Seasonal Affective Disorder
Abstract and Keywords
Winter seasonal affective disorder (SAD) is a subtype of depression, characterized by the recurrence of major depressive episodes in the fall and/or winter months. In North America, SAD prevalence and severity are inversely related to photoperiod, such that SAD is more common at northern latitudes. Photoperiod is the most robust environmental predictor of SAD episode onset. Research has supported a potential role for both physiological and psychological vulnerabilities in the development and maintenance of SAD. Specifically, SAD has been linked to abnormal circadian functioning, retinal sensitivities to low light availability, and maladaptive cognitive and behavioral responses in winter. SAD symptoms can be comparably and effectively treated with different modalities including light therapy, antidepressants, and cognitive–behavioral therapy. Future research should continue to explore and integrate different vulnerabilities as a means to further refine effective treatment and prevention efforts.
Definition of Seasonal Affective Disorder (SAD)
Mammalian behaviors vary according to photoperiod, defined as the time between dawn and dusk, as a means to optimize reproduction and feeding behaviors across seasons. Although amenities of modern living have allowed humans to buffer their dependency on season and natural daylight for survival, we are not fully insulated from experiencing behavioral shifts with the changing seasons. Approximately 95% of individuals report experiencing some degree of physiological, behavioral, or emotional fluctuations across seasons (Kasper, Wehr, & Bartko, 1989). In the general population, complaints of lower activity level, craving carbohydrates, and needing more sleep to feel rested are common during the winter months. Conversely, people tend to be more active, eat healthier, and require less sleep in the summer months (Magnusson, 2000). The degree of seasonality, or seasonal behavior changes, occurs on a continuum ranging from mild to severe. Similar to other mammals, human seasonality has been shown to occur as a function of photoperiod. Higher levels of seasonality are reported at more northern latitudes where photoperiod varies more starkly across the seasons (Magnusson, 2000; Rosen, Targum, & Terman, 1990).
Seasonal affective disorder (SAD) characterizes individuals with a marked degree of seasonality who also experience distress and impaired functioning. First documented by Rosenthal, Sack, and Gillin in 1984, SAD is a form of recurrent major depression that follows a seasonal course. The most common subtype is winter SAD,1 presenting as major depression exclusively in the fall and winter months. Depressive symptoms in SAD vary from patient to patient and can include the full spectrum of symptoms subsumed under major depressive disorder. The majority of SAD patients endorse fatigue, depressed mood, and anhedonia. The (p. 255) atypical presentation, which includes hypersomnia, increased appetite, and weight gain due to carbohydrate craving/consumption, is more common than the melancholic presentation, which features insomnia and weight loss. The term subsyndromal SAD (S-SAD), commonly known as “the winter blues,” applies to individuals who experience moderate seasonality without significant distress or impairment (Kasper et al., 1989). Per the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), SAD is diagnosed as the seasonal pattern course specifier that can be applied to major depressive disorder, bipolar I disorder, or bipolar II disorder (American Psychiatric Association, 2013). To meet full diagnostic criteria, an individual must have experienced a major depressive episode (MDE) in the same season(s) for at least the last two consecutive years with a clear seasonal pattern of full remission or change to mania or hypomania within the 2-year time frame. In addition, the seasonal pattern must be clear over the lifetime with seasonal episodes substantially outnumbering nonseasonal episodes. Given that the intraindividual severity and duration of winter depressions vary from winter to winter (Rosenthal, Sack, et al., 1984), it is reasonable for clinicians to conceptualize cases with a clear seasonal pattern in MDEs as “SAD,” even if symptoms did not meet the full MDE threshold every winter. A diagnosis of SAD is not warranted if the apparent seasonal pattern is attributable to seasonal variations in psychosocial stress (e.g., holiday stress or seasonal unemployment).
The most common spring/summer mood status of SAD patients is full symptom remission. Approximately one-third of patients experience hypomania, and only about 5% experience mania. Outside of winter SAD, another less studied variant of SAD is summer SAD. Summer SAD is characterized by recurrent major depressive episodes during summer months, presumably triggered by heat and humidity, with an estimated prevalence of 0.5–1.2% in adults (Kasper et al., 1989; Rosen et al., 1990; Rosenthal, Sack, et al., 1984). The winter depression syndrome of SAD has a larger research base, supported by a wealth of epidemiological, experimental, and treatment research to date, and is thus the focus of this chapter.
Based on self-report measures of seasonality or retrospective chart review, an estimated 10–20% of all mood disorders follow a seasonal course (Magnusson, 2000). Any epidemiological study on SAD must be considered within the context of the geographic location surveyed and the assessment instrument and criteria used to define caseness. Many studies have relied on the Seasonal Pattern Assessment Questionnaire (SPAQ; Rosenthal, Bradt, & Wehr, 1984), a self-report measure that codes for the respondent’s perceived degree of seasonal change in mood, sleep length, appetite, weight, social activities, and energy. SPAQ studies around the world have yielded prevalence estimates for SAD ranging from less than 1% in the Philippines to greater than 10% in Denmark (Magnusson, 2000).
Despite its ease for large-scale administration in population-based studies and good sensitivity for detecting clinically significant seasonality, the SPAQ overestimates SAD prevalence relative to diagnostic clinical interviews (Magnusson & Partonen, 2010). The National Comorbidity Study, which included over 8,000 respondents aged 15–54 years in the 48 contiguous states, was the first community-based study to estimate SAD prevalence via clinical interview (Blazer, Kessler, & Swartz, 1998). Based on the Composite International Diagnostic Interview, 0.4% and 1.0% of respondents met DSM-III-R criteria for lifetime major and minor depression with a seasonal pattern, respectively. The only other published community-based study using a clinical interview included 781 randomly selected adults aged 20 years and over living in Toronto, Ontario (Levitt, Boyle, Joffe, & Baumal, 2000). In a telephone interview using DSM-III-R criteria for major depression, recurrent with seasonal pattern, 2.9% fulfilled criteria for SAD. When similar methods were applied to the entire province of Ontario (N = 1605), a 2.6% lifetime prevalence of SAD was observed (Levitt & Boyle, 2002). Therefore, SAD prevalence estimates are substantially lower when based on diagnostic clinical interview than when using the SPAQ. As a consequence, the SPAQ is used as a screening device, not as a primary diagnostic instrument, in research and in clinical practice.
Initial studies using the SPAQ suggested that SAD becomes more prevalent as latitude increases. This was interpreted as evidence that photoperiod, which is fully determined by date and latitude, is an environmental trigger for SAD episodes in vulnerable individuals. The first direct test of the latitude hypothesis (Rosen et al., 1990) was a mailed SPAQ survey of over 1,600 randomly selected residents of Nashua, NH (42.5°N), New York, NY (40°N), Montgomery County, MD (39°N), and Sarasota, FL (27°N). SAD prevalence estimates were 9.7%, (p. 256) 4.7%, 6.3%, and 1.4%, respectively. In a meta-analysis of 22 studies in Europe, North America, Asia, and Australia Mersch, Middendorp, Bouhuys, Beersma, and van den Hoofdakker (1999) found that the correlation between SAD prevalence and latitude was low and nonsignificant overall (r = 0.07), but became statistically significant when calculated separately for studies on the North American continent (r = 0.90) with a trend in the same direction among European studies (r = 0.70). Latitude is a crude index of local climatic variables that may be relevant to SAD onset, including indices of luminosity (e.g., minutes of sunshine, cloud cover), temperature, and precipitation. In addition to latitude and climatological variables, research is needed on other factors that might affect SAD prevalence such as time of year assessed, length of residency, acclimatization, sociocultural factors, and within-time zone longitude, which affects wake time relative to sunrise.
