Leo Sher, MD

Whoever wishes to pursue the science of medicine in a direct manner must first investigate the seasons of the year and what occurs in them." --Hippocrates

Since ancient times, people have been aware of seasonal changes in mood and behavior.

 Poets have described the sense of sadness, loss, and lethargy that can accompany the shortening days of fall and winter.

 Many cultures and religions have winter festivals associated with candles or fire. These festivals represent attempts to raise spirits in a season when the days are short.

The concept of seasonal mood disorders dates back to the dawn of medicine.

 Seasonal depressions were described by the Greek physician Hippocrates circa 400 bc.

 About 2000 years ago, the Greek philosopher Posidonius wrote that "melancholy occurs in autumn, whereas mania in summer."

 In the second century, Greco-Roman physicians were treating depression and lethargy with sunlight directed toward the eyes.

 In 1894, explorer Frederick Cook linked seasonal loss of sunlight to a mood disorder.

 Cook described a syndrome characterized by a loss of sexual desire and energy, fatigue, and a profoundly depressed mood. The French neurologist Esquirol

 both described seasonal changes in mood in books published in the years 1845 and 1921, respectively.

Characteristics of seasonal affective disorder

 described the syndrome of "seasonal affective disorder" (SAD), a condition in which depression in fall and winter alternates with nondepressed periods in spring and summer. It was suggested that in order for a diagnosis of  SAD to be made, the following criteria must be met: a history of a major affective disorder; at least 2 consecutive previous years in which depression developed during fall or winter and remitted by the following spring and summer; absence of any other Axis I psychiatric disorder; and absence of any clear-cut, seasonally changing psychosocial variables that would account for the seasonal variability in mood and behavior.

Later, an opposite pattern--depression in the summer and nondepressed periods in the winter ("summer SAD")--was described.

 These 2 types of SAD probably represent a subset of a variety of seasonal behavioral disorders. SAD has been included in 

 as having a "seasonal pattern," an adjectival modifier of any form of seasonally recurrent mood disorder.

The onset of winter SAD usually occurs between the age of 20 and 30 years, but affected people often do not seek psychiatric help for some time.

 Many patients with SAD report disliking winter since their teenage years, although the problem usually becomes severe only in adulthood. Sadness, anxiety, irritability, decreased activity, difficulties at work, social withdrawal, changes in appetite, decreased libido, and changes in sleep are characteristic symptoms of winter SAD.

 Most patients with winter SAD have atypical depressive symptoms such as increased sleep duration, increased appetite, weight gain, and carbohydrate craving. Depressive episodes are generally mild to moderate, but some patients need hospitalization.

The neurovegetative symptoms of subsyndromal SAD are similar to those of SAD, but major depression is absent.

 Patients with winter SAD may experience a reversal of their winter symptoms in summer, including mild hypomania; elevated mood; increased libido, social activity, and energy; and decreased sleep requirements, appetite, and weight.

 Most episodes of SAD occur within unipolar major depressive disorder, a substantial minority have accompanying hypomanic episodes (bipolar II disorder), and very few are associated with manic episodes. Patients with summer SAD usually report typical vegetative symptoms such as insomnia and loss of appetite and weight.

The degree to which season changes affect mood, energy, sleep, appetite, food preference, or desire to socialize with others has been called "seasonality."

 Seasonality can manifest in different degrees in different individuals. It can be viewed as a dimension ranging from the absence of seasonal changes to the occurrence of extreme seasonal changes (eg, some people experience only very mild seasonal changes while others are severely affected).

Children with SAD usually present with fatigue, irritability, difficulty in getting out of bed in the morning, and problems in school.

 Sadness and changes in appetite have also been observed in children with SAD. Children with winter SAD tend to blame the external world (parents, teachers, etc) for treating them poorly.

Seasonality of mood and behavior is common throughout the US population.

 Surveys suggest that the prevalence of SAD in the United States increases with increasing latitude--ranging from 1.4% in Florida to 9.7% in New Hampshire.

