Example 1 — Using a study as evidence, not as an answer

Explain one way in which neuroplasticity has been investigated. [4]

A weak answer:

Maguire studied London taxi drivers and found their hippocampi were bigger. This shows the brain can change.

A strong answer:

Neuroplasticity has been investigated using structural neuroimaging to compare groups with different levels of experience. In the best-known example, MRI scans of experienced London taxi drivers — who must memorise a very large street network — were compared with those of matched controls, and structural differences were found in the hippocampus, a region associated with spatial memory. ✓✓ The reasoning is that if extensive spatial navigation produces measurable structural change, the brain must be capable of reorganising in response to use. ✓ However, the design is correlational: it cannot establish that the navigation caused the difference, because people with pre-existing differences in hippocampal structure may simply have been more likely to succeed at the training. A longitudinal design measuring the same individuals before and after training addresses this, and is the stronger evidence. ✓

4/4.

The difference is not knowledge — both answers know the study. The strong one explains the logic connecting evidence to conclusion, and identifies the specific design limitation with the design that would fix it. That last move — naming the better study — is what turns evaluation from complaint into analysis.

Example 2 — Heritability, stated correctly

Explain what a heritability estimate of 0.5 for a trait means. [3]

It means that in the population studied, under the environmental conditions of that study, approximately 50 % of the variation between individuals in that trait is statistically associated with genetic variation. ✓ It is a property of a population, not of an individual: it does not mean that half of any one person's trait is caused by their genes. ✓ Nor is it fixed. If environmental variation in the population changes — for instance if access to education becomes more equal — the heritability estimate changes too, because there is less environmental variation left for the trait to track. ✓

3/3.

This is the most reliably misunderstood concept in the subject. The three marks correspond to three distinct corrections: variation not amount, population not individual, and environment- dependent not fixed. An answer saying "the trait is 50 % genetic" scores 0, however confidently written, because it states the opposite of what the statistic means.

Example 3 — Paper 2 style: evaluating an unfamiliar study

Stimulus. Researchers recruited 40 university students and measured salivary cortisol before and after a 20-minute public speaking task. Cortisol rose significantly in 34 participants. The researchers concluded that "public speaking causes stress in the general population".

(a) Identify the research method used. [1] (b) Evaluate the researchers' conclusion. [5]

(a)

A repeated measures experiment — the same participants are measured before and after the manipulation. ✓

(b)

What the study supports. The design is a genuine strength: measuring the same participants before and after controls for individual differences in baseline cortisol, which vary widely between people. Cortisol is a physiological measure, so it avoids the demand characteristics and self-report bias that would affect a questionnaire, and the effect was found in 34 of 40 participants, so it is not driven by a few outliers. ✓✓

Where it overreaches. The claim concerns "the general population", but the sample is 40 university students — young, educated, and drawn from one institution. Students are not representative in age, occupation or experience of public speaking, so population validity is weak. ✓ The absence of a control group is a further problem: cortisol follows a diurnal rhythm and falls through the day, so without a comparison group doing a non-stressful task for 20 minutes, some of the change cannot be attributed to the speaking task with confidence. ✓ Finally, a rise in cortisol is evidence of physiological arousal, which is not identical to the subjective experience of stress — the study measures one and concludes about the other. ✓

Judgement. The study provides reasonable evidence that a public speaking task produces physiological arousal in this sample. The conclusion as stated is not supported: it generalises beyond the sample and equates a hormonal measure with a subjective state.

5/5 for (b).

Notice the structure. Strengths first, then limitations organised by type — sampling, design, measurement — and a judgement that says precisely how far the evidence reaches. Note also that the strongest single criticism here is not the sample, which every candidate spots, but the gap between cortisol and the concept of stress. That is a measurement point, and measurement is one of the six course concepts.

Example 4 — Refusing the reductionist trap

Discuss the extent to which the biological approach can explain depression. [8, extract]

Biological explanations identify real and measurable correlates of depression. Neurotransmitter accounts implicate serotonin, supported indirectly by the effectiveness of SSRIs for some patients. Twin studies indicate a genetic contribution, with higher concordance in monozygotic than dizygotic pairs. Chronically elevated cortisol is associated with depressive episodes, and structural differences have been reported in the hippocampus and prefrontal cortex.

Each of these is weaker as evidence than it first appears. That SSRIs help does not establish that low serotonin caused the disorder — inferring the cause from what treats it is the treatment aetiology fallacy, and aspirin relieving a headache does not mean the headache was caused by an aspirin deficit. The serotonin evidence is correlational and the relationship may run the other way. Twin concordance is well below 100 %, so genes are not sufficient. Elevated cortisol may be a consequence of depression as readily as a cause.

More decisively, a purely biological account cannot explain variation the biology does not track: prevalence differs substantially across cultures and has changed over decades far faster than any genetic change could occur, and life events such as bereavement and unemployment predict onset strongly. A gene does not know it has been made redundant.

The defensible position is interactionist, and the diathesis–stress framework states it well: biological factors establish a vulnerability, and environmental stressors determine whether it is expressed. Epigenetics supplies a mechanism, showing that experience can alter gene expression without altering the sequence. On this account the biological approach explains a genuine and necessary part of depression, but not a sufficient one — it describes the terrain on which the disorder develops rather than the whole of what develops.

Why this scores. It takes the biological evidence seriously before criticising it, names a specific fallacy, and uses cross-cultural and historical variation — evidence the biological approach cannot accommodate — rather than merely asserting that other factors matter. The conclusion is an interactionist judgement with a mechanism attached, not a shrug.

Educerie · original worked examples written against the published IB syllabus structure for Psychology Topic 1, first assessment 2027. The stimulus study in Example 3 is fictional, created for this material; other findings referred to are standard in the research literature. Last reviewed 5 September 2026.