Etiology of abnormal psychology

1) Discuss one/evaluate one/one or more study related to etiology of abnormal psychology

Introduction: There are different explanations related to etiology of depression and they are namely: biological,
cognitive and sociocultural.

​Using the example of MDD,The present essay will explain the biological and cognitive factors in development of
depression.

Etiology is the set of causes of a disease or condition. Description in abnormal psychology that is now achieved by
classification systems like ICD-10 or DSM-5. This allows us to reliably diagnose the problem. However, having an
explanation will allow us to predict the course of the disease and the patient’s response to our interventions. ​So
explanations is important as it opens the door

Major depressive disorder or MDD, most commonly known as depression, is a serious mental illness that negatively
affects a person’s emotions and thoughts with extreme cases, causing self harm and suicide. Depression can cause the
loss of interest in activities once enjoyed and hinder a person’s functionality. Symptoms of depression may vary and are
highly subjective.

Biological:
Biological explanations for depression embrace neurochemical factors (neurotransmitters and hormones) and genetic
predisposition.

Firstly, there are three major methods used to establish heritability of traits: twin studies, family studies and adoption
studies. Currently converging evidence from twin studies suggests a 40–50% heritability of depression, whereas family
studies indicate that first-degree relatives of depressed patients are two to three times more likely to have depression
than the general population, Estimation of genetic heritability in twin studies is based on the so-called Falconer model
which assumes that phenotype (observed characteristics such as the presence of presence of symptoms of MDD)
consists of three types of influences: genetics, shared environment
and individual environment. It can be written in the form of:

The falconer model by sullivan et al in meta analysis of studies

found that A = 37% c = 0% and E = 63% The authors concluded
that major depression is a complex disorder that does not result from either genetic or environmental influences

Study: Kendler et al (2006) compared genetic effects on MDD first in males and females and second across different
generations. Results showed that the heritability of MDD was significantly higher in women (A = 42%) than men (A =
29%). No evidence was found for differences in the roles of genetic and environmental factors across generations
spanning almost 60 years. So, the results of the study were in line with the previous estimates of heritability, but it
showed a significant difference between men and women in terms of genetic predisposition to depression.

Gene-environment interaction
The common limitation of research studies based on falconer models is that they ignore complex gene environments.
Gene-environment interaction (GxE) occurs when two different genotypes respond to the same environment in different
ways.

Study: Silberg et al (1999) conducted a longitudinal study, to further understand the reasons for different heritability of
depression in males and females, investigated the trajectories of depressive symptoms among boys and girls from
childhood to adolescence. The authors investigated the link between susceptibility to depression and environmental
factors (stressful life events). Results of the longitudinal analysis showed that the effect of negative life events on
depressive symptoms in adolescent girls was stronger, suggesting that genetic predisposition causes girls at this age to
be more vulnerable to negative or stressful life events. This exemplifies one of the ways in which genes may interact
with the environment: environmental factors serve as necessary mediators or triggers for genetic predisposition.
Molecular genetics allows us to identify specific genes influencing complex psychological disorders, whereas in twin,
family and adoption studies where genes are not “measured” directly we can only talk about some broad, latent,
unspecified genetic predisposition.

Study: Caspi et al (2003) found that a functional polymorphism in a serotonin transporter gene (5-HTT) moderated the
influence of stressful life events on depression The sample was divided into three groups: both short alleles of 5-HTT,
one short allele, one long allele and both long alleles. Individuals who had a short allele of 5-HTT exhibited more
depressive symptoms in relation to stressful life events. More specifically, individuals who carried a short allele whose
life events occurred after their 21st birthday experienced increases in their depressive symptoms from the age of 21 to
26 years, whereas individuals carrying the long/long alleles did not (even though they experienced the same events at
the same time).

Another: Chiao and Blizinsky went further and induced cultural variables. They proposed “culture-gene coevolution
theory” which posits that cultural values buffer genetically susceptible populations from increased prevalence of
affective and mood. They demonstrated that collectivistic cultures were significantly more likely to carry the short allele
of 5-HTT. Additionally, nations with a higher frequency of short allele carriers showed a lower prevalence.

A possible limitations of study is that there is more stigma associated with mental illness in collectivist nations due to
increase cultural pressures to conform to social norms.

