Abstract
Several theories of the underlying mechanisms of Sudden Infant Death Syndrome (SIDS) have been proposed. These theories have born relatively narrow beach-head research programs attracting generous research funding sustained for many years at expense to the public purse. This perspective endeavors to critically examine the evidence and bases of these theories and determine their plausibility; and questions whether or not a safe and reasoned hypothesis lies at their foundation. The Opinion sets specific criteria by asking the following questions: 1. Does the hypothesis take into account the key pathological findings in SIDS? 2. Is the hypothesis congruent with the key epidemiological risk factors? 3. Does it link 1 and 2? Falling short of any one of these answers, by inference, would imply insufficient grounds for a sustainable hypothesis. Some of the hypotheses overlap, for instance, notional respiratory failure may encompass apnea, prone sleep position, and asphyxia which may be seen to be linked to co-sleeping. For the purposes of this paper, each element will be assessed on the above criteria.
Highlights
Background and leading hypothesesBefore committing to this task it is apposite to consider the background and context in which the various hypotheses arose.Beckwith’s 1970 definition of Sudden Infant Death Syndrome (SIDS) [1] created the presumption that SIDS babies were normal
A quite separate approach to SIDS pathogenesis, while containing the fundamental vulnerability of the SIDS infant, age-specific risks, and precipitating factors is the common bacterial toxin hypothesis developed by Morris (1999) [15]. In this we find evidence of the existence of bacterial toxins of common bacteria in SIDS cases compared with healthy babies
In cases where there is a possibility of the existence of, for example, prolonged QT syndrome as being a cause of SIDS
Summary
The pathological findings in SIDS In order to fully examine hypotheses of SIDS causation, it is essential to acknowledge the pathological findings in SIDS. Reasons for the discrepancies between the studies relate to features of the control groups (presence of infection, gestational age, changes in infant nutritional status with socioeconomic development, and so on) These may have negated some organ weight differences between SIDS and normal babies but head and brain size (and possibly thymus) are supported by recent data. Several studies have shown that infants who have apnea in the newborn period are not at higher risk for sudden infant death syndrome (SIDS) [97] Reconciling this would logically mean that brainstem changes found in SIDS babies are not associated with apnea per se and would enforce a conclusion that the anatomical/neurotransmitter changes observed may result in death through a different mechanism.
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