Torrens/Rossi - Mood Disorders and Addiction Flashcards
Comorbidity rate of MD and SUD?
12-80%
What three main explanations are there for the wide range in comorbidity of MD and SUD?
- Sample recruitment characteristics (e.g., general population, differing (non-)treatment enviroments, type of substance used)
- Trends in drug-using population (availability, price, drug treatment policies, presence of other concurrent conditions)
- Methodological differences (diagnostic criteria, instruments, period of time)
Current global prevalence of AUD + lifetime prevalence?
2-4%, 13% (respectively)
lifetime includes dependence and abuse
Comorbidity of alcohol dependence and MD?
“shows a comorbidity as high as”
21%
Two important etiological problems that data suggest with having either MD or AUD?
- Doubles the risk of developing the other disorder
- Increases severity
What other (non-etiological) problems are the comorbidity of MD and AUD associated with?
- Higher risk of suicide (in depressed patients)
- Alcohol addiction as one of the strongest predictors of repeated suicide attempts
Comorbidity rates of MD & heroin/cocaine/cannabis
Respectively, 18-46%, 16-34% & 13.5-38%
Relationship between nicotine dependence and psychiatric comorbidity?
- Depressive disorder = twice the probability to also be nicotine dependent
- People with nicotine dependence have 2-3x the risk of developing a mood disorder (ahoh)
Gender within the relationship between SUD and MD?
- Women with SUD present comorbid with MD more frequently
- Women with SUD are found to have 2x the prevalence of MD compared to the average (European) population
What are four main hypothesis for the high comorbidity of SUD and MD?
- Share common risk factors
- Continued substance use induces neurobiological changes that mediate MD
- SUD as a consequence of MD (self-medication hypothesis)
- Common symptoms (can be mistakenly diagnoses as co-occuring)
What are problems in the diagnosis of MD in substance abusers? (2)
- Substance use effects can mimic MD symptoms (thus: the relationship is difficult to establish)
- MD lacks well-known pathophysiology and associated biological markers (reliance on things like the DSM)
Difference between MD independent from substance, substance-induced MD and expected effects?
Respectively:
- Symptoms in excess of what would be expected/MD onset before use/persistence after abstinence
- Episode occurs entirely during episode of use/within the first 4 weeks after abstinence AND use is relevant to diagnosis/symptoms are greater than expected effects
- Self-explanatory
Is the prevalence of induced or independent MD higher?
Independent
What is a pattern seen in patients diagnoses with induced MD, at follow-up? What could this indicate? (3)
Later re-diagnosed with independent MD
- Higher prob. of being diagnosed with induced when SUD is present
- Diagnosis of induced captures subjects with preexisting higher risk for MD
- SUD precipitated MD (which was then masked by substance use)
Main results from research of comorbid MD and SUD concerning pharmacological treatment? (3)
- Antidepressant drugs improve comorbid depression with alcohol dependence, but not the depression concurrent with cocaine/opiates
- SSRIs are not effective for depression treatment with AUD
- Antidepressants do not directly improve substance use (duh??)
General results for psychosocial interventions for comorbin MD and SUD? (3)
- CBT/MI has seemingly smaller effect sizes than antidepressant treatments
- Number of CBT/MI sessions correlate directly with alcogol abstinence, but not MD outcome
- BRIGHT (residential SUD treatment + group CBT) showed better clinical outcome, higher adherence and improvement in severity of depressive symptoms (compared to what is not mentioned)
Research on BRIGHT is limited
What type of treatment does this chapter advocate for?
Integrated treatment (as evidence supports dual treatment is basically necessary for good outcomes)
