Sudden infant death syndrome may have biologic cause

Newswise — Sudden infant death syndrome (SIDS) is an instance where an apparently healthy infant's demise, unexplained despite extensive inquiry, transpires before their first birthday. The unfortunate event predominantly transpires during the infant's slumber. Although uncommon, it currently stands as the foremost cause of post-neonatal infant mortality in the United States, transpiring in 103 out of every 100,000 live births annually. Despite the initial triumph of nationwide public health campaigns advocating secure sleep surroundings and improved sleep positions for infants in the 1990s, the incidence rates have persisted unchanged throughout the past three decades.

During the designated period from 2004 to 2011, the researchers gathered tissue samples from the San Diego Medical Examiner's Office, specifically pertaining to infant fatalities. Their focus was on examining the brain stems of 70 infants who had passed away within that timeframe, with the objective of identifying any consistent abnormalities through rigorous testing.

The findings of the study indicate that there are noticeable alterations in the serotonin 2A/C receptor in cases of sudden infant death, in comparison to control cases involving infant fatalities. Previous studies conducted on rodents have demonstrated that the signaling of the 2A/C receptor plays a role in arousal and autoresuscitation, which helps maintain optimal oxygen levels in the brain during sleep. This latest research provides further support to the notion that certain infants, due to a biological abnormality, are susceptible to death under specific circumstances.

According to the investigators involved in this study, they hold the belief that sudden infant death syndrome occurs when three factors coincide. Firstly, it happens during a crucial stage of cardiorespiratory development in the infant's first year. Secondly, the child experiences an external stressor, such as sleeping in a face-down position or sharing a bed. Finally, the child possesses a biological abnormality that renders them susceptible to respiratory difficulties while sleeping. It is the convergence of these three elements that is thought to contribute to cases of sudden infant death syndrome.

"The findings presented in this study build upon prior research conducted by our team and other researchers, which have revealed abnormalities in the serotonergic system of certain infants affected by Sudden Infant Death Syndrome (SIDS)," stated Robin Haynes, the lead author of the paper. "While we have identified abnormalities in the serotonin 2A/C receptor in cases of SIDS, we are still uncertain about the precise relationship between these abnormalities and the cause of death. Further investigation is necessary to understand the implications of these receptor abnormalities within the larger network of serotonin and non-serotonin receptors that safeguard vital functions related to cardiac and respiratory control under challenging circumstances. Currently, we lack the means to identify infants with biological abnormalities in the serotonergic system. Therefore, it remains crucial to adhere to safe-sleep practices to mitigate the risk of SIDS."

The paper, “Altered 5-HT2A/C receptor binding in the medulla oblongata in the sudden infant death syndrome (SIDS): part I. Tissue-based evidence for serotonin receptor signaling abnormalities in cardiorespiratory- and arousal-related circuits,” will be available (at midnight on May 25^th) at: https://doi.org/10.1093/jnen/nlad030.