122 Chapter 6 the results. Thereby we do need multiple clinical assays in a row or a full clinical design anyway. Critically, in my opinion the fast fail principle is rather difficult, because even in the case of a clear null-finding it is hard to decide if the intervention did actually fail, since alternative explanations are possible too (e.g., a false negative, or the drug does not work sufficient in only one session), raising a number of new questions. Taken together, the clinical assay is a valuable method to test single session enhancement, with some shortcomings. An alternative design for future studies could therefore be the single case experimental design (SCED), in which the efficacy of an intervention is tested with a small number of participants. In a SCED the intervention can be introduced in a randomized sequential order, it includes repeated measures where participants serve as their own controls and requires special data analyses. This method seems to be very promising in testing new interventions in situations where time and money is limited. Importantly, a SCED is suited to evaluate the process of an intervention (e.g., does the intervention indeed affect the target variable). Moreover, due to the repeated measures it provides researchers with the opportunity to also test interventions that are expected to show slower effects contrary to the clinical assay (see for a guide Krasny-Pacini & Evans, 2018 or a review; Smith, 2012). In sum, the SCED method seems to be a suitable method for future studies testing testosterone enhanced exposure for SAD. Strengths, limitations & future studies Strengths This dissertation has several important strengths that I would like to emphasize. First, as regards our intervention protocols: our proof-of-concept exposure intervention protocols (regardless of enhancements) were successful in establishing reduction in social anxiety symptoms, providing us with the opportunity to test our hypotheses, without applying a full treatment protocol (chapter 3 and 4). In addition, the protocol for administration of a single dose of testosterone was safe and tolerable for our participants. There were no adverse events during the clinical assay or augmentation related drop-out. Drop-out rates were low in both study samples of chapter 3 and 4. As a result, we were able to measure and analyze follow-up results for an almost complete clinical sample. Second and more conceptually, the studies within this dissertation were built on a long fundamental research line evidencing the approach-facilitating properties of testosterone from rodents to patient studies. This groundwork, reviewed in chapter 2, provided a strong starting point for the first proof-of-concept clinical application of testosterone, within an actual treatment setting for individuals with SAD. Relatedly the aim to translate
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