Addiction - A2

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  • Created by: Simba2604
  • Created on: 07-09-17 19:43

Describing addiction

Addiction is:

  • repetetive habit pattern that increases risk of diseases and associated personal + social problems
  • experienced subjectivity as a "loss of control"

= habit patterns give immidiate gratification -----> short term reward

= habit patterns couple with delayed deletrious effects -----> long term costs

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Addiction key terms

Dependancy = the need for a substance/behaviour

  • physical dep = refers to "withdrawal" side. Substance is needed for normal body functions
  • psychological dep = cognitive side (craving) where the individual experiences a mental desire for that behaviour or substance

Tolerance = how much substance/behaviour needed to recieve same effect ---> to be satisfied

  • metabolic tol = how quickly body breaks down and gets rid of substance
  • cellular tol = synaptic changes eg. smoking cig may release dopamine then dopamine receptors become desensitised so more cigs needed to recieve that same effect

Homeostasis = body's tendancy to maintain all its systems in a balanced state for optimal functions

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Withdrawal

Term "withdrawal" refers to the abstinence of use

withdrawal:

  • occurs because body has adjusted in order to counteract effects of substance so, in the absence of the substance there are negative experiences that can ony be overcome by taking or substituting the substance or alternatively, "riding it out"
  • physical withdrawal ---> often opposite effects of effects induced by substance eg. depression in the absence of a stimulant

withdrawal depends on:

1) drug used - each drug has half life (time needed to fully exit body), shorter half life = worse withdrawal

2) amount consumed - larger amounts associated with more intense symptoms

3) drug use pattern - frequent substance use = in body most of time ---> physical dependancy + worse withdrawal

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Synaptic transmission

synaptic transmission = process by which one neuron communicates with another

1) Action potential reaches end of a axon and can travel no further so must travel over synaptic gap

2) nerve impulse is transferred into a chemical message (neurotransmitter) which its contents are released by synaptic vessicles

3) neurotransmitters then carry the signal across the synaptic gap

4) they now bind to the receptor sites on the post synaptic cell

  • if there are more excitatory neurons releases then they trigger a positive change
  • if there are more inhibitory neurons then they trigger a negative change
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Desensitisation hypothesis - Acetylcholine

Researcher = Dani + Heinemann (1996)

Focuses on brain neurochemistry ---> particularly neurons in the brain that produces the neurotransmitter acetylcholine (ACh)

Acetylocholine receptors allow communication across synapses to take place. In neurotransmission, when enough ACh molecules bind with receptors, an electrical impulse is able to continue from one neuron to another. One subtype of ACh is called nicotinic receptor (nAChR), this can bind with ACh and nicotine:

1) ACh molecules bind with the receptors creating an action potential (electrical impulse)

2) Subtype nAChR (nicotinic receptor) binds with both ACh and nicotine

3) Neuron becomes stimulated

4) Immediately after, nicotine receptors shut down and don`t respond to neuroTs (down regulation and desensitisation of the neuron)

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Desensitisation hypothesis - Dopamine

Nicotine addiction occurs because the process triggers release of another neurotransmitter           ---> dopamine

Dopamine creates rewarding and peasurable effects:

  • mild euphoria
  • increased alertness
  • reduction of anxiety

1) nicotine triggers production of dopamine in the nucleus accumbens, which is the reward centre in the brain and part of the mesolimbic system

2) this increases activity in the PFC, which is the common reward pathway

3) constant production of dopamine leads to desensitsation and tolerance

Dopamine is released ---> get used to it ---> chronic desensitisation/metabolic tolerance developed ---> need to up dosage as previous dosages no longer have an impact

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Nicotine regulation model

Nicotine regulation model:

1) smoker goes wihout nicotine for a prolonged period eg. sleep

2) nicotine gets metabolised and disappears out of the body

3) this allows ACh receptors to become functional (upregulation) and neurons to become sensitised again

4) the consequence of this is that there are high levels of ACh in the brain, leading to withdrawal symptoms such as anxiety ---> smoker is thus motivated to avoid upleasant feelings by continuing smoking behaviour

= This is why smokers often describe their first cigarette of the day as the most enjoyable because it follows a period of abstinence. The whole daily cycle of morning upregulation and night time downregulation begins again.

