AQA A-level Psychology Addiction

The AQA A-level psychology specification states you need to revise the following for Addiction:

• Describing addiction: physical and psychological dependence, tolerance and withdrawal syndrome.

Physical dependence occurs with long-term use of many drugs when abused. Dependence can occur with drugs such as heroin and nicotine as well as many prescription drugs such as sedatives and anti-anxiety drugs. Physical dependence often occurs with a drug that sees heavy daily use over several weeks or longer with those physically dependent often needing the drug in order to feel 'normal'. Physical dependence does not necessarily mean the individual is 'addicted' to the drug, however such dependence often accompanies addiction.

A physical dependence is evident by the presence of unpleasant physical symptoms referred to as withdrawal syndrome, when the person suddenly abstains from taking the drug. The person depends on the drug in order to avoid these withdrawal symptoms and function normally. A physical dependence on a drug is often accompanied by increased tolerance for its effects, which requires ever increasing doses in order to obtain the drugs desired effects.

Psychological dependence happens when a drug becomes an important part of the individuals thoughts, emotions and activities. It is usually demonstrated by a strong urge to consume the drug despite awareness of the harmful effects that are associated with its use.

Characteristics of psychological and physiological dependence includes experiencing cravings, which is an intense desire to repeat the experience associated with the drug or activity. Intense cravings are experienced when the individual attempts to abstain or cut down on the drugs usage or set of behaviours behaviours associated. If the cravings are not satisfied, the person begins to feel very anxious, which makes it difficult to stop the addiction. The desire to use the substance or engage in associated behaviour may become so intense that it takes over the individuals thinking completely, causing the individual to feel like they are unable to cope.

Psychological dependence can also occur for non-physical addictions, for example, gambling where individuals are motivated by the thrill of winning money or 'Gymaholic's' who relieve the tension in their lives by spending countless hours in the gym and find changing this habit very difficult to do. Such individuals may experience cravings to gamble or exercise which are just as strong as those experienced by people addicted to drugs.

Tolerance happens when an individuals response to a drug is reduced which requires them to take more and more of the drug to gain the same effect as their initial experience. Tolerance is therefore caused by repeated exposure to the effects of the drug and can be biologically explained using the idea of homeostasis which is a state of acting and feeling normal. Our brain and body attempts to maintain homeostasis where possible and through taking substances, this balance is disrupted. Over time, continuing to consume this substance causes the brain to readjust what it considers to be homeostasis and our 'normal level' and the body raises the bar to compensate for the increased regular substance intake. This results in more of the substance being required to gain the same effects as the body forms a tolerance to the drug with the effects also disappearing more quickly.

• There are different types of tolerance which can occur, one of which is metabolic tolerance. Metabolic tolerance is when the substance is metabolised faster and leaves the body quicker.
• Another type of tolerance is cellular tolerance which is when there are changes in the responsiveness of the neurons due to the brains attempt to recalibrate to higher levels of the drug. 
• A special form of tolerance that can also occur is cross-tolerance which happens when the individuals consumption to one particular type of drug can reduce sensitivity to another type. For example, the consumption of alcohol may lead to a developed tolerance to benzodiazepines. This has also been seen with surgery patients where a tolerance to the sleep-inducing effects of alcohol require higher doses of anaesthetic as a cross-tolerance to them has formed. There are benefits for such in terms of therapy where people may be given benzodiazepines in an effort to help them withdraw from alcohol to reduce withdrawal syndrome.

Withdrawal syndrome refers to a collection of symptoms that are associated with abstaining from a substance where a dependance has formed. The symptoms are generally the opposite of what is created by the drug, for example, withdrawal from nicotine creates irritability, anxiety, restlessness and increased appetite which results in weight gain.

Whenever a dependance has formed with a substance and the addicted individual abstains or does not consume the substance, the symptoms of withdrawal will be experienced by them causing the person to become familiar with them. The motivation to continue taking the substance therefore becomes partly to avoid the withdrawal symptoms that follow abstinence which form a secondary form of psychological dependence.

Withdrawal syndrome can vary in severity and this is determined by several factors including:

1. The drug used. Each drug has a half-life which describes the amount of time it takes to remove the drug from the body. The shorter the half-life of the drug, the more intense the withdrawal from it will be.
2. Amount consumed. If large quantities of the drug are consumed, this will result in greater withdrawal symptoms. 
3. Drug use pattern. If the drug use is frequent and regular, it will be in the body for most of the day. This means the physical dependence that has developed will be greater and consequently the withdrawal effects will also be greater.

For this section on Addiction, you need to know the following for AQA A level psychology:

• Risk factors in the development of addiction, including:
  • Genetic vulnerability, stress, personality,
  • Family influences and peers.

One explanation for why addiction occurs looks at genetic vulnerability. Research has shown that addiction frequently runs in families and a possible explanation is some individuals may be predisposed to addictive behaviours because of genes that have been inherited from their parents that make them vulnerable to such a development. 

This is not to say genes are an inevitable cause for addiction to occur because if an individual is never exposed to such substances, they cannot become addicted to it. Therefore, psychosocial factors are also involved but a genetic vulnerability can help explain why some people may become dependent while others do not as well as explain how progression from occasional use to dependence may also occur.

Two plausible direct genetic mechanisms that might be involved include:

1. The way neurotransmitter dopamine communicates within the brain is dependent on the presence of receptors for dopamine molecules on the surfaces of neurons. Abnormally low numbers of D2 dopamine receptors are thought to be involved in addiction with the proportion of receptors in the brain being determined by genetics. Low levels of dopamine means a decreased ability to activate the reward centre within the brain and therefore anything that can increase dopamine levels (such as substances), would produce strong feels of euphoria.
2. Another explanation suggests some individuals are better at metabolising certain substances and these individuals are at greater risk of developing addictions. Michael Pianezza et al. (1998) found some people lacked a fully functioning enzyme known as CYP2A6, which is responsible for metabolising nicotine. Such individuals were also found to smoke significantly less than those who had a fully functioning CYP2A6 enzyme. As the expression of this enzyme is genetically determined, it is theorised that those with fully functioning versions of the CYP2A6 enzyme are at greater genetic risk of nicotine addiction.

• Research studies appear to a support genetic vulnerability to addiction. For example, Kendler et al. (2012) examined data from the National Swedish Adoption Study and looked at adults who had been adopted away from their biological families where at least one of the parents had an addiction. Such individuals were found to be 8.6% likely to develop an addiction themselves compared to 4.2% for individuals who had no biological parents with any addictions. This is strong evidence for a genetic vulnerability as a risk factor for addiction as those with parents with addictions were more than twice as likely to form one themselves.

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• There appears to be gender differences in genetic vulnerabilities to addiction. While studies of male alcoholics have consistently supported the case for genetic factors in the development of alcoholism, research examining women has produced inconsistent findings (McGue, 1997). McGue points highlights that only two out of the four adoption studies have found a correlation between alcoholism and female adoptees and their biological parents. In addition, only two of the five twin studies found greater concordance rates for alcoholism between identical twins when compared to non-identical twins. This would suggest that genetic factors are less important in the development of alcoholism in women than men.

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• One advantage of genetic explanations is that they can offer an explanation through the diathesis-stress model why some people may develop addictions while others don't, including identical twins. Genetics may make someone vulnerable towards an addiction provided sufficient environmental and psychological factors trigger their expression. For example, the A1 variant of the dopamine receptor gene has been associated with cocaine dependence (Noble et al., 1993), nicotine dependence (Connor et al., 2007) and polydrug abuse (Smith et al., 1992). It is theorised that individuals who inherit this gene variant are more vulnerable to addiction as they have low levels of dopamine which can be increased through drugs that activate the brain-reward pathway. The nature of addiction however would still be dependent on environmental factors and sufficient exposure predicted by the diathesis-stress model.

We've covered stress already as an individual A-level psychology topic but what we didn't cover was how it can also be a risk factor for the development of addictions.

The link between stress being a risk actor for substance abuse has been well established with people dealing with stressful events in their life by engaging in a range of behaviours that help them feel better or cope with stress, which includes substance and drug use.

