New research on sudden infant death syndrome (SIDS, or cot death in other parts of the world) has finally implicated a molecular mechanism for the lethal apnea. It appears that, unlike most children, babies with a serotonin receptor defect aren’t prompted to gasp for air when carbon dioxide levels grow dangerously high:
To find out more, neuropathologist Hannah Kinney of Harvard Medical School in Boston and her colleagues autopsied the brains of 31 SIDS children. They found a lower concentration of a kind of serotonin receptor that specifically controls respiration (other serotonin receptors control sleep, anxiety, and a variety of other functions). The researchers also found nearly twice as many cells that make serotonin in the brain stem as in controls. That made sense: Studies with other chemical messengers often find a higher amount of the messenger can lower the number of its receptors. Furthermore, SIDS boys appeared to have less serotonin bound to serotonin receptors than did the SIDS girls, the team reports today in the Journal of the American Medical Association.
That may explain the higher rate of SIDS deaths in boys, says developmental psychobiologist Michael Myers of Columbia University. Overall, he says, the study further supports the role of serotonin in SIDS, and it’s the first report that has zeroed in on a particular receptor.
Blockbuster stuff. The “Back to Sleep” campaign lowered SIDS rates significantly, now potentially screening for a serotonin receptor abnormality might identify more babies at risk from this unfortunate demise.
More from Dr. Hannah Kinney’s research page at Children’s Hospital, and Dr. David Paterson’s JAMA Abstract…
Flashback: Pacifier Prevents SIDS, RespiSense Buzz detects baby apnea
