Aim

1. To test whether a polymorphism in the 5-HTT serotonin transporter gene moderates the effect of stressful life events on depression.
2. To explain why stressful experiences lead to depression in some people and not in others.

Procedure

1. Participants came from the Dunedin longitudinal cohort of 1037 people in New Zealand, followed from age 3 to age 26.
   1. Retention was high, with 96% of the original cohort still taking part at 26.
2. The 847 Caucasian non-Maori cohort members were genotyped for the 5-HTTLPR polymorphism and grouped by whether they carried a short allele or two long alleles.
   1. The three groups were 147 people (17%) with two short alleles, 435 (51%) with one short and one long, and 265 (31%) with two long.
3. Stressful life events between the ages of 21 and 26 were recorded with a life-history calendar covering 14 kinds of event, and any maltreatment during childhood was recorded too.
   1. Across the sample, 30% reported no such events, 25% reported one, 20% reported two, 11% reported three and 15% reported four or more.
4. Depression at 26 was assessed using the Diagnostic Interview Schedule.

Results

1. There was no difference between the genotype groups in how many stressful events they experienced.
2. Carriers of a short allele had a significantly stronger interaction between life events and depression.
   1. Across the sample, 17% met the criteria for a major depressive episode in the past year and 3% had attempted suicide.
3. Childhood maltreatment predicted adult depression only in those carrying a short allele.

Conclusions

1. Depression here is the product of a gene-environment interaction, because the gene alone does not cause depression.
2. This is a diathesis-stress pattern, in which an inherited vulnerability only shows itself once enough stress arrives.
3. Since exposure to stress did not differ by genotype, the short allele must change sensitivity to stress rather than attract more of it.

Strengths and weaknesses

1. A strength is that the design was longitudinal across a large cohort with very few people dropping out, so the pattern does not rest on a shrinking sample.
2. A second strength is that depression was recorded as a real diagnosis through a clinical interview rather than a quick self-rating.
3. A weakness is that the study is correlational, so it cannot establish that the gene and the life events caused the depression.
4. A second weakness is that the genotyped sample was 847 Caucasian non-Maori members of one New Zealand cohort, so the figures may not generalise to other populations.

Turning this into marks

1. Name the cohort of 1037, the 847 genotyped and the 5-HTTLPR polymorphism when you describe the procedure.
2. The percentages are asked for directly, so learn the three allele groups and the spread of stressful life events rather than rounding them.
3. Say what the study shows, which is that the gene mattered only alongside stress, and name that as gene-environment interaction or diathesis-stress.