One proposed explanation for this is the 'self-medication' model (Gelkopf et al., 2002) which suggests that some individuals intentionally use different forms of pathological behaviour to 'treat' the psychological symptoms they experience because of every day stressors in their lives. For example, research on drug abusers has shown that stress is one of the strongest predictors of relapse (Dawes et al. 2000) and increased drug cravings (Since et al., 2000). Although consuming substances may not decrease the stress the person is under, the perception that it helps is what is believed to be instrumental in the behaviour leading to addiction.

Traumatic stress has also been identified as a potential vulnerability for addictions. For example, Robins et al. (1974) interviewed US soldiers who returned from the Vietnam War and found almost half reported to have used opium or heroin during their tour.  20% reporting a physical or psychological dependency to heroin during their service.

Kessler et al., (1995) conducted a general population study and found that for men who had a history of PTSD, 34% reported drug abuse or dependence compared to 15% of men who did not have PTSD. In women, 27% of those that had a history of PTSD reported drug abuse or dependence compared to just 8% of women who did not have PTSD. This seems to suggest a significant link between traumatic stress and the development of addictions.

• One of the major issues with linking stress to addiction is the difficulty in establishing direct cause and effect within research. High stress levels may well be linked to increasing the likelihood of developing an addiction however it may also just as easily be a by-product of having an addiction. The relative difficulty in disentangling the two and the ethical issues in testing the effects of stress on humans means there is no way of knowing for certain how much of a role stress plays in the development of addiction.

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• If stress contributes to addiction, it stands to reason that coping strategies for stress management should reduce the risk of addictive behaviours. Research by Matheny and Weatherman (1998) found supporting evidence for this suggestion when conducting a follow-up study of 263 smokers who had completed a national smoking cessation programme. Researchers found a strong relationship between stress coping strategies and their ability to maintain abstinence from smoking. This lends support to the notion that it is the effects of stress that contributes to addiction.

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• A limitation of explanations that link stress and addiction is the role of stress varies by the type of addiction. The role stress plays in drug addiction is well established with Dawes et al. (2000) finding that stress was a significant predictor of relapse however its role in other forms of addiction is not as convincing. For example, Arévalo et al. (2008) interviewed over 390 women from substance abuse programmes in Massachusetts and found evidence of a link between stress and drug use, however no such link between stress and alcohol addiction.

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• Understanding the role stress plays in contributing to addiction presents us with real world applications to address such. For example, it is possible to develop a vulnerability measure based on stress levels and coping strategies to determine the likelihood of individuals becoming addicted to substances as well as potential relapse. If coping mechanisms for stress are also found to be effective these can be taught to help equip people from falling into patterns of addictive behaviour too.

The role personality plays in addiction is complex and cause an effect is difficult to establish. This means that it is not always clear whether the addiction has altered a persons personality or whether the personality has contributed to the addiction. 

It is suggested that people who have pathological personalities are more vulnerable to addiction because the drug or behaviour they are addicted to offers them an initial relief. Pathological personalities are characterised by a predominantly negative persona which means they are more prone to becoming stressed and finding life difficult. The temporary high all relief gained from playing a fruit machine or taking substances for example, would likely positively reinforce the behaviour. This means that the personality may trigger the addiction rather than the other way round.

Psychologists generally agree there is no such thing as an 'addictive personality' however individual traits such as hostility and neuroticism have been linked to the formation of addictions (Butler and Montgomery 2004). A strong correlation was also found between antisocial personality disorder (ASPD) and addiction related behaviours. Antisocial personality disorder begins in early adolescence and incorporates many personality-related risk factors, however the key one identified is impulsivity. This is characterised by a lack of planning, a high degree of risk taking behaviour, a preference for immediate gratification of desires, and a chaotic lifestyle. Ivanov et al. (2008) concluded a number of studies strongly supported the link between impulsivity and addiction and it is speculated that this may have a neurological basis or a common genetic component.

• There is evidence from longitudinal studies to suggest that certain traits such as impulsivity are a good predictor for substance use and addiction. For example, McGee et al., (1986) found that adolescents who progressed to higher levels of alcohol abuse also scored highly on scores of impulsivity. This finding was further supported by Blonigen et al. (2011) who found alcohol-prone individuals who scored highly for impulsivity had a greater mortality risk than those who scored low. Impulsivity has been linked to a wide range of health-risk behaviours beyond substance use supporting a case for certain personality traits contributing to addictions.

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• It is important to note that possessing certain personality traits does not necessarily mean that an addiction will occur, it merely highlights a predisposition or vulnerability. There are a number of other factors involved that are psychological in nature and dependent on the environment which influence behaviour and lead to addictions. In addition it may be that the ultimate risk factors that underpin certain behavioural traits are genetic in nature. For example, Lara Ray et al. (2009) found novelty-seeking behaviour, which involves individuals continually seeking new experiences, to be associated with genetic markers for the D4 dopamine receptor. This research demonstrates that individuals with such a trait may be more pre-disposed to use substances due to the rewarding effects of dopamine activation through usage. The personality trait of 'novelty-seeking' may be a proximate risk factor and the immediate influence on addiction, however this may have a genetic basis when examined further.

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• Research has demonstrated that there is a relationship between personality characteristics and addictive behaviours with personality being a key predictor in the initiation, the development and maintenance of substance dependence (Barnes et al., 2000). An implication of this research is that by identifying vulnerable individuals in advance, they can be provided with support before their addictions develop and help prevent the development of substance disorders later. This has real world application as it can help reduce the significant personal costs to those individuals as well as society in the treatment of addictions.

One explanation for how family influences can contribute to increased risk of addictions is through Social Learning Theory (Bandura, 1977).

Social learning is when people learn behaviour by observing role models in their environment and those an individual has the most social contact with. If the individual sees the model rewarded for certain behaviours then this vicarious reinforcement will increase the likelihood of the observer imitating the behaviour themselves. This is proposed to occur with addictive substances within the family, however, it should be noted that the addiction is not the imitated behaviour, it is the desire to try the substance themselves that influences them. 

Parents exert this influence on their children's by being social models for them to learn from as adolescents with substance abusing parents have been found to be more likely to abuse substances themselves (Biederman et al., 2000). Other research has also found that patterns of gambling have been transmitted within families in gendered ways with males disclosing their first experiences of gambling being through their fathers while females reported their mothers (Reith and Dobbie (2011).

Another explanation for parental influence involves the style of parenting involved, particularly in terms of parental control and how much a parent will intervene in their child's life. Parental warmth and how much positive affect a parent shows for their child is also believed to play a role. Authoritative parents show warmth but also exert appropriate control and this type of parenting is associated with psychological resilience and good emotional well-being with lowered levels of substance abuse (Fletcher et al., 1995).

• There is research support for the role of family influences contributing to addiction. Bahr et al. (2005) found the family characteristics that were most strongly associated with an increased prevalence of smoking, drug use and binge drinking were tolerant parental attitudes and sibling substance use. This study also found that adolescents with parents who were tolerant of substance use were also more likely to interact with peers who smoked, drunk or used illicit drugs. These findings demonstrate that family influences and peer influences are not independent of one another but tolerant parental attitudes make it more likely that adolescents will seek peers that endorse substance abuse.

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• Another explanation suggests that substance abuse may actually be due to a lack of parental influence. Stattin and Kerr (2000) proposed that a lack of parental monitoring may result in adolescents disclosing too much information about this substance abuse to the parents. The parents inability to deal with this information may cause them to stop monitoring the children they may perceive as beyond their control. This results in a lack of monitoring and control resulting in the adolescent increasing their substance abuse and becoming more vulnerable to peer influences.

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• A major issue with studies examining the influence of family influences is they are frequently based on correlational data to examine the link between the family and subject. It is not possible to establish cause and effect from such data and there may be other confounding common variables existing within the family setting that are actually the cause. In addition, the relative influence of the family against all other potential influences is extremely difficult to separate. The role of the family will no doubt vary dependent on age and the bond between family members which means there are a number of circumstances under which family influence may play a primary role rather than simply assuming a broad level of influence.

