Cognitive defects accompanying major depression include disrupted attention and short-term memory. Physical (or vegetative) symptoms include weight loss, fatigue, and loss of interest in sex. Vegetative symptoms are usually confined to non-Western cultures, while mood symptoms (those described in the previous paragraph) seem to be restricted to Western cultures. One reason for this difference may be that Western cultures affix on people who are not faring well and various cultures handle death and mourning in different ways. There is a real risk of suicide with people suffering from depression and women are three times more likely to attempt it than men are. However, four times as many men as women actually kill themselves, partly because they choose better methods.
Seasonal affective disorders (SADs) are linked to the amount of sunlight a patient receives. People with this disorder can develop depression in autumn when the days become shorter and develop mania in spring when the days start to become longer. When these patients travel south in the winter or travel north in the summer, their depression seems to improve. SADs seem to be non-existent in equilateral countries. The treatment usually used is to introduce artificial lights in the winter to make up for the drop in sunlight. One possibility for this disorder is that the sleeping-waking cycle is changed and therefore the amount of melatonin secreted by the pineal gland changes. This may have an effect on the mood of the person. There is also evidence to suggest that all depression may involve a disturbance in sleep rhythms, including the overly quick onset of REM sleep (Kupfer, Foster, and Reich, 1976; Wehr and Goodwin, 1981).
We should now ask the question whether mood disorders are caused by organic or psychogenic factors. There is considerable evidence to suggest that the development of mood disorders is based on organic factors. It is likely that many mood disorders have important hereditary components. Studies have shown that concordance rates for identical twins with bipolar disorders are four times higher than those for fraternal twins (Andreasen and Black, 1991; Siever, Davis, and Gorman, 1991). Furthermore, “genetic linkage” studies of extended families with numerous cases of bipolar disorder show that they also seem to be deficient in a particular enzyme and suffer from a type of colour blindness. Both of the anomalies are due to defective genes on the X chromosome and therefore the genes that cause bipolar disorders may be close by (Hodgkinson, Mullan, and Gurling, 1990).
Studies have also shown that patients suffering from one of the disorders (bipolar or unipolar) tend to have relatives with the same disorder but not the other. This suggests that there are separate inheritance pathways for each and makes it likely that they are largely separate disorders (Gershon, Nurnberger, Berrettini, and Goldin, 1985; Torgersen, 1986; Wender, Kety, Rosenthal, Schulsinger, and Ortmann, 1986).
There are strong arguments that biological factors trigger mood disorders, especially bipolar ones. The fact that people suffering from bipolar disorders tend to switch from one extreme mood to another supports this argument. There must be some internal biological switch that triggers this. Some investigations say that the switch is due to instable neuronal membranes (Hirschfeld and Goodwin, 1988; Meltzer, 1986). This may also explain why some medications are successful in controlling these mood swings.
Other hypothesise propose that when important neurotransmitters such as norepinephrine and/or serotonin are in short supply at certain critical sites in the brain, the person becomes depressed. The evidence used to arrive at these conclusions comes from the analysis of the products formed from the metabolic breakdown of these substances. If the levels of these products in the spinal fluid or urine are low then there must have been a low supply of the corresponding neurotransmitters. In addition, analysis also showed that the amount of norepinephrine in the brain increased when the patient became manic (Muscettola, Potter, Pickar, and Goodwin, 1984; Schildkraut, Green, and Mooney, 1985). It seems that these two neurotransmitters may have a direct influence on the mood of the person. Furthermore, antidepressant medications, which help relieve depression, seem to increase the levels of norepinephrine and serotonin.
However, this view has been challenged recently. While some antidepressants cause an almost immediate increase in the relevant neurotransmitter levels, this increase is short-lived. Within a few days, the transmitter levels fall to what they were before the drug was taken. The medication always seems to relieve the depression until at least a week after the drug was administrated. This time lapse means that the supply of neurotransmitters is not actually increased by antidepressants. Studies have shown that these antidepressant medications make the relevant neurones more sensitive to the neurotransmitters, instead of increasing their levels (Schildkraut, Green, and Mooney, 1985).
Organic factors may be a cause of mood disorders but how can it explain a manic person’s exuberance and self-glorification or a depressive person’s despair and self-loathing? Those who regard the disorder as primarily somatogenic believes that what a patient thinks follows her mood. So if low neurotransmitter levels make the patient feel depressed, the person tries to explain why they are depressed. They will then, for example, think that they are no good in this world.
Aaron Beck (Beck, 1967, 1976) believed that the patient’s depression stemmed from a trio of intensively negative and irrational beliefs that the person holds about themselves, the future, and the world around them. These beliefs form the core of a negative cognitive schema in terms of which the patient interprets whatever happens to them. This comes from an accumulation of unsuccessful experiences in earlier life, harsh criticisms from school and home, rejection by peers etc. Because they expect to fail or be defeated at any particular thing, they will eventually fail or be defeated. To defeat this mentality, Beck used a treatment known as cognitive therapy that involved helping the patients overcome these irrational beliefs.
Martin Seligman proposed an approach known as learned helplessness. The concept explains that a series of catastrophic events in life (e.g. bankruptcy, physical disease, death of a loved one) which cannot be prevented leads to the person to believe they are helpless over their own destiny. The depressed patients will have given up and will not take any initiative that might help them cope. However, there are problems with this argument. For example, many people who feel helpless do not go on to become depressed. In addition, if a person were depressed then why would they blame themselves over the things they felt helpless about?
This argument was revised and the attribution style of the person became more important. If a person always feels that they were the cause of unfortunate events then this attitude may lead to depression in later life. A number of critics believe these theories are incorrect as they argue that hopelessness, helplessness and self-blame are the symptoms, not causes, of depression (Coyne and Gotlib, 1983; Lewinsohn, Hoberman, Teri, and Hautzinger, 1985). Cognitive theorists believe, however, that the attribution style of the person is key as to whether they are more likely to become depressed. People with despondant explanatory style are much more likely to become depressed when faced with failure or stress. Other studies have shown that if a person feels that they have nothing to look forward to, the future may look bleak, and this may start a downward spiral towards depression (Alloy, Hartlage, and Abramson, 1988; Abramson, Metalsky, and Alloy, 1989).
It is clear that there are differences in the number of women and men who are diagnosed with depression. Women are diagnosed more than men are by a ratio of 3:2. A biological cause of this might be that there are predisposing genes on the X chromosome (as explained earlier) and this leads to women suffering more from depression than men do. In addition, women endure cyclic hormonal changes, such as drops in the levels of estrogen and progesterone during premenstrual periods, which can lead to depression. There are also some behavioural explanations as to why there is a difference. Men who are depressed may try to suppress it by distracting themselves with physical activities or alcohol. Women, however, may try find out why they are depressed and cry to relieve tension. Women also tend to seek help more than men do and this may explain why more women are diagnosed with depression than men are.
After looking at all the evidence and both sets of view, I am unable to draw to a conclusive answer as to whether mood disorders are biologically determined. However, I believe that the organic explanations, in my view, are far more convincing than the psychogenic explanations. It seems that the levels of norepinephrine and/or serotonin affect the mood of the person and antidepressant medications relieve depression. This suggests that depression and mania are biologically determined. With regard to gender differences, I believe that women tend to be diagnosed more than men due to cultural differences i.e. women tend more often to seek help and therefore are diagnosed more. In conclusion, no current theories have been proved as of yet and I have an open mind as to any other explanations that may cause depression or mania.
