Sanassi, Lorraine A. PA-C, MHS
Seasonal affective disorder (SAD) is a subtype of bipolar disorder or major depressive disorder characterized by recurrent episodes of major depression that occur in a seasonal pattern.1 Predominantly developing in the late fall and winter, SAD also may appear in the spring and summer and is characterized by cyclic onset and cyclic remission of major depressive episodes.1,2 SAD symptoms are predictable and can be expected in the same seasonal pattern in consecutive years; symptoms resolve when light exposure increases.2
SAD is thought to be related to natural seasonal variations in light levels; treatment therefore traditionally has involved light therapy, although recent investigations have explored other options, including antidepressant therapy and CBT. Although SAD is common, it often goes unnoticed in the primary care setting.
SAD affects about 6% of the US population overall and is more prevalent in northern regions, which get fewer hours of sunlight in the winter than southern regions.3,4 Compared with the general population, people who migrate north from southern latitudes may have a higher incidence of SAD because of acclimation problems.5 Patients typically are in their 20s when they first experience SAD, but the condition is common among children and adolescents as well. Women are more likely than men to develop SAD.2,4
Although the exact mechanism of SAD is still under investigation, current evidence supports the phase-shift hypothesis.6 According to this hypothesis, fewer hours of daylight in the winter cause the biological clock, found in the suprachiasmatic nucleus of the anterior hypothalamus, to fall out of synchrony with the solar cycle. This circadian misalignment leads to disturbances in melatonin levels and longer periods of melatonin synthesis at night.5,7–9 Melatonin, the so-called circadian hormone, normally peaks in darkness and helps promote sleep. Patients with SAD may have more daytime melatonin, which contributes to the depressive symptoms of SAD.9 Neurotransmitters under circadian control, such as serotonin, norepinephrine, and dopamine, also may play a role in the mood alterations patients with SAD experience.9 Specifically, levels of serotonin, sometimes called the “happiness hormone,” often decline in winter months.10 Many SAD symptoms, such as increased appetite leading to overeating and weight gain, carbohydrate cravings, and somnolence can be attributed to serotonergic dysfunction. Not surprisingly, selective serotonin reuptake inhibitors (SSRIs) have shown benefit in treating SAD.11
SAD is characterized by typical symptoms of major depression, although atypical depressive symptoms predominate, such as lack of energy, hypersomnia, increased appetite and weight, and a craving for carbohydrates (Table 1).2 Generally, these symptoms precede loss of interest and pleasure in daily activities, excessive fatigue, feelings of guilt, and poor concentration and decision-making capabilities. Symptoms usually resolve in the summer, only rarely progressing to manic episodes of bipolar disorder.4
As with other mental disorders, SAD may also coexist with other psychiatric conditions, generally due to alterations in serotonergic and noradrenergic neurotransmitter activity.12 Possible concomitant mental disorders include bulimia nervosa, generalized anxiety disorder, panic disorder, premenstrual dysphoric disorder, phobias, and alcohol abuse.1,12 SAD also may develop in patients with a family history of mood disorders or first-degree relatives with SAD, or in patients with alcohol-related disorders.12
SAD often is not diagnosed because its symptoms may not be obvious to the provider, especially when routine screening for depressive disorders is not conducted. The US Preventive Services Task Force (USPSTF) recommends such screening, saying that it improves identification of depressed patients in primary care settings.13 The USPSTF suggests using revised versions of standard psychological screening instruments, such as the Seasonal Pattern Adjustment Questionnaire (SPAQ), the Seasonal Health Questionnaire (SHQ), and the Structured Interview Guide for the Hamilton Rating-Seasonal Affective Disorder (SIGH-SAD), which are shorter and more concise than the original screening tools for depression.13
The SPAQ, devised by Rosenthal and colleagues in 1987, is a commonly used screening tool, but its low specificity has contributed to overestimation of the prevalence of SAD.14 With this in mind, Thompson and Lawson devised the SHQ in 2001, and it now is used more often than the SPAQ, although it is more complex than the SPAQ.15 Compared with the SPAQ, the SHQ provides a more realistic estimate of the prevalence of SAD, and research indicates that it has higher sensitivity and specificity for SAD.14 Another commonly used screening tool, the SIGH-SAD, primarily differentiates between SAD and subsyndromal SAD.16 Patients with subsyndromal SAD do not meet the diagnostic criteria for SAD but experience enough seasonal mood disruption and functional impairment to warrant therapy.2
Physical examination and laboratory studies are generally unremarkable in patients with SAD, so diagnosis usually is based on history alone (Table 2).2 Providers also should document the severity of SAD based on the patient's number of symptoms, their intensity, and the level of physical impairment with which they are associated (Table 3).2
Three types of treatments can be used for patients with SAD.
