Key result
Gene-environment interactions, specifically environmental risk factors interacting with genetic polymorphisms, yield phenotypes susceptible to sudden infant death syndrome.
Understanding sudden infant death syndrome requires considering both genetic polymorphisms and environmental risk factors.
May guide SIDS research toward gene-environment models; leaves open clinical translation pending prospective validation.
From the perspective of systems biology, genes and proteins interact to produce complex networks, which in turn interact with the environment to influence every aspect of our biological lives. Recent advances in molecular genetics and the identification of gene polymorphisms in victims of sudden infant death syndrome (SIDS) are helping us better to understand that SIDS, like all other human conditions in health and disease, represents the confluence of specific environmental risk factors interacting in complex ways with specific polymorphisms to yield phenotypes susceptible to sudden and unexpected death in infancy. Failure to consider both genetic and environmental risk factors will impede research progress.
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C E Hunt (2004) conducted a review in Sudden infant death syndrome (SIDS). Gene-environment interactions was evaluated. Gene-environment interactions, specifically environmental risk factors interacting with genetic polymorphisms, yield phenotypes susceptible to sudden infant death syndrome.
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