The use of biological interventions in reducing addictive behaviour

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Varenicline is a prescription medication used to treat nicotine addiction, functioning as a partial agonist for nicotine receptors – stimulating them more weakly than nicotine itself. It both reduces cravings for and decreases the pleasurable effects of nicotine, helping people to quit smoking. Varenicline is usually administered orally, in tablet form.

In a double blind trial, Gonzalez et al (2006) found 44% continuous smoking abstinence during the last 4 weeks of a 12-week treatment in participants taking varenicline, compared to 18% of placebo-treated subjects and 30% of bupropion-treated subjects. After a year, the varenicline group had significantly increased prolonged abstinence compared to other treatments – over double that of a placebo, and slightly more than bupropion. This suggests that varenicline is an effective method of treatment, helping just under half of smokers quit in the short-term, and about a fifth in the long-term.

The fact that they looked at the effects of varenicline over a year, rather than just in the short term, makes this study’s results more valid – showing that varenicline is effective at prolonged rehabilitation from smoking rather than just short-term abstinence.

That 18% of patients managed to quit in the short-term via placebo treatment brings the effectiveness of the drug into question, suggesting that there is more to drug therapy than just biological mechanisms – the belief in having a drug to treat their addiction made them more likely to successfully quit. We cannot definitively say what proportion of those who successfully quit, quit due to the varenicline's effectiveness, or due to the placebo effect.

Aubin et al (2008) compared participants receiving varenicline to those receiving NRT, Nicotine Replacement Therapy. Patients were either on transdermal nicotine patches for 10 weeks, or varenicline for 12 weeks. Prolonged smoking abstinence for the last 4 weeks of treatment was higher for varenicline than nicotine patches – 56% vs. 43%. After a year, rates of prolonged abstinence were still higher for varenicline – 26% vs. 20%. 

Brose et al (2013) compared varenicline and NRT, measuring abstinence using carbon monoxide readings. They found that varenicline was more efficient - 43% compared to 37%.

Unlike many other studies into biological interventions, this study used a scientific, biological and objective measurement of abstinence, rather than self-report surveys and questionnaires, which could give untrue or misleading answers due to a social desirability bias.

Nicotine Replacement Therapy is based around nicotine administration in ways other than smoking tobacco, such as chewing gum, nicotine patches, and e-cigarettes. Rather than acting as a nicotine receptor agonist, they administer nicotine without the multitude of harmful effects associated with smoking, such as lung disease and cancers from chemicals in cigarette smoke.

West (2014) surveyed nearly 6000 smokers in the UK who had tried to quit smoking without the aid of prescription medication or professional support. Participants who used e-cigarettes were 60% more likely to successfully quit than those who used over-the-counter NRT or willpower alone, suggesting that e-cigarettes are the most effective publicly available form of NRT. This effectiveness has been explained by them filling a psychological as well as a biological need – going through a very similar procedure to the action of smoking a cigarette fulfils both, whereas conventional forms of NRT just fulfil a biological need. 

However, it has been suggested that e-cigarettes could increase the risk of future relapse, as they do not break this psychological procedural behaviour pattern of “smoking” like other forms of NRT do.

However, a 2012 study by Harvard University suggested that NRT may not actually be that effective. Surveying nearly 800 adult smokers who had recently quit, they were asked whether or not they had used NRT, joined a quit-smoking program, or received professional help. One-third of quitters surveyed reported to have relapsed, and there was no difference in relapse rate between those who used NRT and those who didn’t, suggesting that NRT might not actually play a role in helping people quit. 

On the other hand, a Cochrane systematic review challenges this, suggesting that NRT may be effective after all – analysing 50000 people over 150 trials of NRT, they found that it increased the chances of stopping smoking from 50% to 70%, but found no difference in effectiveness between different types of nicotine administration method, e.g. e-cigarettes, patches, gum.

The theory of planned behaviour as an intervention into addiction

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This theory assumes that an individual's personal attitudes, subjective norms and perceived control

over their behaviour influence their intention to perform the behaviour. That intention, in turn, predicts whether the behaviour will occur. The TPB assumes a causal relationship between an individual's attitudes about a behaviour, their intention, and the actual performance of that behaviour.  Applied to intervening in the addictive behaviour of smoking, the theory of planned behaviour would reduce addiction in a three step process.

 Firstly, change subjective norms regarding behaviour such as smoking – change the public’s perception to make them believe smoking is harmful, unacceptable and antisocial – through methods such as public health campaigns. Change the law to make public smoking no longer a norm, or tobacco not to be advertised at the point of 

Secondly, change personal attitudes – show the individual that smoking is bad for them and a socially undesirable behaviour - using campaigns like the Toxic Cycle, or graphic warnings on cigarette 

Finally, change their level of perceived behavioural control – show people that they have the power to control and to quit their addictive behaviour – using methods like the Smokefree Products and NHS Quit Kits.

Critics would argue that the theory of planned behaviour is too rational – being able to explain intention, but not behaviour. The majority of people who try to give up smoking fail – due to psychological and physical dependence. The theory of planned behaviour does not take biological dependency into account – the body adjusts to be able to cope with nicotine, and neuroadaptation occurs, causing withdrawal symptoms when they try to quit. 

Armitage (1999) argued that the TPB was too rational an explanation of addiction as it ignored factors such as emotion, compulsion, and social pressures -  for example, many people smoke or drink when under stress or other negative emotions, or in social situations such as being in a group of friends who they usually smoke with.

Armitage & Conner (2001) did a meta-analysis and found that the TPB was good at predicting intention but not actual behaviour - although the theory of planned behaviour may help explain an attitude change which leads to somebody trying to quit their addictive behaviour, this intention change does not directly translate into managing to give up their addictive behaviour.

