Why do difficult life events trigger depression in some people but not others? What makes someone more resilient to depressive symptoms? Psychologists believe that there are both genetic and environmental risk factors associated with depression.
To investigate how these factors may interact, Caspi et al. (2003) looked at the association between the 5-HTT serotonin transporter gene and participants' responses to stressful events. We'll examine how the study was conducted and what the findings suggest about the development of depression.
- First, we will delve into the study of Caspi et al. (2003), discussing Caspi et al (2003) findings
- Following this, we will provide a brief Caspi et al. (2003) summary
- To conclude, we will discuss Caspi et al. (2003) strengths and weaknesses and the ethical considerations
Genetic research reveals how genes can affect behaviour, freepik.com
Caspi et al 2003: Psychology
The study focuses on how both genetic and environmental factors may interact and result in mental health difficulties. It accounts for both the influences of nature and nurture.
The study was carefully designed to control for potential confounding variables and provide evidence for the link between genes, environmental stressors and psychological functioning using a large sample from New Zealand that was followed over 23 years.
Caspi et al 2003: aim
The aim of the study was to examine whether the length of a single gene, the 5-HTT serotonin transporter gene, will moderate the occurrence of depressive symptoms in response to stressful life events. This would be in line with the diathesis-stress model of depression.
The diathesis-stress model
The diathesis-stress model of depression predicts that depressive symptoms develop as a result of an interaction between a vulnerability, which can be genetic, and stressors that trigger the onset of the illness.
According to this model, a genetic predisposition on its own does not determine depression.
For example, among monozygotic twins with the same genetic vulnerabilities, a twin with a large number of stressful experiences is more likely to experience depression compared to a twin with the same vulnerabilities but less stressful experiences.
This model could also account for why different people will experience different reactions to stress.
For example, two people experiencing a relationship loss may respond differently. For a vulnerable person (genetically), such an experience can be devastating and trigger a depressive episode. A person with less vulnerability may experience less severe symptoms, recover quicker and move on almost unscathed.
In this study, the shorter variation in the 5-HTT gene was predicted to be the diathesis due to its involvement in serotonin reuptake.
Hypothesis
Researchers hypothesised that the length of the 5-HTT allele will moderate participant depressive symptoms in response to stress. Specifically, short alleles were thought to impair the serotonergic response and result in greater vulnerability to stress.
Allele refers to one copy of a gene. Each gene has two alleles at the same location of the chromosome. If the two copies are the same we refer to the genotype as homozygous. If the two copies are different we refer to the genotype as heterozygous.
Caspi et al 2003: method
Caspi et al. (2003) conducted a quasi-experiment, which used a longitudinal design to better understand the effects of genetic vulnerability throughout people's life. Participants were a birth cohort of 847 and were tested every few years from the age of 3 to the age of 26.
Birth cohort studies recruit and follow participants born around the same time.
Participants were divided into 3 groups depending on their version of the 5-HTT gene.
Group 1 inherited two short alleles of the 5-HTT gene.
Group 2 inherited one short and one long copy of the gene.
Group 3 inherited two long copies of the gene.
Between the ages of 21 and 26 participants were asked to report stressful life events in a life-event calendar. At 26 participants were assessed for depressive symptoms.
Longitudinal studies follow participants across a period of time, freepik.com
Caspi et al 2003: findings
Caspi et al. (2003) tested whether the variation of the 5-HTT gene would moderate the influence of stressful events experienced in adulthood on depression. Moreover, the association between the gene variation and psychological responses to childhood maltreatment was also tested.
Stressful events in adulthood
Caspi et al. (2003) found that:
The number of stressful life events in adulthood predicted depressive symptoms, depression diagnoses, suicidality and informant reports of depressive behaviour at age 26 for participants with at least one short allele of the 5-HTT gene but not for participants with two long alleles.
Informant reports refer to what other people, the colleagues of participants, reported about their behaviour.
Among the participants with at least one short allele of the 5-HTT gene who experienced four or more stressful life events, 33% qualified for a depression diagnosis at 26.
For participants with both long alleles who experienced at least four stressful life events the prevalence of depression was significantly lower (17%).
