A possible explanation for SIDS?

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Abnormal serotonin receptors, which may cause serotonin levels to dip dangerously and undermine a brain network responsible for regulating the body’s autonomic functions, could be a cause of Sudden Infant Death Syndrome (SIDS), according to new research published in the Journal of the American Medical Association. An estimated two out of every 2,000 children born in the U.S. die each year from SIDS, a tragic condition that causes inexplicable sudden death in babies younger than one-year-old, and most frequently affects babies between the ages of two to four months. Research into risk factors for SIDS—which, notably, include putting babies to sleep on their stomachs or surrounded by soft bedding—prompted awareness campaigns that experts credit with reducing the SIDS mortality rate by 50% since 1990, but that success has tapered significantly as the mortality rate has plateaued in the last decade. If future studies bear out these findings about serotonin deficiency, it could possibly yield promising new techniques for diagnosis and intervention in babies who have the “SIDS abnormality.”

The researchers drew on previous study that showed evidence of abnormal serotonin receptors in a brain system that helps regulates the body’s homeostasis—or its ability to quickly adapt to change and keep things running smoothly—among SIDS infants. In this study, then, they hypothesized that serotonin receptor abnormalities might cripple this vital system, making it difficult for babies to cope in the face of “life-threatening challenges” such as asphyxia, most likely caused by being placed to sleep face-down or getting caught up in plush bedding.

To test this, researchers performed autopsies on 41 babies who had died of SIDS, as well as 7 babies who died of other non-SIDS-related causes. In keeping with previous SIDS research, the investigators found that 39 out of 41 (95%) of the infants had at least one risk factor—such as being born prematurely, being placed to sleep on their stomachs, suffering a slight illness prior to death, etc.—while 36 out of 41 (88%) had two or more.

Yet, beyond external influences on risk for SIDS, the researchers found that babies who died of SIDS had 26% lower levels of serotonin in the part of the brain believed to be home to the regulatory system, compared with infants in the control group. The finding, coupled with the fact that SIDS babies also had lower levels of an enzyme known as TPH2, which plays a role in serotonin production, indicates that serotonin deficiency may be a driving factor for SIDS.

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