 A survey in the Washington, DC, area found that about 4% of the population have winter SAD and over 10% more have subsyndromal features of SAD.

 Twenty-seven percent of respondents reported that changes in the seasons were a problem for them, 66% reported seasonal changes in energy level, 64% reported some seasonal changes in mood, and 49% reported seasonal changes in weight. Another survey, in New York City, indicated that about 6% of the population had seasonal impairment equivalent to that of patients with SAD, 18% reported milder symptoms that were bothersome, and 35% noted symptoms but did not complain.

Many clinical studies report that winter SAD mainly affects women.

 However, the high proportion of women seen in research clinics may be a result of selection bias. Blazer and colleagues

 suggested that SAD with major depressive episodes is more frequent among men, whereas women more commonly experience minor depression with a seasonal pattern.

Identification of a seasonal pattern can only be made if both the patient and physician actively look for it.

 Clinicians should ask the following questions when SAD is suspected. When the seasons change, do you:

If physicians fail to ask these questions, many patients with SAD may be labeled as having a nonseasonal depressive disorder.

Various hypotheses related to the pathophysiology of SAD have been proposed.

 One of these hypotheses suggests that abnormalities of hypothalamic-pituitary-adrenal (HPA)-axis function may contribute to the pathogenesis of SAD. The HPA axis controls the secretion of corticotropin-releasing hormone (CRH), corticotropin (adrenocorticotropic hormone), and cortisol.

 CRH is secreted from the paraventricular nucleus of the hypothalamus as well as from extrahypothalamic sites. It acts on the anterior pituitary gland to cause the release of corticotropin into the bloodstream, where it acts on the adrenal cortex to cause the production and release of cortisol into the bloodstream.

Cortisol has diverse and widespread actions throughout the body and brain. It secondarily inhibits corticotropin and CRH release via negative feedback, although it may augment CRH release in the amygdala. Feedback inhibition is mediated via low-affinity glucocorticoid receptors (GRs) and high-affinity mineralocorticoid receptors (MRs). In the brain, MRs are located primarily in the hippocampus; GRs are more widely distributed in the hypothalamus, pituitary, cortex, and elsewhere. Species from humans to the most ancient organisms share components of the HPA axis.

Release of CRH from the hypothal- amus is influenced by stress, blood levels of cortisol, and the sleep-wake cycle.

 In healthy persons, levels of cortisol rise rapidly after waking, reaching a peak within 30 to 45 minutes. They then gradually diminish over the day, rising again in late afternoon. Cortisol levels fall in late evening, reaching a trough during the middle of the night. The circadian pattern of cortisol release is controlled by the suprachiasmatic nucleus (SCN) of the hypothalamus, also known as the "body clock." Nerve signals from the SCN cause the paraventricular nucleus of the hypothalamus to release pulses of CRH roughly once per hour, resulting in HPA-axis activation and cortisol release. There are also direct links between the SCN and the adrenal gland itself (bypassing the HPA axis) through sympathetic nerve fibers, causing the adrenal gland to become more sensitive to corticotropin stimulation during the morning and further adding to the circadian pattern of cortisol release throughout the day.

Over the past 2 decades, there has been a shift from viewing excessive HPA activity in depression as an epiphenomenon to its having specific effects on symptom formation and cognition.

 Studies have demonstrated that hypercortisolism is involved in the pathogenesis of depressive disorders. Researchers have suggested that HPA dys- regulation is involved in the causality of depression and have proposed that antidepressants may act through normalization of pathologic HPA-axis changes.

 The following clinical observations have been made in patients with depression:

The number of cortisol and corticotropin secretory pulses is increased, which is also reflected in elevated urinary cortisol production rates.

Levels of CRH in the cerebrospinal fluid are elevated.

The number of CRH-secreting neurons in limbic brain regions is increased.

The number of CRH-binding sites in the frontal cortex is reduced as a secondary effect of increased CRH concentration.

