Dependence, tolerance and withdrawal

• Physical dependence — the body has adapted to the presence of the substance, so a withdrawal syndrome occurs when the person stops taking it. Physical dependence is defined by the presence of withdrawal symptoms.
• Psychological dependence — a compulsion to experience the effects of the substance or behaviour. It shows itself as a preoccupation, and in continuing despite obvious harm to health, work and relationships. Psychological dependence generally outlasts physical dependence, which is why relapse is so common.
• Tolerance — the reduced response to a substance after repeated use, so that more is needed to achieve the same effect. Two important sub-types: cross-tolerance (tolerance to one substance produces tolerance to a similar one — a heroin user needs a higher dose of morphine as a painkiller) and behavioural tolerance (a person learns to compensate for the effects, e.g. a heavy drinker who walks in a deliberately straight line).
• Withdrawal syndrome — the set of symptoms experienced when the substance is stopped or reduced. Withdrawal symptoms are typically the opposite of the drug's effects, which is why nicotine withdrawal produces irritability and anxiety when nicotine itself is calming. It has two phases: an acute phase (intense, short-lived) and a prolonged phase (subtler cravings that persist for months and are frequently the cause of relapse).

Risk factors in the development of addiction

• Genetic vulnerability. Addiction is polygenic and moderately heritable. One mechanism is a difference in dopamine D2 receptors: some people inherit fewer D2 receptors, so they get less pleasure from ordinary activities and are more strongly driven to seek the powerful dopamine surge that a drug provides. Genes also influence how quickly a substance is metabolised. Note that genes create vulnerability, not destiny — the individual must still encounter the substance.
• Personality. Certain traits are risk factors, notably impulsivity (acting without weighing consequences, and a preference for immediate reward) and neuroticism. Antisocial personality disorder is over-represented among people with addictions. But the evidence does not support a single 'addictive personality', and the term is best avoided. Chronic and traumatic stress — especially childhood adversity — is a closely related risk factor: the substance is used as self-medication, and stress is one of the strongest triggers of relapse.
• Social influences — family. Perceived parental approval matters: adolescents who believe their parents are relaxed about substance use are more likely to use. Parents also act as models (social learning), and inconsistent or over-strict parenting is a further risk factor.
• Social influences — peers. Peers are the strongest social influence in adolescence. Three mechanisms: peers provide attitudes towards the substance (social learning); they provide opportunity and access; and, crucially, adolescents over-estimate how much their peers are using — a misperceived norm — which then normalises their own use.

Evaluation: risk factor research is almost entirely correlational, so causal direction is uncertain — an adolescent who has already started using drugs will choose drug-using friends, so peer association may be an effect rather than a cause. Risk factors also interact: a genetic vulnerability plus childhood trauma plus a peer group who use is far more predictive than any factor alone. Much of the evidence is also self-report, and admitting to drug use is subject to serious social desirability bias.

Tolerance or withdrawal?

Brain neurochemistry and learning theory

Brain neurochemistry — the dopamine reward system.

• Nicotine is absorbed within seconds and binds to nicotinic acetylcholine receptors (nAChRs) on neurons in the ventral tegmental area (VTA) of the mesolimbic pathway.
• This stimulates the release of dopamine in the nucleus accumbens — the brain's reward centre — producing the pleasurable, mildly euphoric 'buzz'. Dopamine is also released in the prefrontal cortex, which is why smokers report improved concentration.
• The dopamine surge reinforces smoking. But nicotine's effects are short-lived: dopamine levels fall rapidly, producing the craving and irritability that lead to the next cigarette. This is the nicotine regulation model — the smoker smokes to keep nicotine levels topped up and avoid withdrawal.
• With repeated exposure, the number of nAChRs increases (upregulation) and they become desensitised, which explains tolerance.

Learning theory.

• Operant conditioning — the dopamine 'buzz' is positive reinforcement; smoking to relieve the unpleasant symptoms of withdrawal is negative reinforcement. Both increase the behaviour.
• Classical conditioning and cue reactivity. The stimuli repeatedly present when smoking — a coffee cup, a pub, a particular friend, the sight of a lighter — become conditioned stimuli which, on their own, produce a conditioned response of craving and physiological arousal. This is cue reactivity, and it is the reason relapse is so common: an ex-smoker who has been abstinent for months walks past their old pub and the craving returns instantly.
• Social learning — adolescents imitate high-status models who smoke, having observed them being rewarded (with social approval).

Evaluation: the neurochemical account is well supported and explains why nicotine replacement therapy works. But it cannot on its own explain why so many smokers relapse long after all nicotine has left the body and physical withdrawal has ended — for that you need the learning account, and specifically cue reactivity. This is a good example of the two explanations being complementary rather than competing.

Learning theory and cognitive theory

Learning theory: partial (variable ratio) reinforcement. A gambler is not rewarded every time — they are rewarded unpredictably, after a variable number of responses. Skinner showed that a variable ratio schedule produces behaviour that is both high in rate and, crucially, extremely resistant to extinction: because the reward is unpredictable, no run of losses is evidence that the reward has stopped coming. This is precisely why fruit machines and betting apps are designed the way they are.

• Vicarious reinforcement — seeing others win (or seeing the machine's celebration of someone else's win) reinforces gambling in the observer.
• Cue reactivity — the sounds, lights and rituals of gambling become conditioned stimuli that provoke arousal and craving.

