Why do some people struggle emotionally after experiencing stressful events, but not others?
Environmental factors such as stressful life events or trauma often precede the initial onset or relapse of mental health conditions (e.g. Kendler, Karkowski, & Prescott, 1999). However, the experience of such events does not always result in psychopathology; there are individual differences in vulnerability to the effects of stressful events. Similarly, despite mental illnesses being heritable to varying extents, not every person with a genetic risk develops an illness.
This apparent interaction between genes and environment, whereby neither is sufficient in isolation to precipitate psychopathology, is captured by the diathesis-stress model. Developed following observations of individuals with schizophrenia, this model proposes that a stressful event can trigger a vulnerable predisposition (‘diathesis’) to result in mental illness (Bleuler, 1963; Meehl, 1962; Rosenthal, 1963). Consistent with this, a recent study demonstrated that a polygenic risk score for depression interacted with stressful life events to increase the risk of depression (Colodro-Conde et al., 2018). As well as genetic factors, there are other potential vulnerabilities, for example, a pessimistic personality, atypical neurobiology, or an enduring (as opposed to isolated) stressor such as low socio-economic status. Interestingly, these are also influenced by genetic factors (Howard et al., 2018; Nagel et al., 2017; Trzaskowski et al., 2014), so may indicate pathways by which some genes confer their ‘risk’. The diathesis-stress model changed the way that we think about mental illness; highlighting the importance of both nature and nurture in the development of complex disorders. However, it has been criticised for focusing solely on the impact of negative events, missing out the potential role of positive experiences.
The differential-susceptibility model proposes that individuals differ in their sensitivity to the environment, such that genetic factors influence the extent to which an individual is ‘plastic’, or malleable, to events (Belsky, Bakermans-Kranenburg & van IJzendoorn, 2007; Belsky & Pluess, 2009). This model predicts that individuals with genetic factors associated with unhealthy responses to stressful negative environments would conversely demonstrate advantageous responses to positive or enriched environments. Someone who is highly responsive to their environment might be considered to be like an orchid – they will flourish when looked after carefully, but perhaps be more vulnerable to a lack of attention. In contrast, those characterised as a dandelion are hardier and respond less to the environment they lie within. Most existing differential-susceptibility studies have focused on unreliable candidate gene approaches, but we undertook a study of children with anxiety disorders where we reported that a polygenic score of environmental sensitivity moderated the effects of parenting, as well as response to cognitive-behavioural therapy, on emotional problems and anxiety remission (Keers et al., 2016). You can see one of our clinical collaborators explaining these findings in this brief film. This model, therefore, provides a plausible explanation for the individual differences we observe in psychological treatment response. Furthermore, differential-susceptibility could explain resilience; individuals without environmental sensitivity would be protected from the harmful effects of stressful or traumatic events. The differential susceptibility model helps us to understand why some people are especially vulnerable to their environment, and thus are more likely to develop mental health conditions, whilst others remain healthy regardless of their experiences.
Belsky, J., Bakermans-Kranenburg, M. J., & Van IJzendoorn, M. H. (2007). For better and for worse: Differential susceptibility to environmental influences. Current Directions in Psychological Science, 16(6), 300-304.
Belsky, J., & Pluess, M. (2009). Beyond diathesis stress: differential susceptibility to environmental influences. Psychological Bulletin, 135(6), 885.
Bleuler, M. (1963). Conception of schizophrenia within the last fifty years and today [abridged], 945-952.
Colodro-Conde, L., Couvy-Duchesne, B., Zhu, G., Coventry, W. L., Byrne, E. M., Gordon, S., … & Eaves, L. J. (2018). A direct test of the diathesis-stress model for depression. Molecular Psychiatry, 23, 1590-1596.
Howard, D. M., Adams, M. J., Clarke, T. K., Hafferty, J. D., Gibson, J., Shirali, M., … & Shen, X. (2018). Genome-wide meta-analysis of depression in 807,553 individuals identifies 102 independent variants with replication in a further 1,507,153 individuals. bioRxiv, 433367.
Keers, R., Coleman, J. R., Lester, K. J., Roberts, S., Breen, G., Thastum, M., … & Nauta, M. (2016). A genome-wide test of the differential susceptibility hypothesis reveals a genetic predictor of differential response to psychological treatments for child anxiety disorders. Psychotherapy and Psychosomatics, 85(3), 146-158.
Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between stressful life events and the onset of major depression. American Journal of Psychiatry, 156(6), 837-841.
Meehl RE. (1962). Schizotaxia, schizotypy, schizophrenia. American Psychologist, 17, 827–838.
Nagel, M., Jansen, P. R., Stringer, S., Watanabe, K., de Leeuw, C. A., Bryois, J., … & Linnasrsson, S. (2017). GWAS Meta-analysis of neuroticism (N= 449,484) identifies novel genetic loci and pathways. bioRxiv, 184820.
Rosenthal D. (1963). A suggested conceptual framework. In: Rosenthal D(ed). The Genain Quadruplets: A Case Study and Theoretical Analysis of Heredity and Environment in Schizophrenia. Basic Books: NY, USA, 1963, 505–511.
Trzaskowski, M., Harlaar, N., Arden, R., Krapohl, E., Rimfeld, K., McMillan, A., … & Plomin, R. (2014). Genetic influence on family socioeconomic status and children’s intelligence. Intelligence, 42, 83-88.