Major Depressive Disorder is an affective disorder that results in feelings of sadness, difficulties in decision-making and memory, loss of motivation and suicidal ideation.  Biological psychologists argue that there are physiological reasons for the disorder.  Specifically, genetics is seen as a possible explanation of the disorder.  It has long been known that depression seems to run in families; this indicates a possible genetic link.  Since the Human Genome Project, 11 genes have been identified which may be linked to depression. However, there are both strengths and limitations of a genetic explanation of the origin of Major Depression.

One of the largest twin studies was done by Kendler.  Kendler studied over 40.000  twins from the Swedish twin registry.  The study had two interesting findings.  First, monozygotic twins – that is, twins that are from one fertilized egg – had a higher concordance rate for MDD than dizygotic twins (from two separate fertilized eggs).  In addition, females had higher concordance rates than males.  In females, MZ twins had a 44% concordance rate vs. 16% in DZ twins.  For males, it was 31% and 11%.

The study had a large sample size. This means increases the potential external validity of the study.  In addition, the results mirror what is seen in societal – that is, women have a higher rate of depression than males.

This study seems to show that there is a genetic link for depression; however, no specific genes are actually identified.  Also, we cannot know if the twins may have the gene but that it is not expressed. Research on gender differences in depression argue that women are subject to more environmental stressors than men; this could account for the differences in concordance rates - that is, exposure to environmental stressors leads to gene expression.  In order to get a better understanding of whether genes play a role in depression, isolating genes is important.

This was done by Caspi et al who studied the role of the 5-HTT gene.  This gene is responsible for serotonin transport across the synapse.  Caspi looked at a sample of New Zealanders.  The study categorized participants as either having two long 5HTT alleles (normal), one long and one short allele, or two short alleles.  In addition, they were asked to fill out a survey of stressful life events.  Their mental health was measured over a five-year period. Caspi found that those with the two short alleles who also had at least 3 stressful life events were more likely to show signs of depression. This study seems to indicate that inheriting the genetic variation is not enough, but that environmental stressors cause the genes to be expressed.  

This study also had a large sample size and, unlike Kendler’s study, it actually identified a genetic variation that was linked to depression.  The study was longitudinal and took a holistic view of the participants – examining the interaction of environmental and genetic factors.

This study is promising; however, it has its limitations.  First, it is based on the assumption that serotonin plays a role in causing depression. This is not necessarily the case.  SSRIs have mixed results and some argue that depression may lead to lower levels of serotonin, rather than vice versa. Secondly, the symptoms of depression were self-reported – the participants were not actually diagnosed.  This means that the results may not be valid with regard to the actual disorder. Finally, Risch et al carried out a meta-analysis of attempts to replicate the study.  They found that only a few studies were able to get the same results, mostly with small sample sizes. But overall, the results have not been replicated.  This means that the study may have low reliability.

There are limitations of genetic arguments for depression. First, all genetic research is correlational in nature.  No cause and effect can be established.  Also, genes result in physiological changes.  In order for psychologists to understand the origin of a disorder, they must understand how these physiological changes are associated with depression. Another limitation is that it is impossible to isolate biological factors.  Our biology interacts with environmental factors.  In addition, cognitive factors may act as mediating factors for depression. Biological research alone cannot explain this interaction. Finally, depression is a complex disorder.  A genetic explanation could be seen as reductionist.  Although this may be helpful in leading to a successful drug treatment, it also does not explain the wide range of symptoms that are seen in depressed patients.  For example, Kleinman argues that somatic symptoms such as lower back pain is seen in Chinese patients.  It is not clear that all symptoms across all cultures can be explained by genetic arguments alone.

Genetic arguments show great promise in better understanding the origins of depression.  However, with so many different genes potentially involved in depression, it will be difficult to know how these genes interact and if some genes play a greater role than others. If in the future we are able to use genetic markers to study people with depression, we may be able to get a better sense of how genetics – and the physiology that the genes influence – play a role in the onset of the disorder.