Scientists link serotonin deficit to SIDS
The number of babies who die of sudden infant death syndrome has dropped in half over the last 20 years, thanks to a campaign urging parents to put babies to sleep only on their backs. But SIDS is still the leading cause of death in babies between one month and one year old and the number of deaths hit a plateau in 2000, despite greater awareness of risk factors for the baffling disorder.
New research from a team led by a Children's Hospital Boston neuropathologist sheds light on a possible biological cause, pinpointing a defect in the brain that might account for babies who suddenly and unexpectedly die during their sleep. The findings, published in this week's Journal of the American Medical Association, build on previous work that scientists hope will one day lead to a test and treatment.
In the new study, Dr. Hannah Kinney and her colleagues compared the brainstems of 41 babies who had died of SIDS to the brainstems of seven babies who died of other causes and five babies who were hospitalized with low oxygen levels before their deaths. Researchers have suspected that SIDS involves problems with inadequate oxygen, so Kinney wanted to compare the SIDS babies to the two groups. The brainstem is the part of the brain that controls breathing, responds to rebreathing too much carbon dioxide, and regulates blood pressure and body temperature, which are all important in sleeping and waking.
"We found an abnormality in the wiring, in the circuits that control these vital functions," Kinney said in an interview.
In 35 of the 41 SIDS babies, serotonin levels were 26 percent lower than in all the babies who did not die of SIDS and levels of an enzyme that spurs serotonin production were 22 percent lower. Binding to serotonin receptors was 50 percent lower in SIDS babies.
Kinney had previously found differences related to serotonin receptors in SIDS babies' brainstems, but it was not clear whether there was too much or too little of the neurotransmitter that sends signals between nerve cells. An unanswered question was whether the serotonin was there and the babies' brains were unable to use it.
Marian Willinger, who is responsible for the SIDS research program at the National Institute of Child Health and Human Development, called Kinney's results on a serotonin deficit important.
"I think this is an important advance in our understanding of what's wrong with the brainstem of many babies who die from SIDS," she said in an interview. "It helps us ... to understand the pathophysiology, how the baby dies, because we don't really know."
Kinney said the goal is to identify the infants who have this problem.
"We are closer than we have been, but we still have quite a journey to go, to test and then identify it in the living infant and then to have a treatment for it," she said. "Those are long-term goals and we know we are years away from them."
Kinney and Willinger both emphasized avoiding known risk factors parents can control, such as bed sharing, soft bedding, and smoking while research on the biological causes of SIDS continue.
This story was originally published on the Boston Globe's White Coat Notes blog.