Abstract Background Inflammatory bowel disease (IBD) is a chronic inflammatory disorders of the gastrointestinal tract. Up to 30% of people with active IBD experience mood disorders such as depression. Our objective was to identify the pathways associated with the interplay between IBD and depression Methods Detailed information on IBD and depression was gathered from 204 countries and territories spanning 1990 to 2021, sourced from the GBD 2021. Calculations were performed for incidence rates, prevalence rates, disease-adjusted life years (DALYs), years lived with disability (YLDs) and estimated annual percentage changes (EAPCs). In addition, we constructed an age–period–cohort model. We selected three GEO datasets (GSE87473, GSE92415, and GSE112366), Differential expression analysis was performed on the batch-corrected data using the limma package. Furthermore, we curated a list of 153 depression-associated genes from published studies and executed intersection analysis with the identified DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out to investigate biological pathways potentially linking IBD and depression. Finally, GSVA enrichment analysis investigate the underlying molecular biological alterations. Results The incidence of both IBD and depression has been increasing annually globally. Over the past 30 years, the incidence of IBD in China has shown a marked upward trend, while the incidence of depression has exhibited a downward trend. The DALY and YLD rates for both IBD and depression have declined over time. A strong positive correlation between IBD and depression was observed in high-SDI regions and developed countries such as the United States; however, partial correlation analysis controlling for the effect of year revealed no strong linear association between the two. The APC models for IBD and depression indicated that age and period effects play a significant role in the incidence of both diseases. We identified 2560 upregulated and 2593 downregulated genes between IBD and healthy control groups. Intersection of these DEGs with a curated list of 153 depression-related genes revealed 25 overlapping core genes. Then, GO and KEGG enrichment and GSVA analyses highlighted α-Linolenic acid metabolism as a potential key pathway in the IBD-depression comorbidity. Conclusion Although significant progress has been made in the diagnosis and treatment of IBD in China, issues such as delayed identification of depressive symptoms may still persist. Our study discovered α-Linolenic acid metabolism may constitute a critical biological link between IBD and depression, providing novel insights for investigating the shared pathophysiological mechanisms underlying this comorbidity. Reference: none Conflict of interest: Mr. Zhou, Ziru: The authors declare that they have no conflicts of interest. None of the authors have financial, employment, or personal relationships with organizations that could influence the research presented. Zhan, Qiang: The authors declare that they have no conflicts of interest. None of the authors have financial, employment, or personal relationships with organizations that could influence the research presented. Sun, Jing: The authors declare that they have no conflicts of interest. None of the authors have financial, employment, or personal relationships with organizations that could influence the research presented.
Zhou et al. (Thu,) studied this question.