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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%).

Sudden infant death syndrome, in 36 global data sets comprising 67378 postneonatal autopsied cases, has a male fraction of 0.612 which is significantly greater than the male birth fraction of 0.5122. Each of the sex ratios in the 36 data sets cannot be rejected as a random sample from a P = 0.612 binomial distribution. We hypothesize that an X-linked two-allele (a,A) single gene may be responsible for this consistent behavior. The Hardy-Weinberg principle predicts, given a 5% excess male birth rate, that a recessive allele (a) associated with sudden infant death syndrome, having a frequency of q = 2/3, could be responsible for the male fraction of 0.612. The absence of the A allele would be a necessary precondition for sudden infant death syndrome. We hypothesize that the syndrome occurs only with additional rare environmental conditions and rare physiological factors leading to extreme hypoxic stress, which reduces the sudden infant death syndrome rate to the order of 1 per 1000 live births.

Analysis of autopsied cause of death during the London Fog of 1952 indicates that mortality from all respiratory causes, sudden and delayed, had a consistent male fraction of 0.622. Sudden death from heart failure had a similar male fraction of 0.612. However, heart failures after the first day of illness had a male fraction of 0.48. This significant difference in male fraction between sudden (0.61) and delayed (0.48) heart failure suggests different terminal events. Coronary sudden death may be attributable to right-sided heart failure, and the delayed form may be attributable to left-sided failure leading to pulmonary congestion. The male fraction in sudden respiratory and sudden cardiac deaths (0.612) is exactly the same as the male fraction in sudden infant death syndrome-0.612 - which has been posited as being X-linked. It is hypothesized that the same X-linked gene responsible for the 0.612 male fraction in sudden infant death syndrome may be a factor in the respiratory and sudden cardiac mortalities during the London Fog.