addiction Flashcards
What is a physical dependence?
A state of the body due to habitual substance abuse resulting in withdrawal symptoms when drug use is reduced or stopped
What is Tolerance?
A reduction of response to a substance so an individual needs more to achieve the same effect
Behavioural tolerance is when a person learns through experience how to adjust their behaviour to compensate for the effects of a substance
What are withdrawal symptoms?
symptoms that develop when a person stops or reduces substance abuse.
They indicate the presence of physical dependence and may cause a secondary form of psychological dependence.
there are typically two phases:
- Acute withdrawal: within hours of abstaining.
- intense cravings,
- symptoms diminish usually over days
- Prolonged withdrawal: continue for weeks sometimes months or years
- A person is highly sensitive to cues associated with the addiction making relapse common
What is addiction?
A disorder in which an individual takes a substance or engages in a behaviour that is pleasurable but eventually becomes compulsive with harmful consequences.
Marked by physiological and or psychological dependence, tolerance and withdrawal
what are risk factors?
internal or external influences that increase the likelihood of a person starting an addictive substance/behaviour
What are the risk factors of addiction?
Genetic vulnerability
Stress
Personality
Peers
Family influences
Risk factors: Genetic vulnerability
- Two plausible mechanisms creating genetic vulnerability:
- D2 receptor: people with addictions are often found to have a reduced number of D2 receptors so addiction is making up for reduced dopamine
-Nicotine enzyme: Pianezza et al-some people lack a fully functioning enzyme that breaks down nicotine. These people smoke less. The enzyme is genetically determined
Risk factors: evaluate genetic vulnerability
+ Support of adoption studies
> Kendler et al: used data from the national Swedish adoption study
> looked at adults adopted away from families with at least one parent with addiction. They had a greater risk of addiction compared to adopted adults with no family history of addiction
+ support from twin studies
Risk factors: Stress
Anderson and Teicher: highlighted the role of adverse childhood experiences in later addiction.
Argued that early experiences of severe stress have damaging effects on a young brain in a sensitive period of development creating a vulnerability to later stress that will cause someone to self medicate
Risk factors: Evaluate stress
- Studies show strong positive correlation but cant prove causation.
> People can develop addiction despite no great life stress and their addictions then cause great levels of stress producing a positive correlation despite stress not being the cause
Risk factors: Personality
- Most people with APD are also substance abusers
- Robins argued APD is a ‘casual risk factor’ for addiction as they are more likely to break social norms
Risk factors: Evaluate Personality
+ support for the link between APD and addiction
> Bahlmann et al interviewed 55 Alcoholic-dependent people, 18 had APD.
> the researchers found APD had developed on average 4 yrs before the alcohol dependency
Risk factors: Family influences
- Livingston et al: children allowed to drink at home were significantly more likely to drink excessively at collage
- Adolescence who believe their parents have little to no interest in monitoring their behaviour are more likely to become addicted
Risk factors: Evaluate personality
+ research support
> Madras et al found a strong positive correlation between parents who use cannabis and their adolescent children’s use of cannabis.
