Evolution and sudden infant death syndrome (SIDS)

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Abstract
This paper and its subsequent parts (Part II and Part III) build on an earlier publication (McKenna 1986). They suggest that important clinical data on the relationship between infantile constitutional deficits and microenvironmental factors relevant to SIDS can be acquired by examining the physiological regulatory effects (well documented among nonhuman primates) that parents assert on their infants when they sleep together. I attempt to show why access to parental sensory cues (movement, touch, smell, sound) that induce arousals in infants while they sleep could possibly help one of many different subclasses of infants either to override certain kinds of sleep-induced breathing control errors suspected to be involved in SIDS or to avoid them altogether. I do not suggest that solitary nocturnal sleep “causes” SIDS, that all parents should sleep with their infants, or that traditional SIDS research strategies should be abandoned. However, using evolutionary data, I do suggest that an adaptive fit exists between parent-infant sleep contact and the natural physiological vulnerabilities of the neurologically immature human infant, whose breathing system is more complex than that of other mammals owing to its speech-breathing abilities. This “fit” is best understood, it is argued, in terms of the 4–5 million years of human evolution in which parent-infant contact was almost certainly continuous during at least the first year of an infant’s life. Thus, to dismiss the idea that solitary sleep has no physiological consequences for infants does not accord with scientific facts.