Biological embedding occurs when life experience alters biological processes to affect later life health and well-being. Although extensive correlative data exist supporting the notion that epigenetic mechanisms such as DNA methylation underlie biological embedding, causal data are lacking. We describe specific epigenetic mechanisms and their potential roles in the biological embedding of experience. We also consider the nuanced relationships between the genome, the epigenome, and gene expression. Our ability to connect biological embedding to the epigenetic landscape in its complexity is challenging and complicated by the influence of multiple factors. These include cell type, age, the timing of experience, sex, and DNA sequence. Recent advances in molecular profiling and epigenome editing, combined with the use of comparative animal and human longitudinal studies, should enable this field to transition from correlative to causal analyses.

Purpose of Review: To review the literature on the trends in substance use among youth during the coronavirus SARS-CoV-2 (COVID-19) pandemic. Recent Findings: The pandemic has given rise to concerns about the mental health and social well-being of youth, including its potential to increase or exacerbate substance use behaviors. This systematic review identified and included 49 studies of use across alcohol, cannabis, tobacco, e-cigarettes/vaping, and other drugs, and unspecified substances. The majority of studies across all categories of youth substance use reported reductions in prevalence, except in the case of other drugs and unspecified drug and substance use, which included three studies that reported an increase in use and three studies that reported decrease in use. Summary: Overall, the results of this review suggest that the prevalence of youth substance use has largely declined during the pandemic. Youth substance use in the post-pandemic years will require monitoring and continued surveillance.

Gene-by-environment interactions (G×Es) can provide important biological insights into psychiatric disorders and may consequently have direct clinical implications. In this review, we begin with an overview of the major challenges G×E studies have faced (e.g., difficulties replicating findings and high false discovery rates). In light of these challenges, this review focuses on describing examples in which we might begin to understand G×Es on the molecular, cellular, circuit, and behavioral level and link this interaction to altered risk for the development of psychiatric disorders. We also describe recent studies that utilize a polygenic approach to examine G×Es. Finally, we discuss how gaining a deeper understanding of G×Es may translate into a therapeutic practice with more targeted treatments.