Health-Addiction Flashcards
Define drug dependence
‘A cluster of cognitive, behavioural and physiological symptoms indicating that the individual continues use of the substance despite significant substance-related problems’ –DSM-IV-R
The Biological Model of Addiction
-Key principles
(positive reward, tolerance, physical dependency)
- Positive reward theory= addiction occurs because the feelings we get from engaging in the activity are perceived to be pleasant and rewarding.
- Tolerance occurs and the individual needs more to feel the same effects.
- Physical dependence theory= people become addicted because doing without the item or behaviour is unpleasant i.e withdrawal.
The Biological Model of Addiction
-Evaluation
- Helps explain susceptibility at initiation and relapse.
- Complex effects of neurotransmitters are not fully understood, effects of one drug can be diverse e.g. Nicotine increases arousal and decreases stress.
- Too reductionist, ignores social context of addiction. Eg. Drug taking in US soldiers in Vietnam stopped once they returned home (Rubin et al 1975).
Olds and Milner (1954)
They implanted electrodes into rats’ brains, and found that when they gave electrical brain stimulation the rats seemed to experience pleasure.
The rats could press a lever which would deliver a small current deep into its brain.
It was found that they would perform complex and difficult tasks for another dose of stimulation, and would even press the lever up to 2,000 times an hour to the exclusion of eating or drinking.
Neurotransmitters
-Initiation
(RP, memory, dopamine, connecting)
Reward pathway in the centre of the brain is responsible for driving feelings of motivation, reward and behaviour. When a behaviour makes you feel good according to your memory, the brain tells the body to initiate that behaviour. Dopamine is released from reward pathway which gives sense of pleasure. By connecting to regions of the brain that control memory and behaviour, the reward pathway is also responsible for making you repeat the behaviour.
Neurotransmitters
-Maintenance
(addiction induces, release of dopamine, PFC function, over production of dopamine)
Addiction can induce changes in structure and function of reward systems neurons which contribute to tolerance, dependence and craving. Collective stimulation of areas in the medial forebrain produces pleasure and reinforces that behaviour. Most drugs and activities eg gambling release dopamine into the NA area, prompting incentive to continue and increase the behaviour.
PFC function which controls decision making and inhibits risky behaviour is impaired in addicts, so they can choose immediate rewards even in face of long term negative consequences. Continued over production of dopamine leads to desensitisation in receptors to compensate which leads in increased desire to engage so can return to same level of ‘dopamine high’.
Neurotransmitters
-Relapse
Reward pathway linked to memory help make addicts highly sensitive to reminders of past highs, tf vulnerable to relapse when stressed and unable to control urge to repeat addictive behaviour
Biological model
-genes
(susceptibility, pedigrees, treatment, signals/pathways)
Susceptibility to addiction is the results of many interacting genes. Social and environmental factors contribute to this risk of addiction.
Researchers construct pedigrees of large families with addiction which can reveal whether or not a trait has a genetic component by comparing DNA sequences of individuals who have the disease and those who don’t.
As more genes are discovered to make you more susceptible, treatments can be improved. Researchers can focus on one gene product and develop a drug that modifies its activity. So signals or pathways in the brain can be reversed or stabilised to restore proper brain function.
-looking for biological differences that may make someone more or less vulnerable to addiction
The Cognitive Model of Addiction
-Key principles
(Beck, coping, expectancy, self-efficacy, irrational biases)
• Beck et al (2001)-vicarious ‘circle of addiction’:
low mood=using/displaying addictive behaviour=financial/medical/social problems
• Coping= Addictive behaviours to cope with stress and therefore effect
1) mood regulation-increased positive mood.
2) performance enhancement e.g. more alert and can do more
3) distraction- from unpleasant real life
• Expectancy= Expectations affect how and why we ‘do’ some behaviours. E.g Hansen et al (1991)-those who abuse alcohol are likely to be people who perceive fewer negative consequences, while those who expect strong negative consequences are less likely to engage in addictive behaviour.
• Self-efficacy (Bandura)= our beliefs in ourselves, and whether we believe that we are capable of dealing with effects of a particular behaviour. It influences our decisions, goals, effort and perserverance
• Irrational Biases (Griffths, 1994)
The Cognitive Model of Addiction
-Evaluation
- Treatment options-change way people think eg CBT, Education.
- Can explain individual difference-why not everyone becomes addicted.
- Limited for chemical addiction as relapse very biological.
Griffiths (1994)
Aim: to increase understanding of the cognitive processes and behaviour of persistent fruit machine gamblers.
Method:
• Quasi experiment with independent design.
• 2 groups, 30 regular gamblers (29 m and 1 f) play at least once a week.
• Non-regular (15m 15f) play once a month or less.
• Volunteer sample via poster.
• In arcade each participant given £3 to gamble which gave 30 free gambles. Each participant was set objective to stay on fruit machine for 60 gambles to break even and win back £3. If they achieved this, could choose to keep money or carry on gambling.
To measure irrational verbalisations, used ‘thinking out loud technique’. Participants randomly assigned to thinking outloud condition or non-thinking out outloud.
Participants in thinking out loud had their verbalisations recorded.
Results:
• 14 regular gambles managed to break even and 10 stayed on machine until they lost all the money.
• 7 non-regular broke even and 2 stayed on until they lost all their money.
Conclusions:
• Regulars believe they are more skilful than they are and make more irrational verbalizations demonstrating cognitive bias.
Evaluation
+
• Amount and type of data collected. The behavioural data such as fruit machine gambling was quantitative and this allows for comparisons and statistical analysis to be made. Furthermore, the qualitative data collected from the verbalisations were quantified using content analysis again allowing statistical comparisons to be made.
• Carried out in arcade= high EV
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• Demand characteristics as knew they were being studied.
• Thinking out loud method doubtful whether this technique did capture all of the thoughts of the participants.
The learning model of addiction
-Key principles
• Classical conditioning (CC)-learning a new behaviour via the process of association.
• Operate conditioning (OC)-learning by reinforcement.
• Social learning theory and vicarious reinforcement.
• The Cue-reactivity theory- the cues associated with addictive behaviour can trigger responses through CC. e.g lighters for smoker, they are conditioned stimuli.
= if always surrounded by cues will be very hard to stop behaviour.
Classical conditioning applied
- Volkow et al (2006)
- Townsend (1993)
- Volberg (1994)
Volkow et al (2006)
Cocaine addicts watched a video showing cocaine ‘cues’. They experienced increases in the transmission of dopamine in the brain.
Townsend (1993)
Price increase in cigarettes led to decrease in consumption, i.e reduced availability to reduce cues.
Volberg (1994)
Increases in pathological gambling after increase in gambling accessibility.
Aversive agent treatment
Causes an adverse effect such as nausea when the addictive substance is ingested.
Eg. Disulfiram: blocks the enzyme acetaldehyde from converting alchol->acetic acid. Acetaldehyde causes hangovers, therefore Disulfiram causes instand and intense hangover when taken whilst drinking.
Symptoms: shortness of breath, nausea, vomiting.
Krampe et al (2006)
• 9-year study
• Found an abstinence rate of over 50%.
Agonist substitution
Works with the reward pathway.
Stimulates the effects of the addictive substance in a more controlled, less harmful way.
Eg. Methodone: occupies opiate receptor sites, causing a more controlled raising of opiate levels, and causing heroine to have less effect.
Eg. Nicotine patches and gum: reduce cravings by delivering a small quantity of nicotine without all the other harmful ingredients of cigarettes.