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Neurochem approach evaluation1

real life application in the treating of nicotine addiction as it has led to the development of nicotine replacement therapy (NRT) ---> gradually reduces amount of nicotine given to reduce withdrawal symptoms

+ studies show 50-70% reduction in relapse rate 

- NRT does not have 100% reduction in relapse rate ---> neurochemistry cannot be said to be the only factor that affects nicotine addiction 

approach can be said to be reductionist = breaks down complex behaviour (addiction) into a simple concept of neurochemistry 

+ this allows specific treatments to be developed and allows scientific and objective testing.

- fails to acknowledge social and psychological influences such as peers, social smoking, stress

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Neurochem approach evaluation2

biologically deterministric = we have no free will/choice over whether we develop nicotine addiction or not instead isdetermined by neurochemistry in particular, ACh + dopamine

+ predicts causal relationship + allows precise treatment to overcome the addiction (eg. NRT) 

- believing in lack of control may lead individuals lacking motivation to change behaviour or high relapse rates due to approach remiving reponsibility 

Approach does not consider individual differences = assumes everyone reacts same to nicotine however social smokers experience up/down regulation but do not experience withdrawal or repeat behaviour next day

- must be other causal factors that play role in initiation + maintenance of nicotine addiction

approach falls on nature side of nature/nurture debate = states that addiction is purely a result or neurochemistry make up

- nature cannot explain why individuals choose to initiate smoking behaviour whereas SLT (nurture) may explain this as smoker may hevae learned behaviour thru observation/modelling

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Learning theory of nicotine addiction

Initiation:

  • SLT suggests that individuals who observe others smokers will learn how to smoke themselves after seeing the rewards of that behaviour
  • if smokers are percieved to be reinforced for their behaviour through any rewards (VR) then they may come to imitate behav themselves in the hope of similar rewards
  • such rewards may be popularity, attention of improved image
  • this process is known as vicarious reinforcement

Maintenance:

  • smoking is maintained through operant conditioning
  • pleasureable feelings gained through release of dopamine from nucleus accumbens and, acts as positive reinforcer for addict and thus encourages them to smoke
  • over time, maintenance phase driven by urge to avoid withdrawal symp (eg. stress)
  • form of neg reinforcement as smoker smokes to remove/avoid a negative outcome and so smoking is now no longer for pleasure, but rather a necessity
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Learning theory of nicotine addiction2

Relapse:

  • cue reactivity is a type of CC that can be used to explain relapse.
  • this is because the person associates conditioned stimuli such as specific moods, situations or environmental factors (smoking-related cues) with the rewarding effects of nicotine
  • these cues makes quitting difficult and but can also trigger a relapse as they are constantly in the former smoker's environment
  • alternatively, OC can proposes that relapse can be explained through negative reinforcement as the individual wishes to avoid the unpleasant symptoms of withdrawal as these can last for weeks
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Learning theory nicotine addiction evaluation

+ explanations of nicotine addiction through CC and OC have led to development of successful treatments such as Cue exposure and so has real life applications

- theory cannot account for individual differences in relapse as all addicts who attempt to stop are exposed to cues and withdrawal symptoms then attempting to quit however, learning explanations are not able to explain why some are successful and others not

- behaviourist approach is also reductionist as does not consider the role of biology and genetic vulnerability to addiction for which there is strong research evidence

----> also ignores role of cognition and the free will to override urges as well as social contexts

- ppl are presented as simple stimulus response response machines seeking only "rewards" and this is deterministic as it assumes all behaviour is driven for this purpose

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Cog theory of gambling addiction

Cognitive model emphasises the habitual ways of thinking and interpreting events which guide behaviour

Cognitive distortions or maladaptive through processes may lead to inflation + maintenance of addictive behaviour.

Initiation:

  • Duncan's self-medication hypothesis suggests addicts with drug addictions use drugs to help them escape from ongoing state of distress
  • non-drug addictions such as gambling represent similar negatively reinforced behaviour by providing relief from emotional distress

---> if gambling does help relieve boredom or stress then individual is likely to continue to gamble maintaining the addiction

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Cog theory of gambling addiction2

Maintenance:

  • Wagenear (1988) reviewed literature and argued that gamblers gamble because their reasoning in distorted in many ways

Types of cog bias:

  • Availibility = memories of wins can be recalled from memory easier than losses
  • Illusion of control = gamblers feel they have power to exert control over uncertain outcome
  • Confirmation bias = focusing on info that is consistent with belief (being lucky)
  • Flexible attribution = gambler explains wins due to skill + losses due to influence of others
  • Concrete info bias = gambler focuses on events eg. big wins and downplays statistical facts or calculations of losses
  • Hindsight bias = gamblers look back + report they expected a big win/loss ---> gives feeling of control ---> justifies future gambling
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Cog theory of gambling addiction3

