Evidence-Based Reviews

Seasonal affective disorder: How to help patients beat the winter blues

Current Psychiatry. 2002 December;1(12):13-17

If your patient’s depression recurs in autumn and winter, a trial of bright light therapy may provide good results at minimal risk.

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References

1. Partonen T, Magnusson A. Seasonal affective disorder New York: Oxford University Press, 2001;3-134.

2. Lewy AJ, Kern HA, Rosenthal NE, Wehr TA. Bright artificial light treatment of a manic-depressive patient with a seasonal mood cycle. Am J Psychiatry 1982;139(11):1496-8.

3. Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective disorder: A description of the syndrome and preliminary findings with light therapy. Arch Gen Psychiatry 1984;41(1):72-80.

4. Rosenthal NE, Jacobsen FM, Sack DA, et al. Atenolol in seasonal affective disorder: a test of the melatonin hypothesis. Am J Psychiatry 1988;145:52-6.

5. Anderson JL, Rosen LN, Mendelson WB, et al. Sleep in fall/winter seasonal affective disorder: effects of light and changing seasons. J Psychosom Res 1994;38:323-37.

6. Reichborn-Kjennerud T, Lingjaerde O, Dahl AA. Personality disorders in patients with winter depression. Acta Psychiatrica Scand 1994;90:413-19.

7. Mersch PPA, Middendorp HM, Bouhuys AL, Beersma DGM, van den Hoofdakker RH. Seasonal affective disorder and latitude: a review of the literature. J Affect Disord 1999;53:35-48.

8. Wehr TA, Duncan WC, Sher L, et al. A circadian signal of change in patients with seasonal affective disorder. Arch Gen Psychiatry 2001;58:1108-14.

9. Lewy AJ, Sack RL, Singer CM, White DM, Hoban TM. Winter depression and the phase-shift hypothesis for bright light’s therapeutic effects: history, theory, and experimental evidence. J Biolog Rhythms 1988;3:121-34.

10. Avery DH, Kizer D, Bolte MA, Hellekson C. Bright light therapy of subsyndromal seasonal affective disorder in the workplace: morning vs. afternoon exposure. Acta Psychiatrica Scand 2000;103:267-74.

11. Sancar A. Cryptochrome: the second photoactive pigment in the eye and its role in circadian photoreception. Ann Rev Biochemistry 2000;69:31-67.

12. Meesters Y, Jansen JHC, Beersma DGM, Bouhuys AL, van den Hoofdakker RH. Light therapy for seasonal affective disorder: the effects of timing. Br J Psychiatry 1995;166:607-12.

13. Terman M. Internal night. Arch Gen Psychiatry 2001;58:1115-6.

14. Joffe RT, Moul DE, Lam RW, et al. Light visor treatment for seasonal affective disorder: a multicenter study. Psychiatry Res 1993;46(1):29-39.

15. Blashko CA, Moscovitch A, Eagles JM, Darcourt G, Thompson C, Kasper S. A placebo-controlled study of sertraline in the treatment of outpatients with seasonal affective disorder (unpublished data on file with Pfizer Inc.)

16. Thorell LH, Kjellman B, Arned M, Lindwall-Sundel K, Walinder J, Wetterberg L. Light treatment of seasonal affective disorder in combination with citalopram or placebo with 1-year follow-up. Int Clin Psychopharmacol 1999;14(suppl 2):S7-S11.

17. Hilger E. Reboxetine in seasonal affective disorder: an open trial. Eur Neuropsychopharmacology 2001;11(1):1-5.

All of us see patients whose recurrent depressions seem to have a seasonal component. Should we treat them differently than patients whose recurrent depressions are not related to seasons? Is there adequate evidence for the existence of seasonal affective disorder (SAD), or—as it is called in DSM-IV-TR—mood disorder with a seasonal pattern? Is bright light therapy supported by the literature, or is it just some sort of fad?

