Addiction

Describing Addiction

Addiction is characterised by key features:

• Dependence
• Tolerance
Withdrawal symptoms

Addiction is included in the Statistical Manual of Mental Disorders (DSM 5) in the category “Substance-related and Addictive Disorders”.

The only behaviour included is gambling as not enough research on other behaviour such as internet use has been carried out to justify their inclusion.

Dependence (AO1)

Physical dependence: occurs when a person has used a substance so often and in such amount that they experience withdrawal symptoms when they stop using the substance.

Psychological dependence: this is an emotional need to use a substance or perform a behaviour that has no underlying physical need. e.g. when people stop smoking they recover physically in a very short time but their emotional need for nicotine takes a lot longer.

Tolerance (AO1)

Tolerance is shown when a person has diminished response to a drug as a result of repeated use. The individual has to increase the dose of the substance to obtain the same effects as their initial response.

Tolerance is a physical effect of repeated use of a drug, not necessarily a sign of addiction. Tolerance can develop to many types of drugs legal such as benzodiazepam (Valium) and illegal such as cocaine.

The level of tolerance is different for different effects of the substance e.g. to get the euphoric feelings produced by cocaine an individual might have to increase the dose but the effects on the respiratory system increase with the amount taken this can lead to respiratory arrest and death.

Withdrawal Syndrome (AO1)

This occurs in drug and alcohol addicted individuals who discontinue or reduce the use of the drug. This is due to the fact that the brain has adjusted its functioning to the presence of the drug, when the level is reduced, or the drug is absent the brain seeks the substance to bring the level back up.

This can lead to very unpleasant psychological symptoms such as depression and anxiety and physical symptoms such as nausea, loss of sleep, weight loss.

The type and severity of the symptoms depends of the type of drug, the amount used and the length of time the substance has been used. Fear of the withdrawal syndrome often motivate people to carry on using the drug.

Risk factors in the development of addiction (AO1)

Genetic vulnerability AO1

Genetic factors play a role in addiction by predisposing individuals to become addicted to some substances. They do so by influencing the way various substances are metabolised therefore influencing the response to the substance by enhancing the positive or negative effects of the drug.

For example, generally Europeans metabolise alcohol quickly so they do not feel sick but 50% of Asians metabolise alcohol slowly so they feel very nauseous after drinking even a small amount of alcohol as a result they are unlikely to become addicted to alcohol.

There has to be a gene-environment interaction as obviously if the individual is not exposed to the drug, they are not going to become addicted.

Evaluation AO3

• There is support for the influence of genetic factors for example Kendler et al., 1997 carried out a twin study on a 2516 twin Swedish males sample and found a concordance rate of 33% for MZ twins and 15% for DZ twins. This suggests a significant influence of genetic factors.
• However, it also highlights the importance of environmental factors as the concordance rate for MZ twins in all the studies was less than 100%, additionally the studies make the assumption that twins share exactly the same social environment but MZ twins are treated more similarly by their social environment than DZ twins.
• Furthermore, the samples are not representative of the general population as their developmental environment is different from non-twins e.g. before birth they have to share the mother’s nutrients and oxygen which is not the case for non-twins. This could have influenced their development. Furthermore Kendler et al., 2012 found that individuals with one addicted parent who were adopted away from their biological parents had a greater risk to become addicted, 9%, compared to individuals also adopted away from their biological parents who had no addiction, 4%.
• This type of studies is now relatively rare but they are important as they allow us to distinguish the contributions of genetic and environmental factors because biological relatives have only genes in common with the adopted individual and adoptive relatives have only shared environment in common with the adopted individual, the relative influence of genetic and shared environmental factors can be estimated by comparing the incidence of a disorder or the similarity of a trait in biological relatives to adoptive relatives. However, adopted individuals might still have contacts with their biological family, furthermore the individual shared the social family environment until adoption and could have been influenced by it so the influence of shared environment is not completely eliminated.
• The vulnerability varies across substances, so it is specific rather than a general susceptibility to get addicted to any substance. This explanation does not take into account social factors such as social norm, peer pressure, and moral values e.g. some people chose not to take drugs or drink alcohol for moral or religious reasons.
• It is an example of biological reductionism as this explanation suggests that an individual is likely to become addicted to a substance due to their genetic make-up but does not take other factors into account e.g. social factors such as peer pressure social norms and moral values. An interactionist approach combining the genetic influence with social factors would be more appropriate and more likely to lead to more effective ways to deal with addiction.
• It is a determinist explanation as it does not recognise free will in whether an individual develops an addiction.
• It is a socially sensitive explanation as it implies that people are nor responsible for their condition and the consequences e.g. stealing to buy the drugs ….

Stress AO1

High levels of stress make people more vulnerable to addiction. They might turn to substances or behaviour that give them temporary relief as a coping mechanism. However, addiction is less likely in stressful situations if there are mediating factors such as social support.

The stress could be due to the social environment such as family but also where people live. There are more people addicted to drugs in cities than in the countryside however this could be due to the fact that drugs are more easily available in the urban environment. Stress could also be due to childhood trauma such as sexual abuse.

