Revise Abnormal psychology: etiology of disorders for IB Psychology (5.2)

The biological approach locates the origin of depression in physiology — genes, brain chemistry and their interaction with the environment. The core claim for MDD is genetic vulnerability: some people inherit a predisposition that makes them more susceptible to depression. The candidate mechanism is the 5-HTT (serotonin-transporter) gene, which governs how efficiently serotonin is reabsorbed at the synapse. The linked serotonin hypothesis proposes that reduced serotonin activity contributes to depressive symptoms.

Crucially, modern biological accounts are not deterministic. The short allele of the 5-HTT gene does not by itself produce depression; it raises risk only when combined with stress. This is a gene–environment interaction, and it is the biological engine of the diathesis–stress model: genes load the gun, environment pulls the trigger.

The cognitive approach argues that it is not events themselves but how we interpret them that generates depression. Aaron Beck proposed that depressed people hold negative self-schemas — stable, pessimistic beliefs about the self formed early in life — which, once activated by stress, bias interpretation and produce the cognitive triad: automatic negative thoughts about the self ('I am worthless'), the world ('everything is against me') and the future ('nothing will improve').

These schemas drive systematic cognitive biases such as overgeneralisation (one setback means a lifetime of defeat) and arbitrary inference (negative conclusions drawn without evidence). A complementary cognitive account is Seligman's learned helplessness: repeated exposure to uncontrollable stress teaches a person that their actions don't matter, producing the passivity and hopelessness seen in depression — an idea later refined into a negative attributional style (blaming the self, seeing causes as permanent and global).

The sociocultural approach widens the lens to the social world: chronic life stressors (poverty, unemployment, discrimination), the presence or absence of social support, and cultural factors such as gender roles and norms about expressing distress. It explains why prevalence rates differ across groups — for example, the roughly 2:1 female-to-male ratio in reported depression — in terms of environment rather than physiology.

The classic study is Brown & Harris (1978). AIM: to identify social factors linked to depression in women. PROCEDURE: they interviewed a large community sample of women in Camberwell, London. FINDINGS: a severe life event alone rarely triggered depression; risk rose sharply when a severe event met social 'vulnerability factors' — having no close confidant, being unemployed, caring for three or more young children at home, or early loss of one's mother. This is itself a diathesis–stress pattern at the social level: a stressor causes depression mainly when protective support is missing.

Each single-level explanation is incomplete on its own. Biology explains vulnerability but not why identical genes yield depression in one twin and not another; cognition explains the maintaining thought patterns but not where the diathesis comes from; the sociocultural level explains triggers and protection but not why the same stressor devastates one person and barely touches another. The diathesis–stress (biopsychosocial) model resolves this: a biological or cognitive vulnerability is EXPRESSED when it meets social stress. Notice that all three of our studies point the same way — Caspi (gene only matters under stress), Alloy (cognitive style is a diathesis awaiting a trigger) and Brown & Harris (a stressor bites only without support). Arguing this convergence is exactly the developed critical thinking (Criterion D) that lifts an essay into the top band.