Albarracin (2005) criticised the use of self-report questionnaires to measure the TPB, believing them to be unreliable as they are better at assessing attitude and intention rather than actual behaviour. People also tend to give socially desirable answers - for example, addicts tend to play down or under-estimate the extent of their addiction. Alternatively, they may simply be unaware of the extent of their addiction. 

The Cochrane systematic review (2011) found that exposure to tobacco advertising and promotion, including POS displays, increases the likelihood that adolescents will develop a smoking addiction. This supports the assumption of the TPB that social attitudes play a major role in addictive behaviour - subjective norms considering a behaviour acceptable makes it more likely that people will carry out that behaviour.

Klag argued that self-determination theory is a better predictor of quitting, suggesting that people quit an addictive behaviour due to circumstances unique to them – life events such as having a child, or having a relative die due to their addiction - powerful individualistic triggers rather than generic social pressures.

Risk factors affecting vulnerability to addiction

Another application-heavy section here - you'll often be presented with a scenario and asked to identify and explain risk factors that are present, and then evaluate the risk factors using supporting evidence. Remember to specifically signpost any research you take from this as supporting evidence - making sure it counts for AO2 rather than AO1

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Stress: Increased stress levels are positively correlated with an increased vulnerability to developing dependencies, often initiating them as a maladaptive way of coping with stress. The self-medication cognitive model of addiction explains addictive behaviours as initiating in order to alleviate the effects of existing life stressors such as anxiety or a lack of self-confidence, suggesting that people initiate the specific addictive behaviour that they feel will help them best cope with a specific source of stress.

Childs + DeWitt (2010) investigated the effects of stress on cigarette smoking, looking specifically at its effects on cigarette craving, the subjective effects of smoking, and smoking behaviour in daily smokers. A sample of smokers was given a stressful task to complete, and then given a chance to smoke or earn money over a 2-hour period. Both before and after the task, stress was measured both objectively (through heart rate and cortisol levels) and subjectively (through self-reported anxiety and desire to smoke.) These measurements were also taken after they smoked a cigarette when given the chance to. Participants were more inclined to smoke for stress relief than to earn money. Stress did seem to increase cravings to smoke and pleasure obtained from smoking, but did not seem to increase the amount of cigarettes that were smoked.


Cleck + Blendy (2008) reported that people with stress-related psychiatric disorders such as depression and anxiety (that are often related to addictive drug usage and exposure to chronic stressful life conditions such as abuse) have an increased rate of nicotine, alcohol and cocaine usage, suggesting stress is an important factor in determining vulnerability levels to addiction.

These results can also be used to support self-medication cognitive model of addiction – the concept of nicotine taken to alleviate stress and anxiety supports the central concept of self-medication.


Peer group: Peer pressure is a very powerful factor that can influence the behaviour of an individual, especially during childhood and adolescence. Peer pressure can work as a form of operant conditioning – if peer groupings encourage and socially reward addictive behaviours, thrill seeking and experimentation, individuals within the peer group will have an increased vulnerability to both initiation and maintenance of addictive behaviours. Peers also act as a form of social learning, modelling addictive behaviours so others will observe and imitate them, and being rewarded by peer approval as a form of vicarious reinforcement.

Bricker et al (2006) investigated the extent to which childhood friends influenced smoking behaviour. A sample of 4744 children was studied and it was found that close friends influenced them:

• To try smoking 38% of the time
• To move on to monthly smoking 10% of the time
• To move on from monthly to daily smoking 11% of the time.

This study also found that close friends were 12% more influential in the initiation of smoking in the sample children than parents’ smoking was. However, close friends smoking were 16% less influential than parents smoking in the move to daily smoking. This suggests that peers play a role in initiation more than they do maintenance, when the family and parents become more important. This supports the role of social learning theory as an explanation of addictive behaviour initiation – 38% of children initiated an addictive behaviour due to observation and imitation.

Wagner and Anthony (2002) found that cannabis smokers were more likely to progress to cocaine usage due to being in peer groupings where there are opportunities for new drug experiences, suggesting that peers can act as a social context “gateway” to other addictive behaviours. This supports the role of peer groups in the initiation and maintenance of addictive behaviour.

However, cause and effect cannot be established with complete certainty when studying the role of peer groups in addiction – it is possible that instead of peer groups influencing dependency behaviours, individuals who are already dependent will seek out peer groups that accept and encourage their dependent behaviour – social selection rather than social influence.

Gender: it has been suggested that males and females take different factors into consideration when making the decision to initiate smoking. Men tend to be more likely than women to take part in most addictive behaviours and to have a larger repertoire of gambling activity than women.

Amos and Bostock (2007) carried out a qualitative study of 15-16 year old Scottish smokers, and found that smoking played a different role for the two genders, differences revolving around diverse social relationships, interests and activities. For example, boys were more likely to consider the impact that smoking would have on fitness and the ability to play sport, while girls focused more on the aesthetic effects of smoking, such as their clothes and bodies smelling of smoke. This supports the idea that different genders consider different factors when initiating addictive behaviour.

They suggested a real world application from the result of this study: stop-smoking campaigns aimed at girls and boys should be designed differently and with a different message to target the ill effects of smoking that each gender specifically focuses on in order to better target their message to their audience demographic.

Personality: Originally, it was suggested that addiction leads to personality defects, but research has indicated that certain personality traits can predispose an individual to the development of addiction. Traits associated with extroversion, introversion, neuroticism and psychoticism can increase vulnerability to addiction. . Extroversion involves sociability, liveliness, and thrill-seeking, and according to Eysenck’s theories, the thrill-seeking tendencies of extroverts make them more likely to develop an addiction. On the other hand, some introvert traits such as shyness and lack of confidence can make addiction more likely.  

Eysenck and Grosson (1991) used the EPQ (Eysenck Personality Questionnaire) to compare 221 addicts to 310 non-addicts, finding that addicts had many more personality items on the neuroticism scale linked to anxiety and depression. However, cause and effect is an issue here – being addicted to a substance could cause anxiety and depression, rather than anxiety and depression leading to self-medication through addictive substances.

