The Genetics and Epigenetics of Attachment
Attachment emerges as a prototypical nature by nurture interaction – it is influenced by both genetic and environmental factors. This interplay between genetic and environmental factors can nowadays be assessed by combining the study of genetic predispositions (i.e., genetics) with epigenetics (i.e., environment-dependent changes in gene transcription). Thanks to international collaborations, the SoNeAt lab is participating in the investigation of the genetic and epigenetic correlates of attachment in (young healthy) adults.
Interindividual differences in attachment can be understood as meaningful adaptations to specific environmental demands. While infants are born with certain genetic predispositions, it is the environment within which they grow up that determines the extent of gene transcription. The seminal work of Weaver and colleagues in rodents (see original publications from 1999 and 2004) provides the basis of such work. By looking at epigenetic markers (e.g., methylation at CpG sites that control gene transcription) – and by ideally combining such insights with genetic information in the future -, we hope to obtain a better insight into the biological mechanisms underlying environmental adaptations in association with attachment, and in particular secure versus insecure, avoidant and/or anxious attachment dimensions.
In a recent review paper (Attachment and Epigenetics: A Scoping Review of Recent Research and Current Knowledge), Rasmussen & Storebro present a broad perspective on the current state of knowledge in the relatively new and complex field of “attachment and epigenetic processes” in humans. They identified 11 studies since 2009 and summarised the so far available evidence in the format of a narrative / scoping review. While some communalities appear to emerge – such as a focus on the HPA stress axis and glucocorticoids or the oxytocin system – many questions still remain unresolved.
Epigenetics & Attachment in Adults
In a first paper, we looked at epigenetic modification (i.e., degree of methylation) of the oxytocin receptor gene (OXTR) and glucocorticoid receptor gene (NR3C1) promoters as a function of self-reported attachment avoidance and anxiety in a sample of 109 young healthy adolescents. The paper is published and freely available here.
Our findings revealed a specific association between the degree of both OXTR and NR3C1 promoter methylation and attachment avoidance (i.e., in participants who scored high on attachment avoidance but low on attachment anxiety). Attachment avoidance may thus be epigenetically characterised by a less active oxytocin system. The oxytocin system is thought to be implicated in prosocial processes (albeit by no means exclusively – see also here) also comprising mechanisms to cope with stress by seeking proximity to and comfort by others. In addition, attachment avoidance may also be characterised by a more active HPA stress axis and thus sustained stress. This link emerges because the glucocorticoid receptor NR3C1 is generally associated with the negative feedback-loop of the HPA axis to shut down the stress response. Such pattern may be due to the fact that avoidantly attached individuals tend to be self-reliant and to less likely turn to others to help them (co-)regulating stress, which may be a less effective / more costly stress-regulation strategy.
Genetics / Epigenetics & Attachment in Parents and Children
More research in this exciting and new field of research is needed, also comprising replication and extension of the results we obtained in our first study reported above.
To that end, we are carrying out several projects that look at genetics / epigenetics in parents and children using longitudinal designs. Please refer to this page for more information.