Abstract
The aim of this paper is to help draw attention to perceived ideas regarding the risk factors and the implied pathogenesis of Sudden Infant Death Syndrome (SIDS), and SIDS research in general. Our paper shows there is little if any evidence to support the broadly held notion of an association between respiratory function and sudden infant death syndrome. Researchers who hold to this approach to explain the risk factors of bed-sharing and prone sleep position, etc. have failed to meet the standards of scientific endeavour that we would expect of good research. To counter this imbalance we have proposed an evidence-based explanation for SIDS risk factors showing that microbiological studies of SIDS corroborate epidemiologic and pathological data in establishing a plausible pathogenetic mechanism. We reviewed recent publications on current research and the epidemiology of SIDS and publications on the microbiology of SIDS. Conclusion: Comparison of the data presented, suggest that the risk factors of bed-sharing, and smoke exposure, prone sleep position and alcohol can be explained by the theories of a microbiological infection model of SIDS pathogenesis.
Highlights
The ProblemImportant papers such as the recently published one by Mitchell et al (2012) continue to present the risk factors of prone sleep position and bed-sharing in a way that infers respiratory compromise
Researchers who hold to this approach to explain the risk factors of bed-sharing and prone sleep position, etc. have failed to meet the standards of scientific endeavour that we would expect of good research
To counter this imbalance we have proposed an evidence-based explanation for Sudden Infant Death Syndrome (SIDS) risk factors showing that microbiological studies of SIDS corroborate epidemiologic and pathological data in establishing a plausible pathogenetic mechanism
Summary
Important papers such as the recently published one by Mitchell et al (2012) continue to present the risk factors of prone sleep position and bed-sharing in a way that infers respiratory compromise. The findings were congruent with known SIDS risk factors including respiratory infections, central nervous system abnormalities and prone sleeping position Applying these constructs to human babies in terms of cause and effect is not entirely straightforward. If the various factors for SIDS are analysed in relation to infection - age range, gender, prone sleeping position, lack of breast feeding, exposure to cigarette smoke, mild virus infection, ethnic groupthere is evidence to support a role for infections and an infant's inflammatory response to these (Blackwell et al 2005). In relation to bed sharing and smoking, smokers are more heavily colonized by potential pathogens identified in many infant deaths, e.g., Staphylococcus aureus (Musher & Fainstein 1981) It has been previously pointed out how the risk factors can contribute to enhanced colonisation by bacteria, induction of temperature-dependent toxins, and control of inflammatory responses (Blackwell et al 2005).
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