Eysenck linked excess dopamine levels in people with a psychotic personality to addiction, but the rise in dopamine levels caused by many addictive drugs could lead to a rise in personality traits associated with psychoticism such as aggression and impulsivity – can’t determine cause and effect.

Francis (1996) found a link between alcohol, heroin and benzodiazepine and nicotine addictions, and higher than normal neuroticism and psychoticism levels – suggesting that personality factors can affect the likelihood of addictive behaviour developing. 

There is very little empirical evidence to suggest a causal link between the thrill-seeking dimension of extroversion and the initiation of addictive behaviours.

The concept of an addictive personality is supported by the fact that certain individuals can become dependent on many things, either simultaneously or over time. For example, a heroin addict overcoming their heroin dependency and becoming an alcoholic. This idea is also supported by the fact that many recovered addicts develop equally strong compulsions towards other activities not typically seen as addictive behaviours, such as long-distance running, or religious fervour.  

Age: Younger age groups are more likely to engage in online gambling 

The British Gambling Prevalence Survey found high prevalence of online gambling in younger age groups – 15% for those aged 25-34, 1% for those aged 75 or over, across both genders. Across both genders, problem gambling rates did not vary by age, but in men, problem gambling prevalence higher in younger age groups than older – 2.1% in 16-24 age group, 0.4% for 75+ age group. This suggests that belonging to a younger age group can put one at a higher risk for the development of addictive behaviour.

Media: Social Learning Theory suggests that addiction is learnt through observation and imitation, and that figures in the media such as celebrities or fictional characters can act as models for addictive behaviours. If the addictive behaviour is presented in a positive light or the model is rewarded for their behaviour, the viewers are more likely to imitate them and initiate the addictive behaviour themselves, an example of vicarious reinforcement.

Gunsekera et al (2005) carried out a content analysis of 87 popular films released over a period of 20 years. They found that: 8% featured cannabis, 68% featured tobacco, and 32% featured drunken behaviour, and  most that featured them tended to portray these drug-taking behaviours positively.

Dalton et al (2003) surveyed 3547 children aged 10-14, all of whom were non-smokers. 1-2 years later, a follow-up study found that those who had been exposed to the most smoking in films were significantly more likely to have started smoking. Dalton concluded that greater exposure to addictive behaviour in the media leads to an increase risk of developing that addictive behaviour themselves. However, determining cause and effect may be an issue here: it may have been that the type of children likely to start smoking were also more likely to seek out that kind of film. 

Distefan et al (2004) surveyed adolescent smokers and asked them to nominate a favourite film star. One third of participants named a star who smoked on screen – this was seen to play a large part in predicting these adolescents’ own smoking behaviour – particularly among girls. However, this was a correlational study, so we cannot rule out a third variable such as a thrill-seeking personality that could lead children both to start smoking, and to be more drawn to film stars that both smoke and star in more action-based films.

The British Gambling Prevalence Survey of 2011 reported that 73% of the adult population had participated in some form of gambling over the past year, a prevalence increase of 5% from the rate observed in 2007. This correlates with a 600% increase in exposure to gambling adverts on television since the 2005 Gambling Act. Although this is only correlational, it could suggest that the increased media exposure and gambling adverts led to the increase of gambling behaviour in the general public. 

A quick note on the role of the media in addictive behaviour

Questions on the influence of the media on addictive behaviour will either ask about positive, negative, or both effects on addiction. If they ask for the negative effects, use the research studies I outlined in my post on risk factors for addiction (Gunsekera, Dalton and Distefan), and if they ask for the positive effects, use your knowledge of the Toxic Cycle and Gamble Aware campaigns outlined in my post on public health interventions.

Cognitive explanations of addiction

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Cognitions are thoughts, perceptions, reasonings and beliefs. The cognitive approach suggests that addictive behaviours develop due to faulty and irrational thought processes, and suggests several mechanisms for how these thought processes lead to addiction.

Gelkopf developed the self-medication model of addiction, which states that individuals carefully select addictive substances or behaviours based on perceived problems in their life, believing that the substance or behaviour will provide an effective solution to these problems. For example, someone may start smoking to alleviate stress, start drinking alcohol in social situations due to a lack of confidence, or gamble due to financial difficulties.

This model can explain initiation - people start an addictive behaviour due to a pre-existing stressor, maintenance - the behaviour can appear to help in the short term due to associations formed between the addiction and alleviation of the stressor (e.g. nicotine with calmness, alcohol with confidence), and relapse - once someone stops carrying out the addictive behaviour, they will relapse as soon as the initial stressor reoccurs, believing that the stressor has reocurred due to stopping the addictive behaviour.

People often carry out addictive behaviours without any underlying social or psychological hardships to resolve - confident people drink alcohol, non-anxious people smoke, and rich people gamble, so the self-medication model fails to explain initation of addictive behaviours in the absence of a triggering stressor.

Cause and effect is an issue with this model - it is often unclear whether the addictive behaviour develops to medicate for a pre-existing issue, or whether the issue is caused by the addiction. Many pathological gamblers also suffer from depression, and though the model would suggest that people with depression turn to gambling as a form of self-medication escapism, other psychologists have suggested that the causation is the other way round - that depression can develop as a result of poverty brought on by a gambling addiction. Becona (1996) found evidence of major depressive disorders in the majority of problem gamblers, but it is not clear whether the gambling caused the depression or vice versa. A similar cause and effect issue exists with smoking - it could be a self-medication coping response to stress, or stress could be brought on by illnesses caused by smoking.

The self-medication model can explain the disparity between genders in rates of depression and alcoholism reported by the NHS. In the UK, 1 in 4 women will undergo treatment for depression at some time, compared to 1 in 10 men, while men are twice as likely to show signs of alcohol dependency as women. The self-medication model explains this as a result of increased social acceptability of alcoholic self-medication for men - men are more likely to turn to substance abuse to treat their mental health issues than women, who are more likely to seek professional help.

