TY - JOUR
T1 - Gene-environment interactions in cardiovascular disease
AU - Flowers, Elena
AU - Froelicher, Erika Sivarajan
AU - Aouizerat, Bradley E.
N1 - Funding Information:
Funding for Elena Flowers’ doctoral studies was provided by NIH/NIGMS R25 GM56847 and NIH/NCRR/OD UCSF-CTSI Grant TL1 RR024129. Funding for Bradley E. Aouizerat was provided by NIH/NCRR/OD UCSF-CTSI grant number KL2 RR024130.
PY - 2012
Y1 - 2012
N2 - Background: Historically, models to describe disease were exclusively nature-based or nurture-based. Current theoretical models for complex conditions such as cardiovascular disease acknowledge the importance of both biologic and nonbiologic contributors to disease. A critical feature is the occurrence of interactions between numerous risk factors for disease. The interaction between genetic (i.e. biologic, nature) and environmental (i.e. non-biologic, nurture) causes of disease is an important mechanism for understanding both the etiology and public health impact of cardiovascular disease. Objectives: The purpose of this paper is to describe theoretical underpinnings of gene–environment interactions, models of interaction, methods for studying gene–environment interactions, and the related concept of interactions between epigenetic mechanisms and the environment. Discussion: Advances in methods for measurement of genetic predictors of disease have enabled an increasingly comprehensive understanding of the causes of disease. In order to fully describe the effects of genetic predictors of disease, it is necessary to place genetic predictors within the context of known environmental risk factors. The additive or multiplicative effect of the interaction between genetic and environmental risk factors is often greater than the contribution of either risk factor alone.
AB - Background: Historically, models to describe disease were exclusively nature-based or nurture-based. Current theoretical models for complex conditions such as cardiovascular disease acknowledge the importance of both biologic and nonbiologic contributors to disease. A critical feature is the occurrence of interactions between numerous risk factors for disease. The interaction between genetic (i.e. biologic, nature) and environmental (i.e. non-biologic, nurture) causes of disease is an important mechanism for understanding both the etiology and public health impact of cardiovascular disease. Objectives: The purpose of this paper is to describe theoretical underpinnings of gene–environment interactions, models of interaction, methods for studying gene–environment interactions, and the related concept of interactions between epigenetic mechanisms and the environment. Discussion: Advances in methods for measurement of genetic predictors of disease have enabled an increasingly comprehensive understanding of the causes of disease. In order to fully describe the effects of genetic predictors of disease, it is necessary to place genetic predictors within the context of known environmental risk factors. The additive or multiplicative effect of the interaction between genetic and environmental risk factors is often greater than the contribution of either risk factor alone.
KW - Confounding
KW - Environment and public health
KW - Gene expression
KW - Genetic variation
KW - Methods
KW - Phenotype
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U2 - 10.1016/j.ejcnurse.2011.06.001
DO - 10.1016/j.ejcnurse.2011.06.001
M3 - Article
C2 - 21684212
AN - SCOPUS:79958773013
VL - 11
SP - 472
EP - 478
JO - European Journal of Cardiovascular Nursing
JF - European Journal of Cardiovascular Nursing
SN - 1474-5151
IS - 4
ER -