Peer influence for addiction may occur either through direct or indirect encouragement from ones own age group for activities they may not wish to engage in, which can include substance abuse or addictive behaviours. Peers may introduce individuals to risky behaviours or pressure them to take part and then maintain them.

Explanations such as Social identity theory (Tajfel and Turner, 1986) attempts to explain why individuals are likely to be influenced by peer pressure. This explanation suggests that a significant part of an individuals self-identity is formed from the groups ('in-groups') they are a part of. It is thought that being associated with an in-group is important to be socially accepted and this makes the individuals more likely to adopt and replicate their behaviours.

Mary O'Connell et al. (2009) suggested there were three major elements to peer influence as a risk factor for alcohol addiction:

• At-risk adolescent attitudes and norms regarding drinking are influenced by associating with peers that use alcohol.
• Experienced peers provide more opportunities for the at-risk individual to use alcohol.
• The individual over-estimates how much their peers drink and may therefore drink more to keep up with the perceived norm.

What is proposed to be key for influencing substance use is the creation of group norms that favour rule-breaking in a general sense with other substances and addictive behaviours simply being examples of this.

• Research generally supports the idea that peers influence adolescent substance abuse through the modelling of risky behaviour, normative beliefs regarding substance use, and offers to participate in such behaviour through social networks. However, research by De Vries et al. (2006) challenges this idea and instead suggests that similarity in smoking behaviour among adolescents is likely due to friendship selection, i.e. smokers prefer to be friending other smokers rather than smokers influencing non-smokers into the habit. This study found that parental smoking behaviour was a stronger predictor of smoking adoption and peer influence which undermines this explanation.

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• Research into peer influences provide us with real-world applications through social norm interventions. Alcohol abuse among adolescents has become a major health concern and a Finnish longitudinal study of 155 women and 176 men (Pitkänen et al., 2005) on alcohol consumption between the ages of 14 and 42 found that early onset of drinking was a significant risk factor for alcohol dependence in adulthood. Social norm interventions, based on the idea that misperceptions on how peers think and act contribute to this behaviour, were developed to tackle this problem. Correcting such misperceptions (e.g. through media campaigns) is thought to then decrease the problem behaviour and lesson the likelihood of later substance dependence.

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• Peer influences are just one of many possible explanations. Other factors such as economic and social deprivation, intelligence, age and family influences all contribute in complex ways and need to also be considered when assessing levels of vulnerability. This is because it is unlikely that a single dimension such as peer influences will be the sole cause with other factors mitigating their influence. Additionally, it is difficult to distinguish the level of peer influence from other factors mentioned and therefore true cause and effect is impossible to establish.

This section examines explanations for nicotine addiction for AQA A level psychology. The specification states you need to know the following:

• Explanations for nicotine addiction:
  • Brain neurochemistry, including the role of dopamine
  • Learning theory as applied to smoking behaviour, including reference to cue reactivity

Explanations for nicotine addiction have looked at brain neurochemistry and specifically the role of dopamine. Dopamine has been implicated in addiction as using addictive substances or engaging in the addictive behaviour in question, results in a 'high' as it boosts the activity of the brains reward system.

Applying this to nicotine addiction, nicotine is the main ingredient within cigarette tobacco and a typical smoker takes in approximately 1-2mg of nicotine per cigarette. The nicotine is absorbed through the lining of the mouth and nose as well as by inhalation in the lungs. Nicotine reaches peak levels in the bloodstream within 10 seconds and becomes addictive as it activates the brain areas that regulate feelings of pleasure (the brains reward system).

This occurs through nicotine attaching itself to neurons in a region of the brain called the ventral tegmental area (VTA). These neurons trigger the release of the neurotransmitter dopamine in a nearby region of the brain known as the nucleus accumbens (NAc) as well as the release of the neurotransmitter glutamate, which triggers further dopamine release. The release of dopamine produces feelings pleasure which further reinforces the need to repeat the behaviour that led to it (further smoking). It is therefore this pleasure and the drive to repeat the process that leads to nicotine addiction.

Research has also examined why dopamine levels remain high after the direct nicotine stimulus ends and particular focus has been on the neurotransmitters glutamate and GABA. Glutamate speeds up the activity of neurons, whereas GABA slows it down. Research by Zickler (2003) discovered that nicotines effect on glutamate and GABA were responsible for the longer-lasting pleasurable effects of nicotine. Nicotine caused glutamate to speed up dopamine release while also preventing GABA from slowing it down once raised. This combined effect of dopamine release and inhibition of GABA results in increased dopamine and an amplification of its pleasurable effects. 

In addition, cigarette smoke contains an unknown substance that blocks the action go MAO (monoamineoxidase) which is responsible for breaking down dopamine after it's taken effect. Therefore, the blocking of MAO results in even higher dopamine levels which further strengthens the smoking habit by maintaining its feelings of pleasure for longer. Other explanations suggest nicotine addiction develops due to continued activation of the dopamine-enhancing neurons which reduce their sensitivity to nicotine. This results in a higher tolerance and the need for increased usage which ultimately results in dependance and addiction.

• There is research support for the link between nicotine and dopamine. Paterson and Markou (2002) found an epilepsy drug, gamma-vinyl GABA, (GVG) reduced the surge of dopamine in the nucleus accumbens (NAc) which occurred after taking nicotine. This would reduce the addictive tendencies of nicotine and other drugs which may boost dopamine levels. Through counteracting pleasurable experiences that may be gained by increased dopamine, such drugs may offer an alternative way of treating nicotine addiction. Researchers believe GVG can offer a viable alternative to other treatments as it is not addictive, not based on nicotine and has fewer side effects.

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• There is also research support for the role of glutamate and GABA from animal studies involving rats. D'Souza and Markou, (2013) blocked the transmission of the neurotransmitter glutamate resulting in decreased nicotine intake and nicotine seeking behaviour in animals. Nicotine intake and nicotine seeking also decreased when GABA neurotransmission was facilitated. These results are consistent with explanations offered for these two neurotransmitters as glutamate enhances the dopamine-releasing effects of nicotine and therefore blocking it would decrease such effects and make nicotine less rewarding. The inhibition of GABA also keeps the dopamine effect going for longer and therefore its facilitation would overcome the inhibitory effects and also decrease the pleasurable effects of nicotine.

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• A criticism of brain neurochemistry explanations involving dopamine is they are purely biological and as a consequence, ignore psychological aspects of addiction. It is possible that dopamine, although implicated, is not the complete picture and there are many levels to this explanation that include cognitive and social learning explanations. It can therefore be considered reductionist as such dimensions are ignored.

Learning theory as applied to smoking behaviour examines psychological explanations to explain how addiction occurs. Explanations through learning theory include social learning theory as well as classical and operant conditioning.

Social learning theory proposes an individual may start smoking due to them observing role models that engage in the behaviour and experiencing the vicarious reinforcement that occurs. This might include attention, admiration or people thinking "they are cool". This is particularly powerful among young people as this is when most will experience smoking for the first time. Initiation is therefore explained by peer pressure and social influences.

Operant conditioning offers another learning explanation through positive reinforcement. Nicotine addiction can be explained through positive reinforcement, where if a behaviour is seen as rewarding or pleasurable, then the behaviour is likely to be repeated. Nicotine is a powerful reinforcer because of its physiological effects on the dopamine reward system of the mesolimbic pathway. Nicotine stimulates the release of dopamine in the nucleus accumbens which produces a feeling of mild euphoria. This is experienced as a rewarding outcome which positively reinforces the smoking behaviour. Koob and Le Moal (2008) suggest that positive reinforcement can therefore both initiation and maintenance of smoking behaviour.

