Reducing the risk of sudden unexpected infant death: the caffeine hypothesis.

抄録

This review proposes that intermittent hypoxia is the primary pathogenic mechanism driving Sudden Infant Death Syndrome (SIDS). Intermittent hypoxia is a powerful source of molecular and cellular injury and is frequently experienced by infants, especially under conditions associated with known SIDS risk factors such as prone sleeping, respiratory infections, and prenatal nicotine exposure. These factors often trigger hypoxic episodes that may impair autonomic regulation, hinder arousal from sleep, and damage critical neural circuits. By integrating current data, this review highlights the central role of intermittent hypoxia in SIDS pathophysiology. Additionally, it evaluates the potential of caffeine, a respiratory stimulant and adenosine receptor antagonist, as a protective intervention to reduce SIDS risk by enhancing respiratory stability and arousal capacity.