> it may be parents modelling behaviour and this could be generalised to other drugs
Risk factors: Peers
O’Connell et al: there are 3 main elements to peer influence as a risk:
- attitudes and norms around drinking are influenced by associating with peers who drink
- experienced peers provide opportunities to use alcohol
- the individual overestimating how much their peers drink so they drink more to keep up
Risk factors: Evaluate peers
+ real world application
> Using mass media to give an accurate representation of how much people drink can reduce the amount collage kids drink
Biological explanation of nicotine addiction
- nAChR’s are a type of neurotransmitter activated by nicotine
- When activated, the neuron releases dopamine and temporarily shuts down (become desensitised) leading to down regulation and reduction in the number of active neurons
- Dopamine is transmitted along the mesolimbic pathway to the NA triggering the release of more dopamine from the NA to the frontal cortex
- Dopamine is also transmitted along the mesocortical pathway to be released directly into the frontal cortex
- nicotine powerfully activates the dopamine reward system and activates pleasurable effects like mild euphoria, increased alertness, reduced anxiety
- pleasurable effects are associated to smoking through OC
Biological explanation of withdrawal from nicotine
- when a person smokes, their nAChR’s are continuously desensitised
- when a person doesn’t smoke for a prolonged period of time (e.g. sleeping) nicotine disappears from the body so nAChR’s become more functional, dopamine neurons resensitise and become more available (upregulation)
- during upregulation, nAChR’s become overwhelmed with ACh’s because there is no longer any nicotine to bind them
Biological explanation for dependence and tolerance to nicotine
- smoker avoids psychological and physiological unpleasant withdrawal states by having another cigarette
- there is a constant cycle of daytime downregulation and night-time upregulation leading to long term desensitisation of nAChR’s
- continuous exposure of nAChR’s to nicotine permanently changes the brains neurochemistry to decrease the number of active receptors
- tolerance= when the smoker needs more cigarettes for the same effect
Evaluate biological explanations for nicotine addiction
+ research support
> McEvoy et al studied smoking behaviour in people with schizophrenia taking the antipsychotic Haloperidol (a dopamine antagonist
> people taking the drug showed a significant increase in smoking presumably as a form of self medication
CA: Research is increasingly showing a complex interaction of several neurotransmitter pathways e.g. seritonin
> therefore neurochemistry of nicotine addiction cannot be fully understood only looking at dopamine
+ real world application
> real world treatments e.g. NRT (nicotine replacement therapy) allowing reduced withdrawal symptoms
- doesn’t fully explain withdrawal symptoms
> the theory is mainly dependent on the amount of nicotine in the body but Gilbert points out that these factors are not strongly correlated and withdrawal is instead dependent on personality and environment (e.g. people with high neuroticism generally have worse withdrawal symptoms than emotionally stable people)
Learning theory explanation of nicotine addiction
Operant conditioning
- Positive reinforcement: nicotine leads to pleasurable effects from dopamine
- Koob and Le Maol: positive effects of smoking can explain early stages of a smoking addiction
- Negative reinforcement: lessening of nicotine leads to withdrawal symptoms so a person smokes to eliminate negative symptoms
cue reactivity:
- smoking is a primary reinforcer (intrinsically rewarding due to its effects on the dopamine reward system)
- other stimuli like certain environments, people who become associated with the act of smoking are secondary reinforcers and are associated with the pleasurable effects of nicotine
- secondary reinforcer produces a similar effect to nicotine
Evaluate the learning theory of nicotine addiction
+ research support
> Levin et al rats could chose from two water spouts, one with nicotine in, one without, and the rats would more often chose the nicotine lased water
+ research meta analysis
> Carter and Tiffany: 42 studies into cue reactivity typically presented showed smokers shown pictures associated with smoking would have the urge to smoke
+ real world application:
> aversion therapy using counter conditioning to associate pleasurable effects of nicotine with unpleasant stimuli
> Smith had participants give themselves electric shocks when engaging in smoking related activities. after 1yr, 52% were still abstaining reducing strain on NHS (and their 20-25% success rate)
CA: study did not use a control group so is not a valid measure
> comparatively short lived solution (Hajek and Stead)
Cognitive explanations for gambling addiction: expectations
- a person may have expectations about the future benefits out waying the cost or unrealistic expectations on how gambling may help them cope with emotions e.g. boost their mood
Cognitive explanations for gambling addiction: cognitive bias
- continuing to gamble because of a cognitive bias like mistaken belief about luck
- bias influences what gamblers do and don’t pay attention to e/g/overestimating chance of winning
Rickwood classified it into 4 categories: - Skill and judgement: addicted gamblers have an illusion of control that means they overestimate their ability to influence random events
- Personal traits/ rituals: believing their is a greater probability of winning because they are especially lucky or engaged in superstitious behaviour
- Selective recall: gamblers remember the details of their wins but forget/ minimise losses
- Faulty perceptions: gamblers have distorted views about the operation of chance (Gamblers fallacy: a loosing streak must always be followed by a win)
Cognitive explanations for gambling addiction: self efficacy
- refers to expectations on our ability to achieve a desired outcome and is a key element in relapse