Maintenance:

  • Wagenear (1988) reviewed literature and argued that gamblers gamble because their reasoning in distorted in many ways

Types of cog bias:

  • Availibility = memories of wins can be recalled from memory easier than losses
  • Illusion of control = gamblers feel they have power to exert control over uncertain outcome
  • Confirmation bias = focusing on info that is consistent with belief (being lucky)
  • Flexible attribution = gambler explains wins due to skill + losses due to influence of others
  • Concrete info bias = gambler focuses on events eg. big wins and downplays statistical facts or calculations of losses
  • Hindsight bias = gamblers look back + report they expected a big win/loss ---> gives feeling of control ---> justifies future gambling
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Cog theory of gambling addiction evaluation

+ considers that individual differences are important in the formation and maintenance of an addiction whereas other explanations struggle to explain why people's thinking differs

----> therefore, cog explanations are not deterministic unlike bio explanations as they account for ppls ability for conscious thought

+ has real life applications as cog therapy can successfully address faulty thinking to reduce addictive behaviour

- cog theories do not tell us WHY ppl have maladaptive thinking, bio explanations come in and explain that maladaptive thinking occurs because of biochemical imbalances such as dopamine which is released during gambling then gambling becomes viewed in a positive light

- a combined approach between cog and bio explanations may be better suited to gve a more holistic explanation of gambling addiction

- not clear whether cog bias or irrational thoughts are cause or result of gambling therefore, is a telelogical argument

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Expectancy theory + self efficacy

 Expectancy theory = believes ppl initiate an addictive behaviour because they expect it to have a certain outcome

  • addicts believe their behaviour will have + outcome ---> "winning big" 
  • non-addicts believe behaviour will have - outcome ----> loss 

Addicts often deny they have serious problem and may not understand concerns/grievances of others ---> feel treated unreasonably

Self-efficacy:

  • refers to expectations that we have ability to behave in a way that achieves a desired outcome
  • may explain why ppl relapse into gambling after abstaining as they do not believe they are capable of giving up permanently ---> sets up SFP
  • Self fulfilling prophecy ---> behave in a way that then confirms expectations
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Extended knowledge

Factors helping to share an individual's attitude towards gambling:

  • social learning experiences
  • vicarious + participatory exposure to familial + peer related gambling
  • media representations eg. betting ads
  • religiosity + cultural influences
  • personal influences/experiences

Cog regret:

  • regret over ceasing prematurely and missing out on next win
  • concept of cog regret is linked to ratio schedules of reinforcement where next trial unpredictably might result in reward

Thinking aloud technique:

  • where verbalisations during play are audio ---> recorded + analysed for content
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Extended knowledge continued

Gambler's fallacy:

  • belief that a win is due following a series of losses ---> manifest this understanding of the law of averages + law of large numbers

Entrapment:

  • where one is motivated to maintain a course of action having already invested so much to date

Research into verbalisation of gamblers:

  • found that up to 80% of verbalisations made ...
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Learning theory of gambling addiction1

key terms:

  • reinforcement - consequence of behaviour that increases likelihood of being repeated (+/-)
  • partial reinforcement - when behaviour is reinforced only some of the time it occurs (winning at random intervals)
  • variable reinforcement - behaviour is reinforced after unpredictable period of time or number of responses

Initiation:

  • Vicarious reinforcement (SLT) ---> experience of seeing others being rewarded for their gambling, their pleasure + enjoyment + occasional financial rewards
  • Observations can be direct = seeing rewards from peers or indirect = media eg. betting ad
  • broadcasting glamour and excitement of gambling may be enough to trigger a desire for the same reinforcement in someone who hasn't gambled before
  • ppl learn positive effects of gambling through VR and then engage in the behaviour themselves believing they will have similar positive effects
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Learning theory of gambling addiction2

Maintenance:

  • maintained through operant conditioning (+/-)
  • adrenaline ("buzz") and money gained from winning a bet provides + reinforcement
  • distraction from aversive stimuli like the anxieties of everyday life provide - reinforcement
  • however, when ppl gamble they don't always win ---> should cause gambler to stop (stimulus discrimination)
  • but this is prevented by partial + variable reinforcement
  • Partial reinforcement involves winning at random intervals as ppl would get bored of gambling they won small prizes at set intervals ---> bigger unexpected rewards more effective
  • Variable reinforcement involves behaviour being reinforced after an unpredictable period of time or number of responses ---> gambler learnes that they will not win every gamble but will win eventually if they persist (variable ratio schedule)

