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Unit 4 PSYA- 4

1. Models of Addictive BehaviourBiological, cognitive and learning approaches to explaining initiation, maintenance and relapse, and their applications to smoking and gambling

2. Vulnerability to addictionRisk factors in the development of addiction including;PersonalityPeersAgeStressMedia influences on addictive behaviour

3. Reducing Addictive BehaviourModels of prevention, includingTheory of Reasoned ActionTheory of Planned BehaviourHealth Belief ModelTypes of intervention, includingBiologicalPsychologicalPublic Health Interventions and legislation and their effectiveness

Exam Specification for this topic area

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But first ….. A message..

“Research Methods feature heavily in all elements of addictive behaviour and needs to be integrated in all essays- so learn them well you will.”

1. Models of Addictive Behaviour

•Biological, Cognitive & Learning models- including; initiation, maintenance & relapse

•Explanations for specific addictions; smoking & gambling

"Addictive behaviour is a repetitive habit pattern that increases the risk of disease and/or associated personal and social problems....

(Marlatt, Baer, Donovan & Kivlahan, 1988)

Definition of ADDICTIVE BEHAVIOUR

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Watch video

Important information that you will need to use in your EXAM QUESTIONS!!

The need to distinguish between

initiation, maintenance and relapse• You will need to use these three concepts when

describing any of the various models of addiction..

Initiation – factors that affect how the addictive behaviour gets started

Maintenance – factors that keep the behaviour continuing

Relapse - reverting to earlier patterns of the addictive behaviour soon after a

period of abstinence or self-control.

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IT Activity•In groups of two•Use your mobile phone/college ‘flip-camera’ to go out into the college and record examples of addictive behaviour

•Ask permission before filming

•Bring back for the class to email to your teacher

•View next lesson•Email address sgregory@strodes.ac.uk

Biological Model

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Two explanations..

1.Genetics

2.Hijacked brain

Activity- Powerpoint pres.

1. Role of Genetics to explain gambling + evaluation - IMR

2. Role of Neurobiological (“high-jacked brain”) to explain smoking i.e. dopamine/VTA-NA neural pathway + evaluation - IMR

3. Assess the validity of research comparing genetics vs dopamine – smoking /gambling

All need to feature;

initiation maintenance & relapse (IMR)

Clips

Diagrams/pictures to explain theory

FOR INFO..

1. GENETICS

 There are two main ways of investigating genetic factors in human behaviour.

1.To study family relationships including twin studies.

2.To carry out genetic analysis and look for differences in the genetic structure of people with and without addictive behaviours.

A US study by Kendler (2000) found that concordance rates -both twins using, abusing, or being dependent on drugs- were higher for identical than fraternal twins. Some adoption studies (e.g. Heath, 2000) also lend support to the idea that there is a genetic component in addiction..

Han et al (1999)A study of over 300 MZ twins and 200 same

sex DZ twins concluded that the major influences on the decision to use substances was environmental rather than genetic.

Jang et al (2000)Jang showed a connection between genetics and anti-social personality traits and these traits and alcoholism. Similar findings have been claimed for behavioural addictions such as gambling (Coming et al 1996). 

Biological explanations of gamblingTwin studies, DOPAMINE and GENES A large number of studies on twin pairs have found that

shared environmental and genetic factors account for 35-54% of vulnerability to pathological gambling – with genetic factors being more important.

One potential genetic process is through the dopamine D2 receptor gene. A variant to the D2 dopamine receptor (D2A1) has been found to be more prevalent in pathological gamblers compared to the general population. The ‘buzz’ of winning appears to be mediated by a number of neurotransmitters.

For example - dopamine levels rise after a winning streak with activation of the Common Reward or MDP reward system pathways common to other addictions..

Norepinephrine (noradrenaline) - levels rise after gambling episodes

In social gamblers these neuro-chemical

changes typically occur while they are actually gambling, but in pathological gamblers, they occur while anticipating gambling or as a classically conditioned response to a gambling-related stimulus (Shinohara et al 1995)

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Meyer et al (2004) study -

Activity: Complete this research study under the following headings

Aim:To investigate the effect of gambling on cardiovascular (heart rate) endocrine activity

ProcedureTen regular male blackjack players were used – measurements taken during/post matches

Findings•Base heart rate of gamblers was lower than control group at start of arousal but rose significantly during first 30 minutes , then tended to level out up to 60 minutes and ended slightly higher than 30 minute level.

