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 infant before his first birthday remains unexplained even after a thorough investigation. Death usually seems to occur when infants are sleeping.

Although rare, it is the leading post-neonatal infant death in the United States today, occurring in 103 out of 100,000 live births per year. Despite the initial success of national public health campaigns promoting safe sleeping environments and healthier sleeping positions among infants in the 1990s in the United States, case rates have remained the same for the past three decades.

Researchers here collected tissue from the San Diego medical examiner’s office linked to infant deaths between 2004 and 2011. They then examined the brainstems of 70 infants who died during the period and tested them for consistent abnormalities.

They found that the serotonin 2A/C receptor is altered in cases of sudden infant death syndrome compared to control cases of infant deaths. Previous rodent research has shown that 2A/C receptor signaling contributes to wakefulness and self-resuscitation, thereby protecting the oxygen status of the brain during sleep. This new research supports the idea that a biological abnormality in some infants makes them vulnerable to death under certain circumstances.

Investigators believe Sudden Infant Death Syndrome occurs when three things happen together: a child is in a critical period of cardiorespiratory development during their first year, the child is dealing with an outside stressor such as a position face-down sleeping or bed-sharing, and the child has a biological abnormality that makes them vulnerable to breathing problems while sleeping.

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

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

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

The research is published in the Journal of Neuropathology and Experimental Neurology.

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

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