Addiction, tolerance, dependence and withdrawal

• Addiction — compulsive drug-seeking and use that continues despite harmful consequences, with impaired control.
• Tolerance — the same dose produces a smaller effect over time, so the user needs more to get the same result. It arises partly from receptor down-regulation.
• Physical dependence — the body has adapted, so stopping produces a physiological withdrawal syndrome (e.g. tremor, sweating, nausea, seizures in alcohol withdrawal).
• Psychological dependence — a compulsion to use for the mental or emotional effect (craving, relief of anxiety), which can persist long after the physical withdrawal has ended and is a major cause of relapse.

Exam framing: withdrawal explains why people keep using in the short term (they are avoiding an unpleasant state — negative reinforcement), but psychological dependence and cue reactivity explain why people relapse years later, long after detoxification.

The brain's reward pathway

The core biological explanation is the mesolimbic dopamine reward pathway — from the ventral tegmental area to the nucleus accumbens. Drugs of misuse all, by different routes, increase dopamine activity in this pathway, and the behaviour that produced the surge is powerfully reinforced.

• Nicotine binds to nicotinic acetylcholine receptors on neurons in the VTA, increasing dopamine release in the nucleus accumbens. It reaches the brain within seconds of inhalation, which makes the reinforcement very tightly linked to the act of smoking.
• Heroin is an agonist at opioid receptors; it is metabolised to morphine, produces euphoria and analgesia, and indirectly disinhibits dopamine neurons in the VTA.
• Alcohol enhances the inhibitory transmitter GABA and dampens the excitatory transmitter glutamate — which is why it depresses the nervous system and disinhibits behaviour — while also raising dopamine in the reward pathway.
• Genetic vulnerability: twin and adoption studies show heritable differences in risk, e.g. in how alcohol is metabolised and in dopamine receptor genes.

Mode of action

Classic study: Olds and Milner (1954)

Aim: to investigate whether electrical stimulation of certain brain regions acts as a positive reinforcer.

• Method: electrodes were implanted into the brains of rats — notably in the septal area — and the rat could deliver a brief current to its own brain by pressing a lever in a Skinner box.
• Findings: rats with electrodes in the septal area returned repeatedly to the lever and pressed it at very high rates to self-stimulate. The stimulation could also be used to shape behaviour, such as steering the rat towards a particular corner of the box. Stimulation in other regions produced no such effect, or was avoided.
• Conclusion: there are regions in the brain whose stimulation is intrinsically rewarding — evidence for a physiological reward system underlying reinforcement, and the foundation of modern reward-pathway accounts of addiction.

Evaluate it: a controlled, replicable experiment that founded a whole research programme. But it is an animal study — extrapolation to human addiction, which involves cognition, culture and social context, is a real weakness — and it involved invasive surgery, raising serious ethical issues now governed by the Scientific Procedures Act (1986).

Explaining and treating addiction

Tap a card, then tap the category it belongs to.

Learning explanations of addiction

• Operant conditioning: the drug's effect is positively reinforcing (euphoria, relaxation, the nicotine hit). Once dependence has developed, using the drug removes withdrawal symptoms, which is negatively reinforcing — a second, powerful maintenance mechanism.
• Classical conditioning and cue reactivity: the paraphernalia, places and people associated with use (the pub, the lighter, the needle) become conditioned stimuli that trigger conditioned craving responses. This is why an ex-user can relapse simply by walking past an old haunt — and it explains why treatment must address cues, not just chemistry.
• Social learning: initiation is often modelled — a young person imitates high-status peers, siblings or media figures, and vicarious reinforcement (seeing others enjoy it and gain status) increases imitation. Mundt et al. (2012), a contemporary study option, modelled peer selection and peer influence on adolescent alcohol use.

Comparing explanations: the biological account explains the chemistry of dependence but not why some people in identical circumstances never start; the learning account explains initiation, cues and relapse but not tolerance or physical withdrawal. Together they form an interactionist (biopsychosocial) model.

Which mechanism?

Aversion therapy and drug treatments

You need two treatments each for alcohol, heroin and nicotine, and aversion therapy must be one of them.

