115 Summary and General Discussion groups to shed light on the relation between baseline and challenge-reactive testosterone levels. Taken together, these results can be interpreted as providing initial support for the social challenge hypothesis. It extends the hypothesis to a clinically relevant context and supports the relevance of further investigation into exposure-enhancing effects of testosterone in individuals with SAD. This first study on clinical effects of pre-exposure testosterone-reactivity provided promising findings, but it was correlational in nature and provided few insights into the effects of testosterone on in-session fear patterns. To ultimately test whether testosterone levels may be relevant for exposure-treatment in terms of in-session fear levels and symptom reduction, causal evidence is needed. Therefore, following this correlational work, we conducted a pharmacological study using exogenous testosterone administration. More specifically, we conducted a randomized controlled proof-of-concept trial to test the potential of exogenous testosterone as a pharmacological enhancer for exposure for SAD in chapter 4. In this study 55 females meeting the criteria of SAD received two exposure therapy sessions. The first session was supplemented with either testosterone (0.50 mg) or placebo, followed by a second unenhanced exposure session. Transfer effects of testosterone administration on within-session fear and social anxiety symptoms were assessed during the second unenhanced exposure session and at 1 month follow-up. The participants having received testosterone showed a more reactive fear pattern with higher peaks and steeper reductions in fear levels in the unenhanced second session. This pattern appeared to be specific for females with high baseline (endogenous) testosterone, and it was present in the first (enhanced) as well as in the second (unenhanced) session. Participants with low baseline (endogenous) testosterone showed blunted peak fear levels in both sessions. In terms of social anxiety symptom levels we did not observe differences between the placebo and testosterone condition. The results of this study provide preliminary support for the hypothesis that testosterone may act on important fear mechanisms during exposure. However, further exploration of multi-session testosterone-enhanced exposure is needed to better understand the potential of testosterone as an enhancer for exposure treatment for SAD. In the final empirical chapter, we explored the relationship between a core feature of SAD, namely social avoidance behavior, and testosterone-enhanced exposure. Following chapter 2, we first verified whether social avoidance tendencies characterize SAD by contrasting approach and avoidance tendencies for social and non-social stimuli in chapter 5. Critically, we tested whether baseline social avoidance tendencies moderate the efficacy of testosterone-enhanced exposure. For this (pilot) study we analyzed data from a social approach-avoidance task that was assessed pre- and post- treatment in the augmentation study described in chapter 4. Individuals with SAD showed stronger 6
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