A Biological Cause for SIDS?

Susan Gertler of Olympia Fields, Ill., was delighted. Her 15-week-old son, Joey, had slept through the night for the third time. "I can't believe he slept through the night again," she said to her husband, Jeff, when she woke that morning—Jan. 19, 1996. But Joey hadn't slept through the night. He'd stopped breathing around midnight and never started again, a victim of sudden infant death syndrome (SIDS). Gertler administered CPR, while her husband called 911 and summoned a doctor friend down the street, but all their efforts proved fruitless. Joey had been dead too long. "My memories of that morning are all grey, as if someone had turned out the lights," says Gertler, now 46. "You're responsible for your baby's life. You were the one who put them to sleep. It's nobody's fault but your own."

Painful as it sounds, that's what many people used to think. But according to a study appearing Wednesday in the Journal of the American Medical Association, it now seems that there is a biological basis for SIDS, which kills more than 2,100 infants a year in this country. SIDS was long regarded as a mystery disease. But the study by Dr. Hannah Kinney and David Paterson at Children's Hospital Boston and Harvard Medical School provides the strongest evidence to date that babies who succumb to SIDS have specific problems in a part of the brainstem, known as the medulla, that helps regulate automatic functions like heart rate, breathing and body temperature. Kinney says babies with these abnormalities don't react like other babies when carbon dioxide levels in the blood rise too high or oxygen levels fall too low during sleep. "Normally a reflex action would cause them to wake or breathe faster or shift positions to get better air," she says. That apparently doesn't happen in babies with SIDS—particularly when they're sleeping on their stomachs or have their faces covered by bedding, causing them to rebreathe exhaled carbon dioxide. The combination of biological abnormalities and external factors can prove deadly.

The precise chain of neural events leading to SIDS isn't fully understood. But Kinney says the problem relates to abnormalities in the regulation of serotonin, a brain chemical that helps relay messages from one brain cell to the next. Kinney and her colleagues have implicated the brain's serotonin system in SIDS before, finding defects in the way serotonin binds to receptors on brain cell surfaces in SIDS babies. But the new study shows that the problems are more extensive than previously thought. By examining autopsy tissue from the brains of 31 babies in San Diego who died of SIDS and comparing them to brains of 10 infants who died from accidents or known diseases, Paterson and Kinney found that the SIDS babies have fewer serotonin receptors on brain cells in the medulla than normal babies. Curiously, they also have far more neurons devoted to serotonin processing—perhaps the body's attempt to compensate for poor receptor function. They also appear to have insufficient amounts of the so-called serotonin transporter protein, which helps brain cells recycle serotonin for further use.

The findings help explain why certain groups are at greater risk than others. Male SIDS babies outnumber female victims two-to-one. In the new study, the male babies who died of SIDS had lower serotonin-receptor levels than female SIDS infants. Premature babies are also more frequent victims—perhaps because the serotonin system is less developed at birth. And infants of mothers who smoke during pregnancy are also at increased risk. "We know that nicotine and cigarette smoke affect the levels of serotonin, receptors and even numbers of cells devoted to serotonin in the developing fetus," says Kinney.