Sociocultural and genetic factors may also moderate SAD prevalence. For instance, SPAQ-ascertained SAD prevalence was relatively low in Iceland (3.8%, Magnusson & Stefansson, 1993) and in adults of wholly Icelandic descent living in Manitoba, Canada (1.2%) relative to non-Icelandic adults residing at comparable latitudes in the United States (7.4%; Magnusson & Axelsson, 1993). In addition, demographic differences in SAD prevalence have been reported. SPAQ studies have consistently found a higher prevalence of SAD in women relative to men, suggesting that the sex difference in SAD is at least as high as the 2:1 difference in major depressive disorder. Regarding the diagnostic interview studies, the population survey in Toronto observed a 2:1 sex difference in SAD prevalence (Levitt et al., 2000); however, the National Comorbidity Study found that men had a greater risk of major depression with seasonal pattern whereas women had a higher risk of seasonal minor depression (Blazer et al., 1998). Another consistent finding across epidemiological studies with sufficient age range is that the prevalence of SAD increases with age until the early fifties and declines thereafter.
The effects of race and ethnicity on SAD are understudied as the majority of epidemiological research has focused on largely white samples. The National Comorbidity Study reported that white versus “Other” ethnicity was unrelated to risk for a seasonal pattern of major or minor depression (Blazer et al., 1998). SPAQ-determined SAD prevalence among African-American students in the Washington, DC area was comparable to previous estimates for white adults in the same region (Agumadu et al., 2004). Asian studies conducted in tropical climates in the Philippines, Thailand, and Chiang Mai, China have generally found a very low prevalence of SAD (and a higher prevalence of summer than of winter SAD), but this pattern likely reflects the low latitude more so than a low vulnerability to winter SAD among Asians. In support of this, a study in England found that Asian nonindigenous women (i.e., Pakistani, Indian, or Bangladeshi) had more winter depression symptoms than age- and SES-matched white and Asian women born in England (Suhail & Cochrane, 1997).
Photoperiod: The Environmental Trigger for SAD
The latitude hypothesis posits that SAD is causally linked to the short days of winter. Latitude serves as a proxy for photoperiod in epidemiological studies, indirectly informing the association between photoperiod and SAD. In a pooled analysis assessing the effects of climatic variables and photoperiod on the timing of winter depression onset in SAD, photoperiod was the only significant predictor of weekly risk for onset after controlling for other environmental conditions that vary across the seasons (e.g., temperature and indices of light intensity such as daily hours of sunshine and radiation; Young, Meaden, Fogg, Cherin, & Eastman, 1997).
Actigraphy studies examining individual variations in daily light exposure across seasons found that SAD patients spend more time outdoors in summer than winter and show greater seasonal fluctuations in light exposure relative to healthy controls (Eastman, 1990; Graw, Recker, Sand, Krauchi, & Wirz-Justice, 1999). Another study found that SAD patients and nondepressed controls did not differ in winter ambient light exposure patterns, but photoperiod was inversely correlated with winter depression severity only among SAD patients (Oren, Moul, Schwartz, & Brown, 1994). Due to the salience of photoperiod, the majority of etiological research has examined circadian rhythms in SAD, testing whether SAD patients may exhibit distinctive chronobiological responses to short winter photoperiods.
Phase Shift Hypothesis
The circadian pacemaker is located within the suprachiasmatic nucleus (SCN) of the anterior hypothalamus and is responsible for synchronizing (p. 257) physiological processes with the external light/dark cycle. Daily resetting of the biological clock occurs primarily via ocular light input, captured by nonvisual retinal ganglion cells that project photic input to the SCN via the retinohypothalamic (RHT) tract. The pacemaker then emits a neural signal of daylength to other circuits responsible for regulating chronobiological functions such as the timing of hormone secretion, sleep, and alertness, among other behaviors (Wehr, 2001). Circadian phase is most commonly measured as the melatonin onset, or the time of increased pineal melatonin release in evening. In entrained individuals, melatonin release is suppressed by ocular light exposure during daylight hours, and melatonin levels reliably rise in evenings (Benloucif et al., 2008). As a result, melatonin levels are very low during the day and are elevated during the night as long as there are no extraneous factors involved such as shift work. Compared with other biomarkers of circadian phase, such as core body temperature and cortisol level, melatonin is less subject to the confounding effects of sleep/wake and activity/rest cycles (Benloucif et al., 2005).
The leading etiological theory of SAD to date, the phase shift hypothesis (Lewy, Sack, & Singer, 1988), proposes that SAD results when later dawns in winter trigger a pathophysiological phase delay in circadian rhythms relative to the external light/dark cycle and/or the internal sleep/wake cycle. Some studies found that SAD patients exhibited shifted rhythms in winter when depressed, with the circadian phase occurring either earlier (phase advanced) or later (phase delayed) relative to their euthymic circadian phase position following remission with light therapy (Avery et al., 1997; Lewy, Sack, Singer, & White, 1987; Lewy et al., 2003, 2006), or relative to healthy individuals in winter (Dahl, Avery, & Lewy, 1993; Lewy, Lefler, & Emens, 2006). However, several longitudinal studies did not find unique shifts in circadian phase in SAD patients across seasons (Checkley et al., 1993; Koorengevel, Beersma, den Boer, & van den Hoofdakker, 2003; Oren, Levendosky, Kasper, Duncan, & Rosenthal, 1996; Wehr et al., 2001).
Superior efficacy of morning light administration (vs. other times of day) in treating SAD provides indirect support for the phase shift hypothesis, as morning light advances the circadian clock and is thought to correct the circadian phase delay (Eastman, Young, Fogg, & Meaden, 1998; Lewy et al., 1988; Terman, Terman, & Cooper, 2001; Terman, Terman, & Ross, 1998; Terman, Terman, & Quitkin, 1989). However, evening light administration improves SAD symptoms, albeit not as greatly as morning light, and has never been associated with a worsening of SAD symptoms in a clinical trial, as would be expected if it exacerbated a mechanistic phase delay. Light therapy trials have also not observed an association between degree of phase advance across treatment and degree of symptom improvement (Burgess, Fogg, Young, & Eastman, 2004; Eastman, Gallo, Lahmeyer, & Fogg, 1993; Thompson, Childs, Martin, Rodin, & Smythe, 1997).
Recent findings suggest that the timing of the circadian phase relative to the individual’s timing of sleep may be an important marker of SAD. Greater temporal shifts in this phase relationship (i.e., melatonin to sleep) were associated with greater depression severity in winter, whereas the timing of melatonin onset alone was not (Lewy et al., 2006). An estimated two-thirds of SAD patients exhibited a pathophysiological circadian phase delay, whereas one-third of patients exhibited an abnormal phase advance, when depressed (Lewy et al., 2006). There is some evidence for an optimal phase angle between circadian phase and sleep/wake cycle in SAD (i.e., 6 hours between the time of the evening melatonin onset and the midpoint of sleep), corresponding to stable circadian entrainment in healthy adults. To date, two SAD studies have reported that temporal deviation (either fewer or more hours) occurring between the circadian and sleep/wake oscillators is associated with greater SAD severity (Burgess et al., 2004; Lewy et al., 2006). It is yet to be determined whether, and through what mechanism(s), a circadian phase shift is causally linked to depression in SAD. If so, matching the patient’s phase “type” (i.e., delay or advance) with the correct light administration time (i.e., morning or evening, respectively) would be important. Unfortunately, this type of matching is not feasible without a practical measure of the direction of a patient’s circadian phase shift (advance or delay) in response to the short photoperiod of winter relative to summer.
