Sudden infant death syndrome: Study of genes pertinent to cardiorespiratory and autonomic regulation

The "Back to Sleep" campaign, introduced in the U.S. in 1992, identified modifiable environmental risk factors for SIDS and led to a decrease in SIDS incidence from 1.2/1000 live births [46] to 0.529/1000 live births in 2003 [36]. Despite this decline, the final 2003 National Vital Statistics indicate a 2.7 fold increase in SIDS rate among African American infants relative to Caucasian infants (1.152/1,000 livebirths vs. 0.424/1,000 livebirths) [36]. Because of this ethnic disparity and the continued occurrence of SIDS deaths despite improved compliance with modifiable risk factors, investigators considered the possibility of genetic and gene-by-environment interaction to explain the remaining 2,162 SIDS cases in the U.S., alone [36]. Thus far, all genetic studies have been based upon clinical, neuropathological, and epidemiological observations in SIDS victims, with subsequent identification and study of candidate genes. The focus of this chapter will be exclusively on those genes pertinent to cardiorespiratory or autonomic regulation.