Kassel (2007) found that adolescent smokers most commonly reported smoking when they were experiencing negative moods, supporting the theory of addictive behaviours developing as a coping mechanism to deal with stressors and negativities in daily life.

Parrott (1988) explained maintenance and relapse in terms of self-medication to avoid withdrawal symptoms. Abstaining from nicotine, even for a brief period, causes increased stress and anxiety in the form of cravings - smoking immediately relieves this anxiety and stress. This supports the self-medication explanation of smoking - that of nicotine as a coping mechanism for anxiety.

Heuristics are mental shortcuts that allow us to quickly solve problems and come to judgements based on prior experience. Heuristics theory suggests that gamblers maintain their behaviour through the use of a number of irrational heuristics in their information processing, overestimating their ability, overplaying their winnings, and downplaying their losses to support the perceived rationality of their behaviour.

Representative bias (Gambler’s fallacy) suggests that we apply a law of averages to a very small sequence of numbers, assuming that if something happens frequently during a short period of time, it will happen less frequently in the future.

Availability bias suggests that we put too much weighting on information from recent events, claiming that if something can be recalled, it must be important, or at least more important than information from events which are not recalled.

Illusory correlations are where the brain irrationally draws a correlation between two variables where there is none – often as the result of an associative accident. A perception of a relationship between two variables is formed where no relationship exists.


Henslin (1987) found that American players of the dice game Craps would roll the dice slowly when hoping to get a low number, and roll them quickly and hard when attempting to get a high number, even though there is no logical reason to believe that this would affect the outcome. This supports the concept of illusory correlations playing a role in gambling addictions, helping gamblers justify their behaviour to themselves by perceiving themselves to be more in control of outcomes than they actually are.

Griffiths (1994) found that regular gamblers over-estimated their skills, made more irrational verbalisations suggesting cognitive biases and were more likely to engage in machine personification, talking to the machine - supporting the concept of cognitive biases being used by gamblers to justify their own behaviours to themselves.


(Not much AO2 - supporting evidence to go with the final mechanism - cognitive dissonance - so seeing as we aren't asked more than 12 markers on a single aspect of addiction, learning the above in great detail is likely to be more useful than this final approach. It is easier to apply to smoking than Heuristics Theory is, though, so it could be very useful if an application question comes up in that area.)

Cognitive dissonance is another mechanism that cognitive psychology uses to explain addictive behaviour, and it results from a conflict between reasoning and behaviour. When an imbalance in our perception of the risks and benefits of an addictive behaviour occurs, this causes discomfort in the form of cognitive dissonance, so we alter our thought processes to minimise perceived costs and to maximise perceived benefits.

On a rational level, addicts understand smoking to be a negative behaviour, leading to social stigma, health problems and long-term illness. However, they are addicted to the behaviour of smoking, so adapt their belief systems to reconcile their behaviour with their rational understanding. They would make changes to their beliefs such as mentally minimising the risk or maximising the perceived benefits of smoking to help accommodate their addiction – “alleviating their cognitive dissonance” by changing from rational to irrational thinking.

Cognitive dissonance theory can explain maintenance of addiction – why people carry on an addictive behaviour despite being fully aware of the risks involved. They distort their own cognitive processes to to minimise perceived cost and maximise perceived benefit, leading themselves to believe their addictive behaviour is self harmful than it actually is.

It can explain initiation - people with negative views towards a substance or behaviour that feel pressured into starting it could mentally minimise risks and maximise rewards in order to justify their own initiation of the behaviour. 

It can explain relapse - maximising benefits and minimising risks of starting again and alleviating negative conseqences when withdrawal symptoms kick in, making reinitiation of the addictive behaviour seem more desirable than it otherwise would without cognitive dissonance. 

Learning / Behavioural explanations of addiction

You're likely to be asked to apply the learning theories to either the initiation, maintenance and relapse of addiction, or a specific scenario that the question outlines, but generic "discuss the learning approach to smoking/gambling" questions are also possible.

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The behavioural explanation of addiction explains addictive behaviour as a result of three mechanisms: classical conditioning, operant conditioning, and social learning theory. Classical Conditioning explains addiction as being learnt through association: associations form between addictive behaviours and the situation in which a behaviour is carried out, providing a situational cue to trigger the behaviour. For example, one who smokes whenever they're with a certain group of friends will form an association between those friends and smoking, so being with those friends will trigger cravings for nicotine. Cravings can also explain relapse through classical conditioning, as situations trigger cravings due to previously forming associations.

Thewissen (2008) found supporting evidence for classical conditioning's role in the maintenance and relapse of addictive behaviour. Smokers put in a room with cues associated with smoking had significantly more cravings for nicotine than smokers put in a room with cues associated with smoking unavailability - situations where people would normally smoke trigger a continuation of the addictive behaviour, or a relapse if people have attempted to quit. 

Further research support comes from a study on US soldiers in the Vietnam War. The soldiers became addicted to heroin while in Vietnam and experienced withdrawal symptoms while there, but when back in the USA they were far less likely to relapse as they were not experiencing the sight and sound cues that they had association with heroin while there.

This is also an implication for treatment - if certain environmental cues (sights and sounds) make relapse more likely, then a treatment program aimed at exposing the addict to these cues without providing them opportunity to carry out the addictive behaviour will lead to successful treatment, through extinction of the association.

Hogarth (2010) supports classical conditioning as an explanation for maintenance and relapse, through principles of association - cravings significantly increased if a stimulus associated with smoking was presented, providing a cue for carrying out the addictive behaviour.

