1. Comorbidity & Relapse Prevention
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2. Comorbidity Prevalence of AUD: 12M 8.5%, LT 30%
Age of onset of AUD = 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 = 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)

3. 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

4. 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

5. 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)

6. 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?

7. 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

8. 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

9. 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)

10. 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 days)