pain and depression [5]. In a recent systematic review of different studies tackling this matter [108], it was reported that differential effects of stress, depression, and anxiety symptoms may modulate endogenous levels of the eCBs. For example, acute psychological stress increased AEA and other fatty acid ethanolamides in healthy volunteers [114], whereas, in a study involving PTSD patients [115] there was a hypoactive eCB system, notably with decreased AEA and 2-AG, among others, in the plasma of the participants after physical and psychosocial stress. In another study involving patients with treatment-resistant depression or bipolar disorder, before and after electroconvulsive treatment [116], it was noted that the treatment increased AEA in the CSF of patients. In a cohort of students who were carriers of the A allele of the FAAH enzyme, characterized by increased basal AEA, this elevation was shown to facilitate fear extinction and ameliorate extinction of recall [117]. Moreover, it was suggested that the polymorphism in the FAAH gene was associated with bipolar disorder and major depression [118] which is in line with the importance of FAAH activity in depression and suicidal behavior [111].
