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Objective: To determine if the antidepressant effect of 1 hour of light therapy is predictive of the response after 1 and 2 weeks of treatment in patients with seasonal affective disorder (SAD)., Patients: Twelve patients with SAD., Setting: National Institutes of Health Clinical Center, Bethesda, Md., Interventions: Light therapy for 2 weeks., Outcome Measures: Scores on the Seasonal Affective Disorder Version of the Hamilton Depression Rating Scale (SIGH-SAD) on 4 occasions (before and after 1 hour of light therapy and after 1 and 2 weeks of therapy) in the winter when the patients were depressed. Change on typical and atypical depressive scores at these time points were compared., Results: Improvement of atypical depressive symptoms after 1 hour of light therapy positively correlated with improvement after 2 weeks of therapy., Conclusion: In patients with SAD, the early response to light therapy may predict some aspects of long-term response to light therapy, but these results should be treated with caution until replicated.

Background: Information-transducing heterotrimeric G proteins have been implicated previously in the mechanism of action of mood stabilizers and in the pathophysiology of mood disorders. Mononuclear leukocytes of patients with unipolar and bipolar depression have been characterized by reduced measures of the stimulatory and inhibitory G proteins. In this study, patients with seasonal affective disorder (SAD) were measured for mononuclear leukocyte G protein levels while depressed during the winter, following light therapy, and in remission during the summer., Methods: Twenty-six patients with SAD and 28 healthy subjects were assessed in the study. The immunoreactivities of Gs alpha, Gi alpha, and Gbeta subunit proteins were determined by Western blot analysis of mononuclear leukocyte membranes with selective polyclonal antibodies for the various G subunit proteins, followed by densitometric quantitation using an image analysis system., Results: Untreated patients with SAD and winter, atypical-type depression showed significantly reduced mononuclear leukocyte immunoreactive levels of Gs alpha and Gi alpha proteins, similar to previous observations in patients with nonseasonal major depression. The reduced G protein levels were normalized with 2 weeks of light therapy. The same patients while in remission during the summer had G protein levels that were similar to those of healthy subjects., Conclusions: G protein-immunoreactive measures in patients with SAD are suggested as a state marker for winter depression, which is normalized by light treatment and during the summer. We speculate that light may exert its effects via normalization of transducin (Gt protein) levels, which are thought to be reduced in winter depression.

Objective: The authors sought to compare the degree of mood improvement after light treatment with mood improvement in the subsequent summer in patients with seasonal affective disorder., Method: By using the Seasonal Affective Disorder Version of the Hamilton Depression Rating Scale, the authors rated 15 patients with seasonal affective disorder on three occasions: during winter when the patients were depressed, during winter following 2 weeks of light therapy, and during the following summer. They compared the three conditions by using Friedman's analysis of variance and the Wilcoxon signed ranks test., Results: The patients' scores on the depression scale were significantly higher after 2 weeks of light therapy in winter than during the following summer., Conclusions: Light treatment for 2 weeks in winter is only partially effective when compared to summer. Further studies will be necessary to assess if summer's light or other factors are the main contributors to this difference.

Background: Although hypotheses about the therapeutic mechanism of action of light therapy have focused on serotonergic mechanisms, the potential role, if any, of catecholaminergic pathways has not been fully explored., Methods: Sixteen patients with seasonal affective disorder who had responded to a standard regimen of daily 10000-lux light therapy were enrolled in a double-blind, placebo-controlled, randomized crossover study. We compared the effects of tryptophan depletion with catecholamine depletion and sham depletion. Ingestion of a tryptophan-free amino acid beverage plus amino acid capsules was used to deplete tryptophan. Administration of the tyrosine hydroxylase inhibitor alpha-methyl-paratyrosine was used to deplete catecholamines. Diphenhydramine hydrochloride was used as an active placebo during sham depletion. The effects of these interventions were evaluated with measures of depression, plasma tryptophan levels, and plasma catecholamine metabolites., Results: Tryptophan depletion significantly decreased plasma total and free tryptophan levels. Catecholamine depletion significantly decreased plasma 3-methoxy-4-hydroxyphenylethyleneglycol and homovanillic acid levels. Both tryptophan depletion and catecholamine depletion, compared with sham depletion, induced a robust increase (P<.001, repeated-measures analysis of variance) in depressive symptoms as measured with the Hamilton Depression Rating Scale, Seasonal Affective Disorder Version., Conclusions: The beneficial effects of light therapy in the treatment of seasonal affective disorder are reversed by both tryptophan depletion and catecholamine depletion. These findings confirm previous work showing that serotonin plays an important role in the mechanism of action of light therapy and provide new evidence that brain catecholaminergic systems may also be involved.