Evaluation AO3

• Stress could also be due to childhood trauma such as sexual abuse. This is supported by Epstein et al. 1998 found that women with a history of childhood rape had twice as many Post Traumatic Stress Disorder (PTSD) symptoms as did women without who had not been raped. They also had significantly more alcohol symptoms.
• Furthermore, childhood rape victims with PTSD symptoms had twice as many alcohol-related symptoms as did victims without PTSD symptoms. This suggests that PTSD may be one of the contributing factor to alcohol use. It could be that people experiencing PTSD use alcohol to gain relief from the persistent memories of the abuse.
• Tovalacci et al., 2013 found that highly stressed university students (stress measured by a questionnaire) were more likely to smoke, abuse alcohol and were at higher risk of addiction to the internet. This suggests a link between stress and addiction however this was a correlational study so did not show a causal relationship between the two factors. Furthermore, the stress was measured using a questionnaire so social desirability could have influenced the results.

Personality AO1

Eysenck (1997) proposed that some personality types were more prone to addiction. For example, those with high neuroticism (high levels of irritability and anxiety) and those with high psychoticism (aggressive and emotionally detached).

However, this theory is now rejected by most psychologists. The link between personality and addiction is still investigated and one factor seems key in addiction, impulsivity. This is characterised by a lack of planning, risk-taking and the desire for immediate gratification of desire.

Evaluation AO3

• Ivanov et al. 2008, showed a strong link between impulsivity and drug use. Morein-Zamir et al. 2015 found inhibitory difficulties mediated by fronto-striatal circuitry. This suggests that there is a neurological cause for impulsivity which in turn leads to addiction. However more research is needed in this topic.
• One strength of this explanation is that it could help identify individuals at risk of developing addiction and provide them with help before they do. This would reduce personal cost to the individual and to society.

Family influences AO1

Two key features of family influences: Social Learning Theory and perceived parental approval:

Social Learning Theory or social learning - AO1:

The individual (child or adolescent) observes their parents smoking, drinking or …. and the results of the behaviour e.g. the parents feel more relax or seem to experience pleasure, the individual imitate the behaviour to get the same result. Over time and repeated exposures, the individual becomes addicted.

Evaluation AO3

• However, cognitive factors mediate whether the child will smoke or not. He might be influenced by other sources such as health messages, peers … furthermore the influence depends on the age of the individual younger children are more influenced by their family than older ones.
• It also depends on how much he/she identifies with the model of the behaviour.

Perceived parental approval- AO1:

The adolescent perceives that their parents have a positive or at least a permissive attitude towards a particular drug or addictive behaviour such as gambling. This perception might be based on the fact that their parents take the drug themselves or do not monitor their behaviour e.g. let the teenager drink to excess at home.

Evaluation AO3

• Quine and Stephenson 1990 carried out a study on a sample of 2336 10-12 years old Australian children and found that children were significantly more likely than other children to have the intention to drink, or to have drunk a glass of alcohol, if their parents drank at least weekly.
• Furthermore Bonomo et al. (2001) found adolescents who had experienced an alcohol-related injury were 1.8 times more likely than other adolescents to have parents who drank alcohol daily.
• However, it is difficult to separate and measure the influence of the family from all other influences such as peers and the media. Furthermore, these studies are correlational so they do not show cause and effect.

Peers- AO1:

The influence of peers is greater than the influence of the family according to Quine and Stephenson 1990. O’Connell suggests that there three features of peer influence that lead to addiction to alcohol or other drugs.

• An individual is influenced in his drinking or use of drugs by associating with peers who themselves drink or use drugs.
• These peers provide opportunities (and possibly access) to drink or use drugs.
• The individual overestimate how much the peers drink or use and increase their own consumption to keep up.

Evaluation AO3

• It is difficult to test the influence of peers, it could be the choice of peers follow the addiction rather than the addiction being the result of the association with a particular group.
• The influence of peers varies in importance depending on the age of the individual. Peers are more important in teenage years after which their influence decreases.
• It is impossible to disentangle the influence of peers from other social influences such as the influence of the family, media such as raps ….
• This approach does not take into account other possible factors such as social factors such as social deprivation, unemployment and stress.
• The research done is mostly correlational so does not show a causal relationship between the factor studied and addiction.
• No factor is by itself causal of addiction. These and other factors combine in various ways to lead to addiction but also to abstention from drugs, alcohol and gambling. These factors can be social such as social norms, health messages but also personal experience for example an individual who has seen his parents drinking to excess regularly might chose to avoid alcohol and become teetotal others might choose to abstain from drugs and alcohol for moral or religious reasons. So these are risk factors but not causes.
• However, research on this topic is important as it can be the base for preventing and treating addiction for example teenagers who don't use alcohol, cigarettes, and other drugs are less likely to use them as adults. Therefore, targeting prevention health messages to teenagers is an effective way to prevent addiction in adult life.

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Explanations for nicotine addiction

Brain neurochemistry

Desensitisation hypothesis - AO1:

Acetylcholine (ACh) is a neurotransmitter which like all neurotransmitters bind with receptors and activate post-synaptic neurones. One subtype of ACh receptors is called nicotinic receptors, they bind with both nicotine and ACh.

When nicotine binds with nicotinic receptors the neuron becomes become stimulated however almost immediately the receptors shut down and the neuron does not respond to any neurotransmitters (desensitisation).

This also leads to the production of dopamine in the nucleus accumbens. This generates a pleasurable feeling, increased alertness and a reduction of anxiety.

Evaluation AO3

• The Desensitisation hypothesis is supported by Domino, 2004 who using fMRI scans showed a change in the blood flow in the nucleus accumbens, amygdala, and hippocampus immediately after smoking the first cigarette in the morning.
• After smoking the second cigarette, the effects were less than smoking the first. Low-nicotine cigarettes produced fewer changes in the blood flow than those after the first average cigarette. D'souza and Markou, 2013 found that by blocking the transmission of glutamates in rats they reduced their addiction to nicotine.
• These results cannot be extrapolated without caution as animals are physiologically and psychologically different from humans, but it can give rise to research in humans and treatments aiming at blocking the transmission of glutamates to reduce addiction to nicotine.