Operant Conditioning explains addiction as being learnt through positive reinforcement, punishment, and negative reinforcement. In the case of smoking, someone may be alienated and rejected by their social circle due to not taking drugs (punishment). They then initiate the addictive behaviour of drug taking in order to escape this alienation (negative reinforcement), and are rewarded by approval and a sense of belonging to the group (positive reinforcement.) On attempting to quit their addictive behaviour, biological withdrawal symptoms and social rejection may both contribute to relapse by being negative stimuli that can only be escaped by relapsing to the addictive behaviour (escape learning.) Classical and operant conditioning cannot explain initiation very well - the associations can only form and the reinforcements only work once the addictive behaviour has already been initiated.

Griffiths (2009) identified 3 components that serve as positive reinforcement in gamblers, supporting the role of operant conditioning as an explanation of gambling addiction. Physiological rewards such as dopamine release and endorphins from the EOS, social rewards such as attention and congratulations, and financial rewards all make the behaviour of gambling more likely to be repeated and become pathological.

However, Sharpe (2002) criticised operant conditioning's explanation of gambling addiction by claiming that variable ratio reinforcement explains social and casual gambling but cannot explain pathological gambling where sustained, long-term financial losses occur. Variable ratio reinforcement is gambling based around a randomised, average-based payout system rather than a consistent win-loss pattern - explaining why people gamble occasionally if they feel "lucky" but not why they will continue gambling over a prolonged period of time and financial loss.

Mayeux (2008) identified smoking addiction in teenagers as a result of positive reinforcement through social approval and popularity, finding a positive correlation between smoking and popularity in 16-year-old boys. These findings support operant conditioning as an explanation of nicotine addiction - social approval as positive reinforcement that makes future smoking more likely.

Goldberg (1981) found further supporting evidence for the role of operant conditioning in smoking addiction, finding that monkeys in a Skinner box would repeatedly press a lever to receive nicotine, suggesting that positive reinforcement does lead to the development of an addictive behaviour.

Social Learning Theory explains addiction as the result of observation and imitation of role models, as well as vicarious learning through reward or punishment of the model. Models can either be live models, such as parents, peers, or siblings, or symbolic models such as celebrities or fictional characters. If someone observes a model carrying out an addictive behaviour such as gambling, they are more likely to repeat it (imitation) - even more so if the model is rewarded for addictive behaviour, such as winning a large payout from a bet. This explains initiation well - people are likely to start an addictive behaviour by copying a peer, but does not explain maintenance or relapse as well.

Research evidence supports SLT as an explanation of pathological gambling - Lambos (2007) found problem gamblers more likely to have peers and family members who approve of gambling, while Oei and Raylu (2004) found that childrens' attitudes to gambling are influenced by parental attitudes, particularly those of their father.

Karcher and Finn (2005) supports SLT as an explanation of smoking initiation - teens whose parents smoked were nearly twice as likely to start smoking, and nearly thrice as likely if their siblings smoked - observing and imitating the behaviour of family models lead to an addiction developing.

The U.S National Institute of Drug Abuse (NIDA) found that 90% of US smokers started as adolescents through observation of peers, suggesting that SLT is the best explanation of the initiation of smoking.

Murray (1984) found that if parents had strong anti-smoking attitudes, their children were 7 times less likely to start smoking, implicating parents as a very important model in the process of social learning and addiction development.

Overall Evaluation

Children’s attitudes towards and risk of developing addictive behaviours could be a result of social learning from parents, but correlations between addicted parents and addicted children could also suggest a genetic basis to addictive behaviour that is inherited from their parents, rather than the role of learning mechanisms.


Behaviourist theories of addiction could be considered too reductionist, explaining a complex system of behaviours as a result of simple learning processes. Additionally, they ignores evidence for a biological basis for addiction, such as research that suggests the genetic heritability of smoking addiction resulting from the lack of the SLC6A3 – 9 gene.  Addictive behaviour is unlikely to be a result of just biological or environmental factors; it is more likely to be a combination of both systems. 

Classical conditioning suggests that stimulus-response associations form that would put people off drugs if they ever had a negative response to them, but most people who drink alcohol drink anyway despite negative experiences – and many people have especially negative experiences on their first time taking drugs, but continue to take them anyway. This suggests that many more complex factors must play a role, such as cognitive and social motives for indulging in the addictive behaviour.

Operant conditioning and social learning theory do not explain why people carry out addictive behaviours that cause rejection from peer groups or have definite social stigmas associated with them, such as the use of “hard drugs” such as heroin and methamphetamine.

Behaviourist theories of addiction are also overly deterministic, explaining addictive behaviour as being caused entirely by learning processes and leaving very little room for the role of human free will. Lots of people who grow up in areas where drug-taking is a social norm, but do not grow up to take drugs themselves as social learning theory would suggest, implying that free will can play a significant role in the lack of addictive behaviour development.

Aversion therapy as a psychological treatment for addiction

Quite a short topic here - like everything else on addiction, they've never really asked anything more than a 10-marker on this! Be prepared to be asked to apply this for AO2 marks - this can happen.

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Aversion therapy is based on classical conditioning, eliminating the association between the addictive behaviour and pleasure, and forming a new association between the addictive behaviour and unpleasant consequences. Alcohol is often paired with an emetic to induce vomiting and to form a new association, the most commonly used emetic being disulfiram. Usually administered through a tablet or surgical implant, disulfiram prevents the body from metabolising alcohol, causing unpleasant, hangover-type effects whenever a small amount of alcohol is consumed, such as nausea, vomiting, headache, chest pains, weakness ands anxiety. A new association is formed between alcohol and the host of negative of symptoms, replacing pleasure with pain and discouraging people from taking any more alcohol.

While the negative effects such as nausea are actually desired consequences of the treatment, required in order for the association replacement to be successful, disulfiram can have several negative side effects that occur even in the absence of alcohol. These can include liver damage, drowsiness, and fatigue due to the disulfiram metabolite tryptophol, and extrapyramidal symptoms (drug-induced movement disorders) such as muscle spasms and motor irregularity.

