TUESDAY, Feb. 2 (HealthDay News) -- Lack of the brain chemical serotonin may be crucial to sudden infant death syndrome (SIDS), new research finds.
Babies who died of SIDS had significantly lower levels of serotonin -- an important regulator of involuntary functions such as breathing and heart rate -- compared to babies who died of other causes, the study found. This finding may eventually lead to a test that could screen newborns to spot those most vulnerable to SIDS.
"This study is confirming that SIDS is a serotonin problem, and we're getting closer to the fundamental mechanism behind SIDS," said the study's senior author, Dr. Hannah C. Kinney, a neuropathologist at Children's Hospital Boston and a professor of pathology at Harvard Medical School.
"The goal is to develop a test to identify which babies are at risk, and then to find a drug that might be able to help them through the critical period. But these are long-term goals," she said.
Results of the study are published in the Feb. 3 issue of the Journal of the American Medical Association.
SIDS involves the sudden, unexplained death of an infant under one year of age, according to background information in the study. Although the rate of SIDS has decreased in the United States -- largely as a result of a national Back-to-Sleep campaign that encouraged parents to put babies to sleep on their backs one out of every 2,000 American babies is still dying of SIDS, the authors note.
Researchers have long suspected that a lack of serotonin, an important neurotransmitter in the brain, may be a factor in SIDS deaths. Neurotransmitters are chemicals that transmit messages from one brain cell to another. Experts have theorized that a lack of serotonin affects the way a baby responds to a loss of oxygen and a buildup of carbon dioxide while sleeping. In babies with a normally functioning system, the lack of oxygen would cause them to awaken and turn their head to get fresh oxygen.
In babies who die of SIDS, this important protective mechanism is either underdeveloped or lacking, and they don't awaken. That may be one reason why the Back-to-Sleep campaign was so successful in reducing SIDS. By putting babies to sleep on their backs and taking soft, fluffy bedding out of the crib, parents are taking away environmental stressors that may contribute to SIDS, the researchers said.
In the current study, Kinney and her colleagues measured levels of serotonin and trytophan hydroxylase (TPH2) in 35 babies who died from SIDS and in 12 babies who died of other, known causes. TPH2 is an enzyme that helps make serotonin. In the group of babies who had died of other causes, the researchers included infants who had experienced oxygen deprivation near death to rule that factor out as a cause of lower serotonin levels.
They found that serotonin levels were 26 percent lower and TPH2 levels were 22 percent lower in babies who died of SIDS compared to babies who died of other causes.
"This study is getting close to the underlying mechanism," said Dr. Raymond Pitetti, associate director of emergency medicine at Children's Hospital of Pittsburgh.
"The goal would be to develop a screening tests so we can identify someone who might need a monitor or to be more closely watched," he said.
In the meantime, he and Kinney advised parents to continue to put their babies to sleep on their back, to avoid soft bedding, to ensure adequate ventilation in the room where the baby sleeps and maybe even add a ceiling fan to the room. Some research has suggested that putting babies to bed with a pacifier in the mouth may help prevent SIDS, too.
"The most important thing for parents to know is that SIDS is a biological problem. It's a disease process, and right now, there's no way to identify it in advance," said Kinney. That why it's so important to take away any environmental challenges, like soft bedding and sleeping on the stomach, she added.
SOURCE: Hannah C. Kinney, M.D., neuropathologist, Children's Hospital Boston, and professor, pathology, Harvard Medical School, Boston, Mass.; Raymond Pitetti, M.D., associate director, emergency medicine, Children's Hospital of Pittsburgh, Penn.; Feb. 3, 2010 Journal of the American Medical Association