IB Psychology HL Topic 1 — Mental Health Disorders Paper 1 & 2 Biological approach ~9 min read

How Genes Contribute to Depression

Depression runs in families. That much is easy to show. The hard part is that families share far more than DNA — they share homes, money worries, habits and stress. This page shows you how psychologists pull those two things apart, and what the famous twin numbers actually prove.

📘 What you need to know

What we are trying to explain

Before you explain a disorder you have to know what the disorder is. Clinicians look for a set of symptoms that have been there most of the day, most days, for at least two weeks:

Notice that none of these is a brain scan or a blood test. MDD is defined by behaviour and self-report, which will matter later when you evaluate the research.

Learn the symptom list properly. Examiners give credit for a short, accurate description of MDD at the start of an essay, and it costs you about three sentences.

Why psychologists use twins

You cannot run the experiment you would really want. You cannot take a baby, copy their genes, and raise the copies in different homes to see who becomes depressed. Twins are the closest nature gets to that experiment.

The logic works like this:

🧩 The twin-study argument, step by step

  1. MZ twins share 100% of their DNA. DZ twins share about 50%.
  2. Both kinds of twin pair are usually raised in the same home at the same time, so their environment is roughly matched.
  3. So if MZ pairs agree on MDD much more often than DZ pairs, the extra agreement is most likely down to the extra shared genes.
  4. The size of the gap between the two concordance rates is your evidence for a genetic influence.
Concordance for MDD in twin pairs McGuffin et al. (1996), Maudsley twin register 0 20 40 60 80 100 concordance (%) 46% 20% MZ twins (identical) DZ twins (non-identical) 100% shared DNA about 50% shared DNA The MZ bar is more than twice the DZ bar. That gap is the evidence for genes. The missing 54% is the evidence against genes alone.
Read both halves of this chart. The gap between the bars supports a genetic influence; the empty space above the blue bar is why nobody claims MDD is purely inherited.

Research support: McGuffin et al. (1996)

Why blind assessment matters. If the clinician knew a pair was identical, they might unconsciously look harder for symptoms in the second twin and inflate the MZ figure. Removing that knowledge protects the study from researcher bias — an easy, specific strength to write about.

The missing 54% — the point most students skip

If depression were written into the genes and nothing else mattered, MZ concordance would be 100%. Identical DNA would mean identical outcome, every time. It is not 100% in any study ever run.

So the same genotype (the genes you carry) can lead to different phenotypes (how you actually turn out). Something else has to be doing work, and the obvious candidate is life itself.

Same genes, different lives, different endings Identical twins: same DNA Twin A steady home, few big stresses Twin B bullying, job loss, isolation stays well no diagnosis develops MDD same DNA, different life One genotype can produce two different phenotypes. Genes load the dice. They do not throw them.
This single picture answers the most common exam follow-up: if the explanation is genetic, why do identical twins so often differ?

Evaluation of the genetic explanation

Strengths

Limitations

EXAM QUESTION

Discuss one genetic explanation of one disorder. [22]

Here is how to plan it so you cover both command words — explain the idea and weigh it up.

Step 1: define the disorder in 2–3 lines MDD, its main symptoms, and that it is diagnosed from behaviour, not a lab test. Step 2: state the explanation clearly Vulnerability to MDD is partly inherited; heritability is tested using twin and adoption studies and measured with concordance rates. Step 3: use one study in detail McGuffin (1996): 46% MZ vs 20% DZ, blind assessors, Maudsley register. Step 4: discuss — this is where the marks are Two strengths (large sample, blind procedure) and two limitations (never 100%, equal-environment assumption). Finish by linking to diathesis–stress: genes give vulnerability, life events pull the trigger. Never end on “so depression is genetic” End on the interaction. That is the conclusion the mark scheme is looking for.

Link to concepts

Perspective

The genetic account is one level of explanation, not the only one. The same case of depression can also be described as faulty thinking (cognitive), as a loss of rewarding activity (behavioural), or as poverty and isolation (sociocultural). A strong essay says which level it is working at and admits the others exist.

Causality

Twin studies show a relationship, not a cause. Nobody manipulated anyone’s genes, so all we have is a pattern of agreement. Higher MZ concordance is consistent with a genetic cause — it does not prove one.

💡 Exam tip

⚠ Common mix-up

Up next: Neurotransmitters and Depression — if genes only set the risk, what is actually happening in the brain of someone who is depressed? We follow serotonin across the synapse and see how SSRIs work.

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