Negative reinforcement can also help explain nicotine addiction through a process of operant conditioning. Cessation of nicotine leads to acute withdrawal syndrome which has a host of unpleasant symptoms. This can include behavioural effects such as disturbed sleep patterns, agitation, Poor concentration, mood disturbances as well as anxiety and depression. Such symptoms make it difficult for the smoker to abstain so they therefore seek to reduce and eliminate the symptoms by starting to smoke again. Therefore, smoking another cigarette is negatively reinforcing as it stops the unpleasant stimulus i.e. the negative symptoms of withdrawal.

Cue reactivity with regard to smoking involves associations that are made through classical conditioning. For example, cues in the environment include sitting outside a pub drinking, socialising, or going for a meal, all of which would normally be accompanied by smoking behaviour. This forms an association between smoking and numerous behaviours, moods, situations and over time, such repeated associations become secondary reinforcers. The presence of secondary reinforcers can also produce a similar physiological and psychological response to nicotine due to this association. In classical conditioning terms, the secondary reinforcers also act as conditioned stimulus that cue the craving for a cigarette. This association between a number of cues in the environment make it difficult for the individual to give up smoking.

• There is research evidence that supports social learning influences on the development of addiction, For example, peer group influences have been found to be among the primary forms of influence in adolescents who experiment with smoking (DiBlasio and Brenda, 1993). Adolescents that smoked were more likely to socialise with others who also smoked. Research by Karcher and Finn (2005) found that youngsters who had parents that smoked were 1.88 times more likely to start smoking themselves. When such youngsters had siblings that smoked, this increased to 2.64 times more likely and up to 8 times more likely when they had close friends who smoked. This lends support for social learning theory as an explanation for addiction as the presence of models whom they could most identify with, be they parents, siblings or close friends all appear to be associated to the development of addiction.

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• There is also support from non-human animal studies for the role of conditioning and nicotine addiction. Edward Levin et al. (2010) trained rats to self-administer intravenous does of nicotine infusion by licking one of two waterspouts. This behaviour was seen to increase in frequency with every subsequent training session going up to 100 licks per infusion. This lends support for nicotine positively reinforcing self-administration and suggesting a similar process in humans. An issue with such studies however, is animal studies and their findings may not necessarily generalise to human behaviour. Humans are much more complex than rats with cognitive factors, societal factors as well as genetic vulnerabilities that may predispose them to addiction in complex ways beyond just simple conditioning. Therefore such explanations are considered too simplistic in nature to fully account for the complexity of human addiction.

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• Cue reactivity is also supported by Brian Carter and Stephen Tiffany's (1999) meta-analysis of 41 studies that investigated a range of substance addictions. Such studies have typically shown dependent and non-dependent smokers images of smoking related cues, such as lighters, ashtrays and cigarette packets. Self-reported desire or cravings are then measured, along with several physiological indicators of arousal (heart rate etc). Researchers found dependent smokers had a stronger reaction to cues presented to them with higher levels of cravings reported as well as increased physiological arousal. Such findings are consistent with cue reactivity theory predictions and demonstrated how secondary conditioning occurred with addicts demonstrating arousal and cravings to cues even when no nicotine was present.

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• Research study findings also support the idea that negative reinforcement contributes to smoking through negative mood experiences. Shiffman and Waters (2004) found that sudden increases in negative moods were associated with relapse and increased cravings to smoke. This would support the explanation that smoking behaviour is more likely due to experiencing negative moods and addicts relapse into smoking to avoid these negative symptoms.

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• Learning theory as an explanation fails to explain the gender differences in patterns of nicotine addiction. López et al. (1994) found women started to smoke later than men and there were gender-related differences in both the development and context of smoking behaviour. Baewert et al (2014) found women were more likely to smoke during stressful situations as well as become more rapidly nicotine dependent and experience withdrawal effects sooner which makes it harder for them to give up. These gender differences are not fully accounted for by learning explanations.

For explanations for gambling addiction, you need to know the following:

• Explanations for gambling addiction: learning theory as applied to gambling, including reference to partial and variable reinforcement;
• cognitive theory as applied to gambling, including reference to cognitive bias.

Learning theory explains gambling as behaviour that is subject to reinforcement, which in turn strengthens the need to gamble.

One potential explanation is through a process of operant conditioning. Behaviour that produces a rewarding outcome is reinforced positively and increases the chances of it being repeated. The reward may be the money won or the 'buzz' that accompanies the excitement of gambling.

Through a process of negative reinforcement, gambling can also be seen as an escape for some people. This is because gambling may offer them a distraction from other problems they may have in their life and to avoid those negative feelings, people may gamble to replace or avoid such negative thoughts or problems.

Another learning explanation for gambling addiction is through a process of vicarious reinforcement. The experience of observing others being rewarded for gambling through winning, the excitement as well as the pleasure can influence people into gambling. The observation of others may not necessarily be through direct observation and instead through media that portrays the behaviour or outcomes positively. This may trigger a desire for the same reinforcement from the individual for someone that may not have gambled before.

Partial reinforcement also offers an explanation for why gambling behaviour persists even when gamblers do not immediately win. Based on B F Skinner's research with rats and pigeons, a continuous reinforcement schedule that rewarded every desired response did not lead to the most persistent behaviour. Under this condition, once rewards stopped, the desired behaviour disappeared quickly too in a process known as extinction. A partial reinforcement schedule, such as variable reinforcement schedule, see's only some bets rewarded so there is a level of unpredictability and this has been shown to create more persistent behaviour that is consistent with gambling addiction. With variable reinforcement schedules there is no fixed pattern to predict when a payout on a slot or gambling machine will occur as it is random. This explains why gamblers keep going even when they continuously lose as the uncertainty of when a payout is due keeps them going.

Cue reactivity can also explain how behavioural addictions like gambling are maintained or cause relapses. During the course of gambling experiences, the individual will encourager numerous secondary reinforcers that have also become associated with the excitement and arousal caused by gambling. This might include the atmosphere and excitement at a betting shop, the colourful lottery scratch cards, horse-racing on tv or various betting adverts that are displayed. These secondary reinforcers can cue the same arousal that a gambler may crave and offer continuous low-level reminders of the pleasures of gambling to the individual. This makes relapse almost unavoidable and explains why gamblers continuously maintain the behaviour too as they are surrounded by reminders of the addiction through various associations. 

• Research support for the role of positive reinforcement comes from Mark Dickerson (1979). In this study, the behaviours of gamblers in real life gambling environments were observed in two betting offices in Birmingham. Dickerson found that the gamblers who placed the most bets on horse races (high-frequency gamblers) were consistently more likely than low-frequency gamblers to place their bets in the last two minutes before the start of the race. Low-frequency gamblers who waited until this point tended to place their bets on the following race. Dickerson argued that high-frequency gamblers delayed betting to prolong the rewarding excitement they felt, for example the tension built by the radio commentary broadcast in the betting shop. This is offered as evidence for the role of positive reinforcement on gambling behaviour. There are obvious criticisms to this study, one of which being it was an incredibly small sample from one specific location and therefore the behaviours observed may not necessarily generalise to the wider population or universally to other countries.

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• Learning theories may offer reasonable explanations for some types of gambling behaviour but not all. This is because gambling games all vary in terms of the level of skill or luck required with some types, such as fruit machines requiring no skill whatsoever and being based entirely on chance. Many other games such as poker require skill to play however, there is a significant delay between placing bets and the outcome which reduces the chance for any conditioning to take place. It is more difficult to explain in terms of conditioning under this set up however games like fruit machines have no delay between placing the bet and knowing the outcome. These two events occur very close together as required for conditioning to take place unlike poker. Therefore, learning theories lack the ability to explain all types of gambling addiction and may have limited application to only some types.

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• Another criticism for learning theory explanations for gambling addictions is they are unable to account for individual differences between people. Mark Griffiths and Paul Delfabbro (2001) argued that conditioning processes do not occur in the same way in everyone. For example, people respond differently to identical stimuli and have different motivations to gamble with some doing so to relax while others enjoy the arousal. Some individuals are also able to stop gambling and never relapse despite being subjected to cues that cause others to relapse. Such outcomes are not adequately explained by learning theory without considering cognitive features for addiction, such as distorted thinking. For this reason, learning explanations for addiction on their own may not adequately explain gambling addiction.

