Comorbidity & Relapse Prevention 12/10/13

Comorbidity Prevalence of AUD: 12M 8.5%, LT 30% Age of onset of AUD = 19 - 22 y/o AUD with mental health disorders (~50%) AUDs often co-occur with Drug use disorders (OR=9) Mood disorders (OR=2.2) especially bipolar disorder Anxiety disorders (OR=1.9) Antisocial personality disorder (OR=2.9) 12M prevalence of any AUD = 8.5%; LT prevalence of AUD = 30% age of onset AUDs = 19 - 22 y/o Odds Ratios from Hasin et al. (2007) Table 4: increasing odds of having a comorbid disorder given AUD in the last 12M -- these are averages across AD and AA; the OR for AD are highest (Hasin et al., 2007)

Clinical implications of comorbidity More severe and chronic course Associated with more impairment/dysfunction: unemployment, financial problems social isolation, unstable housing suicide risk, exacerbation of psychiatric symptoms legal problems Increases risk of relapse (both ways): Case illustration negative affect states, interpersonal conflict

Implications of comorbidity for treatment Predicts poorer treatment outcomes medication compliance ED use re-hospitalization Associated with poorly coordinated treatment SMI often excluded from substance abuse treatment People with SUDs may not find expertise in MH treatment Integrative care recommended Co-location Cross-trained clinicians Sharing records, reduce barriers Poor coordination of tx: often different payer systems, treatment compartmentalized (I treat the depression, you treat the drinking); sequential (requiring abstinence) often discourages engagement Integrative tx associated with better engagement and retention, better outcomes Barriers to integrated care? Mental health professionals vs peer counselors Treatment system silos Systems of reimbursement

alcohol Relapse curves – aka survival curves = % of people who remain completely abstinent at points past end of treatment. Hunt, Barnett, & Branch (1971): more than half relapsed within 3M, and most by 6M So, of those who receive treatment, the majority of individuals will have at least one drink in the first 12- months following treatment (Maisto, Pollock, Cornelius, Lynch, & Martin, 2003) Survival curves don’t tell the whole story: Trajectories of relapse are heterogeneous with regard to time-to-lapse Post-lapse drinking Small subset (6%) return to frequent heavy drinking Larger subset (12%) taper off to less frequent heavy drinking Majority return to abstinence or infrequent drinking after lapse (Witkiewitz & Masyn, 2008)

Determinants of Relapse (Marlatt & Gordon, 1980) Interpersonal Conflict Social pressure Intrapersonal Negative emotional states (hungry, angry, lonely, tired) Testing personal control/willpower Cravings Positive emotional states (celebrations, familiar cues) Marlatt & Gordon (1980) asked: In what sort of situation did you take the first drink that led to your losing control over drinking? What would you say was the main reason for taking that drink? Can you describe any particular circumstances or set of events which triggered your need or desire to take that first drink? Do you remember any inner thoughts or emotional feelings that triggered your need or desire to take the Erst drink at that time? What did you think after taking your first drink? What sort of feeling did you have after that first drink?

Relapse Prevention Model Guilt + self-blame + loss of control Abstinence violation effect is what happens when a person attempting to abstain from alcohol use ingests alcohol and then endures conflict and guilt by making an internal attribution to explain why he or she drank, thereby making him or her more likely to continue drinking in order to cope with the self-blame and guilt Relapse is not an EVENT, it is a PROCESS LAPSE

Risks for Relapse (Witkiewitz & Masyn, 2008) Distal risks Family history of AUDs Severity of dependence Executive function Proximal risks Immediate triggers of craving, alcohol seeking “straw that broke the camel’s back” Availability of coping behaviors Distal risks = stable predispositions = same factors constituting underlying susceptibility to alcohol abuse/dependence Increase probability of relapse Dependence predicts time-to-first-drink; earlier lapses Proximal risks = immediate precipitants Triggers escalate risk Coping de-escalates risk

Dynamic Model of Relapse Tonic processes = distal risks, characteristic of the person, an individual’s chronic vulnerability for relapse Includes family history (genetic loading for dependence) Includes comorbid psychiatric disorders / general psychological health May lead a person INTO high risk situations at greater rates Phasic responses = situational responses that increase/decrease likelihood of relapse Includes self-regulatory failure (HALT) Includes lack of adequate coping response Witkiewitz & Marlatt (2004)

Implications for treatment Recovery involves cycles through change, relapse, treatment, stability, relapse, etc. Anticipate and plan! Recovery Management Checkup (Scott et al., 2005) Post-treatment monitoring and case management Quarterly “check-ups” = early detection of transitions personalized assessment + feedback Facilitate early linkage and re-entry into treatment Address barriers, motivation Practical facilitation (appointments, transportation) Within each quarter, compared to controls, RMC participants were significantly more likely to return to SA tx (64% vs. 51%) to return sooner (27 vs. 45 days) To have more days in tx (7.75 vs. 4.68 days)