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. (shrink)

An evolutionarily informed perspective on parent-infant sleep contact challenges recommendations regarding appropriate parent-infant sleep practices based on large epidemiological studies. In this study regularly bed-sharing parents and infants participated in an in-home video study of bed-sharing behavior. Ten formula-feeding and ten breast-feeding families were filmed for 3 nights for 8 hours per night. For breast-fed infants, mother-infant orientation, sleep position, frequency of feeding, arousal, and synchronous arousal were all consistent with previous sleep-lab studies of mother-infant bed-sharing behavior, but significant differences (...) were found between formula and breast-fed infants. While breast-feeding mothers shared a bed with their infants in a characteristic manner that provided several safety benefits, formula-feeding mothers shared a bed in a more variable manner with consequences for infant safety. Paternal bed-sharing behavior introduced further variability. Epidemiological case-control studies examining bed-sharing risks and benefits do not normally control for behavioral variables that an evolutionary viewpoint would deem crucial. This study demonstrates how parental behavior affects the bed-sharing experience and indicates that cases and controls in epidemiological studies should be matched for behavioral, as well as sociodemographic, variables. (shrink)

Sudden infant death syndrome (SIDS) has been mainly described from a risk perspective, with a focus on endogenous, exogenous, and temporal risk factors that can interact to facilitate lethal outcomes. Here we discuss the limitations that this risk-based paradigm may have, using two of the major risk factors for SIDS, prone sleep position and bed-sharing, as examples. Based on a multipronged theoretical model encompassing evolutionary theory, developmental biology, and cultural mismatch theory, we conceptualize the vulnerability to SIDS as an imbalance (...) between current physiologic-regulatory demands and current protective abilities on the part of the infant. From this understanding, SIDS appears as a developmental condition in which competencies relevant to self-protection fail to develop appropriately in the future victims. Since all of the protective resources in question are bound to emerge during normal infant development, we contend that SIDS may reflect an evolutionary mismatch situation—a constellation in which certain modern developmental influences may overextend the child’s adaptive (evolutionary) repertoire. We thus argue that SIDS may be better understood if the focus on risk factors is complemented by a deeper appreciation of the protective resources that human infants acquire during their normal development. We extensively analyze this evolutionary-developmental theory against the body of epidemiological and experimental evidence in SIDS research and thereby also address the as-of-yet unresolved question of why breastfeeding may be protective against SIDS. (shrink)