SOME THEORIES ON ADDICTION

November 12, 2007 Kari Poikolainen

www.kolumbus.fi/kari.poikolainenFinnish Foundation for Alcohol Studies

www.alkoholitutkimussaatio.fi

WHAT IS NEEDED?

ConceptsTheoriesExplanationsCorrect 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 ADDICTIONA 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

HYPERBOLIC DISCOUNTING

SOMATIC MARKER HYPOTHESIS: INDUCTION

Bilateral lesion in VM section of prefrontal cortexbefore lesion- normal successful personsafter 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 markers1. no clear winners among markers2. 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 TASKVM 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 thingSubstance dependent individuals- some behave like normal individuals, some like

VM patients

IMPLICATIONSTwo 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

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?