Photoperiodic mammals exhibit a circadian signal of season change (i.e., fluctuation in the duration of nocturnal melatonin release) to inform the timing of seasonal survival behavior, such as eating, sleeping, and mating. The photoperiodic hypothesis proposes that SAD patients may possess the intrinsic ability to track the changing seasons in a manner similar to nonhuman photoperiodic mammals. The one test of this hypothesis to date was supportive. (p. 258) SAD patients, but not healthy controls, exhibited a significantly longer duration of melatonin release in winter relative to themselves in summer (Wehr et al., 2001). Due to the lack of replicated, controlled studies, it remains unclear whether SAD involves an abnormal lengthening of the total duration of nocturnal melatonin release as a unique photoperiodic response and how this might trigger clinical depression.
Retinal Subsensitivity to Light
Another mechanism that could account for the relationship between short photoperiod in winter and risk for SAD, as well as the benefits of light therapy, involves aberrant functioning of retinal photoreceptors. Melanopsin is a recently discovered nonvisual photopigment in the mammalian retinal ganglion cells that projects nonvisually dependent photoreception to the SCN via the RHT as supplementary input to ocular light (Gooley, Lu, Chou, Scrammell, & Saper, 2001; Gooley, Lu, Fischer, & Saper, 2003; Provencio et al., 2000). Experimental studies have demonstrated the necessity of melanopsin input for sufficient circadian functioning (Panda et al., 2002; Provencio, Rollag, & Castrucci, 2002). The retinal subsensitivity hypothesis proposes that SAD patients have impaired retinal adaptation (retinal subsensitivity) or heightened sensitivity (supersensitivity) to low light levels, resulting in problems when photoperiod is short during winter (Beersma, 1990; Remé, Terman, & Wirz-Justice, 1990). Some evidence suggests that SAD patients lack an adaptation to low light availability relative to nondepressed controls (Lavoie et al., 2008; Ozaki, Rosenthal, Myers, Schwartz, & Oren, 1995). A recent finding of diminished pupillary response in winter in SAD further supports the retinal subsensitivity hypothesis (Roecklein et al., 2013). Specifically, SAD patients had a smaller post illumination pupil response (PIPR; i.e., less pupil constriction following a blue relative to a red light stimulus) than controls in winter. Further research is needed to determine how retinal sensitivity aberrations may contribute to circadian functioning and/or depression in SAD.
Some research has pointed to the role of clock gene abnormalities in SAD. For instance, the Leu/Ser polymorphism in Npas2 has been associated with SAD and diurnal preference, but not with seasonality, implicating polymorphisms in susceptibility to certain SAD symptoms (Johannsson et al., 2003). Another study found additive effects of single-nucleotide polymorphisms in three clock genes (Per2, Arntl, and Npas2) shown to be central to pacemaker functioning in predicting risk for SAD, suggesting a possible genetic profile of SAD vulnerability (Partonen et al., 2007). The first study to examine the melanopsin OPN4 gene in SAD found that individuals with a missense variant, the T/T genotype at P10L, were 5.6 times more likely to be in the SAD than in the healthy control group (Roecklein et al., 2009). Although research has implicated the role of the serotonin transporter, 5-HTTLPR, in nonseasonal depression, preliminary studies do not support its role in SAD (see Rohan, Roecklein, & Haaga, 2009). These findings suggest that at least partially different genetic vulnerabilities might underlie SAD versus nonseasonal depression.
Research supports the role of serotonin (5-HT) in SAD. 5-HT fluctuates in humans across seasons, with the highest 5-HT levels in summer and lowest in winter (Carlsson, Svennerholm, & Winblad, 1980; Lambert, Reid, Kaye, Jennings, & Esler, 2002). 5-HT has also been implicated in the circadian system, as it has been shown to mediate the effects of light on the circadian clock via nonvisual pathways (Yannielli & Harrington, 2004). Experimentally induced reductions in both 5-HT as well as norephinephrine (NE) have been shown to produce relapse in SAD patients otherwise remitted with light therapy (Lam et al., 2006; Neumeister et al., 1998). As indirect support for a role of serotonin in SAD, serotonergic pharmaceutical agents have shown some success in treating SAD (Moscovitch et al., 2004; also see Chapter 32 of this book). Future research should aim to further clarify the role of 5-HT and/or NE levels in SAD onset and treatment (see Chapter 17, this volume).
Several studies have found that cognitive vulnerability constructs derived from cognitive theories of depression correlate with SAD (for a review see Young & Yap, 2010). Analogous to the pattern in nonseasonal depression, SAD patients generally show a stronger endorsement of dysfunctional attitudes and a more negative attributional style than never-depressed controls when depressed in the winter, but score comparably to controls on these measures when assessed during summer remission. In addition, individuals with SAD and nonseasonal depression do not differ in dysfunctional attitudes (p. 259) or attributional style when acutely depressed. It is unknown if cognitive reactivity (i.e., change in dysfunctional attitudes across a dysphoric mood induction when euthymic) is relevant to SAD.
In addition to cognitive contents such as dysfunctional attitudes and negative attributions, rumination as a cognitive process (Nolen-Hoeksema, 1991) appears to distinguish SAD and nonseasonally depressed patients from never-depressed controls (see Young & Yap, 2010). Greater endorsement of a ruminative response style as a trait as well as more frequent prospectively assessed ruminative behaviors in the fall are both associated with more severe SAD symptoms the following winter, after controlling for fall depressive symptoms. It is possible that the combination of a strong tendency to ruminate and high levels of fatigue in the winter contributes to SAD onset and/or maintenance. A daily monitoring study over 2 weeks in the winter found that the effect of SAD patients’ daily fatigue on daily mood was moderated by their daily ruminations specifically about fatigue, such that low mood increased as fatigue increased on days with more ruminations about fatigue (Young, Reardon, & Azam, 2008).
Although wintertime anhedonia is a highly prevalent SAD symptom, surprisingly few studies have examined behavioral vulnerabilities to SAD. One study found that SAD patients, but not never-depressed controls, showed variability in response-contingent positive reinforcement across the seasons with the lowest pleasant event frequency/enjoyment in winter and the highest in summer (Rohan, Sigmon, & Dorhofer, 2003). As another behaviorally and/or cognitively mediated potential vulnerability, SAD patients show distinct patterns of emotional responding to light and season visual cues represented in outdoor stimuli across both self-reported affect and psychophysiology (see Rohan et al., 2009 and Young & Yap, 2010 for reviews). Specifically, SAD patients have generally reported more dysphoric mood to overcast and winter scenes and improved mood in response to sunny and summer scenes whereas never-depressed controls do not show affective variation in their responses to these stimuli. In addition, SAD patients uniquely demonstrate psychophysiological changes upon exposure to winter (i.e., increased skin conductance) and to overcast [i.e., skin conductance as well as greater surface facial electromyographic (EMG) responses in the corrugator or brow-pursing muscle] outdoor images (Tierney Lindsey, Rohan, Roecklein, & Mahon, 2011).
