Transcript GEORGE AINSLIE: BREAKDOWN OF WILL

SOME THEORIES ON
ADDICTION
November 12, 2007
Kari Poikolainen
www.kolumbus.fi/kari.poikolainen
Finnish Foundation for Alcohol Studies
www.alkoholitutkimussaatio.fi
WHAT IS NEEDED?
Concepts
Theories
Explanations
Correct assumptions
CONCEPTS
• Concepts
• Definitions
• Operationalizations
Every concept is already a theory
– in a minor way at least
THEORIES
should
• Agree with the known facts
• Give insight
• Predict
• Can be tested, falsified
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 NA
Repeated 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
HYPERBOLIC DISCOUNTING
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
- bankruptcy
Bechara 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 use
2. True addicts: VM disorder - > cannot stop substance use
Cf.: Alcoholism types
1. 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 -> Adolescentonset 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
ANDREASSON 1993
F-up, years
ROHDE
2001
VAILLANT
1982
15
50,465
6.8
1,507
34
456
?
619
56
993
243
110
N of cases at
entry
Lost to
follow up
N of
alcoholics
Dependent hospital
variable
th for
alcoholism
dg alcohol no of alcohol
depend or problems
abuse
PREDICTORS OF ALCOHOLISM
Predictor
Family
history
Conduct
problems
Frequent
anxiety
Smoking
Cultural
background
Parent SES
ANDREASSON 1993
ROHDE
2001
VAILLANT
1982
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↑
↑
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↑
↑
↑
?
0
?
↑
?
?
?
↑
↓
?
0
PREDICTORS OF ADDICTION
• many weak predictors, no strong ones in
unadjusted or partly adjusted studies
• adjustments weaken risk estimates
• interactions E x E, E x G, G x G not yet
much studied
• some mental disorders predict
• is addiction a disease, symptom,
complication or something else?