Download Biological Explanations and Treatments for Depression

Unit 4 – Section B – Psychology in Action
PACK 2
Biological Explanations and Treatments for Depression
Specification:


Clinical characteristics of depression
Issues surrounding the classification and diagnosis of depression, including reliability and validity


Biological explanations of depression, for example, genetics, biochemistry
Psychological explanations of depression, for example, cognitive and psychodynamic

Biological therapies for depression, including their evaluation in terms of appropriateness and
effectiveness
Psychological therapies for depression, for example, psychodynamic and cognitive-behavioural,
including their evaluation in terms of appropriateness and effectiveness

This pack will cover the following part of the specification:

Biological explanations of
depression, for example,
genetics, biochemistry
Note: Research evidence can be used as part of AO1 (particularly
for biological explanations) or as part of AO2.
If you use evidence as AO1 (outline), you only need to describe
the findings/conclusions.
If you use evidence as AO2 (evaluation), you need to explain how
the research supports/contradicts the explanation.

Biological therapies for depression, including their evaluation in terms of
appropriateness and effectiveness
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Biological explanations of
depression:
Note from the mark scheme:
Genetics – genetic explanations are difficult
to describe in detail, so AO1 credit can be
awarded for straight descriptions of family,
adoption or twin studies (eg McGuffin 1996,
Wender 1986) which are used to
demonstrate the genetic explanation.
Genetics
The genetic explanation of depression suggests that we inherit a predisposition towards the disorder from our
parents. Depression seems to run in families and a number of studies have shown an increased risk for
depression in first degree relatives of people with uni-polar depression. There seems to be a link between the
biological closeness of the relationship and the likelihood of developing depression. More recent research has
identified an abnormality in the 5-HTT gene in people who are depressed. This gene is responsible for the
transmission of the neurochemical serotonin. Low levels of serotonin have been implicated in depression. This
means that those who inherit the faulty gene may not produce sufficient levels of serotonin, thus leading to that
individual becoming depressed.
Research evidence
Family studies
Gershon et al. (1982) reported the risk for depression to be higher (over 16%) in first degree relatives
compared to non-relatives (almost 6%).
Weissman et al. (1984) found first degree relatives had a higher risk of suffering depression before the age of
20 (24%) compared to non-relatives (5%).
The evidence points to a genetic component that runs in families, particularly for early onset of depression.
Twin studies
Why study twins and why might twin studies be preferable to family studies?
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Here is a table showing some of the research on twins in relation to depression. In each case, briefly comment
on what the study suggests about genes as a cause for major (unipolar) depression (weak, moderate or strong
evidence).
Allen et al. 1976 (review
of studies)
Mean concordance rate
MZs 40%
DZs 11%
McGuffin et al. 1996
MZs 46%
DZs 20%
Kendler et al. 2006
Largest study, Swedish
42,161 twins including
15,493 complete pairs
MZs 38%
Females 42%
Males 29%
Adoption studies
Wendler et al (1986) found that the biological relatives of adopted sufferers from uni-polar depression were
about 7 times more likely to than adoptive parents to have had the depression themselves.
General evaluation points
Comment on the concordance rates. To what extent do twin studies support the suggestion that major
depression is heritable?
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Explain why concordance rates are not 100% for MZs or 50% for DZs (as would be expected if the cause of
major depression was entirely genetic).
It is possible that females are genetically predisposed to suffer depression more than men. However, there
could be other explanations. What might they be?
Biochemical:
Neurotransmitters
A growing number of researchers believe that genetic factors influence the amount of catecholamines, a group
of neurotransmitters which include noradrenaline [norepinephrine in the US], dopamine and serotonin) in
specific sites in the brain. According to the catecholamine hypothesis, depression is caused by an imbalance
of brain chemicals.
Low levels of serotonin have an effect on noradrenaline and dopamine,
all of which are involved in arousal. Serotonin is thought to be involved
in depression because drugs that increase serotonin levels reduce
symptoms of depression.
Serotonin is broken down by an enzyme (mono-amine oxidase).
There are a number of possibilities for insufficient serotonin. Delete as
appropriate.
a) There may be too much/ too little MAO activity, which clears the synaptic cleft of neurotransmitters
too efficiently
b) Re-uptake of the neurotransmitters may be too efficient /not efficient
c) There may be under production / over production of the neurotransmitters
d) The receiving neuron may be under sensitive / over sensitive (e.g. not enough receptor sites)
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Hormones
An association has been found between the menstrual cycle and depression. 43% of women in one study
suffered depressive symptoms in the pre-menstrual phase.
Cortisol might be involved in depression. In one study, 70% of depressed, hospitalised patients had increased
levels of cortisol, which is a stress hormone.
Further research evidence for biochemical/hormone for depression
Wender and Klein (1981) administered dugs to rats which lower levels of noradrenaline; the behaviour of the
rats became sluggish and inactive.
Mintun et al (2004) used the brain imaging technique of Positron Emission Tomography (PET scan) to compare
the brain activity of severely depressed people to a non-depressed control group. Serotonin receptors are
shown up in the scan by marking them with the chemical tracer of altanserin. The depressed people had fewer
serotonin receptors throughout their brains than the control group.
Anti-depressants such as reboxetine decrease depression in humans; they increase levels of noradrenaline by
inhibiting reuptake. There have been cases were taking reboxetine has led to mania. While the drug has an
immediate effect on the level of noradrenaline in the synapse, they take three to four weeks to work to alleviate
the symptoms of depression. Also Prozac (an anti-depressant) has been found to be effective in reducing
