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Seasonal Affective Disorder: "Shedding Light on Wintertime Blues”

James Odell, OMD, ND, LAc

three adults outside in wintertime

What Is Seasonal Affective Disorder?

Seasonal Affective Disorder, also known as SAD, is a type of recurrent major depressive disorder in which episodes of depression occur during the same season each year. This condition is sometimes called the "winter blues," because the most common seasonal pattern is for depressive episodes to appear in the fall or winter and remit in the spring. SAD is not considered a unique diagnostic entity. Rather, it is a type of recurrent major depression with a seasonal pattern. According to the Diagnostic and Statistical Manual of Mental Disorders DSM-5., criteria for depression with a seasonal pattern include having depression that begins and ends during a specific season every year (with full remittance during other seasons) for at least two years and having more seasons of depression than seasons without depression over a lifetime.1 

How Common Is SAD?

Each year, about 5 percent of the U.S. population experiences seasonal affective disorder, with symptoms present for about 40 percent of the year. It is more common among women than men. While Seasonal Affective Disorder is predominantly an adult condition, estimates are that one million children in North America have it. Interestingly, SAD does not occur in the tropics.

SAD was at first believed to be related to abnormal melatonin metabolism, but later findings did not support this hypothesis. Studies of brain serotonin function support the hypothesis of disturbed activity. This article will outline some of the physiological mechanisms involved and common effective therapies for SAD. 


The identification of seasonal patterns for mood disturbances dates to ancient times, with astute medical observers such as Hippocrates, Pinel, and Kraepelin reporting clear recurrent winter depressive episodes in some of their patients.2 

Historically, depressed mood and low energy levels during the short dark days of winter may have always been experienced by some as an expected part of life, particularly for those living far from the equator. This phenomenon was first identified as a treatable clinical condition during the 1980s when physician Norman Rosenthal moved to the US from his native South Africa. He noticed that he felt much less productive in the winter but returned to normal as soon as spring arrived. He wrote a paper describing its symptoms and proposed etiology.3

In Rosenthal’s work at the National Institutes of Health, he collaborated with Al Lewy, who was researching melatonin, and with Tom Wehr who was researching how light suppressed melatonin and impacted circadian rhythms. 

They conducted a study that described 29 patients with SAD; most of them had bipolar affective disorder, especially bipolar II, and their depressions were generally characterized by hypersomnia, overeating, and carbohydrate craving and seemed to respond to changes in climate and latitude. They found that sleep recordings in nine depressed patients confirmed the presence of hypersomnia and showed increased sleep latency and reduced slow-wave (delta) sleep. Preliminary studies in 11 patients suggest that extending the photoperiod with bright artificial light has an antidepressant effect.4 

Together, they applied and disseminated their findings about how bright light could effectively treat patients with SAD. Since then, numerous studies have been conducted investigating the mechanisms underlying SAD as well as treatment protocols.


People with SAD may suffer from general symptoms of depression including diminished pleasure or interest, psychomotor agitation or retardation, loss of energy, feelings of worthlessness or excessive or inappropriate guilt, diminished ability to think or concentrate, indecisiveness, or recurrent thoughts of death. Symptoms may be from mild to severe. Some of the signs and symptoms of SAD are listed below. But it is different for different people and can vary from season to season. Some individuals might experience other kinds of feelings which are not listed here:

  • Lack of energy.

  • Difficulty concentrating.

  • Not wanting to see people.

  • Feeling sad, low, tearful, guilty, or hopeless

  • Feeling anxious, angry, and agitated

  • Being more prone to physical health problems, such as colds, infections, or other illnesses

  • Sleeping too much, or having difficulty waking up (common with SAD in winter)

  • Sleeping too little, or waking up a lot (common with SAD in summer)

  • Changes in appetite, particularly feeling hungrier, and craving sugar.

  • Losing interest in sex or physical contact

  • Suicidal feelings

Increased appetite is typified by carbohydrate cravings for sugars and starches that are often described as uncontrollable. Binge-type eating can occur, although purging behaviors are uncommon. The increased eating and reduced activity usually lead to significant weight gain. With initial winter episodes, patients lose weight during the summer months when their appetite returns to normal, and they are more active. However, with increasing age, it becomes more difficult to shed the winter weight gain and there is a gradual year-round increase in weight. Those with existing mental health problems might find that things get worse at times when affected by SAD.