Light therapy Several studies have demonstrated the high efficacy and high tolerability of light therapy, even with brief and low doses of at least 2,500 lux.17,18 The light therapy introduced in 1984 used light boxes providing an exposure of about 10,000 lux.9 Early studies observed the effect of bright white light on circadian rhythm, but subsequent research found that less-intense light had a greater capacity to regulate the biological clock than higher-intensity light.17 This is mainly due to melanopsin, a recently discovered photoreceptor in the retina of the eye, which is largely responsible for regulating the biological clock by receiving and interpreting light of low intensities, typically around 480 nm (equivalent to about 5,000 lux).19
Blue light, which has an intensity of about 460 nm, has been found to be more powerful than higher-intensity white light, resulting in significant melatonin suppression, circadian phase shifting, and antidepressant effects.9,19
Light therapy helps reduce fatigue and excessive daytime sleepiness and improves health-related quality of life in patients with SAD, and its beneficial results last for at least 1 month.20 Using a light box, patients can perform this therapy at home in 30 minutes to 2 hours per day, depending on the intensity of the light used. Patients should sit 1 to 3 ft away from the light box and can carry on normal activities as long as they glance at the box periodically.21 Therapy administered in the morning (between dawn and 8 a.m.) provides the best results because early morning light leads to a phase advance in the circadian system, putting it back on track with the normal sleep/wake cycle.9
Clinical improvement can be seen 1 to 2 weeks after light therapy is initiated, and significant clinical improvement often is seen from week 3 onward; however, symptoms usually slowly return to baseline once light therapy is discontinued.22–24 Consequently, patients should continue light therapy until the time of year when their symptoms generally spontaneously remit. Therapy should be tapered before expected symptom remission by reducing the length of daily sessions and number of weekly sessions to ensure symptom control.25 To avoid relapses, the patient should start light therapy as soon as symptoms manifest or at least 2 weeks before she usually experiences seasonal depressive symptoms.25,26 Prices for light boxes range from $100 to $500 and may not always be covered by health insurance plans.27
Pharmacologic therapy SSRIs have been the mainstay of pharmacologic therapy for SAD, but recent studies have investigated other classes of antidepressants, including benzodiazepines, as well as beta-blockers and melatonin.28
Three SSRIs—sertraline, citalopram, and escitalopram—have shown favorable results, with good tolerability and continued control of symptoms until SAD remits spontaneously in the spring.29–31 Mirtazapine, an antidepressant with noradrenergic and selective serotonergic activity, also is well-tolerated and efficacious in achieving nearly full remission.28 Bupropion, which likely enhances noradrenergic activity in the brain, may be useful in preventing the onset of SAD; preventive treatment should start in the early autumn at least 4 weeks before symptoms typically appear.32
Alprazolam, a benzodiazepine, has shown efficacy in improving clinical symptoms of depression, anxiety, and irritability common with SAD but can be habit-forming.28 Beta-blockers such as propranolol and atenolol, which regulate nocturnal melatonin secretion from the pineal gland during sleep, also have proven effective.28
Light therapy and the SSRI fluoxetine are equally effective, but patients may prefer light therapy because its effects are felt more quickly and it is associated with fewer adverse reactions.1,33 If light therapy alone is not successful, some patients may switch to antidepressants alone or may combine antidepressant and light therapy.34 Because patients rapidly undergo a relapse when light therapy is discontinued, administering antidepressant therapy after a brief course of light therapy may be the best way to continue a positive response throughout the winter.35
The newest medication under investigation for treating SAD is agomelatine, a synthetic analog of melatonin that is not yet FDA-approved.36 Agomelatine helps resynchronize circadian rhythms, prevent serotonin reuptake, and decrease anxiety and depressive symptoms.28,36 Agomelatine is generally well-tolerated with fewer adverse reactions than most antidepressants.9
Limited studies have shown that Hypericum perforatum (St. John's wort) is effective in treating SAD and has significant antidepressant effects when combined with light therapy.5 This herbal preparation inhibits serotonin, noradrenaline, and dopamine and has weak monoamine oxidase inhibiting effects, however, so it should not be used in patients on antidepressant therapy.37
Vitamin D has also demonstrated variable and modest results in treating SAD. One study found improvement in patients who took 4,000 IU of vitamin D daily during the winter months.18
COGNITIVE BEHAVIORAL THERAPY
Few studies discuss the effectiveness of CBT for SAD. In general, CBT helps reduce the risk for relapse in all forms of major depression. Patients with SAD who received CBT in combination with light therapy had better outcomes (decreased symptom severity, increased remission rates, and decreased relapse rates) than with CBT alone.38 A preliminary study in 23 patients (and no control group) found that CBT alone, light therapy alone, and CBT with light therapy all significantly improved depressive symptoms of SAD, with the highest remission rate with combination therapy.38 This study suggested that CBT therapy can improve long-term outcomes for patients with SAD with regard to symptom severity, relapse rates, and remission rates in subsequent seasons.
