Addiction

Describing Addiction

Physical dependence occurs when an individual experiences withdrawal symptoms when they stop using a substance. This indicates that their body has adapted to the substance. Psychological dependence occurs when an individual feels compelled to take a substance to gain pleasure or reduce discomfort. Even when the behaviour is harmful, the individual continues to engage in it because it has become a habitual source of reward.

Tolerance occurs when repeated exposure to a substance means that larger doses are required to achieve the same effect. Behavioural tolerance occurs when individuals adjust their behaviour to cope with the effects of the substance. Cross-tolerance occurs when tolerance to one substance reduces sensitivity to another similar substance, such as alcohol reducing sensitivity to benzodiazepines.

Withdrawal symptoms are the physical and psychological effects experienced when a person reduces or stops using a substance. These symptoms are usually the opposite of the rewarding effects of the substance and encourage continued use. Acute withdrawal occurs within hours and involves intense cravings that decrease after a few days. Prolonged withdrawal can last for weeks, months or even years, and individuals remain highly sensitive to cues associated with the substance.

Risk Factors in the Development of Addiction

Genetic Vulnerability

Genetic vulnerability suggests that biological factors increase the likelihood of addiction. Individuals with fewer D2 dopamine receptors have lower dopamine activity, making them more likely to use substances to compensate. The number of dopamine receptors is genetically determined. The CYP2A6 gene also affects addiction because individuals with a poorly functioning version metabolise nicotine less effectively and therefore tend to smoke less.

Personality

Personality is another risk factor. Traits such as neuroticism and hostility have been linked to addictive behaviours. Anti-social personality disorder is particularly associated with addiction because individuals with this disorder tend to be impulsive and engage in risk-taking behaviour.

Social Influences

Stress can lead individuals to self-medicate using drugs or alcohol. Childhood trauma can affect brain development and increase vulnerability to stress later in life. Parental influences are important, as children who grow up around addiction or permissive attitudes towards substance use are more likely to become addicted themselves. Fletcher et al. (1995) found that authoritative parenting reduces the likelihood of substance abuse. Peer influences also play a role. O’Connell et al. (2009) found that socialising with users, having access to substances, and overestimating peer use all increase the likelihood of addiction.

Evaluation of Risk Factors

Kendler et al. (2012) found that children with at least one parent who was addicted were significantly more likely to develop addiction themselves, supporting genetic vulnerability.

However, there is only correlational evidence between stress and addiction, meaning it is unclear whether stress causes addiction or addiction leads to stressful lifestyles.

Bahlmann et al. (2002) found that participants developed anti-social personality disorder before alcohol dependence, suggesting personality may be a causal factor.

Mayes and Suchman (2006) argued that addiction is best explained by a combination of risk factors rather than any single factor alone, and that some influences, such as a supportive family, may act as protective factors.

Explanations for Nicotine Addiction

Brain Neurochemistry

Brain neurochemistry explains nicotine addiction through the role of dopamine and nicotinic acetylcholine receptors (nACHRs). When nicotine stimulates nACHRs, dopamine is released and then the receptors shut down, leading to desensitisation and a reduction in active neurons.

Nicotine stimulates receptors in the ventral tegmental area, causing dopamine to be transmitted along the mesolimbic pathway to the nucleus accumbens and along the mesocortical pathway to the frontal cortex. These pathways form part of the brain’s reward system.

When a person stops smoking, the receptors become resensitised and more available, leading to overstimulation by acetylcholine and the experience of withdrawal symptoms. Continued smoking avoids withdrawal but leads to long-term changes in receptor activity and increased tolerance.

Evaluation of Brain Neurochemistry

McEvoy et al. (1995) found that schizophrenics taking dopamine-blocking drugs increased their smoking, supporting the role of dopamine in addiction.

This explanation has practical applications, as it has led to nicotine replacement therapies such as patches and gum that reduce withdrawal symptoms.

However, the explanation is deterministic because some individuals do not become addicted despite smoking.

Gilbert (1995) found that withdrawal symptoms are not solely related to nicotine levels but are influenced by personality and environmental factors, suggesting that biological explanations are incomplete.

Learning Theory 

Cue reactivity refers to environmental cues becoming associated with smoking. These cues act as secondary reinforcers, such as smoking with friends or in specific places. Cue reactivity involves subjective cravings, physiological responses such as increased heart rate, and behavioural indicators such as patterns of smoking.

Evaluation of Learning Theory

Levin et al. (2010) found that rats repeatedly sought nicotine, supporting the role of positive reinforcement.

Carter and Tiffany (1999) found that dependent smokers showed stronger cravings and physiological responses to smoking cues, supporting cue reactivity.