depression by increasing the availability of serotonin but has no effect on noradrenaline.
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EVALUATION OF BIOLOGICAL EXPLANATIONS
1. Any of the research above can be used as supporting evidence for the biological explanations, just
remember to ground it back to the explanation!
2. Why is it difficult to draw firm conclusions about the role of genes and biochemistry in depression? (Think
about the methods of research – AO3)
3. What are the possible consequences of proposing a biological explanation of depression? Try to make both
a positive and a negative point:
4. Research suggests that drug therapy alone is not as successful at treating depression as drug therapy
combined with cognitive (psychological) therapies. Why does this contradict the view that biology alone is
the cause of depression?
5. Explain why the biological explanations of depression fall on the nature side of the nature/nurture debate
and why this matters.
6. Are there any useful applications of the research?
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Biological treatments for Depression
Drug treatments & ECT
AO1:
Drug treatment
Drug treatments aim to restore the balance of neurotransmitters, particularly by increasing serotonin levels.
Outline how each of these therapies work:
Tricyclics (TCAs)
SSRIs (e.g. Prozac)
Side effects:
SSRIs may cause digestive problems but they usually wear off quite quickly. They can cause drowsiness. They
can also cause withdrawal symptoms if a person stops taking them suddenly.
TCAs: include a dry mouth, constipation, sweating, slight hesitancy in passing urine, and slight blurring of
vision. Quite severe, so SSRIs now preferred.
ECT (you have studied this at AS)
Answer the following questions:
What is it?
How is it administered?
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What is it supposed to do for the patient?
Who is most likely to receive it?
Evaluation: effectiveness and appropriateness of biological treatments
Effectiveness of drug therapies:
Some psychologists claim that antidepressants do not work and they simply act as a placebo, others claim that
they are highly effective; the picture is not clear. Read the article The depressing news about anti-depressants
from the VLE for more information on a view of them not working.
Effectiveness of TCAs versus SSRIs…
Both TCAs and SSRIs have been shown to produce a more significant reduction in depressive symptoms
compared to a placebo (Arroll et al.)
SSRIs may only be effective in cases of severe depression…
Kirsch et al. concluded that only in cases of the most severe depression was there any significant advantage to
using SSRIs over a placebo.
However…
This may be because, among moderately depressed individuals, even the placebo appeared to offer them some
hope, which contributed to a lessening of symptoms. For the severely depressed, the expectation of anything
working was absent, thus removing any placebo effect.
DeRubeis et al. (2005) compared cognitive therapy with drug therapy (an SSRI). After 16 weeks 58% showed
improvement in each group. However, Hollon et al. (2005) followed up on the same patients. They studied
three groups and were interested in relapse.
Cognitive therapy then no further treatment
31% relapse
Drug therapy then no further treatment
76% relapse
Drug therapy – continuing treatment
47% relapse
What does this say about the effectiveness of SSRIs in the long term?
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Turner et al. claim that there is publication bias with regard to the effectiveness of drugs. What would the
publication bias be and why does it matter?
Appropriateness of drug therapies:
Appropriateness of TCAs and SSRIs…
SSRIs have an important advantage over TCAs with respect to tolerability. SSRIs are better tolerated than
TCAs, therefore patients are more likely to continue with treatment and recover (Montgomery et al.).
Antidepressants are not suitable for children and adolescents…
Double blind studies (e.g. Geller et al.) have consistently failed to demonstrate the superiority of antidepressant
medications over placebos when given to children and adolescents.
There may be an increased risk of suicide…
A review of studies (Barbui et al.) found that, although the use of SSRIs increased the risk of suicide among
adolescents, the risk was decreased among adults, and particularly so for adults aged 65+ where it appeared to
have a protection effect against the risk of suicide.
Why drugs may initially be more appropriate than other treatment
Why may drugs not be a suitable long term treatment for depression?
Effectiveness of ECT
Research (e.g. Gregory et al.) have shown that when ECT is compared to ‘sham’ ECT, there tends to be a
significant difference in outcome in favour of real ECT. This suggests that there is no placebo effect from
receiving ECT.
ECT is effective in cases of treatment resistant depression (Folkerts et al.) although other studies have found no
improvement following the administration of ECT for treatment-resistant depression (Hussain).
There are mixed findings regarding its effectiveness. Given the ethical difficulties associated with ECT, it is
questionable whether ECT should be used. Patients may be encouraged to have ECT because it is effective,
when that may not be the case.
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ECT versus antidepressants…
A review of 18 studies with 1,144 patients comparing ECT with antidepressant medication showed that ECT is
more effective in the short-term treatment of depression (Scott). This suggests that ECT is effective compared
with anti-depressants although it may depend on the type of drug offered.
Appropriateness of ECT
It is considered appropriate for treating depression but not for those suffering from schizophrenia or severe
anxiety disorders. However, remember that there can be co-morbidity of disorders (see Diagnosis and
Classification), so it may not always be appropriate for treating depression, particularly if it combines with
anxiety disorders.
Rose et al. concluded that at least one-third of patients complained of persistent memory loss after ECT. A
Department of Health report in 2007 found that, among those receiving ECT in the previous 2 years, 30%
reported that it had results in permanent fear and anxiety.
It may be considered appropriate as a last resort. Why?
In cases of severe depression, a person may be sectioned under the mental health act, particularly if they are
suicidal, in which case a relative would have to give consent to the treatment. It may be ethical to use ECT if the
benefits outweigh the costs.
Do you think they do? How do they compare, ethically, with drug treatments?
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