Abnormal Psychology
General framework (applicable to all topics in the option):
To what extent do biological, cognitive and sociocultural factors influence abnormal
behaviour?
In the biological etiology, it can be argued that short alleles of the serotonin transporter gene increase
one’s sensitivity to stress, which then increases the risk of depression. One gene, the serotonin transporter gene
(5-HTT), stands out in research about genetic risks for depression. Avshalom Caspi work was pivotal and now
used as a model for studying other polymorphisms and behavior. Genetic vulnerability for reacting to stress is
related to polymorphisms in the promoter region of 5-HTT. Promoters are near the genes they regulate and
assist in gene transcription, making sure that normal amounts of serotonin are in the brain. The serotonin
transporter system is important because low levels of the neurotransmitter serotonin are correlated to
depression. Caspi et al 2003, aimed to see the correlation between genetic type, having one short and one long
allele, two short alleles or two long alleles of 5-HTT, with responses on questionnaires about stressful life
events and questionnaires diagnosing depression. The sample used 847 Caucasians from random sample of
New Zealanders, all twenty-six year olds. Participants were placed into one of three groups based on having
one short and one long allele, two short alleles, or two long alleles of the serotonin transporter gene. They
filled out a life history survey with questions about life events such as employment, health, and relationship.
No difference was found in the amount of stressors from participants in the three groups. Another
questionnaire found that 17% of all participants qualified for a major depression diagnosis using DSM-IV.
Data were analyzed with correlations between depression symptoms, genotype, stressful events, and their
interactions. The results were that participants with the two short alleles had a greater risk of depression after
four or more stressful events over a period of five years. Moreover, participants with the two long alleles and
the same number of stressful events had a much lower risk. Reports of low stress environments predicted
lower rates of depression regardless of genotype.
The authors concluded that the gene 5-HTT affects depression greatly, but only as it interacts with stressful
environments. Correlations do not show cause and effect, but the study is part of a large body of research.
About forty independently run studies show that the s allele influences the way people react to stress, giving
them more risk for depression so the conclusion is strong. Some studies did not replicate the findings but
several researchers have identified them as having poor study designs. This depicts the nature side of the
argument that biological factors to some extent do cause depression. This was a very large cohort of males and
females and the age was controlled in order to isolate the variable of number of stressful life events between
the ages of 21 and 26. It was a natural experiment, with the naturally occurring IV being the length of the
alleles. If the results are replicated this would suggest high reliability. However, gene action is highly complex,
and actions of other genes could not be controlled. While the stressful life events were standardised as
employment, financial, housing, health and relationship, whether or not a participant experienced a certain
event as stressful is highly personal. Moreover, the symptoms of depression were self-reported, although one
colleague was contacted for each participant in order to verify the symptoms; self-reporting can be unreliable.
Moreover, researchers should look at a more modest approach towards the study. There were even ethical
issues in the study which limit the credibility of the
General framework (applicable to all topics in the option):
To what extent do biological, cognitive and sociocultural factors influence abnormal
behaviour?
In the biological etiology, it can be argued that short alleles of the serotonin transporter gene increase
one’s sensitivity to stress, which then increases the risk of depression. One gene, the serotonin transporter gene
(5-HTT), stands out in research about genetic risks for depression. Avshalom Caspi work was pivotal and now
used as a model for studying other polymorphisms and behavior. Genetic vulnerability for reacting to stress is
related to polymorphisms in the promoter region of 5-HTT. Promoters are near the genes they regulate and
assist in gene transcription, making sure that normal amounts of serotonin are in the brain. The serotonin
transporter system is important because low levels of the neurotransmitter serotonin are correlated to
depression. Caspi et al 2003, aimed to see the correlation between genetic type, having one short and one long
allele, two short alleles or two long alleles of 5-HTT, with responses on questionnaires about stressful life
events and questionnaires diagnosing depression. The sample used 847 Caucasians from random sample of
New Zealanders, all twenty-six year olds. Participants were placed into one of three groups based on having
one short and one long allele, two short alleles, or two long alleles of the serotonin transporter gene. They
filled out a life history survey with questions about life events such as employment, health, and relationship.
No difference was found in the amount of stressors from participants in the three groups. Another
questionnaire found that 17% of all participants qualified for a major depression diagnosis using DSM-IV.
Data were analyzed with correlations between depression symptoms, genotype, stressful events, and their
interactions. The results were that participants with the two short alleles had a greater risk of depression after
four or more stressful events over a period of five years. Moreover, participants with the two long alleles and
the same number of stressful events had a much lower risk. Reports of low stress environments predicted
lower rates of depression regardless of genotype.
The authors concluded that the gene 5-HTT affects depression greatly, but only as it interacts with stressful
environments. Correlations do not show cause and effect, but the study is part of a large body of research.
About forty independently run studies show that the s allele influences the way people react to stress, giving
them more risk for depression so the conclusion is strong. Some studies did not replicate the findings but
several researchers have identified them as having poor study designs. This depicts the nature side of the
argument that biological factors to some extent do cause depression. This was a very large cohort of males and
females and the age was controlled in order to isolate the variable of number of stressful life events between
the ages of 21 and 26. It was a natural experiment, with the naturally occurring IV being the length of the
alleles. If the results are replicated this would suggest high reliability. However, gene action is highly complex,
and actions of other genes could not be controlled. While the stressful life events were standardised as
employment, financial, housing, health and relationship, whether or not a participant experienced a certain
event as stressful is highly personal. Moreover, the symptoms of depression were self-reported, although one
colleague was contacted for each participant in order to verify the symptoms; self-reporting can be unreliable.
Moreover, researchers should look at a more modest approach towards the study. There were even ethical
issues in the study which limit the credibility of the
