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Am Fam Physician. 2020;102(11):668-672

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Seasonal affective disorder is a mood disorder that is a subtype or qualifier of major depressive disorder or bipolar disorder in the Diagnostic and Statistical Manual of Mental Disorders. It is characterized by depressive symptoms that occur at a specific time of year (typically fall or winter) with full remission at other times of year (typically spring or summer). Possible risk factors include family history, female sex, living at a more northern latitude, and young adulthood (18 to 30 years of age). With the temporal nature of the mood episodes, diagnosis requires full remission when the specified season ends and two consecutive years of episodes in the same season. First-line therapy for seasonal affective disorder includes light therapy, antidepressants, and cognitive behavior therapy, alone or in combination. Commercial devices are available for administering light therapy or dawn simulation. The light intensity and duration of treatment depend on the device and the patient's initial response, but 2,500 to 10,000 lux for 30 to 60 minutes at the same time every day is typically effective. Lifestyle interventions, such as increasing exercise and exposure to natural light, are also recommended. If seasonal affective disorder recurs, long-term treatment or preventive intervention is typically indicated, and bupropion appears to have the strongest evidence supporting long-term use. Continuing light therapy or other antidepressants is likely beneficial, although evidence is inconclusive. Evidence is also inconclusive for psychotherapy and vitamin D supplementation.

Seasonal affective disorder (SAD) is a mood disorder with depressive symptoms that occur at a specific time of year with full remission at other times of year. It typically occurs during fall or winter, although a less common form occurs during spring or summer.1,2 The pathophysiology is unclear, but theories include circadian rhythm disruption, dysregulation of the melanopsin signaling pathway and its impact on serotonin reuptake, and dysfunction of the hypothalamic-pituitary-adrenal axis.35 Studies using interviews and diagnostic criteria in the United States, Canada, and United Kingdom show a lifetime prevalence of 0.5% to 2.4% in the general population.68 Of patients with major depression, 10% to 20% have a seasonal pattern of symptoms consistent with SAD.9

Clinical recommendationEvidence ratingComments
Light therapy, dawn simulation, and cognitive behavior therapy are effective treatments for SAD.25,26,29,30 AConsistent evidence from a Cochrane review
Selective serotonin reuptake inhibitors may play a role in the treatment of SAD.27,28 BLow-quality evidence from two RCTs in a Cochrane review (fluoxetine [Prozac]) and from one RCT (sertraline [Zoloft])
Bupropion (Wellbutrin) may prevent SAD recurrence and is the only pharmacotherapy labeled for this use.35,36 AConsistent evidence from a Cochrane review of three RCTs
There is insufficient evidence to recommend antidepressants other than bupropion, light therapy, mindfulness-based cognitive therapy, or vitamin D supplementation for the prevention of SAD. Interventions should be individualized.33,37,42 BLow-quality evidence from limited RCTs and one non–patient-oriented systematic review

What Are the Risk Factors for SAD?

Evidence for risk factors is mostly weak or limited but suggests that family history, female sex, living at a more northern latitude, and young adulthood (18 to 30 years of age) may increase risk.1015


An Australian study of 4,000 twins compared symptoms in identical twins with symptoms in fraternal twins. Sets of identical twins were twice as likely to have SAD than sets of fraternal twins, suggesting a possible genetic link.10 Specific associated genes have not been identified, but a 2018 meta-analysis revealed ZBTB20 as a potential susceptibility gene for SAD.11

Two large questionnaire studies have shown that individuals living in more northern latitudes have an increased risk of developing SAD.12,13 It is suspected that prevalence increases with increasing latitude, but data are poor, and this conclusion is controversial.12,13

Two studies using the Seasonal Pattern Assessment Questionnaire (SPAQ) found that SAD has a higher prevalence in females, but this is based on poor data.14,15 A 2000 meta-analysis of population studies found that SAD appears to be most prevalent among young adults.9

What Are the Diagnostic Criteria for SAD?

In addition to meeting Diagnostic and Statistical Manual of Mental Disorders , 5th ed., (DSM-5) criteria for major depressive disorder or bipolar disorder, there must be a temporal relationship between time of year and occurrence of mood episodes. Mood episodes are discrete periods during which the patient demonstrates depressive symptoms. Full remission must occur when the specified season ends. There must be two consecutive years of mood episodes in the same season to diagnose fall/winter or spring/summer SAD. In SAD, seasonal mood episodes significantly outnumber nonseasonal mood episodes during the individual's life.1


The DSM-5 does not define SAD as a separate diagnosis and instead includes it as a variant of major depressive disorder or bipolar disorder.1 Typical features of depression include depressed mood, anhedonia, guilt or hopelessness, decreased energy, and impaired mood. Typical features of bipolar disorder include mania, hypomania, depression, irritability, anxiety, mood lability, sleep disturbance, and hyperactivity. SAD is a subtype or qualifier of these mood disorders with a seasonal onset and remission.

The more common fall/winter type of SAD has occasional atypical features, such as increased need for sleep, carbohydrate cravings with increased appetite and weight gain, and extreme fatigue.16 The less common spring/summer type may have the atypical symptoms of increased irritability, poor appetite with weight loss, insomnia, agitation, restlessness, anxiety, and increased violence.17

To meet the diagnostic criteria, psychosocial stressors of a specified season, such as layoffs during the winter season, must not contribute to the mood episodes. Additionally, the diagnosis requires a two-year consecutive pattern of mood episodes during a specified season.1

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