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Small for gestational age infants and sudden infant death syndrome: a confluence of complex conditions
  1. Carl E Hunt
  1. Dr Carl E Hunt, 4550 North Park Avenue, Chevy Chase, Maryland 20815, USA; huntc{at}mail.nih.gov

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Perspective on the paper by Malloy (see page 473)

“All illnesses have some hereditary contribution. Genetics loads the gun and environment pulls the trigger” (Francis Collins, Director, National Human Genome Research Institute, National Institutes of Health, 2006)

New data by Malloy1 further substantiate fetal growth restriction or being small for gestational age (SGA) as a risk factor for sudden infant death syndrome (SIDS). The similar odds ratios for sudden unexpected death in infancy (SUDI) excluding SIDS and for SIDS may reflect at least in part diagnostic shifts based on custom and preference of the medical examiner in classifying infant deaths consistent with SIDS not as SIDS but rather as, for example, “accidental suffocation” or “other ill-defined and unspecified causes”. These new confirmatory data are important, but they provide no new insights regarding potential causal mechanisms for this association between SGA and SIDS. Does being SGA directly increase the risk for SIDS, or is this an indirect association because of an underlying causal biological or environmental risk factor common to both conditions?

Low birth weight is defined as a birth weight <2500 g and can be due to prematurity (<38 weeks’ postmenstrual age) and/or to fetal growth restriction (SGA). SGA, typically defined as a birth weight <10th percentile for gestational age, can be due to a variety of pathophysiological conditions or diseases.2 The growth restriction in SGA infants can be either symmetrical (weight, length and brain size affected) or asymmetrical (brain growth preserved), the former often associated with factors intrinsic to the fetus and the latter often …

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