Describe and Evaluate Explanations of Depression. Refer to Issues Such as Those Raised in the Quotation Above

“Depression tends to run in families and symptoms are similar across cultures, genders and ages. This suggests that biological mechanisms play a strong part in the development of the disorder.”

One explanation which implicates biological mechanisms in the development of depression is the biochemical approach. This suggests that low levels of the neurotransmitter serotonin may be involved. Usually serotonin acts to modulate neural activity and regulates emotional reactions; in patients with noticeably lower levels, symptoms of depression, such as apathy and sadness, can be seen.

Evidence for the role of serotonin has come from studies of patients taking anti-depressants and from PET scans of patients’ brains. Comer (2004) observed that patients who took anti-depressants, which act by increasing the availability of serotonin in the brain, showed reduced symptoms of depression. From this it was suggested that without the drug therapy the patients’ serotonin levels were too low and were causal in their depression. This theory of reduced serotonin levels was supported by the findings of Mann et al.’s (1996) study which used PET scans to observe patients brains, which showed impaired transmission of serotonin.

However, such results cannot prove causation as low serotonin levels could be either a cause or an effect of the depression. If the reduction of serotonin in the brain was caused by the depression, it would not explain how raising levels artificially can be seen to alleviate the symptoms of depression though- it would be expected that under these circumstance there would be no effect. This may lend more weight to the assumption that lower levels of serotonin are a cause rather than an effect.

Equally, it is possible that serotonin is not directly involved in depression. This idea was proposed after it was noted that although anti-depressants significantly raise levels of serotonin within five hours, the drugs take one to two weeks to begin alleviating depressive symptoms. If serotonin was directly implicated it would be expected that as soon as the levels were raised to normal the symptoms would begin to subside. It may be possible that the raise in serotonin causes a chain reaction of chemicals within the brain, so that the initial rise in serotonin levels effects a separate chemical- causing it to rise or lower- which in turn causes another chemical to rise or lower, and so on until the chemical directly linked to depression is finally altered, or the combination of changes makes an impact.

It has been suggested that if depression is associated with psychological problems (mainly expressed in the cognitive model), that the effect of drugs may be due to the “placebo effect”- where the drug is inert yet improvement is seen due to the psychological effect of the power of suggestion; the patient believes the drug will make them feel better, so they do feel better. Studies using the drug Prozac® (an anti-depressant of the SSRI class) have proven that the placebo effect does not occur in the case of depression though. Findings using both Prozac® and a placebo showed that the ...

This is a preview of the whole essay

As a purely biological model, this explanation fails to take account of psychological processes that may be occurring. Some of the symptoms of depression are more associated with psychological aspects of a person rather than physical aspects. For example, weight loss could be explained biologically, however low self-esteem would be better explained by cognitive theories. This suggests that the biological model may not be a complete explanation of depression, and it would be reductionist to consider it possible to explain such a disorder just in biological terms. Ideas from other models may be necessary in order to fully understand the development of depression. The diathesis-stress model attempts to incorporate these different explanations and may be more successful than a completely biological approach.

A second explanation implicated biological mechanisms in the development of depression is the genetic theory. This idea is based on the observation that depression can be seen to run within families, and implicates genes as a causal factor. If a person has genes associated with depression, it may be that the genes influence aspects such as their hormone and neurotransmitters levels, which would cause depression- and so genetic theory can be linked to the biochemical explanation of depression.

Gershon (1990) performed a meta-analysis of ten family studies into depression and found that the rates of unipolar depression amongst first-degree relatives of sufferers were between 7-30%. This is much higher than can be expected in the average population, and so may indicate a genetic link. However, these findings may also have been caused by the environment- it is likely that members of the same family will live in the same or similar environment which may have a negative impact on them, causing a large number of them to develop depression.

Also, family studies are often less reliable than other forms of research, due to the data being retrospective. If the data is self-reported by the family it is possible that the evidence is merely anecdotal and so is unlikely to be completely accurate. If a relative is described as being “depressed” it may be that they did not have clinical depression but instead just a more miserable disposition than others. If reports are taken from medical records it is still possible that the accounts are unreliable, as a judgement may have to be made based on very little evidence- for example if it is simply noted that their mood was lower than usual it must be decided whether this indicates clinical depression or just a bad day. Often a person will not be formally diagnosed in the notes as being clinically depressed, but any notes made may allude to this fact.

By looking at twins it is possible to further examine the role of genes in causing the disorder. Monozygotic twins share 100% of their genes, and so they can be observed for concordance rates of suffering from depression- it would be expected that there would be 100% concordance if depression was caused by genes alone. These results are compared with the results of dizygotic twins, who share only 50% of their genes and so should have a much lower rate of concordance. McGuffin et al. (1996) found a concordance of 46% in MZ twins, compared to a lower 20% concordance in DZ twins. This suggests that genes may be involved in the development of depression; however as MZ twins did not show 100% concordance genes cannot be the only factor.

Such studies are unable to eliminate the effects of the environment though. It is expected that as MZ twins have an identical appearance they are treated as the same person, and so have the same experiences. This does not occur so frequently with DZ twins, and so they would share fewer experiences in common. These differences in shared environments and experiences may account for the differences in rates of concordance, so that genes are not actually the causal factor. It is more ideal to study identical twins that have been separated at birth (so that many environmental factors can be eliminated), however these are very infrequent within the population and it would be unethical to purposefully separate twins for the sake of a psychological study.

Equally, it is possible that having a twin who is depressed may affect the second twin. If they are treated the same, such as with MZ twins, the second twin may develop depression as they are treated as though they already had depression, because their twin is a sufferer (this may be explained through behavioural theories). Having a twin with depression may also be stressful, which could lead to depression, as long periods of stress lead to the secretion of stress hormones such as Cortisol which has also been implicated in the development of the disorder. Also, if the suffering twin is receiving more attention due to their disorder, this may negatively affect the second twin if they become to feel neglected.

As twins, especially identical twins, are rare within the population, the sample size within studies is limited. This means it is hard to generate sufficient data which can firmly prove or suggest if genes are involved in depression. Studies must take place of long periods of time too, which normally leads to high rates of attrition which may have an impact on the data collected.

The theory that genes can cause depression can be criticised as being determinist, as it suggests that if a person has inherited these genes they are unable to prevent themselves from developing depression- once they have the genes they will certainly develop the disorder.

Although these biological explanations are supported by various research studies, there is no conclusive evidence which can determine the precise cause of depression. It is hard to understand whether symptoms of depression such as changes in neurochemical levels are cause or effect, and whether correlational findings from concordance studies imply causation or not. Depression cannot be explained through these biological approaches alone and so needs to be considered from a psychological angle as well. The diathesis-stress model may be more successful in explaining why depression develops as it takes into account both biological predispositions and psychological triggers.

http://pi.lilly.com/us/prozac.pdf