= although gamblers generally lose the contiguity of wins and losses may explain why the behaviour is still maintained despite punishment or lack of reward, this is as wins tend to be bigger and immidiate so are "time contiguous" and therefore the association is greater. However, we're also immidiately punished with losses, these are initially small so the over all neg feeling does not occur until there has been series of losses  so the association is not as strong

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Learning theory of gambling addiction3

Relapse:

  • explained through cue reactivity theory (CC)
  • individual encounters numerous secondary reinforcers = stimuli that become reinforcing due to their association with exciting arousal experienced by gamblers
  • Scratch cards, seeing betting ad or slot machine can generate craving
  • cues saturate in social + media environment ---> offer continuous low-level reminders of pleasures of gambling difficult for abstaining gambler to avoid ---> relapse
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Evaluation of learning theory gambling

- reductionist as it does not consider free will but instead, explains a complex human behaviour as a result of patterns and reward, giving the person themselves a seemily passive role in addiction which would lead to  a lack of motivation in an individual and an increase in the likelihood of relapse

+ reductionist approach means that it is scientific therefore, it identifies causal relationship between addiction and the environment to develop more effective treatments

- learning theory takes a nomothetic approach which means that it creates principles that are generalised to everyone and so does not account for individual differences such as people that do not relapse to gambling despite the presence of cues

+ explains conscious conflict ---> OC does not require our conscious thought, this explains why ppl maintain habits without really thinking about it, and why when they relapse they consciously want to stop but feel compelled to

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Reducing addiction - Drug therapy

Drug therapy:

  • based on idea that addictionhas a biological cause
  • therefore, addiction can be treated using medication

- medication usually treats withdrawal symptoms oof addiction rather than cause

- addict may need to stay in clinic while they undergo treatment (time consuming)

Medications:

= work in 2 ways

  • Agonists ---> activates receptors in brain to mimic drug's effects
  • Antagonists---> attached to receptors without activating the therefore, blocking the pleasureable effect of the drug
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Evaluation of drug therapy

+ allows gradual withdrawal from addiction, minimising withdrawal symptoms and therefore, generally more ethical intervention

- does not address underlying cause for addiction which may lead to individual back into addictive behaviour in future

- research suggests that drug therapy is largely insufficient on its own and shoud be combined with psychological interventions to yield best results, however, this may not be possible due to financial restraints on NHS

- administration of agonists may resut in replacing one addiction with another however, substitute is usually less harmful but this is an issue as nothing changes

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Drug therapy for heroin

Heroin:

  • an opium
  • withdrawal effects are often very severe and mainly physical
  • eg. diahrroea, vomiting, shaking, pain etc
  • methadone (heroin substitute) is used to reduce withdrawal symptoms and prevent relapse
  • methadone = syrup with longer half-life than heroin + helps to reduce craving for herouin by keeping drug level in system consistent
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Research support for heroin (methadone)

McLellan et al (1993)

  • investigated whether methadone alone is sufficient as a treatment or whether it should be administered alongside another substance

= found that 69% of addicts given methadone continued to use heroin

= other groups that recieved methadone and other interventions responded far better

  • suggests that methadone is not an effective agonist
  • only 31% reduction suggets that biological factors are not the only factor in gaining heroin addiction and so there must be other factors in the mind (cognitive) or the environment
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Drug therapy for alcohol

Alcohol:

  • a depressant
  • has mild to moderate symptoms ---> headaches, vomiting, insomnia and rapid HR
  • but also more sever symptoms ----> hallucinations, fever and convulsions

Alcohol addiction treatment:

= benzodiazepines are chosen to treat alcohol withdrawal

  • a class of psychoactive drugs that work to slow doen CNS by activating GABA receptos
  • usual regime is 3 days of long-acting benzos

Types of benzos:

  • chlorodiazepide ---> preffered for its superior anticonvulsant capabilities
  • diazepam ---> preffered for its safety against overdose with alcohol
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Research support for alcohol and problems

Malcolm et al (2006)

  • compared recovery rates of alcoholics taking benzo buspirone with those taking aplacebo
  • found that there were no significant differences in the ammount of alcohol consumed or anxiety levels

= suggests that withdrawal symptoms are psychological so it raises questions about whether benzos are effective or not

Problems with benzos?

