Autor:innen:
Leandra Kuhn, Aachen (Germany)
Hannes Noack, Tübingen (Germany)
Nadine Skoluda, Wien (Austria)
Ann-Kristin Röhr, Aachen (Germany)
Birgit Derntl, Tübingen (Germany)
Vanessa Nieratschker, Tübingen (Germany)
Ute Habel, Aachen (Germany)
Although stress is ubiquitous in both everyday life and psychiatric research, it is still not fully understood. Previous research found an association of the functional promotor polymorphism of the serotonin transporter gene (5-HTTLPR) with stress sensitivity and vulnerability to psychopathology. While most gene x environment studies focused on early life stress, recent studies could already show an effect of 5-HTTLPR on cortisol increase in acute stress situations in the laboratory. However, no study so far investigated the specificity of this effect comparing different types of stressors.
In the present study, we compared the impact of two different stress induction protocols (Maastricht Acute Stress Test, MAST; Smeets et al., 2012 and ScanSTRESS; Streit et al., 2014) and the respective placebo conditions on affective ratings, salivary cortisol levels and cognitive performance. 160 healthy young males were tested in Aachen and Tübingen and were genotyped for the 5-HTTLPR polymorphism.
While physiological stress in the MAST led to a greater cortisol increase compared to the placebo conditions as well as the psychosocial ScanSTRESS Task, subjective stress ratings were highest in the ScanSTRESS condition. Interestingly, only in the ScanSTRESS condition, carriers of the s-allele of the 5-HTTLPR polymorphism exhibited greater post-stress cortisol levels and subjective stress ratings than participants with the l/l genotype. Neither stress induction nor genotype affected working memory capacity in the n-back task or response inhibition in the Stop Signal Task.
Our results are in line with previous research identifying the s-allele as a risk factor for increased stress sensitivity. Additionally, the results indicate that the multidimensional stress response as well as its genetic basis are stressor specific. This can promote new insights into biopsychosocial models for different psychiatric diseases like affective disorders in which stress reactivity plays a role.