addiction

Risk Factors- Genetic Vulnerability

Low number of D2 (dopamine) receptors found in people struggling with depression.

People with ability to metabolise nicotine enzyme (CYP2A6) smoke more than those without (Pianezza et al)- tolerance.

Monozygotic more likely to be pathological gamblers- interviews with 2889 pairs of twins (Slutske et al)

AO3:

+ Support from adoption studies (Kendler et al)

• data from National Swedish Adoption Study- more likely to have addiction if at least one biological parent with one.

- Correlational, not causational

+ Support from Vink et al

• 1572 Dutch twins, nicotine 75% genetic.

- Inconsistent findings (Slutske et al)

• 49% male vs 55% female monozygotic twins both had.

Risk Factors - Stress

Self medication (Gekopf et al) - pathological behaviour viewed as being able to alleviate stress, strong predictor of relapse (Dawes et al).

Traumatic stress- Robins et al interviewed US soldiers a year after Vietnam (almost ½ used heroin, 20% dependent during war), Kessler et al (34% men with PTSD addicted, 15% without VS 27% women with PTSD, 8% without).

AO3:

+ Research support - Kessler Robins.

- Doesn’t explain why those without PTSD can become addicted.

- Retrospective studies - relying on memory of stressful events.

- Causation not established, unclear order of stress/ addiction.

Risk Factors - Personality

Personality traits (e.g. impulsivity, external LOC).

Addiction-prone personality - Barnes et al developed APP scale, found it to be an indicator of ‘heavy’ marijuana use.

Personality disorders (e.g. Anti-social) cause traits that link with addiction.

AO3:

+ Support for link of APD with addiction

• Bahlmann et al interviewed 55 alcohol-dependent, 18 diagnosed.

+ Support for addiction-prone personality

• Barnes et al - connection between personality and addictive behaviours, can prevent addiction by identifying.

- Lack of control of external variables.

- Minimised blame/self-fulfilling prophecy.

Risk Factors - Family Influence

Lack of (perceived) monitoring from parents.

SLT (Bandura) - behaviour learned through observation of those we interact socially with the most.

Parenting style (parental control/warmth), they are social models for their children.

AO3:

+ Research support (Reith and Dobbie)

• interviews with 50 gamblers - boys learnt from fathers (sports betting), girls learnt from mothers (bingo, machines).

- Resilience to parental control/ supervision not quantifiable.

- Lack of consideration for siblings’ influence/ access to addictive material.

Risk Factors - Peer Influence

Peer pressure/ peers introducing to addictive material.

Latkin et al - addiction more likely in circles where behaviour is present, framed as desirable.

Shakya et al - indirect peer influence, parents influence child who influences their peers.

Conformity - NSI with peers.

SLT - identifies with admirable peers, positive reinforcement.

AO3:

+ Research support (Moreno et al)

• 56% of 400 MySpace profiles (17-20 years) referenced alcohol.

- Peer influence may be overstated (De Vries et al)

• smoking within friend group more likely due to friend selection than influence on non-smokers.

+ Real-world application (Pitkanen et al)

• longitudinal (14-42 years), early onset of drinking → addiction.

• social norm intervention - challenge misconceptions and decrease alcohol consumption.

Genetic Explanation - Nicotine Addiction

Brain imaging = fewer D2 receptors → more likely to become addicted (Volkow).

Genes = 75% of inclination to start smoking (Volkow).

Genes CD2 receptors (DRD2) = initiation + inability to quit, increased tolerance and avoidance of withdrawal = maintenance.

AO3:

+ Genetic tests = early prevention/treatment.

+ Research support (Schachter)

• ½ Ps given high-nicotine cigarettes, other ½ low-nicotine.

• Ps with low-nicotine wanted more.

• body regulates + causes desire to smoke and avoid withdrawal.

- SLC6A3-9 (smoking gene) has 40% inheritability rate.

• can’t purely be biological, must be partially learnt.

• too reductionist.

Neurochemical Explanation - Nicotine Addiction

Nicotine receptors triggered by its presence → release of dopamine in nucleus accumbens (pleasure centre).

Built up tolerance = need for more.

Nicotine paradox = smoking appears to relax people but it is a stimulant.

AO3:

- Reductionist

• biological model = oversimplified, suggests addiction is inevitable.

• COUNTER: environmental factors not always relevant.

- Ignores individual difference - access to nicotine, desire to use, etc..

+ Research support from twin studies

• 108 MZ twins raised separately = 75% concordance for smoking status.

• similar found in MZ raised together.

+ Real-life application - new treatment

• nicotine replacement therapy (e.g. gum, patches) deliver controlled dose - binds with neurons and mimics effect.

Learning Theory Explanation - Nicotine Addiction

Classical conditioning = initiation:

• Sitting with friends who smoke (UCS) + Nicotine inhalation (NS) → nucleus accumbens triggered, pleasure.

• Nicotine inhalation from smoking (CS) → nucleus accumbens triggered, pleasure.

Operant conditioning (positive reinforcement) = maintenance.

Pleasure of smoking = primary reinforcer, stimuli present at same time = secondary reinforcer (rewarding on their own).

Situations where smoking is common (e.g. pub) = cues, produce same effects as smoking.

Wikler - group of opiate addicts experienced withdrawal symptoms in places associated with former drug use.

