New study identifies biomarkers that could prevent sudden infant death syndrome

Sudden Infant Death Syndrome | Image Credit: © dizain - © dizain - stock.adobe.com.

Groundbreaking research from the University of Virginia School of Medicine has identified critical biomarkers in blood samples that could revolutionize the early detection and prevention of Sudden Infant Death Syndrome (SIDS). This development is a significant leap forward in addressing a condition that remains the leading cause of death in infants aged one month to one year.¹

The study, the largest of its kind, analyzed the blood serum of 300 infants from two major sources: the Chicago Infant Mortality Study and the National Institutes of Health’s NeuroBioBank. Researchers examined 828 metabolites associated with vital biological processes, including nerve cell communication and stress response. Their findings identified 35 key biomarkers linked to SIDS, offering invaluable insight into its underlying causes and potential diagnostic tools.²

“Our study is the largest study to date that has attempted to detect how these small molecules in the blood may serve as biomarkers for SIDS,” said researcher Keith L. Keene, PhD, founding director of UVA’s Center for Health Equity and Precision Public Health. “Our findings support a role for multiple key biological pathways and provide insight into how those biological processes may contribute to increased risk or serve to diagnose SIDS.”¹

Understanding SIDS through metabolomics

Metabolomics, the study of small molecules called metabolites, offers new perspectives on complex diseases like SIDS. By investigating substances linked to nerve function, stress responses, and hormone regulation, the UVA team pinpointed critical metabolites. Notable among them was ornithine, essential for ammonia elimination, and lipid metabolites crucial for brain and lung health.²

The study identified disruptions in lipid profiles, particularly sphingomyelins, which are critical for brain and lung development. “Differences in these fats may disrupt these critical processes, placing some infants at risk for SIDS," said Chad Aldridge, DPT, MS-CR, of the School of Medicine’s Department of Neurology.¹

Another significant finding was the association of ribitol and arabitol, compounds linked to energy metabolism, with increased SIDS risk. These results underscore the multifactorial nature of the syndrome and the importance of metabolic pathways in its onset.²

A step toward prevention

The significance of this research lies in its potential to develop a simple blood test that could identify infants at heightened risk. Such a breakthrough could enable targeted interventions and proactive monitoring. However, the researchers emphasize the need for further research to confirm these biomarkers' roles in causing or predicting SIDS.

“The results of this study are very exciting–we are getting closer to explaining the pathways leading to a SIDS death,” said Fern R. Hauck, MD, MS, study researcher, family medicine physician at UVA Health, director of the Chicago Infant Mortality Study, and a leading expert on SIDS. “Our hope is that this research lays the groundwork to help identify –through simple blood tests–infants who are at higher risk for SIDS and to save these precious lives.”¹

While the findings are promising, researchers stress that they are only the beginning. Further studies are required to validate these biomarkers and explore their implications across diverse populations. The study’s insights into lipid and amino acid metabolism, stress responses, and other pathways offer a foundation for future research aimed at unraveling SIDS's mysteries.¹

References:

1. University of Virginia Health System. SIDS discovery could ID babies at risk of sudden death. Eurekalert. January 22, 2025. Accessed January 22, 2025. https://www.eurekalert.org/news-releases/1071193

2. Aldridge CM, Keene KL, Normeshie CA, Mychaleckyj JC, Hauck FR. Metabolomic profiles of infants classified as sudden infant death syndrome: a case-control analysis. EBioMedicine. 2025;111:105484. doi:10.1016/j.ebiom.2024.105484