Krampe et al (2006) found supporting evidence for the effectiveness of aversion therapy in their double blind, longitudinal study of 180 alcoholics attempting to quit, comparing a group taking disulfiram to a group taking a placebo. An abstinence rate after 9 years of at least 50% was found in the disulfiram group, far higher than that of a placebo, suggesting that drug-assisted aversion therapy is a very effective method of reducing alcoholism.

Fuller et al (1986) carried out a controlled blind study of 605 men, assigned to disulfiram, a placebo, or no treatment. There were no significant long-term differences between groups in total abstinence, social stability, or time until relapse – disulfiram was found to reduce drinking frequency after relapse, but did not make patients more likely to successfully remain abstinent – challenging the drug’s reported effectiveness as a stimulus in aversion therapy.

Jørgensen et al (2011) carried out a meta-analysis and found Disulfiram to be more effective than placebos or other treatments on rates of abstinence, days until relapse and number of drinking days, suggesting that drug-assisted aversion therapy is a very effective alcoholism reduction method. However, one limitation of the analysis was that the vast majority of the studies only studied the effectiveness of Disulfiram over a short period of time.

Tablets might be better due to psychological establishment of routine daily actions based around ending alcoholism, implants might be better due to not being removable – if people really want to relapse on tablets they can just stop taking them, and there’s no option like this with an implant.

The use of public health interventions in reducing addictive behaviour

Considering merging clinical and public health interventions into a single post once I've covered all the clinical interventions content, I'll see how much there is and if it's not too much then I'll redo this post to include them both. Another likely candidate for application questions, so make sure you know how to apply these in order to access top AO2 marks!

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Purple: My notes/hints/tips

The Toxic Cycle Campaign

In 2013, Public Health England launched this campaign to remind smokers of the physical damage caused by tobacco smoking. Through television, radio and online advertising, the campaign dramatised the harms of smoking by showing how it affects the whole of the body, from the heart to the lungs, blood and brain. It aimed to increase awareness by highlighting the immediate damage done by every cigarette, focusing on the toxins in cigarette smoke polluting the blood and increasing the chance of heart attacks and strokes.

The campaign used both ‘harm’ and ‘hope’ messaging, by showing the harm caused by smoking to encourage smokers to quit, and, at the same time, providing a way for them to do so in the form of support from Smokefree. The advertising encouraged smokers to go online to find their way out of smoking, and order free support in the form of the Quit Kit, Smokefree app, text and emails. Partnership with pharmacies was a key part of the campaign strategy, and over 75% of pharmacies across England were provided with a new product – ‘Quit Cards’,  to act as a conversation starter to help  them engage with  smokers and promote the full range of Smokefree products to help them quit.

The campaign achieved a national awareness of 87%, with 84% of smokers who saw the campaign reporting that it was aimed at people like them. The messages cut through similarly well, with 68% of people agreeing that "these adverts made me think that every cigarette is harmful", 87% agreeing that "cigarettes cause heart attacks and strokes", and 30% taking action to quit smoking, by either ordering a Quit Kit, stopping smoking, or talking about it with family or friends.

During the campaign, approximately 172'000 Smokefree products were ordered, including 84'000 Quit Kits and 50'000 downloads of the Smokefree mobile app. 420'000 Quit Cards were distributed by pharmacies across England.

These figures suggest that the public health campaign was a success, and that it motivated a significant number of people to try and quit smoking, as well as raise awareness of the harmful effects of tobacco smoke on the body.

The Gamble Aware Campaign

Also known as "Bad Betty", this campaign by the Senet Group used television, radio, digital press and gambling shop window posters to highlight the warning signs of problem gambling and the benefits of staying in control, using the slogan: "When the fun stops, stop!" Aiming to prevent problem gambling, the campaign advised gamblers to only bet what they can afford, not gamble when they're angry, never chase losses, and not put gambling before their friends.

The campaign resulted in high levels of awareness, with over 1/3 of gamblers who recall the campaign saying it made them approach their gambling more responsibly, and 1/6th of people who recall the campaign being prompted to "warn other people about their gambling habits.", suggesting that it also influenced public perceptions of gambling and made people more aware of the risks. The campaign achieved an awareness of 34% in the general population, a significant percentage usually only achieved with double the levels of funding that Gamble Aware was granted.

The phrases "when the fun stops, stop" and "Bad Betty" were recited by millions following the campaign, and occupied a significant place in the consciousness of gamblers that prompted them to approach their habit with more caution.

Changes to the UK smoking laws

The 2007 public smoking ban prohibited smoking cigarettes in indoor workplaces, indoor public places, and on public transport. These laws were later amended in 2015 to prohibit smoking in a vehicle carrying children, punishable by on-the-spot fines. These law changes have resulted in significant health benefits, as well as changes in behaviour and attitudes towards smoking.

In the year following the introduction of the smokefree laws, there was a 2.4% reduction in hospital admissions for heart attacks in England, saving the NHS £8.4 million in a single year. In the same year, there was a 12.3% reduction in hospital admissions for childhood asthma cases, equivalent to 6800 admissions over the next 3 years.

The ban proved to be successful and popular, even among smokers. A YouGov survey commissioned by ASH in 2014 found that 82% of adults in the UK support the smokefree laws, including 54% of smokers.

In addition to support for the smokefree laws, people are now less willing to expose themselves to smoke in private dwellings. In 2009, 78% responders to an ASH YouGov survey did not allow smoking anywhere in their home or in enclosed areas on their property, and this had increased to 86% of respondents by 2014, suggesting that the law changes were responsible for a decrease in the social acceptability of smoking, leading to it being a less desirable behaviour among the public.

Since April 2012, it has been illegal to display tobacco products at the point of sale (POS) in large shops, and since 2015 it has been illegal to display them at any point of public sale. This was inspired by the idea that openly displaying tobacco products in shops contributed to the normalising of smoking by society, and the hope that banning this display would reduce the social acceptability of smoking.

