40 Chapter 2 also possible that the training increases prefrontal control over amygdala-driven approach–avoidance responses. Single-dose testosterone administration in SAD might aid the training process by biasing the brain towards social approach, although this effect is likely specific for social threat faces. All these studies would be helped by increased clarity on the neuroendocrine mechanisms underlying deviations in social motivational behavior in SAD. Research featuring neuroimaging techniques should shed more light on this matter. Future studies could combine social approach and avoidance tasks with fMRI, endogenous hormone/neuropeptide measurements (e.g., Volman, Toni, et al., 2011), and/or testosterone/oxytocin administration to find out how these neuroendocrine agents modulate social approach/ avoidance behavior in SAD. In addition, it would be interesting to try to probe the functioning of the emotion-network (e.g., fear reduction by GABA-ergic mechanisms) and the reward network (dopaminergic mechanisms) in SAD, by using single photon emission computed tomography (SPECT) or positron emission tomography (PET) scanning (e.g., Schneier, Kent, Star, & Hirsch, 2009; van der Wee et al., 2008), in combination with testosterone administration. It would be particularly interesting to add genotyping for androgen and dopaminergic receptor genes. Furthermore, future research featuring EEG or magnetoencephalography (MEG) should further elucidate the temporal dynamics of these processes in both healthy individuals and those with SAD. The same line of reasoning holds for aggression-related disorders, such as psychopathy, for which identification of biological underpinnings of subtypes and adaptive treatment is still in its infancy (e.g., Brazil et al., 2016). More research is needed to obtain starting points for studying the effects of hormone manipulations on the management of social aggression. Pioneering evidence in autism spectrum disorders, where aggression plays an important role as well, suggests that oxytocin has the potential to enhance motivation and attention to social cues in patients with autism spectrum disorder (Yamasue, 2016). A recent review and meta analyses concluded that studies on autism did show significant effect sizes (combined effect size of d = 57, e.g., medium effect); however, oxytocin seemed less effective in other psychopathologies (Bakermans-Kranenburg & Van IJzendoorn, 2013; Guastella & Hickie, 2016). On the other hand, no significant meta-analytic effect of oxytocin on the social domain in autism was found by Ooi and colleagues (Ooi, Weng, Kossowsky, Gerger, & Sung, 2017). More sophisticated and targeted clinical trials are required, due to a limited number of studies and small sample sizes. Whether similar interventions may be effective for aggression-related disorders, such as psychopathy, remains to be determined. It is conceivable that the social salience enhancing effects of oxytocin could make matters worse in psychopathy.
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