Gene-Environment Interactions in Human Health

Mechanic, Leah E.; Hutter, Carolyn M.

doi:10.1007/978-1-4471-6678-8_10

Cited by 2 publications

(2 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is not surprising because genes might not be directly related to psychopathology but may lead to increased risk in interaction with specific environmental factors (Rutter, 2012). Effect sizes of G × E are, however, often not much larger (Mechanic & Hutter, 2015; Rutter, Moffitt, & Caspi, 2006), as was also evident from our present analyses. Testing G × E involves measuring how much behavioral variation is attributed to the interaction and will therefore be subject to a lot of noise.…”

Section: Resultssupporting

confidence: 85%

DRD4 and DRD2 genes, parenting, and adolescent delinquency: Longitudinal evidence for a gene by environment interaction.

Chhangur¹,

Overbeek²,

Verhagen³

et al. 2015

Journal of Abnormal Psychology

View full text Add to dashboard Cite

Gene by environment (G × E) research has been increasingly appreciated as it relates to the development of psychopathology. In particular, interactions between dopaminergic genotypes and maladaptive parenting have been prominently in the spotlight. In this study, we investigated whether high parental psychological control and low support would be differentially related to the development of delinquency in adolescents based on their genetic background (i.e., DRD4 and DRD2 genotypes). Data were derived from a 5-wave longitudinal survey among adolescents (N = 308; Mage = 13.4 at Time 1). After accounting for possible passive genetic effects (i.e., parents' genotype, Parents' Genotype × Adolescents' Genotype, and Parents' Genotype × Parenting, cf. Keller, 2014), latent growth modeling revealed a significant interaction of DRD2 × Parental Support, indicating that adolescents with the DRD2 A2A2 genotype were more vulnerable for low parental support, developing more delinquent behavior as a consequence. No significant interactions emerged for DRD4 with parental support and psychological control, nor for DRD2 with parental psychological control. The observed effect size of the identified DRD2 × parental support interaction was modest, emphasizing that replication is essential to confirm the present evidence.

show abstract

Section: Resultssupporting

confidence: 85%

DRD4 and DRD2 genes, parenting, and adolescent delinquency: Longitudinal evidence for a gene by environment interaction.

Chhangur¹,

Overbeek²,

Verhagen³

et al. 2015

Journal of Abnormal Psychology

View full text Add to dashboard Cite

show abstract

“…Building on and extending the ‘Hallmarks of Cancer’ framework proposed by Hanahan and Weinberg [ 36 ], an international team of 170 scientists participating in the Halifax project recently evaluated the contributions to carcinogenesis of low-dose exposures to individual compounds and mixtures of environmental chemicals on each of the proposed hallmark phenotypes [ 37 ]. Other recent reviews have focused on the importance of evaluating: non-monotonic dose-response relationships, especially between EDCs and health outcomes [ 38 ]; timing of exposures to environmental toxicants, with an emphasis on fetal to adolescent exposures to EDCs and later development of diseases [ 39 – 41 ]; environmental carcinogenesis from the perspective of disruptions of cell-cell (e.g., stromal-epithelia) interactions [ 42 , 43 ]; gene-environment interactions [ 44 , 45 ]; the importance of using the principles of basic endocrinology in establishing mechanistic models for examining health impacts of exposures to EDCs [ 46 , 47 ] and the relevance for these mechanisms in understanding the growing appreciation of the links between environmental toxicants and increased risk for many diseases, including breast cancer [ 48 – 52 ].…”

Section: Introductionmentioning

confidence: 99%

State of the evidence 2017: an update on the connection between breast cancer and the environment

et al. 2017

View full text Add to dashboard Cite

BackgroundIn this review, we examine the continually expanding and increasingly compelling data linking radiation and various chemicals in our environment to the current high incidence of breast cancer.AbstractSingly and in combination, these toxicants may have contributed significantly to the increasing rates of breast cancer observed over the past several decades. Exposures early in development from gestation through adolescence and early adulthood are particularly of concern as they re-shape the program of genetic, epigenetic and physiological processes in the developing mammary system, leading to an increased risk for developing breast cancer. In the 8 years since we last published a comprehensive review of the relevant literature, hundreds of new papers have appeared supporting this link, and in this update, the evidence on this topic is more extensive and of better quality than that previously available.ConclusionIncreasing evidence from epidemiological studies, as well as a better understanding of mechanisms linking toxicants with development of breast cancer, all reinforce the conclusion that exposures to these substances – many of which are found in common, everyday products and byproducts – may lead to increased risk of developing breast cancer. Moving forward, attention to methodological limitations, especially in relevant epidemiological and animal models, will need to be addressed to allow clearer and more direct connections to be evaluated.

show abstract

Gene-Environment Interactions in Human Health

Cited by 2 publications

References 78 publications

DRD4 and DRD2 genes, parenting, and adolescent delinquency: Longitudinal evidence for a gene by environment interaction.

DRD4 and DRD2 genes, parenting, and adolescent delinquency: Longitudinal evidence for a gene by environment interaction.

State of the evidence 2017: an update on the connection between breast cancer and the environment

Contact Info

Product

Resources

About