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Resilience and Vulnerability to Trauma 359Foa, Rothbaum, and colleagues at the University of Pennsylvania designed apsychotherapeutic treatment specifically for PTSD called prolonged exposure (PE)(Foa & Rothbaum, 1998). PE is a manualized, exposure-based cognitive-behavioraltechnique based on principles of learning theory (habituation and extinction). Thecore of the treatment is exposure therapy, including imaginal exposure to the traumaticmemory (i.e., having the participant repeatedly retell the story of the trauma)and in vivo exposure (exposing the participant to previously avoided situationsthat may trigger the conditioned fear). The treatment also involves skill-basedinterventions, including psychoeducation about common reactions to trauma andbreathing retraining. PE can thus be seen as a form of active coping and stressinoculation, in that it exposes the participant to traumatic memories and avoidedsituations within a manageable/masterable context. It requires the participant toface fear through repeated retelling of the traumatic story and engaging in feared(but not dangerous) activities. PE also assists the participant in addressing distortedcognitions (e.g., self-blame) and maladaptive behaviors (e.g., avoidance,passive coping) that perpetuate the symptoms of PTSD. In recent comparison studies,PE has been found to have longer-lasting symptom reduction than other modalities(e.g., Stress Inoculation Training, supportive counseling, and waiting listconditions; Foa et al., 1999a, 1999b).Recent research indicates that extinction actually represents new learning, ratherthan the attenuation of the old fear-conditioned association. Facing fears throughexposure ideally leads to extinction of the conditioned fear. Davis and Myers(Davis, 2002; Davis & Myers, 2002) have demonstrated in animal models thatthe neurotransmitters gamma-aminobutyric acid (GABA) and glutamate are criticalcomponents of this process. GABA may exert an inhibitory influence on theamygdala (central to fear leaning), and glutamate, acting at N-methyl-D-aspartatereceptors (NMDA) may facilitate this GABA-mediated inhibition (Davis &Myers, 2002). These neurobiological findings have potentially meaningful implicationsfor exposure therapy outcomes.Physical ExerciseAttending to physical well-being is part of good self-care; exercising as a meansof relieving stress and dealing with negative affect is part of an active coping style.Consistent physical exercise has consistently been shown to have positive effectson physical hardiness, mood, and self-esteem. Individuals who exercise regularlyreport lower depression scores than those who do not exercise (Brosse et al., 2002;Camacho et al., 1991). In addition, exercise is associated with a number of neurobiologicaleffects that contribute to resilience. It is related to increases in plasmamonoamines and tryptophan (precursor to serotonin) levels, and attenuates HPAactivity in response to stress. Exercise also increases release of endorphins, whichcontributes to mood elevation. From a genetic perspective, physical exercise isthought to induce the expression of several genes related to neuroplasticity and