Abbate et al report success in limiting adverse cardiac remodeling after acute myocardial infarction by blockade of interleukin-1. This promising new approach used anakinra, a natural substance.

Their report also has significance for another noncardiac disorder, sudden infant death syndrome (SIDS). In 1989, I suggested that interleukin-1 was the intermediary causing prolonged sleep apnea and SIDS during respiratory infections. Interleukin-1 and infections cause fever, activation of the immune system, and increased slow-wave sleep. As any parent knows, mild respiratory infections are common in infants and children, usually only a nuisance, but they have a statistical correlation with SIDS, and SIDS almost always occurs during sleep. The combination of respiratory infection and deep sleep may cause prolonged apnea and, if not interrupted by arousal, lead to hypoxic apnea and death.

This possibility of involvement of interleukin-1 was supported by a Norwegian group in 1995, who found that at autopsy, SIDS cases had increased interleukin-6 in the cerebrospinal fluid. The prevention of SIDS theoretically might be possible if anakinra were given to infants with respiratory infections at bedtime, but that is not justified, unlike the “back-to-sleep” positioning of all sleeping infants, which lowered the rate of SIDS by 50% and has no side effects.