Pathophysiological Mechanisms of SAD

Despite SAD’s long observed history in medicine, its pathophysiological mechanism(s) have not been completely identified and may be more complex than previously thought. People with SAD may have trouble regulating their levels of serotonin, a neurotransmitter that influences mood. Research has also suggested that people with SAD may produce less vitamin D in response to sunlight. Vitamin D is believed to play a role in serotonin activity; thus, an insufficient vitamin D level can be associated with clinically significant depression symptoms.5 

Vitamin D concentration is assessed by serum 25-hydroxyvitamin D (25-OH D) levels: with optimal levels being at 50 nq/mL; insufficient levels at less than 30 ng/mL; and severely deficient levels at less than 20 ng/mL Low levels of vitamin D are usually due to insufficient dietary intake or lifestyle issues such as little outdoor exposure to sunshine. During the winter months of November through February, those living about 33 degrees north or 30 degrees south of the equator are not able to adequately synthesize vitamin D due to light deprivation.

Another explanation is that the mammalian pineal gland appears to be a major endocrine component in the regulation of photoperiodic responses. The circadian pattern of secretion of the pineal hormone, melatonin (5-methoxy-N-acetyltryptamine), is regulated by the nervous system. Changes in photoperiod, as occur in the winter, act on the nervous system, and alter the temporal pattern of melatonin secretion. The changes in secretion patterns convey information about day length from neural components of the circadian system to the reproductive system, and probably to other physiological systems.6

Pineal melatonin secretion happens almost solely at night; the duration of nocturnal melatonin pulse is inversely related to day length, i.e., a long melatonin pulse signals short days leading to behavioral changes preparing the animals for the cold winter climate, e.g., weight gain, decreased activity, and inhibition of reproduction. 

Although the validity of the melatonin hypothesis has not been conclusively validated or refuted, research findings tend to suggest at least an indirect role of melatonin in the etiology of SAD.

Additionally, there may be a genetic propensity to SAD. The short-allele polymorphism for serotonin transporter is more common in patients with SAD than in healthy people.7, 8, 9

Specifically, a functional polymorphism in the serotonin promoter gene region (5-HTTLPR) has been found to influence serotonin transporter (5-HTT) expression in human cell lines.10, 11 This may explain why some individuals are more prone to experience SAD and why it is more prevalent in certain families.

In short, the similarity between the symptom constellation of SAD and these seasonal physiological changes seen in animals, e.g., weight gain, hypersomnia, and lack of energy, as well as the observation that bright light, while being able to alleviate SAD symptoms and suppress nocturnal pineal melatonin secretion has led to the speculation that SAD is associated with an abnormal body response to the seasonal change in day length.12 Consequently, treatment for SAD has now been focused on lengthening the photoperiod by presenting bright artificial light in the morning and then in the evening to extend the photoperiod.



Because winter depression may be a reaction to lack of sunlight, broad-band light therapy is frequently used as a treatment option. Light treatment has been shown to significantly improve SAD symptoms and may be used as prophylaxis before the subsequent autumn and winter seasons. Light therapy is generally well tolerated, with most patients experiencing clinical improvement within one to two weeks after the start of treatment. To avoid relapse, light therapy should continue through the end of the winter season until spontaneous remission of symptoms in the spring or summer. Pharmacotherapy with antidepressants and cognitive behavior therapy are also appropriate treatment options and have been shown to be as effective as light therapy. Because of the comparable effectiveness of treatment options, first-line management should be guided by patient preference. 

Light Therapy Studies

There have been dozens of positive efficacy studies of light therapy. Two recent systematic reviews have rigorously addressed the light therapy efficacy. The first used Cochrane Collaboration methodology to review 14 randomized controlled trials (RCTs) of light therapy versus control conditions.13

The second was commissioned by the Council on Research of the American Psychiatric Association (APA).14 

Both meta-analyses found that bright light was superior to credible control conditions, with an odds ratio of 2.83 (indicating almost 3 times better odds of achieving response with light therapy) and an effect size of 0.83 (indicating a medium to large treatment effect), respectively. These results show that the therapeutic effects of light therapy are equal to, or greater than, those found in most antidepressant pharmacotherapy trials. 