The dexamethasone suppression test (DST), CRH stimulation test, combined DST-CRH stimulation test, and other neuroendocrine function tests indicate the presence of HPA dysregulation.

The DST showed that a high proportion of patients with various affective disorders have elevated cortisol levels, thus escaping the suppressive effect of dexamethasone.

 After CRH became available for clinical studies, the DST was combined with CRH administration.

 In this test, patients are pretreated with a single dose of dexamethasone at 11 pm and receive CRH intravenously at 3 pm the following day. The resulting DST-CRH stimulation test proved to be much more sensitive in detecting HPA system alterations than the DST alone. Several studies showed that depressed patients pretreated with dexamethasone reacted with an exaggerated corticotropin and cortisol response.

 A number of studies found that cortisol can affect mood and behavior and disrupt memory and recall.

 For example, cortisol administration in healthy volunteers alters processes associated with prefrontal cortex functions such as inhibitory control, atten- tion regulation, and planning.

Most seasonal investigations into cortisol have found the highest levels to be present in winter.

 Quarterly measurements of morning and evening cortisol levels were determined in a longitudinal study of healthy male and female volunteers.

 There was a season-al variation in cortisol levels with significantly higher levels found in winter and fall than in spring and summer. Walker and associates

 also reported that in healthy men, winter plasma cortisol levels were significantly higher than summer values. Studies that investigated the circadian profile of cortisol in healthy individuals indicated that circadian rhythm was delayed in winter.

 In an Antarctic study, the circadian rhythm of cortisol showed low am- plitude and a phase advance in summer when compared with other seasons.

The circadian rhythms of cortisol obtained without a "constant routine" (a protocol used in circadian rhythms or sleep studies to minimize exogenous effects such as changes in body position, temperature, and meals) were found to be similar in SAD patients and controls in both phase and amplitude; the rhythms did not change with successful bright light therapy.

 Since sleep has a suppressing effect on cortisol,

 those cortisol data do not reflect the unmasked endogenous circadian rhythm of cortisol.

 assessed cortisol rhythms during a constant routine in patients with winter SAD and in healthy controls. After sleep was standardized for 6 days, the subjects were sleep-deprived and restricted to bed rest for 27 hours while cortisol levels were assessed. The minimum level of the cortisol rhythm was phase-delayed in the SAD group compared with the control group; however, with bright light treatment, the minimum level advanced. Another study reported that SAD patients had normal cortisol and corticotropin levels but their responses to CRH were delayed and significantly reduced.

 With bright light therapy, the responses of cortisol and corticotropin to CRH increased significantly.

We have studied the question of whether there are circannual effects on clinical parameters, baseline cortisol and prolactin levels, and cortisol and prolactin responses to fenfluramine hydrochloride administration in subjects with nonseasonal major depression.

 We compared subjects experiencing major depressive episodes in fall or spring (the spring/fall group) with subjects experiencing major depressive episodes in summer or winter (the winter/summer group) and found that baseline cortisol levels were significantly higher in the spring/fall group compared with the winter/summer group.

Our observation that baseline plasma cortisol levels were higher in the spring/fall group than in the winter/ summer group suggests that these 2 groups may represent different biologic subtypes of major depression. This hypothesis is supported by the observation by Beck-Friis and associates,

 who examined the per-month frequency of patients with one or more depressive episodes registered yearly from first onset of illness. The frequencies--calculated from the patients' previous records--were a percentage of the maximum number of patients and were separated for patients with normal and abnormal results on the DST. The authors demonstrated a trend for higher incidences of depression during spring and fall among the patients with normal DST results, whereas the distribution of depressive periods during the year in the abnormal DST group was more uniform.

Another study of depressed patients showed a significantly biannual rhythm in the postdexamethasone cortisol values in depressed men, with peaks in June and December and troughs in March and September.

 The hypothesis that the spring/fall group and the winter/summer group represent different biologic subtypes of major depression is also supported by the observation that the number of binding sites to serotonin receptors during spring and fall is 12% higher than in winter and summer.