As December brings the shortest days of the year, we shine the spotlight on SAD and examine the latest evidence on its causes, diagnosis, and treatment.

Moods with a seasonal rhythm

Moods have been observed to change with the seasons since ancient times (Box 1).¹ As recently as 25 years ago, however, seasonal affective disorder was not recognized as a psychiatric diagnosis.

In the early 1980s, when researchers at the National Institute of Mental Health (NIMH) were studying the effect of bright light on melatonin secretion, they were contacted by Herbert E. Kern, a research engineer who suffered from recurrent depression. A methodical person, Kern had kept a journal of his mood variations and noticed a pattern that appeared to follow the seasons. His depression worsened in the fall and winter and improved in the spring and summer. Kern subsequently participated in an NIMH trial with phototherapy, his mood improved, and the results were published in 1982.²

Box 1

‘LAPP SICKNESS’ AND THE EFFECT OF LIGHT ON MOOD

Hippocrates, with his knack for keen observation, observed the variation of moods with the seasons. Aretaeus went a step further in the 2nd century by proposing that “lethargics are to be laid in the light and exposed to the rays of the sun.”

More recently, the physicist Angstrom—for whom the unit of light wavelength is named—was one of the first to mention the Swedish word “Lappsjuka,” which means “Lapp sickness” (Lapp refers to Scandinavian aborigines). He wrote, “Many people are sensitive to the lack of light, while others are less so. The former will in arctic winters suffer from Lappsjuka.”¹

Two years later, the researchers published the first paper that described SAD as a psychiatric diagnosis.³ Criteria for the diagnosis included:

presence of a major affective disorder
affective episodes occurring during fall or winter and remitting in spring or summer for at least 2 consecutive years.

The paper also discussed treatment of winter depression with phototherapy.

DSM-IV-TR describes SAD as a course specifier for mood disorders, including major depressive episodes in bipolar I and II disorders and major depressive disorder (Box 2). In other words, as used in DSM-IV-TR and this article, SAD is not an independent disorder but a type of major affective disorder.

Characteristics of SAD

Symptoms. Patients with SAD suffer the typical symptoms of depression—decreased energy, guilt, and decreased libido—as well as atypical symptoms—carbohydrate craving, hypersomnia, and weight gain. They also appear less likely to exhibit psychotic symptoms and may be at lower risk for suicide than persons with major mood disorders but without SAD.¹

Changes in sleep patterns also have been observed. Rosenthal et al⁴ found increased sleep latency and increased total sleep time in patients with SAD. Delta or slow-wave sleep—the restorative part of the sleep cycle—decreased by nearly one-half (mean 46%). REM latency did not change, contrary to typical findings in depressed patients. Anderson et al⁵ also reported no change in REM latency in patients with SAD.

Comorbid conditions. Eating disorders—particularly bulimia nervosa—are more prevalent in patients with SAD.¹ Binge eating tends to worsen in the fall and winter.

Personality disorders are also common in these patients, with cluster C over-represented. Avoidant personality disorder is most common. In a sample of 45 patients with SAD, Reichborn-Kjennerud et al⁶ found any personality disorder in 58% and avoidant personality disorder in 31%. Patients with comorbid personality disorders were less likely to respond to bright light therapy.

Prevalence. The prevalence of SAD in North America is approximately 1 to 6 %, with four times as many women affected as men.¹ Data on the effect of latitude on prevalence of SAD are inconclusive.⁷

Making the diagnosis

For patients with depression, clinicians should ask about seasonality of symptoms. Onset of major depressive symptoms in the fall or winter for at least two consecutive years or remission of depressive symptoms in the spring for two consecutive years (without onset of depressive syndromes during the spring or summer) probably merits a diagnosis of SAD. The diagnosis is confirmed if seasonal patterns of depressive symptoms substantially outnumber nonseasonal occurrences over the patient’s lifetime. The diagnosis may not be appropriate if there are obvious seasonal psychosocial stressors, such as anniversary reactions in posttraumatic stress disorder.