Background Module 1 Flashcards
How does the National Institute on Drug Abuse (NIDA) define addiction?
A chronic, relapising disorder, characterized by compulsive drug seeking, continued use despite harmful consequences, and long-lasting changes in the brain
What happens to the brain changes due to addiction, after a person has quit the drug?
Changes persist long after they quit
- Note that improvements have been observed in some systems/functions
What is the relapse rate (+ time-frame) of GHB?
70% within 3 months after detoxification
What is an important factor for the relapse rate on an individual level?
Co-morbidity; e.g., alcohol abuse + anxiety disorder = greater risk for relapse
What is a critique against the current relapse rates?
Many people recover from addiction without formal treatment, thus, high relapse rates may be in part attributable to only included clinical samples.
What is spontaneous remission?
Sudden/unexpected recovery (without formal treatment)
Which model, regarding addiction, is currently most prevalent?
The brain disease model
What was the prevalent addiction model in the 19th century (1800s) & what did it entail?
entail = includes treatment of addicts/reasoning/etc.
Moral Model:
- Addiction = moral weakness (didn’t they used to soak tampons in opium and belladonna?)
- People with an addiction were locked up in prison/re-education institutions (“under challenging circumstances” = abuse)
- For obvious reasons, not scientifically supported.
Occasionally reappears (smh)
Which addiction model arose during the mid 19th century (~1850s) and what did it entail?
Pharmacological model:
- Movement against sale/use of spirits > addiction attributed to the substance and not the addict
- Addictive characteristic of substance causes addiction (treatment = prohibition)
- Prohibition of America (1920-1933)
- Model is viewed as one-sided = the availability and use is insufficient for the development of addiction (current view, not fact)
- Still widely used for certain substances (e.g., heroin)
What addiction model arose in 1930-1950 and what did it entail?
Symptomatic model:
- Psychoanalytically inspired (Freud…)
- Addiction is not a condition, but a symptom of an underlying character-neurosis/personality disorder
- Treatment = long-term, insight-oriented psycho-therapeutic treatment of character-neurosis
- Treatment still used in some communities
This feels like a step back towards the moral model ngl
What addiction model arose during 1940-1960 and what did it entail?
The disease Model (Jellinek):
- Fundamental biological/psych differences between addicts and non-addicts
- Addicts are unable to use substances in moderation because of the above differences
- Uncontrolled use + physical dependence
- Treatment = full abstinence for (latent) addicts
- Representatives = AA & The Minnesota Model
What addiction model arose in 1960-1970 (short-lived, damn) and what did it entail?
Learning Theory Model:
- Behaviourist roots
- Addiction is a maladaptive learned behaviour (can be unlearned)
- Treatment = Behavioural therapeutic interventions
- Aversion therapy & cue exposure as interventions (little success)
What addiction model arose in 1970-1990 and what did it entail?
Bio-psycho-social development model:
- Interplay of biological, psychological and social factors
- Heroin Vietnam veteran addicts that underwent spontaneous recovery when coming back = basis for this model
- Innate vulnarability + personal development + circumstances = continues interaction in both onset and termination
- Multi-modal interventions (i.e., all factors are included in treatment)
- “Dependence syndrome” based on this model
What addiction model arose in 1990 (still prevalent) and what does it entail?
Brain Disease Model:
- Link between brain, genetic risk factors and (risk for) addiction
- Medical-biological aspects of the 1970 model
- Innate vulnarability (= basis) + brain changes because of repeated use
- Pharmacological and behavioural therapeutic interventions
“Criticisms” against the Brain Disease Model?
- Does it come at the expense of analysis of the level of environmental/social/societal factors in addiction
- Can the biological basis peacefully co-exist with behavioural research (This feels less like a critique and more like a philosophical question)
A new model that has come to the forefront in recent years + what it entails?
Complex Systems Model:
- Biological/psych/social factors play a role in a dynamic fashion
- Resistance to change depends upon the relationship between relevant factors
- Unique to the individual
Model gives vague description
Three defined types of substance categories?
- Sedatives (calm + relaxed)
- Stimulants (Invigorating- unless you have ADHD lol)
- Psychedelics (atler conscious/perception states)
What substances constitute sedatives?
Alcohol, barbiturates (???), benzodiazepines and opiates (opium, heroin, morphine)
What substances belong to stimulants?
Caffeine, nicotine, amphetamine and cocaine
Not me being on three of these rn, goddamn
What constitutes psychedelics?
Cannabis, extasy, LSD
What important feature do all of the defined substance categories have in common?
Directly or indirectly result in a release of dopamine in the nucleus accumbens, which plays an important role in their addictive effect
- I wonder if this is a factor that makes substance abuse more common in ADHD + why substance affects ADHD peeps differently (mostly)
Evolutionary view on the reward system & its development?
- Enables us to anticipate rewards
- Reinforces desirable/adaptive behaviour
What role does dopamine play in our reward system? How do drugs affect the reward system?
Dopamine:
- Anticipation of reward = release of dopamine
- Noticably in the nucleus accumbens, part of the mesolimbic pathway
Drugs:
- Much stronger dopamine activity than normal
- Thus, enormous rush; “hijacks the reward system”
Addiction & reward system?
Lower sensitivity to natural rewards
What is the reward deficiency syndrome (RDS) account? Explanatory account made for people suffering what?
RDS as explanation for:
- Chronic definiciency of dopamine D2 receptors in the ventral striatum (nucleus accumbens) are less sensitive to simple natural rewards
- May look for stronger stimuli to compensate above
- Has been linked to a genetic predisposition (I think? lowkey lost)
Note:
- People with high density of D2 receptors are less likely to take drugs
- D2 density may be a consequence of substance abuse
Which type of learning mechanism plays an important role in addiction? How so (basic)?
Pavlovian conditioning > stimuli that predict a reward can evoke conditioned responses/craving
What is a prominent theory about the role of craving in addiction and what does it entail?
Incentive-sensitization theory:
- Drug-associated stimuli acquire incentive salience, thus the drug itself becomes attractive
- Leads to wanting (craving) > elicits targeted acquiring behaviour
- Wanting does not equate liking (necessarily)
- In addiction, wanting increases, while hedonic experience (liking) decreases
- Theory may explain relapse (drug-associated cues stay after withdrawal symptoms have dissipated)
- Dopamine in the mesolimbic system plays a crucial role in wanting
What traditional theory accounts for withdrawal/relapse in addiction, what does it entail and how is this theory regarded now?
Opponent-process theory:
- Initial drug use for pleasure (positive reinforcement), but tolerance occurs and drugs are taken to avoid withdrawal symptoms (negative reinforcement)
- I.e., explains relapse as an avoidance of withdrawal symptoms
- As relapse often occurs long after withdrawal symptoms (mostly) dissapate, this theory cannot fully account for the reasoning
Which seven addiction models, not including the complex systems model, can be seen throughout time? Include intervention(s)
Give this in chronological order
this question poses as an extra exercise
- Moral Model, imprisonment/re-education institutions
- Pharmological model, prohibition of substance sale/use
- Symtomatic model, insight-oriented psycho-therapeutic treatment of character-neurosis
- Disease model, (latent) addicts should be completely abstinent
- Learning theory model, aversion therapy and cue exposure
- Bio-psycho-social development model, multi-modal interventions
- Brain disease model, pharmacological and behavioural interventions
