Transcript 1 Biological model 2013 - Psychology: Teaching and Learning

Unit 4
PSYA- 4
1
Exam Specification for this topic area
1. Models of Addictive Behaviour
2. Vulnerability to addiction
3. Reducing Addictive Behaviour
Biological,
cognitive
and
learning
approaches
to
explaining
initiation,
maintenance and relapse, and their
applications to smoking and gambling
Risk factors in the development of addiction
including;
Personality
Peers
Age
Stress
Media influences on 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
2
But first ….. A message..
“Research Methods
feature heavily in all
elements of addictive
behaviour and needs
to be integrated in all
essaysso learn them well you
will.”
1. Models of Addictive Behaviour
•Biological, Cognitive & Learning modelsincluding; initiation, maintenance & relapse
•Explanations for specific addictions; smoking &
gambling
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
6
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.
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 [email protected]
9
Biological Model
10
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
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).
 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 antisocial personality traits and these traits and
alcoholism. Similar findings have been claimed for
behavioural addictions such as gambling (Coming et
al 1996).

Some people are more
likely to develop an
addiction because of their
genetic predisposition.
Other research
It may be that people who are sensitive to
addiction have inherited a more sensitive
mesolimbic dopamine pathway – Liebman and
Cooper 1989. 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.
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.
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)
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..
 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)
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
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
25
 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).
Relapse
Idea of genetic
vulnerability to
addictions may
explain why some
people are more
resistant to
treatment and more
likely to relapse
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
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)
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 BrainNeurobiological approach
The brain gets “Hi-jacked”
By a “need” to engage in
addictive activities…
I really
need a
drink..
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
NEURAL PATHWAYS IN
THE BRAIN..
Responsible for maintenance
of addiction
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)
From last year…
Key features of the biological approach to abnormality
Biological Approach
All mental illnesses have
a physical cause
Genetic inheritance
Mental illnesses can be
described and diagnosed
in terms of clear-cut
symptoms
Biochemistry
ICD 10
Infection
Brain damage
DSM IV
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.
Initiation and 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 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.’
Brain
imaging..
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
“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.
Time for some drawing…
Insert the following into the ‘addicted’ brain in your
learning pack;
Common Reward Pathway
Pre-Frontal Cortex
Amydala
The VTA-NA ‘common reward’
pathway
“Addicted” Brain
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).
Amygdala
Dopamine movement
“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)
• 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
The Common Reward Pathway
VTA
NA
Amygdala and prefrontal cortex
Watch video
Video clip
Reward pathways
4mins 52 secs
51
The Role of the Pre-Frontal
Cortex (PFC)
Pre-Frontal Cortex (PFC) - RELAPSE
The PFC, which is involved in decisionmaking 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.
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.
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).
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).
Also….
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
Utube CLIPS..
Video 1
Video 2
Video 3
59
Additional info..
Explaining Tolerance
Watch video
SENSITISATION AND DESENSITISATION
Excessive activation and chronic movement beyond its natural, balanced
state causes neurochemical changes to occur in the brain
1min12 secs
Desensitisation
1. Neural mechanisms become more and more tolerant as
addiction progresses
2. 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 behaviour
5. 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.
61
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
EVALUATION
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 nonbiological factors such as conditioned responses and cognitive processes64
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 biochemistry 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
74
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)
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..
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.
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.
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)
Other sample EXAM questions
Outline a key research study carried out to
investigate the physiological effects of gambling
behaviour
(3 + 3 marks)
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)
Possible Plans..
PLAN 1. Outline and evaluate one explanation (biologicalgenetics) 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, PFCplanning 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 ..
Cognitive model
-RP model
Behavioural
(Learning) model
-classical cond.
-operant cond.
Biological model
- Genes
- Twins
- Pathway
- VTA-NA + MDP
Personality
Peers
Age
Stress
Initiation
Maintenance
Relapse
1. Models of addictive
behaviour
Media
Influences
2. Vulnerability to
addiction
Addictive Behaviour
3. Reducing addictive
behaviour
Types of
intervention
Models of prevention
TRA / TPB/ HBM
Biological
psychological
Public
Health +
legislation