Etiologies: Major Depression Disorder

Biological
Introduction
Etiology is the scientific study of the origins of disease or abnormal behaviour.
This allows psychiatrists to ensure that the appropriate treatment is used as to
directly treat the cause of the behaviour, whether it be biological, cognitive or a
result of sociocultural factors.
Depression is an affective disorder which is characterised by symptoms of
loneliness, hopelessness, etc. Biological factors which may influence depression
in individuals is genetic components and biochemical factors.

Catecholamine Hypothesis (serotonin hypothesis)

The catecholamine hypothesis suggests that low levels of norepinephrine,
dopamine and serotonin lead to depression. In particular, the serotonin
hypothesis falls under this and more particularly explores the specific effect of
serotonin on symptoms of depression. This can be seen through studies which
show that decreased levels of serotonin results in feelings of sadness, mood
swings, insomnia and many other symptoms of major depressive disorder.

Mann et al (1996)
Findings:

They found evidence of impaired serotonin transmission in depressed

people.
This would account for the low levels that their findings found
Findings showed low levels of serotonin can result in OCD-like symptoms
e.g. obsessive thoughts and compulsive behaviours
Other effects include an increase in impulsivity, suicidal feelings and
thoughts, and an increase in aggressive behaviour
Lower levels of serotonin were found to be linked to mood swings,
increases in worrying, insomnia, and sadness

Teuting et al (1981)
Procedure:

Individuals with depression were asked to provide urine samples, along

with individuals with no depression
These were analysed by researchers, in which a compound produced when
serotonin and noradrenaline are broken down by enzymes is present in
urine, so researchers searched for evidence of this compound

Findings:

Found that there was a significantly lower level of serotonin found in the
depressed individuals samples compared to the non-depressed

However, there is also more recent research which argues against the effect of
serotonin levels on depressive moods.

Evaluation of catecholamine hypothesis:

Strengths
There are several longitudinal
case studies and animal studies
which support these theories.
Practical application of the
theories have led to successful
drug treatments that have
improved peoples lives (e.g.
Prozac)

Limitations
Correlational research means that
causation cannot be established
and bidirectional ambiguity
cannot be resolved.
The treatment etiology fallacy
the mistaken notion that the
success of a given form of
treatment reveals the cause of the
disorder.
Biological explanations cannot
explain the range of symptoms
associated with depression.
There may be cultural and
cognitive factors which also
influence this. Thus the biological
explanation can be argued as a
reductionist approach to a
complex human behaviour.

Genetic Predisposition
Genetic predisposition is another possible biological influence on susceptibility
to depression and suggests that vulnerability to a particular behavioural
abnormality has a genetic basis. This can be explored through research into
genetic markers, in which DNA mrorkers can be used to identify genes that are
involved in depression. The human genome project has suggested that there are
11 possible genes which appear to correlate with major depressive disorder. One
of these is the 5-HTT gene.

Caspi et al. (2003)

Aim: To investigate whether the 5-HTT (5-hyroxy-tryptamine) gene inf1 luences
depression.
Method: Correlation study
Procedure: Participants with a normal 5-HTT gene were compared to
participants with a mutation of the 5-HTT gene in terms of their symptoms of
depressive behaviour after stressful events.
Findings: Participants who carried the mutated 5-HTT gene indicated a higher
vulnerability to depression after stress compared to those who had a normal 5HTT gene.

Conclusion: The gene 5-HTT may be partly responsible in the responding

behaviour to certain environmental situations (such as depression following a
stressful event). Therefore the gene 5-HTT influences behaviour.
Strengths: The study successfully showed a correlation between the presence
of a mutation in the 5-HTT gene and depression.
Limitations: Due to using a correlational study, it isnt possible to draw a causeeffect relationship between the gene and behaviour. However, it was also found
that some of the people who did not carry the mutated gene indicated that they
had depression this may suggest that there are other factors which influence
behaviour apart from only genes.
Evaluation of genetic predisposition argument:

Strengths
Twin studies have been used and
are highly reliable in analysing
results of concordance.
Modern research has allowed us
to actually locate the genetic
variations using very large sample
sizes.
Modern research recognizes the
interaction of environmental and
biological factors.

Limitations
Correlational studies do not
establish a causal relationship.
In twin studies, which are often
used to investigate the
relationship between genetics and
behaviour, there are issues of
validity as samples are small.
It is impossible to isolate the
variables within effects on
depression, social/cultural and
cognitive factors cannot be
separated out.
The argument is reductionist and
does not account for the
variations in the symptomology of
depression.
It is not yet clear how the 11
genetic markers interact.