Evidence from different disciplines suggests that acute and chronic stress--related mechanisms play an important role in both the development and the chronic, relapsing nature of addiction (Baumeister 2003; Baumeister et al. 1994; Brady and Sinha 2005). Stress is defined as the physiological and psychological process resulting from a challenge to homeostasis by any real or perceived demand on the body (Lazarus and Fokman 1984; McEwen 2000; Selye 1976). Stress often induces multisystem adaptations that occur in the brain and body and affect behavioral and social function. The resulting dynamic condition is a dysregulated physiological state maintained beyond the homeostatic range. This definition and conceptualization of stress was further developed to explain the chronic abuse of substances and comfort foods and has been studied in the context of behavioral addiction (i.e., pathological gambling) (Dallman et al. 2005; Koob and Le Moal 1997; Koob 2003). Persistent challenges to an organism through chronic substance use may ultimately lead to an altered set point across multiple systems. This hypothesis is consistent with evidence that suggests adaptations in brain reward and stress circuits, and local physiology (e.g., energy balance) can contribute to addictive processes. Cravings or urges, decreases in self-control, and a compulsive engagement in unhealthy behaviors each characterize patients with addiction (Dallman et al. 2005; Kalivas and Volkow 2005; Koob et al. 2004; Sinha 2001). Alternatively, a person's ability to successfully cope with high stress is reflected in adaptive physiological and psychological responses (Charney 2004; MacQueen et al. 2003).
Resilience, defined as the absence of psychopathology despite exposure to high stress, can be studied by examining interindividual differences in stress responsivity across an organism's various types (i.e., at multiple phenotypic levels). Responsivity ranges from psychological differences in the way individuals cope with stress to differences in neuro-chemical or neural circuitry function (Cicchetti and Blender 2006). Variability within the genetic makeup and quality of early-life experience, as well as interactions between the two, are known to contribute to differences in stress resilience (Enoch 2010; Heim and Nemeroff 2001). Genetic influences can stem from gene--environment interactions, changes in gene expression influenced by the environment (i.e., epigenetic changes), or variation within the actual genetic code. Some examples of genetic influences on resilience include variability in the genes involved in the body's stress response (i.e., those controlling the hypothalamic-pituitary-adrenal [HPA] axis). These include those coding for the corticotropin-releasing factor (CRF) type 1 receptor or the glucocorticoid receptor (GR) (which cortisol can activate) as well as the serotonin transporter cathecol-O-methyltransferase (COMT), neuropeptide Y (NPY), and brain-derived neurotrophic factor (BDNF) genes (Feder et al. 2009) Genetic variation in the gene encoding the CRH1 receptor was found to moderate the impact of stress, for example, among adolescents engaging in heavy drinking (Blomeyer et al. 2008; Schmid et al. 2010). This gene-by-environment interaction predicted the initiation of drinking in adolescence as well as progression to heavy drinking by young adulthood (Schmid et al. 2010). The following sections highlight resilient responses to stress in studies in which stress was identified as an important factor contributing to the neurobiology of alcohol dependence.
Psychosocial Factors Associated With Resilience
Early studies of children exposed to adversity (Masten 2001; Masten and Coatsworth 1998; Rutter 1985) as well as more recent studies in resilient adults (Ahmad et al. 2010; Alim et al. 2008; Bonanno 2004) have identified a range of psychosocial factors associated with successful adaptation to stressful or traumatic events. …