About: Gene–environment interactions likely account for a large portion of the “missing heritability” or “dark matter” of genetic associations with traits and diseases. In concert with the powerful methods and scale of genomic population analyses, a complementary effort is needed to capture data about behavioral and environmental variables acting on the genetic substrate and contributing importantly to disease risk. Examples from environmental exposures to foods and food additives, infectious agents, inhaled pollutants, pesticides, pharmaceuticals, sensory stimuli, and allergic and sensitizing agents are summarized. Epigenomics and protein folding/misfolding are recently recognized mechanisms for some of these interactions and effects. Keywords asthma, cancers, eco-genetics, epigenomics, evolution, gene–environment interactions, genome-wide association studies, heritability, host susceptibility, nutrigenomics, pathogens, toxicogenomics

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About: Gene–environment interactions likely account for a large portion of the “missing heritability” or “dark matter” of genetic associations with traits and diseases. In concert with the powerful methods and scale of genomic population analyses, a complementary effort is needed to capture data about behavioral and environmental variables acting on the genetic substrate and contributing importantly to disease risk. Examples from environmental exposures to foods and food additives, infectious agents, inhaled pollutants, pesticides, pharmaceuticals, sensory stimuli, and allergic and sensitizing agents are summarized. Epigenomics and protein folding/misfolding are recently recognized mechanisms for some of these interactions and effects. Keywords asthma, cancers, eco-genetics, epigenomics, evolution, gene–environment interactions, genome-wide association studies, heritability, host susceptibility, nutrigenomics, pathogens, toxicogenomics Goto Sponge NotDistinct Permalink

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value	Gene–environment interactions likely account for a large portion of the “missing heritability” or “dark matter” of genetic associations with traits and diseases. In concert with the powerful methods and scale of genomic population analyses, a complementary effort is needed to capture data about behavioral and environmental variables acting on the genetic substrate and contributing importantly to disease risk. Examples from environmental exposures to foods and food additives, infectious agents, inhaled pollutants, pesticides, pharmaceuticals, sensory stimuli, and allergic and sensitizing agents are summarized. Epigenomics and protein folding/misfolding are recently recognized mechanisms for some of these interactions and effects. Keywords asthma, cancers, eco-genetics, epigenomics, evolution, gene–environment interactions, genome-wide association studies, heritability, host susceptibility, nutrigenomics, pathogens, toxicogenomics
part of	Chapter 4 Gene–Environment Interactions Eco-Genetics and Toxicogenomics
is abstract of	Chapter 4 Gene–Environment Interactions Eco-Genetics and Toxicogenomics

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