A review was published (1991) of 19 retrospective case-control studies that had investigated the relationship between prone sleeping position (on the stomach) and the sudden infant death syndrome (SIDS). These studies, which had been conducted between 1965 and 1990 in New Zealand, Australia, England, France and the Netherlands, showed an overall higher rate of SIDS in infants who usually slept prone. In those countries, vigorous community intervention to change babies' sleep position away from the prone has resulted in marked declines of 50 per cent or more in the rate of SIDS. Such encouraging reports from many countries prompted the American Academy of Pediatrics to recommend that infants be placed to sleep on their backs to reduce the risk of SIDS. This was followed by a successful campaign in the United States between mid-1994 and 1998. Despite the decreased incidence, SIDS remains the leading cause of death in infants 1 month to 1 year of age of industrialized nations of the world. Studies have been conducted in human infants, mechanical models and animal models to learn the role of risk factors in prone sleeping infants. Soft bedding, thermal stress and biologic risk factors such as impaired ventilatory and arousal responsiveness are among many factors that have been investigated. Hunt states that there is not a single unifying factor that explains increased SIDS in prone sleeping infants. Two major studies conducted in the 1970s showed: (1) muscle weakness in the upper half of the body in infants who subsequently died of SIDS, and (2) shoulder hypotonia in near-miss for SIDS infants. An infant sleeping face-down in the prone position could be jeopardized if he lacked the muscle strength to shift his position or turn his head to rescue himself from a life-threatening situation. In contrast, recent studies in neonates sleeping in the prone position report that normal infants can spontaneously arouse and turn their heads. Some data support the hypothesis that magnesium deficiency contributes to SIDS. Muscle strength is seriously impaired in the young magnesium deficient subject, while magnesium rapidly reverses muscle weakness. In rats, marginal deprivation in dietary magnesium reduces exercise capacity, an early effect of magnesium deficiency which is preventable by consuming magnesium-enriched mineral water. It is concluded that magnesium deficiency is at least one major unifying factor that explains increased SIDS in prone sleeping infants.