Habitual coffee intake and risk for nonalcoholic fatty liver disease: a two-sample Mendelian randomization study
- PDF / 662,374 Bytes
- 7 Pages / 595.276 x 790.866 pts Page_size
- 72 Downloads / 204 Views
ORIGINAL CONTRIBUTION
Habitual coffee intake and risk for nonalcoholic fatty liver disease: a two‑sample Mendelian randomization study Yang Zhang1 · Zhipeng Liu2 · Tasnim Choudhury1 · Marilyn C. Cornelis3 · Wanqing Liu1,4,5 Received: 20 April 2020 / Accepted: 19 August 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Purpose Epidemiological studies support a protective role of habitual coffee and caffeine consumption against the risk of non-alcoholic fatty liver disease (NAFLD). We aimed to investigate the causal relationship between coffee intake and the risk of NAFLD. Methods We performed a two-sample Mendelian randomization (MR) analysis using SNPs associated with habitual coffee intake in a published genome-wide association study (GWAS) as genetic instruments and summary-level data from a published GWAS of NAFLD (1122 cases and 399,900 healthy controls) in the UK Biobank. The causal relationship was estimated with the inverse weighted method using a 4-SNP and 6-SNP instrument based on the single largest non-UK Biobank GWAS (n = 91,462) and meta-analysis (n = 121,524) of GWAS data on habitual coffee intake, respectively. To maximize power, we also used up to 77 SNPs associated with coffee intake at a liberal significance level (p ≤ 1e-4) as instruments. Results We observed a non-significant trend towards a causal protective effect of coffee intake on NAFLD based upon either the 4-SNP (OR: 0.76; 95% CI 0.51, 1.14, p = 0.19) or 6-SNP genetic instruments (OR: 0.77; 95% CI 0.48, 1.25, p = 0.29). The result also remains non-significant when using the more liberal 77-SNP instrument. Conclusion Our findings do not support a causal relationship between coffee intake and NAFLD risk. However, despite the largest-to-date sample size, the power of this study may be limited by the non-specificity and moderate effect size of the genetic alleles on coffee intake. Keywords Coffee · Nonalcoholic fatty liver disease (NAFLD) · Causal effect · Mendelian randomization · Genome-wide association study (GWAS) Yang Zhang and Zhipeng Liu are contributed equally. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00394-020-02369-z) contains supplementary material, which is available to authorized users. * Wanqing Liu [email protected] 1
Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI, USA
2
Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN, USA
3
Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
4
Department of Pharmacology, School of Medicine, Wayne State University, Detroit, MI, USA
5
Integrative Biosciences Center, Wayne State University, Room 2401, 6135 Woodward Ave., Detroit, MI 48202, USA
Introduction Nonalcoholic fatty liver disease (NAFLD) is defined as the development of an abnormal accumulation of fat in the liver without sig
Data Loading...
