<abstract xmlns="http://www.w3.org/1999/xhtml"><bold>Introduction:</bold> 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.<bold>Methods:</bold> We use U.S. published infant mortality data from <ext-link ext-link-type="uri" xmlns:xlink="http://www.w3.org/1999/xlink" xlink:href="http://wonder.cdc.gov">wonder.cdc.gov</ext-link> 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.<bold>Results:</bold> 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.<bold>Conclusion:</bold> 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.</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.

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

WHO, Division of Environmental Health, Geneva, CH (now Newark, DE, USA) 18 W Periwinkle Lane. Newark DE

Corporación Infancia Colombia Calle 127C # 7 A -32 - Bogotá DC, Colombia

Servicio de Neonatología del Hospital Italiano de San Justo Agustín Rocca. Av.Presidente Perón 2231. San Justo. Provincia de Buenos Aires Argentina., 4959.0200

Dupont Haskell Global Centers for Health & Environmental Sciences, Newark, DE, USA, 18 W. Periwinkle Lane. Newark DE. 19711-6212. USA

Scandinavian Journal of Forensic Science

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"The Role of Respiratory Infection in Sudden Infant Death Syndrome (SIDS)"}

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,...

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

Published Online: Jul 01, 2016

Page range: 15 - 20

DOI: https://doi.org/10.1515/sjfs-2016-0004

Keywords
physiological anemia, X-link recessive, respiratory infection, 4-parameter lognormal age distribution, cohabiting family members

© 2016 David T. Mage et al., published by De Gruyter Open

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

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

Published Online: Jul 01, 2016

Page range: 15 - 20

DOI: https://doi.org/10.1515/sjfs-2016-0004

Keywordsphysiological anemia, X-link recessive, respiratory infection, 4-parameter lognormal age distribution, cohabiting family members

© 2016 David T. Mage et al., published by De Gruyter Open

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Keywords
physiological anemia, X-link recessive, respiratory infection, 4-parameter lognormal age distribution, cohabiting family members