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• Blaszczynski and /Nower (2002) argued it is possible that there are different pathways to gambling addiction with some becoming 'behaviourally conditioned' through role models or peer groups and a process of social learning and reinforcement and this being just one possible route. Other routes into gambling may be due to anxiety, depression, history of poor coping skills as well as negative experiences and life events that produce an emotionally vulnerable individual that becomes susceptible. This would explain the different profiles of individuals that become addicted where the principles of learning theory do not appear to apply.

The cognitive approach to gambling behaviour sees problematic behaviour being the result of cognitive distortions or maladaptive thought processes. Cognitive explanations attempt to identify the thought processes occurring within addicts to explain gambling addiction and how it may start as well as become maintained.

One proposed cognitive theory for gambling addiction is through cognitive biases which involve a distortion of attention, memory and thinking processes that are linked to common beliefs held by gambling addicts. Cognitive biases may include an overestimation in ones ability to influence the outcome of random events (illusions of control), expectations that they are due a win after successive losses (gamblers fallacy), selective recall of winning and losing (recall bias) and seeing 'nearly winning' as encouragement for further gambling (near miss bias).

• The gamblers fallacy: This is a distortion or cognitive bias where the gambler believes that completely random events are influenced by recent events. For example, the tossing of a coin and believing that the run of particular outcomes such as two or three heads in a row, will be balanced out by the opposite outcome.
• The illusion of control: The illusion of control among gamblers is demonstrated through the performance of various superstitious behaviours which they believe will help them control the outcome of the event in their favour. Pathological gamblers may also have an exaggerated sense of self-confidence in their ability to 'beat the system' and influence random outcomes. This may be due to the different attributions they have about their gambling with success being attributed to ability or skill, and failure or losses attributed to chance factors or bad luck.
• The 'near miss' bias: This type of distortion is when gamblers get close to winning, for example, if a gamblers horse comes second in a race or the slot machine displays 2 of the 3 desired outcomes. Due to these near misses, the gambler does not see himself as constantly losing but instead 'constantly nearly winning' (Griffiths, 1991). Near misses are thought to still have some rewarding value for the gambler despite the lack of any monetary reinforcement.
• The recall bias: Pathological gamblers tend to suffer from a recall bias where they have the tendency to remember and overestimate their wins while simultaneously forgetting, ignoring, underestimating or rationalising their losses (Blanco et al., 2000). Such individuals believe they will eventually win or be rewarded for their efforts and may be motivated to continue gamble due to the belief they 'deserve' to win or are overdue one after successive losses.

Key Research: Mark Griffiths (1994) Cognitive Bias in Fruit Machine Gambling

Mark Griffiths examined whether regular gamblers thought and and behaved differently to non-gamblers due to cognitive bias.

• Procedure: The study was carried out in a natural setting in an arcade with 30 regular gambler participants that gambled once or more per week. They were compared with 30 non-regular gamblers who played less than once a month. Each participant was given £3 to gamble on the fruit machines with each gamble costing 10 pence resulting in a total of 30 gambles. They were given the objective of staying on the fruit machine for 60 total gambles and try and win back the £3. Participants were asked to verbalise any thoughts that passed through their minds as they gambled. A content analysis was used to classify these responses into either rational statements or irrational statements. A semi-structured interview was also conducted to assess how skilful participants thought they were.
• Findings: No differences between regular gamblers and occasional gamblers in objective behavioural measures were found e.g. regular gamblers did not win more money. They did however, make almost six times as many irrational verbalisations than occasional gamblers (14% compared with 2.5%). Regular gamblers were also more prone to an illusion of control believing they were more skilful than they actually were as well as overestimate the amount of skill required to win on slot machines, while considering themselves to be especially skilful at doing so compared with occasional gamblers.

• A major criticism of cognitive explanations for gambling addiction is they are heavily dependent on self-reports that attempt to capture cognitive bias. Delfabbro (2004) examined the evidence for cognitive bias and argued they were difficult to falsify, idiosyncratic and context bound. Verifying cognitive distortions objectively is almost impossible as they are dependent on introspection that may or may not be accurate.
  

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• When the cognitive styles of problematic and social gamblers are examined, differences have been observed. However, we are assuming it is distorted cognitive styles that underpin addiction to gambling when in fact these differences may be a consequence of such. There is no way to establish cause and effect from such research and it is possible that faulty cognitive styles may simply be a by-product of being a gambling addict. Cognitive theories for gambling also do not explain why problematic gamblers have distorted cognition that is different and only highlights such potential differences. This is where biological explanations and vulnerabilities through bio-chemical imbalances such as dopamine may offer a credible explanation. Dopamine offers a rewarding sensation and gambling may increase this which in turn leads to individuals having positive thoughts about gambling. Therefore a combined approach between cognitive and biological explanations may be better suited to give a more holistic explanation of gambling addiction.
  

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• Cognitive theories present us with real world applications and interventions based on cognitive behavioural therapy (CBT) that can be developed to treat gambling addiction. CBT can be used to help individuals recognise and challenge their faulty or irrational beliefs. For example, skills such as self-talk can be used by the gambler themselves to challenge their own recognised cognitive bias and maintain abstinence with the help of therapists.
  

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• The is significant evidence demonstrating the high rates of cognitive biases in populations of problem gamblers. Ladouceur et al., (2002) found that up to 80% of gambling-related verbalisations made by problem gamblers seeking treatment would be classified as irrational where as recreational gamblers did not show a high degree of cognitive biases. This supports the cognitive explanation that irrational beliefs sustain the gambling behaviour and make people more vulnerable to develop such addictions (Petry, 2005).
  

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• A strength of cognitive explanations for gambling is they help us better understand individual differences which other explanations struggle to explain as peoples thinking differs. Therefore cognitive explanations are not deterministic unlike biological explanations as they account for peoples ability for conscious thought.

This section examines explanations for reducing addiction for AQA A level psychology. The specification states you need to know the following for the addiction topic:

• Reducing addiction: drug therapy
• Behavioural interventions, including aversion therapy and covert sensitisation
• Cognitive behaviour therapy

Drug therapy is a biological intervention for treating addiction and it is most commonly used to treat addictions to drugs such as alcohol and heroin. There are three types of drug therapy that are commonly used which are aversives (aversion therapy), agonists and antagonists.

The main effect of aversion therapy is to produce unpleasant consequences when the addicted substance is consumed. Examples include vomiting or as drugs like dsulfiram cause, hypersensitivity to alcohol where the severe effects of hangover are felt within 10 minutes of consuming an alcoholic drink.

Agonists are drug substitutes that bind and activate neuron receptors to produce similar effects to the addictive drug itself. Methadone is one example which is used to treat heroin addiction by satisfying the individuals craving for the buzz they receive from heroin. The benefit of agonists is they generally have fewer side effects and are cleaner as they are administered medically rather than provided through the black market on the streets. The agonists stabilise the addict by helping them control withdrawal symptoms and over time, their dosage can be gradually reduced to ween them off the substitute.

Antagonists treat addiction by binding to neuron receptor sites and blocking them so the drug individuals are addicted to cannot have it's normal effects, such as the feeling of euphoria they experience. One such drug is Naltrexone which is an opiate antagonist and is used to treat addiction to heroin.

For detoxifying alcoholics, Benzodiazepines (BZ’s) like valium are used to gradually reduce alcohol intake by relaxing addicts and stopping the shakes that occur from withdrawal. Benzodiazepines basically depress the central nervous system and cause drowsiness and sleepiness while enhancing gamma-amino butyric acid (GABA) which slows down nerve impulses throughout the whole body. Alcoholics, when attempting to reduce their intake, will suffer from Alcohol Withdrawal Syndrome which has painful effects such as seizures, hallucinations, palpitations, vomiting and various other unpleasant side-effects. Benzodiazepines help reduce the impact of Alcohol Withdrawal Syndrome to help make it more manageable.

