Beer Intake is Positively, While Cheese and Dried Fruit Intake Are Negatively Genetically Correlated with Psoriasis:...

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.

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.

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.

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.