Nicotine regulation model - AO1:

When the smoker does not take nicotine for a prolonged period of time, the nicotine is metabolised and excreted, and the nicotinic receptors become sensitised again giving rise to feelings of agitation and anxiety (withdrawal symptoms) which motivate the individual to smoke.

Additionally, the ACh increased transmission is accompanied by a decrease of dopamine activity. The repetition of this cycle creates a chronic desensitisation of the nicotinic receptors, so the intake of nicotine has to increase to produce the same effects (tolerance).

Furthermore, the prolonged use of nicotine results in an increase of the number of nicotinic receptors. Nicotine also stimulates the releases of glutamates which also increase and speed up the release of dopamine thus increasing the rewarding effects of nicotine.

Evaluation AO3

• The link between the use of nicotine and dopamine is also supported by the study of patients with Parkinson’s disease (this disorder is due to the loss of dopamine producing cells). Research shows that smokers are less likely to develop Parkinson’s disease than non-smokers.
• This suggests that nicotine has a protective effect against the development of Parkinson’s disease and supports the existence of a link between nicotine and dopamine. Cosgrove et al.,2014 compared the brain of men and women while smoking using PET scans and found that the dopamine effect took place in different regions of the brain. This suggests that men and women might smoke for different reasons. This is not taken into account by this explanation.
• This explanation is limited as research shows that there are many more neurotransmitters involved in the addiction to nicotine such as serotonin and GABA. This research is very important as addiction to smoking leads to very serious disorders such as cancer of the lungs which can be fatal and is very expensive to treat so by the development of treatments based on this research can contribute to individuals’ well-being and to the economy.
• This explanation is reductionist it focuses only on neurochemical processes and fails to take into account social and psychological factors so it cannot explain why, as Choi et al. (2003), found the teenagers who were the most likely to get addicted to nicotine were individuals who felt that they were underachieving. It cannot explain either individual differences for example some people can be and remain occasional smokers while others get addicted to nicotine very quickly.

Learning Theory

The learning theory explanation of nicotine addiction aims to explain the initiation, maintenance and relapse of nicotine addiction.

Initiation-> Social Learning Theory (SLT)

Maintenance -> Operant conditioning

Relapse -> Cue reactivity

Social Learning Theory (SLT) - AO1:

SLT suggests that people begin to smoke, particularly when they are young, due to learning from their social environment. They observe people e.g. peers or parents smoking and the consequences of the behaviour e.g. they enjoy it, they look “cool” and are popular (vicarious reinforcements).

So they imitate the behaviour- smoking- to get the same reinforcements. Mayeux et al. (2008) carried out a longitudinal study and found significant positive correlations between smoking at 16 and popularity two years later in boys, however they found a negative relationship in girls between smoking at 16 and popularity at 18.

This suggests that popularity might act as a vicarious reinforcement then a direct positive reinforcement for boys but not for girls.

Evaluation AO3

• DiBlasio & Benda (1993) found that adolescents who smoked associated themselves with other smokers and were more likely to conform to the social norm of a smoking group.
• This explanation accounts for the motivation to start smoking but does not explain why smoking continues despite the consequences -punishments-such as the cost, the health warnings and the health difficulties resulting from smoking.
• This explanation has practical applications in the prevention of smoking individuals could be taught the skills necessary to resist social influence (Botvin, 2000).

Operant conditioning - AO1:

Operant conditioning explains why smoking continues after initiation. When an individual smokes, he/she gets positively reinforced by the action of nicotine on the dopamine reward system.

Nicotine leads to a release of dopamine in the nucleus accumbens, this produces a mild feeling of euphoria thus rewarding the behaviour (smoking).

However not smoking gives rise to feelings of agitation and anxiety, this acts as a negative reinforcement therefore the behaviour – smoking- is more likely to be repeated to avoid the withdrawal symptoms.

Evaluation AO3

• Levin et al., 2010 trained rats to self-administer nicotine by licking one of two waterspouts. The number of licks increase with each training session which suggests that the effects of nicotine (higher dopamine leading to mild euphoria) reinforce the behaviour of taking nicotine.
• However, this study was carried out on animals so we cannot extrapolate to humans without caution as we are different both psychologically and physiologically so the effects might be different in humans.
• Furthermore the study used only nicotine but real cigarettes and other tobacco products contain many other constituents which might also affect the behaviour so the results might not represent the response to tobacco as a whole.

Cue reactivity- Classical conditioning - AO1:

Cue reactivity is the theory that people associate situations (e.g. meeting with friends)/ places (e.g. pub) with the rewarding effects of nicotine, and these cues can trigger a feeling of craving.

These factors become smoking-related cues. Prolonged use of nicotine creates association between these factors and smoking. This is based on classical conditioning. Nicotine is the unconditioned stimulus (UCS) and the pleasure caused by the sudden increase in dopamine levels is the unconditioned response (UCR).

Following this increase, the brain tries to lower the dopamine back to a normal level. The stimuli that have become associated with nicotine were neutral stimuli (NS) before “learning” took place but they became conditioned stimuli (CS), with repeated pairings.

They can produce the conditioned response (CR). However, if the brain has not received nicotine the levels of dopamine drop, and the individual experiences withdrawal symptoms therefore is more likely to feel the need to smoke in the presence of the cues that have become associated with the use of nicotine.

