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)

Postnatal parent-infant physiological regulatory effects described in the previous paper (Part I) are viewed here as being biologically contiguous with events that occur prenatally, preparing and sensitizing the fetus to the average microenvironment into which the infant is expected, based on its evolutionary past, to be born. Following McKenna (1986), evidence (some of which is circumstantial) is presented concerning fetal hearing and fetal amniotic liquid breathing as they are affected both by maternal cardiovascular blood flow sounds in the uterus and (...) by fluctuating maternal blood sugar levels. These data are linked in turn to the infant’s postulated postnatal responsivity to parental sensory cues, including auditory and vestibular respiratory cues that may assist infants as they “learn” to breathe and, for some, to resist a SIDS event. Data on the respiratory and vocalizing behavior of normal and hearing-impaired persons are used to show that not all forms of human breathing are innate; some forms develop with experience. These data reveal how human infants learn, for example, to coordinate higher and lower brain respiratory nuclei in the context of learning initially to cry with intent and purpose and later to speak. Voluntary, cortex-based breathing emerges at the same time that infants are most likely to die from SIDS, between 2 and 4 months of age. This switch between voluntary and involuntary breathing during both sleep (while dreaming) and wake cycles, which depends on the integration of higher cortical and lower brain stem nuclei, is complex and is possibly the basis of the human species’ unique susceptibility to SIDS—a syndrome as yet unrecognized in other species. These human infant vulnerabilities, including delayed maturity, can explain in part why natural selection ought to favor increased infant sensitivity to parental sensory cues provided by a caregiver—stimuli available in the evolving parental care environment that included parent-infant co-sleeping for more than 4–5 million years of human evolution. (shrink)

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)