Understanding gene × early adversity interactions: possibilities for insight in the biology of psychiatric disorders

Examining the independent and joint effects of molecular genetic liability and environmental exposures in schizophrenia: results from the EUGEI study

“…Second, they may open up promising research lines for further exploration of gene‐environment interactions in the biological context, such as using biologically‐informative pathway scores instead of an aggregate genetic risk score for disease phenotype. These studies may help us investigate both hypotheses for biologically plausible pathways impacted by distinct exposures (e.g., hypoxia‐ischemia pathway x obstetric complications and childhood adversities x hypothalamic‐pituitary‐adrenal axis), and putative common final pathways, such as the broad inflammatory pathway which may be influenced by many exposures cumulatively.…”

<p>Attention Deficit Hyperactivity Disorder And Borderline Personality Disorder In Adults: A Review Of Their Links And Risks</p>

“…Another subgroup, probably characterized by higher levels of hyperactivity/impulsivity and emotional problems, seems more prone to develop the comorbid BPD+ADHD clinical presentation70 It is unclear to what extent these clinical pictures are linked to either different neurobiological vulnerabilities, and/or their interaction with an unfavorable environment. Emerging evidence on the latter topic suggests that while childhood adversity may increase the risk of overall psychopathology124 it is likely that repeated exposure to physical abuse in particular might be associated with the persistence of ADHD into adulthood, while emotional or sexual abuse might be particularly involved in the development of BPD or comorbid BPD+ADHD117 Moreover, although still speculative, it is possible that ADHD symptoms in childhood, especially when untreated, may increase the odds of severe negative childhood experiences, and this, in turn, may predispose to the development of BPD in adulthood in a subgroup of individuals 8…”

“…In addition to different types of adversity, timing of exposure during different developmental periods could be an important factor for differential disease risk123 and could be mediated by differential vulnerability of certain systems during developmental periods124 This means that investigating the differential disease risk relative to type of adversity, but also timing of exposure in BPD, ADHD, and BPD+ADHD could be particularly relevant to the understanding of their specific developmental pathways.…”

“…Given the increasing evidence supporting the role played by adverse and traumatic events on the emergence of psychopathology124 there has been a shift in ongoing research in psychiatric disorders from identifying “vulnerability genes” to identifying genes that can be influenced by the environment and contribute to adult psychopathology125 Epigenetics, which refer to the study of modifications of gene expression rather than alteration of the genetic code itself, has been investigated in relation to childhood adversities mainly in BPD. Genes involved in the regulation of the hypothalamic–pituitary–adrenal (HPA) axis have shown promising results126 However few studies have investigated this issue in ADHD and few epigenetic changes in relation to early life adversities have been shown to be shared between ADHD and BPD 125…”

Using interaction-based phenotyping to assess the behavioral and neural mechanisms of transdiagnostic social impairments in psychiatry

“…This characterization is reflected by the kind of research that has and is being conducted in psychiatry and the clinical neurosciences. Indeed, this research has focused on the genetic contributions to psychiatric disorders, but more recently also on the epigenetic factors, i.e., gene × environment interactions, which are relevant in shaping mental ill health [1]. In spite of the important advances and new insights that have been gained as a result of focusing more strongly on the interplay between social and biological factors [2], our understanding of how social factors influence the 'social brain' and how this could inform individual diagnosis and treatment is still limited.…”