For nicotine addiction and smoking, nicotine replacement therapy (NRT) uses gum, inhalers or patches that deliver nicotine into the bloodstream at lower levels without the harmful chemicals that are found in cigarettes. Released nicotine operate neurochemically by binding to nicotinic acetylcholine receptors in the mesolimbic pathway of the brain. This stimulates the release of dopamine in the nucleus accumbens in the same way cigarette smoking affects individuals. Over time, using nicotine replacement therapy the dosage of nicotine can be reduced by using smaller and smaller patches to manage withdrawal syndrome and avoid the aversiveness of quitting.

For gambling, no drugs have yet been approved in the UK but research suggests they can help reduce cravings to gamble. The main type of drug therapies used to treat gambling are antagonists, antidepressants and mood stabilisers.

Opioid antagonists act upon opioid receptors which are important pathway for processing dopamine, the neurotransmitter that activates the brains feeling of reward. Once bound to opioid receptors, this results in them becoming blocked which results in individuals being prevented from experiencing the reward response that is associated with the behaviour of gambling. For example, drugs like Naltrexone which target the D2 dopamine pathway were administered in a study by Kim et al. (2002) during a 12-week double-blind placebo controlled trial with 45 pathological gamblers. Researchers found that naltrexone was effective in reducing the frequency and intensity of gambling urges, as well as gambling behaviour itself. It was also more effective in gamblers with severe urges to gamble.

Antidepressants act under the assumption that serotonin dysfunction is related to pathological gambling (George and Murali, 2005). Some research has shown that gamblers that have been treated with antidepressants that increase serotonin levels (selective serotonin reuptake inhibitors or SSRIs) have shown significant improvement in their gambling behaviour when compared to control groups. SSRIs reduce the symptoms of anxiety and depression which is believed to be one pathway into gambling behaviour that occurs in response to stressors in their lives. Reducing these symptoms associated with stressors is thought to reduce the urge to gamble. Another way SSRIs help is by reducing impulsivity which has been linked to a wide range of addictive behaviours that includes gambling. Low levels of serotonin have been found in individuals that lack impulse control including pathological gamblers. Administering SSRIs helps raise serotonin levels and should in turn reduce impulsive behaviour that relates to pathological gambling.

• There is significant research support for the effectiveness of nicotine replacement therapy. Stead et al. (2012) investigated it's effectiveness compared to a placebo across 150 studies. They concluded all the different types of nicotine replacement therapies, whether a patch, gum or inhaler, were effective in helping people stop their nicotine habit and 70% more effective than the placebo. The nicotine replacement therapy was independent of any other additional support that was provided to the individuals which suggests people being able to stop was a consequence of the treatment alone.

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• There is criticisms for clinical trials of nicotine replacement therapies that argue they are not truly 'blind'. It is argued that patients that receive the nicotine recognise the sensation while those receiving the placebo feel the withdrawal effects of no nicotine. Mooney et al. (2004) found that of 73 double-blind placebo controlled studies into nicotine replacement therapy, only 17 had conducted blinding assessments where they asked participants whether they believed they were using real nicotine or a placebo. Researchers found that of the 17 that did conduct blinding assessments, two-thirds were confident they had not received real nicotine patches. The lack of effective blinding means conclusions about the effectiveness of nicotine replacement therapy are not as certain as claimed.

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• A benefit of using drug therapies to abstain from substances is they are generally cheap when compared to rehabilitation clinics or other interventions. They also help the addict avoid the need to seek out harmful and illegal drugs which means they are more likely to remove themselves from criminal influences. This can not only improve their own life, but also the lives of people around them such as their family, friends and society.

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• The use of opioid antagonists such as naltrexone to stop the dopamine reward system can make other normal activities less pleasurable. For example, this drug works by blocking the brains reward system when they engage in gambling behaviour however this drug will also stop dopamine for other perfectly normal activities such as sport, socialising or even sex. The drugs tendency to make fun activities 'uninspiring' is a side-effect of using naltrexone and why it may not be appropriate, but also overall less effective in tackling the issues of individuals.

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• There are methodological issues that arise in using drug therapies for gambling addiction. Blaszcynski and Nower (2007) argue research into this area is plagued with small sample sizes, high dropout rates and low numbers of female pathological gamblers to study. Many studies do not include control groups or randomly assign gamblers to different treatment conditions. The other issue is of comorbidity where participants may have other disorders or illnesses and the response to treatment. This all makes it difficult to draw conclusions on how effective drug therapies alone are.

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• There are some ethical issues that arise when using biological interventions. Patients may not be of sound mind to give consent to biological treatments that alter their bodily chemicals due to their addic- tions which raises the issue of informed and reasoned consent. Another weakness is biological treatments may only treat the symptoms rather than cause of addiction. Many people develop addictions due to psychological issues and therapies such as CBT and counseling may be more effective with some patients. Overall a more effective approach may be to combine biological interventions with psychological ones such as CBT.

Behavioural interventions for addiction, and effectively any disorder, work under the assumption that the addictive behaviours are learned  through a process of reinforcement and can therefore be unlearned, reduced or eliminated by changing the consequence of the undesired behaviours.

People are believed to engage in addictive behaviours such as substance abuse and gambling because they find it pleasurable in some way as they associate the behaviour with some form of reward. Once this association occurs, the individual will form a desire or urge to engage in the same behaviour in the future.

Behavioural interventions attempt to change a persons motivation to engage in the behaviours and does this in one of two ways. The first is through aversion therapy and secondly, through covert sensitisation.

Using aversion therapy, either a real unpleasant association is introduced in what is known as 'overt sensitisation' or an imagined unpleasant association through 'covert sensitisation'. Aversion therapy is based on the principles of classical conditioning where an individual learns to associate an aversive stimulus with an action they had previously enjoyed such as the addictive behaviour (smoking, drinking, gambling).

During aversion therapy, the individual is asked to engage in the undesired behaviour while at the same time, they are exposed to something unpleasant that is foul smelling and makes them feel nauseous, disgusted or generally disliked like mild electric shocks. This can even include emetic drugs like Antabuse for alcohol addictions that cause vomiting once alcohol is consumed. Over time, the undesired behaviour becomes associated with this unpleasant stimulus and becomes a conditioned stimulus. Gradually the unpleasant stimulus is reduced in frequency and ultimately stopped when it is thought that engaging in the undesired addictive behaviours will produce the same negative feelings that were associated with the unpleasant stimulus.

Covert sensitisation is similar to aversion therapy and involves eliminating an undesired behaviour by creating an association between the behaviour in question (gambling for example, or drinking) and an aversive stimulus. The key difference however is that instead of being exposed to a real aversive stimulus, patients are asked to imagine them instead as well as the accompanying negative sensations. 

Once this association is firmly established, it is hoped the undesired behaviour will no longer be appealing and lead to decreased urges or desires and its avoidance in the future.

• Research findings for aversion therapy are mixed with some studies showing supporting evidence while others highlight methodological issues. For example, Smith and Frawley (1993) studied 600 patients that were being treated for alcoholism using aversion therapy across three addiction treatment hospitals in the US. From the 600 patients, 75 were also being treated for cocaine dependence. At least 12 months after they had completed the treatment, they were contacted to examine their progress with 65% being found to be totally abstinent from alcohol at this point. The abstinent rate at 12 months for cocaine was 83.7% and this study showed significant support for the effectiveness of aversion therapy in reducing alcohol and drugs.

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• Research by Peter Hajek and Lindsay Stead (2001) identified methodological issues with aversion therapy when reviewing 25 studies that used the therapy to treat nicotine addiction. They concluded it was impossible to determine the effectiveness of aversion therapy because the reviewed studies suffered from methodological issues such as the failure to 'blind' the procedures. This means the researchers that evaluated the outcomes of the studies knew whether the participants were in a therapy group or placebo group and inbuilt biases may have made the therapy seem more effective than it was. In addition, by modern standards, most of the studies into aversion therapy are dated and it is now rarely used with covert sensitisation being the primary choice.

