Seasonal Affective Disorder (SAD) 

Updated: Nov 15, 2016
Author: David R Michael, DO; Chief Editor: Randon S Welton, MD 

Overview

Background

Seasonal Affective Disorder (SAD) is a syndrome typically used to describe a recurrent, seasonal pattern of depressive episodes. SAD may also describe other affective episodes (mania or hypomania) that occur in a seasonal pattern.[1]

SAD was first described in 1984 by Rosenthal as a “syndrome characterized by recurrent depressions that occur annually at the same time each year.”[2] In this study, funded by the NIMH, Rosenthal et al. described a group of 29 patients, 27 of whom had bipolar illness who reported a history of atypical depressive symptoms during the winter time which remitted during the spring and summer. It was also noted that 23 of the participants had traveled north or south during their depressive episodes. Twenty-nine of them noticed a change in mood after traveling and showed improved mood within a few days of traveling south, which deteriorated when traveling back north. Eleven of these patients were started on bright light therapy with all showing some response within three to seven days after treatment was started (though all but one relapsed when the light was discontinued). 

Seasonal affective disorder is not listed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) as a separate condition. Instead it is listed as a specifier "with seasonal pattern" under Major Depressive Disorder, recurrent and the Bipolar Disorders.[1] This article will focus on recurrent, seasonal depressive episodes, which may be found in either Major Depressive Disorder or the Bipolar Disorders.

SAD is a relatively common syndrome with significant effects on mood and psychosocial functioning. It is particularly problematic as it is, by definition, a recurring syndrome with symptoms that may last 40% of the year. SAD is usually more common in the fall/winter (Winter SAD), though it may occur during the spring/summer (Spring SAD). Winter-onset SAD is more common and is often characterized by atypical depressive symptoms including; hypersomnia, increased appetite, and craving for carbohydrates. On the other hand, spring/summer also seen and is more frequently associated with typical depressive symptoms including insomnia and loss of appetite.[3]

Seasonal affective disorder is not without controversy. A recent study questions the very existence of SAD.[4]  In this study, the 2006 CDC survey of about 34,000 adults, which included depression screening questions was analyzed. The authors of the study could not find any evidence of seasonal or light-dependent increases in depression scores, thus calling in to question the very existence of SAD. The authors did note that screening for SAD might be difficult to detect on a population level and that screening for depressive symptoms is not necessarily the same as screening for SAD symptoms.

Pathophysiology

The etiology of SAD is not completely understood. A combination of physiologic, psychologic, genetic and environmental factors likely play a role.[5] Circadian phase delay, retinal subsensitivity to light, altered neurotransmitter release (e.g., serotonin, melatonin, dopamine), hypovitaminosis D and genetic variations in clock, monoamine and retinal photopigment genes have all been proposed mechanisms underlying the etiology of SAD.[6] It is important to note that SAD may be a heterogeneous condition and that some factors may play a role in some individuals with the disorder and not others.[7]

Circadian Rhythms and Photoperiod

Given the change in photoperiod length (longer nights and shorter days) and that bright-light therapy has an antidepressant effect, circadian rhythms have been hypothesized to contribute to the onset of SAD. A number of studies have found a correlation between photoperiod length and depression severity.[5]

Circadian phase shifts have also been proposed as a mechanism for the precipitation of SAD. Most commonly, SAD is associated with a phase-delay in circadian rhythms. Most of the research has tested the hypothesis that aberrations in circadian rhythm leads to alterations in melatonin release from the pineal gland. Bright light is a zeitgeber (external time cue) that affects melatonin release. Light is conveyed by the retina, through the retinohypothalamic tract to the pineal gland where it suppresses melatonin release. Internal or circadian cues come from the suprachiasmatic nucleus, which is also linked to the pineal gland. Interestingly, Wehr et al showed that controls did not demonstrate differential melatonin secretion during the winter while those with SAD demonstrated seasonal variation in melatonin secretion, with longer duration of secretion in the winter than during the summer.[8]  

Later dawn during the fall and winter might contribute to a phase delay (i.e., melatonin is released later) in the timing of melatonin release at night while earlier dawn might contribute to a phase advance (earlier onset of melatonin release).Most patients with SAD appear to be be phase-delayed and this might be part of the reason that bright-light therapy exerts an antidepressant effect. 

Genetics

Numerous studies have looked for genetic variation in those with SAD. Although data is inconclusive at this time, there have been some differences noted in the 5-HTTLPR gene and the 5-HT2A gene. Additionally, one study has found polymorphic differences in circadian clock genes, specifically Period3 and NPAS2.[9]  Another possible genetic variation might be related to differences in retinal light sensitivity and that those with SAD might have decreased sensitivity to light. It has been proposed that retinal photopigments such as melanopsin or cryptochrome might be involved in the pathophysiology of SAD and this is an active area of research.