The Status of SAD Etiology: Summary and Integration
Although studies using remitted depression paradigms can inform factors associated with SAD maintenance, the field of SAD vulnerability research as a whole is lacking the kinds of designs (i.e., prospective longitudinal studies of initially SAD-free individuals who later develop the condition) to make definitive statements about the etiology of initial SAD onset. It seems unlikely that any one biological or psychological vulnerability factor will explain all cases of SAD. It appears more plausible that one or more seasonally linked environmental stressors triggers a cascade of underlying vulnerabilities that differ in presence and sequence across individuals with SAD and perhaps even differ across episodes within individuals.
In an expansion of Young’s dual vulnerability model (Young, Watel, Lahmeyer, & Eastman, 1991), Rohan et al. (2009) proposed the integrative cognitive-behavioral model of SAD as a comprehensive framework for future work that integrates biological, cognitive, and behavioral vulnerabilities to understand SAD onset, maintenance, and remission. According to the model, the first step in the chain of events leading to a given SAD episode occurs when there is sufficient environmental provocation (e.g., reduced photoperiod, cues that the seasons are changing such as leaves changing color or trigger calendar dates such as the end of daylight saving time) and/or when the individual experiences a conditioned negative anticipation of the winter. Therefore, down-spiraling into a SAD episode could be initially precipitated by a purely autonomous process in reaction to an environmental stressor or more of a reactive psychological process. However, these two components might be interrelated (e.g., someone with a history of SAD might begin to have catastrophic negative thoughts about the coming winter in reaction to certain calendar dates or cues signaling the end of summer). Based on the model, the presence of one, the other, or both of these initial triggers leads to the same result: activation of the psychological and biological vulnerabilities to SAD described above, giving rise to the affective, behavioral, cognitive, and somatic symptoms that comprise the clinical manifestation of SAD. The model assumes that symptoms persist until there is sufficient environmental change (e.g., longer photoperiods, cues signaling the arrival of spring such as the first crocus) and/or positive expectations surrounding the occurrence of spring/summer, triggering a gradual reversal of symptoms.
(p. 260) Treatment
The most studied treatment for SAD is light therapy, involving daily exposure to bright artificial light. Traditional light boxes tested in the majority of clinical trials emit 10,000 lux2 of full-spectrum or cool white fluorescent light, with ultraviolet rays filtered out, and with a surface of at least one square foot. Some newer studies are testing smaller devices containing either white or blue light-emitting diodes (LEDs). A recent study found that LEDs emitting short wavelength, LED blue-spectrum light (468 nm) suppressed melatonin levels acutely and reduced SAD severity as compared to a dim red light placebo (654 nm; Glickman, Byrne, Pineda, Hauck, & Brainard, 2006). However, widespread adoption of blue light therapy remains controversial in the field due to concerns about possible retinal toxicity. Clinical practice guidelines recommend daily light therapy from first symptom onset until the typical time of spontaneous remission in the spring (Lam & Levitt, 1999). Given that light therapy requires consistent use to be effective, compliance with this regimen during the symptomatic months is considered crucial. A retrospective follow-up study reported that only 41% of SAD patients treated in a light therapy trial continued using the treatment over subsequent winter seasons (Schwartz, Brown, Wehr, & Rosenthal, 1996). There is expert consensus that light therapy should be supervised by a clinician with some basic knowledge of chronotherapeutics and that the daily duration and timing of light therapy should be tailored to the individual (see Terman & Terman, 2013). Thirty minutes in the morning upon waking is a common starting dose, but this may need to be titrated up to elicit a response, temporarily reduced to alleviate side effects (e.g., headache, eye strain, mania/hypomania), or shifted to the evening to reduce an evident phase advance.
In a meta-analytic review of randomized, controlled light therapy trials, Golden et al. (2005) found that light therapy was associated with significantly greater improvements in depressive symptoms relative to credible controls. A larger proportion of SAD patients fully remit with morning light therapy administration (53%), as compared with evening light (38%), midday light (32%), or placebo (11%; Terman et al., 1989). The best response might be achieved by very early exposure (i.e., rise 30 minutes earlier than usual to initiate light therapy). However, light administration immediately upon waking is typically used in research and practice to avoid sleep disruption (Terman et al., 2001).
The mechanism underlying light therapy’s antidepressant effect on SAD (e.g., correcting circadian misalignment according to the phase shift hypothesis) remains unknown. By suppressing pineal melatonin production, bright light acts as the primary time cue for the circadian clock. Bright light exerts circadian phase shifts according to a phase response curve, such that morning light advances, and evening light delays, the circadian rhythm (Czeisler et al., 1989). As mentioned earlier, the superiority of morning light exposure to evening light administration indirectly supports the phase shift hypothesis. However, results remain mixed regarding whether phase shifts are necessary for an antidepressant response in SAD, as some studies have found that the degree of phase shift is predictive of treatment outcome (Terman et al., 2001), whereas others have not (Burgess et al., 2004; Eastman et al.,1993). Future research is needed to identify the causal mechanism of light therapy and to identify strategies that might yield greater long-term patient compliance.
Antidepressants are comparably effective to light therapy in the treatment of SAD. In a multisite Canadian study (Lam et al., 2006), 96 SAD patients were randomly assigned to receive 8 weeks of light therapy (10,000 lux) and a pill placebo or fluoxetine (20 mg, daily) and placebo light (100 lux). There were no treatment group differences in the proportions of responses or remissions. Bupropion XL is the only FDA-approved drug for SAD, specifically for SAD recurrence prevention. Three double-blind, placebo-controlled trials allocated 1,042 SAD patients to receive either 300 mg of bupropion XL or pill placebo prior to SAD symptom onset in fall, continuing through March (Modell et al., 2005). The proportion of recurrences was significantly smaller for bupropion (16%) than placebo (28%), although both were quite low.
Cognitive–behavioral therapy (CBT) is the only type of psychotherapy that has been empirically tested for SAD. The protocol for conducting CBT tailored to SAD (CBT-SAD; Rohan, 2008) was modeled on cognitive therapy for depression (Beck, Rush, Shaw, & Emory, 1979). It retains the traditional treatment components of behavioral activation (i.e., identifying and scheduling enjoyable (p. 261) activities), cognitive restructuring (i.e., recording and modifying negative automatic thoughts and core beliefs using the Socratic method), and relapse prevention (i.e., using the skills learned in therapy to prevent relapse/recurrence). In CBT-SAD, these intervention components are framed as ways to foster proactive coping with the fall/winter season and associated environmental stimuli (e.g., short photoperiod, cues that the seasons are changing such as fall foliage, triggering dates such as the end of daylight savings time) so that depression can be alleviated in the present and prevented during future fall/winter seasons. Therefore, unlike cognitive therapy for nonseasonal depression, the intervention components have a “seasonal twist” (e.g., problem-solving wintertime activities that are available and enjoyable; cognitive restructuring of negative thoughts about the winter season and their associated meanings; explicitly implementing recurrence prevention efforts as summer transitions to fall). The protocol consists of 12 1-½ hour sequenced group therapy sessions, delivered at a rate of twice per week over 6 weeks during the fall and/or winter and completed ahead of spontaneous springtime remission.