Cognitive theory: the biases of the gambler. Cognitive explanations propose that gamblers hold irrational beliefs about their chances of winning, and that these distortions maintain the behaviour:

• The gambler's fallacy — the mistaken belief that a run of losses means a win is 'due' (or that a run of reds on a roulette wheel makes black more likely). In reality, each spin is independent.
• The illusion of control — the belief that one's own skill, ritual or system can influence a purely chance outcome (throwing the dice harder for a higher number; using 'lucky' numbers).
• The near-miss bias — two jackpot symbols and a third just above the payline is objectively a loss, but it is experienced as 'almost a win'. Near misses activate the same reward circuitry as wins, and encourage continued play. Machines are deliberately engineered to produce them.
• Recall bias — gamblers remember and over-estimate their wins and forget or rationalise their losses ('I was unlucky'), which sustains an inflated sense of their own success.

Evaluation: the cognitive approach has strong support from the 'thinking aloud' method, in which gamblers verbalise their thoughts while playing: such studies find that gamblers make far more irrational statements than non-gamblers. It also has direct application — it is the theoretical basis of CBT for gambling, and it works. But the evidence is largely correlational, and it is possible that cognitive biases are a consequence of problem gambling (a way of justifying the behaviour) rather than its cause. Learning theory, meanwhile, explains why gambling persists but struggles to explain why most people who gamble on variable ratio schedules do not become addicted.

Explain the fruit machine

Drug therapy, behavioural interventions and CBT

• Drug therapy — agonists. An agonist mimics the drug's effects by binding to the same receptors, satisfying the craving without the harm. Nicotine replacement therapy (NRT) — patches, gum, inhalators — delivers nicotine without the carcinogens of tobacco smoke, and can be tapered downwards. Methadone is an agonist used to treat heroin addiction.
• Drug therapy — antagonists. An antagonist blocks the receptors, so the drug produces no effect and the reinforcement is removed. Naltrexone is used in this way for gambling addiction and for alcohol dependence, by blocking opioid receptors and reducing the reward.
• Drug therapy — aversives. Disulfiram for alcohol addiction: it produces a violently unpleasant reaction (nausea, vomiting, palpitations) if alcohol is consumed, deterring drinking.
• Aversion therapy — a classical conditioning treatment. The addictive substance or behaviour (CS) is repeatedly paired with a genuinely unpleasant stimulus (UCS) — for example an emetic drug that induces vomiting, or an electric shock — so that the substance itself comes to produce an aversive conditioned response. Gamblers may receive a shock while reading out gambling-related phrases.
• Covert sensitisation — the same principle, but the aversion is imagined rather than real. The client, deeply relaxed, is guided through a vivid, disgusting scenario in which the addictive behaviour leads to nausea, vomiting and humiliation, followed by an imagined 'relief' scene of walking away. It is much more ethically acceptable and less traumatic than aversion therapy, and can be practised as homework.
• CBT — cognitive restructuring challenges the irrational beliefs (the gambler's fallacy, the illusion of control) directly, and the behavioural component teaches specific skills: identifying and avoiding high-risk situations, refusing offers, managing boredom and stress, and planning for relapse.

Evaluation: drug therapies are effective and easy to adhere to, but they treat the symptoms, not the underlying causes, and they have side effects. Aversion therapy raises serious ethical objections (deliberately harming a client) and is undermined by poor evidence of long-term effectiveness — the aversion often fails to generalise beyond the clinic, because the client knows perfectly well that they will not be shocked at home. Covert sensitisation avoids the ethical problem but relies on the client's imaginative engagement. CBT has the best evidence for lasting change, but it is expensive, demands high commitment, and has a high drop-out rate. In practice, the best outcomes come from combining drug therapy with a psychological therapy.

Prochaska's six-stage model of behaviour change

Prochaska's six-stage model (the transtheoretical model) treats behaviour change as a process, not an event. People move through the stages cyclically, frequently relapsing and re-entering the cycle — and, crucially, a different intervention is appropriate at each stage.

• 1. Precontemplation — the person is not thinking about change in the next six months. They may be in denial about the harm, or demoralised by previous failed attempts. Therapeutic goal: get them to think about change — provide information, explore the consequences.
• 2. Contemplation — aware of the problem and thinking about it, but deeply ambivalent, weighing the costs against the benefits. People can remain here for years. Goal: tip the balance towards change.
• 3. Preparation — the person believes change is necessary and intends to act within about a month, but does not yet know how. Goal: help them construct a concrete, realistic plan.
• 4. Action — the person has actively done something about the addiction within the last six months. Goal: teach the skills needed to avoid relapse — identifying and avoiding high-risk situations and cues.
• 5. Maintenance — the change has been sustained for more than six months, and the focus shifts to maintaining it. The person is more confident and needs less support, but remains vulnerable.
• 6. Termination — the new behaviour is automatic, there is no temptation to return, and the person has complete self-efficacy. Prochaska accepted that many people never reach this stage and instead remain permanently in maintenance.

Evaluation. The model's great strength is that it treats relapse as a normal part of the cycle, not as failure — which is far more realistic and far less demoralising for the client — and it has genuine practical value, because matching the intervention to the person's stage improves outcomes (there is no point handing a detailed quit plan to someone in precontemplation). But the six-month boundaries are arbitrary and have no psychological justification, and people frequently do not move through the stages in order: they skip stages, or jump straight from precontemplation to action after a health scare. Some critics argue the 'stages' are simply an artificial slicing of what is really a continuous process, and that the model describes change without explaining what causes someone to move from one stage to the next.

Spec check: the theory of planned behaviour (Ajzen) has been removed from 7182 v1.4. The specification now names only Prochaska's six-stage model.

Which stage?

Physical or psychological?

Which stage?

Where does nicotine act?

Why is gambling so hard to extinguish?

Agonist or antagonist?

Aversion or covert sensitisation?

Prochaska's insight

Sort the concept

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Term and meaning

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The big ideas to know

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