Wang et al. (2023) utilised the stress-diathesis model to investigate how genetic
predispositions interact with environmental stressors (e.g., childhood trauma, loneliness,
stressful life events) to contribute to onset and severity of anxiety and depression.
The study found stress-related exposures explained a significant portion of variance in
depression and anxiety. The polygenic risk score (PRS) for depression significantly predicted
−16
depression scores (β = 0.11, p < 2.2 × 10 ), with significant interactions found between
PRS and all five stress-related exposures. Stronger effects were seen for individuals with high
stress exposure. Depression scores increased 63% in individuals with high long-term
difficulties, compared to 33% in those with low exposure. Additionally, reduced social
support amplified genetic risk of depression. Similarly, the PRS for anxiety significantly
−16
predicted anxiety scores (β = 0.19, p < 2.2 × 10 ). Significant interactions were found
between PRS and stress-related exposures (i.e., loneliness, stressful life events, long-term
difficulties and reduced social support), except childhood trauma. Conclusively, the study
found that individuals with both high genetic risk and high stress exposure were significantly
more likely to develop depression and anxiety .While genetic vulnerability plays a role, the
influence of stress, particularly in early life, can significantly shape one’s mental health
trajectory.
A strength of this paper is its large dataset. The sample size allowed the study to
examine nuanced interactions between genetic and environmental factors, increasing
reliability of the conclusions. Additionally, the longitudinal nature of the data allowed an
assessment of how stress exposure and genetic predisposition influence mental health over
time. This allowed for an observation of how different individuals respond to stress over
time, making it possible to identify patterns of resilience or vulnerability that might be missed
in a single-time point study. Lastly, the study integrated multiple levels of analysis,
predispositions interact with environmental stressors (e.g., childhood trauma, loneliness,
stressful life events) to contribute to onset and severity of anxiety and depression.
The study found stress-related exposures explained a significant portion of variance in
depression and anxiety. The polygenic risk score (PRS) for depression significantly predicted
−16
depression scores (β = 0.11, p < 2.2 × 10 ), with significant interactions found between
PRS and all five stress-related exposures. Stronger effects were seen for individuals with high
stress exposure. Depression scores increased 63% in individuals with high long-term
difficulties, compared to 33% in those with low exposure. Additionally, reduced social
support amplified genetic risk of depression. Similarly, the PRS for anxiety significantly
−16
predicted anxiety scores (β = 0.19, p < 2.2 × 10 ). Significant interactions were found
between PRS and stress-related exposures (i.e., loneliness, stressful life events, long-term
difficulties and reduced social support), except childhood trauma. Conclusively, the study
found that individuals with both high genetic risk and high stress exposure were significantly
more likely to develop depression and anxiety .While genetic vulnerability plays a role, the
influence of stress, particularly in early life, can significantly shape one’s mental health
trajectory.
A strength of this paper is its large dataset. The sample size allowed the study to
examine nuanced interactions between genetic and environmental factors, increasing
reliability of the conclusions. Additionally, the longitudinal nature of the data allowed an
assessment of how stress exposure and genetic predisposition influence mental health over
time. This allowed for an observation of how different individuals respond to stress over
time, making it possible to identify patterns of resilience or vulnerability that might be missed
in a single-time point study. Lastly, the study integrated multiple levels of analysis,