Research shows that POS display has a direct impact on young people smoking. In 2006, 46% of UK teenagers were aware of tobacco display at POS, and those who admitted an intention to start smoking were more likely to recall brands seen at POS.

The Cochrane systematic review (2011) found that exposure to tobacco advertising and promotion, including POS displays, increases the likelihood that adolescents will develop a smoking addiction, justifying the hypothesis that POS bans decrease the prevalence of smoking.

An evaluation of the POS ban in Ireland found that it had an immediate impact on young peoples' attitudes towards smoking. The proportion of young people believing that more than 1/5th of their age group smoked decreased by 16%, and 38% of teenagers thought the law would make it easier for children not to smoke, suggesting that the bans had significant effects on the public perception of smoking and helped to de-normalise it.

A study by Cancer Research UK in 2010, just after the laws had been passed, found 73% support for the removal of POS displays, whereas a larger poll of British adults found 64% support. These results both suggest that the public is in favour of banning these displays as a way of reducing young peoples' exposure to tobacco advertising.

Issues with public health interventions

There are methodological issues in attempting to judge the effectiveness of public health campaigns. When multiple public health measures (e.g. Fit for Life, 5-a-day) are introduced within a short period of time, it is difficult to establish cause and effect as we cannot pin down which campaigns are responsible for specific changes in public behaviour, perceptions of smoking and gambling, and overall changes in health. For example, the 2.4% reduction in hospital admissions for heart attacks may not necessarily be due to the introduction of the public smoking ban, but rather due to a greater overall focus on a healthy lifestyle in the media.

We don't know how closely peoples' reported attitude changes, awareness of addiction, or planned changes in behaviour reflect their actual actions - in responses judging the effectiveness of the Toxic Cycle campaign,  people could have overestimated their own likelihood of quitting, or simply lied and reported stopping smoking for the purpose of giving a socially acceptable survey answer. Many people accessed Smokefree and NHS Stop Smoking services to attempt to quit, but this does not necessarily mean that the system was effective at helping them quit rather than just providing an incentive (30% took actions such as ordering a Quit Kit, but there is no figure for how many successfully stopped smoking.)

Biological explanations of addiction

Thought I'd make a start on the addiction topic! AO2 in this can come from two styles of question - the first being evaluation (of theories or studies), the second being application. Questions can give a specific scenario and ask you to apply your knowledge to the situation - make sure you specifically reference the situation they describe in order to gain AO2 credit for application. They can also ask about either smoking or gambling in specific detail - so make sure to learn points relating to both addictions rather than just one or the other. You can also be asked about addiction, maintenance and relapse as separate elements of addiction - so make sure you can specifically apply theory to each of the three stages!

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points/IDAs
Purple: My notes/hints/tips

Dopamine Reward System (DRS)

According to this hypothesis, when the brain experiences pleasure dopamine is released from the mesolimbic pathway in the midbrain. The original purpose of this was to promote behaviours that aided survival and reproduction, such as eating, drinking, and sex. However, the use of certain drugs such as alcohol or nicotine, or events such as winning money when gambling, can also trigger mesolimbic dopamine release, as well as a glutamate release from the limbic system, stimulating areas of the prefrontal cortex responsible for memory - creating a memory of pleasurable feelings.

Continued drug use has been shown by Volkow et al (1999) to reduce the sensitivity and activity of the D2 dopamine receptors in the brain's reward system. This can explain the maintenance and progression of an addictive behaviour - it is suggested that this leads people to taking more or "harder" drugs in order to compensate for their decreased sensitivity.

Pontieri et al (1996) found supporting evidence for the role of the DRS in addiction. They found that nicotine produces its pharmacological effects through the activation of nicotinic acetylcholine receptors (nAChRs). The activation of these receptors then increases dopamine levels, causing pleasurable feelings.

The Parkinson’s Disease Society estimates that 14% of patients who take drugs such as Pergolide, which increase dopamine activity, will develop compulsive behaviours such as gambling. (Breen 2008)  Similarly, Grosset (2009) found that dopamine agonists used to treat Parkinson’s disease turned 10% of patients in to compulsive gamblers. This suggests that dopamine levels can play a role in the initiation of addictive behaviour  - this is far higher than in the general population, implying that rather than just being released by addictive behaviours, dopamine plays a role in triggering these behaviours in the first place. Supporting this, Kim & Grant (2001) found that administering Naltrexone, a dopamine antagonist, was successful in reducing compulsions to gamble. These results also help explain initiation of addictive behaviour - drug induced deviations from normal drug levels can stimulate or kill urges to initiate an addictive behaviour.

Cocaine inhibits the action of a protein called DAT (which controls the removal of excess dopamine from the junctions between nerve cells in the brain). This leads to nerve cells being overloaded with dopamine, which contributes to the "high" associated with taking cocaine - supporting the hypothesis that behaviours that cause a dopamine surge will be registered as "pleasurable" and become addictive.

However, Volkow et al (1997) found that while drugs increased dopamine activity the limbic systems of addicted participants, they also raised dopamine levels in non-addicted controls to an even greater degree without them becoming addicted, suggesting that raised dopamine levels cannot entirely explain addiction, and it is overly reductionist to suggest this - there must be other factors that cause somebody to develop a dependence after just taking the drug.

Prefrontal Cortex

The prefrontal cortex (PFC) deals with rational decision-making and social behaviour. It also plays a role in regulating the emotionally-driven and impulsive limbic system. Raised dopamine levels suppress the PFC, leading to it being unable to regulate the more primitive amygdala, leading to risk-taking and impulsive behaviour such as drug-taking.

Research has found a grey matter reduction in the frontal lobes in addicts to heroin, cocaine and alcohol, damaging "synaptic plasticity"  which then leads to a loss of PFC function. This explains maintenance of addiction - drug addiction damages our own ability to regulate our addictive behaviours, making us less likely to be able to quit.