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• The use of aversion therapy as a treatment has raised significant ethical concerns. For example, some forms of the treatment can cause extremely uncomfortable consequences for an individual such as vomiting and nausea. Such effects may lead to poor engagement with the treatment and high dropout rates which decreases the effectiveness of the treatment. There is also a risk that the negative association can become generalised to other stimuli inadvertantly. This means a participant may suffer from psychological harm given this would be an unwanted by-product of the treatment. Critics also question whether the treatment is appropriate from a moral point of view given it deliberately exposes people to feel unwell and uncomfortable with certain stimuli.

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• There is support for covert sensitisation being effective and given this does not expose addicts to any real unpleasant stimulus, this may be a better ethical option in comparison to aversion therapy. Kraft and Kraft (2005) used hypnotic suggestion to associate feelings of nausea with problem behaviours such as cigarette smoking, alcoholism and chocolate addiction. They found that while not all people responded to this form of therapy, it was claimed by them to be effective in 90% of cases. They concluded that covert sensitisation was a rapid and effective form of treatment to tackle undesired behaviours.

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• There are concerns that behavioural interventions such as aversion therapy or covert sensitisation only treat the symptoms and not the cause. The treatments are devised under the assumption that addictive behaviours are learned and ignores other factors such as cognitive, social or biological influences. As the treatments only tackle the learned behaviours, they ignore all other psychological and potentially biological causes. This is because addictions are often complex in their reasons for development and likely underpinned by a number of influences and behavioural therapies will tackle merely what is expressed. This may explain why it's long-term effectiveness has been questioned by McConaghy et al. (1991) who found that aversion therapy was effective in reducing gambling behaviour and cravings in the short-term. Examining the long-term impact after between two and nine years, it was deemed to be no more effective than a placebo.

Cognitive behavioural therapy ('CBT') is based on the idea that undesired or addictive behaviours are caused and maintained by maladaptive, irrational or distorted thoughts. The main goal of cognitive behavioural therapy is to help people change their thought processes concerning their addiction, as well as learn new ways in which they can cope with the circumstances that led them into these behaviours. 

Cognitive behavioural therapy promotes the recognition of thought processes for addicts, as well as raise their self-awareness about the triggers that help maintain the behaviour. The therapy also looks to teach skills that can be used to deal with their triggers such as drug-refusal skills, cognitive restructuring and relapse prevention training. Generic skills include relaxation, assertiveness, problem solving and self-talk.

Cognitive behavioural therapy starts with a functional analysis where the therapist and client working together to identify high-risk situations in which the client is likely to engage in the addictive behaviours be it gambling, using substances or consuming alcohol. The relationship between the client and therapist is crucial and needs to be warm, collaborative and responsive so distorted cognitions can be challenged. The client is encouraged to recall what they were thinking before, during and after they have engaged in the behaviour. Functional analysis is an on-going process and helps the client identify triggers or reasons for their addictions in the early phases of treatment. It is also useful in the later stages of therapy where the client may need further help to work out the circumstances in which they may still be struggling.

Dependent on the situation and need, different skills are drawn upon to abstain. Drug refusal skills help equip addicts with specific strategies that help them say no to their addictive substance or avoid social pressures to conform. For example, through role playing scenarios and rehearsing common risky situations with the therapist, this can help them resist temptation and social pressures.

Cognitive restructuring requires the client to examine the thought processes prior to their addictive behaviour and to reshape the way they think. This might involve the client recognising the triggers and accompanying thoughts that lead to the undesired behaviour. As triggers cannot always be removed, cognitive restructuring allows the client to learn ways to change their thought patterns, their perception of their actions and ultimately their behaviour.

Relapse prevention training is another skill that can be taught and is closely related to the theory of planned behaviour to help address their undesired behaviours over the long-term. The practitioner works with the client to identify the beliefs in their addiction which includes their motivation and attitude towards their treatment as well as their beliefs about themselves. When beliefs are faulty or unhealthy, the practitioner will challenge them in an effort to help the client improve the control they feel they have about their addiction. The hope is through addressing their beliefs that underpin their faulty thinking, this will make them less susceptible to slipping back into their addictive patterns of behaviour.

Relaxation skills can help manage stress and anxiety which produce a physiological response. Some addicts will use substances or engage in addictive behaviours to self-medicate, for example consuming opiates or drinking alcohol to help them relax. Learning relaxation skills means they do not have to take such substances and instead learn techniques that help lower their physiological arousal. Through practice, they can use these skills at a point they recognise they are at risk of using substances again, which will allow themselves to rationalise their actions and avoid relapsing.

• Cognitive behavioural therapy has been shown to be effective in the treatment of a number of addictions. Magill and Ray (2009) conducted a meta-analysis examining CBT trials finding that it was effective in reducing alcohol and illegal drug addiction. The therapy was also effective in the treatment of gambling addiction in both individual and group settings as well as more effective than referrals to 'Gamblers Anonymous' (Petry et al., 2006) and drug therapy (Ravindran et al., 2006).

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• However, a criticism is that CBT may only be this effective when patients are able to engage with the practitioner and those suffering from withdrawal symptoms for substance addictions may struggle with focus and concentration. Combining CBT with biological interventions such as methadone for drug addiction, may be more effective in improving engagement and managing withdrawal. Another strength of CBT is its effectiveness in dealing with the root cause better than other interventions which may merely deal with the symptoms. Many people with addictions have reported psychological problems such as low self-esteem, confidence or problem solving skills which trigger their addictive behaviour and CBT can help tackle this effectively leading to longer lasting change when the root cause is determined to be psychological in nature.

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• A major problem with psychological interventions is that they are extremely time consuming and costly compared to biological therapies such as drug interventions. Particularly with CBT, it can take time for addicts to open up to form a trusting relationship and it takes a long time for effective change to be noticed. For many psychological therapies to be effective it may be dependent on the skill level of the practitioner and this may vary or there may be availability issues for such specialistic resources. Drop-out rates for CBT can be up to five times greater than other treatment groups and this may be due to its demanding nature (Pim Cuijpers et al. (2008). Lack of adherence to the treatment is a major obstacle that makes it difficult for us to understand how truly effective it is 

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  Cognitive behavioural therapy as a treatment for addiction offers a number of advantages over other treatments. For example, addicts often suffer from negative thought patterns which contribute to their feelings of helplessness and the development of positive ways of thinking can help them address these. Another advantage is the addicts are taught a number of skills that can help them resist peer pressure, such as assertive communication, which can increase their confidence in resisting activities that have led to their addiction. In contrast to drug therapies, there are no side effects for this form of therapy and the skills can be long-lasting and drawn upon whenever required. 

The theory of planned behaviour (Ajzen, 1989) attempts to explain decision making and motivation and can be applied to addictive behaviours as well as prevention and treatment. The theory has 3 main components which shape a persons intention thus translating into actual behaviour. The 3 components are behavioural attitudes, subjective norms and perceived behavioural control.

Behavioural attitudes concern how the person views the behaviour itself and the expected outcomes of it. The behaviour may be perceived positively or negatively based on the beliefs around consequences of engaging in the behaviour. These consequences then shape the persons attitude towards the behaviour. If the consequences are deemed positive then the attitude towards the behaviour would be positive. If the consequences are seen to be negative, then the attitude would also be negative.

Subjective norms refers to the behavioural expectations within the persons own social group. This is a product of social influence as well as the individuals own set of beliefs of what is perceived to be right in the eyes of others (injunctive norm) as well as what people are actually doing (descriptive norm).

Perceived behavioural control is the individuals belief around their own ability to carry out the behaviours (self-efficacy) taking into account internal and external factors that help or hinder performance. Perceived behavioural control along with intention (willingness) may be used to predict behaviour itself. Those with higher perceived control and self-efficacy will have stronger intention and try harder than those with less perceived control.

The theory of planned behaviour when applied to addiction, can help us understand the processes that lead to addiction, prevention and treatment. This means programmes can be devised that can help bring about long-lasting changes in addictive behaviour. 

