The Role of Respiratory Infection in Sudden Infant Death Syndrome (SIDS)

Abstract

Abstract:Introduction: The Sudden Infant Death Syndrome (SIDS) is not likely to be explained by a currently measureable presence in all cases and absence in controls, as otherwise it would have been solved already. Indeed, any proposed physiological model for SIDS causation must explain the constant mathematical and statistical properties of SIDS age and gender. We have shown previously that SIDS are characterized by a common 4-parameter lognormal age distribution sparing neonatal infants, by a nominal 50% male excess, and by a higher rate in winter than summer. We test now whether SIDS is closely related to a fulminating prodromal Acute Respiratory Infection (ARI) by a common increasing rate with the infants increasing Live Birth Order (LBO), all remaining the same, independent of the change in preferred sleeping positions of the infants, prone or supine. Methods: We use U.S. published infant mortality data from wonder.cdc.gov and other countries (Colombia, U.K., Europe, Australasia) to make comparisons between the two causes of death (ARI and SIDS) to evaluate how closely ARI resembles the characteristics of SIDS. Results: Gender: SIDS male excess 50%, ARI male excess 50%; Ages: SIDS 90% post-neonatal, ARI 96% post-neonatal; Seasonality: SIDS and ARI are higher in winter than summer; Live birth order: SIDS and ARI rates increase with increasing LBO with similar mathematical relationship. Conclusion: Our results show that all SIDS are very likely relatable to a single cause tied to a fulminating prodromal ARI in a physiologically anemic infant who is genetically (X-link recessive) susceptible to cerebral anoxia. An alternative cause of all SIDS death by a collection of subsets of different causes, such as brainstem-related respiratory abnormalities and cardiac QT abnormalities, is not supported because they cannot all have the same age-gender-seasonal-familial-distributions of SIDS, required by Cramér's Theorem.

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

“…As shown here, and in our other papers cited, the following mathematical relationships that SIDS display must be explained by any proposed cause for SIDS: The constant SIDS 50% male excess rate compared to the female rate for equal numbers of infants at risk. Given the nominal 5% excess male birth rate, this leads to the observed male fraction of 0.612 ( 8 ); The SIDS left-censored 4-parameter lognormal (Johnson S B ) age distribution that has 3rd and 4th parameters of order −0.31 and 41.2 months, respectively, with median of approximately −1.0 and approximate SD of 0.30; Maximum SIDS rate in winter months and minimum rate in summer months ( 10 ); The increased risk of SIDS with the infant’s increasing numbers of older siblings, proportional to the factor (1 − 0.9 CFM ), where CFM = 2 parents + (LBO − 1) siblings ( 13 , 14 ); The SIDS X-linkage model predicts the 5/9 male fraction of all infant mortality for equal numbers of males and females at risk ( 13 , 14 ). …”

“…The increased risk of SIDS with the infant’s increasing numbers of older siblings, proportional to the factor (1 − 0.9 CFM ), where CFM = 2 parents + (LBO − 1) siblings ( 13 , 14 );…”

“…The SIDS X-linkage model predicts the 5/9 male fraction of all infant mortality for equal numbers of males and females at risk ( 13 , 14 ).…”

“…Whereas traditional medicine repeatedly autopsies SIDS over and over again, expecting to find its cause, we took an engineering approach and looked to the numerical structure of SIDS vital statistics data for an insight. We propose that probability models of risk factors show that: (1) an X-linkage may create the 50% male excess SIDS rate ( 7 , 8 ); (2) the observed same 4-parameter lognormal age distribution for both males-and-females and prone-and-supine sleepers, is predicted by Cramér’s Theorem ( 3 , 9 , 10 ) (NB: because total of all SIDS ages have a normal transform distribution, any subsets of SIDS must also have the same normal transform distribution); (3) SIDS and ARI have the same seasonal pattern ( 11 ); and (4) the increasing SIDS rate with live-birth order (LBO) is related to increased probability of ARI brought home to the infant by family members ( 12 , 13 ). The X-linkage model can then predict the 5/9 male fraction of all infant mortality for equal numbers of males and females at risk ( 14 – 16 ).…”