•Base heart rate of control group was higher than gambling group at start of arousal but fell significantly during the first 30 minutes and ended slightly lower than 30 minute level

Conclusion:Sympathetic consequences of gambling may reinforce future gamblingRelevance of increased cortisol for maintenance of gambling unclearGambling enhances mood – cortisol may contribute to mood alteration

The gene DRD2 (dopamine receptor D2) has been found in 42% of people with alcoholism, 50% of pathological gamblers, 45% of people with Tourette’s syndrome and 55% of people who have autism.

However, it has also been found in 25% of the general population. This means that DRD2 appears more frequently in people with these behavioural syndromes, but it cannot be the sole explanation for the behaviour (Comings, 1998).

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Smoking initiation and maintenance

Initiation and maintenance of smoking behaviour

Recently, there has been an increasing interest in smoking in children. Because a lot of children and adolescents try a puff of a cigarette, it is difficult to distinguish between actual initiation and maintenance of smoking behaviour.

Cigarette smoking is addictive. It is classified as a substance related disorder in DSM-IV-TR (see page 410) and is referred to as a Nicotine-Related Disorder since nicotine is the addicting agent of tobacco

Biological FactorsThere is some evidence of a genetic factor in

smoking behaviour.

Shields (1962) looked at 42 twin pairs who had been reared apart; chosen to separate out the effects of genetics from family influence. Only nine pairs were discordant for smoking behaviour (suggesting genes might play a part)

DRD2 Gene This gene occurs in alcoholics and pathological

gamblers as well as individuals who have Tourette’s syndrome and autism. This poses a problem for the idea that DRD2 is a ‘reward’ gene because individuals with Tourette’s syndrome and autism are not thought to be particularly ‘pleasure seeking.’

Explaining individual differences. Genetic explanations can explain why some people

become addicted yet others who have the same environmental factors do not. Some people are more vulnerable to develop an addiction because of their genetic disposition (the diathesis-stress model). This idea of genetic vulnerability may also explain why some people are more resistant to treatment for the addictive behaviours and are more likely to relapse.

A reductionist approach. Ignores social context, therefore highly

reductionist

2. Hi Jacked Brain- Neurobiological approach

The brain gets “Hi-jacked”

By a “need” to engage in addictive activities…

I really need a drink..

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THE HI-JACKED BRAIN

DEFINITION of ‘hijacked’ - effect of addictive substances onnormal brain functioning•activate and can subvert areas of our brain which evolved to regulate and sustain the most basic aspects of our existence.

i.e. the same brain circuitry which subserves feeding, sex and other essential survival behaviours, also underlies the development and maintenance of substance abuse. (Claridge and Davis 2003)

•Also because these non-natural behaviours ‘trick’ the brain into thinking that a survival need has been met, addicts typically have a diminished sexual libido and appetite for food.

NEURAL PATHWAYS IN THE BRAIN..

Responsible for maintenance of addiction

Exam Question January 2011Topic: The Psychology of Addictive Behaviour

11) “Outline and evaluate the Biological model as an explanation for the maintenance of one addictive behaviour” (4 marks + 4 marks)

From last year…

Key features of the biological approach to abnormality

Biological Approach

All mental illnesses have a physical cause

Mental illnesses can be described and diagnosed

in terms of clear-cut symptoms

ICD 10 DSM IVGenetic inheritance Biochemistry

Infection Brain damage

Neurotransmitters

Neurotransmitters (chemicals in the brain) play an important role in behaviour.

Imbalances of these chemicals may be involved in certain mental illnesses.e.g. An excess of dopamine has been detected in the brains of schizophrenics.Low serotonin levels are often found in people with depression.

Nerve cells

The neurotransmitter dopamine plays a major role in addiction.

Increased levels of dopamine are associated with pleasure. The desire for the rewarding pleasurable feeling may account for the initiation and maintenance of addictive behaviour.

