4 sample essays on exam questions on unipolar depression (one of the optional mental disorders to pick from) worth 20 marks each
including evaluation on biological and non-biological explanations and treatments.
provides a structure for 20 markers on questions about unipolar depression
UNIPOLAR DEPRESSION
EVALUATE 1 BIO EXPLANATION OF DEPRESSION (20)
1 weakness of monoamine hypothesis is that it suffers from treatment aetiology fallacy. The
monoamine hypothesis proposes that low levels of serotonin cause the levels of other
monoamines such as noradrenaline and dopamine to drop as well, leading to anxiety and
lack of pleasure, and hence some symptoms of depression. The issue is that it is unclear
whether the erratic brain function such as low levels of monoamine neurotransmitters cause
depression or whether depression causes low levels of monoamines. This means that the
cure of antidepressants that work by boosting monoamine levels doesn’t necessarily imply
that the low levels of monoamine was the cause of depression in the first place. This is a
weakness as it points out that the monoamine hypothesis isn’t a causal explanation of
depression but is just a description of the symptoms of depression. On the other hand,
double-blind trials testing noradrenaline reuptake inhibitors (NRIs) and placebo drugs have
shown that NRIs led to mood improvement in patients with depression compared to placebo
drugs. This implies that low levels of monoamines must be involved in the development of
depression as correcting these also improved the depressed mood characteristic of
depression.
One strength of the monoamine hypothesis is that it has research support. Low levels of
monoamines mean that there is little stimulation of postsynaptic receptors, therefore an up-
regulation in sensitivity of these receptor sites on synapses in relevant pathways occurs to
process as much monoamine as possible. When antidepressants are administered, the
receptors sites are desensitised, so down-regulation occurs to prevent damage of the
receptors. For example, Andreoli et al. (2002) demonstrated that antidepressants
increasing serotonin levels are just as effective as other drugs increasing noradrenaline
levels. This means that serotonin and noradrenaline are key monoamines involved in
depression as these once corrected, were more effective in treating depression when
antidepressants are used. This is a strength as it provides evidence for the monoamine
hypothesis that serotonin and noradrenaline levels are characteristic of depression.
However, NRIs and SSRIs do not work for all patients with depression, implying that other
factors must be involved in the development of depression as well.
One weakness of the monoamine hypothesis is that it is reductionist. This hypothesis
proposes that only 3 neurotransmitters are involved in depression, which are serotonin,
noradrenaline and dopamine which all regulate mood. For example, people with an under-
active form of the gene 5-HTT are more likely to suffer depression after stressful life events
due to little production of serotonin. This implies that low serotonin levels are the sole
predictor of whether someone will develop depression or not. This is a weakness because
this explanation ignores the role of any psychological or environmental factors, since people
in lower-income households might still end up getting depression even though they may
have normal levels of serotonin. On the other hand, it could be argued that the progress of
depression may still be due to faulty biological processes in the body such as excess cortisol
levels, contributing to a lot of stress which may lead to fatigue and loss of concentration –
symptoms of depression.
One strength of the monoamine hypothesis is that it has supporting evidence. Monoamine
oxidase A (MAO-A) recycles monoamines that are not needed from the synapse through
reuptake. Too high levels of MAO-A lead to reuptake of monoamines which are needed for
mood regulation, leading to low levels of monoamines. Mann (2003) reported reduced
serotonin levels in patients who committed suicide in his post-mortem studies. This implies
that depression is characterised by low serotonin as shown by these studies. This is a
strength as it provides scientifically credible evidence for the monoamine hypothesis since it
, describes exactly what the hypothesis would predict, such as low levels of serotonin.
However, not all suicides are caused by depression, meaning that low serotonin levels may
also be caused by another factor and not necessarily by depression. This contradicts the
hypothesis as depression may not always be due to low levels of serotonin.
One weakness of the monoamine hypothesis is that there are other more suitable
explanations for depression. Serotonin regulates sleep, therefore low levels may cause
insomnia or hypersomnia – changes in sleep patterns as seen as one of the symptoms of
depression in the DSM-V. However, abnormalities in the neuroendocrine system might
explain symptoms of depression better than the explanation of neurotransmitters. For
example, the hypothalamic-pituitary-adrenal system regulates the body’s response to stress.
The hippocampus controls levels of CRH hormones and consequently levels of cortisol.
Severe stress and depression lead to a constant release of CRH and cortisol, affecting the
hippocampus. This results in a vicious cycle of releasing more stress hormones such as
CRH and cortisol. This means that depression is not a consequence of abnormal
neurotransmitter levels, but rather results from the excessively high levels of stress
hormones in the body since CRH and cortisol are constantly being released by the
hippocampus. This disproves the monoamine hypothesis as hormones not neurotransmitters
might be the main culprit in causing depression. However, if NRIs have been shown to be
more effective than placebo drugs, then monoamines must have a role in the development
of depression as once corrected, the symptoms of depression improve resulting in mood
improvement.
In conclusion, the monoamine hypothesis taught us that low levels of monoamines that
regulate mood are involved in the development of depression since low noradrenaline
results in anhedonia and low dopamine results in anxiety, both which are symptoms of
depression. It isn’t possible to conclude that abnormal levels of neurotransmitters are the
sole cause of depression since no studies have found whether abnormal levels of
monoamines were present before the development of depression in patients as it’s hard to
predict who will have depression. However, placebo studies have demonstrated that
monoamines should at least have a role in depression since the placebo effect didn’t result
in mood improvement greater than the effect of NRIs. This implies that monoamines are
involved in depression but may not be the sole cause of it. To improve this hypothesis,
further neurotransmitters should be investigated as it is too simplistic to narrow down a
complex mood disorder like depression with many affective and cognitive symptoms to just 3
neurotransmitters as the interaction between many neurotransmitters and the environment
the person is in is a more credible explanation of depression.
Evaluate 1 non-bio expl. of a disorder other than SZ (20)
One strength of negative thinking as an explanation for unipolar depression is
that it has scientifically credible evidence. Beck (1967) proposed that depression is
caused by 3 patterns of negative thinking: negative automatic thinking, selective
attention to negative thoughts and negative schemas. Negative schemas are a set of
beliefs and feelings about the client that they developed through unpleasant
experiences in childhood such as critical relationships with parents or traumatic
events such as abuse. Rayner et al. (2016) conducted brain scans of 59 patients with
depression and found overactivity in the prefrontal cortex when the patients had
unpleasant memories and felt guilt, and less activity in areas of the brain to do with
concentration and decisiveness. This suggests that negative thinking can be
observed in brain scans and is not hence an abstract concept. This provides
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