Evaluation AO3

• This can explain the maintenance of smoking and relapse in individuals who had given up smoking but cannot explain why people start smoking.
• Carter and Tiffany, 1999 support the cue reactivity theory, they carried out a meta-analysis reviewing 41 cue-reactivity studies that compared responses of alcoholics, cigarette smokers, cocaine addicts and heroin addicts to drug-related versus neutral stimuli. They found that dependent individuals reacted strongly to the cues presented and reported craving and physiological arousal.
• Calvert,2009 found that when smokers were shown packets of cigarettes they experienced strong activation in the nucleus accumbens. This supports cue reactivity as the cigarette packets acted as a cue and elicited the same activation pattern than the intake of nicotine produces

Social Learning Theory (SLT) - AO3:

• There are practical applications: some treatments such as aversion therapy and covert sensitisation are derived from this explanation (see reducing addiction).
• These treatments have been shown to be effective. It does not explain why men and women show some differences for example women find giving up smoking more difficult than men and are more likely to relapse than men. It does not explain why many people start smoking but do not become addicted. This suggests that other factors are involved which are not considered by this theory.
• Operant conditioning and classical conditioning are deterministic explanations however SLT does accept that the individual might decide not to imitate the behaviour displayed by the models so some free will is recognised in this instance.
• This theory does not take into account other negative environmental factors. Robin (1973) carried out a research on American Vietnam veterans. About 20% of American soldiers were using heroine during the Vietnam war however when they returned home she found that “only 5% of the men who became addicted in Vietnam relapsed within 10 months after return, and only 12% relapsed even briefly within three years”.
• These results are supported by Alexander et al. (1981). They placed rats in a cage in which they could drink from two dispensers. One dispenser contained a morphine solution and the other plain tap water.
• When the rats were on their own they drank 19 times more of the morphine solution than they did when they were with other rats. These studies suggest that negative environmental factors can lead to drug use and maintain addiction.

Explanations for gambling addiction

Learning theory explanation for gambling addiction

Social Learning Theory (SLT)

SLT suggests that people begin to gamble due to learning from their social environment. They observe people e.g. peers or parents gambling and the consequences of the behaviour e.g. they enjoy the excitement, they win money (vicarious reinforcements). So they imitate the behaviour- gambling- to get the same reinforcements.

Operant conditioning

The behaviour, gambling is maintained by direct positive and negative reinforcements. A reinforcement is anything that makes a behaviour more likely to be repeated.

Positive reinforcement: anything that rewards the behaviour, e.g. winning money, the excitement of betting, the social life associated with betting e.g. in casinos and betting shops. Negative reinforcement: anything unpleasant that is avoided by performing the behaviour e.g. gambling can offer an escape from a stressful life, loneliness.

Schedule of reinforcement

Continuous reinforcement: Skinner’s research with rats and pigeons showed that when the behaviour e.g. pecking a disc was reinforced by food every time it was performed (fixed ratio), the behaviour was repeated but when the rewards stopped the behaviour quickly ceased (extinction).

Variable ratio reinforcement: When the behaviour was only rewarded unpredictably (only now and then and it is impossible to say when the reward will occur) then the behaviour took longer to learn but once learnt it was very resistant to extinction.

Variable ratio reinforcement is a type of partial reinforcement. Applying the theory to gambling: A fruit machine might be set to give a pay out on average every 30 games.

However, an individual might win at the 5th game and then not until the 47th game (variable ratio) but the individual will carry on playing despite the losses waiting for the reward.

Evaluation (AO3)

• It could be argued that operant conditioning does not explain why people continue gambling when they lose more often then they win as the loss are punishments therefore should make gambling less likely.
• However, the magnitude of the losses is less obvious than the magnitude of the wins e.g. in a fruit machine the losses are a few pounds at a time so are not so obvious but the win might be £50 at once so is more noticeable.
• Furthermore, the loss being relatively small each time does not give rise to a lot of anxiety, but the win gives rise to a feeling of euphoria so the association between the behaviour and the feeling of triumph is greater. Parke & Griffiths,2004 found support for the reinforcing role of winning but also of “near-win” (coming very close to winning e.g. the horse comes second). This means that gambling is rewarded not only by winning but also by nearly winning which makes it more addictive.
• Operant conditioning cannot explain how people start gambling (see SLT) but can explain how the behaviour is maintained. Operant conditioning requires a contiguity between the behaviour and the consequences (short delay between the gambling and the win or loss).
• However, in some gambling activities such as poker or betting on the outcome of a sports game or a horse race there is a fairly long delay between the two so the association between the behaviour and the consequences should be weaker than for fruit machines, but this does not seem to be the case as both types of gambling seem to be equally addictive. This theory cannot explain why many people gamble at some point during their lives and experience reinforcement only a relatively small number of people become addicted to gambling.
• This suggests that other factors are involved in the formation of gambling addiction. This theory is beta biased (it does not acknowledge the difference between men and women). According to a study of gambling in Victoria, Australia by Hare, 2009 using a sample of 15 000 adults 1.3% of men were addicted to gambling but only 0.6% of women.
• They also found that men were more likely than women to gamble for social reasons or for general entertainment, but women were more likely to gamble to relieve stress, loneliness and boredom. This suggests that there are differences between gender which cannot be explained by the theory.
• This theory is reductionist, it does not take into account the physiological rewards experienced by gamblers such as the adrenaline and dopamine involved in the ‘buzz’ of winning. Operant conditioning is deterministic, it does not recognise free-will, the behaviour is determined by the consequences but SLT recognises that the individual might not want to imitate the gambling behaviour observed for moral or religious reasons.
• This explanation has practical applications: some treatments such as aversion therapy and covert sensitisation are derived from the learning explanation (see reducing addiction). These treatments have been shown to be effective.