- a person has a biased belief that they cannot permanently abstain. They expect to gamble again, so do, reinforcing the view they cannot permanently abstain
Cognitive explanations for gambling addiction: research into cognitive bias
- Griffiths: used the ‘thinking aloud’ method
- had participants verbalise any thought they had and did a content analysis classifying them into rational and irrational
- did a semi structured interview to ask participants the degree of skill required to win on slot machines
Findings - there was no difference between regular and occasional gamblers in objective measure (e.g. winning money) but regular gamblers made almost 6 times more irrational utterances, were more prone to the illusion of control and overestimated the amount of skill required to win a slot machine, and their skill at doing so
Evaluate Cognitive explanations for gambling addiction
+ Research support
> Michalczuck et al studied 30 addicted gamblers compared with 30 non addicts
> Adicted gamblers showed significantly higher levels of gambling related cognative bias and were more impulsive and likely to prefer immediate reward to later larger gain
> supports the idea of a strong cognative componant
CA: Cognative bias in this study was measured using the GRCS which could mean gamblers have a tendency to use their beliefs as justification and it isn’t what they acctually believe
+ Research support
>McCusker and Gettings used a modified Stroop task to have participants quickly identify the ink colour of words (they had to pay attention to the ink colour and ignore the meaning of the words)
> Addicted gamblers were slower at this only when the words related to gambling suggesting they have a cognative bias to pay attention to gambling
- Methodological issues
> Dickerson and O’connor: what people say in gambling situations do not necessarily represent deeply held beliefs
Learning theory of gambling addiction: Vicarious reinforcement
Seeing someone else get rewarded for gambling (even through media not directly) may be enough to trigger a desire for the same reinforcement in someone who has never gambled.
Learning theory of gambling addiction: Direct positive and negative reinforcement
Positive: Money, the gambling ‘buzz’
Negative: anxiety/ need to be distracted
Learning theory of gambling addiction: Partial reinforcement
Skinner: once the rewards stopped, the rats and pigeons stopped displaying the target behaviour.
The unpredictability of gambling is enough to maintain it without wins.
Learning theory of gambling addiction: Variable reinforcement
Behaviour is reinforced intermittently producing the most persistent learning
It takes longer to establish learning but is much more persistent when learnt. They have learnt they wont win every time but will eventually if they persist
Learning theory of gambling addiction: Cue reactivity
Secondary reinforcements like betting shops may cause relapse and cue the craved arousals.
Learning theory of gambling addiction: Evaluate
+ Research
> Dickerson observed behaviour of gamblers in two betting offices.
> Found high frequency gamblers were more likely to place bets in the last 2 mins before the start of the race
> suggested gamblers find the build up exiting and delay betting to prolong it
CA: Methodological issues
> Gambling behaviour was observed over 14 weeks by 1 observer
: there is no way of checking reliability
- Limited explanation:
> explains addiction in games with no delay between bet and outcome but not delayed outcomes where the conditioning should be less effective
+ Explains failure to stop
> the conditioning does not require and active actions so their conflicting want to give up gambling causes them to do it more (NR)
Drug therapy for addiction: what are the 3 types?
Aversive: produce unpleasant consequence e.g. vomiting
> disulfiram is used to treat alcoholism by creating a hypersensitivity
Agonists: activate neuron receptors to produce similar effect to the substance
> methadone to creates feeling of euphoria to treat heroine addiction
Antagonist: block receptor sights so drug cannot have its usual effect.
> Naltrexone against heroine addiction
> other methods should be used a long side
Drug therapy: Nicotine addiction
NRT provides a clean, controlled dose of nicotine that can be reduced slowly over time reducing withdrawal symptoms
Drug therapy: Gambling addiction
No officially approved drug but ongoing research into opioid antagonists like Naltrexone is promising
Neurochemical explanation of gambling addiction is that it taps into the same dopamine reward system as nicotine addiction so opioid antagonists enhance GABA reducing dopamine release
Drug therapy: Evaluate
+ research support
> Hartmann-Boyce: meta analysis os 136 high quality studies concluding all forms of NRT were significantly more effective in helping smokers quit than a placebo and increase quitting nicotine by up to 60%
CA: publication bias may cause studies that don’t show positive results to not be published leading to misleading data
- side effects
> NRTs can have side effects like dizziness, headaches,
> Naltrexone can have side effects like spasms, anxiety, depression
+ reduces Stigma
> many people believe addiction is a psychological weakness
> continuing usefulness of drug therapy changes perspectives and reduces stigma
Behavioural interventions: Aversion therapy
Alcohol: a client takes an aversive drug like disulfiram that reacts with alcohol to cause vomiting and nausea - instant hangover
Gambling: giving gamblers a cards to read and a 2 second shock for any gambling related ones
Behavioural interventions: Covert sensitisation
A client is encouraged to relax and the therapists leads to a script
client sees themselves smoking and then the most unpleasant consequence described in in graphic detail
McMurran: a habitual slot machine user with a phobia of snakes:
- Imagined snakes coming out of the slot machine instead of money
- they are then instructed to imagine a scene where they turn their back on it causing relief.