Hypovitaminosis D

It has been proposed that low vitamin D may play a role in the development of SAD. Vitamin D may be involved with the functioning of the suprachiasmatic nucleus as well as the synthesis of serotonin and dopamine. Vitamin D levels do appear to fluctuate in a seasonal pattern due to changes in light exposure. At this time, studies assessing the effects of vitamin D have either been negative or inconclusive at this time.[10, 11]

Epidemiology

SAD is considered to be a relatively common disorder. The prevalence of SAD tends to vary across populations. The prevalence of SAD appears to be most linked to photoperiod and as such tends to be more prevalent with higher latitudes, though the evidence is not equivocal. In the United States, prevalence estimates range from 0.4% to as high as 10% depending on the methodology being used.[12]  There is significant evidence that people who migrate from lower to higher altitudes are more susceptible to SAD.[13]  SAD seems to affect women more commonly than men (4:1 ratio) and appears to decrease in prevalence with age.[14]

Winter-onset SAD is more common (often characterized by atypical depressive symptoms including; hypersomnia, increased appetite, and craving for carbohydrates). On the other hand, spring/summer also seen and is more frequently associated with insomnia and loss of appetite.[3]

Prognosis

SAD is, by definition, a recurrent disorder. It has been estimated that 67% of those diagnosed with SAD will face recurrence the following winter,[15] and after 5–11 years 22–42% of patients will still be suffering from SAD, 33–44% will develop non-seasonal depressive episodes, and remission is seen in approximately 14–18% of patients.[16]

 

Presentation

History

About 70% of depressed people feel worse/complain of more intense symptoms during the winter and less intensive symptoms during the summer. To meet the DSM-5 diagnostic criteria for major depressive disorder with seasonal pattern, depression should be present only at a specific time of year (e.g., in the fall or winter) and full remission occurs at a characteristic time of year (e.g., spring).[1] An individual should demonstrate at least 2 episodes of depressive disturbance in the previous 2 years, and seasonal episodes should substantially outnumber nonseasonal episodes. Winter-onset SAD is more common and is often characterized by atypical depressive symptoms including: hypersomnia, increased appetite, and craving for carbohydrates. On the other hand, spring/summer SAD is also seen and is more frequently associated with insomnia and loss of appetite.[3]

Cases where there is an obvious effect of seasonally related psychosocial stressors (e.g., seasonal unemployment, or specific anniversaries or losses) do not meet the diagnostic criteria. For example: Tom works a seasonal construction job that he enjoys. Living in a northern climate, work is much more slow in the winter and he notices that his mood is more down when he is less busy and does not have the money to do the activities that he most enjoys.  

Diagnosing seasonal affective disorder in children is difficult because they experience the recurrent universal stressor of beginning school every autumn.

 

DDx

Diagnostic Considerations

The primary diagnostic consideration is to differentiate “regular” major depressive disorder or bipolar spectrum disorder from the additional specifier of “with seasonal variation.” To meet the DSM-5 diagnostic criteria for major depressive disorder with seasonal pattern, depression should be present only at a specific time of year (eg, in the fall or winter) and full remission occurs at a characteristic time of year (eg, spring). An individual should demonstrate at least 2 episodes of depressive disturbance in the previous 2 years, and seasonal episodes should substantially outnumber nonseasonal episodes.[1]  Additionally, cases where there is an obvious effect of seasonally related psychosocial stressors (eg, seasonal unemployment) do not meet the diagnostic criteria.

 

Treatment

Approach Considerations

Available treatments for SAD include light therapy, pharmacotherapy and psychotherapy, used either alone or in combination. No one treatment has been proven to be more efficacious than the others and are often used in combination. Therefore, it is reasonable to guide therapy based on patient preference[24] and prior response. According to the American Psychiatric Association, SAD (Major Depressive Disorder, with seasonal pattern) can be treated with the entire range of treatments available to treat Major Depressive Disorder.[17]  Of note, if bipolar disorder is evident, winter depression should not be the only target of treatment. The full spectrum of the disorder should be treated, including mania or hypomania that may be evident during the spring and summer months.

Bright-Light Therapy

Bright-light therapy (BLT) has an established role in the treatment of seasonal affective disorder and is often referred to as the treatment of choice.[3]  The American Psychiatric Association (APA) recommends that for milder forms of seasonal affective disorder, bright-light therapy can be recommended as a 1–2 week time-limited trial as primary treatment.[17]  For more severe forms of SAD, the APA views BLT as an adjunctive treatment. While there is no data to suggest that BLT is associated with retinal or ocular damage, ophthalmologic examinations prior to initiating BLT and at regular follow-up visits for patients with pre-existing retinal disease, those taking photosensitizing medications, and those with systemic disease that involve the retina are recommended.[14] Patients often respond to BLT in as little as 1–2 weeks. Typically, BLT is continued until the time of their usual spring remission.[18]

BLT for SAD is used at an intensity of 10,000 lux for 30–90 minutes daily, usually within 1 hour of arising in the morning. Like any effective antidepressant, BLT has the potential to precipitate a hypomanic or manic episode in susceptible individuals. Other common adverse effects include eye irritation, restlessness, and transient headaches. These lamps are not a significant source of ultraviolet (UV) light.

