Update on Seasonal Affective Disorders: Clinical Issues and Treatment Strategies

February 20, 2014

In this CME article, the focus is on persons with a formally recognized recurrent wintertime mood disorder that rises to such a level that it merits a diagnostic title and clinical intervention.

Premiere Date: February 20, 2014
Expiration Date: February 20, 2015 [Expired]

This activity offers CE credits for:
1. Physicians (CME)
2. Other

All other clinicians will either receive a CME Attendance Certificate or may choose any of the types of CE credit being offered.

ACTIVITY GOAL

This article provides information on seasonal affective disorder (SAD) and its treatment, with an emphasis on light therapy.

LEARNING OBJECTIVES

At the end of this CE activity, participants should be able to:

1. Identify the seminal research on SAD.

2. Define SAD.

3. Differentiate between the 2 primary treatment modalities.

4. Describe the various forms of light therapy.

TARGET AUDIENCE

This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.

CREDIT INFORMATION

CME Credit (Physicians): This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians.

CME Outfitters designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

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Dan A. Oren, MD, is a Board Member of the non-profit Center for Environmental Therapeutics (CET). He receives no financial or material compensation for his work related to CET.

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The human condition is such that all of us may be vulnerable to seasonal affective disorder (SAD). If placed in an environment sufficiently deprived of light, we would all develop a reversible syndrome of major depression.

SAD emerged into the modern lexicon in 1984 in a landmark paper by Rosenthal and colleagues.1 The work on SAD, however, began a few years earlier in Thomas Wehr’s research program at the National Institute of Mental Health (NIMH). At the time, National Institutes of Health scientists were encouraged to do work that could not or would not be done anywhere else. The group published 2 seminal papers in Science. In one paper, Wehr and colleagues2 demonstrated that a “phase advance” of the circadian sleep-wake cycle could serve as an antidepressant. That is, a manipulation of the internal biological clock to cause people to wake earlier in the day was shown potentially to have antidepressant psychiatric effects.

In the other paper, Lewy and colleagues3 shined a bright light on study participants, which led to rapid and reversible suppression of nocturnal pineal gland production of melatonin. Melatonin was already known to be a critical light-regulated seasonal and circadian hormone in animals, and this research raised the question of its having a similar role in humans.

Although articles on current research that links biological clock disruption to psychiatric illnesses are published with precise molecular genetic detail and appear at a frequency that resembles clockwork, 3 decades ago such work was highly controversial. At the time, Kripke4 was conducting pioneering research that suggested bright white light could rapidly reduce depressive symptoms even in usually sun-filled climates.

Closely following the scientific literature was a brilliant Bell Labs researcher named Herbert E. Kern who had recognized a pattern in his own seasonal depressive episodes that recurred as the days shortened each summer. A founding member of the American Society for Photobiology in 1972, Kern contacted Lewy in 1980 for evaluation.

Lewy, Kern, Rosenthal, and Wehr5 demonstrated that bright artificial light in midwinter could successfully treat Kern’s depression. They published the first modern case report on the efficacy of bright white light for the treatment of a seasonal winter depression. Kern’s seasonal depression and response to bright light led the NIMH group to look for a pattern in others. They found that winter seasonal depression was not uncommon, and they conducted the first of many placebo-controlled trials that described the syndrome and showed the efficacy of light treatment.1

Related content: Mini Quiz: Light Therapy for Winter Blues

 SAD may have existed for as long as humans have walked the temperate climates of this earth: records of melancholy associated with autumn and mania with summer go back millennia, as recorded in the fourth century by the clinician Posidonius.

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In 1921, Emil Kraepelin

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observed patients with recurrent winter depression (and spring hypomanias): “Repeatedly I saw in these cases moodiness set in in autumn and pass over in spring, ‘when the sap shoots in the trees,’ to excitement.” (For a more thorough historial review, I recommend Wehr’s chapter on the historical background of SAD.