The initial randomized clinical trials included a total of 87 acutely symptomatic adults with SAD in the greater Washington, DC area and found that CBT-SAD, light therapy, and their combination showed comparable outcomes and were all superior to a wait-list control across a 6-week intervention trial in the winter (Rohan, Tierney Lindsey, Roecklein, & Lacy, 2004; Rohan et al., 2007). At follow-up the next winter, solo CBT-SAD was associated with fewer depression recurrences and less severe symptoms than solo light therapy, but the combination of CBT-SAD plus light therapy did not do as well as solo CBT-SAD (Rohan, Roecklein, Lacy, & Vacek, 2009). A recent clinical trial randomized 177 SAD patients in Vermont to CBT-SAD or light therapy. The study included an ecologically valid sample that allowed for some comorbidities and stable antidepressant use and enlisted community therapists to deliver CBT-SAD. Both treatments showed large and comparable improvements in SAD symptoms during the acute 6-weeks treatment phase and very similar remission proportions at treatment endpoint (47.6% in CBT-SAD vs. 47.2% in LT; Rohan et al., 2015). The treatments did not differ on outcomes the next winter, perhaps due to the frequent assessment protocol over the first year. However, two winters after treatment, CBT-SAD showed fewer depression recurrences (27.3% vs. 45.6%) and less severe symptoms than light therapy (Rohan et al., 2016). The evidence base for CBT-SAD is promising, especially with regard to long-term SAD outcomes.
Dawn simulation uses a device to program the onset of an artificial summer dawn by gradually increasing ambient light intensity in the bedroom up to 250 lux by the desired wake time. Most direct comparisons found that standard light therapy was more effective than dawn simulation as a stand-alone SAD treatment; however, a recent SAD trial found that light therapy and dawn simulation (0.0003–250 lux in the pattern of May 5 at 45° North latitude) yielded similar improvements (Terman & Terman, 2006) and comparable phase advances (~30 minutes; Terman & Terman, 2010).
Negative Air Ions
Although it is not known how or why negatively charged ions (i.e., air particles) would have antidepressant effects, some clinical trials for SAD have tested the efficacy of negative ion generators, which produce negatively charged ions at a high flow rate to maintain an overall high density of negative relative to positive ions in the immediate vicinity. The treatment is administered either first thing in the morning or during the end of sleep using a grounded conductive bed sheet. A recent trial found that high-density negative ions are comparably effective to light therapy in treating SAD and that both active treatments are more effective than low-density negative ions (Terman & Terman, 2006). Similar to dawn simulation, the efficacy of negative air ions in SAD treatment requires replication.
Some have speculated that physical activity and exercise might be antidepressant for SAD through chronobiological mechanisms similar to those proposed for light therapy (see Peiser, 2009). Only two clinical trials have tested an exercise intervention for SAD. Pinchasov, Shurgaja, Grischin, and Putilov (2000) found that women with SAD randomized to 1 week of daily afternoon treatment with either light therapy or aerobic exercise on a stationary bike (i.e., two 27-minute pedaling sessions, separated by a 5-minute rest, including a 5-minute warm up, 12 minutes of basic pedaling, and 10 minutes of pedaling at 75% maximal heart rate) showed comparable improvements in depression, and both improved more than an untreated control group.
(p. 262) In a nonrandomized SAD trial comparing natural (i.e., outdoor) morning light exposure to a low-dose morning light therapy placebo control group, the active intervention consisted of going outdoors daily for an hour “as early in the morning as possible” (Wirz-Justice et al., 1996). Although activity was not prescribed while outdoors for natural light treatment, it was reported that “nearly all walked most of the time (none were joggers).” After 2 weeks, the natural light group showed greater improvements in depression and a larger proportion in remission relative to the placebo light therapy group. Because the active intervention group generally engaged in some form of physical activity concurrent with natural light exposure, it is not known which intervention component(s) were associated with improvements. The field of exercise intervention for SAD is small and inconclusive presently, but warrants further study.
SAD is a fascinating subtype of recurrent depression in that its predictably recurrent pattern facilitates the study of antecedents, concomitants, and consequences of winter depression. The camps of researchers working in the field range from photobiologists to psychiatrists and clinical psychologists, setting the stage for potentially exciting multidisciplinary collaborations toward a better understanding of SAD. As existing studies to date rely on already diagnosed SAD patients, little is known about more distal vulnerabilities for initial development of seasonal symptoms. Effective treatment options are available, but no single treatment produces full remission in all cases. There is more work to be done in terms of developing new treatments and possibly sequencing treatments to optimize outcomes acutely and in the long term.
Questions for Future Research
Future research should investigate which vulnerabilities (chronobiological, cognitive, or a combination) best predict the initial development (i.e., first onset) and annual recurrence of SAD. The field would benefit from stronger integration of theory and treatment. For example, research should examine whether any of these vulnerabilities predict the most effective treatment modality for a given patient or constitute a mechanism of action underlying effective treatment. In addition, SAD patients would benefit if researchers adopt a long-term perspective on the disorder, geared toward optimizing treatment to prevent annual recurrence.
Agumadu, C. O., Yousufi, S. M., Malik, I. S., Nguyen, M. C., Jackson, M. A., Soleymani, K., … Postolache, T. T. (2004). Seasonal variation in mood in African American college students in the Washington, D.C., metropolitan area. American Journal of Psychiatry, 161, 1084–1089. http://www.ncbi.nlm.nih.gov/pubmed/15169697 Find this resource:
American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders: DSM-V. Washington, DC: American Psychiatric Association.Find this resource:
Avery, D. H., Dahl, K., Savage, M. V., Brenglemann, G. L., Larsen, L. H., Kenny, M. A., … Prinz, P. N. (1997). Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression. Biological Psychiatry, 41, 1109–1123. doi:10.1016/S0006-3223(96)00210-7Find this resource:
Beck, A. T., Rush, J. A., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression. New York, NY: Guilford Press.Find this resource:
