Abstract

The cause of the sudden infant death syndrome (SIDS) is perhaps the oldest of unsolved mysteries of medicine, possibly dating back to Exodus in Biblical times when Egyptian children died in their sleep as if from a plague. It occurs when infants die unexpectedly with no sufficient cause of death found in a forensic autopsy, including death scene investigation and review of medical history. That SIDS is an X-linked recessive death from infectious respiratory disease of a physiologically anemic infant and not a simple anomalous cardiac or neurological condition is an extraordinary claim that requires extraordinary evidence. If it were by a simple cause, it would have already been solved, with over 11,000 papers on SIDS listed now in PubMed. Our aim is to use mathematical models of SIDS to explain: (1) its 50% excess male death rate; (2) its 4-parameter lognormal distribution of ages at death; (3) its winter maxima and summer minima; and (4) its increasing rate with live-birth order. From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We, then, compare these SIDS properties to infant death from acute respiratory infection (ARI), and infant death from encephalopathy, unspecified (EU). Comparisons show that SIDS are congruent with ARI and are not consistent with EU and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life. SIDS are not rejected as an X-linked disease involving ARI and are not explained by a triple risk model that has been commonly accepted by the SIDS medical community, as implicating a neurological causation process in a subset of SIDS.

Highlights

  • The sudden unexpected death of an apparently healthy and wellnurtured infant or young child during sleep – that in modern times remains unexplained after forensic autopsy, medical history review, and death scene investigation – is a phenomenon that has appeared throughout human history

  • In the pooled data sets, we have analyzed, the numbers of observations are very large totaling from tens of thousands up to a few million, so the means of the data sets closely approach the means of the underlying distributions

  • Given the nominal 5% excess male birth rate, this leads to the observed male fraction of 0.612 (8); (2) The sudden infant death syndrome (SIDS) left-censored 4-parameter lognormal (Johnson SB) age distribution that has 3rd and 4th parameters of y = Log[(m + 0.31)/(41.2 - m)]

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Summary

BACKGROUND

The sudden unexpected death of an apparently healthy and wellnurtured infant or young child during sleep – that in modern times remains unexplained after forensic autopsy, medical history review, and death scene investigation – is a phenomenon that has appeared throughout human history. The SIDS’ parents or other caregivers have no premonition that their infant is at immediate risk of imminent death, so the precipitating fatal event in SIDS must occur suddenly without warning, or they would have sought prompt medical help We propose it is an occult prodromal respiratory infection that fulminates lethally in the infant (12) with unmeasured asymptomatic physiological anemia (total Hb < −2σ), autopsied without blood or lung viral or bacterial cultures (17), or with such testing leading to a culture-negative sepsis (12, 18). We noted that Carpenter and Gardner (28) reported in their Table 1, for England and Wales 1965–1976, that all infant deaths from non-respiratory anomalies were 5,653 males and 5,369 females, a 5.3% male excess, similar to the nominal 5% male live-birth excess This should have indicated to those looking for autosomal variants related to SIDS that androgen interactions were unlikely.

Male mortality
Age ma
Seasonal Pattern of SIDS
Respiratory Infection and SIDS
November December
Infants at risk
SUMMARY
England and Wales
CONCLUSION
AUTHOR CONTRIBUTIONS
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