Light therapy is recommended as a first-line treatment for SAD in expert and consensus clinical guidelines.

 It is possible that light therapy reduces HPA-axis abnormalities associated with SAD.

It has also been shown that antidepressants may prevent and treat SAD.

 A recent report suggests that light treatment showed earlier response onset and lower rates of some adverse events relative to fluoxetine, but there were no other significant differences in outcome between light therapy and antidepressant medication.

 Another study concluded that it is possible to prevent recurrence of SAD episodes by beginning bupropion treatment early in the season while patients are still well.

 Antidepressants may act by normalizing the pathologic changes in HPA function in SAD patients. Also of interest, a recent report suggests that mifepristone,

 a steroid antagonist, may be useful for the treatment of SAD.

Increased cortisol secretion caused by major and minor stressful events may contribute to the development of SAD and other depressive disorders in vulnerable individuals.

 Therefore, one of the goals of prevention of such stress-related disorders is to help individuals to be more competent in managing their behavior and emotions in reaction to the negative aspects of their environment.

Dr Sher is an associate clinical professor of psychiatry at Columbia University College of Physicians and Surgeons and a research psychiatrist in the department of neuroscience at the New York State Psychiatric Institute in New York City. He reports no conflicts of interest regarding the subject matter of this article.

Winter Blues: Everything You Need to Know to Beat Seasonal Affective Disorder.

 Rev ed. New York: Guilford Press; 2006.


2. Wehr TA. Seasonal affective disorder. A historical overview. In: Rosenthal NE, Blehar MC, eds. 

Seasonal Affective Disorders and Phototherapy.

3. Oren DA, Rosenthal NE. Seasonal affective disorders. In: Paykel ES, ed. 

 2nd ed. New York: Guilford Press;1992: 551-567.


4. Hippocrates. Aphorisms. In: Jones WHS, trans-ed. 

 Vol. 4. Cambridge, Mass: Harvard University Press; 1931:128-129.


The Extant Works of Aretaeus, the Cappadocian.

 Adams F, trans-ed. London: Sydenham Society; 1856.


On Acute Diseases and On Chronic Diseases.

 Drabkin IE, trans-ed. Chicago: University of Chicago Press; 1950.


8. Cook FA. Gynecology and obstetrics among the Eskimo. 

 Hunt EK, ed. Philadelphia: Lea and Blanchard; 1845.


 Barklay RM, trans, Robertson GM, Livingstone E, Livingstone M, eds. Edinburgh: E&S Livingstone; 1921.


11. Rosenthal NE, Sack DA, Gillin JC, et al. Seasonal affective disorder. A description of the syndrome and preliminary findings with light therapy. 

12. Wehr TA, Sack DA, Rosenthal NE. Seasonal affective disorder with summer depression and winter hypomania. 

Diagnostic and Statistical Manual of Mental Disorders, 3rd ed rev.

 Washington, DC: American Psychiatric Publishing; 1987:224.


Diagnostic and Statistical Manual of Mental Disorders, 4th ed

. Washington, DC: American Psychiatric Publishing; 1994: 389-390.


15. Partonen T, Lonnqvist J. Seasonal affective disorder. 

16. Kasper S, Wehr TA, Bartko JJ, et al. Epidemiological findings of seasonal changes in mood and behavior. A telephone survey of Montgomery County, Maryland. 

17. Rosenthal NE, Carpenter CJ, James SP, et al. Seasonal affective disorder in children and adolescents. 

18. Magnusson A. An overview of epidemiological studies on seasonal affective disorder. 

19. Rosen LN, Targum SD, Terman M, et al. Prevalence of seasonal affective disorder at four latitudes. 

20. Terman M. On the question of mechanism in phototherapy for seasonal affective disorder: considerations of clinical efficacy and epidemiology. 

21. Blazer DG, Kessler RC, Swartz MS. Epidemiology of recurrent major and minor depression with a seasonal pattern. The National Comorbidity Survey. 

