Sudden infant death syndrome: a genetically determined impaired maturation of the photoneuroendocrine system. A unifying hypothesis.
Sudden Infant Death Syndrome (SIDS) is the unexpected, and after autopsy, unexplained death of an apparently healthy infant. SIDS exhibits circannual, circadian, and ontogenetic features which may reflect an impaired maturation of the photoneuroendocrine system caused by a genetic absence or mutation of the enzyme N-acetyltransferase which is the rate-limiting enzyme for the biosynthesis of the hormone melatonin in the pineal gland. The failure of normal pineal gland development and subsequent impaired production of its main secretory product, melatonin, may cause a lethal imbalance in the chemical interactions among serotonin, progesterone, and catecholamines. The result of this chemical imbalance, culminating in SIDS, involves the neurotoxic and cardiomyotoxic effects of abnormally elevated catecholamines and intracellular calcium ions.
Weissbluth
L
L
Department of Pediatrics, Northwestern University Medical School, Chicago, IL 60611.
Weissbluth
M
M
D000123:Acetyltransferases / Q000235:genetics; D001921:Brain / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D002940:Circadian Rhythm; D006801:Humans; D007223:Infant; D008550:Melatonin / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009490:Neurosecretory Systems / Q000254:growth & development* / Q000503:physiopathology; D010870:Pineal Gland / Q000254:growth & development* / Q000503:physiopathology; D011374:Progesterone / Q000378:metabolism; D012621:Seasons; D012701:Serotonin / Q000378:metabolism; D013398:Sudden Infant Death / Q000097:blood / Q000235:genetics*
D002395:Catecholamines; D012701:Serotonin; D011374:Progesterone; D000123:Acetyltransferases; D008550:Melatonin; D002118:Calcium