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UNIT 2
PSYCHOPATHOLOGY
UNIT TWO
EXPLANATIONS OF DEPRESSION
BIOLOGICAL EXPLANATIONS OF DEPRESSION
Specification requirements
LEARNING OBJECTIVES: You will be able to:
-Outline the biological explanations for depression, for example, genetics, biochemistry
-Evaluate the biological explanations for depression.
INTRODUCTION
There are several reasons why biological factors are strongly implicated in the origins of
depression:
 The symptoms of depression usually include physical changes (weight loss/gain,
fatigue, sleep disturbance etc.
 Depression runs in families
 Biological therapies such as the use of antidepressant drugs are helpful in alleviating
symptoms of depression
 Certain drugs used in the treatment of other medical conditions can induce
symptoms of depression in non-depressed individuals. Similarly, certain head injuries
and other illnesses can give rise to depression.
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GENETIC FACTORS
Psychologists are divided as to whether depression is something that can be passed on via
our genes or whether the reasons for depression are more psychological.
Research on the heredity of depression within families, shows that some individuals are
more likely to develop the disorder than others.
Individuals with a parent or sibling with clinical depression are 1.5 to 3 times more likely to
develop the condition than those who do not have a close relative with the condition. This
suggests there may be some kind of genetic factor in the cause for depression.
A genetic factor can be investigated by:
Twin studies
Concordance rates can be compared between MZ twins (monozygotic – identical sharing
100% genes) and DZ twins (dizygotic – fraternal twins sharing 50% genes like any other
siblings).
The genetic basis is strongest for bipolar disorder where almost 60 per cent of MX twins will
develop the same bipolar disorder as their co-twin.
Research has been less consistent for unipolar disorder but they are still of interest:
McGuffin et al., 1996 used the Maudsley Hopsital Twin Register and found concordance
rates of 46% in MZ twins and 20% in DZ twins.
Evaluative commentary
Both of these rates are considerably higher than the normal lifetime risk of developing
depression that applies to the general population. However, the concordance rates are
never 100 per cent so genetics cannot offer a complete explanation. Twins usually share a
very similar life experience (even more so for identical twins who will always be the same
sex, maybe dressed in the same outfits and can even pose as each other).
There appears to be strong evidence that a predisposition to mood disorders is genetically
transmitted (Andrew et al., 1998) but this is likely to be a general predisposition rather than
for a specific mental disorder.
The diathesis-stress model suggests that certain individuals have a strong genetic
predisposition which makes them more susceptible to developing depression when they are
exposed to environmental stressors.
Kendler et al., 1995 provided support for this model in their Virginia twin study. They found
that women who were genetically predisposed to depression (i.e. they had a twin already
diagnosed with the disorder) were far more likely to develop depressive symptoms when
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faced with negative life events than women who were at less risk of depression (i.e. they
had a twin who did not have the disorder.
BIOCHEMICAL FACTORS
Introduction
Psychologists have established that levels of certain biochemicals in the body can seriously
affect a person’s moods. Recreational drugs are taken by many individuals because of the
effect they have on their moods, and these drugs work by altering the levels of certain
biochemical in the body and brain. Knowing this, many researchers proposed that if
increasing these biochemicals can improve mood, then decreasing them can cause
depressive symptoms. It is very possible then that low levels of these could be a
contributory factor in the development of depressive disorder.
Amine Hypothesis
Neurotransmitters are chemical messengers in the nervous system and are known to be
particularly active in parts of the brain associated with reward and punishment. They help to
regulate the hypothalamus, which is a crucial link between the nervous system and the
endocrine system and is involved in sleep, appetite, sexuality and physical movement all of
which are, areas, affected in depressive disorders.
One of the most famous neurochemical theories was proposed by Joseph Schildkraut in the
1960s and was named the ‘catecholamine hypothesis’.
This suggests that depression is caused by low activity of certain monoamine
neurotransmitter – noradrenaline. The link between noradrenaline and depression was
established way back in the 1950s by accident. A number of drug trials were being done to
explore the effectiveness of certain drugs to lower blood pressure. One of these drugs,
reserpine also lowered noradrenaline as a side effect. It was observed that participants
whose noradrenaline levels were lowered seemed to develop periods of acute depression.
