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Abstract Details
Habitual coffee intake and risk for nonalcoholic fatty liver disease: a two-sample Mendelian randomization study
Eur J Nutr. 2021 Jun;60(4):1761-1767. doi: 10.1007/s00394-020-02369-z.Epub 2020 Aug 27.
Yang Zhang#1, Zhipeng Liu#2, Tasnim Choudhury1, Marilyn C Cornelis3, Wanqing Liu456
Author information
1Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI, USA.
2Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, Purdue University, West Lafayette, IN, USA.
3Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
4Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI, USA.
5Department of Pharmacology, School of Medicine, Wayne State University, Detroit, MI, USA.
6Integrative Biosciences Center, Wayne State University, Room 2401, 6135 Woodward Ave., Detroit, MI, 48202, USA.
#Contributed equally.
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.