What Causes Seasonal Affective Disorder?
Researchers aren’t sure what causes seasonal affective disorder. Three main theories have been put forth, and there is contrasting evidence both for and against each of these theories: the Melatonin Hypothesis, the Phase Shift Hypothesis, and the Serotonin Hypothesis.
The Melatonin Hypothesis argues that seasonal affective disorder (SAD) is due to too much melatonin being secreted in response to the long, dark days of winter. Some studies have supported this theory, while others have disputed it.
Phase Shift Hypothesis
Advocates of the Phase Shift Hypothesis, proposed in 1986, contend that in patients with seasonal affective disorder (SAD), circadian rhythms [see Sleep & Circadian Rhythm Disorders section] have been desynchronized to the light-dark cycle, and that appropriately timed bright light reverses SAD Symptoms by realigning these rhythms. Again, there is evidence on either side of the debate.
In the Serotonin Hypothesis, the idea is that serotonin levels in the brain are much lower during the winter months in patients with seasonal affective disorder (SAD) than they are either in people without SAD or in SAD patients during the spring and summer months. This hypothesis came about from researchers observing that SAD patients tend to feel energized after carbohydrate consumption (which increases serotonin levels), whereas people without SAD generally feel more lethargic after eating carbohydrates. Whether serotonin is ‘the cause’ of SAD or not, there is currently a wide body of evidence to suggest that it does play a major role in the disorder.
Other neurotransmitters (dopamine and noradrenaline, for example) may also be involved, as well as other hormones (thyroid, corticotrophin-releasing hormone). The role of these other neurotransmitters and hormones, though, requires further research.