The understanding of the pathophysiology and treatment of SAD has come a long way since the condition was defined in the 1980s. As the hours of daylight decrease in the fall and winter, depressive symptoms become obvious in patients with SAD and the application of light therapy provides significant relief.2,20,24 Because the prevalence of SAD varies geographically, epidemiologic statistics have been difficult to obtain.3–5 More studies need to be conducted worldwide to determine if prevalence is increased at high latitudes. The prevalence of SAD in children, young adults, and older adults also should be investigated.
For years, light therapy has been the foundation of therapy, with increasing evidence showing that lower-intensity light can be more beneficial than higher-intensity light because of retinal receptor factors.17,19 Given that morning light therapy is most effective in decreasing fatigue and excessive daytime sleepiness and increasing quality of life, the role of light therapy on night-shift workers with SAD needs to be investigated.9 Do these workers have different symptoms than patients who work daytime hours? Should the timing of light therapy and its intensity be changed to remedy their symptoms? These are some of the intriguing questions to be answered.
Although few studies have focused on drug therapy for SAD, available studies have demonstrated that these light and drug therapies have comparable effects.30 SSRIs, which have been studied the most, have been shown to improve SAD symptoms considerably. Similar effects have also been seen with other classes of antidepressants and with benzodiazepines, beta-blockers, and melatonin.28 The best outcomes result from the use of light therapy used concurrently with antidepressant therapy until symptoms spontaneously remit in the spring or summer. Over-the-counter medications such as St. John's wort and vitamin D have also demonstrated some positive effects, especially when used in combination with light therapy, although more empiric studies are needed to characterize the benefit and risks of these supplements.
The role of CBT in treating SAD has not been investigated thoroughly, but studies have shown that CBT has a general positive effect on depression.38 In patients with SAD, CBT alone has demonstrated positive effects but has greater effect when combined with light therapy.38 More studies need to be conducted to validate these findings. Implementing CBT as part of the management of SAD also may help prevent SAD in subsequent seasons.38
SAD is one of the few psychiatric disorders with clearly defined causes and a predictable course, with clear reversal of symptoms with light therapy and antidepressants. Clinicians can do a better job of screening for this disorder in the fall and winter, allowing for prompt initiation of treatment with light therapy, pharmacotherapy, and/or CBT.
1. Lurie SJ, Gawinski B, Pierce D, Rousseau SJ. Seasonal affective disorder. Am Family Physician
2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders
, 5th ed. Arlington VA: American Psychiatric Publishing; 2013.
3. Targum SD, Rosenthal N. Seasonal affective disorder. Psychiatry (Edgmont)
4. Magnusson A, Partonen T. The diagnosis, symptomatology, and epidemiology of seasonal affective disorder. CNS Spectr
5. Miller AL. Epidemiology, etiology, and natural treatment of seasonal affective disorder. Altern Med Rev
6. Lewy AJ, Rough JN, Songer JB, et al. The phase shift hypothesis for the circadian component of winter depression. Dialogues Clin Neurosci
7. Boyce P, Barriball E. Circadian rhythms and depression. Aust Fam Physician
8. Sullivan B, Payne TW. Affective disorders and cognitive failures: a comparison of seasonal and nonseasonal depression. Am J Psychiatry
9. McClung CA. Circadian genes, rhythms, and the biology of mood disorders. Pharmacol Ther
10. Gupta A, Sharma PK, Garg VK, et al. Role of serotonin in seasonal affective disorder. Eur Rev Med Pharmacol Sci
11. Sher L. Seasonal affective disorder and seasonality: a review. Jefferson J Psychiatry
12. Partonen T, Magnusson A. Seasonal Affective Disorder: Practice and Research
. New York, NY: Oxford University Press; 2001.
