Vicios en la fase ejecutiva

No empirical research that we know of has examined how treatment change is related to the process of offender re-entry; therefore, this study is exploratory. To investigate the possibility that the re-entry process mediates the relationship between treatment change and recidivism, below I consider what is targeted for change in treatment and make conceptual connections to the factors that influence the re-entry process (i.e., stable and acute dynamic risk factors and protective factors).

The primary goal of offender rehabilitation is to reduce offenders’ levels of criminality by altering their antisocial attitudes and beliefs, reducing their ties with criminal peers, and shifting the balance of rewards and costs for criminal and non- criminal activities so that non-criminal activities become the preferred option

(Andrews & Bonta, 2010). However, for these changes to be meaningful, they need to be sustained beyond the end of the programme (Serin, Lloyd, Helmus, Derkzen, &

Luong, 2013). If changes are not maintained after release, then within-treatment change is unlikely to be related to a reduction in recidivism. We know from prior research that patterns of change during treatment do not necessarily parallel patterns post-treatment. In our study of 35 life-sentenced prisoners, some men were unable to maintain change in the months following the programme (Yesberg & Polaschek, 2014). Thus, examining the relationship between within-treatment change and change on stable dynamic risk factors after release (e.g., antisocial attitudes, peer associations) might help to explain the relationship between treatment change and recidivism. Consistent with the ITDSO, we would expect that the desisting offender would still be actively engaged in the change process during re-entry (Göbbels et al., 2012).

Another goal of offender rehabilitation is to prepare offenders for release by teaching them practical skills to manage acute risk factors during the re-entry period (e.g., loss of a job, relationship problems). Offenders are taught to recognise their own high-risk situations and develop strategies to effectively manage them (Andrews & Bonta, 2010; King, Creamer, Tiller, & Williams, 2007). Although measures of treatment change capture this learning, the relationship between treatment change on stable dynamic risk factors and the actual management of acute risk during re-entry is unclear. As Serin and Lloyd (2009) note “success can only be claimed if offenders are able to take their new skills and apply them to high-risk situations in the community” (p. 359).

Zamble and Quinsey’s (1997) Coping Relapse Model provides a framework for understanding how treatment change might be indirectly related to recidivism through acute risk in the community. Their model suggests that recidivism is preceded by a complex series of cognitive, emotional, and environmental events. In particular, the model postulates that recidivism is triggered by one or more acute dynamic risk factors: variables that can change rapidly and increase risk of recidivism. Acute dynamic risk factors may initially be environmentally based (e.g., marital discord, job loss), but such environmental catalysts often lead to a second series of internal acute dynamic

responses, whereby the individual engages in cognitive appraisals and experiences a range of emotionally based outcomes (e.g., stress, negative mood). Subsequently, the individual will attempt to implement stable dynamic response mechanisms (e.g., coping responses). Hence, the model suggests there is an interaction between stable and acute dynamic risk factors: offenders with better coping responses (and lower stable dynamic risk in general) will be more equipped to deal with environmentally and emotionally based acute stressors and less likely to recidivate. Therefore, we might expect that offenders who make more change in treatment will be better able to manage acute dynamic risk factors pertinent to the coping relapse model.

Lastly, effective treatment is not just about reducing deficits; it also involves building up strengths, such as family support and identification with prosocial models (Andrews & Bonta, 2010). Serin et al. (2013) suggest that programmes are unlikely to bring about long-term change “unless they link the offender to helpful community and relationship factors” (i.e., informal social controls, p. 50). Therefore, we might expect that change in treatment would be related to an offender’s level of protective factors during re-entry: factors that promote desistance from crime (i.e., facilitators to re- entry; Göbbels et al., 2012). As Serin and Lloyd (2009) note, “an offender’s cessation of crime is not directly tied to the extinction of risk factors that led to his initial

involvement in crime” (p. 355). Taking into account facilitators to successful re-entry may help to explain the relationship between treatment change and recidivism.

6.4 Study Objectives

The objective of this study is to test an explanation for why treatment change was not directly related to reductions in recidivism in Study 2. I propose that the re- entry process might mediate the relationship between treatment change and recidivism (i.e., treatment change may have an indirect relationship with recidivism through its relationship to the DRAOR). Because there is a lack of consensus regarding the best methodology to assess the different types of dynamic re-entry factors included in the

DRAOR (e.g., is variability in acute risk more predictive than one score in isolation?), three different types of DRAOR data will be used as possible mediating variables or intermediate outcomes: (1) one score in isolation (i.e., “initial” scores from Study 3), (2) variability in scores during the re-entry period, and (3) net change during re-entry (the first score minus the last score within 100 days of release). I hypothesise that people who make more changes in VRS scores in treatment will: (1) have lower risk and higher protective factor scores immediately following release, (2) show less variability in their scores during re-entry, particularly in the acute risk factors, and (3) make more positive change during the re-entry process. I also hypothesise that at least some of these relationships will explain the relationship between treatment change and recidivism.

6.5 Method