SOME THEORIES ON ADDICTION November 12, 2007 Kari Poikolainen Finnish Foundation for Alcohol...
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Transcript of SOME THEORIES ON ADDICTION November 12, 2007 Kari Poikolainen Finnish Foundation for Alcohol...
SOME THEORIES ON ADDICTION
November 12, 2007
Kari Poikolainen
www.kolumbus.fi/kari.poikolainen
Finnish Foundation for Alcohol Studies
www.alkoholitutkimussaatio.fi
CONCEPTS
• Concepts• Definitions• Operationalizations
Every concept is already a theory – in a minor way at least
EXPLAINING ADDICTION
A good theory should explain• Causes of the onset• Causes of the course – “natural” history• How to intervene with the course - treatment• When not to intervene
UNDERLYING ASSUMPTIONS
Addiction is
• A category, distinct of non-addiction• An unitary entity, not several different ones True or false?
ADDICTION AS A CHRONIC BRAIN DISEASE
• Cause: Repeated drug use
+ genetic disposition + learned environmental associations with drug use
Kalivas PW & Volkow ND. Am J Psychiatry 2005;162:1403
ADDICTION AS A CHRONIC BRAIN DISEASE
Process: “Normal”: drug high <-> dopamine release in NARepeated use -> switch from dopamine to glutamate-based
behaviour -> cellular adaptations in glutamatergic projection from the prefrontal cortex to NA
-> prefrontal regulation of behaviour and decision-making reduced except
-> stimuli predicting drug availability - > activate!! activate!! activate!!
-> uncontrollable urge to obtain drugs
What causes repeated use? What kind of repeated use causes addiction?
BRAIN DISEASE – IMPLICATIONS
• Permanent defect in the brain - > maintenance treatment• Only drug-related stimuli salient -> disinterest for other activities
BRAIN DISEASE – CONFLICT WITH FACTS
• Chronic and relapsing... * a good deal of DSM-addiction cases recover, many without treatment – remission or permanent?• Permanent defect... * memory improves by abstinence• Salience...* maintenance pat's active in work and social life
HYPERBOLIC DISCOUNTING
• rational choice theory (Becker and Murphy) presumes exponential discounting of future utilities -> order of preferences does not change
• if true, addicts are rational• experiments show that discounting in humans
and lower animals is hyperbolic -> order can change
• leads to voluntary temporary preferences (TP)• short ones may seem to be involuntary but are
not
SOMATIC MARKER HYPOTHESIS: INDUCTION
Bilateral lesion in VM section of prefrontal cortex
before lesion
- normal successful persons
after lesion
- good or normal IQ, memory and problem solving abilities
- decide against their best interests
- bankruptcyBechara A. Sem Clin Neuropsychiatry 2001;6:205
Normal VM prefrontal cortex
1. couples exteroceptive complex stimuli with
2. emotional (somatic) states previously associated with those stimuli
3. these (2) mark behaviour options with values
4. high values help in selecting good responses
SOMATIC MARKER HYPOTHESIS: PATHOLOGY
If there are no somatic markers
1. no clear winners among markers
2. no rapid on-line decisions, therefore either
- slow reasoned decision-making, or
- inaction, or
- decision based on the immediate reward of an option -> addiction
GAMBLING TASK
VM patients
- do not learn to predict and avoid high risk options
- do not develop anticipatory SCR responses
- make bad choices despite realizing the consequences of the action
- say the right thing but do the wrong thing
Substance dependent individuals
- some behave like normal individuals, some like VM patients
IMPLICATIONS
Two types?1. Abusers: no VM disorder - > can stop or revert to
social use2. True addicts: VM disorder - > cannot stop substance use
Cf.: Alcoholism types1. Adult-onset, mild, low hereditability <- self-medication <-
anxiety 2. Adolescent-onset, severe, high hereditability <- antisocial
<- impulsivity <- difficult temperament
Catechol-O-methyltransferase (COMT) gene polymorfism
“Warriors” have Val158
- stress and pain resistant
- worse executive cognitive performance in most conditions
- impulsivity, antisocial behaviour -> Adolescent-onset alcoholism?
“Worriers” have Met158
- pain sensitive
- prone to anxiety -> Adult-onset alcoholism?
PREDICTORS OF ALCOHOLISM – FOLLOW-UP STUDIES
ANDREASSON Andréasson S et al. Predictors of alcoholism in young Swedish men. Am J Public Health 1993;83:845 ROHDE Rohde P & al. Natural course of alcohol use disorders from adolescence to young adulthood. J Am Acad Child Adolesc Psychiatry 2001;40, 83-90. VAILLANT Vaillant & Milofsky. The etiology of alcoholism. American Psychologist 1982:37:494
PREDICTORS OF ALCOHOLISM – FOLLOW-UP STUDIES
ANDREAS- SON 1993
ROHDE 2001
VAILLANT 1982
F-up, years 15 6.8 34 N of cases at entry
50,465 1,507 456
Lost to follow up
? 619 56
N of alcoholics
993 243 110
Dependent variable
hospital th for alcoholism
dg alcohol depend or abuse
no of alcohol problems
PREDICTORS OF ALCOHOLISMPredictor ANDREAS-
SON 1993 ROHDE
2001 VAILLANT
1982
Family history
↑ ↑ ↑
Conduct problems
↑↑↑ ↑ ↑
Frequent anxiety
↑ ? 0
Smoking ? ↑ ? Cultural background
? ? ↑
Parent SES ↓ ? 0