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)

Milder recurrent winter depressions that did not meet MDD criteria were also found to be responsive to bright light therapy.9 A century earlier, polar explorers noted that darkness appeared to trigger depression in winter and the return of sunlight sparked improvements in mood and energy.10 Such observations raised the question of whether vulnerability to winter darkness represents human physiology that becomes pathophysiological in the case of winter SAD but, at its core, is part of our evolutionary responses to sunlight and to seasonal change.11

In this article I focus on persons with a formally recognized recurrent wintertime mood disorder that rises to such a level that it merits a diagnostic title and clinical intervention. This is the population with recurrent wintertime SAD, or, as coded in DSM-5, patients with a recurrent pattern of MDD during the winter months, associated with remission (or entrance to mania or hypomania) in the spring or summer. The syndrome requires a clear and regular temporal relationship between the onset of the depressive episodes and the time of the year and full remission (or changes to the manic side) at a characteristic time each year (additional details are published in DSM-5).

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Written in memory of Herbert E. Kern, formerly of Florham Park, New Jersey, born May 14, 1917, who died at age 96 on September 9, 2013.

Understanding SAD

The behavioral pattern associated with SAD has strong biological underpinnings seen across many forms of animal life, and precise physical mechanisms, even if not yet fully understood, are rapidly being found to explain the molecular connections between light and melatonin.12 The most frequent symptoms associated with SAD (seen in over 80% of patients) are recurrent wintertime sadness, decrease in activity, social difficulties (eg, withdrawal), anxiety, irritability, occupational difficulties, and daytime tiredness. Most patients with winter SAD also report a seasonally recurrent increase in sleep, weight, and appetite; carbohydrate craving; and decrease in libido.

Although each person’s symptom profile is unique, in the Northern hemisphere, depressive episodes typically begin in September to November, depending on the latitude, and usually do not resolve until the following spring. For many patients, symptoms are at their worst in January and February, despite the fact that the days are getting longer during these months. The relatively darker days brought on by the weather in January and February have been proposed as one explanation for this pattern. Some patients also report that brief stretches of dark weather in summer or light-deprived working conditions are associated with the return of depression.

Although most patients with winter SAD may lose their unique winter seasonal pattern of recurrence over time, the syndrome is fairly common.13 The prevalence of the syndrome in North America ranges up to approximately 2.5% in Canada and is associated with distance from the equator.14 The increase in prevalence is presumably related to the shorter hours and lower intensity of daylight in the northern latitudes during the winter. Winter SAD has been described worldwide, but the influence of latitude on prevalence appears to be more limited outside of North America, perhaps because most of the European areas that have been studied lie north of the United States.15

Although SAD does occur in men, as with other forms of MDD, it is seen more often in women.16 The average age of onset of winter SAD is in the early 20s, but many patients with SAD recall wintertime depressive symptoms going back to their early teens. The diagnosis is often missed because health care professionals usually do not consider the diagnosis.17

Treatment

Anecdotally, patients with winter SAD (and many others) report their mood improves dramatically if they travel to a sunny place in winter. If one thinks of sunlight as a health supplement, no less important to life than water or food, one would want to be in an environment with sufficient sunlight. Despite the clear efficacy of many of the treatments for winter SAD, their effectiveness rarely fully matches the effects of summer or of a sunny climate in winter.

More realistic than moving to a sunny climate, the leading treatments are medication or various forms of light therapy. Which of these treatments might be used is more a question of personal convenience and patient preference than of one being more effective than another. A Canadian study determined that the difference in total health care costs (at least in the Canadian medical system) between the 2 modalities was relatively modest.18 It may therefore be reasonable to let patients’ personal preference (which might well affect compliance) influence the choice of initial treatment modality. In many cases, patients report an optimal response from a combination of light therapy and antidepressant medication.

Medications. The first and only medication approved by the US FDA for the prevention of winter SAD is bupropion XL. Patients who received 150 to 300 mg of bupropion daily before the onset of the winter seasonal episode were, on average, 44% less likely to have a winter depressive episode than those who received placebo throughout the winter.17 Fluoxetine and sertraline have also been found to be effective.19 The adverse effects associated with various antidepressant drugs are well recognized.

Light therapy. For patients who prefer physiological treatment, various forms of light therapy-intended to deliver light to the eyes-may be considered. Some experts suggest beginning the daily treatment about 2 weeks before the patient’s winter symptoms typically begin and then continuing the treatment throughout the season. As the days lengthen and brighten in the spring and patients begin to receive enough natural light, they can decrease or eliminate the daily dose of light treatment.