Smith (1988) found that aversion therapy was effective in reducing smoking, demonstrating real-world applications of learning theory.

Explanations for Gambling Addiction

Learning Theory

Learning theory explains gambling through vicarious reinforcement, where individuals observe others being rewarded. Partial and variable reinforcement schedules make gambling resistant to extinction because rewards are unpredictable. Cue reactivity also contributes, as environmental stimuli associated with gambling trigger cravings.

Evaluation of Learning Theory

Dickerson (1979) found that frequent gamblers delayed their bets to prolong excitement, supporting reinforcement explanations.

However, learning theory does not fully explain why some individuals do not become addicted, suggesting that other factors are involved.

Brown (1987) argued that individual differences influence susceptibility to reinforcement.

Cognitive Theory

Cognitive theory suggests that gamblers develop distorted thinking patterns. They overestimate their chances of winning and underestimate losses.

Rickwood et al. (2010) identified four types of cognitive bias. Skill bias involves overestimating control over random events. Personal beliefs involve superstition or beliefs about luck. Selective recall involves remembering wins and forgetting losses. The gambler’s fallacy involves believing that losses must eventually be followed by wins.

Self-efficacy also plays a role. Individuals who believe they cannot stop gambling are more likely to relapse, creating a self-fulfilling prophecy.

Evaluation of Cognitive Theory

Michalczuk et al. (2011) found that addicted gamblers showed higher levels of cognitive bias, supporting the theory.

However, self-report measures may not accurately reflect genuine thought processes.

Dickerson and O’Connor (2006) argued that verbal reports may not reflect actual thinking.

McCusker and Gettings (1997) found that gamblers showed attentional bias in a Stroop task, supporting cognitive explanations.

Reducing Addiction

Drug Therapy

Drug therapy includes aversive drugs, agonists, and antagonists. Aversive drugs such as disulfiram create unpleasant effects when combined with substances, leading to conditioned aversion. Agonists mimic the effects of the addictive substance to reduce withdrawal symptoms, while antagonists block receptors to prevent the substance from producing its effects.

Nicotine replacement therapy acts as an agonist that stimulates receptors and releases dopamine in a controlled way. Naltrexone is sometimes used for gambling addiction because it affects similar reward pathways.

Evaluation of Drug Therapy

Hartmann-Boyce et al. (2018) found that nicotine replacement therapy increased quit rates by approximately 60 per cent compared to placebo groups.

However, drug therapies can produce side effects such as headaches, nausea and sleep disturbances. Naltrexone may cause depression and muscle spasms.

A strength is that drug therapies reduce stigma by emphasising biological causes of addiction.

Behavioural Interventions

Aversion therapy involves pairing addictive behaviour with unpleasant consequences to create a new association. Disulfiram causes nausea when alcohol is consumed, while electric shocks may be used in gambling treatments.

Covert sensitisation involves imagining unpleasant consequences rather than experiencing them directly.

Evaluation of Behavioural Interventions

Fuller et al. (1986) found no significant long-term difference between disulfiram and placebo groups, suggesting limited effectiveness.

Some argue that aversion therapy is unethical due to psychological and physical harm.

McConaghy et al. (1983) found that covert sensitisation was highly effective, with 90 per cent of participants reducing gambling behaviour.

However, behavioural interventions may only address symptoms and lead to symptom substitution.

Cognitive Behavioural Therapy

Cognitive behavioural therapy involves identifying high-risk situations and challenging faulty thinking patterns. Functional analysis helps identify triggers, while skills training teaches strategies such as assertiveness and coping skills.

Evaluation of CBT

Cowlishaw et al. (2012) found CBT reduced gambling behaviour in the short term, but effects were not maintained long term.

CBT is demanding and has high dropout rates, limiting its effectiveness.

It is also possible that changing behaviour alone is sufficient, without targeting cognition.

Prochaska’s Six Stage Model of Behaviour Change

Prochaska and DiClemente (1983) proposed that individuals move through six stages when changing addictive behaviour.

In precontemplation, individuals are not considering change. In contemplation, they recognise the need to change but focus on costs. In preparation, they plan to change. In action, they actively attempt to stop. In maintenance, they sustain change for more than six months. In termination, abstinence becomes permanent. However, individuals may relapse or move between stages.

Evaluation of Prochaska’s Model

The model is realistic because it acknowledges relapse and views behaviour change as a process.

It has strong face validity because it reflects real-life experiences of recovery.

However, Taylor et al. (2006) found that the model is no more effective than other behaviour change models and lacks strong empirical support for distinct stages.

A limitation is that the model assumes rational decision-making, which may not apply to individuals affected by addiction and cognitive biases.