In clinical practice, the preferred device for light therapy is the full spectrum light box that produces light intensities of greater than 2,500 lux. The lux is the unit of illuminance, or luminous flux per unit area, in the International System of Units (SI). It is equal to one lumen per square meter. In photometry, this is used as a measure of the intensity, as perceived by the human eye, of light that hits or passes through a surface. 

For comparison, indoor evening room light is usually less than 100 lux while a brightly lit office is less than 500 lux. In contrast, outdoor light is much brighter: a cloudy gray winter day is around 4,000 lux and a sunny day can be 50,000 to 100,000 lux or more.15 

For light therapy to be effective the individual must be awake with their eyes open during light exposure, but they are not required to look directly at the light source, i.e., they can read or eat during the light treatment. The standard “dose” of light is 10,000 lux for 30 minutes per day. There appears to be a relationship between intensity and duration of exposure, so light boxes rated at 2,500 lux require 2 hours of daily exposure for the same response.

Light therapy is usually administered in the early morning as soon as possible upon arising, e.g., at 7:00 am or earlier because most studies and meta-analyses have found that early morning exposure is superior to other times of the day.16, 17,18

The onset of action of light therapy is usually rapid with significant clinical improvement found in studies of 1 or 2 weeks’ duration. However, individual patients may require 2–3 weeks to show clear responses to light therapy. When light therapy is discontinued, most patients will relapse after a similar period of a couple of weeks. Patients are therefore encouraged to use light therapy regularly during their symptomatic winter season until the time of their usual spring-summer remission. There are no contraindications to light therapy (although retinopathies are a relative contraindication) and no evidence that light therapy is associated with ocular or retinal damage with current dosing guidelines.19

Choosing a Light Box

When it comes to choosing a light box, there are many offerings on the marketplace. These are the important considerations in choosing a lightbox:

  1. It should be of a certain size – the surface area from which the light comes should be at least one-foot square. Smaller boxes may be less effective – though this has not been thoroughly researched.

  2. Fluorescents are best. The new LED-based light boxes have not been tested as well for safety and efficacy either.

  3. Full-spectrum white is better than blue. Although blue may seem cool, it has not been as well tested as white light, and some experts have voiced safety concerns about blue.

In addition to light therapy, a diet rich in quality proteins, vegetables, unprocessed foods, and complex carbohydrates may be helpful. It may be also advisable to plan winter trips to sunny locales before winter sets in.


Seasonal Affective Disorder (SAD) is a form of recurrent depressive disorder, with episodes that vary in severity typically occurring in the autumn and winter with remission in the spring or summer. Lack of sunlight plays a critical role in decreased serotonin activity, affecting melatonin production, disrupting circadian rhythms, and reducing levels of Vitamin D. SAD was at first believed to be primarily related to abnormal melatonin metabolism, but this has not been definitively confirmed. It is possible that several other mechanisms may also be involved, such as a lack of vitamin D, and genetic abnormalities relating to melatonin. The short-allele polymorphism for serotonin transporter is more common in patients with SAD than in healthy people. Full spectrum light therapy is effective for most people affected by SAD, and the standard treatment regimens include a “dose” of 10,000 lux light for 30 minutes per day. 

Many websites now offer helpful advice and resource materials for the clinical use of light (e.g.,,,


  1. American Psychiatric Association, Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), American Psychiatric Association, Arlington, Va, USA, 2013.

  2. Wehr TA: Seasonal affective disorders: A historical overview. In Rosenthal NE, Blehar MC (eds): Seasonal Affective Disorders and Phototherapy 1989; New York, Guilford Press, 11–32

  3. Rosenthal, N. "What is seasonal affective disorder? Answers from the doctor who first described the condition." Dr. Rosenthal’s personal website, http://www. normanrosenthal. com/seasonal-affective-disorder.

  4. Rosenthal, Norman E., David A. Sack, J. Christian Gillin, Alfred J. Lewy, Frederick K. Goodwin, Yolande Davenport, Peter S. Mueller, David A. Newsome, and Thomas A. Wehr. "Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy." Archives of general psychiatry 41, no. 1 (1984): 72-80.

  5. Anglin, Rebecca ES, Zainab Samaan, Stephen D. Walter, and Sarah D. McDonald. "Vitamin D deficiency and depression in adults: systematic review and meta-analysis." The British Journal of Psychiatry 202, no. 2 (2013): 100-107.

