Genetic Susceptibility in Sudden Infant Death Syndrome (SIDS): A Narrative Review of Emerging Evidence

Sudden Infant Death Syndrome (SIDS) continues to be one of the most challenging and tragic causes of infant mortality in developed countries. While public health interventions have reduced its prevalence, the underlying mechanisms contributing to SIDS remain largely unclear. The biological basis of SIDS is widely believed to be multifactorial in nature, involving inherited genetic vulnerabilities, including mutations in cardiac ion channels and genes associated with brainstem serotonin function, metabolic enzymes, and inflammatory mediators. This review presents a comprehensive analysis of genetic studies relating to SIDS, incorporating recent findings from molecular autopsies, genome-wide association studies and functional assays. It also explores how gene–environment interactions, polygenic risk scores, and multi-omic strategies are reshaping our understanding of this complex condition. The review aims to integrate recent insights from molecular autopsy, genomic profiling, and gene–environment interactions to offer a framework for better risk assessment and the stratification of vulnerable infants who could benefit from targeted clinical and public health interventions.