Moniek Hutschemaekers

126 Chapter 6 et al., 2017; Rodebaugh et al., 2013; Van Der Flier et al., 2019) and the earlier discussed EPT (Foa & Kozak, 1986; Foa et al., 2005), the more recent theoretical model of exposure therapy: ILT (see also introduction) suggests that inhibitory learning and maximizing expectancy violation are crucial for exposure success. Fear activation may be useful for expectancy violation, but according to ILT it is not a necessity (Craske et al., 2008, 2014a, 2022). As such, a suggestion for a future study would be to use an alternative outcome for exposure success, for example an index of expectancy violation. Currently, I would not argue that an index of expectancy violation would be a better outcome compared to fear reduction, since studies testing the value of expectancy violation as a marker for exposure success find mixed results (Buchholz et al., 2022; de Kleine, Hendriks, Becker, Broekman, & van Minnen, 2017; Elsner, Jacobi, Kischkel, Schulze, & Reuter, 2022; Guzick, Reid, Balkhi, Geffken, & McNamara, 2020; Pittig et al., 2022; Scheveneels, Boddez, Van Daele, & Hermans, 2019), and there is not yet consensus on how to assess expectancy violation. Furthermore, as described in the introduction and chapter 2, the HPG-axis and its end-product testosterone do not work in isolation. For example, there are complex interactions between the HPG and HPA-axis. Although the HPG and HPA axis work in conjunction during high acute stress-exposure, the HPG-axis can also work in antagonism with the hypothalamus-pituitary-adrenal (HPA) axis in such a way that cortisol, the end product of the HPA-axis, may disrupt the production and inhibits actions of testosterone which in turn inhibits the stress induced activation of the HPA-axis (Viau, 2002). Moreover, testosterone also interacts with neuropeptides such as oxytocin. Therefore, it is worthwhile to take into account the assessment of other hormones, peptides and -if possible- neurotransmitters in future studies to further understand the interplay between different hormones in social anxiety disorder and its treatment. For example, there is some support for a dual process hypothesis that states that the HPA and HPG-axis interact to regulate several behavioral domains including dominance and social status (Mehta & Josephs, 2010; Mehta & Prasad, 2015). Specifically, the dual process hypothesis states that testosterone is positively related to dominance and social status related behaviors, but only in individuals with low cortisol levels, which may be of relevance in an exposure context too. To conclude, the current dissertation is part of a novel line of research in which different pharmacological enhancers are being tested to improve exposure efficacy for SAD as well as other (anxiety) disorders. Different enhancers appeared to be promising candidates such as DCS (Hofmann et al., 2019; Rodebaugh et al., 2013; Rosenfield et al., 2019), but replication is often difficult and therefore these augmentation strategies are not (yet) considered effective for SAD (De Cagna et al., 2019; Pelissolo, Abou Kassm, &

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