Seasonal Affective Disorder: Cause, Effect and Treatment

Season Affective Disorder


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Seasonal affective disorder is a psychological mood disorder that is characterized by lethargy and depression dependent upon the seasons of the earth. There are two different subtypes of the disorder. They are winter seasonal affective disorder and summer seasonal affective disorder. Winter SAD is more common and it occurs in the months of winter and it spontaneously disappears in the springtime. Summer SAD is just the opposite; Depression occurs in the spring and the symptoms recede in the winter. Subsyndromal SAD is similar to seasonal affective disorder but has milder symptoms and does not disturb a person’s ability to function. (Partonen & Lonnqvist, 1998). This paper will focus mainly on winter seasonal affective disorder. The Diagnostic and Statistical Manual of Mental Disorders lists SAD as “a specifier of either bipolar or recurrent major depressive episodes,” (Partonen & Lonnqvist, 1998).


This disorder only affects a small number of people each year. Seasonal affective disorder is estimated to only be diagnosed in 5% of the population. Geographical location does play an important factor in prevalence of the disorder. The disorder is more common among people who experience a longer winter and less hours of sunlight than people closer to the equator. (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998) While people in all areas of the United States can be diagnosed with seasonal affective disorder, it mostly affects people that live north 40 degrees in latitude. Interestingly, people native to Alaska are less likely to be diagnosed than people that relocate to that area. (Timby & Smith, 2005).

SAD is 4 times more common among females than males. This may be due to differences in each sex in biochemical responses to climatic changes. In a study by Buget, Gati, and Soubiran, males adapted to climate changes by decreasing their metabolism. Females, on the other hand, showed variable metabolic reactions to temperature increases (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This may mean that males are more effective at responding to climatic variables than women due to a biological difference.

Seasonal affective disorder usually develops around the age of 20 to 30 years old and also shows evidence of significant familial predisposition to developing the disorder. 50-60% of patients with SAD have first degree relatives that have a major affective illness (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This demonstrates an important genetic role in the disorder that can also be a predictor for a higher risk of SAD.

After following up with patients with SAD 5-11 years after diagnosis, 38-42% of patients routinely experience the symptoms of SAD. (Partonen & Lonnqvist, 1998). This suggests that patients with the disorder can be treated effectively without relapsing with the same symptoms.


The symptoms of seasonal affective disorder are present during the winter and are not experienced in the spring and summer. Frequent symptoms of SAD are “Social withdrawal; decreased activity; sadness; anxiety”, fairly frequent symptoms are “carbohydrate craving; decreased libido; poor quality of sleep; increased sleep; irritability; increased weight; increased appetite” Fairly infrequent symptoms are “Suicidal thoughts; decreased sleep; decreased appetite” (Partonen & Lonnqvist, 1998). These atypical depression symptoms can be life altering and should be treated.


It is believed that seasonal affective disorder is triggered by a decreased exposure to sunlight. Its underlying cause is not clear but there are many theories to what causes SAD.

Melatonin is a hormone that is important in circadian rhythms and the sleep wake cycle. Seasonal affective disorder was originally believed to be an abnormal melatonin metabolism, but patients with SAD did not have any abnormalities in their levels of melatonin secretion. Yet, it is suggested that patients with SAD have abnormal insensitiveness to light and may have light induced suppression of melatonin during the night. (Partonen & Lonnqvist, 1998). It has been observed that bright light can inhibit nocturnal melatonin secretion of the pineal gland. The studies on melatonin and seasonal affective disorder suggest melatonin may play a small part in the disorder but it is not believed to be the main cause (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998).

Another theory is that the biological clock is disrupted during the winter months. The circadian rhythms of patients with SAD seems to be more irregular than healthy individuals. Their patterns within the circadian rhythms deviate from normal and do not show the same times of peak as people without the disorder. (Partonen & Lonnqvist, 1998). There is evidence that the circadian rhythm disturbances “… are worsened by shorter periods of daylight, exposure to cold weather, and ageing” (Partonen & Lonnqvist, 1998). The differences in circadian rhythms of patients with SAD may be explained by the shorter daylight experienced in the winter months.

