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啤酒摄入与银屑病呈正向遗传相关,而奶酪和干果摄入呈负向遗传相关:基于condFDR/conjFDR的GWAS汇总统计研究

 

Authors Liu G , Gong F , Yang G, Luo Q 

Received 4 November 2025

Accepted for publication 20 January 2026

Published 29 January 2026 Volume 2026:19 578871

DOI https://doi.org/10.2147/CCID.S578871

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

Editor who approved publication: Dr Monica K. Li

Guo Liu,1,2 Fengjuan Gong,1 Guanhu Yang,2 Qinghua Luo2,3 

1Department of Dermatology, Qionglai Hospital of Traditional Chinese Medicine, Chengdu, 611530, People’s Republic of China; 2Faculty of Chinese Medicine, Macau University of Science and Technology, Macau, 999078, People’s Republic of China; 3Clinical Medical College, Jiangxi University of Chinese Medicine, Nanchang, 330004, People’s Republic of China

Correspondence: Guo Liu, Department of Dermatology, Qionglai Hospital of Traditional Chinese Medicine, Chengdu, 611530, People’s Republic of China, Email zgsccdlg@163.com

Background: Previous epidemiological investigations have reported associations between beer, cheese, and dried fruit intake and the incidence of psoriasis (PS). Nevertheless, the extent of shared genetic architecture underlying these associations remains insufficiently characterized. Therefore, it is essential to examine their molecular relationships from a genomics perspective.
Methods: A stratified, stepwise analytical framework was applied, utilizing genome-wide association study data for PS and three dietary intake patterns (beer, cheese, and dried fruit intake). In the initial phase, linkage disequilibrium score regression, genetic covariance analysis, and high-definition likelihood approaches were employed to quantify genome-wide genetic correlations. Subsequently, local genetic overlap analyses were conducted to delineate chromosomal regions harboring relevant associations. Finally, the conditional/conjunctional false discovery rate (condFDR/conjFDR) methodology was implemented to identify potential shared genetic loci (genetic overlap) across the phenotypes.
Results: The analysis revealed consistent genome-wide genetic correlations between psoriasis (PS) and the three dietary intake traits across LDSC, GNOVA, and HDL. PS showed a significant positive genetic correlation with beer intake (Rg = 0.1082 [LDSC], 0.0796 [GNOVA], and 0.144 [HDL]), whereas negative genetic correlations were observed for cheese intake (Rg = − 0.1523, − 0.1089, and − 0.1866) and dried fruit intake (Rg = − 0.2187, − 0.1639, and − 0.2623). Local analyses further identified multiple chromosomal regions with shared genetic signals. Finally, condFDR/conjFDR analyses supported these overlaps and enabled the identification of several significant shared loci between PS and the dietary traits.
Conclusion: This study systematically investigated the genetic associations between PS and three dietary intake patterns from a genomic perspective and characterized their genome-wide and local genetic overlap. The shared loci identified enhance the understanding of nutrition–disease molecular mechanisms and provide genetic evidence to inform future mechanistic research and risk-modification strategies.

Keywords: psoriasis, dietary intake patterns, genetic correlation, genetic loci, genetic overlap