Epigenetics of Stress-Related Psychiatric Disorders and Gene × Environment Interactions

Abstract

A deeper understanding of the pathomechanisms leading to stress-related psychiatric disorders is important for the development of more efficient preventive and therapeutic strategies. Epidemiological studies indicate a combined contribution of genetic and environmental factors in the risk for disease. The environment, particularly early life severe stress or trauma, can lead to lifelong molecular changes in the form of epigenetic modifications that can set the organism off on trajectories to health or disease. Epigenetic modifications are capable of shaping and storing the molecular response of a cell to its environment as a function of genetic predisposition. This provides a potential mechanism for gene-environment interactions. Here, we review epigenetic mechanisms associated with the response to stress and trauma exposure and the development of stress-related psychiatric disorders. We also look at how they may contribute to our understanding of the combined effects of genetic and environmental factors in shaping disease risk.

Clinical Diagnosis of Mental Disorders Immediately Before and After Cancer Diagnosis

“…As the outcome of interest, we defined a composite group of the 5 most commonly diagnosed mental disorders among patients with cancer, 13 including Tenth Swedish Revision of the International Classification of Disease Codes for stress reaction/adjustment disorder (code F43), depression (codes F32-F33), anxiety (codes F40-F41), substance abuse (codes F11-F16 and F18-F19), and somatoform/conversion disorder (codes F44-F45), which have also been suggested as potentially related to psychological stress. [28][29][30] Because alcohol consumption and tobacco use are known risk factors for multiple cancers, 31,32 we excluded alcohol and tobacco abuse or dependence from the group of substance abuse disorders.…”

Potential of Environmental Enrichment to Prevent Transgenerational Effects of Paternal Trauma

“…Such experiences often increase the risk to develop psychiatric and cognitive disorders in adulthood (Klengel and Binder, 2015). Further, their effects can be transmitted to subsequent generations and affect the offspring similarly to the ancestors in the absence of any trauma or stress exposure (Bohacek and Mansuy, 2015;Metz et al, 2015).…”

Epigenetics of Addiction: Current Knowledge, Challenges, and Future Directions

“…Causal inference may be strengthened by capitalizing on cross-species designs, using findings from experimental/mechanistic animal models to inform the investigation of DNAm markers in humans. Studies will also need to better quantify the relative contribution of genetic and environmental factors on DNAm (e.g., via twin, GCTA [genome-wide complex tract analysis], and G × E [Gene × Environment] analyses; Klengel & Binder, 2015;Trzaskowski & Plomin, 2015) and use prospective designs to examine whether DNAm patterns predict substance use liability as well as addiction risk. Specifically, this will require the use of longitudinal designs that make it possible to compare pre-versus post-exposure methylomic signatures during adolescence, a key period of vulnerability for the development of substance use disorders (Crews et al, 2007).…”