Sudden infant death syndrome: selenium administered above dietary needs stabilizes the electrocardiograms of subjects deprived of exercise stimuli to the brain.

The human foetus begins preparation for extrauterine life in the 26th week of gestation. Victims of sudden infant death syndrome (SIDS) were described as having less-intensive reactions to environmental stimuli than their siblings. They were described as less-active physically and more breathless and exhausted during feeding. These foetal-like qualities are similar to the microgravity deconditioning of the space traveller and the autonomic dysfunction of hypokinetic humans. During quiet sleep, a group of near-miss SIDS victims displayed a faster heart-rate and a decreased movement-time, compared to controls. Another group of SIDS victims linked delayed repolarisation and sympathetic overactivity of the nervous system. The excessive Q-T wave intervals, cardiac instability and autonomic dysfunction tended to coincide with the peak incidence of SIDS which is the normal period of autonomic transformation at 2-3 months of age. Sympathetic hyperactivity transforms the subject into an energy-intensive species with an accelerated heartbeat, intensive vasoconstriction and general reactions to a hostile environment. Energy-intensive species (flight-oriented species) were sensitive to selenium (Se) deficiency. Altered mitochondrial structure and defective electron transport of heart mitochondria were features of this syndrome. Runaway excessive sympathetic autonomic activity transforms the subject into an energy-intensive species responsive to selenium. Groups of Se-deficient lambs confined for eight weeks developed abnormal electrocardiograms (ECGs). Groups exercised daily on a treadmill or Se-supplemented groups retained virtually normal ECGs. Foetuses and subjects unreactive to the environment are space travellers lacking parasympathetic stimuli to the brain. Decreased movement-time deprives the brain receptors of the stimulus induced by gravity.