Genes vs environment in inflammatory bowel disease: an update

ABSTRACT

Introduction

Inflammatory bowel diseases (IBDs) are known to be caused by a combination of genetic and environmental factors that vary in their influence on the development of the disease. Environmental exposures seem to influence IBD susceptibility, whereas genetic background is thought to modulate the impact of the environment on disease course and phenotype.

Areas covered

A broad review of the involvement of genes and the environment in IBD pathogenesis was performed, and information regarding the main genetic and environmental factors – categorized into lifestyle factors, drugs, diet, and microbes – was updated. Monogenic very early onset IBD (VEO-IBD) was also discussed.

Expert opinion

In the upcoming years, better understanding of gene-environment interactions will contribute to the possibility of a better prediction of disease course, response to therapy, and therapy-related adverse events with the final goal of personalized and more efficient patient management.

KEYWORDS:

• Environment
• gene
• inflammatory bowel disease
• risk factor
• very early onset inflammatory bowel disease

Article highlights

• The exact cause of IBD is still unknown. The most validated hypothesis is based on the interactions between genetic susceptibility, environmental and dietary factors, gut microbiome alterations, and dysregulated immune response.

• To date, approximately 240 susceptibility loci for IBD have been discovered, which individually contribute only a small percentage of the expected heritability in IBD.

• Among the environmental factors linked to the development of IBD are lifestyle, drugs, dietary factors, and bacterial exposures. Nonetheless, evidence is often conflicting and/or of poor quality.

• More research is needed to corroborate existing data and solve knowledge gaps, such as the exact mechanisms by which environmental exposures cause IBD.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.