Moniek Hutschemaekers

18 Chapter 1 ed in alleviation of gaze avoidance toward angry facial expressions in individuals with SAD (Enter, Terburg, et al., 2016). Participants showed less aversion of gaze towards the eye-regions of negative facial expressions after testosterone versus placebo. Moreover, testosterone administration led to increased approach behavior toward social threat (e.g., angry faces) on a social approach avoidance task (Enter, Spinhoven, et al., 2016). Finally in an EEG study, it was found to result in reduced automatic threat processing of angry faces in individuals with SAD versus healthy controls (van Peer, Enter, van Steenbergen, Spinhoven, & Roelofs, 2017). In light of these consistently established prosocial and approach enhancing properties of testosterone in general and specifically in SAD, testosterone may be a potential candidate to boost exposure effects in SAD, by targeting within session avoidance behavior. This is exactly what I aim to investigate using the current dissertation. Boosting treatment effectiveness by means of testosterone would extend a vast line of research conducted over the past two decades on pharmacological enhancement of CBT. Among potential pharmacological enhancement methods, various randomized controlled trials have found most support for D-cycloserine (DCS), a partial N-methyl-D-Aspartate (NMDA) receptor agonist, associated with fear extinction consolidation (Hofmann et al., 2006; Rodebaugh, Levinson, & Lenze, 2013; Smits et al., 2020). Additionally, few studies examined effects of pharmacological enhancers such as Yohimbine and Oxytocin in SAD (Guastella et al., 2009; Smits, Rosenfield, Davis, et al., 2013). These enhancement strategies all aimed to target the process of (extinction) learning in SAD. Although the results are encouraging, none of these pharmacological enhancers directly acts on acute within-session social-approach behavior, essential for effective exposure. This brings me to the next section, on the potential mechanism of action of testosterone in exposure therapy. Testosterone as a potential enhancer of exposure therapy As mentioned, one of the proposed mechanisms of action of exposure is that individuals with SAD learn that exposure to a feared stimulus (e.g., a social situation) does not lead to their feared outcome (social rejection). To learn this, it is needed that individuals with SAD approach the feared situation, rather than avoiding it. That is, they have to approach the social interaction and have to get engaged in it. The social challenge hypothesis (Wingfield et al., 1990, 2001) states that testosterone levels rise in preparation to a socially challenging situation (such as exposure) and thereby initiates approach motivation. Testosterone reactivity may therefore be important for successful exposure treatment by stimulating within-session approach behavior. Crucially, testosterone reactivity can be experimentally manipulated for example by testosterone administration, resulting in social approach behaviors in individuals with SAD (Enter, Spinhoven, et al.,

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