Gene environment correlation

Gene-environment interaction recognizes that both genes and environment are important in determining the
development of a mental disorder. There are 3 ways in which genes influence the environment: the passive
environment correlation where parents are not only genotype but also a rearing environment, the evocative
gene-environment correlation where genotype influences the response you receive, the active gene correlation
where an individual may actively select certain environment

“serotonin hypothesis” states that low levels of serotonin in the brain play a causal role in developing MDD. Mostly this
hypothesis has been based on two types of finding. Certain drugs (prescribed for completely different purposes) that
were known to deplete levels of serotonin in the brain were also found to have depression-inducing side effects and that
Certain drugs such as monoamine oxidase inhibitors (MAO inhibitors) were found to be effective against symptoms of
depression. Another class of drugs is selective serotonin reuptake inhibitors, these chemicals inhibit the reuptake of
excess serotonin, increasing synaptic concentration of serotonin, SSRI have shown to be effective against symptoms of
depression. However, these findings are based on “treatment etiology fallacy” where treatment X targets chemical Y.
This might not be true

Evaluation: Not all patients benefit from drugs, antidepressants in some people do not produce any effect and in a
small number of patients this is negative. The link between neurotransmitters and depressive symptoms are mediated
by other variables. Even following recovery from depression, levels of serotonin in many patients tend to remain low.
Also that drugs increase levels of neurotransmitters within minutes, but effects on moods are not fast. Therefore the fact
that antidepressants do not take effect immediately suggest that influence of serotonin on depression might be indirect

Cognitive:
Aaron Beck’s (1967) Beck’s theory identifies three elements of depression: the cognitive triad which includes
deeply grounded beliefs about three aspects of reality which includes: self, the world and the future. The
cognitive triad interferes with automatic thoughts, making them unrealistically pessimistic. The other is
negative self-schema which can be the result of childhood experiences such as excessive criticism, abuse in
the family or bullying. Lastly, faulty thinking patterns which are the negative beliefs that lead to a number of
cognitive biases that people with depression often resort to when they interpret their daily experiences, some
of faulty thinking patterns common for depression include: arbitrary interference, selective abstraction,
overgeneralization, personalisation and dichotomous thinking. According to Beck, the thinking of irrational
elements and biases. biases. Becoming aware of these irrational elements and replacing them with more
logical thinking is a way to overcome these negative thinking habits, which forms the basis of cognitive
behavioral therapy (CBT).

The study of Alloy et al, 1999 quasi and field experiment, demonstrated that people’s cognitive style
influences their vulnerability to depression. Healthy college freshmen were examined for 5.5 years after
splitting them into a group of high risk and another of low risk based on their cognitive styles. Self report
questionnaires and semi structured interviews were conducted during this period on a regular basis. Results
showed that 17% of the high risk group developed depression compared with the 1% from the low risk group,
which shows that negative cognitive correlates with vulnerability to depression. However, the study did not
take into account biological or social factors that could have influenced the results. Hence, the internal validity
of the study is low as the results could have been influenced with a factor other than cognition. The results
showed 17% of the high risk group who have developed MDD, however the rest, the majority, of the group
has not, which suggests the role of other factors. Overall, Alloy demonstrated that negative cognition can
increase the risk of developing MDD, however the study was not controlled and other factors such as biology
and the social environment were not taken into account, weakening its results and reducing their validity.

Another study, the study of Brown and Harris, 1978, aimed at outlining how vulnerability factors can interact
with triggering stressors and therefore increase the risk of developing MDD. The study involved 458 women
from London who underwent semi structured interviews on their history of depressive episodes. The findings
showed that there were four vulnerability factors that were likely to provoke depression in women. The first
one was the presence of three or more children under the age of 14, the second was the lack of intimacy in
their relationship, the third was lack of employment and finally the loss of a mother before 11 years of age.
The study demonstrated how social factors contribute to the development of depression. A disadvantage of
the study is that it is gender biased towards women and therefore the results can not be generalized to men.
A strength of the study is that it was replicated multiple times and the same results were obtained and shown.
The study is also supported by Patten, 1991 that showed that the risk of developing depression can increase
by 3.7 times with the lack of an intimate relationship whereas the other factors double the risk. In conclusion,
the study of Brown and Harris demonstrated that factors outside cognitive etiology such as the sociocultural
environment, significantly contribute to the risk and the vulnerability to depression.