The best-established light treatment is delivered with “light boxes.” These portable light fixtures deliver bright polychromatic white light in an attempt to make up for the relative darkness of winter. Patients typically sit in front of the light box for a fixed time each morning and “bathe” their eyes in indirect light shining from the lamps. While sitting in front of the light box, patients can easily use the time efficiently with such activities as eating breakfast, reading a newspaper, watching television, or responding to email. Some enterprising patients set up their light boxes on a stand, so they can use an elliptical trainer or the like to enhance their physical and mental health at the same time. A response often occurs within days and may strengthen over the course of a few weeks; more immediate responses have also been reported.20

Small handheld light devices are also being marketed for the treatment of wintertime dysphoria or anergy, but the safety and efficacy data to support their use are limited. The evidence is limited, but self-contained light visors or light caps are also available and might be beneficial when a patient is traveling.21

The “dawn simulator” serves to replicate the natural spring profile of a slowly brightening dawn and gradually brightens the room of a sleeping patient before he or she awakes.22 Its chief advantage over the light box is that it provides treatment during the last hours of the patient’s sleep and does not take time away from normal wintertime waking hours. Its chief disadvantage is that the light from the device might wake a sleeping partner.

There have been extensive studies and debates over the optimal timing, duration, and intensity of bright light therapy. Although there are individual exceptions, early morning light therapy for under an hour at 10,000 lux intensity provides good results. The intensity can be reduced to 2500 lux (by increasing the distance to the light) if glare makes the brighter light uncomfortable. Thirty-minute sessions are a typical starting duration, which can be adjusted upward or downward depending on clinical response. There might be an optimal specific time at which to administer light treatment because of a correlation between the timing of the internal body clock and the optimal timing of light administration. A quickly administered test to estimate an optimal time for daily light treatment is the Morningness-Eveningness Questionnaire (MEQ), which is free and can be accessed online.23

CASE VIGNETTE

Jane, a 32-year-old woman, is referred to a psychiatrist for the treatment of depression. Because of her husband’s job transfer, she moved to Maine several years ago. She visits her native sunny southern California every January.

She is euthymic in summer, but beginning around the time when daylight saving time ends she senses a lessening of her energy and an inability to complete daily tasks. After several weeks, she notes inexplicable and dominant periods of sadness or irritability. By early December, she begins to feel increasingly sleepy and starts to crave carbohydrates, which leads to weight gain. She enjoys her time in California but within 1 week of returning home, her depressed mood returns. February, despite being a short month, always feels to her as if it is the longest month of the year. The depression typically lasts until mid-April, when she begins to feel as if she is coming out of a fog. She denies suicidal ideation, and she has never been hospitalized for a psychiatric illness.

Last January, she began treatment with 10,000 lux light therapy at 6:30 AM each morning. Two weeks later her mood and energy improved and she became highly productive at work. She continues to use the light therapy throughout the winter. At the beginning of April she tells her psychiatrist that she spontaneously stopped using the light box 2 weeks earlier because she felt that she was receiving enough natural light and did not need to supplement it with a light box.

A number of studies have examined whether particular wavelengths (colors) of light might be optimally effective for winter SAD. Although individual treatment studies have shown efficacy with bright green light, most of the trials in the literature have used “broad spectrum” white light (composed of multiple wavelengths to give a white appearance). There is no evidence that blue light is more effective than white light for such treatment. Moreover, blue light may pose a risk of macular degeneration or other adverse ocular effects.24 Some patients who have used a specific color of light have reported that after the light treatment they have a short but temporary uncomfortable aftereffect of seeing abnormally colored objects (likely a result of temporary bleaching of certain cone photoreceptors).

Ultraviolet light is unnecessary for effective light treatment and does not appear to provide additional benefits.25 It might also increase the risk of cataracts or other adverse ocular effects.24,26 Patients with macular degeneration should use bright light treatment only with the review or guidance of an ophthalmologist.