• should change routine in recovery to avoid this.

Goldberg

• monkeys repeatedly pressed lever to receive nicotine → reinforcement.

• - generalisability?

Calvert - smokers shown cigarette packet had greater biological activation.

• - based on self-report - social desirability, subjective.

• + physical signs (e.g. sweat, heart rate) = objective

Learning Theory AO3 - Nicotine Addiction

- Slightly reductionist

• simple, but ignores biological, social, cultural

- Deterministic

• ignores cognition, individual choice, neurochemistry outside of dopamine (e.g. GABA).

+ Initiation clearly explained, not in other approaches.

+ Real-life application

• suggests smoking can be ‘unlearned’ since it is learnt.

- Ethical + generalisation issues of animal studies

Learning Theory Explanation - Gambling Addiction

Reinforcement:

• vicarious, positive, negative.

• partial = win only percentage of times.

• variable = uncertain form of partial- most effective.

Cue reactivity = secondary reinforcer → stimulus (e.g. flashing lights).

Gambling environment = excited/inviting atmosphere.

‘Big win’ hypothesis = win early in experience → increased desire to gamble.

‘Near miss’ hypothesis = encouragement to ‘try again’ from excitement.

Learning Theory AO3 - Gambling Addiction

- Can’t explain all stages of initiation + maintenance- incomplete explanation.

- Suggests all initiating cues will continue to work

• Griffiths - interactionist approach, cues = vulnerable, psychological risks = stressors.

+ Research support for positive/vicarious reinforcement (Dickenson)

• high frequency gamblers placed bets 2 minutes before race - pre-race buzz.

- Doesn’t explain transition from behaviour to addiction - some gamble but do not become addicted.

Cognitive Explanation - Gambling Addiction

Expectancy theory = initiation - outcome > cost.

Self efficiacy = belief that belief → desired outcome, explains relapse- don’t believe they can lose.

Cognitive biases = irrational beliefs that don’t reflect reality.

Gambler’s fallacy = luck influenced by random recent events.

Illusions of control, recall bias (only recall wins).

Griffiths - 30 non-regular vs 30 regular gamblers given £3 for fruit machines, more irrational verbalisations from regulars.

+ Research support (Burger + Smith)

• people with high level of ‘control motivation’ = more gamblers.

+ Real-life application - treatment

• CBT directly addresses irrationalities.

- Individual difference (fruit machines + online > sports + horses).

- Methodological issues (self-report).

Drug Therapy - Reducing Addiction

Aversive drugs = cause negative consequences, e.g. antabuse.

Agonists = mimic effect on neurotransmitters but less harmful, e.g. methadon.

Antagonists = blocks neurotransmitters (and effect of drugs), should be accompanied by counselling, e.g. naltrexone.

Nicotine:

• agonists - patches, gum, inhaler = stimulate release of dopamine, slowly reduced.

• antagonists - varenicline = reduces craving, blocks rewards.

- Ineffective, many relapse over withdrawal, relies on patient.

+ Less commitment, less impact on economy (time off/cigarette breaks), less expensive than CBT.

+ 60% relapse rate, less than placebo patches.

- Ethical issues (cardiovascular change with gum and patches, dependency on replacements).

Prochaska’s 6 Stage Model (Prochaska + DiClementes)

Overcoming addiction is cyclical not linear - stages may be repeated or skipped altogether.

Depends on readiness to quit, stage of recovery.

1. Precontemplation

• not considering changing behaviour (unmotivated, denial).

• focus on recognising need for change.

2. Contemplation

• thinking about change sometime in next month.

• focus on pros > cons.

3. Preparation

• undecided on how/when to change.

• focus on constructing a plan.

4. Action

• have done something to change (therapy, meaningful action).

• focus on developing coping skills to quit.

5. Maintenance

• kept changes for > 6 months.

• focus on relapse prevention, avoiding cues.

6. Termination

• newly acquired behaviours become automatic.

• may not be realistic in all cases.

Prochaska’s Model AO3

+ Dynamic process

• recognises importance of time, recycling stages, skipping them.

• COUNTER: arbitrary stages, no evidence to distinguish. Kraft = precontemplation + all others - may mean less useful for treatment reccomendations.

+ Positive view of relapse

• relapse is inevitable but also impactful on recovery.

• face validity - realistic.

- Contradictory research (Taylor et al)

• review for NICE (meta analysis) = no more effective than alternatives.

• defined stages cannot be validated.

Theory of Planned Behaviour (Ajzen)

Behaviour is under conscious control of individual

• increased perceived control = intention to try harder.

Personal attitudes = degree to which behaviour is positively/negatively viewed/

• 2005 - ONDCP = ad campaign to decrease teenage cannabis use, attributed success to teenage attitudes.

Subjective norms = social pressure to be involved/not

• anti-drug campaigns use real stats to challenge misconceptions about how common behaviour is.

Perceived behavioural control = presence of factors that help/hinder performance.

• prevention programmes focus on effort/willpower

ToPB AO3

- Problems determining intention from self report

• social desirability bias.

+ Research support

• all 3 factors tested + predicted intention to limit drinking to national guidelines (1 month + 3 months).

• COUNTER: wasn’t so successful for all addictions (e.g. binge drinking).

- Doesn’t consider external factors

• e.g. personality + culture.

- Invalid evidence

• much is based on self report.