Key Takeaways & Executive Findings
- •• Vitamin D and appendicular lean mass show negative genetic correlations with inflammatory bowel disease and its subtypes. • Mendelian randomization reveals a positive causal effect of serum magnesium on inflammatory bowel disease and small intestine Crohn’s disease. • Cross-phenotype analysis identifies shared genetic loci, particularly in the HLA region, influencing both nutritional status and inflammatory bowel disease. • Targeted nutritional management may be crucial for slowing inflammatory bowel disease progression.
Abstract
BACKGROUND: Inflammatory bowel disease, encompassing ulcerative colitis and Crohn’s disease, is a chronic condition linked to malnutrition, sarcopenia, and disease severity, with limited research on their genetic associations. OBJECTIVE: To systematically explore the common genetic basis and causal relationships between nutrition, nutritional status, and inflammatory bowel disease using advanced statistical genetics. METHODS: Single nucleotide polymorphism data for nutritional markers (minerals, vitamins, albumin, hemoglobin, fatty acids) and sarcopenia traits (appendicular lean mass and hand grip strength) were obtained from the GWAS Catalog, and inflammatory bowel disease and its subtypes from the FinnGen database R10. Advanced statistical genetics methods, including linkage disequilibrium score regression, cross-phenotype association analysis, and Mendelian randomization, were used to infer associations. RESULTS AND CONCLUSION: Significant genetic correlations were found: vitamin D with inflammatory bowel disease (rg=-0.080, P=0.029) and ulcerative colitis (rg=-0.087, P=0.027); appendicular lean mass with inflammatory bowel disease (rg=-0.100, P=0.0002), ulcerative colitis (rg=-0.100, P=0.0002), and small intestine Crohn’s disease (rg=-0.081, P=0.035); hand grip strength with small intestine Crohn’s disease (rg=-0.125, P=0.035). Mendelian randomization indicated a positive causal effect of magnesium levels on inflammatory bowel disease (OR=1.41, P=0.036) and small intestine Crohn’s disease (OR=1.78, P=0.035). Cross-phenotype analysis identified shared single nucleotide polymorphisms, particularly in the human leukocyte antigen region, affecting both nutritional status and inflammatory bowel disease. These findings further explain the genetic link between nutrition, sarcopenia, and inflammatory bowel disease, suggesting that targeted nutritional management may be key to slowing disease progression. This study provides new perspectives for personalized treatment and has potential implications for prevention strategies of inflammatory bowel disease.
1. Introduction
Inflammatory bowel disease, encompassing ulcerative colitis and Crohn’s disease, is a chronic inflammatory condition of the gastrointestinal tract, with rising incidence in recent years, imposing a substantial burden on individuals, families, and society [1-2]. Patients with inflammatory bowel disease often experience reduced nutritional intake, malabsorption, dysbiosis, and increased energy expenditure due to immune-inflammatory responses, leading to poor nutritional status, weight loss, and low muscle mass [3]. Sarcopenia, characterized by rapid decline in muscle mass and strength, is associated with disease progression in inflammatory bowel disease [4]. Additionally, multiple serum nutritional markers, including minerals, vitamins, hemoglobin, albumin, and lipids, are linked to the severity of inflammatory bowel disease [5-8]. Although dietary calcium supplementation is considered potentially beneficial in alleviating symptoms [9] and has been supported in animal experiments [10-11], randomized controlled trials have not demonstrated significant efficacy [12]. Serum albumin levels have been shown to be negatively correlated with disease activity, but most existing studies are cross-sectional and lack prospective evidence [8,13]. Research on the impact of sarcopenia on inflammatory bowel disease severity is also limited and inconclusive.
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Liao Guibin, Wu Yixuan, Tang Jing, Huang Jinke, Wang Jun, Yan Ziqi, Liu Shujun, Zhang Haiyan (2026). Shared genetic basis and causal relationship between nutrition, nutritional status and inflammatory bowel disease. Chinese Journal of Tissue Engineering Research. https://doi.org/10.12307/2026.21251
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Frequently Asked Questions
What is the main finding of this study?
The study reveals significant genetic correlations between vitamin D, appendicular lean mass, and inflammatory bowel disease, and identifies a positive causal effect of serum magnesium on inflammatory bowel disease and small intestine Crohn’s disease.
What methods were used?
Advanced statistical genetics methods including linkage disequilibrium score regression, cross-phenotype association analysis, and Mendelian randomization were applied to GWAS summary statistics.
What are the implications for clinical practice?
The findings suggest that targeted nutritional management, particularly monitoring and optimizing magnesium and vitamin D levels, may be important for slowing disease progression and could inform personalized treatment strategies.
What are the limitations of the study?
The study relies on genetic data from European populations, and the Mendelian randomization analysis may be subject to horizontal pleiotropy and weak instrument bias. Further research is needed to validate findings across diverse populations and to explore underlying mechanisms.
How can this research be extended?
Future studies could investigate the causal role of other nutritional factors, explore the shared genetic architecture in more detail, and conduct functional experiments to validate the identified loci and pathways.
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