  6. Goldman, Bruce D., and Janet M. Darrow. "The pineal gland and mammalian photoperiodism." Neuroendocrinology 37, no. 5 (1983): 386-396

  7. Rosenthal, Norman E., Chiara M. Mazzanti, Robert L. Barnett, Todd A. Hardin, Elise H. Turner, Garrett K. Lam, Norio Ozaki, and Dana Goldman. "Role of serotonin transporter promoter repeat length polymorphism (5-HTTLPR) in seasonality and seasonal affective disorder." Molecular psychiatry 3, no. 2 (1998): 175-177.

  8. Willeit, M., N. Praschak-Rieder, A. Neumeister, P. Zill, F. Leisch, J. Stastny, E. Hilger et al. "A polymorphism (5-HTTLPR) in the serotonin transporter promoter gene is associated with DSM-IV depression subtypes in seasonal affective disorder." Molecular psychiatry 8, no. 11 (2003): 942-946.

  9. Thierry, Nikolaus, Matthäus Willeit, Nicole Praschak-Rieder, Peter Zill, Kurt Hornik, Alexander Neumeister, Elisabeth Lenzinger et al. "Serotonin transporter promoter gene polymorphic region (5-HTTLPR) and personality in female patients with seasonal affective disorder and in healthy controls." European Neuropsychopharmacology 14, no. 1 (2004): 53-58.

  10. Heils, Armin, Andreas Teufel, Susanne Petri, Gerald Stöber, Peter Riederer, Dietmar Bengel, and K. Peter Lesch. "Allelic variation of human serotonin transporter gene expression." Journal of neurochemistry 66, no. 6 (1996): 2621-2624.

  11. Lesch, Klaus-Peter, Dietmar Bengel, Armin Heils, Sue Z. Sabol, Benjamin D. Greenberg, Susanne Petri, Jonathan Benjamin, Clemens R. Müller, Dean H. Hamer, and Dennis L. Murphy. "Association of anxiety-related traits with a polymorphism in the serotonin transporter gene regulatory region." Science 274, no. 5292 (1996): 1527-1531.

  12. Lewy, Alfred J., Thomas A. Wehr, Frederick K. Goodwin, David A. Newsome, and S. P. Markey. "Light suppresses melatonin secretion in humans." Science 210, no. 4475 (1980): 1267-1269.

  13. Lam, Raymond W., Minnie Y. Teng, Young-Eun Jung, Vanessa C. Evans, John F. Gottlieb, Trisha Chakrabarty, Erin E. Michalak, Jill K. Murphy, Lakshmi N. Yatham, and Dorothy K. Sit. "Light therapy for patients with bipolar depression: systematic review and meta-analysis of randomized controlled trials." The Canadian Journal of Psychiatry 65, no. 5 (2020): 290-300.

  14. Golden RN, Gaynes BN, Ekstrom RD, Hamer RM, Jacobsen FM, Suppes T, Wisner KL, Nemeroff CB: The efficacy of light therapy in the treatment of mood disorders: A review and meta-analysis of the evidence. Am J Psychiatry 2005; 162:656–662

  15. Kripke, Daniel F. "Light treatment for nonseasonal depression: speed, efficacy, and combined treatment." Journal of affective disorders 49, no. 2 (1998): 109-117.

  16. Terman M, Terman JS: Light therapy for seasonal and nonseasonal depression: Efficacy, protocol, safety, and side effects. CNS Spectr 2005; 10:647–663.

  17. Penders, Thomas M., Cornel N. Stanciu, Alexander M. Schoemann, Philip T. Ninan, Richard Bloch, and Sy A. Saeed. "Bright light therapy as augmentation of pharmacotherapy for treatment of depression: a systematic review and meta-analysis." The primary care companion for CNS disorders 18, no. 5 (2016): 26717.

  18. Pjrek, Edda, Michaela-Elena Friedrich, Luca Cambioli, Markus Dold, Fiona Jäger, Arkadiusz Komorowski, Rupert Lanzenberger, Siegfried Kasper, and Dietmar Winkler. "The efficacy of light therapy in the treatment of seasonal affective disorder: a meta-analysis of randomized controlled trials." Psychotherapy and Psychosomatics 89, no. 1 (2020): 17-24.

  19. Gallin PF, Terman M, Reme CE, Rafferty B, Terman JS, Burde RM: Ophthalmologic examination of patients with seasonal affective disorder, before and after bright light therapy. Am J Ophthalmol 1995; 119:202–210

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