Behavioural interventions: Evaluate Aversion therapy
- Methodological issues
> Hajek and Stead: its impossible to judge the effectiveness of aversion therapy because of the methodological issues like failure to use ‘blind’ procedures - Poor long term effectiveness
> Fuller et al: gave a group a disulfiram every day for a year and another group a placebo and weekly counselling. there was no significant difference after 6 months
Behavioural interventions: Evaluate Covert sensitiseation
+ research support
> McConaghy et al: after a year participants who underwent covert sensitiseation were more likley to not be addicted than those who underwent aversion therapy
CA: no control group
> non learning causes that are not treated
Cognitive behavioural therapy: cognitive
Functional analysis:
- client and therapist identify high risk situations
- therapist reflects on what the client is thinking before, during and after the situation to challenge the belief
- client-therapist relationship should be warm, collaborative but not cosy
- CBT programs aim to change addiction related cognitive bias
- identifying triggers is a useful starting point
Cognitive behavioural therapy: Behavioural
Skills training
specific: skills allowing the client to cope with triggers e.g. assertiveness training, anger management
Social: help clients in social situations and with refusing their addiction without fuss/ embarrassment
Cognitive behavioural therapy: Evaluate
- short term solution
> Cowlishaw et al: meta analysis of 11 studies showing CBT had medium to large effect up to 3 months but after 9-12 there is no significant difference between CBT and control groups
CA: There is some high quality research challenging this
Petry et al randomly allocated pathological gamblers to a control group or treatment condition and the CBT group gambled significantly less after 12 months - High drop out rate:
> Cuijpers et al: drop out rates are 5x higher than other forms of therapy
+ relapse prevention
> relapse is part of CBT so helps with dealing with it
Theory of planned behaviour
1 personal attitude
- if a persons attitude is less favourable towards their addiction they are less likely to do it
2 subjective norms
- what the client thinks the people around them would think of their addiction
- adolescent overestimate the substance abuse of their peers. campaigns against this may reduce substance abuse
3 perceived behavioural control
- influences behaviour indirectly via intentions and directly
- increasing self efficacy increases likelihood of quitting
Theory of planned behaviour: evaluate
+ research support
> Hagger et al: 486 participants completed questionnaires about alcohol related behaviours and again a month later and three months later
- attitudes towards subjective norms and perceinved behavioural control was significantly correlated with intention to limit drinking
CA: the study failed to preduct some alcohol related behaviours
- short term effect
> McEachan et al: meta analysis of 237 tessts of TPB and found strength of correlation between intention and behaviour varied according to the legth of time between the two.
> it can only predict ab 5 weeks
- Intention-behaviour gap
> doesn’t explain how the behaviour is caused
> Miller and Howel: studied gambling behaviour of teens and found strong support for some areas of TPB but not intentions related to actual gambling behaviour
Prochaska’s model: 6 stages
Precontemplation: person does not think ab their addiction bc they don’t believe they have one or are not motivated to change
Contemplation: A person is aware of the need to change but also the cost and have not necessarily decided to change
Preperation: a person believes the benefits outweigh the costs and are ready to change
Action: a person has done something in the last 6 months to substantially reduce their risk
Maintenence: a person has maintained changed behaviour for at least 6m
Termination: new behaviours become automatic, no intervention required
Prichska’s model: evaluate
+ Dynamic
> emphisises importance of time and recycling backwards or missing stages
> realistic
CA: stages are arbitrary and no research to destinguish one from the other
> argument for reduction to two stages: precontemplation and all the others
> model is of little use
+ posetive view of relapse
> does not view relapse as a failure and does not underestimate its potential to blow change off course
> Face validity with clients
- contradictory research
> Taylor et al analysed 24 revies concluding it was no more effective than appropriate alternatives in nivotine addiction and the defined stages choulld not be validated by available data
