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