22. Sher L. Genetic studies of seasonal affective disorder and seasonality. 

23. Magnusson A, Boivin D. Seasonal affective disorder: an overview. 

24. Hauger RL, Datzenberg FM. Regulation of the stress response by corticotropin-releasing factor receptors. In: Conn PM, Freeman ME, eds. 

Neuroendocrinology in Physiology and Medicine.

 Totowa, NJ: Humana Press; 2000:261-287.


25. Tsigos C, Chrousos GP. Hypothalamic-pituitary- adrenal axis, neuroendocrine factors and stress. 

26. Van Cauter E, Turek FW. Endocrine and other biological rhythms. In: De Groot LJ, ed. 

 Philadelphia: WB Saunders;1995:2497-2548.


27. Van Cauter E, Speigel K. Circadian and sleep control of hormonal secretions. In: Turek FW, Zee PC, eds. 

Regulation of Sleep and Circadian Rhythms.

 New York: Marcel Dekker, Inc; 1999:397-425.


29. Shatzberg AF, Garlow SL, Nemeroff CB. Molecular and cellular mechanisms of depression. In: Davis KL, Charney D, Coyle JT, Nemeroff C, eds. 

Neuropsychopharmacology: The Fifth Generation of Progress.

 Philadelphia: Lippincott, Williams & Wilkins; 2002:1039-1050.


30. Holsboer F. The corticosteroid receptor hypothesis of depression. 

31. Holsboer-Trachsler E, Stohler R, Hatzinger M. Repeated administration of the combined dexamethasone-human corticotropin releasing hormone stimulation test during treatment of depression. 

32. Keeney A, Jessop DS, Harbuz MS, et al. Differential effects of acute and chronic social defeat stress on hypothalamic-pituitary-adrenal axis function and hippocampal serotonin release in mice. 

33. Sher L, Oquendo MA, Galfalvy HC, et al. Age effects on cortisol levels in depressed patients with and without comorbid post-traumatic stress disorder, and healthy volunteers. 

Articles

The degree to which season changes affect mood, energy, sleep, appetite, food preference, or desire to socialize with others has been called "seasonality." Identification of a seasonal pattern can only be made if both the patient and physician actively look for it.

Cortisol and Seasonal Changes in Mood and Behavior

Light therapy, in one form or another, has been used as a treatment for a number of conditions since ancient times. Nearly 2,000 years ago, Greco-Roman physicians were treating depression and lethargy with sunlight directed toward the eyes. During his Arctic expeditions in the 1890s, Frederick Cook, M.D., noticing the profound influences of light on the voyagers and Alaskan natives, described a syndrome characterized by depressed mood, fatigue, and loss of energy and sexual desire. In 1946, H. Marx reported the use of bright artificial light to treat four men who had become depressed during an Arctic winter.

Contemporary light therapy involves daily scheduled exposure to bright artificial light (Lam et al., 1999b; Partonen, 2001; Rosenthal and Matthews, 1999). The term 

 is used to differentiate light therapy for psychiatric disorders from phototherapy for other conditions, such as hyperbilirubinemia or psoriasis.

Since the first study of light therapy in winter seasonal affective disorder (SAD) (Rosenthal et al., 1984), a syndrome in which depression developed during fall or winter and remitted the following spring or summer for at least two successive years, numerous studies have concluded that bright light therapy is an effective treatment for SAD (Lam et al., 1999b; Magnusson and Boivin, 2003; Oren and Rosenthal, 1992; Partonen, 2001).

Light therapy is commonly administered by means of a light box--a metal structure containing fluorescent tubes behind a plastic diffusing screen (Lam et al., 1999b; Partonen, 2001; Rosenthal and Matthews, 1999). The dose of light exposure can be measured with the intensity and duration of the exposure. Efficacy is dose dependent to some extent, with both duration and intensity being important. Many studies used 2,500 lux light that was usually administered for two to six hours per day (Lam et al., 1999b; Partonen, 2001). Studies of 10,000 lux fluorescent light yielded similar results to studies using 2,500 lux for two hours (Magnusson and Kristbjarnarson, 1991; Partonen, 2001; Terman et al., 1990). To some degree, there is an inverse relationship between the intensity used and the duration required. Thus, 30 minutes of exposure to 10,000 lux may be as good as two hours of exposure to 2,500 lux, although such a linear relationship does not necessarily apply (Rosenthal and Matthews, 1999). The 10,000 lux fluorescent light box is usually used in clinical practice (Lam et al., 1999b).

