Genetic factors
Mood disorders tend to run in families, and the same type of disorder is generally found among members of
the same family. Recent research supports the idea that there is indeed a familial genetic link for
depression. When one identical twin suffers from depression the other twin has a fifty percent or higher
chance of also suffering from it. With fraternal twins the likelihood of another twin suffering from
depression or a mood disorder is about twenty percent. Even amongst adopted individuals, research suggests
that depression is still more common with adopted children whose biological family members have suffered
from depression.
STUDY TO SUPPORT
Goodwin & Guze 1984 found the concordance rate for bipolar disorder was 72% for MZ twins compared to
14% for DZ. By contrast the rate for unipolar disorder was 40% MZ and 11% DZ. This is evidence for
genetic influence on mood disorders. Some studies have shown that the concordance rates for mood
disorders is higher in woman than in men (Kendler et al, 2001), however other studies have shown no
differences. So far it has not been possible to pin point a single gene responsible for MD’s, however
Wilhelm et al (2006) found that an abnormal serotonin transporter (SERT) gene could play a key role. The
present view is that MD’s result from multi gene action and not single gene action.
EVALUATIONs
The problem with twin studies is that 100% concordance rates are never found which suggests maybe it is
not genes that is the cause of depression at all. Maybe the similar concordance rate is in fact due to the
environment, i.e the fact that twins are reared identically in their homes and treated similarily most their
lives could be the explanation instead.
Brown and Harris (1978) also believe that social factor contribute to the development of unipolar depression
in particular. For example, unemployment, divorce, single parenting.
STUDY
Egeland (1987) has also provided some evidence of genetic involvement in depression – manic depression in
particular. He studied the Amish communities in USA and using a technique called chromosome mapping he
found from family DNA samples that all those family members with depression had similar abnormalities on
chromosome 11 – again suggesting depression is caused by genes.
Neurotransmitters
Depression has been linked to problems or imbalances in the brain with regard to the neurotransmitters
serotonin, norepinephrine, and dopamine. For example, the neurotransmitter serotonin is involved in
regulating many important physiological functions, including sleep, aggression, eating, sexual behavior, and
mood. Current research suggests that a decrease in the production of serotonin can cause depression in
some people, and more specifically, a mood state that can cause some people to feel suicidal.
In the 1960s, the "catecholamine hypothesis" was a popular explanation for why people developed
depression. This hypothesis suggested that a deficiency of the neurotransmitter norepinephrine (also known
as noradrenaline) in certain areas of the brain was responsible for creating depressed mood. More recent
research suggests that there is indeed a subset of depressed people who have low levels of norepinephrine.
For example, autopsy studies show that people who have experienced multiple depressive episodes have
fewer norepinephrinergic neurons than people who have no depressive history. However, research results
also tell us that not all people experience mood changes in response to decreased norepinephrine levels.
Some people who are depressed actually show hyperactivity within the neurons that produce norepinephrine.
More current studies suggest that in some people, low levels of serotonin trigger a drop in norepinephrine
levels, which then leads to depression.
The neurotransmitter dopamine is also linked to depression. The neurotransmitter dopamine is also linked to
depression. Dopamine plays an important role in regulating our drive to seek out rewards, as well as our
ability to obtain a sense of pleasure. Low dopamine levels may in part explain why depressed people don't
derive the same sense of pleasure out of activities or people that they did before becoming depressed.
Klimek et al 1997 carried out a post mortem study which investigated the role of noradrenaline in
depression. They compared the brains of fifteen patients who had suffered from depression and fifteen
controls (who hadn’t) and found significant differences between the two groups in the structure of the
locus coeruleus part of the brain. Where there was a reduction in the amount of norepinephrine.
EVALUATIONS
The problem with these findings is the cause and effect issue. We do not know if low levels of serotonin
cause depression or if depression causes low levels of neurotransmitters.
Hormones
Cortisol is a hormone secreted from the adrenal glands. These adrenal glands are located near the kidneys.
Adrenal glands assist us in our reactions to stressful events, i.e. stand up to fight or flee from the
situation…. It is believed that the secretion of cortisol hormone is related to clinical depression. It is found
that the people who are clinically depressed, about half of them have the excess of cortisol hormone. And
usually the high levels of cortisol are reducing to a normal level once the depression disappears. This means
that the depressive episodes continue in the absence of any obvious external stressful events.
EVALUATIONS
Researchers knew that people with depression have high levels of cortisol but it not clear whether this was
a cause or an effect of the problem.
Evidence against hormones comes from research on Post natal depression. Evidence that depression in
women is linked to the menstrual cycle, the post-partum period (immediately after birth) and the menopause
has not strongly supported the idea that the hormones oestrogen and progesterone are the cause. With
respect to premenstrual depression, the research indicates that whilst a higher percentage of women may
experience depression at this time, it is usually the case that they have a history of depression not related
to the menstrual cycle.
Around one in ten women experience post-partum depression, but this has not been linked to levels of
hormones such as oestrogen. Research has focused on life events, marital problems and difficult babies
rather than a biological problem (Hendrick et al, 1998).
General evaluations

Biological explanations of depression are deterministic – and this can have negative implications for
the treatment of mental disorders – i.e. if the individual believes that the mental disorder is
controlled by factors outside of their control – i.e. biology/genes etc…. which means it removes the
persons choice of free will – they may believe they cannot help themselves to recover and so may not
even try.

On a positive note determinism can have positive implications – it removes the guilt and hopefully the
stigmatisation away from blaming yourself for the development of the mental disorder.

The biological explanations of depression are reductionist – it doesn’t seem reasonable to simplify
the causes of depression due to just one factor – i.e. genes or neurotransmitters or hormones etc –
especially when the evidence is so varied and contradictory. Other explanations of depression – i.e.
the cognitive explanations would propose that it is the development of negative schemas…….

Other support for the biological explanations comes from the recovery rates of patients undergoing
biological treatments. Drug therapy has shown fast acting relief to patients within 2 weeks by
targeting the neurotransmitters. Thus giving proof to neurotransmitters being the cause in the first
place.

Diathesis stress model might explain depression – or all mental disorders, i.e. the person must have a
genetic pre disposition to that disorder which is then triggered by a stressful life event. So some
people might be vulnerable to depression but because they have never encountered a stressful
situation – they do not develop the disorder.
EXAM QUESTION
Discuss the biological explanations for depression. Refer to empirical evidence in your answer. (12
marks)