HookHomosexuality was a mental disorder until 1973 — the day the definition changed
Until 1973, homosexuality was an official mental disorder. It sat in the American Psychiatric Association's diagnostic manual, the DSM, alongside phobias and depression, and psychiatrists were paid to 'treat' it. Then, after years of protest and a floor vote at the APA's annual meeting, it was deleted. Nobody's brain had changed overnight. What changed was the social norm — the shared, unspoken agreement about what counts as acceptable behaviour. And there, in one embarrassing episode, is the whole problem the Psychopathology topic exists to solve: how do you decide, without prejudice, that a mind is disordered?
AQA's answer is that there is no single definition that works, so you learn four, each with a fatal flaw the examiner wants you to expose. Then the topic narrows to three specific disorders — phobias, depression and OCD — and asks you to explain and treat each one through a different lens: the behavioural approach for phobias, the cognitive approach for depression, and the biological approach for OCD. The pattern is deliberate. By the end you can argue that the way you explain a disorder dictates the way you treat it — that a fear learned by association is unlearned by exposure, while low serotonin is corrected by a pill. Get that spine and every 16-mark essay in this topic becomes the same three moves: describe the explanation, tie the therapy to it, then evaluate whether the therapy actually works.
ModelFour definitions of abnormality, four fatal flaws
AQA gives you four ways to define abnormality, and the marks come from knowing where each one breaks. Deviation from social norms labels behaviour that violates a society's unwritten rules — but norms are culturally and historically relative, which is exactly why homosexuality was 'abnormal' in 1972 and normal in 1974, and why the diagnosis could be abused to control people who were merely different. Failure to function adequately (Rosenhan and Seligman) labels people who can no longer cope with everyday living — signalled by personal distress, maladaptive behaviour, irrationality and observer discomfort — but distress is subjective, and some seriously ill people feel no distress at all.
Statistical infrequency defines abnormality as being statistically rare — more than two standard deviations from the mean, which is how an IQ below 70 flags intellectual disability. Its flaw is obvious once stated: rare is not the same as undesirable (a genius IQ of 150 is equally rare) and common conditions like depression are not statistically infrequent at all. Deviation from ideal mental health (Jahoda) flips the question, listing six criteria for good mental health — self-actualisation, accurate perception of reality, autonomy, resistance to stress, environmental mastery and a positive self-attitude — and calls their absence abnormal. But almost nobody meets all six, so the definition sets an impossibly high bar and is culturally biased towards Western individualism. The exam-ready judgement is that no single definition is sufficient; clinicians use several together.
DataThe 3-by-3 grid — behavioural, emotional and cognitive characteristics
AQA describes each disorder along three columns — how the person behaves, how they feel (emotional) and how they think (cognitive) — and questions reliably ask for characteristics in one named column. Learn it as a grid. Phobias: behaviourally, avoidance and panic; emotionally, disproportionate anxiety and fear; cognitively, irrational beliefs and selective attention to the phobic stimulus. Depression: behaviourally, reduced activity, disruption to sleep and eating, sometimes aggression; emotionally, persistent low mood, worthlessness and anger; cognitively, negative self-concept, absolutist 'black-and-white' thinking and poor concentration.
OCD: behaviourally, compulsions (repetitive actions like handwashing) and avoidance; emotionally, high anxiety, distress and accompanying depression; cognitively, obsessive intrusive thoughts, awareness that the obsessions are irrational, and hypervigilance. The examiner's trap is the column label: a question asking for two cognitive characteristics of OCD earns nothing for naming the compulsion (a behaviour). The discipline that scores is to file every feature under the correct heading as you learn it, so that under exam pressure you retrieve from the column the question actually names.
MechanismPhobias — learned by association, treated by exposure
The behavioural approach explains phobias through Mowrer's two-process model: they are acquired by classical conditioning and maintained by operant conditioning. Watson and Rayner's 'Little Albert' (1920) is the classic acquisition case — an eleven-month-old was shown a white rat (a neutral stimulus) paired repeatedly with a frightening loud noise (an unconditioned stimulus), until the rat alone produced fear (a conditioned response). The phobia then persists because avoiding the feared object reduces anxiety, and that relief negatively reinforces the avoidance — you never stay near the object long enough for the fear to fade.
Because the fear is learned, the treatments unlearn it through exposure. Systematic desensitisation (Wolpe) works up a graded anxiety hierarchy while the patient stays deeply relaxed, using reciprocal inhibition — you cannot be relaxed and afraid at once — so the calm response counter-conditions the fear step by step. Flooding does the opposite: immediate, prolonged exposure to the worst-case stimulus with no escape, until the fear response physically exhausts itself and extinguishes. Flooding is faster and cheaper but far more traumatic, which raises an ethical objection and makes it unsuitable for many patients.
Here is a worked chunk of a 16-mark essay ('Discuss the behavioural approach to treating phobias', 6 marks AO1 + 10 marks AO3). AO1 first, precise: 'Systematic desensitisation reduces phobic anxiety through counter-conditioning. The therapist and patient build an anxiety hierarchy from least to most feared situations, teach a deep relaxation technique, then work up the hierarchy while relaxed. Because relaxation and fear are incompatible responses — reciprocal inhibition — the calm gradually replaces the fear.' Then AO3, each point a claim plus evidence plus consequence: 'A strength is effectiveness: Gilroy et al. followed spider-phobics treated with SD and found reduced fear at three and thirty-three months, showing the improvement lasts rather than relapsing. A further strength is that SD is preferred by patients over flooding because it is less traumatic, so drop-out rates are lower — treatment people actually complete is treatment that works. However, SD may only treat the symptom, not an underlying cause; if the phobia is a symptom of something deeper, symptom substitution could occur, a criticism the behavioural model cannot easily answer because it ignores cognition.' Notice the shape: quantified, named-study AO1, then evaluation that always ends on why it matters for the therapy — never a bare 'this is good'.
