Sudden Infant Death Syndrome (SIDS)

Lewis P. Lipsitt is a well-known scholar and developmental researcher with broad interests in infant learning and perception, perinatal risk, and the behavioral contributions to crib death. As a professor emeritus of psychology, medical science, and human development and a research professor at Brown University, he continues to direct a long-term longitudinal study of newborns begun in 1959. His awards and honors are numerous and include the Nicholas Hobbs Award for “science in the service of children,” the American Association for the Advancement of Science (AAAS) Lifetime Achievement Award, the Distinguished Contribution Award of the New England Press Association (NEPA), and the 2003 Urie Bronfenbrenner Award from American Psychological Association's Division 7. In addition to publishing more than 200 journal articles and book chapters, Lipsitt founded and coedited Advances in Child Development and Behavior and Advances in Infancy Research, as well as the journal Infant Behavior and Development. His awards, publications, and major editorial achievements reflect his applied developmental focus, and he has made significant contributions to multiple fields within developmental science. A full description of his life and work has been presented in an autobiography series of the great developmental psychologists in history (Lipsitt, 1996).

Lipsitt's work has advanced both empirical and theoretical research on the study of sudden infant death syndrome (SIDS), including the development of a complete analysis of the syndrome (Burns & Lipsitt, 1991). In the following, a summary of Lipsitt's proposal that behavioral factors in combination with biology are responsible for SIDS will be provided (Lipsitt, 1977, 1978). Second, the significance and impact of this hypothesis will be highlighted.

Sudden infant death syndrome is defined as the sudden death of an infant, younger than 1 year of age, which is unexplained following a complete review of clinical history, autopsy reports, and death scene examinations. Large numbers of epidemiological studies conducted over the past 30 years have tested various medical/biological hypotheses concerning the causes of SIDS, varying from hypersensitivity to cow's milk to air pollution. Generally, these studies have led to no significant interventions resulting in a reduction of SIDS.

Lipsitt's biobehavioral model proposed that behavior of the infant in concert with early constitutional vulnerability were responsible for SIDS. More specifically, the argument was that eventual SIDS victims begin life with a constitutional fragility, manifested in central nervous system impairments resulting from known risks (e.g., maternal smoking, prematurity, poor prenatal care, etc.) (Burns & Lipsitt, 1991; Lipsitt, 2003). This vulnerability limits infants' critical learning experiences related to respiratory processes. These learning experiences would ordinarily, and do in the surviving infant, “immunize” the child by providing appropriate defensive responses against threats of respiratory occlusion. The absence of learned defensive behaviors, which are necessary for clearing the air passages for breathing between 2 and 5 months of age, becomes highly critical when so much of self-regulatory behavior matures from predominantly subcortical mediation to cortical regulation. Thus, according to the Lipsitt biobehavioral model, the rarity of SIDS during the first 2 months is due to the fact that before 2 months, even the vulnerable infant has adequate (sub-cortical) reflexes to defend against respiration-blocking substances (mucous) or objects (a pillow, crib carrier). The period between 2 and 5 months marks the ascendancy of cortical mediation and thus a transition from unlearned defensive behaviors (e.g., the respiratory occlusion reflex) to learned behaviors (e.g., coughing and volitional head turning). Lipsitt's hypothesis is a biobehavioral model, as both the physiological dispositions of the child and early environmental factors, including learning experiences, are presented as critical for self-regulation of respiration.

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