Childhood maltreatment
The effects of childhood maltreatment depended on the gene variation.
For participants with at least one copy of the 5-HTT gene, childhood maltreatment predicted depression, and participants with two short alleles were most vulnerable.
For participants with two long alleles, childhood maltreatment did not predict depression.
Caspi et al 2003: conclusion
The interaction found between the variations of the 5-HTT gene and stressful life events on the occurrence of depression supports the diathesis-stress model. The gene itself didn't directly predict depression. Similarly, stressful life events didn't directly predict depression.
Both stressful events in adulthood and childhood maltreatment predicted depression only for participants with a short variation of the gene. The results suggest that inheriting two long alleles of the gene is protective against developing depression.
Caspi et al. (2003): Summary
Caspi and colleagues investigated the interaction of a variation of the 5-HTT gene and stressful life events in the development of depression using a longitudinal birth cohort study. Participants who inherited one or two short alleles of the gene showed significantly greater vulnerability to developing depression in response to stressful life events.
A similar vulnerability was not observed in participants with two long alleles. This study supports the diathesis-stress model of depression.
Caspi et al. (2003): Strengths and weaknesses
A number of strengths and weaknesses of this study can be identified.
Strengths of Caspi et al. (2003)
Using a longitudinal birth cohort design helps control for potential developmental and contextual differences between participants. Following participants from birth to adulthood allowed researchers to account for previous events in their life like childhood maltreatment. Moreover, effects found in longitudinal studies can indicate causal links between variables with more confidence compared to cross-sectional studies.
Researchers used both self-reports and informant reports to assess depressive symptoms, since both measures resulted in the same findings, it can be concluded that the measure of depression was reliable.
Weaknesses of Caspi et al. (2003)
Causality cannot be inferred as the study was observational and the independent variables (stressful life events and genetic variations) were not manipulated by the researchers. Participants were also not randomly allocated to study conditions, other factors (e.g. other genes) could have influenced the findings.
It can be argued that people have personal interpretations of what they consider to be a stressor. Since depression is associated with negative thinking and catastrophising, people's existing depressive symptoms could have influenced their reports of stressful events.
Caspi et al. (2003): Ethical considerations of the study
Due to the observational nature of longitudinal studies, researchers don't interfere with participants' life. In this study, some participants were found to be subjected to severe childhood maltreatment. By not intervening it can be argued that the study failed to protect children from harm.
Caspi et al. (2003): Ethical considerations of genetic screening
Knowing one has a genetic predisposition and lower resilience to stress can make people think that there is nothing they can do about it and lose hope about their future mental health outcomes. A belief that one's outcomes are predetermined often leads people to exert less effort trying to, for example, engage in protective behaviours.
Moreover, stigmatisation of vulnerable people is possible, not only by their relatives or friends but also by medical professionals. This could result in people being treated differently e.g. when seeking medical treatment for an unrelated issue.
On the other hand, by screening and identifying vulnerable people clinicians would be able to target people that could benefit most from psychological interventions. Such interventions could help people with genetic vulnerabilities cope with stressful life events.
Caspi et al 2003 - Key takeaways
- The diathesis-stress model of depression predicts that depressive symptoms develop as a result of an interaction between a genetic vulnerability and stressors that trigger the onset of the illness. This model is supported by the study of Caspi et al. (2003).
- The aim of the study was to examine whether the length of the 5-HTT serotonin transporter gene will moderate the occurrence of depressive symptoms in response to stressful life events.
Caspi et al. (2003) concluded that depression develops as a result of an interaction between the 5-HTT gene and the number of stressful life events. For participants with a short 5-HTT gene allele, the number of stressful life events was predictive of depressive symptoms. For participants with long 5-HTT variations, stressful life events didn't predict depression.
Strengths of the study of Caspi et al. (2003) include the use of a longitudinal, birth cohort design and reliance on both self-reports and informant reports of depression. However, we can't infer causality from their findings.
The study can be criticised for failing to protect participants from harm. Moreover, there are important ethical implications of the study findings in relation to genetic screening.
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