Interleukin-1 as intermediary causing prolonged sleep apnea and SIDS during respiratory infections

Abstract

Two epidemiologic features of sudden infant death syndrome, respiratory infections and prolonged sleep apnea, have not been linked by a known mechanism. Muramyl peptide, acting through interleukin-1, is proposed as that link. Both agents produce fever, activation of the immune system, and of particular significance, increased deep or slow wave sleep. Although sleep apnea is universal, prolonged apnea can, if uninterrupted by arousal, lead to hypoxic apnea, coma, and death. Infants in the first six months of life are particularly vulnerable when arousal mechanisms may not be fully developed, after 9 months of fetal life when life does not depend on respiration.