Biological Explanations of Unipolar Depression.
Genetic Influences (from Psychology in Focus):
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Medical mode sees psychological problems as illnesses with physical causes
Genes are often singled out as 1 of the causes of depression. People with a particular genetic makeup
are seen to have a predisposition to depression.
Family Studies:
o Appears to be a tendency for depression to run in families
o Suggests a possible genetic component
o The closer the genetic relationship, the more likely people are to share a diagnosis of depression.
o 1st degree relatives: brothers, sisters, sons, daughters, fathers and mothers share 50% of their
genes
o 1st degree relatives of people diagnosed with depression are 2-3 times more likely to receive a
similar diagnosis than 1st degree relatives of those who haven’t received a diagnosis of depression
(Oruc et al, 1998)
Twin Studies:
o MZ twins share 100% of their genes
o DZ twins share around 50% of their genes
o If genes are a factor in depression, we would expect a higher proportion of MZ twin to share
disorder
o A number of studies have supported this. For example, a study based on nearly 200 pairs of twins
found that when a MZ twin was diagnosed with unipolar disorder, there was a 46% chance that the
other twin would receive a similar diagnosis
o The figure for DZ twins was 20% (McGuffin et al, 1996)
Adoption Studies:
o Most twins and 1st degree relatives share same environment for part of their lives, therefore it’s
difficult to separate genetic and environmental influences
o Studies compare people who have been adopted at an early age with their biological and adoptive
relatives
o Since they were raised apart from biological relatives, similarities with those relatives would
indicate genetic influences
o Most studies of adoptees diagnosed with depression show that their biological relatives are more
likely than their adoptive relatives to have a similar diagnosis. 20% of biological relatives compared
with 5-10% of their adoptive relatives, which is the rate for the general population (Harrington et
al, 1993)
Linkage Studies:
o Studies attempt to identify sequences of genes that appear to be inherited along with a
predisposition to develop depression
o Study of Amish community in Pennsylvania found 4 extended families had a high likelihood of
developing depression
o From 81 people studied, 14 diagnosed to as having bipolar disorder
o Disorder appeared to be linked with a specific genetic marker on chromosome 11 (Egeland et al,
1987)
o Later research both within Amish community and in other populations failed to replicate finding
(Kelsoe et al, 1989)
Genetic Influences (from Psychology A New Introduction (2nd edition))
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Adopted children who later develop a mood disorder appear to be much more likely to have a biological
parent who has a mood disorder, becomes alcoholic or commits suicide, even though adopted children
are raised in very different environments (Wender et al, 1986)
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Cells use a gene called SERT to make a serotonin transporter protein, which plays an important role in
transmission of information between neurons. (Ogilvie et al, 1996)
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In most people, part of this gene contains 10 or 12 repeating sections of DNA
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In a significant number of people with depression, part of this gene has only 9 repeating sequences
The fact that serotonin is strongly implicated in depression and that newer anti-depressants interact with
serotonin transporter protein, offers 1 of the strongest hints that genes may be involved in depression
(Frisch et al, 1999), although research disputes SERT’s role (Seretti et al, 1999)
AO2:
Although genes appear to be involved, role of genetic factors in depression is complex
Don’t know which genes are involved for which people
Don’t know what these genes do or how they are inherited
Biochemistry (from Psychology for A2 Level):
Much interest in possibility that depressed patients might have either elevated or reduced levels of various
neurotransmitters
There are many theories put forward in this area
Many are based on the notion that low levels of noradrenaline and serotonin may play a role in
development of depression
The Permissive Amine Theory:
o Kety (1975), put forward the permissive amine theory of mood disorder
o According to this theory, level of noradrenaline is generally controlled by level of serotonin.
