Sudden Infant Death Syndrome (SIDS) is a perplexing phenomenon where healthy infants die unexpectedly, often during sleep, before their first birthday. It remains the leading cause of post-neonatal infant death in the U.S., with fixed rates despite ongoing safe-sleep campaigns since the 1990s. Recent research has discovered abnormalities in the serotonin 2A/C receptor in tissue samples from 70 infants who died between 2004 and 2011, linking these abnormalities to critical functions like arousal and autoresuscitation. This suggests that infants may be particularly vulnerable to SIDS due to a combination of developmental factors, external stressors (e.g., sleeping position), and biological predispositions.
The study highlights the Triple-Risk Model for SIDS, which posits that three conditions must coincide for SIDS to occur: an infant in a critical developmental period, exposure to external stressors, and the presence of biological vulnerabilities in respiratory control. While the exact relationship between the serotonin receptor abnormalities and SIDS is unclear, the findings underscore the ongoing necessity for safe-sleep practices to mitigate risks, as there currently isn’t a way to identify infants with these biological abnormalities.
