Subscribe to Clinical Compass™ Volume 3, Issue 22 - October 21, 2008

Beating the Winter Blues: Brief Update on Seasonal Affective Disorder

by Lisa Brauer, PhD

Seasonal affective disorder (SAD), also called the "winter blues," is a subtype of major depression with a seasonal component. Symptoms begin in the fall or winter, and lessen or remit during spring and summer. SAD affects 1% to 3% of adults, mostly women. Ratios between 1.8:1(1) and 4:1(2) have been reported for female predominance. The prevalence of SAD is highest during the reproductive years. For some, SAD lasts a lifetime; for others, it remits or may turn into some other type of depression. SAD can be very disabling in terms of both social and occupational function,(3) and can markedly impair quality of life.

SAD shares some symptoms with major depressive disorder (MDD), including depressed mood, anergia, difficulty concentrating, and fatigue, but also has some atypical features. For example, SAD is associated with increases in appetite, weight gain, and hypersomnia, carbohydrate craving, and intense daytime sleepiness in spite of increased sleep.(1) The atypical symptoms of SAD often make it difficult to distinguish from hypothyroidism, chronic fatigue syndrome, or other forms of atypical depression. A key diagnostic factor for SAD is the seasonal variation and cyclic nature of symptoms.

The pathophysiology of SAD is not well understood, but there appears to be a genetic component to vulnerability, with heritability between 29% and 60% across studies.(1) There is evidence that individuals with SAD show dysregulation in the serotonin, melatonin, and circadian systems. It has been shown that patients with SAD show retinal subsensitivity to light.(1) Consequently, they "respond to artificial light as if it were the equivalent to darkness and that's why they need more light," according to Dr. Norman E. Rosenthal, a private practice psychiatrist in Maryland who has been credited with first describing SAD.(2)

The standard first-line treatment for SAD is light therapy (phototherapy), usually with light boxes in which the light is 20 times brighter than normal indoor light. In a typical regimen, patients look into a light box when they first wake up in the morning. A large number of studies as well as several meta-analyses have shown that light therapy has a clinical response rate of about 65%.(1) Therapy should be given throughout winter and can be varied in intensity, wavelength, duration and timing of exposure.(1) According to Dr. Rosenthal, the light sends messages to the brain to simulate chemical changes.

Although light therapy is the gold standard, it is not always feasible or preferable for patients with SAD. A number of other strategies, including pharmacologic agents, also have been studied, including those used to treat typical depression. Bupropion XL is the only agent with FDA approval for the treatment of SAD, and it has been shown that early treatment may prevent recurrence. One report of data from three randomized controlled trials of 1042 patients showed that treatment with 150 mg or 300 mg of bupropion in the fall had a 44% risk reduction for winter depression.(4) A number of other pharmacologic agents have since been evaluated, some in open-label trials, including the SNRI duloxetine,(5) the SSRIs fluoxetine, sertraline, and escitalopram,(6) the norepinephrine reuptake inhibitor reboxetine,(7) and the melatonin receptor agonist agomelatine.(8) Each has shown to have promise in the treatment of SAD, and to date, antidepressants have had similar efficacy to light therapy. In a multi-center randomized controlled trial in Canada, 96 patients who met DSM-IV diagnostic criteria for seasonal depression were randomly assigned to 8 weeks of treatment with either 10,000-lux light treatment, or the same light treatment in combination with fluoxetine. Although response to light treatment occurred somewhat earlier, phototherapy and fluoxetine had similar response and remission rates, as well as overall number of adverse events.

Given the fact that SAD can be quite disabling, has a predictable course, and that there are effective therapies available for both preventing and managing symptoms, recognition and early identification are important. Physicians need to take a careful history in patients with relevant symptoms, and particularly to ask about seasonality. Experts agree that patients are unlikely to spontaneously report—or even to notice—the seasonality of their symptoms.(1) Once a diagnosis of SAD has been confirmed, physicians should discuss treatment options with their patients in order to match appropriate and acceptable treatments (i.e., light therapy or medication) to particular patients. According to Westrin and Lam, "SAD is a common condition with significant psychosocial impairment. Clinicians should be vigilant in recognizing seasonal patterns of depressive episodes because there are effective, evidence-based treatments for SAD."(9)

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References

  1. Magnusson A, Boivin D. Seasonal affective disorder: an overview. Chronobiol Int 2003;20:189-207.
  2. Woznicki K. Seasonal affective disorder, a common but shadowy condition. Medpage Today 2005;http://www.medpagetoday.com/Psychiatry/Depression/2397.
  3. Lam RW, Levitt AJ, Levitan RD, et al. The Can-SAD study: a randomized controlled trial of the effectiveness of light therapy and fluoxetine in patients with winter seasonal affective disorder. Am J Psychiatry 2006;163:805-812.
  4. Modell JG, Rosenthal NE, Harriett AE, et al. Seasonal affective disorder and its prevention by anticipatory treatment with bupropion XL. Biol Psychiatry 2005;58:658-667.
  5. Pjrek E, Willeit M, Praschak-Rieder A, et al. Treatment of seasonal affective disorder with duloxetine: an open-label study. Pharmacopsychiatry 2008;41:100-105
  6. Pjrek E, Winkler D, Stastny J, Praschak-Rieder N, Willeit M, Kasper S. Escitalopram in seasonal affective disorder: results of an open trial. Pharmacopsychiatry 2007;40:20-24.
  7. Hilger E, Willeit M, Praschak-Rieder N, Stastny J, Neumeister A, Kasper S. Reboxetine in seasonal affective disorder: an open trial. Eur Neuropsychopharmacol 2001;11:1-5.
  8. Pjrek E, Winkler D, Konstantinidis A, Willeit M, Praschak-Rieder N, Kasper S. Agomelatine in the treatment of seasonal affective disorder. Psychopharmacology 2007;190:575-579.
  9. Westrin A, Lam RW. Seasonal affective disorder: a clinical update. Ann Clin Psychiatry 2007;19:239-246.

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