Cognitive theory explanation for gambling addiction AO1

The cognitive theory explains gambling in terms of irrational/ maladaptive thought processes. It focuses on the reasons people give for gambling.

According to the cognitive theory the behaviour- gambling- can be explained by cognitive biases. A Cognitive Bias is a pattern of thinking and processing information about the world that produces distorted perceptions, attention and memory of people and situations around us.

These biases operate at an automatic and pre-conscious level but they influence attention and memory linked to the behaviour.

Rickwood et al. (2010) identified four main categories of cognitive biases:

1. Skill and Judgement: Gamblers tend to over-estimate the amount of control they have over their chances of winning even with random forms of gambling such as the lottery. They may look back over recent draws and believe they can spot patterns in the winning numbers.
2. Personal characteristics and Rituals: Gamblers sometimes believe themselves to be naturally more lucky than other people. They engage in ritualistic behaviours prior to or during gambling which they believe may influence the odds in their favour e.g. they have a lucky number.
3. Selective Recall: The tendency to overestimate wins and underestimate losses and to see big losses as totally inexplicable.
4. Faulty perceptions: these include Gambler’s fallacy, the idea that random events equal themselves out over time e.g. “I haven’t won for three weeks so it should be my turn soon”.

Evaluation (AO3)

• Griffiths (1994) carried out a study to find out if regular fruit-machine players behaved and thought differently from non-regular gamblers (the control group). They gave each of the participants £3 to spend on the fruit machine and the Ps were asked to “talk aloud” so that their cognitive activity could be assessed. Later they were interviewed to assess their perceived skill level.
• They found that the regular gamblers saw themselves as more skilful than non-gamblers- in fact there was no difference. They made more irrational statements such as statements suggesting that the machine had a personality or moods (this machine does not like me). They were also more likely to explain losses as near misses or even as near wins.
• The theory is also supported by Michealczuk et al (2011). They compared 30 addicted gamblers to 30 non-gamblers whilst each group played fruit machines. The gamblers were far more likely to have cognitive distortions and have a much greater sense of control. The results of these two studies support the cognitive explanation as it shows the presence of cognitive biases expected and the irrational beliefs e.g. attributing personality and moods to a fruit machine in the addicted gamblers.
• However, it could be argued that what the participants uttered whilst using the slot machines did not represent what they really thought but as these biases operate at a pre-conscious level it is very difficult to access these beliefs in any other way. It is impossible to know if the cognitive biases are a cause or the symptoms of the gambling addiction. If they come before the addiction, the theory does not explain how these biases occur or why they occur in some people and not others.
• This theory is beta biased. According to a study of gambling in Victoria, Australia by Hare, 2009 using a sample of 15 000 adults 1.3% of men were addicted to gambling but only 0.6% of women. They also found that men were more likely than women to gamble for social reasons or for general entertainment, but women were more likely to gamble to relieve stress, loneliness and boredom. This suggests that there are differences between gender which cannot be explained by the theory.
• This explanation is reductionist it sees the gamblers in isolation from their social environment for example if people are struggling financially it might makes sense to buy lottery tickets regularly in the hope of a big win which would solve their problems. Furthermore, it does not take into account the physiological rewards experienced by gamblers such as the adrenaline and dopamine involved in the ‘buzz’ of winning.
• A more holistic explanation combining cognitive, physiological and social factors would be more complete. The knowledge of how gamblers think has practical applications for example cognitive behavioural therapy aims at addressing these biases and irrational beliefs to reduce gambling addiction.

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Reducing addiction

Drug Treatments

There are three basic types of drug treatments:

1. Aversives: These drugs produce unpleasant consequences e.g. vomiting and nausea if taken with specific drugs. For example, if people consume alcohol while taking disulfiram, an antabuse drug they experience nausea, vomiting, dizziness, blurred vision and severe headache. They work on the principle of counterconditioning the behaviour, replacing pleasant associations with unpleasant ones.
2. Agonists; These drugs are in fact drug substitutes, they act as a less harmful replacement for the drug on which people are dependent. They have fewer side effects. They bind to the same neurones receptors than the addictive drugs and produce similar effects. They allow a gradual and controlled withdrawal from the substance. One example is methadone for the treatment of heroin addiction.
3. Antagonists: These drugs block the neural receptors sites thus preventing the drug of addiction to have its usual effects such as the feeling of euphoria. Example naltrexone for the treatment of heroin addiction.

Drug therapy for nicotine addiction - AO1:

Nicotine replacement therapy (NRT) uses patches, gums and inhalers to deliver nicotine, the psychoactive substance in tobacco in a less harmful and more controlled way than smoking.

NRT uses “clean” means to release nicotine in the bloodstream, although it still increases heart rate and blood pressure, it is not being taken with the cocktail of other harmful chemicals that are found in tobacco products such as cigarettes.

The nicotine acts in the same way than in tobacco products, it stimulates the nicotinic receptors, releasing dopamine in the nucleus accumbens thus producing sensations of pleasure and reducing anxiety. Over time the amount of nicotine is reduced gradually for example the patches are reduced in size so the withdrawal symptoms are managed over a period of two to three months.

Stead et al. (2012) reviewed 150 trials, including 50 000 people and found that chances of stopping smoking were increased by 50 to 70% by the use of NRT compared to the placebo and no treatment groups.