For example, behavioural attitudes can be reshaped to see addiction to substances and gambling differently. The US Office of National Drug used this understanding to launch a campaign in 2005 to lower teenage marijuana use. A review by Slater et al., (2011) attributed the campaigns success to its influence on attitudes as it aimed to create view that marijuana use was inconsistent with making your own choices and achieving aspirations.

Subjective norms can also be changed with actual data to dispel what people thing is normal to do. For example, anti-drug campaigns can target adolescents with actual data about the percentage of young people engaging in drug taking to show them it is not the norm for teenagers. If they were a part of a group that engaged in such, it would help them see this is not normal behaviour for people of their age.

Perceived behavioural control can be promoted as often addicts do not believe they have the willpower or control to stop. Programmes can be devised that help increase peoples confidence so they come to accept they have control over their behaviour and also increase their intention to stop by highlighting their goals. Cognitive behavioural therapy is really effective for this and could be one way in which this is done.

• Armitage et al highlighted that a major criticism of the theory of planned behaviour is it is too rational and fails to account for humans to be governed by irrational thoughts or emotions as the model assumes behaviours are always conscious, reasoned and planned which is not always true with addicts. The role of free will and ability to reason against even rational choices is not factored into this model which is another weakness.
  

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• Completing questionnaires regarding attitudes or intentions lacks internal validity as it cannot fully account for actual behaviour in real life. Experiencing strong emotions for example can explain irrational behaviour that goes against intended behaviour such as wanting to quit drinking even when the person knows it is in their best interest (Albarracin et al., 2005). The model also ignores the influence of alcohol and drugs which can produce a discrepancy between measured intention and actual behaviour. The attitudes and intentions of individuals are usually measured when sober, whereas risky behaviours are performed under the influence of substances. This means in practice, the model lacks internal validity as it would struggle to measure what it intends to measure, which is the real attitudes and intentions of individuals that influence addictive behaviours.
  

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• Armitage et al. (2001) conducted a metal-analysis of studies using the theory of planned behaviour and found the model was better at predicting intention rather than actual behaviour which is another weakness as the model may be better suited at gauging intention initially which may later translate into actual behaviour through other processes.
  

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• Another weakness of the theory of planned behaviour is it ignores other factors which are thought to be influential in addiction. Topa and Moriano (2010) suggest group variables, such as identification with peers plays a mediating role addictive behaviours. Also motivation appears to give a more consistent measure of recovery according to Klag (2006). Studying 350 substance abusers in Australia, recovery was more successful in people who had decided to quit themselves rather than be coerced into quitting due to a court sentence. Self-determination Theory may therefore offer a better explanation for addiction as it emphasises the importance of internal motivation which the theory of planned behaviour ignores.

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• One major strength for the theory of planned behaviour is it offers real world practical applications as clinicians can use it to tailor treatments to individual need which is another strength of the model. It is also the most popular and widely used social cognition model within health psychology which is another testament to its validity. However a major methodological weakness is TPB may lack internal validity as it relies so heavily on self-reports which may be subject to social desirability bias with addicts not being honest about the true extent of their dependency. Another issue is most research relies on correlation data which links positive or negative outcomes to behaviours but it is not clear if changes are due to behavioural attitudes changing or not as we cannot establish cause and effect between such due to possible confounding variables such as motivation or peer influence as Topa et al. (2010) suggests.

Prochaska's stages of change, also known as Prochaska and DiClemente's (1983) six-stage cycle for change, sees people pass through six transitional stages when attempting to change addictive behaviours such as substance abuse or gambling. Unlike other models, Prochaska's model highlights that overcoming addiction is rarely the result of a single decision to change and instead comes through subtle, often complex progression.

The first three stages in Prochaska six-stage model of change represents the person's intention to change their behaviour and are considered the 'pre-action' stages. The latter three stages are all 'post-action' stages and represent the duration of the change. Individuals may move through these stages in order, however on occasion, relapse and revert back to an earlier stage before repeating the cycle again.

The six stages of change are as follows:

Stage 1: Precontemplation - In this stage, individuals are not thinking about addressing their addiction anytime in the next six months. They may be unaware their behaviour is problematic or be in a stage of denial. The person may also lack the motivation due to previous failed attempts at change. Intervention at this stage would focus on helping the individual recognise the need for change.

Stage 2: Contemplation - During this stage, individuals show an awareness of their problem and that they need to take action but have yet to make a commitment to do anything about it. The person begins to think about making a change in their behaviour and desire the benefits this would bring, but they are also aware of the barriers for such change. Individuals can be stuck in this stage of contemplation for long periods of time as they are aware of what they need to do but do not act on this.

Stage 3: Preparation - At the preparation stage, the individual has accepted change is required and are ready to take steps towards this believing the benefits outweigh the barriers they will face. While they may still be engaging in their problematic behaviours, they may begin to reduce the frequency of them. The most helpful thing to do at this stage would be to formulate a plan or consider options to begin the process.

Stage 4: Action - The action stage is characterised by changes to address the undesired or problematic behaviour. The behaviour in question, whether it is substance abuse or gambling stops. Effective intervention at this stage focuses on developing the skills needed to quit and maintain the change of behaviour. The person is classed as being in the action stage of the cycle of change once they have altered their behaviour for a period between one day and six months.

Stage 5: Maintenance - During the maintenance stage, the individual has maintained a change of behaviour for more than six months and the focus is on relapse prevention. The individual will actively avoid situations where cues might trigger a relapse. The individual grows in confidence that the changes can be maintained over the longterm as they become a way of life. Intervention at this stage helps the client to apply the skills they have earned and continue using sources of support.

Stage 6: Termination - The final stage sees the new set of behaviours related to abstinence become automatic. The person is no longer tempted to revert to past undesired behaviours and is completely confidence in maintaining the change. Relapse may occur for some as they may be required to work through earlier stages when this does happen although they may move through them more quickly this time. No intervention is required at this stage.

• Prochaskas stages of change model is useful as it highlights different strategies that can help reduce addiction dependent on where the individual is at in the cycle of change. This is supported by Hallam and Draper (2000) who found women further along the cycle of change were more receptive towards the dangers of smoking during pregnancy. In contrast, women that were in the first stage of Prochaska and DiClementes cycle of change were most resistant to making positive health changes during pregnancy. Pregnant women assessed as being further along the cycle of change were more convinced in regards to the health risks of smoking while pregnant. This offers real world applications as interventions can be tailored to an individuals stages of change for most effectiveness.

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• Research evidence in support of the model has been mixed. A major review of available evidence for the National Institute for Health and Care Excellence (NICE) by David Taylor et al. (2006) concluded that stage-based approaches are no more effective than alternatives for treating nicotine addiction. A followup study by Kate Cahill et al. (2010) found the same conclusion with the overall impression of stage models being negative and Robert West (2005) remarking "the problems with the model are so serious, it should be discarded" and "The model has been little more than a security blanket for researchers and clinicians". This undermines the validity of the model as a tool to understand and tackle addictive behaviours.

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• Another weakness of Prochaska and Diclementes cycle of change model is the differences between the stages are too arbitrary. Stephen Sutton (2001) highlights that if an individual plans to stop drinking in 30 days time, they are in the preparation stage however, if they plan to give up drinking in 31 days time, they are in the contemplation stage. Bandura (1997) argued the first two stages, pre contemplation and contemplation, are not qualitatively different because the only difference is how much the individual wants to change. Kraft et al. (1999) argued the six stages could be reduced to just two useful ones consisting of precontemplation, and all the others grouped together as one.

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• Another weakness with Prochaskas stages of change model is it suffers from cultural bias and is mostly geared towards western cultures while ignoring the social norms in other cultures that influence addictive behaviours. For example, Daoud et al. (2015) found that in Arab cultures, social smoking was incredibly difficult to quit as cigarettes would be distributed at social events such as weddings and funerals. 62% Arab male smokers were in the precontemplation stage while only 14% were in the preparation stage. Compared to the US and Europe, 40% of smokers were in the precontemplation stage and 20% in the preparation stage. This would suggest that lower readiness to quit smoking behaviour may be a product of social norms and pressures that limit the effectiveness of therapeutic interventions.