Describe and evaluate biological explanations of depression There are many different explanations for depression, including biological. Links have been found between biochemical, genetics and hormonal imbalances with depressed people. In the biochemical explanation, a link has been found between neurotransmitter imbalances and depression. Serotonin is associated with pleasure and mood. Mann et al found impaired transmission of serotonin in people with depression. However Julian disagrees with this statement and says depression may be due to neuron damage rather than a neurotransmitter reduction.

The problem with this approach is that it implies correlation and not causation, there may be a link but something else could be causing both depression and low serotonin. There is the chicken and egg problem – does low serotonin cause depression or does depression cause low serotonin? In other areas of psychology low serotonin has been linked with increased aggression and eating disorders, as well as anxiety. Someone that has low serotonin does not necessarily become depressed. There is also the problem where people are depressed but have normal serotonin levels.

This shows that depression is not fully down to biochemical imbalances but other things as well. It is a very simplistic and reductionist model and should only be included as a vulnerability and not the whole answer to depression. Another explanation is a genetic problem. Through many family studies Gershon states there is a clear inheritable component to depression, especially in bipolar disorder. Weisseman et al supports this by saying that for if a child has a parent with depression, the risk of the child having depression is increased by three times compared to the general population.

This is a strong finding but as the children share the same environment as their parents, there is a possibility that the child has learnt the behaviour through the social learning theory of imitating and observing and not through genetics. Kendler et al studied over 15000 twins in Sweden and found that if one twin has depression, there is a 38% chance that the other twin will have it too. This has strong methodology and is supported by many twin studies who have found similar results. On the other hand the twins share the same environment and so environmental influences may still be possible.

The results were nowhere near 100% showing that depression is not fully down to genes, the people may have a genetic vulnerability but it takes something to trigger, perhaps. It is also unclear as to how exactly genes play a role in depression, without knowing the exact genes involved. Another way to access the significance of genes is through adoption studies. Wender found that a child is seven times more likely to have depression if the biological parents were depressed and the adoption parents were not.

They found little evidence of depression being learnt. However Wender got his information about biological relatives just from hospital records and so there could be error of misdiagnosis or short-term depression only. The knowledge of whether a person has a genetic vulnerability to depression can be useful as the person is able to take preventative measures (change in lifestyle, diet to bring positivity to avoid depression), but it could be fatalistic as they understand they are more likely to become depressed – leading to depression.

Diathesis-stress model says that depression can be better understood as an interaction between genes and environmental factors. Carroll found that high levels of the hormone cortisol are found in those suffering from depression and techniques known to suppress cortisol secretion have been found to be successful in depressive patients. However cortisol is released when stressed and so the high levels could be due to the high levels of stress the person has when they are depressed.

As depression is twice as common in women as men, it could be due to the differences in sex hormones. Post-natal depression could be due to the high levels of oestrogen and progesterone that are released during pregnancy and then rapidly decrease once the baby is born which may account for an imbalance of hormones. Cooper disagrees with this statement as there was very little difference in the number of women suffering from depression after childhood and a control group of non-pregnant women at the same age.

If imbalance of hormones was the cause then most mothers should get this type of illness but it is only a small number that get it. Menopausal depression is where oestrogen levels drop and hormone replacement therapy appears to be affective in treating many (but not all) women who suffer from this type of depression. However this could be due to the negative thoughts of getting older rather than the hormonal imbalance. Through the biological approach there are many possibilities. I think it is a mixture of biological vulnerabilities and stressful environments.