Both psychological and biological factors seem to play a role for the development of SUD after experiences of CAN, but many aspects of this relationship remain poorly understood. Among the most important mediators are comorbid mental disorders, namely posttraumatic stress disorder (PTSD). Their important role for the development of SUD was initially suggested by proponents of the ‘self-medication hypothesis’ (Khantzian, 1985), and has been confirmed in many studies with different methodological approaches over the past two decades (Coffey, Stasiewicz, Hughes, & Brimo, 2006; Gielen, Krumeich, Tekelenburg, Nederkoorn, & Havermans, 2016; Kaysen, Stappenbeck, Rhew, & Simpson, 2014; Stewart, Conrod, Samoluk, Pihl, & Dongier, 2000). More recently, psychological consequences of CAN that could be important for different diagnostic entities have received increasing attention. This refers, for instance, to emotion regulation (ER) difficulties as a consequence of trauma (Ehring & Quack, 2010), which are also a potential predictor for SUD (Aldao, Nolen-Hoeksema, & Schweizer, 2010). Only few studies exist, however, on the interaction between ER deficits and subsequent craving and relapse in patients with SUD (Fox, Hong, & Sinha, 2008), and the impact of childhood trauma in this context (Banducci, Hoffman, Lejuez, & Koenen, 2014; Mandavia, Robinson, Bradley, Ressler, & Powers, 2016). Another promising perspective concerns alterations of the neuroendocrine responses to stress in victims of CAN (Tyrka, Burgers, Philip, Price, & Carpenter, 2013) that could also play an important role in the development of SUD (Enoch, 2011). Again, little empirical evidence exists regarding potential interactions between CAN and the neuroendocrine response to stress in patients with SUD (Moran-Santa Maria et al., 2010; Schäfer et al., 2010).