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%).