Despite a decreasing incidence,
sudden infant death syndrome (
SIDS) is still the most frequent cause of death in industrial nations during the first year of life.
Hypoxia plays a major role in the pathogenesis, but the exact mechanism is not fully understood.
METHODS: This study was based on personal considerations and a selective online literature search.
HYPOTHESIS: Especially in combination, all risk factors for
SIDS favour an
ATP-deficiency by increasing
ATP-catabolism and/or by diminishing
ATP-synthesis. Prenatal chronic hypoxaemia and an insufficient supply with nutrients lead to low birth-weight, reduced adipose tissue, elevated haemoglobin F, increased sympathetic activity, hypermetabolism, and diminished
hypoxia tolerance in the neonates. Because of reduced adipose tissue, more energy for thermogenesis is needed after birth. In reaction to hypoxaemia, infants with risk factors show
hyperventilation instead of hypoxic hypometabolism and
respiratory depression. Enhanced breathing, however, requires additional
ATP and causes increasing
oxygen affinity, which is elevated physiologically during the first months of life. Thereby, tissue-
hypoxia and diminished
ATP-synthesis may arise. Besides, enhanced sympathetic activity leads to hypermetabolism and increased
ATP-catabolism. While innate risk factors may reduce
ATP-production in burdening situations, like food deprivation, postnatal
hyperthermia and stress augment
ATP-catabolism by
hyperventilation and hypermetabolism and empty energy stores. For term newborns, the peak incidence of
SIDS might be explained by the haemoglobin nadir of physiological anaemia and by the therefore reduced capacity for
oxygen transport. Thereby, the risk of tissue-
hypoxia, which follows increased
oxygen affinity and vanishing ability to hypoxic hypometabolism, is further enhanced. The almost identical symptoms of
SIDS and
ATP-
deficiency diseases like hypophosphataemia,
heat stroke, and
carbon monoxide poisoning support the presented hypothesis.