113 Summary and General Discussion Aims of this dissertation The main aim of this dissertation was to test the potential of the steroid hormone testosterone as an enhancer for exposure treatment efficacy for social anxiety disorder (SAD). As described in the previous chapters, persistent avoidance is an important factor hindering the extinction of fear during social situations, which is why reducing avoidance behavior is the core target of exposure therapy, the treatment of choice for SAD. However around 45-55% of the individuals with SAD do not profit sufficiently from treatment (Carpenter et al., 2018; Loerinc et al., 2015). Therefore, the intervention leaves room for improvement. Based on pre-clinical research, the steroid hormone testosterone yielded promise to enhance exposure therapy effects for those suffering from SAD. From a literature review in chapter 2 we concluded that testosterone is an important regulator of social approach behavior, it alleviates social avoidance and facilitates prosocial approach and dominance-seeking behavior (Hermans & Van Honk, 2006; Maner et al., 2008; Mazur & Booth, 1998). Therefore, in our first empirical study we tested whether pre-exposure increase in endogenous testosterone is predictive of exposure efficacy in males and females with SAD. Next, we conducted a randomized controlled proof-of-concept trial in which we tested whether a single dose of exogenous testosterone could improve exposure efficacy in females with SAD. Lastly, we examined whether social avoidance tendencies moderate testosterone-enhanced exposure efficacy. This final chapter summarizes the results of these theoretical and empirical chapters, presents an integration and discussion of the findings as well as the clinical implications. Additionally, I will describe the strengths and limitations of this dissertation, followed by a conclusion. Summary of chapters There is a wealth of fundamental neuroendocrinological research in animals and humans pointing to the relevance of the HPG- and HPA-axis in the regulation of social motivational behavior. In Chapter 2, we explored the relevance of those fundamental insights for our understanding of social motivational deficiencies characterizing social motivational disorders such as SAD and psychopathy. Specifically, we presented a literature review regarding the role of the steroid hormones testosterone and cortisol and provided converging evidence that SAD as well as aggression-related psychopathologies present with an imbalance in these steroid hormones. This imbalance shows an interesting symmetry with alterations in social approach and avoidance in healthy individuals but particularly in relation to social motivational disorders, such as SAD and psychopathy. A 6
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