Biological Explanation of Unipolar Depression

One biological explanation for unipolar depression is the monoamine hypothesis. The monoamines are a group of neurotransmitters which include serotonin, noradrenaline and dopamine. You will recognise the latter, dopamine, from the biological offering of an explanation for schizophrenia. The monoamines are believed to regulate mood. One of the functions of serotonin is to regulate the other neurotransmitters. Without the regulation provided by serotonin, erratic brain functioning and thinking patterns occur.

Low levels of serotonin produces low levels of noradrenaline (a neurotransmitter needed for alertness, energy, anxiety and attention to life). Evidence suggests that low levels of noradrenaline cause depression, and high levels cause mania, which suggests it is involved both in unipolar and bipolar depression. Dopamine is also related to feelings of alertness, motivation and attention, and so it is suggested low levels of dopamine similarly are linked to depression.

Essentially the monoamine hypothesis suggests that low levels of dopamine and low levels of noradrenaline result in depressive moods, and low levels of serotonin mean low levels of noradrenaline. It can therefore be low levels of dopamine or noradrenaline that result in depression, or a mixture of both. The hypothesis is used to work with drug treatment, so that the correct drugs (antidepressants) can be prescribed based on the particular monoamine in question. In other words, when a clinician is presented with a patient, they will choose the correct drug that alleviates the presented symptoms of depression.

Most antidepressants work by increasing levels of serotonin. It cannot be concluded that the explanation for depression is strictly biological. The diathesis-stress model explains how some mental disorders can have a biological underlying cause but require an environmental trigger to become active. Evaluation: One strength of the biological explanation of depression is that there is further empirical support provided by Ogilvie et al. (1996). They showed that cells use a gene called SERT to make serotonin transporter protein which plays an important role in the transmission of information between neurons.

In most people, part of this gene called the second intron contains 10-12 repeating sections of DNA. However, people with depression, only have 9 repeating sections of DNA. This suggests that there is wider academic support for the idea that serotonin is strongly associated with depression. There is much sound evidence to support the theory, particularly in treatment – if the hypothesis suggests the symptoms are due to monoamine deficiencies and drugs which replace those monoamines alleviate the symptoms, there is evidence for the hypothesis Kraft et al. 2005) studied 96 depressed patients treated over 6 weeks with SNRI (increases levels of noradrenaline) had a reduction in depressive symptoms compared to those treated with a placebo. Leonard (2000) drugs that lower noradrenaline levels have been found to bring about depressive states. Therefore increasing noradrenaline should decrease depressive symptoms . However, The influence of noradrenaline is recognised by the effects of antidepressant drugs which aim to increase levels of noradrenaline.

However, these drugs may also affect other neurotransmitters, so it is difficult to find a clear connection and can be interlined with the critiscism that it is difficult to establish cause and effect. It the chemical imbalance in the brains of depressed people the cause of the depression or the effect of depression? This issue is further complicated by the fact that the answer may be different for different types of depression. In endogenous depression perhaps the chemical imbalance comes first, but the other way round in reactive depression.

Supporting evidence for the biochemical explanation of depression is that it has practical applications From research into the effectiveness of treatments such as ECT and drugs. ECT supports the biochemical explanation because one shock of 110 volts is passed through the brain of depressives for up to 4 seconds. This results in convulsions of up to 2 mins. 6-9 treatments are given of 2-4 weeks. For 60-70% of people with depression, ECT works quickly and effectively. As drugs and ECT alter the balance of chemicals in the brain, it suggests clinicians can improve the quality of people’s lives.

One weakness of the biological explanation of depression is that there are individual differences. Not everyone who suffers from depression is helped by serotonin-based drugs, which suggests that there are other causes of the disorder. It is also not clear why some people become depressed when their serotonin or norepinephrine level is low, whereas others with the low neurotransmitter level remain depression-free. This suggests that the results gained from such research cannot be generalised to the whole population. Another weakness of the research is that it is biologically deterministics.

The reason for this is because it suggests that individuals who have low levels of serotonin are determined to suffer from depression in later life, however, people have a choice about their behaviour and whether they want to do anything about it. This suggests that the biological explanation does not account for free will. A final weakness of the biological explanation of depression is that it is reductionist. The reason for this is because it explains depression in terms of genes (SERT) and neurotransmitters (serotonin) and ignores psychological factors such as learning.

This suggests that the biological explanation is oversimplistic when explaining depression. Alternative explanations for depression is cognitive explanations which is accounted by Beck (1974) who , cognitive theories assume that people’s attributions for events, their perceptions of control and self-efficacy, and their beliefs about themselves and the world influence their behaviors and emotions when reacting to a situation. In general, an individual with various maladaptive beliefs and attitudes becomes more vulnerable to depression because of his or her generalized negative belief pattern.