Helicobacter pylori may be linked to sudden infant death syndrome (SIDS) through synthesis of inflammatory cytokines, particularly interleukin-1, which can produce fever, activation of the immune system, and increased deep sleep. A relatively minor respiratory or enteric infection, together with overwrapping and prone sleep position could then induce terminal hypoxemia. Alternatively, H. pylori produces large amounts of urease which, if aspirated in gastric juice, could reach the alveolae, react with plasma urea, and produce ammonia toxicity leading to respiratory arrest. Epidemiological similarities between H. pylori and SIDS are presented along with possible transmission mechanisms for H. pylori which support this hypothesis.