A Unifying Theory for SIDS

Abstract

The Sudden Infant Death Syndrome (SIDS) has four distinctive characteristics that must be explained by any theory proposed for it. (1) A characteristic male fraction of approximately 0.61 for all postneonatal SIDS in the US; (2) a distinctive lognormal-type age distribution arising from zero at birth, mode at about 2 months, median at about 3 months, and an exponential decrease with age going towards zero beyond one year; (3) a marked decrease in SIDS rate from the discovery that changing the recommended infant sleep position from prone to supine reduced the rate of SIDS, but it did not change the form of the age or gender distributions cited above; (4) a seasonal variation, maximal in winter and minimal in summer, that implies subsets of SIDS displaying evidence of seasonal low-grade respiratory infection and nonseasonal neurological prematurity. A quadruple-risk model is presented that fits these conditions but requires confirmatory testing by finding a dominant X-linked allele protective against cerebral anoxia that is missing in SIDS.

Figure 1

US postneonatal SIDS during period of change from prone to supine sleep position showing that the male fraction remains constant at or about 0.61.

Figure 2

Age distribution from 15 global data sets combined versus month attained of 19,949 SIDS [21].

Figure 3

Venn Diagram for a Quadruple Risk Model of SIDS. These four probability factors involved with SIDS explain the age and gender distributions invariant with different sleep position, and subsets of SIDS found with and without neurological prematurity and respiratory infection. It is proposed that a prone infant is susceptible to SIDS anywhere in the intersection between the genetic (Pg) and anemia-related apnea (Pa) factors, but a supine sleeping infant is only susceptible to SIDS if it is in the intersection of all four factors (Pa, Pg, Pi, Pn).