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Having described addiction and examined the biological, learning and cognitive models that explain it, this lesson turns to the practical question of how addiction can be reduced. The interventions follow logically from the models: where addiction is understood biologically, drug therapies target its neurochemistry; where it is understood as learned, behavioural interventions (aversion therapy, covert sensitisation) try to recondition it; and where it is understood cognitively and motivationally, structured approaches such as the theory of planned behaviour and Prochaska's transtheoretical (six-stage) model explain and support the process of change. For the AQA specification, the focus falls on drug therapy, behavioural interventions, and the two named models of behaviour change. A recurring evaluative theme is the contrast between interventions that suppress the symptoms of addiction (drug therapy managing withdrawal) and those that target its causes and the change process itself (behavioural and cognitive approaches), and the consistent finding that combined and well-matched approaches outperform any single one. Smoking, alcohol and gambling are used as examples, and the topic is treated clinically and objectively, without operational detail about substance misuse.
Key Definition: A theory of behaviour change is a model that specifies the factors and stages involved in moving from an addictive behaviour to abstinence or controlled use; the AQA-specified examples are Ajzen's theory of planned behaviour and Prochaska's transtheoretical (six-stage) model.
This lesson addresses the following points from the AQA A-Level Psychology (7182) specification, Paper 3, Section D — Addiction:
It develops drug therapy (nicotine replacement and aversive drugs), the two behavioural interventions, and the two theories of behaviour change, preparing you to describe (AO1) and evaluate (AO3) approaches to reducing addiction. Questions are usually split AO1/AO3 only, with no AO2 unless a scenario stem is provided — this lesson flags that distinction. The content applies the conditioning principles from the learning model and the brain mechanisms from the biological model directly to treatment.
Drug therapies follow from the biological model: if addiction is driven by the action of substances on the brain's reward and receptor systems, then drugs that modulate those systems should help. They fall into broad types.
Nicotine replacement therapy (NRT) supplies controlled nicotine without the harmful combustion products of cigarette smoke, via patches, gum, lozenges, inhalers or sprays. It works by:
NRT maps neatly onto the desensitisation account from the biological model: by keeping nicotinic receptors gently stimulated, it prevents the sharp craving state that drives the next cigarette, then reduces the level slowly enough for the upregulated receptors to readjust. A further advantage of separating the nicotine from the cigarette is that it begins to break the behavioural habit — the hand-to-mouth ritual, the conditioned cues of lighting up — even while withdrawal is being managed, so NRT works on both the biological and (indirectly) the conditioned components of smoking. This is one reason NRT is more effective when combined with behavioural support and with the kind of cue management that the learning model recommends.
Other drug therapies work by blocking reward or by creating aversion:
| Drug type | Example and mechanism | Application |
|---|---|---|
| Partial agonist | A drug that partly stimulates nicotinic receptors (easing withdrawal) while blocking nicotine's full effect (reducing the reward from smoking) | Smoking cessation |
| Antagonist | An opioid antagonist that blocks reward receptors, reducing the pleasurable effects of alcohol (and reducing urges) | Alcohol dependence; also trialled for gambling urges |
| Aversive | A drug that blocks alcohol metabolism so that drinking produces highly unpleasant effects (nausea, flushing), deterring use | Alcohol dependence (an aversive, not a reward-blocker) |
The logic of these drug therapies is instructive. Substitution (NRT) eases the path to abstinence by removing withdrawal as an obstacle; antagonists attack the addiction at the point of reward, so that using the substance no longer "pays"; and aversives add a deterrent cost to use. They therefore target different points in the addiction cycle, which is one reason the choice of drug depends on the substance and the individual.
For gambling, drug therapy is much less established: there is no approved pharmacological treatment specific to gambling disorder, though reward-blocking (opioid-antagonist) drugs have shown some promise in reducing urges — consistent with the shared dopamine reward mechanism. This gap is itself revealing: because gambling has no ingested chemical to substitute or metabolise, the substance-focused logic of much drug therapy has little to grip onto, which is precisely why psychological approaches (cognitive and behavioural) carry more of the load in treating behavioural addictions.
Key Definition: In addiction pharmacology, an agonist/substitute supplies or mimics the substance to reduce withdrawal and craving (e.g., NRT); an antagonist blocks the reward; and an aversive makes use unpleasant. All three target the biological mechanisms of addiction.
Behavioural interventions follow from the learning model: if addiction is conditioned, it can in principle be reconditioned. Both named interventions use classical conditioning to attach an aversive response to the addictive substance or behaviour — the reverse of the appetitive conditioning that helped create the addiction. Where cue reactivity attached craving to substance-related cues, aversion methods aim to attach revulsion instead, so that encountering the substance or thinking about the behaviour elicits discomfort rather than desire. This is sometimes described as counter-conditioning: replacing an existing conditioned response (craving) with an incompatible one (aversion).