In addition to its established role in seasonal affective disorder, BLT may be effective in nonseasonal depression or as an augmenting agent with antidepressant medication. One study found that the combination of 30 minutes of BLT a day plus 20 mg of fluoxetine significantly improves nonseasonal major depressive disorder. Data also show that light therapy alone is more effective than antidepressant monotherapy.[19]

Studies have demonstrated benefit of BLT for treatment of nonseasonal depression in pregnant patients and elderly patients.[20, 21]

Psychotherapy

Psychotherapy, particularly cognitive-behavioral therapy (CBT) may play a role in the treatment of SAD. Though data are limited, a recent study did find that CBT was as effective as bright-light therapy for the acute treatment of SAD.[22]  Psychotherapy may be useful as an adjunct or monotherapy for the treatment of SAD. One small study did find that those participants who did CBT had a lower recurrence rate of depression the next winter than those who did bright-light therapy alone.[23]

 

Consultations

While there is no data to suggest that bright-light therapy (BLT) is associated with retinal or ocular damage, ophthalmologic examinations are recommended prior to initiating treatment and at regular follow-up visits for patients with pre-existing retinal disease, those taking photosensitizing medications, and those with systemic disease that involve the retina.[14]

Prevention

Preventative treatment for seasonal affective disorder (SAD) is important considering the recurrent nature of the disorder. Unfortunately, current data is limited with regards to the effectiveness of preventative measures. 

The best data for prevention of SAD episodes comes from the clinical trials that resulted in the FDA approval of bupropion XL for the prevention of SAD.[15] In this case, bupropion XL is usually initiated in the autumn prior to the onset of depressive symptoms and is continued until the spring. Data on the use of other antidepressants for the prevention of SAD is lacking.[15]

With regard to psychotherapy, one small study did find that those participants who did CBT had a lower recurrence rate of depression the next winter than those who did bright-light therapy (BLT) alone. 

There is some data showing that initiating BLT prior to the onset of a depressive episode can reduce recurrence.[24] However, a recent Cochrane review found only low-quality evidence for using BLT for the prevention of SAD and suggested that its use for this purpose be guided on patient preference.[25]

Once again, it should be noted that according to the American Psychiatric Association, SAD (Major Depressive Disorder, with seasonal pattern) can be treated with the entire range of treatments available to treat Major Depressive Disorder.[17]

 

Medication

Medication Summary

The data are limited with regard to psychoactive medications and their use in the treatment of seasonal affective disorder. At the present time, the serotonin reuptake inhibitors (SSRIs) fluoxetine and sertraline have been the most studied and appear to be effective.[3]

According to the American Psychiatric Association, SAD (Major Depressive Disorder, with seasonal pattern) can be treated with the entire range of medication treatments available to treat Major Depressive Disorder.[17]   

Of note, while bupropion XL is an established treatment for the prevention of SAD (and is FDA approved for this indication), the evidence for the treatment of SAD is more limited.[3]

Antidepressants, SSRIs

Class Summary

SSRIs potentiate the pharmacologic effects of serotonin (5-hydroxytryptamine [5-HT]) in the central nervous system (CNS).

Fluoxetine (Prozac, Prozac Weekly)

Fluoxetine is an antidepressant agent that is chemically unrelated to the tricyclic, tetracyclic, or other available antidepressants. It selectively inhibits presynaptic serotonin reuptake with minimal or no effect on the reuptake of norepinephrine or dopamine.

Paroxetine (Paxil, Paxil CR, Pexeva)

Paroxetine is a potent selective inhibitor of neuronal serotonin reuptake. It also has a weak effect on norepinephrine and dopamine neuronal reuptake. For maintenance therapy, adjust the dosage to maintain the patient on the lowest effective dosage, and reassess the patient periodically to determine the need for continued treatment.

Sertraline (Zoloft)

Sertraline selectively inhibits presynaptic serotonin reuptake, with minimal or no effect on reuptake of norepinephrine or dopamine.

Citalopram (Celexa)

Citalopram is an SSRI used to treat depression. It is similar to fluoxetine, sertraline, and paroxetine. A highly selective reuptake inhibitor of serotonin, citalopram has little effect on other neurotransmitters.

Escitalopram (Lexapro)

Escitalopram is an SSRI and an S-enantiomer of citalopram. It is used for the treatment of depression. The drug’s mechanism of action is thought to be the potentiation of serotonergic activity in the CNS resulting from the inhibition of CNS neuronal reuptake of serotonin.

