Seasonal Affective Disorder (SAD)

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.

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-HT_2A 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]}

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]

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]