However, it is difficult to establish cause and effect here - an alternate explanation is that a reduction in PFC activity pre-dates addiction, and is actually responsible for the loss of control and impulsive behaviours such as gambling and drug-taking, rather than drug-taking causing PFC damage.

Frontal lobe volume loss has been found in cocaine addicts (Franklin et al 2002), alcoholics (Jernigan et al (1991) and heroin addicts (Liu 1998), suggesting that drugs which increase dopamine levels cause damage to the PFC's frontal lobes.

Endogenous Opioid System

The opioid system controls pain, reward and addictive behaviours. Opioid receptors in the brain are activated by a family of endogenous peptides such as enkephalins and endorphins, released by neurons that are stimulated by addictive behaviours such as gambling and smoking - the activation of this system causes a pleasure response similar to that of the mesolimbic pathway's dopamine reward circuit.

Herz (1997) found that endogenous opioids play a key role in the addictive properties of alcohol, as results showed that opioid antagonists (reducing EOS activity) reduce both pleasure from and urge to drink alcohol.

Karras and Kane (1980) found that tobacco smoking and cravings are reduced in humans when they are given naloxone, a narcotic opioid antagonist. The resulting suppression of the EOS resulted in less urge to carry out an addictive behaviour and fewer withdrawal symptoms (cravings), suggesting that the EOS has a role in both the formation and relapse of addictive behaviour.

Pierzchala et al. (1987) showed that repeated short-term administration of small doses of nicotine to male rats produced significant increases in enkephalin, supporting the central idea of the EOS playing a role in the pleasurable feelings from addictive drugs and behaviours.

Anthropomorphism is an issue with Pierzchala's study, as research carried out on rats cannot necessarily have its results accurately applied to humans. The physiological differences between rats and humans could mean that the biological mechanisms that influence addiction such as the EOS function differently too.

Research into the endogenous opioid system can only explain maintenance and relapse of addictive behaviour (see Karras + Kane - EOS suppression reduced cravings.) It cannot explain initiation of an addictive behaviour, as one must take a drug first in order to know that it has pleasurable effects stemming from opioid release - we don't know that something will be pleasurable until we try it.

Genes

There are certain genes or combinations of genes that have been implicated in increasing or decreasing the likelihood that an individual will engage in addictive behaviours. There is also evidence suggesting that the concordance for many addictions rises as people become more genetically similar.

Breen (2006) identified a variant of a gene responsible for inhibiting the production of DAT, which controls dopamine levels. It was found that those who had 2 copies of the variant gene were 50% more likely to become addicted to cocaine, suggesting that genetics can play a role in addiction.

Studies have identified the presence of the gene SLC6A3-9 as reducing the risk of starting smoking, pushing back the age of beginning, and making quitting more likely to succeed - also causing a lower dopamine release from nicotine. This gene reduces the risk of "thrill-seeking" behaviour such as smoking, gambling and drug-taking.

Lerman (1999) compared the DNA of non-smokers and chronic smokers, and found that non-smokers were more likely to have the SLC6A3-9 gene present, and smokers with the gene were less likely to have started below age 16, suggesting that the gene's absence powerfully influences the risk of nicotine addiction. 

Hamer (1999) studied smokers, former smokers, and non-smokers. Participants with the SLC6A3-9 gene scored 1 point lower in the "novelty seeking" index and were rated as less impulsive, deriving less of a "thrill" from nicotine.

These studies that identify SLC6A3-9 absence as a genetic risk factor can certainly help explain initiation of addiction. The absence of this gene makes people more likely to indulge in thrill-seeking and impulsive behaviours such as trying smoking or drugs for the first time, starting up a habit that can quickly develop into addiction.

Shields (1962) investigated 42 pairs of monozygotic twins raised apart, to control for environmental factors in their upbringing, and found a 79% concordance rate for smoking addictions. Due to being able to control for environmental factors such as peer groups that could have played a role in addiction initiation, this is strong supporting evidence for the role of genes providing an inherent susceptibility to nicotine addiction.

Neuroadaptation

Neuroadaptation is the process whereby the body compensates for the presence of a chemical in the body so that it can continue to function normally. As a person uses a drug more regularly, the body will become used to the presence of the substance and adapt its normal responses accordingly, meaning somebody develops tolerance to a drug, and needs more of the substance to give a desired effect. Tolerance leads to dependence and addiction - significant changes occur in the brain to support the constant presence of drugs in the body, and a person will feel withdrawal symptoms when the drug is removed from their system. Withdrawal symptoms occur because the body has adapted to the drug's presence, and now requires it in order to maintain normal functioning.

With nicotine, withdrawal symptoms that can lead to relapse include anger, anxiety, depression, insomnia, weight gain and an inability to concentrate.

While neuroadaptation can explain the maintenance and relapse of addiction, with the body adjusting to a constant level of the drug in its system and suffering withdrawal when it is removed, it cannot explain addiction. 

Only really bring up neuroadaptation if the question asks about maintenance or withdrawal, as there really isn't anything in this theory that explains initiation. There isn't much AO2 here - so use it sparingly. It's very useful for application questions, though.

Overall

Biological explanations of addiction can be considered overly reductionist, ignoring environmental factors such as the role of the peer group, and cognitive processes such as self-medication in the process of addiction. Social factors such as the peer group are very important in the initiation of addiction - most addicts are first exposed to the drug through a member of their peer groups, and many people take a drug only in a specific social scenario.

Biological explanations of addiction are also overly deterministic, suggesting that people are completely controlled by their neurological systems such as the DRS and the EOS, as well as inherited genetic predispositions. Not everyone with a thrill-seeking personality due to genetics goes on to develop an addiction, and nor does everyone with raised dopamine levels - free will must play a powerful part in addiction formation.

Generally, genes best explain initiation, EOS and DRS best explain maintenance, and neurodaptation/withdrawal best explain relapse.