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Cause of Seasonal Affective Disorder

What Cause Seasonal Effective Disorder? Explanations of SAD are almost uniquely biological.

Genetic factors

There is now increasing evidence of genetic processes in the aetiology of SAD. In one population study, Madden et al. examined the prevalence of SAD in MZ and DZ twins, concluding that about 29 per cent of the variance in the risk for developing SAD was attributable to genetic factors. Interestingly, given the apparent different aetiology between non-seasonal depression and SAD (see below), biological studies have implicated genes related to serotonergic transmission  as well as those that infl uence circadian rhythms.

Circadian hypothesis

According to the circadian hypotheses, the key to SAD is a hormone known as melatonin. Release of melatonin from the pineal gland in the base of the brain is triggered by darkness, and it is found mainly in the midbrain and hypothalamus. It controls sleep and eating. In mammals that are living wild, the release of melatonin as the nights get longer reduces their activity, slows them down and prepares them for winter rest or hibernation. Early melatonin models thought that SAD resulted from an excess production or responsiveness to melatonin. However, evidence of differences in levels of melatonin in people with and without SAD have not proven conclusive. As a consequence, Lewy et al. (1998) suggested that rather than the level of melatonin being the determinant of mood, it is the times at which it is secreted that are important. In their circadian hypothesis, they suggested that ‘normal’ depression can result from poor sleep resulting from disruption of the circadian wake–sleep cycle. In the case of SAD, changes in the times of dawn and dusk in the transition from summer to winter affect the time that melatonin is released, shifting the circadian rhythm of sleep, and taking it out of alignment with other biological rhythms. The goal of therapy is to rephase the wake–sleep cycle to that of the summer.

According to Lewy and colleagues, this may be achieved through exposure to light early in the morning, which helps maintain the summer wake–sleep cycle and delays the secretion of melatonin until later in the day. This, combined with earlier times of sleep in the evening, should prove an effective treatment for SAD. Their own work supported this hypothesis, with fi ndings that light therapy in the morning was more effective than if it was provided in the evening: an effect that seems to hold as long as the individual maintains their summertime waking and sleeping times. Countering this hypothesis, however, are data from, for example, Terman et al. who have found bright light treatment in the morning and evening to be equally effective allowing the possibility that there may be two sub-groups of SAD: one with a general melatonin disorder, and one with a distorted circadian rhythm.

Serotonin hypothesis

A final hypothesis suggests that at least some of the mechanisms underlying SAD may not be particular to this syndrome, and may be those that underpin other forms of depression. A number of factors tie serotonin to the aetiology of SAD. Serotonin is involved in the control of appetite and sleep, and is a precursor to melatonin. Serotonin levels vary seasonally, and reducing serotonin levels by removal of a precursor to serotonin known as tryptophan from the diet results in depressive symptoms during the summer in people who typically develop winter SAD. Further evidence of a role for serotonin has come from treatment trials involving SSRIs. Both sertraline and fl uoxetine have proven moderately effective in the treatment of SAD. However, these are generally not as effective as light therapy or may work best with people who have not responded to light therapy, suggesting that while serotonin levels may be implicated in SAD, they do not provide the entire picture.

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