Download Outline and evaluate biological explanations for depression. 8 + 16

Outline and evaluate biological explanations of depression.
8 + 16 marks
One biological explanation of depression is genes. This suggests that depression is
inherited. Research shows that individuals with a depressed relative (parent/sibling)
are 1.5. to 3 times more likely to develop depression than those without a depressed
relative. Twin studies show a concordance rate of 46% for MZ (identical) compared
with 20% for DZ (non-identical) twins. This suggests that genes have a role in
whether people develop depression or not.
However, concordance rates are never 100% for identical twins so this suggests
that genes can’t be a full explanation because MZ twins share 100% of their genes
and so if genes were the only cause of depression there would be a 100%
concordance. This means that there must be other factors involved for example
environmental ones such as upbringing and interaction with parents and family
members. Higher concordance rates for MZ twins could be explained by the fact
that being identical, they are more likely to share a more similar life experience than
non-identical twins. It makes sense to take a mixed approach; the diathesis-stress
model shows how there can be a genetic predisposition which is triggered by
environmental cues such as life experience. Research has shown that women who
were genetically predisposed to depression (had an identical twin suffering with
depression) were more likely to develop depressive symptoms when faced with
negative life experiences than women who were at less risk, i.e. not genetically
predisposed.
A methodological problem with twin studies is sample size because it can be
difficult to find depressed twins which leads to a problem of inappropriate
overgeneralisation. The relatively small number of participants available may not
always be representative of people generally. Furthermore, it would take a
longitudinal study over many years to establish accurate concordance rates as,
while one twin may not be depressed at the time of the study, they may on to
develop depression later on.
Biochemistry can also explain depression. The amine hypothesis suggests that an
imbalance of neurotransmitters in the synapses in the brain may bring about low
mood. For example, it was discovered by accident, during drug trials, that the
neurotransmitter noradrenaline may be involved in depression. Reserpine (used to
treat high blood pressure) resulted in lowered levels of noradrenaline and patients
in the drug trial suffered acute depression.
Evidence for the amine hypothesis comes from the effectiveness of medications
which raise the levels of this neurotransmitter. MAOIs and Tricyclics, work by
either inhibiting the flushing away of noradrenaline from the synapse or blocking its
reuptake into the presynaptic neuron. This ensures that more noradrenaline
remains available in the synapse to bind with the receptor sites on the post-synaptic
neuron. Such drugs seem to be effective in relieving symptoms of depression.
However, while the drugs raise levels of the noradrenaline immediately the
symptoms of low mood take a couple of weeks at least to be relieved. This suggests
that there must be other factors involved. As Tricyclics work on serotonin as well
as noradrenaline, it was considered that serotonin may have a part to play in
regulating mood which led to another group of drugs being produced – SSRIs
which specifically target serotonin and block its reuptake. The effectiveness of
these drugs and the lack of side effects made them a popular alternative to
MAOIs and Tricyclics. However, they do not work for everybody and if depression
was simply caused by amines we would expect to see less variation in how people
respond to them. Furthermore, it isn’t even certain whether these chemicals are
the cause of depression or whether it is the depression which brings about changes
in their levels.