudinal community-based study of 13 039 participants from the ARIC (Atherosclerosis Risk in Communities) study who had 25(OH)D and lipids measured at baseline (1990-1992) and lipids remeasured in 1993 to 1994 and 1996 to 1998. Mixed-effect models were used to assess the association of 25(OH)D and lipid trends after adjusting for clinical characteristics and for baseline or incident use of lipid-lowering therapy. Risk for incident dyslipidemia was determined for those without baseline dyslipidemia. RESULTS: Baseline mean ± SD age was 57 ± 6 y and 25(OH)D was 24 ± 9 ng/mL. Participants were 57% women, 24% black. Over a mean follow-up of 5.2 y, the fully adjusted average differences (95% confidence interval [CI]) comparing deficient (<20 ng/mL) to optimal (≥30 ng/mL) 25(OH)D were: total cholesterol (TC) -2.40 mg/dL (-4.21 to -0.60), high-density lipoprotein cholesterol (HDL-C) -3.02 mg/dL (-3.73 to -2.32) and the ratio of TC to HDL-C 0.18 (0.11-0.26). Those with deficient compared with optimal 25(OH)D had modestly increased risk for incident dyslipidemia in demographic-adjusted models (relative risk [RR], 1.19; 95% CI, 1.02-1.39), which was attenuated in fully adjusted models (RR, 1.12; 95% CI, 0.95-1.32). CONCLUSIONS: Deficient 25(OH)D was prospectively associated with lower TC and HDL-C and a greater ratio of TC to HDL-C after considering factors such as diabetes and adiposity. Further work including randomized controlled trials is needed to better assess how 25(OH)D may affect lipids and cardiovascular risk.
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