Life Stress, Coping and Comorbid Youth: An Examination of the Stress-Vulnerability Model for Substance Relapse
ABSTRACT The stress-vulnerability model of addiction relapse states that the impact of life stress on alcohol and other drug use is influenced by several types of psychosocial risk and protective factors. Coping skills have been shown to be protective against alcohol or other drug use in adolescents and adults. To date, the influence of life stress and coping on addiction relapse has not been investigated among substance use disordered youth with comorbid Axis I psychopathology. In the present study, 80 adolescents, ages 13 to 17, were followed six months after treatment for substance use and Axis I disorders. Participants completed measures of psychopathology, substance use, life stressors and coping during treatment and at three and six months following treatment. Coping ability best predicted youth substance use at six months. Negative life events moderated the relation between coping and frequency of substance use. These results suggest that coping is a protective factor for return to substance involvement post-treatment, particularly for comorbid youth who have experienced high levels of life stress.
- SourceAvailable from: Sarah Dow-Fleisner
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- "Multiple research studies have identified a number of objective and subjective individual factors that predict treatment response and are related to substance use outcomes and relapse (Anderson, Ramo, & Brown, 2006; Ramo and Brown, 2008; Chung & Maisto, 2006; Kelly, Dow, Yeterian, Kahler, 2010; Sussman et al., 2008; Wei, Heckman, Gay, & Weeks, 2011). Some objective predictors have included prior treatment experiences, criminal justice system involvement, and psychiatric comorbidity; subjective factors have included perceived substance involvement and impairment, motivation for abstinence, self-efficacy, and coping skills (Anderson et al., 2006; Dennis, Scott, Funk, & Foss, 2005, Godley, et al., 2007; Kelly et al, 2010; Sussman et al., 2008). Importantly, just as adolescents entering treatment have varying levels of motivation for abstinence, coping skills, and abstinence self-efficacy, as well as unique substance use histories, they may also report different reasons for their substance use. "
ABSTRACT: National efforts have focused on improving adolescent substance use disorder (SUD) treatment outcomes, yet improvements remain modest. Because adolescents are noteworthy for heterogeneity in their clinical profiles, treatment might be enhanced by the identification of clinical subgroups for which interventions could be more effectively tailored. Some of these subgroups, such as those based on abstinence motivation, substance involvement, and psychiatric status are promising candidates. This study examined the unique predictive utility of adolescents' primary reason for alcohol and other drug use. Adolescent outpatients (N = 109; 27% female, aged 14-19) were assessed at treatment intake on their reason for substance use, as well as demographic, substance use, and clinical variables, and reassessed at 3, 6, and 12 months. Reason for use fell into two broad domains: using to enhance a positive state (positive reinforcement [PR]; 47% of youth) and using to cope with a negative state (negative reinforcement [NR]; 53% of youth). Compared with PR patients, NR patients were significantly more substance involved, reported more psychological distress, and had a more extensive treatment history. It is important to note that NR patients showed a significant treatment response, whereas PR patients showed no improvement. PR-NR status also uniquely predicted treatment response and outcome independent of a variety of other predictors, including abstinence motivation, self-efficacy, coping, and prior treatment. Adolescents' primary reason for substance use may provide unique clinical information that could inform treatment planning and patient-treatment matching. (PsycINFO Database Record (c) 2012 APA, all rights reserved).Psychology of Addictive Behaviors 12/2012; 27(4). DOI:10.1037/a0031065 · 2.09 Impact Factor
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- "This environmental modulation of sensitization is especially interesting because it is well known that environmental cues trigger craving and drug-seeking behavior in humans (Childress et al., 1986; Niaura et al., 1988; Carter and Tiffany, 1999). Several animal studies and some human laboratory studies have suggested that exposure to stress increases drug use and is associated with craving and relapse in addicts (Sinha, 2001; Sinha et al., 2006; Anderson et al., 2006; Grusser et al., 2007). Stress/negative affect and drug cues produce increases in anxiety associated with craving, producing a dissociable psychobiological state involving subjective emotional, cardiovascular, and cortisol responses (Sinha et al., 2006; Fox et al., 2007). "
ABSTRACT: Several substances that inhibit the induction or expression of behavioral sensitization have been proposed, but patients who present for treatment often have already an established sensitized drug response. Serotonergic agents, including serotonin-2 (5-HT(2)) antagonists, reverse cocaine sensitization, but there is no evidence for the same effect with ethanol, although serotonin involvement in ethanol sensitization has been well reported. To evaluate a 5-HT(2C) antagonist effect on reversing established ethanol sensitization, three experiments were performed assessing locomotor activity of mice under different treatments. First, mice received daily intraperitoneal saline (S), mianserin 10 (M1) or 20 mg/kg (M2), ethanol 2 g/kg (E), or ethanol+mianserin for 21 days. Then, each treatment was withdrawn for 3 days, and mice were randomly challenged with S, E, M1, or M2. During the next 7 days, S and E groups were subjected to daily treatment with S, E, M1, or M2. On the eighth day, all rats were tested under ethanol challenge. The saline group expressed sensitization under ethanol challenge similarly to the ethanol group. Mianserin+ethanol blocked the development of sensitization, suggesting an involvement of the 5-HT(2C) receptor subtype on ethanol-induced sensitization. Ethanol challenge to the chronic mianserin group did not express sensitization, implicating a role for mianserin in protection against stress. Mianserin did not reverse established ethanol sensitization, suggesting that cocaine- and ethanol-induced sensitization involved different mechanisms.Pharmacology Biochemistry and Behavior 03/2008; 88(4):456-64. DOI:10.1016/j.pbb.2007.10.002 · 2.78 Impact Factor
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- "Any change in these factors may influence the development and expression of sensitization , either by improving or impairing behavior. Furthermore , several animal studies and some human laboratory studies have suggested that exposure to stress increases drug use and is associated with craving and relapse in addicts (Sinha 2001; Anderson et al. 2006; Sinha et al. 2006; Grusser et al. 2007). "
ABSTRACT: Drug-induced sensitization has been associated with enhanced self-administration and may contribute to addiction. The possible association between sensitization and voluntary ethanol consumption using an addiction model was investigated. Mice (n = 60) were individually housed with ad libitum access to food and had free choice between ethanol (5% and 10%) and water in a four-phase paradigm: free choice (12 weeks), withdrawal (2 weeks), re-exposure (2 weeks), and quinine-adulteration (2 weeks). Control mice (n = 10) had access to water. Mice were characterized as addicted (n = 10, ethanol preference without reducing intake with adulterated ethanol), heavy (n = 22, ethanol preference but reduced intake with adulterated ethanol), and light (n = 21, water preference). Oral ethanol then was withdrawn, and 24 h later mice received a 2 g/kg ethanol (i.p.) challenge dose or saline, and ambulation was evaluated 10 min later. Half of the classified mice received daily 2 g/kg ethanol injections for 14 days, and ambulation was assessed 10 min after the last dose. Acute ethanol increased ambulation in all groups compared to the control group, and chronic ethanol induced sensitization, showing no difference among ethanol-treated mice. The data suggest that independent neural mechanisms are responsible for the development of addiction and sensitization.Journal of Neural Transmission 02/2008; 115(1):43-54. DOI:10.1007/s00702-007-0843-0 · 2.40 Impact Factor