Genetic factors: McGuffin et al
- Using the Maudsley Hospital Twin Register, concordance rates of 46% were found in MZ twins and 20% in DZ twins.
- These rates considerably higher than for the lifetime risk of developing depression that applies to the general population.
- However, it is not 100% so it would indicate other factors are at play.
Genetic factors: adoption studies
Adoption studies are one way of disentangling genetic and environmental factors, since they look at depressed people who have been adopted at an early age and brought up away from the influence of their biological families.
Most of these studies have shown an increased risk in the biological relatives of people with depression rather than the adoptive relatives.
For example, Wender et al (1986) found that biological relatives were eight times more likely to have depression than adoptive relatives.
Genetic factors: Diathesis stress model
The DIATHESIS-STRESS MODEL states that having a genetic predisposition for depression will make depression more likely in response to environmental stressors.
- Not reductionist because it focuses on nature and nurture, doesn't simplify it
Genetic factors: Kendler et al
KENDLER ET AL: VIRGINIA TWIN STUDY. They found that women who were genetically predisposed to depression were far more likely to develop depressive symptoms when 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: neurotransmitters
Depression may be the result of low levels of certain neurotransmitters – namely, noradrenaline and serotonin. These neurotransmitters are known to be associated with the parts of the brain involved in reward (pleasure) and punishment and they help to regulate the hypothalamus which controls physiological arousal and some of the key areas affected by depressive disorder (eg sleep, appetite, and sexuality).
- Anti-depressant drugs are an effective treatment for depression and work by increasing the action of noradrenaline and/or serotonin in the brain
- Conversely, depression is an unwanted side-effect of Reserpine, a drug used to treat high blood pressure. This drug reduces levels of noradrenaline. Thus, suggesting that neurotransmitters could be the cause of depression.
- Anti-depressant drugs exert an immediate effect on neurotransmitter levels in the brain but it takes several weeks for the person to start feeling better
- It may be that lower levels of noradrenaline and serotonin are an effect rather than a cause of depression
- This is supported by research evidence. Dogs are restrained in a harness and given electric shocks from which they cannot escape, eventually show symptoms of depression. However, it is only AFTER such symptoms have appeared that levels of noradrenaline and serotonin are found to drop – not before, which is what you would expect if low levels of these neurotransmitters cause depression.
High levels of the stress hormone cortisol are often found in depressed people and levels return to normal when they are over the depressed episode.
When noradrenaline levels are low, the hypothalamus loses its ability to regulate Cortisol levels. After depression, when noradrenaline levels return to normal, the hypothalamus can again control cortisol levels.(high levels)
- 10-15 % of women meet the criteria for major depressive disorder after child birth – post-natal depression. This has led to speculation that ovarian hormones may play a role
- The problems with stating that high levels of cortisol cause depression are that it could be a consequence rather than a cause of depression (e.g. person feels stressed about their depression).
- However, it has been found that the majority of women who experience post-natal depression also experience other problems (eg adjusting to the role of being a mother) and have had prior episodes of depression.
People who have suffered head injuries or strokes in the frontal lobes of the brain have a strong likelihood of developing depression. This part of the brain is associated with planning and judgement as well as playing a role in emotion and motivation.
Based on research with stroke patients, STARKSTEIN AND ROBINSON (1991) suggest that damage may disrupt noradrenaline and serotonin pathways that connect the frontal lobes to other brain structures that regulate mood.
In turn, this has led to speculation that brain abnormality may be a cause of depression in people who have not suffered brain damage and brain scans have revealed some frontal lobe abnormality in people with unipolar disorder.