MechanismDepression — faulty thinking, corrected by challenge
The cognitive approach blames depression on how the person thinks, not on events themselves. Beck (1967) identified three cognitive vulnerabilities: a negative self-schema (a template of self-blame built in childhood), faulty information processing such as overgeneralisation and catastrophising, and the negative triad — automatic negative views of the self, the world and the future that feed each other in a downward spiral. Ellis (1962) offered the complementary ABC model: an Activating event triggers not the emotion directly but a Belief about it, and it is an irrational belief (his 'musturbation' — the tyranny of 'I must succeed') that produces the depressive Consequence. The same rejection letter leaves one person disappointed and another devastated, because the belief in between differs.
If faulty beliefs cause depression, correcting them cures it, which is the logic of cognitive behaviour therapy (CBT). The therapist helps the patient identify negative automatic thoughts, then disputes them — Ellis's logical, empirical and pragmatic challenges — treating the patient as a scientist who tests beliefs against evidence ('you say everyone dislikes you; what is the evidence?'). Behavioural activation adds gradual re-engagement with rewarding activity. CBT is the frontline NHS talking therapy for depression, though it demands motivation and effort many severely depressed patients cannot summon, and critics argue it can overlook genuinely difficult life circumstances by locating the fault inside the patient's head.
CaseOCD — genes and chemistry, corrected by drugs
OCD is AQA's showcase for the biological approach, where the explanation is genetic and neural and the treatment is drugs. The genetic explanation is polygenic and diathesis-stress: OCD runs in families (Lewis found 37% of OCD patients had a parent with OCD), and candidate genes such as the serotonin-transporter gene 5-HTT and the dopamine-regulating COMT gene are implicated, but no single gene causes it — inherited vulnerability is triggered by environmental stress. The neural explanation points to abnormally low serotonin (which regulates mood and would explain the accompanying anxiety) and to overactivity in a brain circuit linking the orbitofrontal cortex and basal ganglia — the so-called 'worry circuit' that fails to switch off, so intrusive thoughts are not filtered out.
Because the fault is chemical, the treatment is chemical. SSRIs (selective serotonin reuptake inhibitors, e.g. fluoxetine) block the reabsorption of serotonin at the synapse, raising its concentration and, over three to four months, reducing symptoms. Tricyclics such as clomipramine and, for anxiety, benzodiazepines are alternatives. Drug therapy is cheap, non-disruptive and backed by placebo-controlled trials — but it treats symptoms not causes, carries side effects (nausea, insomnia, reduced libido) that drive people to stop taking it, and the very evidence that low serotonin is the cause is weakened because raising serotonin does not help everyone, hinting the chemistry is a correlate rather than the root.
A model evaluation paragraph for 'Discuss the biological approach to explaining OCD', showing the top-band move of turning a treatment fact into an argument about the explanation: 'Support for the neural explanation comes from the success of SSRIs: because drugs that raise serotonin reduce OCD symptoms, low serotonin is implicated in the disorder — treatment aetiology working backwards as evidence. However, this reasoning is circular and only correlational; SSRIs also fail for a substantial minority, so serotonin cannot be the whole story. The genetic explanation is better framed as diathesis-stress than as biological determinism, because twin concordance is well below 100%, showing inherited vulnerability needs an environmental trigger — which is why a purely biological account is reductionist and an interactionist model fits the data better.' The examiner rewards this because each sentence does analytical work: it weighs the evidence, names the flaw (circularity, correlation, reductionism) and lands a defensible judgement.
VocabularyKey terms the mark scheme pays for
TrapsMisconceptions that cost marks
ExamWhat examiners want
AQA Psychology essays are marked out of 16 as 6 marks AO1 (accurate, detailed knowledge) plus 10 marks AO3 (evaluation), in four levels — the top band (13–16) demands that evaluation is thorough and effective, not a bulleted list of strengths. Budget your time to match: roughly one-third describing, two-thirds evaluating. The commonest fatal error in this topic is writing a beautiful description of Beck or the two-process model and then stopping — a pure-AO1 answer caps at the bottom of the mark range however accurate it is.
Tie the therapy to the explanation explicitly, because that link is where analysis marks live: say why exposure treats a conditioned fear, or why an SSRI targets a serotonin deficit. For AO3, use the PEEL discipline — Point, Evidence, Explain, Link — and always finish each paragraph on the consequence for the theory or therapy ('...which means the treatment addresses symptoms but not the cause'). Name real evaluative concepts the mark scheme rewards: reductionism, determinism, cause-versus-correlation, symptom substitution, cultural relativism, and the diathesis-stress alternative to purely biological accounts.
On application questions (AO2), a short stem describes a named patient — you must quote details from that stem and attach the concept to them (identify the compulsion as behavioural, the intrusive thought as cognitive), because AO2 marks are only released when the concept is connected to the scenario rather than defined in the abstract. And when a question specifies a characteristic column — behavioural, emotional or cognitive — answer only from that column; a feature filed under the wrong heading scores zero.