Light therapy for SAD is usually innocuous. Adverse events associated with bright light therapy in more than 10% of patients include eye irritation, headache, and nausea. These can usually be resolved by increasing the distance of the eyes from the light or by reducing the daily duration of light therapy.20 As with antidepressant medications, light therapy usually reduces suicidal ideation, although cases of mania or suicidality associated with light therapy have been reported.27

Device choices. One question that frequently arises is the choice of a specific brand of light fixture. Because all of the light device manufacturers currently market products that are intentionally described not as medical treatment devices but rather as light fixtures (which anyone may buy), these devices do not fall under FDA regulation. Advising patients on the use of a particular model is complex because of a limited database. Although price is a consideration for most people, it is a mistake to assume that a less costly device is just as effective and as safe as a more expensive device; the reverse is also true. In the absence of regulation, we live in a “caveat emptor” universe of light boxes. In my own practice, I usually refer patients to the non-profit Center for Environmental Therapeutics Web site, or to one of the established manufacturers whose data have been published in some of the well-respected studies described in this review.

Summer mood disorders

Anecdotal reports suggest that light therapy may also be useful in patients with seasonally worsening mood disorders who have a double depression manifested by year-round dysthymia or depressed mood that worsens in winter. Just as recurrent winter depression can be associated with the absence of light, the abundance of spring-summer light can be associated with hypomania or mania. Patients with winter depression might respond to light therapy in winter and have a springtime episode of mania aborted by wearing dark wraparound sunglasses to minimize bright light exposure. Dark therapy may prove to be a useful adjunctive treatment for a manic episode.28

The phenomenon of recurrent summer depression appears to be much rarer than winter SAD and is much more poorly understood; descriptions of the syndrome and its treatment are limited. Excessive summer exposure to heat, rather than overabundant light, may be central to the disorder. Treatment with repeated cold showers may be effective.29 In the absence of controlled trials of temperature manipulations for summer SAD (and the inconvenience of taking multiple cold showers daily), standard antidepressant treatment approaches are appropriate.

Conclusion

What is the mechanism by which light therapy has its antidepressant effect in winter SAD? This is a question of immense interest and discussion and, I would argue, critical physiological importance. I would direct the interested reader to a review paper in the December 2013 issue of The American Journal of Psychiatry, which considers this topic from an evolutionary and molecular viewpoint and leads in a surprising direction.11 In that article, my coauthors and I review a model of humoral phototransduction. Our findings suggest that using plant responses to light as a model for human chronobiological behavior identifies hemoglobin and bilirubin as mediators of some of light’s antidepressant and chronobiological effects. From this standpoint, the past century’s worth of advances by botanists in understanding plant behavior may prove useful models for understanding critical aspects of the molecular regulation of animal and human behavior.

Regardless of mechanism, the research that grew out of Wehr’s group showing that bright light can suppress melatonin in humans and that it successfully treats winter SAD sprang from a biological hypothesis rather than being a serendipitous occurrence.30 Subsequent clinically practical chronobiological treatments for nonseasonal depression include sleep deprivation (wake therapy) and triple chronotherapy that combines wake therapy, bright light therapy, and sleep phase advances.31

Yet, without Herbert Kern, an entire line of research and treatment might have lain fallow for years. Instead, the connection between light and the biological clock and human physiology and depression is at the cutting edge of scientific advances. And Mr Kern had the privilege of living to see this corner of medicine blossom.

[This CME is expired]

Disclosures:

Dr Oren is Associate Professor (Adjunct) of Psychiatry at Yale University, New Haven, Conn, and Medical Director of BHcare, Inc, North Haven, Conn.

References:

1. 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;41:72-80.

2. Wehr TA, Wirz-Justice A, Goodwin FK, et al. Phase advance of the circadian sleep-wake cycle as an antidepressant. Science. 1979;206:710-713.

3. Lewy AJ, Wehr TA, Goodwin FK, et al. Light suppresses melatonin secretion in humans. Science. 1980;210:1267-1269.

4. Kripke DF. Photoperiodic mechanisms for depression and its treatment. In: Perris C, Struwe G, Jansson B, eds. Biol Psychiatry. Amsterdam: Elsevier-North Holland Biomedical Press; 1981:1249-1252.

5. Lewy AH, Kern HA, Rosenthal NE, Wehr TA. Bright artificial light treatment of a manic-depressive patient with a seasonal mood cycle. Am J Psychiatry. 1982;139:1496-1498.

6. Roccatagliata G. A History of Ancient Psychiatry. Westport, Conn: Greenwood Press; 1986.

7. Kraepelin E. Manic-Depressive Insanity and Paranoia. Edinburgh: E & S Livingstone; 1921:139.

8. Wehr TA. Seasonal affective disorders: a historical overview. In: Rosenthal NE, Blehar MC, eds. Seasonal Affective Disorders and Phototherapy. New York: Guilford Press; 1989:11-32.