A number of studies have found that morning light exposure was superior to evening light exposure (Eastman et al., 1998; Lam et al., 1999b; Lewy et al., 1998; Terman et al., 1998). It is important to note that evening light exposure was still significantly superior to placebo (Eastman et al., 1998; Terman et al., 1998). It is reasonable to start light therapy with morning exposure. Light treatment should not be administered late in the evening because it may cause insomnia.

Studies suggest that younger age and atypical symptoms such as hypersomnia, increased appetite, weight gain and increased carbohydrate consumption are associated with good response to light therapy (Lam et al., 1999b). The early response to light therapy partially predicts long-term response (Sher et al., 2001). If replicated, this observation may provide a simple test that will allow clinicians to predict which patient will respond best to light therapy.

Before starting light therapy, an ophthalmologic consultation is recommended for patients with a pre-existing retinal or eye disease (e.g., retinal detachment, retinitis pigmentosa, glaucoma, previous cataract surgery and lens removal) or a systemic illness that affects the retina (e.g., diabetes mellitus) (Lam et al., 1999b; Partonen, 2001). Side effects of light therapy include headaches, eyestrain, fatigue and insomnia (Lam et al., 1999b; Partonen, 2001; Rosenthal and Matthews, 1999). Most of these side effects respond to dose reduction. Hypomania and mania are uncommon, but serious, side effects. If a patient has prior history of mania, the risk of switch into mania might be minimized with a mood stabilizer (Kripke, 1991; Lam et al., 1999b).

Light treatment is best prescribed by psychiatrists who have experience in its use and can appropriately evaluate the indication for light therapy and monitor the response to treatment. Some individuals buy light boxes using the Internet or from stores and carry out the treatment without prior consultation and adequate supervision. Patients should be discouraged from treating themselves without medical supervision. However, patients can be encouraged to participate in establishing an optimal light protocol. For patients with SAD, light therapy should be regarded as the first-line treatment, but other treatments including antidepressants, stress management, exercise and psychotherapy may also be useful (Lam et al., 1999b).

The biological mechanisms of SAD and light therapy are not clear. Various studies suggested the involvement of serotonergic, dopaminergic and noradrenergic pathways; the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid axes; and changes in circadian rhythm and melatonin secretion in the neurobiology of seasonal changes in mood and behavior and effects of light therapy (Enns et al., 1999; Magnusson and Boivin, 2003; Oren and Rosenthal, 1992; Rosenthal and Matthews, 1999). For example, Lambert et al. (2002) reported that the rate of production of serotonin by the brain was directly related to the prevailing duration of bright sunlight and rose rapidly with increased luminosity.

A psychobiological response to seasonal changes is a result of interacting environmental and genetic factors (Lam et al., 1999b; Sher, 2001). Genetic factors can interact with environmental factors in different ways, and two such mechanisms have been described: 

genetic control of sensitivity to the environment

genetic control of exposure to the environment

 (Kendler, 1998). Genetic control of sensitivity to the environment suggests that genes, in part, render individuals relatively vulnerable to the effects of seasonal and lighting conditions. For example, the effect of light deprivation may be substantially greater in those at high genetic risk for seasonal changes in mood and behavior (Sher, 2003). Genetic control of exposure to the environment suggests that genetic factors influence the probability that individuals will select themselves into certain environments. For example, the genetic risk factors for seasonality may express themselves by influencing the probability that individuals will spend more time indoors (Sher, 2003).