They found no overall difference in effectiveness between different forms of NRT (patches, spray or gums). This supports the effectiveness of the treatment but also supports the biological explanation of nicotine addiction.

Drug treatment for gambling addiction - AO1:

There is no specific drug as to treat gambling addiction however naltrexone, usually used for the treatment of heroin addiction is used in the U.S and because of the similarities between gambling addiction and substance abuse.

Like nicotine, heroin and other drugs, gambling leads to the release of dopamine thus activating the reward system. Naltrexone, an opiate antagonist, reduces the release of dopamine in the nucleus accumbens therefore decreasing the feeling of pleasure and increases the release of GABA in the mesolimbic system which is a neurotransmitter which decreases the cravings.

In the UK naltrexone is used only for the treatment of heroin addiction, however, in the USA it is becoming more widely used for other addictions. A significant issue with the use of naltrexone is that this drug can have serious side-effects such as anxiety, drowsiness, fatigue, panic attack and depression.

Furthermore, this drug could also stop patients feeling pleasure in all other areas of their life which leads to non-compliance (the patients stop taking the drug) this reduces the effectiveness of the treatment.

Kim, 2001 carried out a 12-week double-blind placebo-controlled trial of naltrexone and found that a dose of188mg/day reduced the frequency and intensity of gambling urges, as well as the behaviour itself in 45 pathological gamblers compared to the placebo group.

Another group of drugs, the Selective Serotonin Reuptake Inhibitors (SSRIs) is also used. The serotonin system is associated with impulse control, by inhibiting the reuptake of serotonin these drugs make more of it available in the synapses therefore should increase impulse control and reduce gambling.

This is supported by Hollander et al. (2000) who found a significant improvement in the experimental group compared with the group given placebo however Saiz-Ruiz et al. (2005) found no difference.

Evaluation (AO3)

• Drug treatment is cheaper than other form of treatment such as CBT as it requires only prescription and medical supervision. However, the use of drugs raises ethical issues as there are serious side-effects to some of the drugs used.
• This should be clearly discussed with the people treated. Though, some drug addicts might not have the mental capacity to give informed consent because of the damage caused by the drugs. This treatment requires people to take their tablets/injections regularly and this might be difficult for drug addicts who lead a very disorganised life or whose memory has been damaged by the use of drugs such as cannabis, ecstasy, and cocaine.
• Drug treatment might not be effective on its own for example McLellan et al. (1993) found that a group of drug addicts on methadone receiving also psychological intervention responded better to the treatment than a group treated with methadone but without psychological help.
• By focusing only on the biological problem rather than considering addiction as a choice, this approach removes the stigma of addiction and the blame culture that surrounds it.
• On the other hand, it does not address the difficulties that might have led to addiction in the first place e.g. stress, loneliness or other social problems such as unemployment.
• Furthermore, it does not address the issue of cognitive biases which are involved in some addictions such as gambling.

Behavioural interventions

Aversion therapy - AO1:

This is based on classical conditioning. According to the learning theory two stimuli become associated when they occur frequently together (pairing). In addiction the drug, alcohol or behaviour in the case of gambling becomes associated with pleasure and high arousal.

Aversion therapy uses the same principle but changes the association and replaces the pleasure with an unpleasant state (counterconditioning).

Aversion therapy and alcohol addiction

Patients are given an aversive drug which causes vomiting-emetic drug. They start experiencing nausea at this point they are given a drink smelling strongly of alcohol, they start vomiting almost immediately.

The treatment is repeated with higher dose of the drug. Another treatment involves the use of disulfiram (e.g. Antabuse). This drug interferes with the metabolism of alcohol. Normally alcohol is broken down into acetaldehyde and then into acetic acid (vinegar).

Disulfiram prevents the second stage from occurring leading to very high level of acetaldehyde which is the main component of hangovers. This results in severe throbbing headache, increased heart rate, palpitations, nausea and vomiting. (bad hangover x 10  !!!)

Aversion therapy for gambling addiction For behavioural addiction such as gambling electric shocks are used, these are painful but do not cause damage. The gambler creates cue cards with key phrases they associate with their gambling and then similar cards for neutral statements.

As they read through the statements they administer a two-second electric shock for each gambling related statement. The patient set the intensity of the shock themselves aiming to make the shock painful but distressing.

Covert sensitisation - AO1:

This is more likely to be used now than aversion therapy. It is also based on the principle of counterconditioning. Rather than experiencing electric shocks or vomiting, the client is asked to imagine how it would feel to experience these. This is called in vitro conditioning.

The client is asked first to relax then to imagine an aversive situation, for example feeling sick, vomiting or seeing a snake coiled around their drink if they are afraid of snakes. The therapist encourages the client to go into a lot of detail, mentally picturing the colour, texture, smell….

Then they imagine themselves smoking, drinking or gambling whilst thinking about the unpleasant consequences. These might include smoking cigarettes smeared with faces. The aim is to get the scene as vivid as possible to create a strong association, it is thought that the more negative the imagined situation the greater the chance of success.

