Moniek Hutschemaekers

118 Chapter 6 The role of baseline testosterone When studying the effects of endogenous and pharmacological testosterone reactivity, it is relevant to take inter and intra-individual differences in baseline testosterone levels into account (see also Geniole & Carré, 2018 for a review). In chapter 3 low baseline testosterone seemed linked to stronger symptom reduction, an effect that we could not replicate in chapter 4. In chapter 4, we found a moderating role of baseline testosterone on testosterone enhancement. Specifically, low baseline testosterone was linked to blunted fear levels within both exposure sessions with no transfer to social anxiety symptoms. On the one hand one could argue that individuals with low baseline testosterone benefit from testosterone enhancement as they show lower fear during exposure. This could be interpreted as indicating that for individuals with relatively low endogenous baseline testosterone, administration of testosterone vs placebo works fear-reducing. However, individuals with high endogenous baseline testosterone levels showed an interesting fear level pattern as well. That is, they showed increased peaks and steeper reductions in fear levels at the end of the first session and interestingly this pattern showed transfer to the second, unenhanced exposure session (see Fig 4.2). The latter may suggest that an important mechanism of exposure is more manifested, since from theoretical models of exposure therapy (Emotional Process Theory, [EPT] and Inhibitory Learning Theory [ILT]) one can derive that higher initial fear levels during exposure are beneficial since they are important for good learning (e.g., fear activation in EPT and optimal expectancy violation in ILT), resulting in a better long term response to treatment (Craske et al., 2008; Craske, Treanor, Conway, Zbozinek, & Vervliet, 2014a; Foa & Kozak, 1986; Foa, Huppert, & Cahill, 2005). Although speculative at this point, one could imagine that follow-up research with repeated testosterone-enhanced exposure in individuals with high baseline testosterone is promising. This more reactive fear level pattern was present also when not taking baseline testosterone into account, in the second unenhanced session. Therefore, we conclude that future research using multiple enhancement sessions is needed to investigate whether the promising effects of testosterone administration on in-session fear levels transfer to symptom-level effects in the long run. The observation that individual differences in baseline testosterone modulate these effects are worth further exploration as they could provide a promising starting point towards individualized treatments that could be specified based on biomarkers such as endogenous testosterone levels.

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