Sudden infant death syndrome (SIDS) may have a biological mechanism that could, at least in part, help explain the condition’s cause.
Researchers have identified a brainstem abnormality affecting serotonin receptors, which they believe, alongside other biological and environmental factors, may increase an infant’s risk of SIDS.
Also known as “cot death”, SIDS is the sudden, unexpected, and unexplained death of a seemingly healthy baby under one year of age that usually occurs while they are sleeping.
It is rare, but is still the leading cause of post-neonatal infant death in the United States, affecting around 38 out of 100,000 live births in 2020, according to the Centers for Disease Control and Prevention.
Its cause is unknown, despite a wealth of research and even some breakthroughs. So, researchers, led by Robin Haynes at Boston Children’s Hospital, Massachusetts, embarked on a study to learn more.
They collected and analyzed the brainstem tissue of 70 deceased infants, 58 of whom died of SIDS and 12 of other causes between 2004 and 2011.
When comparing the tissues, the team noticed differences in how serotonin – a chemical that sends signals between nerve cells and is involved in modulating numerous biological processes including mood and sleep – binds to receptors.
These same receptors – called 5-HT2A/C receptors – have previously been associated with arousal and autoresuscitation in rodents and so may have a protective function during sleep.
The researchers found that the binding of serotonin to these receptors was altered in the lower brainstems of babies who died of SIDS, compared with those who died of other causes.
They speculate that these abnormalities, in at least a subset of SIDS, may lead to “failure across multiple vital respiratory, cardiovascular, and autonomic brainstem systems that are necessary for successful reoxygenation and perfusion of the developing brain in response to [low oxygen].”
Such a biological vulnerability, in conjunction with other factors such as a child’s sleeping position and age, may all contribute to their increased risk of SIDS, the team believes.
“The work presented builds upon previous work by our laboratory and others showing abnormalities in the serotonergic system of some SIDS infants,” Haynes said in a statement.
“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 in determining the consequence 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.”
It is hoped that such research could help us to one day predict an infant’s risk of SIDS. However, “we have no means to identify infants with biological abnormalities in the serotonergic system [at present],” Haynes added, stressing the importance of adhering to safe-sleep practices.
Last year, the American Academy of Pediatrics updated its guidelines on infant sleeping for the first time in six years, providing up-to-date safe-sleep recommendations and advice on lowering the risk of SIDS.
This includes laying infants flat on their backs on non-inclined surfaces and avoiding bedsharing. More information can be found here.
The study is published in the Journal of Neuropathology & Experimental Neurology.