Evaluation of behavioural interventions as a way to reduce addiction (AO3)

• Meyer & Chesser (1970) found that with aversion therapy 50% of alcoholics abstained for at least a year and that the treatment was more successful than no treatment. This supports the effectiveness of interventions based on classical conditioning.
• However, Hajek and Stead (2011) reviewed 25 studies of the effectiveness of aversion therapy and found that all but one had significant methodological flaws which means that their results have to be treated with caution. Compliance to the treatment is low due to the unpleasant nature of the stimuli used e.g. inducing violent vomiting.
• There are ethical issues associated with the use of aversion therapy such as physical harm (vomiting can lead to electrolyte unbalance) and loss of dignity for this reason covert sensitisation is now preferred to aversion therapy.
• Ashem et al. (1968) found that 40% of a group of alcohol addicts receiving covert sensitisation were still abstaining after 6 months compared to a control group in which all carried on their normal drinking pattern. McConaghyy et al. (1983) found that after 1 year 90% of gamblers who received covert sensitisation had reduced their gambling activities compared with on 30% of the participants who had received aversion therapy.
• This suggests that the effect of covert sensitisation has a longer-term effect than aversion therapy. However, relapse is a problem for both therapies. Away from the controlled environment where the associations between behaviour/drug and unpleasant stimuli are formed, it is common for addictions to return.
• Behavioural therapies are mostly used in combination with other therapies [(CBT) or biological (drugs)] it is therefore difficult to evaluate their effectiveness. Behavioural interventions focus on the behaviour but do not address the underlying cause of addiction such as biological factors, cognitive biases or social environment (i.e. the thing that is leading them to addictive behaviour in the first place) a more holistic approach might be more effective to achieve a lasting improvement.

Cognitive behavioural therapy (CBT)

The assumption of CBT is that behaviour, addiction, is determined by our ways of thinking. Therefore, the aim of the therapy is to identify and change the way people think about their addiction to a more adaptive way (functional analysis).

The second aim is to help the client to develop strategies to avoid situations that trigger addiction behaviour (skills training).

Functional analysis - AO1:

The client and the therapist identify the situations in which he/she is likely to gamble/take drugs or drink alcohol. They explore the thoughts and motivations before, during and after the event in an attempt to help the patient to identify “faulty thinking”, cognitive distortions or cognitive biases.

These are challenged by the therapist. Functional analysis is ongoing throughout the treatment to assess the success of the therapy and guide its future direction.

Skills training - AO1:

People who are addicted usually respond to the challenges of everyday life by turning to their addiction. CBT helps by suggesting other strategies. Cognitive restructuring: the treatment helps the client in modifying their irrational beliefs and cognitive biases.

Specific skills: The aim is to enable the client to cope with situations that leads to drink/gambling or drug use. The skills taught vary depending on the client’s needs. They may include assertiveness training to help an alcoholic firmly but politely refuse a drink offered at a party.

Social skills: These skills help people avoid situations likely to result in a lapse managing social situations more effectively. The therapist explains and models the behaviour then the client imitates the behaviour in a role play.

Evaluation of cognitive interventions as a way to reduce addiction (AO3)

• Ladouceur et al. (2001) randomly allocated 66 gamblers to either a CBT group where their irrational thoughts about gambling were challenged and they were given training in relapse prevention and a control group where the participants were placed on a waiting list for treatment.
• The results show that 86% of those in the CBT group reduced their gambling to the point where they were no longer defined as addicts. This improvement was maintained at a one year follow up.
• This supports the effectiveness of CBT. This is also supported by Petri (2006) who compared pathological gamblers attending Gambler’s Anonymous (GA). They either had GA and CBT or just GA. A year later those from the CBT group were gambling significantly less than the GA group.
• However, Cowlishaw et al.(2012) reviewed 11 studies on the effectiveness of CBT and found that there are medium to large positive short-term effects (3 months) but there was no difference after 12 months.
• CBT is carried out over 10-15 one-hour weekly sessions. Furthermore, one important aspect of this therapy is the “homework” as after each session the client will be asked to practise new skills in real life situations. This makes CBT time consuming and it also requires commitment from the client, this might be a problem for certain types of addicts such as drug addicts who lead very disorganised life. This leads to a high rate of drop out. Cuijpers (2008) found that the drop-out rate is five times greater for CBT than for other types of therapies. So only very motivated clients are likely to benefit from the therapy.
• CBT does not take into account the influence of biological factors however, it can be used with other treatments such as drugs to help with the withdrawal symptoms.
• A strength of CBT is that, unlike other therapies, it provides skills to resist social pressure and to deal with everyday situations without engaging in drugs or alcohol.
• A further limitation of CBT is that it does not deal with the stressors in the social environment which might have led to the addiction or maintain the addiction such as demanding job, difficult home life or housing problems. A more effective solution to addiction needs to take a wider approach addressing the social environment.
• Furthermore, individuals with a long history of abuse face other difficulties such as unemployment and homelessness, drugs/ alcohol are part of their culture and environment. They might not have the skills and resources to change to a new life and require more than CBT to adjust.

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Applying theories of behaviour change to addictive behaviour

Theory of planned behaviour (TPB)

This is a cognitive theory by Azjen and Fishbein (1975) that proposes that an individual’s decision to engage in a specific behaviour such as gambling or stopping gambling can be predicated by their intention to engage in that behaviour.

According to theory of planned behaviour intentions are determined by three variables:

Personal attitudes- This is our personal attitude towards the particular behaviour. It is the sum of all our knowledge, attitudes, prejudices …. positive and negative that we think of when we consider the behaviour. For example, our individual attitude to smoking might include tobacco is relaxing and makes me feel good but it makes me cough in the morning, costs a lot of money and smells bad.

Subjective norms- This considers how we view the ideas of other people about the specific behaviour e.g. smoking. This could be the attitude of family and friends and colleagues to smoking. It is not what other people think but our perception of others’ attitudes.

