The X-linkage hypotheses for SIDS and the male excess in infant mortality.
Sudden Infant Death Syndrome is characterized globally by a 50% excess in males per 1000 live births of each gender. We previously hypothesized that this male excess may arise from a single X-linked gene locus with a dominant allele (p = 1/3) that is protective against potentially terminal cerebral anoxia by catalyzing anaerobic oxidation and a recessive allele (q = 2/3) that is unprotective. We now hypothesize this same terminal mechanism for all other causes of infant respiratory death (50% male excess) and that infant cardiac death is equally probable for males and females (0% male excess). With these hypotheses, we model the male excess of all infant mortality (under 5 years) as 25% per 1000 live births of each gender. We show for the USA (1979-2000) that this model of a 25% male excess accurately predicts the male excess mortality under 1 year (24.15%), from 1 to 4 years (25.42%), and under 5 years (24.51%).
Mage
David T
DT
Institute for Survey Research, Temple University, 1601 N. Broad Street, Philadelphia, PA 19122-6099, USA. david.mage@temple.edu
Donner
Maria
M
D002423:Cause of Death; D002675:Child, Preschool; D041321:Chromosomes, Human, X; D005260:Female; D008040:Genetic Linkage; D006801:Humans; D007223:Infant; D007226:Infant Mortality; D007231:Infant, Newborn; D008297:Male; D008957:Models, Genetic; D011237:Predictive Value of Tests; D011247:Pregnancy; D011256:Pregnancy Outcome; D015203:Reproducibility of Results; D012189:Retrospective Studies; D012727:Sex Characteristics; D012744:Sex Ratio; D013398:Sudden Infant Death / Q000453:epidemiology* / Q000235:genetics*; D014481:United States / Q000453:epidemiology