Rewarding experiences, such as drug taking, trigger the release of dopamine and effectively telling the brain ‘to do it again.’

Initiation and maintenance

Brain imaging..

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THE ADDICTED BRAIN (CLARIDGE AND DAVIS, 2003) Box 9.1 Pages 392 – 393 Textbook

•Drugs boost activity of brain’s reward system•Chronic drug use can induce long term changes in structure/function of reward systems neurons•Changes contribute to tolerance, dependence and craving

“Common – Reward” or “VTA-NA” Pathway

• The VTA-NA pathway acts as a ‘rheostat of reward’, i.e. it tells other brain centres how rewarding an activity is. The more rewarding, the more likely the organism is to remember it and repeat it..

Activity: Using page 393 of textbook-complete the following;

VTA= A key part of the brain’s reward system is the pathway extending from dopamine - producing neurons in the ventral tegmental area (VTA) to…NA= dopamine-sensitive neurons in the nucleus acumbens (NA)There are also pathways linking the VTA and NA with other brain regionsthat can help make addicts sensitive to reminders of past highs (such as places where they scored) vulnerable to relapse when stressed, and unable to control the urge to seek drugs.

Time for some drawing…

Insert the following into the ‘addicted’ brain in your learning pack;

Common Reward PathwayPre-Frontal Cortex Amydala

“Addicted” Brain

Prefrontal cortex (PFC)Part of the frontal lobe that is involved in many cognitive functions, including memory, language and decision making.

The VTA-NA ‘common reward’ pathway

Nucleus Accumbens – (NA)A small region in the forebrain with ancient evolutionary origins, which helps regulate survival drives like food and thirst.Affected by drugs includingcocaine, amphetamine,cannabinoids (e.g cannabis)and opioids (e.g. heroin).

Ventral Tegmental Area– (VTA)Found in the midbrain, thisarea produces dopamineand forms part of one of fourmajor dopamine pathways inthe brain. Affected by drugs including; nicotine, alcohol and opioids (e.g. heroin).

Dopamine movement Amygdala

Striatum

Dopamine binding to

receptors in the nucleus

accumbens (NA)

• Activation brings pleasure

• Activation reinforces Links to other brain regions develop sensitivity to and reminders of past highs and make vulnerable to relapse

• Drug and activity abuse stimulates extracellular dopamine in this area

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VTAVTANA

The Common Reward Pathway

Amygdala and prefrontal cortex

4mins 52 secs

Watch videoVideo clip

Reward pathways

The Role of the Pre-Frontal Cortex (PFC)

Drives the addict to do anything necessary to obtain a fix.

Addicts have learned to expect a rewarding experience from their addictive behaviour, e.g. drug taking and this can make it difficult for an individual who is trying to abstain from a drug if s/he is surrounded by cues and reminders of the behaviour that leads to the pleasurable state caused by the release of dopamine. The presence of these cues and

the impaired decision making can lead to relapse.As a result of this down regulation more and more of

the drug is needed to trigger the reward pathway (e.g. Koob and Kreek 2007).

Relapse..

Also….

Other CUES for RELAPSE..

Cues that may cause an addict to relapse for smoking and gambling addictions.

Smoking – smell, finishing eating, others

smokingGambling – adverts, sporting pages in a

newspaper, sports on TV

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Video 1Video 2Video 3

Utube CLIPS..

Additional info..

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Explaining ToleranceSENSITISATION AND DESENSITISATION

Excessive activation and chronic movement beyond its natural, balanced state causes neurochemical changes to occur in the brain

Desensitisation1.Neural mechanisms become more and more tolerant as

addiction progresses2.Prolonged and repeated increases in extracellular dopamine

causes the brain to compensate for the excessive stimulation by changing its function in some way

3.Dopamine receptors at the post-synaptic level become less sensitive i.e. they begin to close down

4. One of the consequences of this neuroadaptation is an increased desire for more extensive addictive behaviour5.The individual needs larger and more frequent doses to achieve the initial or desired effect of the behaviour.6.Reduced activity in the PFC also occurs – This reduced activity makes it difficult for

addicts to resist impulses to use drug, nicotine etc.

Watch video

1min12 secs

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Sensitisation

•Plays an important role in supporting addictive behaviour.

