1. The Psychology of Addictive Behaviour
Unit 4 PSYA- 4

2. Exam Specification for this topic area
1. Models of Addictive Behaviour
Biological, cognitive and learning approaches to explaining initiation, maintenance and relapse, and their applications to smoking and gambling
2. Vulnerability to addiction
Risk factors in the development of addiction including;
Personality
Peers
Age
Stress
Media influences on addictive behaviour
3. Reducing Addictive Behaviour
Models of prevention, including
Theory of Reasoned Action
Theory of Planned Behaviour
Health Belief Model
Types of intervention, including
Biological
Psychological
Public Health Interventions and legislation and their effectiveness

3. But first ….. A message..

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

5. 1. Models of Addictive Behaviour
Biological, Cognitive & Learning models-
including; initiation, maintenance & relapse
Explanations for specific addictions; smoking &
gambling

6. Definition of ADDICTIVE BEHAVIOUR
"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)
Watch video

7. initiation, maintenance and relapse
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..

8. Maintenance – factors that keep the behaviour continuing
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.

9. 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 to your teacher
View next lesson
address

10. Biological Model 10

11. Two explanations..
Genetics
Hijacked brain

12. Activity- Powerpoint pres.
Role of Genetics to explain gambling + evaluation - IMR
Role of Neurobiological (“high-jacked brain”) to explain smoking i.e. dopamine/VTA-NA neural pathway + evaluation - IMR
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

13. FOR INFO..

14. 1. GENETICS

15. Biological model – initiation 2
Some adoption studies (e.g. Heath, 2000) lend support to the idea that there is a genetic component in addiction.
A US study by Kendler found that concordance rates -both twins using, abusing, or being dependent on drugs- were higher for identical than fraternal twins (see chart on next slide).

16. Genetics
 There are two main ways of investigating genetic factors in human behaviour.
To study family relationships including twin studies.
To carry out genetic analysis and look for differences in the genetic structure of people with and without addictive behaviours.

17. Twin Studies
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.

18. Genetics
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).

19. Some people are more likely to develop an addiction because of their genetic predisposition.

20. Other research
It may be that people who are sensitive to addiction have inherited a more sensitive mesolimbic dopamine pathway – Liebman and Cooper The reward pathway functions in much the same way in mice as it does in people. When researchers discover a gene in mice that plays a role in addiction, they can then identify the counterpart gene in humans by comparing DNA sequences.

21. Other research
Increased expression of the Mpdz gene results in mice experiencing less severe withdrawal symptoms from sedative-hypnotic drugs such as barbiturates.
Mice bred to lack the serotonin receptor gene Htr1b are more attracted to cocaine and alcohol.

22. Other research
Disease model – reward centre in brain stimulated by addictive drugs (mesolimbic pathway). Incentive sensitisation theory (Robinson and Berridge, 1993) – repeated exposure leads to increased sensitivity to drug desirability.
The opioid system may also be implicated in addiction (encephalin and endorphins). These systems may be directly stimulated by drugs such as heroin, alcohol and nicotine. (e.g. Krishnan-Sarin et al 1999)

23. Biological explanations of gambling
Twin 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..

24. 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)

25. Activity: Complete this research study under the following headings
Aim:
To investigate the effect of gambling on cardiovascular (heart rate) endocrine activity
Procedure
Ten 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 gambling
Relevance of increased cortisol for maintenance of gambling unclear
Gambling enhances mood – cortisol may contribute to mood alteration
Meyer et al (2004) study - 25

26. Specific Genes
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).

27. Relapse
Idea of genetic vulnerability to addictions may explain why some people are more resistant to treatment and more likely to relapse

28. Smoking initiation and maintenance
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
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. 28

29. Biological Factors
There 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)

30. Evaluation of Genetic explanations
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.’

31. Evaluation of Genetic explanations
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

32. 2. Hi Jacked Brain- Neurobiological approach

33. The brain gets “Hi-jacked”

34. By a “need” to engage in addictive activities…

35. I really need a drink..

36. DEFINITION of ‘hijacked’ - effect of addictive substances on
THE HI-JACKED BRAIN
DEFINITION of ‘hijacked’ - effect of addictive substances on
normal 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. 36

37. NEURAL PATHWAYS IN THE BRAIN..
Responsible for maintenance of addiction

38. 11) “Outline and evaluate the Biological model as an explanation
Exam Question January 2011
Topic: 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)

39. From last year…

40. Key features of the biological approach to abnormality
All mental illnesses have a physical cause
Mental illnesses can be described and diagnosed in terms of clear-cut symptoms
Genetic inheritance
Biochemistry
ICD 10
DSM IV
Infection
Brain damage

42. Neurotransmitters
Nerve cells
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.

43. Neurotransmitters, Pleasure Centres and Reward Pathways
Initiation and maintenance
Neurotransmitters, Pleasure Centres and Reward Pathways
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.’

44. Brain imaging..

45. (CLARIDGE AND DAVIS, 2003) Box 9.1 Pages 392 – 393 Textbook
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 45

46. “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 regions
that 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.