Use of light treatment for nonseasonal depressive disorders is growing (Kripke, 1998; Lam et al., 1999a, 1997; Tuunainen et al., 2004). There may be a role for light therapy in treating nonseasonal depression, especially in cases where antidepressants are not tolerated or where the patient preference is for nonpharmacological treatment. A recent Cochrane report suggested that bright light therapy offers a modest, though promising, antidepressant effect (Tuunainen et al., 2004). Treatment is particularly effective when administered in the morning during the first week and as an adjunct to sleep deprivation. Light therapy may be useful as an augmentation strategy for antidepressant nonresponders (Levitt et al., 1991).

A recent study found that there were seasonal influences on morning cortisol levels in patients with major depression (Sher et al., 2004). It is interesting to speculate that the hypothalamic-pituitary-adrenal system is involved in the biological mechanisms of light therapy in nonseasonal depression.

Recent reports suggest that bright light therapy has an antidepressant effect on patients with antepartum depression (Epperson et al., 2004; Oren et al., 2002). Evening bright light for two premenstrual weeks decreases depression and tension in patients with premenstrual dysphoric disorder (Lam et al., 1999a). Light treatment appears to decrease depressive symptoms in patients with nonseasonal bipolar disorder (Bauer, 1993).

Exposure to bright light is important for psychological well-being of healthy people (Bauer et al., 1994; Lambert et al., 2002; Partonen et al., 1998). In the modern industrial world, many people spend a lot of time indoors. They are light-deprived and have a sedentary lifestyle. Combined exposure to bright light and physical exercise can be especially effective for improving mood- and health-related quality of life (Partonen et al., 1998). Various outdoor activities may provide opportunities to improve psychological and physical health.

The increased clinical and research interest in light treatment appears well justified. There is sufficient research evidence to support the efficacy of light therapy in SAD. Light therapy has a promising potential role in the treatment of nonseasonal depressive disorders. We are in the early chapters of our understanding of how light affects humans.

I would like to conclude with advice from A. Cornelius Celsus, a Roman medical writer: "Live in rooms full of light. Avoid heavy food. Be moderate in the drinking of wine. Take massage, baths, exercise, and gymnastics."

 Bauer MS (1993), Summertime bright-light treatment of bipolar major depressive episodes. Biol Psychiatry 33(8-9):663-665.
 

 Bauer MS, Kurtz JW, Rubin LB, Marcus JG (1994), Mood and behavioral effects of four-week light treatment in winter depressives and controls. J Psychiatr Res 28(2):135-145.
 

 Eastman CI, Young MA, Fogg LF et al. (1998), Bright light treatment of winter depression: a placebo-controlled trial. Arch Gen Psychiatry 55(10):883-889 [see comments].
 

 Enns MW, Levitan RD, Levitt AJ et al. (1999), Diagnosis, epidemiology, and pathophysiology. In: Canadian Consensus Guidelines for the Treatment of Seasonal Affective Disorder, Lam RW, Levitt AJ, eds. Toronto: Clinical & Academic Publishing, pp20-63.
 

 Epperson CN, Terman M, Terman JS et al. (2004), Randomized clinical trial of bright light therapy for antepartum depression: preliminary findings. J Clin Psychiatry 65(3):421-425.
 

 Kendler KS (1998), Anna-Monika-Prize paper. Major depression and the environment: a psychiatric genetic perspective. Pharmacopsychiatry 31(1):5-9.
 

 Kripke DF (1991), Timing of phototherapy and occurrence of mania. Biol Psychiatry 29(11):1156-1157 [letter].
 

 Kripke DF (1998), Light treatment for nonseasonal depression: speed, efficacy, and combined treatment. J Affect Disord 49(2):109-117.
 

 Lam RW, Carter D, Misri S et al. (1999a), A controlled study of light therapy in women with late luteal phase dysphoric disorder. Psychiatry Res 86(3):185-192.
 

 Lam RW, Tam EM, Gorman CP et al. (1999b), Light treatment. In: Canadian Consensus Guidelines for the Treatment of Seasonal Affective Disorder, Lam RW, Levitt AJ, eds. Toronto: Clinical & Academic Publishing, pp64-88.
 