•Repeated, intermittent exposure to drugs that stimulate the ability for people to move (called psychomotor stimulants) produce increased behavioural and neurochemical responses to subsequent drug exposure.

•In animals their activity levels increase.

•Sensitisation also functions at the level of associative learning (classical conditioning to be explained in the next model on learning)

One way of studying desensitization is to examine the brains of former drug addicts after death. These post-mortems reveal a reduced density of dopamine receptors compared to normal brains

EVALUATION

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Substantial Empirical Support (A03 - Reliability) Considerable research evidence to support the role of various brain structures and pathways in addictive behaviour

Methodological problems (A03 – Internal Validity)•Difficult to infer causality from post-mortem studies of human addicts•Animal experiments subject to usual ethical issues associated with use of animals generally•Difficulties in interpreting behaviour of organisms that cannot communicate feelings (inferences made from their overt behaviour)

A reductionist Approach (A03 - Reductionism)Biological approach ignores non-biological factors. Implies identification of brain structures and functions fully explain addiction when they do notBecause same brain activity triggered when addicts not directly involved in addictive behaviour as when they are suggests psychological factors are also involved.Neurobiological approaches are reductionist because they exclude non-biological factors such as conditioned responses and cognitive processes

EVALUATION OF THE BIOLOGICAL APPROACHActivity: Complete the following Evaluations from Page 397 of

textbooks

Finish evaluation with research support – at home..

Some sample .. exam questions

a) Outline the systems involved in the ‘common reward pathway’ (10 marks)

b) Evaluate the biological model of addictive

behaviour (14 marks)

a) Outline the systems involved in the ‘common reward pathway’ (10 marks)

“The key area of the brain’s reward system is the pathway extending from dopamine producing neurons in the Ventral Tegmental Area (VTA) in the mid brain, to dopamine sensitive neurons in the Nucleus Acumbens (NA) deep beneath the frontal cortex – also known as the Universal Addiction Site. The neurons in the VTA send messages to other brain regions like the pre-frontal cortex (PFC) as well as to the NA. These regions are known as the ‘Common Reward Pathway’ and their activation is experienced as pleasurable and reinforcing this is important in understanding what causes the initiation and maintenance of addictive behaviours.

The VTA-NA pathway acts as a ‘rheostat of reward’ telling other brain centres how rewarding an activity is. PET scans show that the NA in cocaine addicts ‘lights’ up when shown stimuli of people snorting cocaine. The ‘memory’ of these sensations partly explains maintenance of drug-taking…

Continued..

..These brain centres help our understanding of how addiction is initiated and maintained. Chronic drug use can induce changes in the structure and function of these reward system neurons and these changes can contribute to tolerance, dependence and craving – a process called downgrading. This results in stress, characterised by withdrawal symptoms like anxiety; resulting in a negative state causing the user to continue taking substances to achieve pleasure (positive reinforcement) and to avoid a negative state (negative reinforcement).

Addiction also changes the function of the Prefrontal Cortex in judging the consequences of actions. Claridge and Davis state impairment to PFC causes addicts to choose immediate rewards even if the consequences are negative. However whether there is a genetic fault with the PFC causing addiction or whether the fault is a result of addictive behaviour is unclear. Jentsch and Taylor 1999 found addicts show a reduced ability to self-regulate their behaviour and lose inhibitions, as well as being unable to adapt to new situations because of prior conditioned responses.”

b) Evaluate the biological model of addictive behaviour (14 marks)

“The Biological model of addictive behaviour’s features heavily in the nature versus nurture scientific debate as its’ reliance on using genetics and brain bio-chemistry to explain addiction comes into conflict with the behaviourist ‘environmental’ view of addiction. The use of family and twin studies has been made to demonstrate a genetic factor in the initiation to addiction. Heritability estimates of 50 – 60 % contribute to the development of alcohol dependence (McGue, 1999). In addition, Kendler et al (2000) researched twins and round a common genetic factor contributed to the total variance in alcohol dependence and drug dependence. They concluded that genetic influence on addictions reveals itself in a predisposition towards behaviours that can lead to drug and alcohol dependence. There is considerable research evidence to support the role of bio-chemistry (i.e. various brain structures/pathways) in addictive behaviour (many using animals).

