Abstract

Objective: Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in developed nations and is independently associated with increased overall morality from all causes as well as from CVD. Growing evidence support that low serum 25-hydroxyvitamin D ((25OH)D) is associated with NAFLD. However, significant racial/ethnic differences exist in serum 25(OH)D and the prevalence of NAFLD: African Americans have lower 25(OH)D than Caucasians, and NAFLD prevalence is higher in Caucasians. We tested whether the association between 25(OH)D and NAFLD vary by race/ethnicity, adjusting for common risk factors for low 25(OH)D and NAFLD. Methods: Participants were from the MESA study, who were free from CVD and liver conditions, were not taking oral corticosteroids, did not report heavy alcohol intake (>7 drinks/week for women and > 14 drinks/week for men), and had serum 25(OH)D and upper abdominal non-contrast CT images available at baseline. 25(OH)D was adjusted for season. NAFLD was defined if liver-to-spleen Hounsfield units ratio was <1. Logistic regression was used for statistical analyses. Final models were adjusted for study site, age, gender, education, income, BMI, triglycerides, high-density lipoproteins, systolic blood pressure, smoking, diabetes, interlukine-6 and C-reactive protein. Results: The study included3,484 participants (mean age (SD): 62.7(10.4) Yr; 44% of participants were male; 38.4% Caucasian, 27.8% African American, 23.5% Hispanic, and 10.3% Chinese American). Serum 25(OH)D significantly varied by race/ethnicity; with Caucasian have the highest levels and African American have the lowest levels (mean(SD): 29.5(10.4)ng/ml vs. 19.6(9.1)ng/ml, respectively, p<0.0001). NAFLD was present among 17.5% (n=611) of the participants; with Hispanic showing the highest prevalence rate (26.2%) followed by Chinese American (19.8%), Caucasian (15.8%) and African American (11.7%), P=<0.0001. In unadjusted and final models, the association of 25(OH)D with NAFLD differed significantly by race/ethnicity (P<0.01). Stratification analyses showed significant negative association only in Causations; such that lower 25(OH)D was significantly associated with higher risk of NAFLD (adjusted OR (95% CI):1.23(1.03, 1.47) per 1 SD decrease in serum 25(OH)D). For other racial/ethnic groups, BMI, triglycerides, diabetic status and/or smoking, but not serum 25(OH)D, were common independent risk factors for NAFLD. Conclusions: The association of 25(OH)D with NAFLD varies by race/ethnicity. Future studies should assess if targeting vitamin D deficiency in Caucasians may reduce their higher risk of NAFLD above and beyond controlling other modifiable risk factors, whereas, controlling modifiable risk factors, excluding vitamin D, may be more important in reducing NAFLD risk in other racial/ethnic groups.

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