Perceived behavioural control- This is the extent to which we believe we can control our behaviour (self-efficacy). This depends on our perception of internal factors such as our own ability and determination and external factors such as the resources and support available to us.

The theory argues that our perception of behavioural control has two effects: It affects our intentions to behave in a certain way i.e. the more control we think we have over our behaviour, the stronger our intention to perform the behaviour. It also affects our behaviour directly, if we perceive that we have a high level of control we will try harder and longer to succeed.

Evaluation AO3

• TPB is the model most used in health psychology. It has been useful in predicting intentions relating to smoking and drinking as supported by Hagger et al. (2011). He found that the three of the components of the model (personal attitudes, subjective norms and perceived behavioural control) correlated with alcohol addicts’ intentions to limit or stop their drinking. He also found that those intentions were reflected in their behaviour and could predict the approximate number of units consumed after 1 and 3 months. However, it did not predict binge drinking.
• Penny (1996) found that smokers were less likely to believe they would quit smoking and therefore were less likely to try, the more times they have failed to quit previously. This shows the importance of perceived behavioural control in shaping our intentions as predicted by TPB.
• However, Webb et al. (2006) carried out a meta-analysis of 47 studies and found that although there is a link between intention and actual behaviour, that link is small. This suggests that there is a significant gap between intentions and behaviour.
• There are methodological problems associated with research on this theory. All the components of the model are assessed using questionnaires or interviews, so the answers are influenced by social desirability. Furthermore, these interviews or questionnaires are done when the participants are not under the influence of drugs/ alcohol but when they are in the situations which triggers their addiction behaviour (pub, party ….) their intentions might soon be forgotten and the behaviour resumed.
• A strength of TPB is that it takes into account the influence of peers (subjective norms) which is significant in both the beginning of the behaviour and its maintenance (SLT and operant conditioning).
• TPB assumes that all behaviours are conscious, reasoned and planned however it does not consider the role of emotions such as sadness, frustration … which can play an important role in influencing behaviour.
• TPB has been used in health education campaigns. Anti-drug campaigns often give data about the percentage of people engaging in risky behaviour such as smoking or drug use to change the subjective norm. for example, teenagers who smoke are usually are part of a peer group who smoke, therefore they might think smoking is the norm however most teenagers don’t smoke, so exposure to statistics showing them the true extent of smoking should change their subjective norm.

Prochaska’s six-stage model of behaviour change

Prochaska and DiClemente (1983) noticed that the change from unhealthy behaviour (smoking) to healthy behaviour (not smoking) is complex and involves a series of stages.

These stages do not happen in a linear order, the process is often cyclical. Some stages may be missed, or the addicts might go back to an earlier stage before progressing again. The model considers how ready people are to quit the addiction and adapts intervention to the stage the client is at.

Stages of Prochaska’s model of behaviour change

1. Precontemplation

At this stage people are not considering changing their behaviour in the near future. They might be in denial or feel demotivated by their failure in previous attempts. Intervention at this stage should focus at helping them realise that they have a problem

2. Contemplation

People become increasingly aware that they need to change. They consider the advantages and the cost of changing. This stage can last for a long time. At this stage intervention should help the client see that the pros outweigh the cons.

3. Preparation

At this stage, the individual has decided to change but has not got a plan on how to do it yet. Any intervention should focus on helping the client to decide which support will be needed to achieve the change successfully e.g. contact GP, specialised clinics or helpline.

4. Action

At this stage people change their behaviour e.g. they get rid of all tobacco products, lighters …. Relapse can happen. Intervention should focus on supporting the individual by practical help, praise, rewards .. to maintain the change.

5. Maintenance

The individual has maintained the change for at least 6 months and is growing in confidence that the change can be permanent. Intervention at this stage focuses on strategies learnt to prevent relapse e.g. emphasizing the benefits of stopping the addiction…

6. Termination

The change is permanent and stable. Abstinence is now automatic, there is no relapse. Some people do not achieve this stage and remain at the maintenance stage for many years. Relapse for them is still possible.

Evaluation AO3

• The model is flexible and dynamic. It reflects the changing emotions and attitudes that addicts have towards their condition. Sometimes they appear to be in denial and at other times they recognise that their addiction is a problem.
• It also offers a different focus of intervention at every stage, this should lead to more individually tailored interventions which are more likely to be successful than a “one size fit all” approach.
• However, the research carried out on the effectiveness of this model is inconclusive. Velicer et al. (2007) reviewed 5 studies and found a 22-26 success rate which compared well with other interventions. Furthermore, Aveyard et al. (2009) found that tailoring intervention to the stages of change did not increase its effectiveness in individuals who were trying to stop smoking. Similarly, Baumann et al. (2015) carried out a study on randomly allocated alcohol addicts to an experimental group and to a control group. They found no beneficial effect to staged intervention.
• The model encourages a more realistic view of relapse, which is seen as an inevitable part of the process rather than a failure on the part of the client. This is a strength as it avoids the low self-confidence and demotivation likely to arise if the client sees relapse as a failure.
• One weakness of the model is that the difference between stages is often “blurry” e.g. the difference between contemplation and preparedness is vague. So it is questionable whether they are in fact two distinct stages.
• A further weakness is that the model neglects the influence of social factors for example living conditions and unemployment within this environment. It also fails to recognise the influence of wider social norms such as in some societies it is expected that when people socialise they will drink alcohol so abstaining would be very difficult.

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About the Author

Elisabeth Brookes is an A-level psychology teacher, and author of her own website http://www.psychbug.co.uk/

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