Even small changes in the sleep-wake cycle can have significant effects on mood. Mood is influenced by the circadian rhythm and the hours spent awake. Abnormal sleep patterns are reported by many individuals with seasonal affective disorder. While SAD patients have a regular homeostatic regulation of sleep, changes in sleep-related event are experienced. The sleep related events could be body temperature, increased rapid eye movement, and less efficient sleep (Partonen & Lonnqvist, 1998).This information displays how small changes in sleep can greatly affect a person’s mood and may be the cause of SAD.

It is thought that light during different times of the day may be a cause of seasonal affective disorder. Tests that observed light therapy during varying times of the day have been completed. The results of study showed morning light administration to be effective in alleviating symptoms of seasonal affective disorder (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). Times and duration of sunlight are altered depending on the seasons of the year. Different phases of light during the day in different seasons may explain why patients experience depressive symptoms during certain parts of the year.

While this study would explain seasonal affective disorder, other studies have not have the same results. For that reason, we cannot claim that these changes in light times cause seasonal affective disorder. It is argued that people with SAD do not all have the same need for light at the same times of the day; their circadian rhythms may be advanced or delayed. For example, some patients may need more light in the morning, and others need more light in the evening (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This makes it difficult to determine whether these light phases during the day are the cause of seasonal affective disorder.

Decreased serotonin function in the brain may be another explanation for seasonal affective disorder. Patients with SAD or recurrent major depression show depressive symptoms when brain serotonin function is lowered by depletions of tryptophan from the diet, unlike normal individuals. Another study that regulated hormonal responses with a serotonin-releasing agent reported that patients with SAD had diminished prolactin and cortisol changes. There is also evidence that abnormalities in the serotonin transporter are more common in people with SAD than people without the disorder. (Partonen & Lonnqvist, 1998). Patients with SAD display different serotonin patterns than normal individuals. This abnormality may be the cause of seasonal affective disorder (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998).

This is supported by a study that “reported that consumption of carbohydrates increased the plasma content of tryptophan, as well as serotonin synthesis in the rat brain. Based on this observation, they proposed that the excessive carbohydrate intake in SAD patients might reflect a form of self-medication that temporarily relieves the vegetative symptoms via an increased central serotonergic activity” (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This finding is important in discovering the cause of seasonal affective disorder as well as an effective treatment. Carbohydrate consumption increases in patients while they are experiencing the symptoms of SAD. This may be explained by a decrease in serotonin levels; patients eat excessive carbohydrates to compensate for this decrease.

More support for this theory is shown by the use of specific serotonin reuptake inhibitors. These medications are effective in the treatment of seasonal affective disorder while other medications for depression are not. (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). They work by blocking serotonin from being reabsorbed, therefore increasing the amount of serotonin being used. This leads people to believe that serotonin is a factor of the disorder as well.

Another interesting theory is that seasonal affective disorder “… may relate to rod shortening due to deficient photostatic adjustment, leading to decreased absorption of quanta of light, leading to insufficient light energy believed to be necessary for maintaining a normal mood” (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This means that a decreased photoperiod of sunlight in the winter does not give people with the shorter rods enough time essential to cultivate a healthy mood. Still, this theory has not been proven to be the underlying cause of seasonal affective disorder (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998).

Brain activity of SAD patients vary from healthy individuals. Positron emission tomography or PET scans of patients with SAD show a lower metabolism within the brain than healthy individuals. The patients with SAD had more metabolic activity on the left side of their brain in the medial prefrontal cortex. On PET scans of normal individuals, there is decreased blood flow after bright-light treatment. Patients with SAD showed an increase in blood flow following this treatment. (Partonen & Lonnqvist, 1998). This is not only important is determining the cause of the disorder, it is also relevant to treatment efficacy. Patients with SAD respond well to bright-light therapy. Unique brain activity is observed in these patients and should be further explored to determine the underlying cause. Although the true cause is not known, all of these organic changes elude to an imbalance of biological factors.


