79 The enhancing effects of testosterone in exposure treatment for social anxiety disorder proach boosting effects of testosterone in patients with social anxiety disorder (Enter, Spinhoven, et al., 2016; Enter, Terburg, et al., 2016). Then again, acute testosterone-augmentation effects depended on endogenous testosterone levels. This is consistent with evidence showing that individual differences in basal testosterone and proxies of fetal testosterone exposure (2D:4D ratio) moderate the effects of exogenous testosterone on various pertinent behavioral processes, including social approach, aggression, dominance, and risk-taking (Carré et al., 2015b; Carré & Robinson, 2020; Geniole & Carré, 2018; van Honk et al., 2011; Welling et al., 2016). The interaction between endogenous testosterone levels and exogenous testosterone administration was interesting and deepen our understanding of the primary results, in that exclusively the participants with low baseline concentrations having received testosterone reported blunted peak fear levels. This is in line with earlier findings regarding the anxiolytic properties of testosterone (Bos, Panksepp, et al., 2012; Hermans, Putman, Baas, Koppeschaar, & van Honk, 2006). Together, these findings suggest that women with relatively low endogenous testosterone show lowered threat response following testosterone supplementation that transfers to the non-enhanced session. In contrast, although the women with higher basal testosterone reported similar fear levels at the end of the enhanced session, they arrived there via a different, more fear-reactive route that appeared to be transferred to the unenhanced session. Arguably, the testosterone-induced effects (e.g., higher peak fear) in women with higher endogenous levels could be interpreted as negative. However, in theoretical accounts of exposure therapy (i.e., EPT (Foa & Kozak, 1986b; Foa et al., 2005) and inhibitory learning theory (Craske et al., 2008, 2014b)) high fear levels during (initial) exposure sessions are deemed beneficial for a good response, prompting the hypothesis that, it may facilitate essential exposure mechanisms in those with high basal levels. In the present proof of concept study we cannot yet verify such qualification of patterns as beneficial or not, particularly as our single session-enhancement did not result in lower SUD levels at the end of the second exposure, in the testosterone compared to placebo group. We can only make speculations based on theoretical grounds and clearly, treatment protocols with more exposure sessions are needed to further elucidate the effects of exogenous testosterone on fear activation and reduction within and across exposure sessions. That endogenous testosterone moderates the effects of exogenous testosterone may be explained by trait factors, including individual differences in the sensitivity of the androgen receptor (AR), where relative AR insensitivity has been reported for people with low basal concentrations (Hogervorst, Bandelow, & Moffat, 2005; Holland, Bandelow, & Hogervorst, 2011). Moreover, testosterone administration can lead to AR downregulation 4
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