- potential for dependance + abuse

- symptoms of benzos are quite similar to those of alcohol withdrawal

- only recommended for short term treatment of alcohol withdrawal  

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Drug therapy for nicotine

Nicotine:

  • cessation of smoking is a big industry with nicotine gum, patches, lozenges, sprays and e-cigs all used as a method of nicotine replacement therapy (NRT)
  • NRT provides use with a clean, controlled dose of nicotine that binds to Ach receptors in the mesolimbic pathway stimulating dopamine release in the nucleus accumbens
  • this can be removed over time to manage withdrawal symptoms
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Research support for nicotine

Stead et al (2012)

  • reviewed 150 high quality research studies into the effectiveness of NRT
  • concluded that all forms of NRT are significantly more effective than placebo, with nasal sprays being the most effective
  • NRT clients were 70% more likely to still be abstaining from smoking, 6 months after quitting + also adds validity for neurochem

- however, wasn't 100% so must be individual differences

- used meta-analysis = secondary data ---> so cannot know if all variables were controlled

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Reducing addiction - behavioural interventions

Behavioural interventions:

  • based on the premise that addiction is learned through experience and environmental factors
  • as a result, interventions are based on principles of OC + CC

Aversion therapy:

  • works on principles of CC
  • used primarily with addiction that have biological action ---> alcohol, drugs, nicotine etc
  • aims to break pleasurable association and replace it with a negative one so that the addict no longer desires the substance
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Behavioural interventions evaluation

- AT could be argued to be unethical ---> concerns whether an addict can give consent let alone understand the often extreme adverse consequences of AT such as violent vomiting etc.

+ CD may be more appropriate as it is much more ethical

- however, CD requires motivation of individual to continue the mental imagery, if this individual is not motivated to do this regularly then it will not work

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Aversion therapy for alcohol addiction

  • uses the drug antabuse ---> emetic drug (causes vomiting)
  • Anatbuse (UCS)
  • Vomiting (UCR)
  • when antabuse is given at the same time as alcohol it evokes sickness which becomes associated with it

= means that in future, when alcoholic encounters alcohol they will feel sick even though antabuse is not present

= Alcohol becomes CS and vomiting becomes CR

- aversion therapy is less effective in people who aren't motivated to change behaviour as they could choose not to take antabuse so they can drink

- ethical issues associated with AT ---> no pfph as electric shocks/vomiting is used

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Covert desensitisation

Covert desensitisation:

  • similar to aversion therapy, but in vitro
  • rather than actually experiencing the unpleasant stimulus (shock/vomiting), pps are asked to imagine how it feels

1) client told to relax

2) therapist reads a script instructing the client to imagine an aversive situation whilst they are smoking

= the more graphic, the more effective

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Research support for covert desensitisation

Researcher = McConaghy et al (1983)

  • compare CD and electrical AT a a treatment for gambling addiction
  • 12 months later ---> CD = 79% reported control over gambling compared to AT = 50%

= suggests that not only is CD a more ethical traetment, it is also more effective in the long term

Researcher = Danaher (1977)

  • tested effectiveness of aversion therapy with 50 habitual smokers over 3 weeks
  • As the US, researchers used smoke from cigs + asked pps to inhale deeply till they felt sick
  • this worked well for some but not others

= suggests that there may well be individual differences in efficacy of aversion therapy

- small time frame therefore, not a valid measure of true relapse

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Cognitive interventions

Cog interventions:

  • CBT is built on premise that addiction is a result of maldaptive thought processes
  • therefore, these interventions aim to identify and change this faulty cognition
  • variety of methods/skills are taught to allow the addict to recognise their faulty processing, identify potential triggers to relapse and implement their new skils to overcome potential relapse situations

Cognitive restructuring:

  • all CBT programmes include element of cognitive restructuring to tackle the biases that operate even below the client's level of awareness
  • so in gambling addiction, training addresses the client's faulty beliefs about probability, randomness, control, gains and losses
  • these are confronted and challenged by therapist
  • together, therapist and client develop strategies that help increase self-control etc to deal with cravings
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Cog interventions - skills training

Cognitive restructuring:

  • CBT's cog restructuring to tackle biases that operate below the client's level of awareness
  • so in gambling addiction, training addresses the client's faulty beliefs about probability, randomness, control, gains and losses
  • these are confronted and challenged by therapist

Specific skills:

