IB Docs (2) Team
Epigenetics and depression
Modern biologists do not simply argue that a gene “causes” a behaviour; instead, they recognize what is known as the gene-environment interaction. This is part of a field of study known as epigenetics. Epigenetics argues that in order for a behaviour to occur, genes must be “expressed.” Genetic expression is a complex chemical reaction to environmental or physiological changes that allow a gene to “do its job.”
We do not need to understand the exact process of gene expression for IB psychology, but it is important to know that environmental factors such as stress, exercise or diet, may result in genetic expression, or the lack of genetic expression. This also means that an individual may have a gene that could lead to a behaviour, but if the gene is never expressed, then this behaviour will not occur.
When looking at twin research, when studying behaviour, the concordance rate of MZ twins is never 100%. What is the reason for that? When we look at twin studies, we have to remember that genes need to be expressed. So, MZ twins have the same genes, but they may not have been exposed to the same environmental stressors, and thus the same genes may not be expressed. The fact that concordance rates are higher for MZ than DZ twins also makes sense. Twins do share some genes, so it is possible that DZ twins both share genes related to a behaviour like depression. But not all DZ twins would. In addition, in the DZ twins that do share those genes, some would not be expressed. This accounts for the significantly lower rate of concordance among DZ twins.
Genetic arguments for depression
Depression – officially known as Major Depressive Disorder - is considered the common cold of mental health. In the abnormal option, you may study this disorder in depth. Here, we are using it as an example of how genetic research is applied to understand human behaviour.
Genetic researchers argue that genetic predisposition can partly explain depression. We know that mood disorders tend to run in families, so one of the ways to investigate this is twin studies. Kendler el al (2006) carried out a twin study of 15,493 complete twin pairs from the Swedish national twin registry to determine the level of heritability of depression. They found that the average concordance rate for MZ male twins was 31 percent and for MZ female twins 44 percent, while for DZ twins it was 11 and 16 percent respectively. Overall, Kendler concluded that the heritability of depression is estimated to be 38%. The fact that the concordance rate for MZ twins is far below 100 percent indicates that depression may be the result of a genetic predisposition - also called genetic vulnerability. The fact that the concordance rate for MZ twins is below 100 % does not contradict the argument that depression is genetically inherited. It may mean that the gene is there, but both twins have not experienced the same level of stress and thus both twins have not "expressed their genes." The fact that some of the DZ twins also both had depression is also explained by the fact that they do share some of the same genes.
Since twin studies leave a lot of questions unanswered, modern research in genetics focuses on genetic mapping. Recent research has used DNA markers to try and identify the gene or genes that are involved in depression. The Human Genome Project allowed us to see that there are up to 11 genetic markers - or variations - that seem to be correlated with Major Depressive Disorder.
Research in psychology: Caspi et al (2003)
Caspi et al (2003) examined the role of the 5-HTT gene in depression. This gene plays a role in the serotonin pathways that scientists believe are involved in controlling mood, emotions, aggression, sleep, and anxiety. Caspi hypothesized that people who inherit two short versions of the 5-HTT gene are more likely to develop major depression after a stressful life event.
Caspi and his team looked at a sample of 847 New Zealand 26-year-olds. The study was a prospective, longitudinal study. All were members of a cohort that had been assessed for mental health on an every-other-year basis until they were 21. They were divided into three groups based on their 5-HTT alleles: Group 1 had two short alleles; Group 2 had one short and one long allele; Group 3 had two long alleles. The mutation of the 5-HTT gene has the shorter alleles.
The participants were asked to fill in a "Stressful life events" questionnaire which asked them about the frequency of 14 different events - including financial, employment, health, and relationship stressors - between the ages of 21 and 26. They were also assessed for depression.
People who had inherited one or more short versions of the allele demonstrated more symptoms of depression and suicidal ideation in response to stressful life events. The effect was strongest for those with three or more stressful life events. Simply inheriting the gene was not enough to lead to depression, but the genes interacting with stressful life events increased one's likelihood of developing depression.
The study is correlational, so no cause-and-effect relationship can be determined.
The study makes an assumption that serotonin causes depression.
Information about life events was self-reported. It may be the salience of the negative life events that plays a role in depression - that is, those that recalled them more easily may have a tendency toward depression. Those who are more resilient, may not recall negative life events as easily.
The theory acknowledges the interaction between both biological and environmental factors in depression. This is a more holistic approach, not reductionist.
There were some participants who did not carry the gene mutation who became depressed; therefore, we cannot say that gene expression alone can cause depression.
There are several strengths to genetic arguments for depression. First, twin studies have been shown to be highly reliable in their results. In addition, modern research has allowed us to locate genetic variations using very large sample sizes. Finally, modern research is not reductionist; it recognizes the interaction of environmental and biological factors in depression.
However, there are several limitations. Firstly, genetic arguments are correlational – they do not – and cannot – establish a cause-and-effect relationship. Secondly, as mentioned earlier, twin studies have a problem with population validity. The samples are not representative of the general population – and they tend to be small.
Population validity is a type of external validity that describes how well the sample can be generalized to a population.
In addition, it is impossible to isolate variables and to separate out the role of environmental factors. Finally, although genetic markers have been identified, it is not clear how these genetic markers interact to produce the behaviours associated with depression.
Possible exam question
Paper 1, section B
To what extent may genetic inheritance influence behaviour?
This question uses the command term “to what extent.” This means that you need to look at the strength of genetic arguments as well as look at other potential arguments. In this case, you should look at the role of environment vs. genetics. You should present evidence from research and you should arrive at a conclusion based on the arguments presented.
Checking for understanding
The field of epigenetics studies ....
Epigenetics looks at the gene - environment interaction and gene expression.
Why is the concordance rate of monozygotous (MZ) twins almost never 100%
MZ twins by defintion have the same DNA. It is just that they do not have the same genetic expression. It is true that MZ twins are not a representative sample, but this is not due to social desirability efect.
What assumption does Caspi et al (2003) make about the origin of depression?
Notice that the study is not of a "depression gene" - it is of a serotonin transporter gene. This means that Caspi assumes that serotonin is linked to the origin of this disorder. You will learn later in the course that this is a highly debated theory with very little actual support. This assumption may be problematic for the validity of this study.
What conclusion did Caspi et al draw from their study of the 5-HTT gene?
The researchers found that 80 per cent of those with two short 5-HTT genes been diagnosed as depressed after three or more negative life events in a year, whereas those with two long genes appeared resilient - only 30 per cent developed the illness in similar situations.
Which of the following variables could have an effect on the results of the study by Caspi et al?
All of these variables could have an effect on the validity of the study. We have to assume that the diagnosis of MDD is valid for all of those who were diagnosed as having the disorder. If people are more resilient, then they may not develop the disorder, which may actually account for the rates being lower than 100%. Culture also plays a role in how we cope with stress and manifest symptoms of mental illness.
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