Beersma, D. G. M. (1990). Do winter depressives experience summer nights in winter? Archives of General Psychiatry, 47, 879–880. http://www.ncbi.nlm.nih.gov/pubmed/2393349 Find this resource:
Benloucif, S., Burgess, H. J., Klerman, E. B., Lewy, A. J., Benita, M., Middleton, B., … Revell, V. L. (2008). Measuring melatonin in humans. Journal of Clinical Sleep Medicine, 4(1), 66–69. http://www.ncbi.nlm.nih.gov/pubmed/18350967 Find this resource:
Benloucif, S., Guico, M. J., Reid, K. J., Wolfe, L. F., L’Hermite-Baleriaux, M. L., & Zee, P. C. (2005). Stability of melatonin and temperature as circadian phase markers and their relation to sleep times in humans. Journal of Biological Rhythms, 20(2), 178–188. doi:10.1177/0748730404273983Find this resource:
Blazer, D. G., Kessler, R. C., & Swartz, M. S. (1998). Epidemiology of recurrent major and minor depression with a seasonal pattern. The National Comorbidity Survey. British Journal of Psychiatry, 172, 164–167. doi:10.1192/bjp.172.2.164Find this resource:
Burgess, H. J., Fogg, L. F., Young, M. A., & Eastman, C. I. (2004). Bright light therapy for winter depression: Is phase advancing beneficial? Chronobiology International, 21(4–5), 759–775. doi:10.1081/CBI-200025979Find this resource:
Carlsson, A., Svennerholm, L., & Winblad, B. (1980). Seasonal and circadian monoamine variations in human brains examined post mortem. Acta Psychiatrica Scandinavica Supplement, 280, 75–85. doi:10.1016/S0140-6736(02)11737-5Find this resource:
Checkley, S. A., Murphy, D. G., M., Abbas, M., Marks, M., Winton, F., Palazidou, E., … Arendt, J. (1993). Melatonin rhythms in seasonal affective disorder. The British Journal of Psychiatry, 163, 332–337. doi:10.1192/bjp.163.3.332.Find this resource:
Czeisler, C. A., Kronauer, R. E., Allan, J. S., Duffy, J. F., Jewett, M. E., Brown, E. N., & Ronda, J. M. (1989). Bright light induction of a strong (type 0) resetting of the human circadian pacemaker. Science, 244, 1328–1333. doi:10.1126/science.2734611Find this resource:
(p. 263) Dahl, K., Avery, D. H., & Lewy, A. J. (1993). Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression. Acta Psychiatrica Scandinavica, 88, 60–66. doi:10.1111/j.1600-0447.1993.tb03414.xFind this resource:
Eastman, C. I. (1990). Natural summer and winter sunlight exposure patterns in seasonal affective disorder. Physiology & Behavior, 48(5), 611–616. doi.org/10.1016/0031-9384(90)90199-EFind this resource:
Eastman, C. I., Gallo, L. C., Lahmeyer, H. W., & Fogg, L. W. (1993). The circadian rhythm of temperature during light treatment for winter depression. Biological Psychiatry, 34(4), 210–220. http://www.ncbi.nlm.nih.gov/pubmed/399817 Find this resource:
Eastman, C., Young, M. A., Fogg, L. F. & Meaden, P. M. (1998). Bright light treatment for winter depression. Archives of General Psychiatry, 55, 883-889. http://archpsyc.ama-assn.org/cgi/content/full/55/10/883 Find this resource:
Glickman, G., Byrne, B., Pineda, C., Hauck, W.W., & Brainard, G.C. (2006). Light therapy for seasonal affective disorder with blue narrow-band light-emitting diodes (LEDs). Biological Psychiatry, 59, 502–507. http://www.ncbi.nlm.nih.gov/pubmed/16165105 Find this resource:
Golden, R. N., Gaynes, B. N., Ekstrom, R. D., Hamer, R. K., Jacobson, F. M., Suppes, T., … Nemeroff, C. B. (2005). The efficacy of light therapy in the treatment of mood disorders: A review and meta-analysis of the evidence. American Journal of Psychiatry, 162, 656–662. http://www.ncbi.nlm.nih.gov/pubmed/15800134 Find this resource:
Gooley, J. J., Lu, J., Fischer, D., & Saper, C. B. (2003). A broad role for melanopsin in nonvisual photoreception. Journal of Neuroscience, 23, 7093–7106. doi: 10.1038/nature10206Find this resource:
Gooley, J. J., Lu, J., Chou, T. C., Scammell, T. E., & Saper, C. B. (2001). Melanopsin in cells of origin of the retinohypothalamic tract. Nature Neuroscience, 4, 1165. Doi: 10.1038/nn768Find this resource:
Graw, P., Recker, S., Sand, L., Krauchi, K., & Wirz-Justice, A. (1999). Winter and summer outdoor light exposure in women with and without seasonal affective disorder. Journal of Affective Disorders, 56, 163–169. doi:10.1016/S0165-0327(99)00037-3Find this resource:
Johannsson, C., Willeit, M., Smedh, C., Ekholm, J., Paunio, T., Kieseppa, T., … Partonen, T. (2003). Circadian clock-related polymorphisms in seasonal affective disorder and their relevance to diurnal preference. Neuropsychopharmacology, 28, 734–739. doi:10.1038/sj.npp.1300121Find this resource:
Kasper, S., Wehr, T. A., & Bartko, J. J. (1989). Epidemiological findings of seasonal changes in mood and behavior: A telephone survey of Montgomery County, Maryland. Archives of General Psychiatry, 46, 823–833. http://www.ncbi.nlm.nih.gov/pubmed/2789026 Find this resource:
Koorengevel, K. M., Beersma, D. G., den Boer, J. A., & van den Hoofdakker, R. H. (2003). A mood regulation in seasonal affective disorder patients and healthy controls studied in forced desynchrony. Psychiatry Research, 117, 57–74. http://www.ncbi.nlm.nih.gov/pubmed/12581821 Find this resource:
Lam, R. W., & Levitt, A. J. (1999). Clinical guidelines for the treatment of seasonal affective disorder. Vancouver, BC: Clinical & Academic Publishing.Find this resource:
Lam, R. W., Levitt, A. J., Levitan, R. D., Enns, M., Morehouse, R. L., Michalak, E. E., & Tam, E. M. (2006). The CAN-SAD study: A randomized controlled study of light therapy and fluoxetine in patients with winter seasonal affective disorder. American Journal of Psychiatry, 163, 805-812. http://www.ncbi.nlm.nih.gov/pubmed/16648320 Find this resource:
Lambert, G., Reid, C., Kaye, D., Jennings, G., & Esler, M. (2002). Effect of sunlight and season on serotonin turnover in the brain. Lancet, 360, 1840–1842. doi:10.1016/S0140-6736(02)11737-5Find this resource:
Lavoie, M., Lam, R. W., Bouchard, G., Sasseville, A., Charron, M., Gagne, A., … Hébert, M. (2008). Evidence of a biological effect of light therapy on the retina of patients with seasonal affective disorder. Biological Psychiatry, 66, 253–258. doi:10.1016/j.biopsych.2008.11.020Find this resource:
Levitt, A. J., & Boyle, M. H. (2002). The impact of latitude on the prevalence of seasonal depression. Canadian Journal of Psychiatry, 47, 361–367. http://www.ncbi.nlm.nih.gov/pubmed/12025435 Find this resource:
Levitt, A. J., Boyle, M. H., Joffe, R. T., & Baumal, Z. (2000). Estimated prevalence of the seasonal subtype of major depression in a Canadian community sample. Canadian Journal of Psychiatry, 45, 650–654. http://www.ncbi.nlm.nih.gov/pubmed/11056828 Find this resource:
Lewy, A. J., Lefler, B. J., & Emens, J. S. (2006). The circadian basis of winter depression. Proceedings of the National Academy of Sciences USA, 103, 7414–7419. doi:10.1073/pnas.0602425103Find this resource:
Lewy, A. J., Lefler, B. J., Hasler, B. P., Bauer, V. K., Bernert, R. A., & Emens, J. S. (2003). Plasma DLMO10 zeitgeber time 14: The therapeutic window for phase-delayed winter depressives treated with melatonin. Chronobiological International, 20, 1215-1216.Find this resource:
Lewy, A. J., Sack, R. L., & Singer, C. M. (1988). Winter depression and the phase shift hypothesis for bright light’s therapeutic effects: History, theory and experimental evidence. Journal of Biological Rhythms, 3(2), 121–134. http://www.ncbi.nlm.nih.gov/pubmed/2979635 Find this resource:
Lewy, A. J., Sack, R. L., Singer, C. M., & White, D. M. (1987). The phase shift hypothesis for bright light’s therapeutic mechanism of action: Theoretical considerations and experimental evidence. Psychopharmacology Bulletin, 23(3), 349–353. http://www.ncbi.nlm.nih.gov/pubmed/3324148 Find this resource:
Magnusson, A. (2000). An overview of epidemiological studies on seasonal affective disorder. Acta Psychiatrica Scandinavica, 101, 176–184. doi:10.1034/j.1600-0447.2000.101003176.xFind this resource:
Magnusson, A., & Axelsson, J. (1993). The prevalence of seasonal affective disorder is low among descendants of Icelandic emigrants in Canada. Archives of General Psychiatry, 50, 947–951. http://www.ncbi.nlm.nih.gov/pubmed/8250680 Find this resource:
Magnusson, A., & Partonen, T. (2010). Prevalence. In T. Partonen & S. R. Pandi-Perumal (Eds.), Seasonal affective disorder: Practice and research (2nd ed., pp. 221–234). New York, NY: Oxford University Press.Find this resource:
Magnusson, A., & Stefansson, J. G. (1993). Prevalence of seasonal affective disorder in Iceland. Archives of General Psychiatry, 50, 941–946. http://www.ncbi.nlm.nih.gov/pubmed/8250679 Find this resource:
Mersch, P. P. A., Middendorp, H. M., Bouhuys, A. L., Beersma, D. G. M., & van den Hoofdakker, R. H. (1999). Seasonal affective disorder and latitude: A review of the literature. Journal of Affective Disorders, 53, 35–48. http://www.ncbi.nlm.nih.gov/pubmed/10363665 Find this resource:
Modell, J. G., Rosenthal, N. E., Harriett, A. E., Krishen, A., Asgharian, A., Foster, V. J., … Wightman, D. S. (2005). Seasonal affective disorder d its prevention by anticipatory treatment with buproprion XL. Biological Psychiatry, 15, 658–667. doi: 10.1016/j.biopsych.2005.07.021Find this resource:
(p. 264) Moscovitch, A., Blashko, C. A., Eagles, J. M., Darcourt, G., Thompson, C., Kasper, S., & Lane, R. M. (2004). A placebo-controlled study of sertraline in the treatment of outpatients with seasonal affective disorder. Psychopharmacology (Berl), 171, 390–397. doi:10.1007/s00213-003-1594-8Find this resource:
Neumeister, A., Turner, E. H., Matthews, J. R., Postolache, T. T.,Barnett, R. L., Rauh, M., … Rosenthal, N. E. (1998). Effects of trypophan depletion vs catecholamine depletion in patients with seasonal affective disorder in remission with light therapy. Archives of General Psychiatry, 55, 524–530. doi:10.1001/archpsyc.55.6.524Find this resource:
Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal Psychology, 100(4), 569–582. http://www.ncbi.nlm.nih.gov/pubmed/1757671 Find this resource:
Oren, D. A., Levendosky, A. A., Kasper, S., Duncan, C. C., & Rosenthal, N. E. (1996). Circadian profiles of cortisol, prolactin, and thyrotropin in seasonal affective disorder. Biological Psychiatry, 39, 157–170. http://www.ncbi.nlm.nih.gov/pubmed/8837977 Find this resource:
Oren, D. A., Moul, D. E., Schwartz, P. J., & Brown, C. (1994). Exposure to ambient light in patients with winter seasonal affective disorder. American Journal of Psychiatry, 151(4), 591–593. http://www.ncbi.nlm.nih.gov/pubmed/8147459 Find this resource:
Ozaki, N., Rosenthal, N. E., Myers, F., Schwartz, P. J., & Oren, D. A. (1995). Effects of season on electro-oculographic ratio in winter seasonal affective disorder. Psychiatry Research, 59(1–2), 151–155. http://www.ncbi.nlm.nih.gov/pubmed/8771230 Find this resource:
Panda, S., Sato, T. K., Castrucci, A. M., Rollag, M. D., DeGrip, W. J., Hogenesch, J. B., … Kay, S. A. (2002). Melanopsin (Opn4) requirement for normal light-induced circadian phase shifting. Science, 298 (5601), 2213–2216. doi:10.1126/science.1076848Find this resource:
Partonen, T., Treutlein, J., Alpman, A., Frank, J., Johansson, C., Depner, M., … Schumann, G. (2007). Three circadian clock genes Per2, Arntl, and Npas2 contribute to winter depression. Annals of Medicine, 39, 229–238.Find this resource:
Peiser, B. (2009). Seasonal affective disorder and exercise treatment: A review. Biological Rhythm Research, 40(1), 85–97. doi:10.1080/09291010802067171Find this resource:
Pinchasov, B. B., Shurgaja, A. M., Grischin, O. V., & Putilov, A. A. (2000). Mood and energy regulation in seasonal and non-seasonal depression before and after midday treatment with physical exercise or bright light. Psychiatry Research, 94(1), 29–42. http://www.ncbi.nlm.nih.gov/pubmed/10788675 Find this resource:
Provencio, I., Rodriguez, I. R., Jiang, G., Hayes, W. P., Moriera, E. F., & Rollag, M. D. (2000). A novel human opsin in the inner retina. Journal of Neuroscience, 20(2), 600–605. http://www.ncbi.nlm.nih.gov/pubmed/10632589 Find this resource:
Provencio, I., Rollag, M. D., & Castrucci, A. M. (2002). Photoreceptive net in the mammalian retina: This mesh of cells may explain how some blind mice can still tell day from night. Nature, 415(6871), 493. http://www.ncbi.nlm.nih.gov/pubmed/11823848 Find this resource:
Remé, C. E., Terman, M., & Wirz-Justice, A. (1990). Are deficient retinal photoreceptor renewal mechanisms involved in the pathogenesis of winter depression? Archives of General Psychiatry, 47, 878–879. http://www.ncbi.nlm.nih.gov/pubmed/2393348 Find this resource:
Roecklein, K. A., Rohan, K. J., Duncan, W. C., Rollag, M. D., Rosenthal, N. E., Lipsky, R. H., … Provencio, I. (2009). A missense variant (P10L) of the melanopsin (OPN4) gene in seasonal affective disorder. Journal of Affective Disorders, 114, 279–285. doi:10.1016/j.jad.2008.08.005Find this resource:
Roecklein, K. A., Wong, P., Ernecoff, N., Miller, M. A., Donofry, S., Kamarck, M., … Franzen, P. (2013). The post illumination pupil response is reduced in seasonal affective disorder. Psychiatry Research, 210, 150-158. doi: 10.1016/j.psychres.2013.05.023.Find this resource:
Rohan, K. J. (2008). Coping with the seasons: A cognitive-behavioral approach to seasonal affective disorder. Therapist guide. New York, NY: Oxford University Press.Find this resource:
Rohan, K. J., Mahon, J. N., Evans, M., Ho, S., Meyerhoff, J., Postolache, T. T., & Vacek, P. M. (2015). Randomized trial of cognitive-behavioral therapy vs. light therapy for seasonal affective disorder: Acute outcomes. American Journal of Psychiatry, 172, 862-869. doi: 10.1176/appi.ajp.2015.14101293Find this resource:
Rohan, K. J., Meyerhoff, J., Ho, S., Evans, M., Postolache, T. T., & Vacek, P. M. (2016). Outcomes one and two winters following cognitive-behavioral therapy or light therapy for seasonal affective disorder. American Journal of Psychiatry, 173, 244–251. doi:10.1176/appi.ajp.2015.15060773Find this resource:
Rohan, K. J., Roecklein, K. A., & Haaga, D. A. F. (2009). Biological and psychological mechanisms of seasonal affective disorder: A review and integration. Current Psychiatry Reviews, 5, 37–47. doi:10.2174/157340009787315299Find this resource:
Rohan, K. J., Roecklein, K. A., Lacy, T. J., & Vacek, P. M. (2009). Winter depression recurrence one year after cognitive-behavioral therapy, light therapy, or combination treatment. Behavior Therapy, 40, 225–238. http://www.ncbi.nlm.nih.gov/pubmed/19647524 Find this resource:
Rohan, K. J., Roecklein, K. A., Tierney Lindsey, K., Johnson, L. G., Lippy, R. D., Lacy, T. J., & Barton, F. B. (2007). A randomized controlled trial of cognitive-behavioral therapy, light therapy, and their combination for seasonal affective disorder. Journal of Consulting and Clinical Psychology, 75, 489–500. doi:10.1037/0022-006X.75.3.489Find this resource:
Rohan, K. J., Sigmon, S. T., & Dorhofer, D. M. (2003). Cognitive-behavioral factors in seasonal affective disorder. Journal of Consulting and Clinical Psychology, 71, 22–30. doi:10.1037/0022-006X.71.1.22Find this resource:
Rohan, K. J., Tierney Lindsey, K., Roecklein, K. A., & Lacy, T. J. (2004). Cognitive-behavioral therapy, light therapy, and their combination in treating seasonal affective disorder. Journal of Affective Disorders, 80, 273–283. doi:10.1016/S0165-0327(03)00098-3Find this resource:
Rosen, L. N., Targum, S. D., & Terman, M. (1990). Prevalence of seasonal affective disorder at four latitudes. Psychiatry Research, 31, 131–144. http://www.ncbi.nlm.nih.gov/pubmed/2326393 Find this resource:
Rosenthal, N. E., Bradt, G. H., & Wehr, T. A. (1984). Seasonal Pattern Assessment Questionnaire. Bethesda, MD: National Institute of Mental Health.Find this resource:
Rosenthal, N. E., Sack, D. A., & Gillin, J. C. (1984). Seasonal affective disorder: A description of the syndrome and preliminary findings with light therapy. Archives of General Psychiatry, 41, 72–80. http://www.ncbi.nlm.nih.gov/pubmed/6581756 Find this resource:
Schwartz, P. J., Brown, C., Wehr, T. A., & Rosenthal, N. E. (1996). Winter seasonal affective disorder: A follow-up study of the first 59 patients of the National Institute of Mental Health Seasonal Studies Program. American Journal of (p. 265) Psychiatry, 153, 1028–1036. http://www.ncbi.nlm.nih.gov/pubmed/8678171 Find this resource:
Suhail, K., & Cochrane, R. (1997). Seasonal changes in affective state in samples of Asian and white women. Social Psychiatry and Psychiatric Epidemiology, 32, 149–157. doi:10.1007/BF00794614Find this resource:
Terman, M., & Terman, J. S. (2006). Controlled trial of naturalistic dawn simulation and negative air ionization for seasonal affective disorder. American Journal of Psychiatry, 163, 2126–2133. doi:10.1176/appi.ajp.163.12.2126Find this resource:
Terman, M., & Terman, J. S. (2010). Circadian rhythm phase advance with dawn simulation treatment for winter depression. Journal of Biological Rhythms, 25, 297–301. doi:10.1177/0748730410374000Find this resource:
Terman, M., & Terman, J. S. (2013). Chronotherapeutics: Light therapy, wake therapy, and melatonin. In J. J. Mann, S. P. Roose, & P. J. McGrath (Eds.), Clinical handbook for the management of mood disorders. New York, NY: Cambridge University Press.Find this resource:
Terman, M., Terman, J. S., & Cooper, T. B. (2001). Circadian time of morning light administration and therapeutic response in winter depression. Archives of General Psychiatry, 58, 69–75. http://www.ncbi.nlm.nih.gov/pubmed/11146760 Find this resource:
Terman, M., Terman, J. S., & Quitkin, F. M. (1989). Light therapy for seasonal affective disorder: A review of the efficacy. Neuropsychopharmacology, 2, 1–22. http://www.ncbi.nlm.nih.gov/pubmed/2679625 Find this resource:
Terman, M., Terman, J. S., & Ross, D. C. (1998). A controlled trial of timed bright light and negative air ionization for treatment of winter depression. Archives of General Psychiatry, 55, 875–882. http://www.ncbi.nlm.nih.gov/pubmed/9783557 Find this resource:
Thompson, C., Childs, P. A., Martin, N. J., Rodin, I., & Smythe, P. J. (1997). Effects of morning phototherapy on circadian markers in seasonal affective disorder. The British Journal of Psychiatry, 170, 431–435. doi:10.1192/bjp.170.5.431Find this resource:
Tierney Lindsey, K., Rohan, K. J., Roecklein, K. A., & Mahon, J. N. (2011). Surface facial electromyography, skin conductance, and self-reported emotional responses to light- and season-relevant stimuli in seasonal affective disorder. Journal of Affective Disorders, 133, 311–319. doi:10.1016/j.jad.2011.04.016Find this resource:
Wehr, T. A. (2001). Photoperiodism in humans and other primates: Evidence and implications. Journal of Biological Rhythms, 16(4), 348–364. http://www.ncbi.nlm.nih.gov/pubmed/11506380 Find this resource:
Wehr, T. A., Duncan, W. C., Sher, L., Aeschbach, D., Schwartz, P. J., Turner, E. H., … Rosenthal, N. E. (2001). A circadian signal of change of season in patients with seasonal affective disorder. Archives of General Psychiatry, 58, 1108–1114. http://www.ncbi.nlm.nih.gov/pubmed/11735838 Find this resource:
Wirz-Justice, A., Graw, P., Kräuchi, K., Sarrafzadeh, A., English, J., Arendt, J., & Sand, L. (1996). “Natural” light treatment of seasonal affective disorder. Journal of Affective Disorders, 37, 109–120. http://www.ncbi.nlm.nih.gov/pubmed/8731073 Find this resource:
Yannielli, P., & Harrington, M. E. (2004). Let there be “more” light: Enhancement of light actions on the circadian system through non-photic pathways. Progress in Neurobiology, 74, 59–76. doi:10.1016/j.pneurobio.2004.06.001Find this resource:
Young, M. A., Meaden, P. M., Fogg, L. F., Cherin, E. A., & Eastman, C. I. (1997). Which environmental variables are related to the onset of seasonal affective disorder? Journal of Abnormal Psychology, 106, 554–562. doi:10.1037/0021-843X.106.4.554Find this resource:
Young, M. A., Reardon, A., & Azam, O. (2008). Rumination and vegetative symptoms: A test of the dual vulnerability model of seasonal depression. Cognitive Therapy and Research, 32, 567–576. doi:10.1007/s10608-008-9184-zFind this resource:
Young, M. A., Watel, L. G., Lahmeyer, H. W., & Eastman, C. I. (1991). The temporal onset of individual symptoms in winter depression: Differentiating underlying mechanisms. Journal of Affective Disorders, 22, 191–197. doi:10.1016/0165-0327(91)90065-ZFind this resource:
Young, M. A., & Yap, B. J. (2010). Psychological and biological traits in seasonal affective disorder. In T. Partonen & S. R. Pandi-Perumal (Eds.), Seasonal affective disorder: Practice and research (pp. 189–208). New York, NY: Oxford University Press.Find this resource:
(1.) We use the generic term “SAD” to refer to winter-type SAD (i.e., recurrent winter major depression) unless otherwise stated.
(2.) The intensity of light in light therapy is substantially greater than ordinary lighting conditions provided by indoor lamps and fixtures in the home or office (typical range at night = 300–700 lux), but is less than natural outdoor light intensity (i.e., up to 100,000 lux on a summer day with a clear sky).