13. United States Preventive Services Task Force. Screening for depression in adults: US Preventive Services Task Force recommendation statement. Ann Intern Med
14. Thompson C, Thompson S, Smith R. Prevalence of seasonal affective disorder in primary care: a comparison of the seasonal health questionnaire and the seasonal pattern adjustment questionnaire. J Affect Disord
15. Thompson C, Cowan A. The Seasonal Health Questionnaire: a preliminary validation of a new instrument for seasonal affective disorder. J Affect Disord
16. Laskoski J. Is bright light therapy effective for improving depressive symptoms in adults with seasonal affective disorder (SAD). Internet Journal of Academic Physician Assistants
. Accessed November 9, 2013.
17. Shirani A St. Louis EK. Illuminating rationale and uses for light therapy. J Clin Sleep Med
18. Bertone-Johnson ER. Vitamin D and the occurrence of depression: causal association or circumstantial evidence. Nutr Rev
19. Meesters Y, Dekker V, Schlangen LJ, et al. Low-intensity blue-enriched white light (750 lux) and standard blue light (10,000 lux) are equally effective in treating SAD. A randomized controlled study. BMC Psychiatry
20. Rastad C, Ulfberg J, Lindberg P. Improvement in fatigue, sleepiness, and health-related quality of life with bright light treatment in persons with seasonal affective disorder and subsyndromal SAD. Depress Res Treat
21. Golden RN, Gaynes BN, Ekstrom D, et al. The efficacy of light therapy in the treatment of mood disorders: a review and meta-analysis of the evidence. Am J Psychiatry
22. Bauer MS, Kurtz JW, Rubin LB, Marcus JG. Mood and behavioral effects of four-week light treatment in winter depressives and controls. J Psychiatr Res
23. Eastman CI, Young MA, Fogg LF, et al. Bright light treatment of winter depression: a placebo-controlled trial. Arch Gen Psychiatry
24. 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
25. Kurlansik SL, Ibay AD. Seasonal affective disorder. Am Fam Physician
26. Meesters Y, Beersma DG, Bouhuys AL, van den Hoofdakker RH. Prophylactic treatment of seasonal affective disorder (SAD) by using light visors: bright white or infrared light. Biol Psychiatry
28. Pjrek E, Winkler D, Kasper S. Pharmacotherapy of seasonal affective disorder. CNS Spectr
29. Pjrek E, Winkler D, Stastny J, et al. Ecitalopram in seasonal affective disorder: results of an open trial. Pharmacopsychiatry
30. Moscovitch A, Blashko CA, Eagles JM, et al. A placebo-controlled study of sertraline in the treatment of outpatients with seasonal affective disorder. Psychopharmacology (Berl)
31. Martiny K, Lunde M, Simonsen C, et al. Relapse prevention by citalopram in SAD patients responding to 1 week of light therapy. A placebo-controlled study. Acta Psychiatr Scand
32. Modell JG, Rosenthal NE, Harriett AE, et al. Seasonal affective disorder and its prevention by anticipatory treatment with buproprion XL. Biol Psychiatry
33. Westrin A, Lam RW. Seasonal affective disorder: a clinical update. Ann Clin Psychiatry
34. Howland RH. Somatic therapies for seasonal affective disorder. J Psychosoc Nurs Ment Health Serv
35. Westrin A, Lam RW. Long-term and preventative treatment for seasonal affective disorder. CNS Drugs
36. Howland RH. Agomelatine: a novel atypical antidepressant. J Psychosoc Nurs Ment Health Serv
. 2007;45(12), 13–17.
38. Rohan KJ, Lindsey KT, Roecklein KA, Lacy TJ. Cognitive-behavioral therapy, light therapy, and their combination in treating seasonal affective disorder. J Affect Disord
39. Singh T, Williams K. Atypical depression. Psychiatry (Edgmont)
© 2014 American Academy of Physician Assistants.