The most common treatment for seasonal affective disorder is phototherapy. Phototherapy or light therapy “involved exposure to visible light producing at lead 2500 lx at eye level” (Partonen & Lonnqvist, 1998). According to Merriam Webster dictionary, Lux or lx is “a unit of illumination equal to the direct illumination on a surface that is everywhere one meter from a uniform point source of one candle intensity or equal to one lumen per square meter” (Merriam Webster). This light must be obtained by special lighting because lighting with the home is usually around 100 lx. According to Timby & Smith, “The frequency and duration for phototherapy can vary, but a common prescription is for the patient to sit by the light source from 30 minutes to 2 hours per day, preferably in the early morning hours” (2005). Also, direct eye contact with the light is not required. A convenient form of treatment is phototherapy light in the bedroom that are set to an automatic timer. They illuminate at a predawn schedule. The light passes through the eyes and is thought to trigger a decline in melatonin, which may alleviate seasonal affective disorder symptoms (Timby & Smith, 2005).

According to Partonen & Lonnqvist, phototherapy for 2 hours in the morning for seven consecutive days “… led to improvements of 67% of patients with mild depressive episodes and 40% of those with moderate to severe depressive episodes” (1998). The treatment has a relatively quick onset and only takes about 4 days to begin observing symptoms remission. This treatment does not cure the patient of seasonal affective disorder. Symptoms will return if the treatment is ceased. This treatment is also effective for children and adolescents.

In respect to the type of light, full spectrum light is not required for seasonal affective disorder treatment. White and green light are superior for treatment to red light. Also, ultraviolet or UV light is not required for treatment. In fact, ultraviolet light is more effective in treating atypical symptoms such as those seen with SAD (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998).

While this treatment seems optimal, some believe that the positive effects are only seen due to the placebo effect. Others suggest that the placebo effect was not the reason for success. Rosenthal states “that a placebo explanation of the therapeutic effect of light would not be plausible, since a placebo tended to result in a more rapid and variable time course of response and relapse, a gradual decline in treatment efficacy with time, and a variable difference between treatment effect of bright and dim light” (Lee, Chen, Chan, Paterson, Janzen & Blashko, 1998). This therapy may also be effective because the light is a conditioned stimulus that creates a euthymic states as a response. Patients may believe that they are experiencing depressive symptoms as a result of lack of light. Their mood may be elevated due to the conditioned stimulus of the light. This is thought to be wrong because the effects of light therapy last longer than hypnosis.

Although this treatment seems ideal, there are negative side effects. Eye-strain and headache are common complaints of patients prescribed with light therapy. (Partonen & Lonnqvist, 1998).

Medications are also used as treatment for seasonal affective disorder. These treatments are usually used if light therapy does not work. Antidepressants are effective at treating SAD. Selective serotonin reuptake inhibitors are considered effective while other antidepressants are not.

Simple lifestyle changes may be an easy way to mitigate the depressive symptoms associate with season affective disorder. Timby & Smith note these lifestyles changes as:

“Take walks outside, preferably around noon. Try to go outside for an hour a day.
Avoid using sunglasses or contact lenses that are coated to shield UV radiation because this interferes with light transmission to the pineal gland.
Add more lamps and brighter lights at home and work.
Trim shrubs and trees from around windows to let in more light.
Use translucent curtains or shades rather than heavy drapes.
Sleep and work in east-facing rooms” (2005)

These simple lifestyle changes could be an effective treatment for those experiencing milder symptoms and may reduce symptoms of SAD.


Seasonal affective disorder is a psychological disorder in which depression occurs during the same time every year. Usually patients experience symptoms in the winter months, but other time cycles are possible. It only affects a small number of people but its atypical depression symptoms can be life altering. The direct cause of the disorder is unknown but is thought to be due to a variations in the amount of light each day. Light therapy is an efficacious treatment for seasonal affective disorder. Other treatments include antidepressant medication and lifestyle changes. This information is essential in learning how to identify the disorder and ways to treat patients.


Lee, T., Chen, E., Chan, C., Paterson, J., Janzen, H., & Blashko, C. (1998). Seasonal affective disorder. American psychology association,5(3), 275-290.

Merriam-Webster. (2014).Lux. Retrieved from

Partonen, T., & Lonnqvist, J. (1998). Seasonal affective disorder.The lancet,352, 1369-1374.

Timby, B., & Smith, N. (2005). Seasonal affective disorder: Shedding light on the wintertime blues.Nursing,35(1),

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