This suggested that low levels of noradrenaline may be implicated in depression.
Evaluation of the catecholamine hypothesis
There is a great deal of research that supports the catecholamine hypothesis. However,
much research also contradicts Schildkraut’s hypothesis. While there does seem to be a
relationship between low levels of noradrenaline and MDD, levels of noradrenaline do not
affect the moods of everyone in the same way, if they affect them at all. This variability can
be further seen in sufferers of depression who are prescribed drugs which increase the
levels of noradrenaline in the body, but have little effect on the depressive disorder.
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Support for this idea has come from drug therapy
 Antidepressant drugs such as tricyclics and MAOIs, which work by increasing the
available amount of noradrenaline and 5HT (serotonin receptors) in the brain were
found to be effective in alleviating the symptoms of depression.
 Selective Serotonin Reuptake Inhibitors (SSRIs e.g. Prozac) work by increasing the
availability of serotonin and work well for some people in reducing the symptoms of
depression. They have a negligible effect on noradrenaline.
 Conversely, depression is an unwanted side-effect of reserpine, a drug used to treat
high blood pressure, which acts by depleting levels of noradrenaline.
Such findings led to the idea that depression is simply caused by a depletion of the amines,
primarily noradrenaline and serotonin, while mania is caused by too much of these amines.
However, it now seems that the mechanism is more complex than that. One problem for the
original theory is that antidepressant drugs do not simply target these particular
neurotransmitter levels – they have other effects in the brain as well. This means that we
can’t be sure that it is the change in the neurotransmitter levels that accounts for the
effectiveness of the drug. It follows that we cannot conclude that these neurotransmitters
cause the depression in the first place.
Another problem to consider is that they exert an immediate effect on neurotransmitter
levels but take several weeks to have an effect on the mood symptoms of depression. It is
also the case that newer, equally effective antidepressant medications do not work by
increasing neurotransmitter availability in the same way as the first generation of drugs.
These problems with the simple, basic theory have led researchers to suggest that
depression arises from a much more complex interaction of neurochemical factors.
Research into the amine hypothesis continues, but the precise link to depression is not yet
clear. It could even be the case that the dysregulation of the amine system is the result of
depression rather than the cause.
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Neuroendocrine factors
The hypothalamic-pituitary-adrenal (HPA) axis is important in our reaction to stress.
A consistent finding when comparing depressed and non-depressed individuals
shows differences in the functioning of the HPA.
A stress reaction leads to the production of cortisol, a key hormone in arousal. In
normal people, a homeostatic mechanism prevents excessive or prolonged arousal
in response to a stressor.
Cortisol levels are often found to be elevated in people with depression and levels
drop again once the depressive episode is over.
This might be linked to the amine hypothesis – when noradrenaline levels are low,
the hypothalamus loses its ability to regulate cortisol levels. When noradrenaline
levels rise again (i.e. when the depressive episode is over) the hypothalamus can
again start to control cortisol levels. However, high levels of cortisol are not specific
to depression as they are also found in people with anxiety disorders. It is not clear
whether raised levels of cortisol are an effect of depression or a contributory factor.
Neuroanatomical factors
It has been observed that people who have head injuries or strokes in the frontal
parts of the brain have a strong likelihood of developing depression. Post-stroke
depression is associated particularly with lesions in the front region (Starkstein and
Robinson, 1991). The frontal lobes have an important role in planning and
judgement as well as being involved in emotions and motivation.
Starkstein and Robinson have suggested that stroke-induced damage to the amine
pathways which connect the frontal lobes to the limbic system might be responsible
for the depressive symptoms. These findings in stroke patients have led to
speculation that there might be similar brain abnormalities in other depressed
patients.
Some evidence to support this has been found form neuro-imaging studies and from
electro-physiological recording (EEG). Powell and Miklowitz reviewed some of these
studies (1994) which found evidence of structural abnormalities in the frontal lobes
of patients with unipolar disorder, but they cautioned against assuming that there is
a direct causal connection.
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