Seasonal affective disorder (SAD) is recognized as a type of depression that occurs in the affected population on a recurring annual basis. It was first described by Rosenthal and colleagues in 1984 and identified as a syndrome associated with depressive symptoms that reoccur during fall and winter, with full remission in spring and summer.1

The features of SAD can be characterized by symptoms of hypersomnia, increased appetite, weight gain, and carbohydrate craving.1,2 The syndrome is more likely to be identified in females versus males (4:1), but it tends to decline among older adults, with prevalence being equal among older men and women.1,3,4 In any given year, it is estimated that about 5% of the United States population will experience SAD, with symptoms being present for about 40% of the time that year.5,6 

While the etiology and pathophysiology of SAD are not clearly understood, it has been proposed that there may be several underlying factors that lead to its presentation. One leading theory is that a circadian phase delay or advance may trigger SAD depression. This is known as the phase shift hypothesis and is the presumed cause based on much of the current literature,.5,6 Often attributed to Lewy, the phase shift hypothesis is the most prominent model for SAD, but it is not the only one.7

Other proposed theories include retinal sensitivity to light, neurotransmitter dysfunction, generic variations that can have an influence on circadian rhythms, and serotonin levels.6,7 Ultimately, SAD is viewed as a complex disorder that can result for a variety of factors involving biologic and psychological mechanisms such as an individual’s vulnerability to stress.7 Other predisposing risk factors for SAD may include having a first-degree relative with symptoms of depression or living in northern altitudes.8 The manifestations of SAD can cause significant burden, and a lack of adequate or effective therapeutic intervention can contribute to increased utilization of health care services by sufferers in comparison to their age-matched controls without SAD.9,10

There are currently 2 evidence-based treatments that have been identified for SAD: antidepressants and light therapy. Other off-label interventions can also be utilized to treat SAD. The efficacy of the use of antidepressants and light therapy have been demonstrated in randomized controlled trials.11-13 Light therapy is considered to the first-line treatment for SAD, while antidepressant medication is considered to be a secondary treatment.14

Multiple systematic reviews and meta-analyses that have examined the influence of light therapy have shown an impact on phase advance and efficacy for the short-term treatment of SAD.15,16 Its comparison to credible controls showed that light therapy was associated with a significant reduction of depressive symptoms during the initial autumn months.16 While studies have shown light therapy, pharmacotherapy, and even cognitive behavioral therapy to be appropriate therapeutic options for SAD, no studies have identified 1 treatment or a combination of treatments to be effective in all patients.17

The mechanism for light therapy is to diminish the levels of melatonin in the bloodstream when natural light isn’t sufficient to do so. In healthy individuals, the sleep hormone melatonin is released in the evening hours, with decrease in natural lighting to induce somnolence. The light of the sun will stop the release of melatonin in the morning hours in order to induce wakefulness, especially in sunny climates and seasons of the year. In addition, the grogginess associated with residual melatonin in circulation is thought to cause SAD.

For certain individuals, and at extreme latitudes, melatonin release may not be turned off upon waking because of insufficient lighting in the morning hours. It is now known that photosensitive ganglion cells in the retina respond primarily to light and communicate directly with the pineal gland which, in turn, controls melatonin release in the bloodstream. Thus, artificial lighting that includes these wavelengths can wake the individual up, reducing SAD symptoms. However, artificial lighting can also lead to insomnia at night.

Light therapy is considered to be an established first-line SAD treatment, with clinical practice guidelines recommending the use of light therapy at first symptom presentation each fall or winter through springtime remission.18 A pooled analysis of light therapy studies showed that 53% of individuals with SAD overall, and 43% of moderate to severe SAD cases, met the remission criteria by the end of the light therapy trials.19

The standard light therapy involves positioning patients about 12 to 18 inches from a white, fluorescent light source at a standard dosage of 10,000 lux for 30 minutes per day in the early morning, This protocol has demonstrated statistically significant clinical improvement after 1 to 2 weeks of therapy, but with discontinuation of therapy, most patients can experience a relapse.20 Treatment is to be continued until spontaneous remission is observed in the spring or summer.20 Light therapy appears to be well-tolerated by most individuals, Some uncommon adverse effects may include blurred vision, nausea, agitation, eye strain, or headache, but these effects are generally mild and transient.20,21

Recently, there has been evidence that a much less bright blue light may be all that is necessary to combat SAD. The theory is as follows: it is known that patients with SAD have increased levels of melatonin in the bloodstream during the fall and winter months. Melatonin induces somnolence and is released into the bloodstream when there is not enough high-energy blue light, such as in the nighttime. The high color temperature bluish white light of the morning sun deactivates melatonin release, but may not be sufficient at northern latitudes in the winter.

The results of most randomized controlled clinical trials on pharmacotherapies for SAD have shown that the use of second-generation antidepressants such as selective serotonin reuptake inhibitors and serterotin-norepineprine reuptake inhibitors resulted in the reduction of depression scores when compared to placebo.17,20,22 In randomized controlled trials on short-term treatment of SAD with antidepressants such as fluoxetine 20 mg per day and sertraline 50-200 mg per day, there was evidence of efficacy in treating the disorder. Other comparative studies have also shown antidepressants such as bupropion, reboxetine, and moclobemide to be effective.17,21,22

The initiation of antidepressants can be associated with adverse effects such as nausea, vomiting, headache, anxiety, nervous, weakness, or heart palpitation. Similar to light therapy, these effects can be self-limiting. In individual patients, there may be occasions where these effects do not disappear or become serious, such as increased risk of suicidal ideation and serotonin syndrome, both of which require immediate intervention.23,24  

Melatonin, the major hormone of the pineal gland, has also been said to play a role in mood disorders and disturbances, in addition to its proven role in circadian rhythms and sleep. Taken at bedtime, it can also play a role in SAD. Melatonin possesses the properties of a circadian rhythm-regulating factor, as a well as a hormone that has been attributed to the regulation of sleep, and it may be important in the control of mood and behavior.

Because SAD is recognized as a condition that has the potential to induce substantial psychosocial impairments, it is important for clinicians to be able to evaluate the signs and symptoms and apply evidence-based treatments. Currently, SAD can be difficult to treat, though there is evidence to support the use of antidepressants and light therapy, which have demonstrated positive outcomes in many patients.

Given SAD's predicable patterns, one of the best strategies to curtail its development is through prevention, which can be achieved by implementing therapy before the onset of symptoms. The use of light therapy or antidepressant therapy can help to reduce recurrence and the severity of depressive symptoms. 27,28
 
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