Sudden infant death syndrome may have a biological cause

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Sudden infant death syndrome (SIDS) is a case where the death of an apparently healthy baby before his first birthday remains unexplained even after a thorough investigation. Death generally seems to occur when babies are asleep.

Although rare, it is today the leading postneonatal infant mortality rate in the United States, occurring in 103 of 100,000 live births each year. Despite the initial success of national public health campaigns promoting safe sleep environments and healthier infant sleeping positions in the United States in the 1990s, the number of cases has remained steady over the past three decades.

Researchers here collected tissue from the San Diego Medical Examiner’s Office linked to infant mortality between 2004 and 2011. They then examined the brain stems of 70 babies who died during the period and tested them for consistent abnormalities.

They found that the serotonin 2A/C receptor is altered in SIDS cases compared to infant death control cases. Previous research in rodents has shown that 2A/C receptor signaling contributes to arousal and autoresuscitation, protecting the brain’s oxygen state during sleep. This new research supports the idea that a biological abnormality in some babies leaves them vulnerable to death under certain circumstances.

The researchers here believe that SIDS occurs when three things happen together: a child is in a critical period of cardiorespiratory development in its first year, the child is confronted with an external stressor such as a face-down sleeping position or sharing a bed, and the child has a biological abnormality that makes them vulnerable to breathing problems while sleeping.

“The work presented builds on previous work by our lab and others that showed abnormalities in the serotonergic system of some SIDS infants,” said the paper’s lead author, Robin Haynes.

“While we have identified serotonin 2A/C receptor abnormalities in SIDS, the relationship between the abnormalities and cause of death remains unknown.”

“Much work remains to determine the consequences of abnormalities in this receptor in the context of a larger network of serotonin and non-serotonin receptors that protect vital functions in cardiac and respiratory control when challenged. Currently, we have no resources to infants with biological abnormalities in the serotonergic system, so adherence to safe sleep practices remains critical.”

The research has been published in Journal of Neuropathology & Experimental Neurology.

More information:
Robin Haynes et al., Altered 5-HT2A/C receptor binding in the medulla oblongata in sudden infant death syndrome (SIDS): part I. Tissue-based evidence for serotonin receptor signaling aberrations in cardiorespiratory and arousal-related circuits, Journal of Neuropathology & Experimental Neurology (2023). DOI: 10.1093/jnen/nlad030

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