 Lam RW, Terman M, Wirz-Justice A (1997), Light therapy for depressive disorders: indications and efficacy. Mod Probl Pharmacopsychiatry 25:215-234.
 

 Lambert GW, Reid C, Kaye DM et al. (2002), Effect of sunlight and season on serotonin turnover in the brain. Lancet 360(9348):1840-1842.
 

 Levitt AJ, Joffe RT, Kennedy SH (1991), Bright light augmentation in antidepressant nonresponders. J Clin Psychiatry 52(8):336-337.
 

 Lewy AJ, Bauer VK, Cutler NL et al. (1998), Morning vs evening light treatment of patients with winter depression. Arch Gen Psychiatry 55(10):890-896 [see comments].
 

 Magnusson A, Boivin D (2003), Seasonal affective disorder: an overview. Chronobiol Int 20(2):189-207.
 

 Magnusson A, Kristbjarnarson H (1991), Treatment of seasonal affective disorder with high-intensity light. A phototherapy study with an Icelandic group of patients. J Affect Disord 21(2):141-147.
 

 Oren DA, NE Rosenthal NE (1992), Seasonal affective disorders. In: Handbook of Affective Disorders, 2nd ed., Paykel ES, ed. London: Churchill Livingstone pp551-567.
 

 Oren DA, Wisner KL, Spinelli M et al. (2002), An open trial of morning light therapy for treatment of antepartum depression. Am J Psychiatry 159(4):666-669.
 

 Partonen T (2001), Light therapy. In: Seasonal Affective Disorder. Practice and Research, Partonen T, Magnusson A, eds. New York: Oxford University Press, pp65-78.
 

 Partonen T, Leppamaki S, Hurme J, Lonnqvist J (1998), Randomized trial of physical exercise alone or combined with bright light on mood and health-related quality of life. Psychol Med 28(6):1359-1364.
 

 Rosenthal NE, Matthews JR (1999), Seasonal affective disorder and light therapy. In: Encyclopedia of Neuroscience, 2nd ed., Adelman G, Smith BH, eds. Amsterdam, Netherlands: Elsevier, pp1828-1831.
 

 Rosenthal NE, Sack DA, Gillin JC et al. (1984), Seasonal affective disorder: a description of the syndrome and preliminary findings with light therapy. Arch Gen Psychiatry 41(1):72-80.
 

 Sher L (2001), Genetic studies of seasonal affective disorder and seasonality. Compr Psychiatry 42(2):105-110.
 

 Sher L (2003), Bright light, serotonin turnover, and psychological well-being. Can J Psychiatry 48(7):499 [letter].
 

 Sher L, Matthews JR, Turner EH et al. (2001), Early response to light therapy partially predicts long-term antidepressant effects in patients with seasonal affective disorder. J Psychiatry Neurosci 26(4):336-338.
 

 Sher L, Oquendo MA, Galfalvy HC et al. (2004), A study of seasonal effects on cortisol and prolactin levels in patients with major depression and healthy volunteers. Biol Psychiatry 55(8 suppl 1):86S.
 

 Terman JS, Terman M, Schlager D et al. (1990), Efficacy of brief, intense light exposure for treatment of winter depression. Psychopharmacol Bull 26(1):3-11.
 

 Terman M, Terman JS, Ross DC (1998), A controlled trial of timed bright light and negative air ionization for treatment of winter depression. Arch Gen Psychiatry 55(10):875-882 [see comments].
 

 Tuunainen A, Kripke D, Endo T (2004), Light therapy for non-seasonal depression. Cochrane Database Syst Rev 2:CD004050.

Although light therapy is an old treatment, new therapeutic uses are being researched. What is the optimal time and strength of light treatment to best help patients with depressive disorders?

Author | Leo Sher, MD

Articles

Cortisol and Seasonal Changes in Mood and Behavior

Light Therapy for Depressive Disorders