Banks et al (2008) showed success in addictive research by treating monkeys ‘on cocaine’ with a substitute drug that was less addictive but mimicked the action of cocaine…

Continued..

• However the external validity of animal research has been criticized. Hackam and Redelmeier (2006) argue that translating information from animal studies to humans is speculative. Even high quality animal research does not replicate in human research. In addition ethical issues are associated with animal use, as well as the fact that only overt behaviour can be assessed as they cannot communicate feelings. There are also problems with post mortem studies of human addicts because it is not possible to infer causality (did the addiction cause changes in the brain or did inherited brain problems cause the addiction). The biological model cannot explain individual differences.

• For example, why some people become addicted but why others, who have the same environment and life pressures, do not. The diathesis stress model goes some way to explaining this suggesting that people with genetic predisposition combined with stressful life events makes them more vulnerable to becoming addicts. This model can also explain why people are resistant to treatment and likely to relapse.

Continued..

Volkow (2001) found that individual differences are clear when using a drug that lifted dopamine levels – some volunteers liked the rush given and some hated it. In the former, brain scans showed these volunteers had fewer dopamine receptors and concluded that those who hated it had a brain circuitry that couldn’t take the additional stimulation…

It is has been claimed (Smith, 1998) that the model is reductionist because complex addictive behaviours are reduced to a relatively simple level of explanation. Reducing addiction to the action of brain structures or specific genes ignores other non-biological factors such as cognitive processes (irrational thoughts) social and environmental influences, e.g. the Learning model shows that mere anticipation of addictive behaviour can trigger the same brain activity as when they are directly involved.

Or…Potential Answer to a)

• The common reward pathway is initiated by the brain’s Ventral Tegmental Area (VTA) where the neurotransmitter dopamine is produced. Dopamine production is stimulated here by the use of addictive behaviours, e.g, drugs. Dopamine is transmitted via the amygdala to the Nucleus Acumben’s Area (NA) where food/drink intake is affected (i.e. usually reduced). Neurotransmitter transmission also affects the Prefrontal cortex (PFC) where cognitive functions such as memory, language and decision making are dealt with. In addictive behaviours this explains the maintenance of behaviour as memory reminds the person of the dopamine ‘high’ and can be responsible for them relapsing

Other exam questions

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Total for this question: 24 marks(a) A recent large survey on behalf of the Gambling Commission

provided a number of interesting findings about gambling behaviour in Great Britain. For example, 57% of the population had gambled on the National Lottery Draw in 2007, although the rate of problem gambling in the adult population was only about 0.6%.

(i) Explain some of the difficulties of gathering data about problem gambling. (5 marks)

ii) Outline and evaluate one explanation of gambling addiction. (4 marks + 6 marks)

b) ‘The relapse rate for smokers in the first three months after trying to give up is estimated at 70%.’Discuss reasons why relapse occurs in people with addictive behaviour (4 marks + 5 marks)

Plan

i)Stigma- problem gambling is a socially sensitive problem whereby people might not want to disclose it..

so .. Social desirability bias – (less inclined to give full disclosure of problem gambling condition

And low reliability of results

Discuss reasons why relapse occurs in people with addictive behaviour. (5 marks + 5 marks)

• Relapse – describe

• Describe Behavioural or cognitive or biological explanation

• Compare this with the others using research

• Criticise research findings..

• First part must be put in context – answers not in context did not attract many marks (max basic = 2)

• Outline and evaluate – balance of answer should be thought about. Depth vs. breadth (can do ‘learning theory’ or ‘classical conditioning’ or if you prefer could do just one personality factor. This is fine as long as the candidate writes enough to attract the marks.

• It might be harder to get high band marks if you choose the depth approach as it may be that it is more difficult to includes issues and debates etc.

• Could include general approach or limit it to initiation, maintenance/relapse.

• If question asks for reasons it means at least two – candidates must take notice of this requirement.

• Just because the q was about smoking it didn't mean that they only have to write about this – the stem is just designed as a stimulus to get them started.

• For AO2/3, studies, individual differences, and methodology as well as practical implication can be discussed.

