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Check your homework answers for the evaluation points of the Theory of Planned Behaviour: A strength of the theory of reasoned action (TPB) is that it.

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Presentation on theme: "Check your homework answers for the evaluation points of the Theory of Planned Behaviour: A strength of the theory of reasoned action (TPB) is that it."— Presentation transcript:

1 Check your homework answers for the evaluation points of the Theory of Planned Behaviour: A strength of the theory of reasoned action (TPB) is that it has research studies to support the fact that it can explain addictive behaviour. A meta-analysis by Armitage and Connor (2001) found that perceived behavioural control more accurately predicted individual’s intention to behave when compared to looking at attitudes and subjective norms alone. This shows that the principles of the TPB can accurately predict how people will behave in terms of their likelihood to engage in addictive behaviour.

2 However, a limitation of this research is that it may not predict actual addictive behaviour accurately. This is because their meta-analysis showed research into the TPB found it was only accurate in predicting intention to change rather than actual behavioural change – therefore explaining how people may be motivated to change and intend to change but may not lead to a change in their behaviour. This limits the extent to which TPB can be applied to the accurate prediction of health behaviours in clinical settings, as it may be primarily an account of intention formation rather than clearly specifying the processes involved in translating intention into action.

3 However, a further strength of the TPB is that it is supported by the principles of the cognitive model of addiction. This model assumes that humans are in control of their own behaviour and have the free will to choose whether to engage in an addictive behaviour or not. This is in contrast to a deterministic view such as the biological perspective that states addictive behaviour is the result of ‘faulty’ genes or an imbalance of neurotransmitters or hormones. Thus, both the TPB and the cognitive approach acknowledge the complexity of human thought processes and their influence on addictive behaviour.

4 However, a limitation of the TPB is that there is research evidence that other models may provide better alternatives for explanations of behaviour change. For example, ‘Stages of change’ model suggests an individual must be ready for change and tries to get them to a position where they are highly motivated to change behaviour, taking into account that most people who take action to change an addiction are not successful at first. Moreover, this model has been successfully used in smoking cessation clinics. Therefore, this model may be more productive at explaining non- conscious behaviours such as addiction as opposed to the TPB which could be said to fail to take into account emotions and compulsions of addiction.

5 On the other hand, a weakness of the TPB is that the very existence of approaches other than the cognitive model of addiction suggests that this theory alone is not enough to account for and prevent addictive behaviour. This model only explains addictive behaviour at the level of thought processes and behavioural intentions and fails to acknowledge that addiction may be learned through the process the operant conditioning, when addicts engage in addictive behaviour because of the positive reinforcement they receive (e.g. feeling relaxed or high). In order to explain the complex nature of addiction, a more holistic view should be taken that encompasses a bio-psych-social perspective.

6 Task Complete pages 51 – 54 in your booklets on biological interventions to treat addiction.

7 Main neurotransmitters for addiction Serotonin - helps regulate mood (e.g. anxiety and depression). Too little has been associated with depression (neurons using this found in pons) Dopamine - plays a role in mood, particularly motivation and reward (as well as cognition, learning and memory). Endorphins - produced in pituitary gland during exercise, excitement and pain.

8 Dopamine agonists Dopamine antagonists

9 Treatment for smoking 1. NRT – replace nicotine from cigarettes with nicotine from safer sources (patches, gum, spray, inhalers). Small amounts of nicotine contained within the gum or patch which is absorbed into the blood, giving body nicotine it thinks it needs. Purpose behind NRT to slowly reduce dosage. Little by little, less nicotine until, eventually, you not needed anymore. A02 - May double rates of quitting. BUT smokers may continue to smoke in addition to intervention.

10 2. Varenicline – drug that acts as nicotine receptor partial agonist; attaches to receptors to partially stimulate receptor, without creating full nicotine effect to alleviate craving and withdrawal symptoms and reduce rewarding effects of smoking. Secondly, blocks the ability of nicotine to stimulate the central nervous mesolimbic dopamine system. A02 – Varenicline: side effects are common, has been associated with depression and suicide – patients need careful monitoring

11 3. Antidepressants - e.g. bupropion and nortriptyline (tricyclic antidepressants) – inhibits the reuptake of dopamine, serotonin and noradrenaline, allowing chemicals to stay in the brain for longer A02 - Hall et al (1988) found antidepressant nortriptyline assisted quitting, especially if used alongside CBT, BUT have more serious side effects than newer SSRIs (which are not effective in treating smoking)

12 Treatment for gambling 1. Opioid antagonists – prevent the pleasure experienced when gambling by attaching to (i.e. blocking) dopamine receptor sites, therefore diminishing desire to gamble (theory is that repeated lack of effects from gambling breaks the habit) A02 - Grant and Kim (2006) found gamblers experience rush of excitement and that naltrexone reduced thoughts about gambling and urge to gamble, and at higher doses, reduced actual gambling.

13 2. SSRIs – gamblers been found to have low levels of serotonin (more likely to engage in sensation-seeking behaviour) – as serotonin is low SSRIs should be effective. A02 - Kim et al (2002) found SSRIs reduced gambling symptoms compared to placebo condition.

14 3. Mood stabilisers (e.g. Lithium) –target impulsivity associated with impulse-control disorders such as gambling by altering the way the body breaks down neurotransmitters: increases effect of serotonin (a neurotransmitter that plays a role in stabilizing moods) and also decreases the levels of the neurotransmitters norepinephrine and dopamine, and prevents the nerve receptors from becoming overly sensitive to the effects of dopamine.

15 AO2 A02 - Hollander et al (2005) found Lithium more effective than placebo at reducing gambling urges over 10 weeks. BUT, drug group did not lose less money or gamble less than placebo group A02 – drug treatments for gambling still at early stage and remain experimental

16 Task - homework Listen to the pod cast and fill in the missing information (page 54) on evaluation of biological interventions. Identify the main point of each evaluation paragraph.

17 Optional - Exam question Discuss one type of intervention aimed at reducing addictive behaviour. (4 + 8 marks)


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