Aversion therapy repeatedly pairs the addictive substance or behaviour with an unpleasant stimulus so that the substance itself comes to elicit an aversive response:
graph LR
A[Addictive substance: CS] --> C[Paired repeatedly]
B[Aversive stimulus: UCS] --> C
C --> D[Substance alone triggers nausea / revulsion: CR]
D --> E[Reduced desire to use]
Aversion therapy can also be applied to gambling, where, for example, gambling-related stimuli or behaviours are paired with an aversive stimulus so that the urge to gamble becomes associated with discomfort.
Covert sensitisation is a less invasive, imagery-based form of aversion therapy. Instead of physically experiencing an aversive stimulus, the client vividly imagines the addictive behaviour followed by extremely unpleasant consequences (e.g., imagining taking a drink and then becoming violently nauseous and vomiting in public), so that the aversive imagery becomes associated with the behaviour. Because it is conducted "covertly" in imagination, it avoids the physical discomfort and many of the ethical problems of in-vivo aversion therapy, though its evidence base is more limited and largely drawn from case studies.
Key Definition: Covert sensitisation is an imagery-based behavioural therapy in which the addictive behaviour is repeatedly paired, in imagination, with aversive consequences, to condition an aversion to it without physically administering an unpleasant stimulus.
Ajzen's theory of planned behaviour (TPB) is a cognitive model of how intentions to change behaviour are formed and translated (or not) into action. Applied to reducing addiction, it identifies three influences on the intention to quit or cut down, and one influence on whether the intention becomes behaviour:
graph TD
A[Attitudes towards quitting] --> D[Intention to change]
B[Subjective norms] --> D
C[Perceived behavioural control] --> D
D --> E[Behaviour change: e.g. quitting]
C --> E
Together, attitudes, subjective norms and perceived behavioural control shape the intention to change, and perceived behavioural control also directly influences the behaviour itself. The model implies that interventions should work on all three components — improving attitudes (health education about the harms of smoking, alcohol or gambling and the benefits of stopping), shifting norms (denormalising smoking and gambling, emphasising that most people do not smoke), and strengthening perceived control (building self-efficacy and concrete coping skills so the person believes quitting is achievable). A practical strength of TPB is therefore that it gives intervention designers a clear set of modifiable targets rather than treating the decision to quit as a single, mysterious act of will. Its key caveat, developed in the evaluation, is that strengthening intention does not guarantee changed behaviour, because intentions can be overridden by the automatic, craving-driven processes that characterise addiction.
Prochaska and DiClemente's transtheoretical model (TTM) describes behaviour change as a process through stages rather than a single event, and is widely used to match support to the individual's readiness to change.
| Stage | Description | Implication for intervention |
|---|---|---|
| 1. Pre-contemplation | Not yet considering change; may not see a problem | Raise awareness; provide non-confrontational information |
| 2. Contemplation | Aware of the problem and considering change, but ambivalent | Explore the pros and cons; help tip the balance |
| 3. Preparation | Intending to change soon and starting to plan | Help set goals and develop a concrete plan |
| 4. Action | Actively changing behaviour (e.g., has quit) | Support and reinforce the new behaviour; teach coping skills |
| 5. Maintenance | Sustaining the change over time and avoiding relapse | Consolidate gains; relapse prevention |
| 6. Relapse | Returning to the behaviour; re-enters the cycle at an earlier stage | Normalise the setback; avoid demoralisation; re-engage |
graph LR
A[Pre-contemplation] --> B[Contemplation]
B --> C[Preparation]
C --> D[Action]
D --> E[Maintenance]
E --> F[Relapse]
F --> B
Two features are central. First, the model treats relapse as a normal, expected part of the cycle rather than as failure — a person who relapses re-enters at contemplation or preparation rather than starting from scratch, which reduces the demoralisation that can otherwise drive a full return to use. Second, it implies that interventions must be stage-matched: pushing action-oriented techniques onto a pre-contemplator is likely to fail, whereas the same person may respond to awareness-raising. This is the rationale behind motivational approaches that meet the individual "where they are" rather than assuming readiness to change.
It helps to see how the two behaviour-change theories relate to the practical interventions. The theory of planned behaviour and Prochaska's model are not themselves "treatments" but frameworks that explain and structure the change process, and they make the interventions more effective when combined with them. For example, drug therapy reduces withdrawal and craving, but whether a smoker even attempts to quit depends on the TPB precursors (a positive attitude to quitting, supportive norms, a sense that quitting is achievable); and when to offer intensive, action-oriented support depends on the person's Prochaska stage. In practice, then, a well-designed programme might use Prochaska's model to gauge readiness, the theory of planned behaviour to strengthen the intention to change, drug therapy to manage the biology of withdrawal, and behavioural or cognitive techniques to recondition cues and challenge distortions — an integrated package in which the theories and the treatments do different jobs.
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