• Reasons for smoking addiction (AO2 = 6)

• Theory of reasoned action (AO1 = 5)

• Public health interventions (AO1 = 4)

• Effectiveness of PH interventions (AO2/3 = 10)

Other sample EXAM questions

Outline a key research study carried out to investigate the physiological effects of gambling behaviour (3 + 3 marks)

  

 

Group 1 - Outline and evaluate one explanation (biological-genetics) of gambling addiction (4 + 6 marks)

Half-term 2013 A2 Psychology homework

Group 2 -Outline the systems involved in the ‘common reward pathway’ (10 marks)

Group 3 - Evaluate the biological model of addictive

behaviour (14 marks)

Possible Plans..

PLAN 1. Outline and evaluate one explanation (biological-genetics) of gambling addiction (4 + 6 marks)

• Method - Twin studies - look for differences – explain why..

(genetic structure of people with and without addictive behaviours.) • Initiation = Describe Mpdz gene and DRD2 (dopamine receptor

D2).• A variant to the D2 dopamine receptor (D2A1) has been found to be

more prevalent in pathological gamblers compared to the general population.

• Maintenance = The ‘buzz’ of winning appears to be mediated by a number of neurotransmitters.

• Research- A US study by Kendler (2000) found that concordance rates -both twins using, abusing, or being dependent on drugs- were higher for identical than fraternal twins.

• Heath, 2000 also lends support to this idea….• However.. Han et al (1999) study of over 300 MZ twins and 200

same sex DZ twins concluded that the major influences on the decision to use substances was environmental rather than genetic.

PLAN 2 - Outline the systems involved in the ‘common reward pathway’ (10 marks)

Initiation & maintenance •The neurotransmitter dopamine plays a major role in addiction. •Increased levels of dopamine are associated with pleasure. The desire for the rewarding pleasurable feeling accounts for the maintenance of addictive behaviours. •Rewarding experiences, such as smoking, trigger the release of dopamine and effectively telling the brain ‘to do it again”•Describe process of VTA-NA pathway including; dopamine release, amygdala-memory, NA-evolutionary area, VTA-pleasure, PFC-planning actions

Relapse •Cues for relapse – cravings e.g. smoking – smell, finishing eating, others smoking. Gambling – adverts, sporting pages in a newspaper, sports on TV

PLAN 3 - Evaluate the biological model of addictive behaviour (14 marks)

Substantial Empirical Support (A03 - Reliability)

•Considerable research evidence to support the role of various brain structures and pathways in addictive behaviour

Methodological problems (A03 – Internal Validity)

•Difficult to infer causality from post-mortem studies of human addicts

•Animal experiments subject to usual ethical issues associated with use of animals generally

•Difficulties in interpreting behaviour of organisms that cannot communicate feelings (inferences made from their overt behaviour)

A reductionist Approach (A03 - Reductionism)

•Biological approach ignores non-biological factors. Implies identification of brain structures and functions fully explain addiction when they do not

•Because same brain activity triggered when addicts not directly involved in addictive behaviour as when they are suggests psychological factors are also involved.

•Neurobiological approaches are reductionist because they exclude non-biological factors such as conditioned responses and cognitive processes

Explaining individual differences

•Genetic explanations can explain why some people become addicted yet others who have the same environmental factors do not. Some people are more vulnerable to develop an addiction because of their genetic disposition.

DRD2 Gene

•This gene occurs in alcoholics and pathological gamblers as well as individuals who have Tourette’s syndrome and autism. This poses a problem for the idea that DRD2 is a ‘reward’ gene because individuals with Tourette’s syndrome and autism are not thought to be particularly ‘pleasure seeking.’

Now..

• Complete this summary mindmap ..

Biological model-Genes-Twins-Pathway-VTA-NA + MDP

Initiation MaintenanceRelapse

1. Models of addictive behaviour

Addictive Behaviour

Cognitive model-RP model

Behavioural (Learning) model-classical cond.-operant cond.

2. Vulnerability to addiction

3. Reducing addictive behaviour

PersonalityPeersAgeStress

Media Influences

Models of prevention

TRA / TPB/ HBMBiologicalpsychological

Public Health + legislation

Types of intervention