Insomnia may be either secondary to another disorder or a disorder in its own right.

Primary insomnia occurs on its own for at least one month which has no obvious medical or psychiatric cause (e.g. drugs or mental disorder). If there is no obvious cause of the insomnia, then it may be classified as primary insomnia. Secondary insomnia is a form of insomnia which has an environmental, medical or psychiatric cause. This could be that the insomnia is the secondary consequence of another problem. One explanation given for primary insomnia is that some people have a genetic vulnerability towards sleeping difficulty. This genetic vulnerability may predispose a person to be more likely to experience hyperarousal (high physiological arousal when awake and asleep). Hyperarousal would make it more difficult for a person to get to sleep which may initiate insomnia. The insomnia then may be maintained and perpetuated as a result of these people expecting to have sleep difficulty. In other words, these people have come to expect that they will have sleep difficulties which further raises their stress and arousal which makes the insomnia worse. One cause of secondary insomnia is psychological disorders and states such as depression and anxiety. Weiss (1962) found that 72% of psychiatric patients in their study reported sleep disturbance, compared to 18% of their control sample. Insomnia and depression in particular are closely related because insomnia is one of the criteria that can be used to diagnose depression. As such, it has been suggested that depression and insomnia may share common underlying mechanisms. Benca and Peterson (2008) suggested that depression and insomnia shared neurochemical imbalances. For example, people with depression generally show lower levels of serotonin which is a neurotransmitter involved in the regulation of the circadian rhythm. As such, low serotonin level may influence sleeping patterns. There is a growing amount of evidence for a genetic predisposition towards primary insomnia. Beaulieu-Bonneau (2007) reported that 34.9% if insomniacs surveyed indicated that they had a first degree relative with a current or recent problem with insomnia. This suggests that insomnia may have a genetic influence although it is difficult to isolate the effects of genes and the environments in family studies. The findings of family studies though have been supported by twin studies. In a study of over 2000 twins, Watson (2006) found MZ twin insomnia was highly correlated (0.47) whereas DZ insomnia was poorly correlated (0.15). This suggests that there is a strong genetic influence on primary insomnia, although they do not completely predict insomnia sufferers. This may suggest a diathesis-stress model for primary insomnia. That is, that genes (nature) give someone a predisposition towards suffering from insomnia but this must somehow be triggered by environmental factors (nurture). There is evidence that depression and anxiety are some way involved in insomnia. Gregory (2006) looked at the relationship between family conflict and the later development of insomnia in a longitudinal study. They found that the degree of family conflict experienced in childhood was significantly correlated with the experience of insomnia at 18. This suggests a possible causal connection between conflicts and later sleep problems. It could be that insecurity may lead to a tendency to focus of family problems which in turn leads to anxiety which in turn effects sleep. However, this evidence is correlational which means that cause and effect cannot be determined between family conflicts and later sleep problems, it may be that family conflicts cause sleep problems due to the anxiety they cause, or it could be that the underlying mechanism which cause

sleep problems later on in life cause anxiety, which is revealed because of family conflicts. In addition, whilst the sample size was large, only 15% of the sample experienced insomnia at 18 meaning that it was a relatively small group from which to identify the variables affecting sleep. One problem for the idea that insomnia and depression share common biological mechanisms is the fact that there are many sufferers of insomnia that do not suffer from depression. Equally, there are many sufferers of depression that do not experience insomnia. If the two conditions shared the same cause, you would expect there to be a much larger comorbidity in the sufferers. As such, the serotonin hypothesis seems to be too simplistic and reductionist. There is also little research into gender differences and sleep disorders. This is an issue because much of the research into the causes of insomnia has focused on women because they are far more likely to seek treatment for insomnia. This means that there could be a gender bias because there is an assumption that the results from studies with females will automatically apply to males. Conditions like Chronic Insomnia are highly complex and unlikely to be explained by one single factor. The large numbers of factors makes it very difficult to conduct meaningful research because studies find only small effects. In addition there are so many different causes for insomnia- stress, depression, age, gender and so on, that it is very difficult to draw any firm conclusions from the research.