  • functional analysis reveals client lacks specific skills that prevent them to cope with situations that trigger drug abuse
  • assertiveness training could be used to help client confront interpersonal conflicts in a controlled and rational way instead of using avoidance, manipulation or aggression

Social skills:

  • addicts eg. alcoholics will inevitably meet situations where alcohol is present
  • social skills training helps clients to learn how to refuse the offer or the temptation
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Evaluation of cog interventions

+ research support from Nancy petry et al (2006) where gamblers were treated with CBT and shown to gamble significantly less than the control pps up to 12 months

+ for clients who do stuck with therapy, BCT appears to be especially effective at preventing relapse (motivated clients)

- there are conflicting studies that show no significant differences in outcome between CBT and control groups ---> therefore, CBT is effective in reducing gambling behaviour, but the durability of therapeutic gain is unknown

- Pim Cuijpers et al (2008) indicate that drop-out rates in CBT treatment groups can be up to 5x greater than other forms of therapy ---> lack of treatment adherence is major obstacle to a full understanding of how effective CBT is for reducing addictions

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Evaluation of cog interventions2

+ CBT may yield longer lasting results than other therapies such as drug therapy, because it provides individual with skills + techniques that deal with cog distortions that may underpin maintenance of addiction ---> beneficial because addict can apply skills to handle high risk situations and therefore, deal with with the craving to relapse

+ can be practically applied to treat number of addictions, because precursor to relapse such as the craving/drive to perform/consume a substance or behaviour is similar in each addiction therefore, providing individuals with skills needed to overcome these feelings

  • beneficial because addicts tend to have multiple addictions simultaneously
  • therefore, equipping with skills that can be tailored to suit other addictions which is more empowering + economical than using variety of treatments/prescribing loads of drugs

+ encourages addict to responsibility for behaviour, because they learn that it is only them that can change their maladptive thought processes + cog biases

  • however, could be disadv as it places blame on individual + won't work if patient isn't motivated
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Risk factors of addiction - Genetic vulnerabi

Genetic vulnerability:

  • idea that an individual is more likely to become an addict due to their genetic makeup
  • therefore, anyone with a close relative that suffers from an addiction may have a higher risk of having an addiction themselves, also indicate that addictions may be hereditary
  • genetics can also influence the way our body responds to a drug and therefore, increase likelihood of addiction
  • ---> may explain why one person can take drugs for pleasure now and again whilst another develops an addiction

Researcher = Kendler + Prescott (1998)

  • compared CR of drug abuse amongst 2000 MZ and DZ twins
  • found CR significantly higher in MZ than DZ
  • cocaine abuse ---> MZ = 47% DZ = 8%
  • cocaine dependancy ---> MZ = -35% DZ = 0%
  • indicates a genetic link to drugs
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Evaluation of genetic vulnerability

+ huge wealth of research gathered using scientific methods such as gene mapping ---> increases validity of the research ---> provides credibility of psych as a science

- may be argued that environmental/circumstantial factors that family members share may be the reason they develop addictions

- perhaps biology provides genetic predisposition to develop adiction but needs environmental triggers for the onset of addiction

---> this is supported by the fact that no twin study has ever found 100% CR even in MZ twins

- difficult to seperate the influence of environment and genes in twins studies as it is almost certain that MZ twins will be treated more similarly than DZ twins

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Risk factors of addiction - Stress

Stress:

  • state of mental/emotional strain or tension resulting from adverse/demanding circumstances
  • drugs and substances may act as a coping mechanism as they act as a temporary relief
  • however, some people are more at risk from the effects of stress and so may not necessarily be the level of stress experienced but one's ability to cope with it

Piazza et al (1989):

  • tested rats for vulnerability to stress by pinching their tails
  • found that were more likely to seek out/ingest amphetamines the more stressed they got
  • shows that stress can lead to addictive behaviours

+ controlled research ---> confounding variables can be controlled, increasing internal validity

- lacks generaliseability ---> cog processes in rats differ greatly to humans, also physiological differences in brain + reward centres

- unethical ---> causes pain to animals and forcing them to ingest dangerous substances

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Stress + addiction evaluation

- majority of supporting research is correlational ---> therefore, dificult to establish c+e relationship

---> stress may increase likelihood of becoming addicted but may also be true that addiction can cause stress due to personal, social and financial implications of it

- research is also carried out on animals due to ethical issues of causing stress in humans, therefore difficult to apply the research