• Aversion therapy (classical conditioning): pair the drug with something unpleasant so it becomes a conditioned stimulus for disgust. For alcohol, disulfiram blocks the breakdown of acetaldehyde, so drinking produces flushing, nausea and vomiting. For smoking, rapid smoking makes the act itself aversive. It can work quickly, but effects often extinguish outside the clinic, drop-out is high, and it raises clear ethical concerns about deliberately causing harm.
• Drug therapy — heroin: methadone is a long-acting opioid agonist given as substitution/maintenance: it prevents withdrawal without the rapid high, so users can stabilise. It keeps the person dependent on an opioid, which some criticise.
• Drug therapy — nicotine: nicotine replacement therapy (patches, gum) delivers nicotine slowly, without the smoke, breaking the tight drug-behaviour reinforcement link and easing withdrawal.
• Psychological therapy: CBT (identifying triggers and high-risk situations, coping strategies, relapse prevention) and contingency management (an operant token-based reward for clean tests).

Which treatment principle?

Anti-drug campaigns and the psychology behind them

You must know one campaign and the psychological strategies it uses.

• Fear appeals: graphic images of harm are intended to change attitudes. Protection motivation theory says a fear appeal only works if the person believes the threat is severe, that they are vulnerable to it, and — crucially — that they are able to act (self-efficacy). Fear without an achievable action tends to produce defensive avoidance instead of change.
• Social norms marketing: correcting the false belief that 'everyone is doing it' reduces use, because much adolescent initiation is driven by perceived norms and social learning.
• Providing credible information (e.g. the FRANK service) treats the audience as decision-makers rather than targets to be frightened.

Evaluating campaigns: effectiveness is hard to measure (self-report, no control group, many confounding influences), effects are often short-lived, and campaigns can backfire by making a drug seem exciting or normal. This is a strong practical issues in research design and usefulness point.

Match the term to its meaning

Tap a term on the left, then its correct definition on the right.

Using animals to study drugs

• Why animals: extremely high control (dose, genetics, environment), the ability to use invasive procedures that would be unethical in humans (implanting electrodes, lesioning), and shorter lifespans allowing generational studies. Olds and Milner could not have been done on humans.
• Why not: extrapolation is the central problem — human addiction involves expectation, culture, identity and social context that a rat in a box does not have. Animals in barren cages may also self-administer more than they otherwise would.
• Ethics: the Scientific Procedures Act (1986) and Home Office regulation require licences, cost-benefit review, and the 3Rs — replacement, reduction, refinement.
• Human drug studies: two methods, e.g. laboratory experiments (control, but artificial), longitudinal and correlational designs (real users, but no causal inference), case studies and cross-cultural comparisons (do addiction rates track culture rather than chemistry?).

Animal research

Determinism, social control and social sensitivity

• Nature-nurture: genetic vulnerability and dopamine chemistry versus modelling, peer influence and availability. The evidence supports an interactionist (biopsychosocial) position — genes may set vulnerability, environment pulls the trigger.
• Determinism and free will: if addiction is a brain disease, is the user responsible? This has direct consequences for whether we punish or treat, and for how addicts are treated by the NHS and the courts.
• Social control: methadone maintenance, mandated treatment and drug campaigns all raise the question of who is being served — the individual or society.
• Socially sensitive research: studying drug use in particular communities (as Dixit et al., 2012, did in urban and rural India) risks stigmatising them, and findings may be used to justify discriminatory policing.

Evaluating a claim

Which treatment for which drug?

How Topic 8 is assessed

Health psychology is one of three options and, if you take it, is assessed in Section B of Paper 2, alongside the compulsory clinical psychology in Section A.

• The spec is explicit: one biological and one learning explanation for each of alcohol, heroin and nicotine, and two treatments each — one of which must be aversion therapy. Build a grid and learn it.
• You must know one anti-drug campaign and the psychological strategies behind it, and be able to evaluate whether it worked.
• Olds and Milner (1954) is examinable in full, with the ethics of animal research.

Mode of action is the phrase examiners use. Be able to say where in the synapse each drug acts — receptors, reuptake, agonist or antagonist.

The big ideas to know

That is Topic 8 — remember it is one of three options for Section B of Paper 2. Press Finish to see your score.