Depression is multifactorial — biological, cognitive and social factors all contribute. GCSE focuses on two main approaches: biological and psychological (cognitive and learning theories).
Biological theory
Genetic vulnerability
Depression runs in families.
- Family studies — first-degree relatives of people with depression have ~2–3× the population risk.
- Twin studies — concordance rate ~40–50% in monozygotic (MZ) twins vs ~10–25% in dizygotic (DZ) twins. Suggests substantial genetic contribution but not 100% MZ concordance, so environment matters too.
- Adoption studies — biological parents' depression predicts adopted children's risk better than adoptive parents'.
The inheritance pattern is polygenic — many genes each contribute small effects (e.g. variants of the 5-HTT serotonin transporter gene).
The serotonin (monoamine) hypothesis
Low levels or reduced activity of certain neurotransmitters — especially serotonin, but also noradrenaline and dopamine — are linked to depressive symptoms.
- Drugs that lower serotonin (e.g. reserpine in the 1950s) can produce depressive symptoms.
- SSRIs (selective serotonin reuptake inhibitors) raise serotonin levels in the synapse and improve symptoms over weeks.
- Caspi et al. (2003) — the short allele of the 5-HTT gene combined with stressful life events increased depression risk; gene × environment interaction.
Limitations of the simple chemical-imbalance idea: SSRIs raise serotonin within hours but symptoms only improve over weeks — suggesting downstream effects on neuroplasticity matter, not just monoamine levels.
Psychological theories
Beck's cognitive theory: negative schemas and the cognitive triad
Aaron Beck (1967) proposed that depression arises from negative schemas — automatic, distorted patterns of thinking — formed in childhood through criticism, loss or failure. These schemas drive the cognitive triad:
- Negative view of the self ("I'm worthless").
- Negative view of the world ("Everyone is unfair to me").
- Negative view of the future ("Things will never improve").
Cognitive distortions maintain the schemas: overgeneralisation, catastrophising, personalisation, all-or-nothing thinking. Therapy targets these (P2.PS.4 — CBT).
Attribution theory and learned helplessness
Martin Seligman (1967) observed that dogs given inescapable shocks later failed to escape even when escape became possible — learned helplessness. He argued depression in humans involves a similar belief that nothing one does affects outcomes.
Reformulated attribution model — people prone to depression make negative attributions about causes:
- Internal ("it's my fault") rather than external.
- Stable ("it always happens") rather than unstable.
- Global ("it affects everything") rather than specific.
This pessimistic explanatory style predicts later depression risk.
Strengths and weaknesses
Biological strengths: solid genetic and pharmacological evidence; explains family clustering; supports drug treatments. Weaknesses: ignores psychosocial triggers; doesn't explain why some people with the genes don't develop depression.
Cognitive strengths: testable cognitive distortions; evidence base from CBT outcomes; explains why two people with similar life events differ. Weaknesses: chicken-and-egg problem — does negative thinking cause depression or vice versa? Addresses cognition but underweights biology.
Modern integrative view (diathesis–stress)
Most researchers now favour a diathesis–stress model: a biological vulnerability (the diathesis) interacts with stressful life events to trigger depression in susceptible individuals. Caspi et al. (2003) is the headline evidence.
⚠Common mistakes— Common errors
- Treating biological and cognitive theories as either/or — they complement each other.
- Saying "depression is caused by low serotonin" — the simple chemical-imbalance account is now considered too narrow.
- Confusing learned helplessness with hopelessness — the modern attribution version is the closer fit for depression.
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