Gene-environment interplay
Environmental factors can cause deviations from expected gene expression, which ultimately impact cellular processes, such as cell signaling.
[5] For instance, one study on children in middle childhood found that a child's innate desire for autonomy partially determined the degree of maternal control evoked.
This is done through the disturbance of histone acetylation and DNA methylation which is correlated with increased rates of cancer, autoimmune diseases, and neurological disorders.
While the mechanism is not fully understood, it could involve the formation of reactive oxygen species, leading to oxidative stress and cellular signaling cascade or increased fetal cortisol levels.
[19] The alteration in DNA methylation patterns can elevate the risk of developing metabolic disorders and type II diabetes mellitus.
[21] Malnutrition can also significantly impact gene expression in the small intestine, leading to alterations in nutrient transporters, digestive enzymes, barrier function, immune responses, and metabolic adaptation.
Research indicates that individuals that reside in impoverished communities or those who belong to marginalized racial and ethnic groups may encounter limited access to nutritious food options.
This suppression can help prevent the development of chronic inflammation and associated age-related diseases due to excess inflammatory cytokines.
[28] These alcohol-induced changes in DNA methylation during pregnancy contribute to the distinct set of traits seen in Fetal Alcohol Spectrum Disorder (FASD).
[28] Other instances of prenatal environment impact on fetal epigenetic state include maternal folic acid, stress, and tobacco smoking during pregnancy.
[32] GRs play a critical role in the HPA axis by aiding in the restoration of normal physiological state after stress exposure.
Down regulation of GRs expression occurs through histone modifications and DNA methylation of the GR gene, resulting in dysregulation of the stress response, including prolonged inflammation and cellular damage.
[33] Additionally, numerous studies have linked early life stress with later-life psychiatric disorders, including anxiety and depression, through epigenetic modulation of genes involved in the HPA axis.
[34] Socioeconomic disparities, discrimination, and cultural factors prevalent within minority communities can contribute to heightened levels of stress and adversity, impacting gene expression and health outcomes.
These studies typically involve the comparison of identical (monozygotic) and fraternal (dizygotic) twins to determine the extent to which genetic factors and environmental influences contribute to variations in traits or behaviors.
[38][39] Animal models provide a controlled and manipulable environment in which researchers can investigate the complex interactions between genes and environmental factors, shedding light on various biological and behavioral outcomes.
For example, one study has demonstrated the utility of mouse models in understanding gene-environment interactions in schizophrenia due to the genetic similarities.
For instance, gene-environment interactions have a prevalent role in mental health disorders; specifically, evidence has found a link to alcohol dependence,[39] schizophrenia,[42] and psychosis.