o When level of serotonin is low, levels of noradrenaline are less controlled, and so they may
fluctuate wildly
o Dopamine is also involved
o Noradrenaline, serotonin and dopamine are all neurotransmitters of monoamine group
(catecholamine), which explains the name “permissive amine” theory
o Neurotransmitters act as synapses or junctions between neurons in the brain. They may facilitate
or block nervous transmission
o Noradrenaline associated with physiological arousal in general
o Serotonin is also related to arousal and sleep. Increases in serotonin generally reduce arousal
o Dopamine is normally inhibited by serotonin. It has also been linked to schizophrenia
o Under normal conditions all 3 neurotransmitters play a role in arousal and are related to mood
o It’s been suggested that in depression, serotonin levels are low as a consequence of individual
differences inherited and abnormal serotonin levels prevents adequate control of the other 2
neurotransmitters
o Support for this hypothesis comes from studies that establish a link between mood and these
monoamines, and from studies of effects of anti-depressant drugs
Mood and monoamine transmitters:
o Teuting, Rosen and Hirschfield (1981) compared substances found in urine of depressed patients
and normal patients
o Compounds that are produced as a by-product of action of enzymes on noradrenaline and
serotonin were present in smaller amounts in the urine of depressed patients
o Finding suggest that depressed patients have lower levels of noradrenaline and serotonin
AO2:
It’s hard to know whether high or low levels of noradrenaline and serotonin helped to cause depression, or
whether depression altered levels of those neurotransmitters
Antidepressant drugs such as monoamine oxidase inhibitors (MAOIs) increase active levels of
noradrenaline and serotonin in depressed patients, and typically reduce symptoms of depression
Drugs rapidly affect neurotransmitter levels, but take much loner to reduce symptoms of depression or
mania
It’s possible that MAOIs reduce depression by increasing sensitivity of receiving neurons and it takes time
for this increased sensitivity to occur.
Biochemistry (from Psychology in Focus):
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People don’t inherit depression as such. Nor do they directly inherit the tendency for depression or the risk
of depression
We inherit genes, genes make up proteins, both neurotransmitters and neurotransmitter receptors are
proteins
Genetic difference could therefore present themselves as differences in biochemistry and thus influence
depression
Neurotransmitters:
o Antidepressant drugs are often effective in reducing symptoms of unipolar disorder
o 1 group of antidepressant increases levels of serotonin and noradrenaline
o Findings formed the basis of 1 main biochemical theory of depression
o Unipolar depression is caused by low levels of noradrenaline and serotonin
o How low levels of serotonin and noradrenaline affect depression isn’t clear
o For example, 1 theory states lower levels of both neurotransmitters can lead to depression.
Another theory states it’s the balance between neurotransmitters and their relationship to other
neurotransmitters that contributes to depression (Barlow and Durand, 1999)
o Further research is needed to discover the exact biochemical mechanisms of depression
Biochemistry (from Psychology A New Introduction (2nd edition)):
Schildkraut (1965) proposed that too much noradrenaline at certain sites causes mania and too little
causes depression
Later research suggested that serotonin plays a similar role
There is some evidence supports Schildkraut’s proposals:
o For example, non-humans given drugs that diminish noradrenaline production become sluggish and
inactive, 2 symptoms of depression (Wender and Klein, 1981)
o Similar effects occur when humans are given reserpine to treat high blood pressure
Drugs that are effective in reducing depression increase the brain’s level of noradrenaline and/or serotonin
(Lemonick, 1997)
Drugs that alleviate depression increase noradrenaline and serotonin levels only do so in the period
immediately after taking the drug
Within a few days, levels return to baseline
Problem with Kety’s theory is that antidepressants effects don’t occur during the period when transmitter
levels are elevated
All antidepressants take some time before they alleviate depression
It suggests that depression cant be explained in terms of change in neurotransmitter levels
It’s more likely that drugs act to reduce depression by increasing sensitivity of receiving neurons, thereby
allowing them to utilise limited transmitter supplies in a more effective way (Kennett, 1999)
Antidepressants aren’t always effective in reducing depression, not everyone suffering from depression
shows reduced neurotransmitter levels
It’s likely that neurotransmitters play a role in mood disorders, findings that determine their exact role
remains to be determined (Wolpert, 1999)