An Anthropological Perspective on the Sudden Infant Death Syndrome: The Neurological and Structural Bases of Speech Breathing and Why SIDS Appears to Be a Species-Specific Malady, Part II

This paper extends the evolutionary-based arguments proposed in a previous
paper (see McKenna 1987, Part I) but concentrates on why the sudden infant death syndrome is not found
among other animal species, and cannot be experimentally replicated, and thus why it appears to be a speciesspecific, unique human infant malady. Data from studies of the breathing and vocalizing difficulties of normalhearing and hearing-impaired persons are used to argue that, to a degree unparalleled in other species, certain
breathing behaviors are cortically controlled and learned by way of both internal and external auditory
processes. While the neurophysiological and neurostructural voluntary-involuntary nerve conduit upon which
this system depends is a prerequisite for human language, or more specifically, for speech breathing, it makes
human infants more vulnerable to any number of breathing control errors, one of which may be SIDS. Hence,
this perspective attempts to explain why SIDS is so circumscribed by age since speech breathing begins to
occur as the infant begins to assert increasingly voluntary control over its crying behavior at two to four months
when SIDS rates peak. By seven months, well before the infant utters its first words, it has mastered the
voluntary pulmonic manipulations required for speech. While making no suggestions about the primary causes
of SIDS, this paper like the previous one provides a heuristic model and rationale for new data-based research
questions on a malady that has resisted our attempts to understand it for over 20 years. Finally, for some but
not all infants, it is suggested that the evolutionary old microenvironment of sustained and continuous parentinfant contact, including cosleeping, provides the safest context within which such a system could evolve.