9. Kasper S, Rogers SLB, Yancey A, et al. Phototherapy in individuals with and without subsyndromal seasonal affective disorder. Arch Gen Psychiatry. 1989;46:837-844.

10. Kane EK. Arctic Explorations in the Years 1853-1855. Philadelphia: Childs and Peterson; 1856.

11. Oren DA, Koziorowski M, Desan PH. SAD and the not-so-single photoreceptors. Am J Psychiatry. 2013;170:1403-1412.

12. Yamaguchi Y, Suzuki T, Mizoro Y, et al. Mice genetically deficient in vasopressin V1a and V1b receptors are resistant to jet lag. Science. 2013;342:85-90.

13. Sakamoto K, Nakadaira S, Kamo K, et al. A longitudinal follow-up study of seasonal affective disorder. Am J Psychiatry. 1995;152:862-868.

14. Rosen LN, Targum SD, Terman M, et al. Prevalence of seasonal affective disorder at four latitudes. Psychiatry Res. 1990;31:131-144.

15. Mersch PPA, Middendorp HM, Bouhuys AL, et al. Seasonal affective disorder and latitude: a review of the literature. J Affect Disord. 1999;53:35-48.

16. Magnusson A, Partonen T. Prevalence. In: Partonen T, Pandi-Perumal SR, eds. Seasonal Affective Disorder: Practice and Research. 2nd ed. Oxford, England: Oxford University Press; 2010:221-234.

17. 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.

18. Cheung A, Dewa C, Michalak EE, et al. Direct health care costs of treating seasonal affective disorder: a comparison of light therapy and fluoxetine. Depress Res Treat. http://www.hindawi.com/journals/drt/2012/628434/. Accessed January 9, 2014.

19. 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.

20. Partonen T, Halonen L, Eloholma M. Light exposure. In: Partonen T, Pandi-Perumal SR, eds. Seasonal Affective Disorder: Practice and Research. 2nd ed. Oxford, England: Oxford University Press; 2010:267-279.

21. Desan PH, Weinstein AJ, Michalak EE, et al. A controlled trial of the Litebook light-emitting diode (LED) light therapy device for treatment of Seasonal Affective Disorder (SAD). BMC Psychiatry. 2007;7:38.

22. Terman M, Terman JS. Controlled trial of naturalistic dawn simulation and negative air ionization for seasonal affective disorder. Am J Psychiatry. 2006;163:2126-2133.

23. Morningness-Eveningness Questionnaire (MEQ). http://www.ubcmood.ca/sad/MEQ.pdf. Accessed January 7, 2014.

24. Reme CE, Rol P, Grothmann K, Kaase H, Terman M. Bright light therapy in focus: lamp emission spectra and ocular safety. Technol Health Care. 1996;4:403-413.

25. Oren DA, Brainard GC, Johnston SH, et al. Treatment of seasonal affective disorder with green light and red light. Am J Psychiatry. 1991;148:509-511.

26. Oren DA, Rosenthal FS, Rosenthal NE, et al. Exposure to ultraviolet B radiation during phototherapy. Am J Psychiatry. 1990;147:675-676.

27. Lam RW, Tam EM, Shiah IS, et al. Effects of light therapy on suicidal ideation in patients with winter depression. J Clin Psychiatry. 2000;61:30-32.

28. Barbini B, Benedetti F, Colombo C, et al. Dark therapy for mania: a pilot study. Bipolar Disord. 2005;7:98-101.

29. Wehr TA, Giesen H, Schulz PM, et al. Summer depression: description of the syndrome and comparison with winter depression. In: Rosenthal NE, Blehar MC, eds. Seasonal Affective Disorders and Phototherapy. New York: Guilford Press; 1989:55-63.

30. Wirz-Justice A, Terman M, Oren DA, et al. Brightening depression. Science. 2004;303:467-469.

31. Wirz-Justice A, Benedetti F, Terman M. Chronotherapeutics for Affective Disorders: A Clinician’s Manual for Light and Wake Therapy. 2nd rev ed. Basel, Switzerland: Karger; 2013.