----> also difficult to measure stress in animals and therefore, stress levels are assumed, making research less valid

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Risk factors of addiction - Personality

Personality:

  • ppl with pathology personalities are more liely to become addicts because addicts because their addiction offers them a relief
  • pathological personalities (mainly neg persona, more stressed) may be more attracted to susbtance abuse to help them to escape the everyday stresses of life that don't bother psychologically fit people
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Risk factors for Addiction - Personality2

Eysenck (1997):

  • outlined psychological resource model, which proposes that dependencies arise as addictive behaviours fulfil needs related to personality type
  • believed that there was biological basis to personality and that individuals who inherited personality with high levels of neuroticism (moodiness/irritability/anxiety) and high levels of psychotism (aggressiveness/emo coldness/impulsivity) may be more vulnerable to addiction

Colinger's tri-dimensional theory of addictive behaviour (1987) suggests that there are 3 key traits that make someone vulnerable to addiction:

  • novelty seeking ---> need for change + stimulation, seek new environments and experience therefore, more likely to seek sensation of drugs
  • harm avoidance ---> amount of time  person worries and sees neg elements of situation
  • reward dependance ---> how quickly someone reacts and learns from rewarding situation, high reward dependancy increases likelihood of addictiond sd they experience reward more quickly and easily
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Personality + addiction evidence

Howard et al (1997) - completed meta-analysis:

  • found that novelty seeking does predict alcohol abuse in teens and young adults but harm avoidance and reward dependance are not clearly linked

+ provides us with research that can be practically applied to reduce teenage alcohol abuse eg. public health campaigns

- meta-analysis ---> secondary data that may show positive bias as only significantly positive studies may be selected

Wan-Sen Yan et al (2013):

  • found high levels of neuroticism and psychotism and low levels of extraversion were linked to internet addiction
  • supports Eysenck's theory but refutes Cloninger's as extraversion would suggest novelty seeking so Cloninger would suggest high levels of extroversion would increase addiction, not low
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Personality + addiction evaluation

+ idea of an addictive personality is supported by fact that certain individuals can become dependant on many things, simultaneously or over time

+ idea that addiction is linked to personality is supported by fact that many recovering addicts develop equally strong compulsions towards other activities (eg. running) that are not seen as harmfully addictive

- evidence to suggest personality is implicated in an individual's likelihood to becoming addicted is less plausible and not supported by research evidence

- evidence suggests certain traits predict addictive behaviour but cannot explain underlying cause therefore, theory is incomplete and limited

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Risk factors of addiction - Family influences

Family influences:

= social learning - learning of behaviour through observing role models

  • and so if individual sees a familial model rewarded for consuming addictive substances then the vicarious reinforcement increases likelihood of the observer copying the behaviour

= expectancies - associations we make from observing environment around us

  • expectancies are formed through experience and learning and form our schemas
  • if ur expectancies of taking a substance are positive due to things we've seen/heard in our home environment then we will be more likely to do so
  • eg. parents may ask for alcohol after stressful experience so we may believ that alcohol reduces stress, therefore when confronted by fure stressful situations, our response may be to drink alcohol as we expect it to reduce stress
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Family influences + addiction evidence

Akers + Lee (1996):

  • found SLT was important in explaining smoking behaviours in adolescents
  • investigated smoking behaviours of 454 ppl aged 12-17 over 5 year
  • found that social influences affected likelihood of pps trying, continuing or quitting smoking

+ longitudinal study increasing validity of finding as gives greater insight into longetivity of behaviour and identify patterns

- lacks external validity as influences, cultural and familial expectations have changed a lot over last 22 years and may not influence smoking behaviour more or less

Christiansen et al (1989) - showed expectancies can be used to predict future drinking problems

  • found expectancies of 11-14 yo were indicator of how often they drank a year later
  • shows importance of environmental influence, including the family
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Family influences + addiction evaluation

- familial influences are not constant, influences of family will vary depending on the age and strength of the relationship

---> family may be greater influence in initiating in or abstaining from behaviours at younger age than older

- observing a behaviour does not equate to imitation, there are mediating factors that also influence if a behaviour is copied or not

- difficult to specify and measure impact of family as it is impossible to seperate from other factors such as genetics, personality and stress therefore, at best, we can conclude that family may influence addiction but to what extent it may do so is unknown

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Risk factors for Addiction - Peers

Peers:

  • their impact is potentially great due to contribution of social influence
  • if individual observes a peer partaking in addictive behaviour and recieves a reward, they may be motivated to imitate that same behaviour to recieve same reward
  • peers influential at the initiation stage of addiction as may provide access to drugs or encourage a relapse

Bullers et al (2010) - conducted longitudinal study

  • found that selection of a peer group followed addiction and therefore, peers did not play an influential role in initiation of addiction

Kobus (2003) - reviewed literature

  • found that effect of peer influence on smoking was more subtle than often thought
  • did believe that peer influence can encourage and deter smoking behaviour but that mediational cognitive processes needed further investigation
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Peers + addiction evaluation

+ has real life applications, many treatment programmes now take peer group and social context into consideration when rehabilitating addicts back into own environments

- issue of proving causation as addiction may be influenced by peer groups but similarly, the choice of peer groups may be influenced by addction

- peer group is just one social influence and other factors such as economic/social deprivation should be considered when assessing levels of vulnerability

- influence of peers is likely to differ according to age as peer influence during adolescence is far greater and therefore the initiation of substance abuse in adolescence is much more likely to happen here rather than as adults

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Theory of planned behaviour

Theory of planned behaviour:

  • Azjsen attempts to explain decision making + motivation
  • can be applied to addictive behaviours as well as prevention and treatment
  • theory has 3 components which shape person's intention thus translating to actual behaviour

1) behavioural attitude - how an individual views behaviour itself and the expected outcomes of it ---> behaviour may be percieved + or - based on beliefs around consequences of engaging in that behaviour, if the consequences are deemed positive then attitude towards behaviour are likewise positive

2) subjective norms - refers to behavioural expectations within persons own social group ---> product of social influence also what they believe to be right in eyes of others (injunctive norm)

3) percieved behavioural control - individuals belief around own ability to carry out behaviours (self efficacy) taking into account internal/external factors that help/hinder performance

---> ppl with higher percieved control + self-efficacy will have stronger intention and try harder

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Research evidence for TOPB

Walker (2006):

  • interviewed gamblers to assess whether theory of planned behaviour could explain their gambling
  • found that behavioural + normative beliefs were important but percieved control wasn't
  • intention, however, was found to be a good predictor of behavioural change

- self report technique used ---> may give biased results due to social desireability, interviewer influence, failure to tell truth

Web + Sheeran (2006) - conducted meta analysis of 47 studies using TOPB

  • found that level of intention is linked to behavioural change but the link is very small

- meta-analysis so using secondary data which may be influenced by publishing bias or data may be flawed due to different sample sizes and methods used in the studies

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Prochaska's 6 stage model

Prochaska:

  • prior to this, he felt behavioural change was often portrayed as an immediate jump from unhealthy to healthy
  • argued that there are series of changes in the lead p, during and after behavioural

1) pre-contemplation - aware behaviour is unhealthy but don't feel they need to do anything

2) contemplation - individuals acknowledge they need to take action but do not act upon it

3) preparation - beginning to plan and prepare behaviour change, behaviours that are planned and obstacles such as social events etc prepared for mare more likely to succeed

4) action - individual puts plan to action eg. thinking of how to stop smoking/drinking                ---> ppl are deemed to be in this stage for at least 6 months unless they relapse

5) maintenance - lengthy stage which includes no. of strategies and efforts to stay here, relapse is still possible

6) termination - there's no temptation and no efforts needed to abstain from former addiction

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Research evidence for 6 stage model

Velicer et al (2007)

  • showed that smoking cessation programmes based on 6 stage model showed 22-26% success rate which compares favourably with other interventions
  • there were no demographic differences in the success of the programme

= shows that model can be successful and is equally as effective regardless of individual differences but 26% is still low showing it fails for a large majority

Aveyard et al (2009) - randomised control trial

  • found that there was no increase in effectiveness if an intervneton was tailored to stages of change to the individual trying to stop smoking

= suggests that the efficacy of the model may be overestimated

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Evaluation of 6 stage model

+ looking at change as a series of stages means that iterventions can be designed to match the stage that the individual is currently in ---> can be argued to mean that interventions incorporating the model should work better

+ has led to measures being developed to identify which stage individuals are currently in, the most widely used is the URICA scale therefore, allowing practical application

- evidence is mixed so it's usefulness is not clear

eg.  Noel (199) developed modified version of the model which proposed that behavioural change is not linear as the model suggests, eg. someone may be in action stage for long period of time but then revert to contemplation stagebriefly before resuming behaviour (inconsistent views about model)

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