Antidepressants, SNRIs

Class Summary

The mixed serotonergic and noradrenergic drugs have effects on serotonin, norepinephrine, and, in some cases, dopamine and even on nicotinic acetylcholine systems. Because of the empirical nature of psychopharmacology, they may be used as first-line drugs or as follow-up agents when SSRIs fail.

Duloxetine (Cymbalta)

Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake. Its antidepressive action is theorized to be due to serotonergic and noradrenergic potentiation in the CNS.

Venlafaxine (Effexor XR)

Venlafaxine is structurally unrelated to other available antidepressants. It inhibits serotonin reuptake at select receptors, as well as the reuptake of norepinephrine.

Desvenlafaxine (Khedezla, Pristiq)

Desvenlafaxine is a strong and selective serotonin and norepinephrine reuptake inhibitor.

Levomilnacipran (Fetzima)

Active enantiomer of milnacipran. A strong inhibitor of norepinephrine and serotonin reuptake.

Antidepressants, Dopamine/Norepinephrine Reuptake Inhibitors

Class Summary

The mixed serotonergic and noradrenergic drugs have effects on serotonin, norepinephrine, and, in some cases, dopamine and even on nicotinic acetylcholine systems. They may be used as first-line drugs or as alternative agents when other antidepressants cause undesired side effects.

Bupropion (Aplenzin, Wellbutrin XL, Wellbutrin SR, Forfivo XL)

Bupropion inhibits neuronal dopamine reuptake, but it is also a weak blocker of serotonin and norepinephrine reuptake. A low incidence of sexual dysfunctions occurs with this medication.

Antidepressants, TCAs

Class Summary

TCAs are used when SSRIs are ineffective. They are structurally related to the phenothiazine antipsychotic agents and exhibit 3 major pharmacologic actions in varying degrees: amine pump inhibition, sedation, and anticholinergic action (peripheral and central). They inhibit reuptake of norepinephrine or serotonin at the presynaptic neuron.

Imipramine (Tofranil)

Imipramine inhibits the reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) in the central nervous system by inhibition of their reuptake by the presynaptic neuronal membrane.

Nortriptyline (Pamelor)

Nortriptyline works by inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, thus increasing the synaptic concentration of these neurotransmitters in the central nervous system (CNS). Pharmacodynamic effects such as the desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors also appear to play a role in its mechanisms of action.

Amitriptyline (Elavil)

Amitriptyline inhibits the reuptake of serotonin and/or norepinephrine at the presynaptic neuronal membrane, thus increasing the concentration of these neurotransmitters in the CNS.

Doxepin

Increases concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by presynaptic neuronal membrane. Inhibits histamine and acetylcholine activity and has proven useful in treatment of various forms of depression associated with chronic pain.

Trimipramine (Surmontil)

Antidepressant effects may result from postsynaptic sensitization to serotonin.

Desipramine (Norpramin)

Desipramine my inhibit the reuptake of norepinephrine, and possibly, serotonin in the central nervous system, thereby increasing their synaptic concentration. May also desensitize adenyl cyclase, down regulate beta-adrenergic receptors, and down regulate serotonin receptors.

Protriptyline (Vivactil)

Protriptyline has efficacy for migraine prophylaxis that is independent of its antidepressant effect. It inhibits activity of such diverse agents as histamine, 5-HT, and acetylcholine.

Antidepressants, MAO Inhibitors

Class Summary

Their main advantages are a low risk of dependence and a lesser anticholinergic effect than is seen with TCAs. Their main disadvantage is the higher number of adverse effects, including sexual difficulty, hypotension, and weight gain. A diet low in tyramine must be followed to avoid a hypertensive crisis. Over-the-counter medications should be used with great caution.

Tranylcypromine (Parnate)

Tranylcypromine inhibits the enzyme monoamine oxidase, which is responsible for the breakdown of neurotransmitters, thereby increasing endogenous concentrations of epinephrine, norepinephrine, and serotonin.

Phenelzine (Nardil)

Phenelzine is the most commonly used MAOI for anxiety disorders. Phenelzine is usually reserved for patients who cannot tolerate or do not respond to TCAs or SSRIs. Inhibits the enzyme monoamine oxidase, which is responsible for the breakdown of neurotransmitters, thereby increasing endogenous concentrations of epinephrine, norepinephrine, and serotonin.

Isocarboxazid (Marplan)

Inhibits the enzyme monoamine oxidase, which is responsible for the breakdown of neurotransmitters, thereby increasing endogenous concentrations of epinephrine, norepinephrine, and serotonin.

Selegiline (Eldepryl, Zelapar, Emsam)

Selective inhibitor of MAO type B, which plays a major role in metabolism of dopamine. May also increase dopaminergic activity by interfering with dopamine reuptake at the synapse.