47. Time for some drawing… Insert the following into the ‘addicted’ brain in your learning pack; Common Reward Pathway Pre-Frontal Cortex Amydala

48. “Addicted” Brain The VTA-NA ‘common reward’ pathway
Prefrontal cortex (PFC)
Part of the frontal lobe that is involved in many cognitive functions, including memory, language and decision making.
Striatum
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 including
cocaine, amphetamine,
cannabinoids (e.g cannabis)
and opioids (e.g. heroin).
Ventral Tegmental Area– (VTA)
Found in the midbrain, this
area produces dopamine
and forms part of one of four
major dopamine pathways in
the brain. Affected by drugs including; nicotine, alcohol and opioids (e.g. heroin).
Dopamine movement
Amygdala

49. Dopamine binding to receptors in the nucleus accumbens (NA)
“Common – Reward” or “VTA-NA” Pathway
Dependence maintenance
The Ventral Tegmental Area sends neuron projections into the medial forebrain connecting to the Nucleus accumbens, amygdala and Pre Frontal Cortex.
Stimulation of the VTA, NA, amygdala and PFC areas collectively, produces pleasure and reinforcement of that behaviour.
Most drugs (such as nicotine which is a psychoactive drug) and activities such as gambling release dopamine into the NA area, prompting the incentive to continue and increase the behaviour.
Dopamine binding to receptors in the nucleus accumbens (NA)

50. 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

51. The Common Reward Pathway
VTA NA
The Common Reward Pathway
Amygdala and prefrontal cortex
Watch video
Video clip
Reward pathways
4mins 52 secs 51

52. The Role of the Pre-Frontal Cortex (PFC)

53. Pre-Frontal Cortex (PFC) - RELAPSE
The PFC, which is involved in decision-making and the inhibition of risky behaviours is impaired in addicts, allowing them to choose immediate rewards even in the face of long term negative consequences.
Continued over-production of dopamine leads to desensitisation in receptors to compensate. This leads to increased desire to engage in the addictive behaviour to return to the same level of ‘dopamine high’ i.e. the person is becoming tolerant.
Drives the addict to do anything necessary to obtain a fix.

54. PFC
Long term exposure to drugs/alcohol can lead to a reduction in the reward pathway activity (this is called downregulation). This results in withdrawal symptoms.

55. Relapse..
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).

56. Cues for RELAPSE - Cravings
The negative withdrawal state then results in drug cravings – the user is not trying to get positive reinforcement but to avoid the bad feelings (many smokers say this is how they feel – they don’t smoke to make them feel better, rather it is to stop them feeling bad).

57. Also….

58. Other CUES for RELAPSE..
Cues that may cause an addict to relapse for smoking and gambling addictions.
Smoking – smell, finishing eating, others smoking
Gambling – adverts, sporting pages in a newspaper, sports on TV

59. Video 1
Video 2
Video 3
Utube CLIPS.. 59

60. Additional info..

61. SENSITISATION AND DESENSITISATION
Watch video
Explaining Tolerance
SENSITISATION AND DESENSITISATION
Excessive activation and chronic movement beyond its natural, balanced
state causes neurochemical changes to occur in the brain
1min12 secs
Desensitisation
Neural mechanisms become more and more tolerant as
addiction progresses
Prolonged and repeated increases in extracellular dopamine
causes the brain to compensate for the excessive stimulation
by changing its function in some way
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 behaviour
The individual needs larger and more frequent doses to achieve the initial or desired
effect of the behaviour.
Reduced activity in the PFC also occurs – This reduced activity makes it difficult for
addicts to resist impulses to use drug, nicotine etc. 61

62. 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 62

63. EVALUATION

64. EVALUATION OF THE BIOLOGICAL APPROACH
Activity: Complete the following Evaluations from Page 397 of textbooks
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 64

65. Finish evaluation with research support – at home..

66. 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)

67. 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…

68. 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.”

69. 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…

70. 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.

71. 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.

72. 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

73. Other exam questions

74. 74

75. Complete this exam question
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)

76. 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

77. Describe Behavioural or cognitive or biological explanation
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..

78. Comments from examiners
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.

79. Comments from examiners
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.

80. Exam questions Reasons for smoking addiction (AO2 = 6)
Theory of reasoned action (AO1 = 5)
Public health interventions (AO1 = 4)
Effectiveness of PH interventions (AO2/3 = 10)

81. Other sample EXAM questions
Outline a key research study carried out to investigate the physiological effects of gambling behaviour (3 + 3 marks)   

82. Half-term 2013 A2 Psychology homework
Group 1 - Outline and evaluate one explanation (biological-genetics) of gambling addiction (4 + 6 marks)
Group 2 -Outline the systems involved in the ‘common reward pathway’ (10 marks)
Group 3 - Evaluate the biological model of addictive behaviour (14 marks)

83. Possible Plans..

84. 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.

85. 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

86. 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.’

87. Now..
Complete this summary mindmap ..

88. Addictive Behaviour Models of prevention 2. Vulnerability to
Cognitive model
-RP model
Behavioural (Learning) model
-classical cond.
-operant cond.
Media Influences
Personality
Peers
Age
Stress
Initiation
Maintenance
Relapse
Biological model
Genes
Twins
Pathway
VTA-NA + MDP
2. Vulnerability to
addiction
1. Models of addictive behaviour
Addictive Behaviour
3. Reducing addictive
behaviour
Models of prevention
Types of intervention
TRA / TPB/ HBM
Public Health + legislation
Biological
psychological