Objective: To evaluate the efficacy of light therapy for the treatment of pediatric seasonal affective disorder (SAD)., Method: 28 children (aged 7 to 17 years) at two geographically distinct sites were enrolled in a double-blind, placebo-controlled, crossover trial of bright-light treatment. Subjects initially entered a week-long baseline period during which they wore dark glasses for an hour a day. They were then randomly assigned to receive either active treatment (1 hour of bright-light therapy plus 2 hours of dawn simulation) or placebo (1 hour of clear goggles plus 5 minutes of low-intensity dawn simulation) for 1 week. The treatment phase was followed by a second dark-glasses phase lasting 1 to 2 weeks. After this phase, the children received the alternate treatment. Response was measured using the parent and child versions of the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorders version (SIGH-SAD)., Results: Data were analyzed as change from baseline. SIGH-SAD-P total depression scores were significantly decreased from baseline during light therapy compared with placebo (one-way analysis of variance, rho = .009), and no differences were found between the placebo and control phases. Subscores of atypical and typical depression were also significantly decreased during the active treatment (rho = .004 and .028, respectively). A similar trend was noted with the SIGH-SAD-C, but this did not reach significance. At the end of the study, 78% of the parents questioned and 80% of the children questioned rated light therapy as the phase during which the child "felt best.", Conclusion: Light therapy appears to be an effective treatment for pediatric SAD.

Background: Multiple lines of evidence suggest that brain serotonergic systems may be disturbed in seasonal affective disorder (SAD). Previously, we found that the serotonergic agent meta-chlorophenylpiperazine (m-CPP) produced increases in activation and euphoria in depressed patients with SAD, but not in patients with SAD following light treatment or in the summer, nor in healthy control subjects in any condition. In the present study, we attempted to replicate and extend this finding using better methods., Methods: Seventeen outpatients with SAD and 15 control subjects underwent successive 3-week periods of bright light treatment and light avoidance in a randomized order. During the third week of each condition, on 2 different occasions, subjects were admitted to the hospital for a night of sleep (core temperatures were recorded), followed by infusions of m-CPP (0.08 mg/kg) or placebo the next morning. Dependent measures included the 24-item National Institute of Mental Health Self-Rating Scale, plasma corticotropin, cortisol, prolactin, growth hormone, and norepinephrine concentrations, and core temperatures., Results: Meta-chlorophenylpiperazine produced (1) significant increases in "activation-euphoria" ratings only in depressed patients with SAD in the untreated condition and (2) blunted corticotropin and norepinephrine responses in patients with SAD compared with controls across both light treatment conditions. In both groups, light treatment was associated with significant reductions in nocturnal core temperatures, which were correlated with similarly significant reductions in mean diurnal growth hormone concentrations. In patients with SAD, (1) the reductions in nocturnal core temperatures also were correlated with the reductions in baseline depression ratings and (2) the reductions in mean growth hormone concentrations were significantly smaller compared with controls., Conclusions: The abnormal m-CPP-induced activation-euphoria responses represent a replicated state marker of winter depression in patients with SAD. The blunted m-CPP-induced responsiveness of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system may represent traitlike abnormalities. The improvements in mood following light treatment in patients with SAD seem to be associated with the lowering of nocturnal core temperatures. The findings, although not easily explained based on a uniform abnormality of serotonin receptors, are nonetheless compatible with the notion that selected regions of the central nervous system are deficient in serotonin transmission during winter depression.

Objective: The purpose of the study was to ascertain whether phototherapy light visors provide an effective treatment for seasonal affective disorder. Previous studies have demonstrated a moderate response rate but have failed to find any difference in efficacy between light intensities., Method: Subjects were randomly assigned to receive, over a 2-week treatment period, 30 minutes of morning phototherapy with a light visor that emitted either a dim (30-lux) red light or a bright (600-lux) white light. Raters were blind to treatment, and patients were unaware of the alternatives. Response was assessed by using the structured 21-item Hamilton Depression Rating Scale, with an eight-item addendum for atypical depressive symptoms. Fifty-seven patients were enrolled across two sites., Results: Patients assigned to the different visors had similar baseline depression scores and similar expectations of outcome. Hamilton depression scale scores declined by 34.6% for subjects given bright white light and by 40.9% for subjects given dim red light. Scores for atypical depressive symptoms fell by 44.1% for patients assigned the bright white light visors and by 49.0% for patients assigned the dim red light visors. Altogether, 39.3% of the patients who received red light and 41.4% of the patients who received bright white light showed a full clinical response., Conclusions: There were no significant differences in therapeutic response between patients who were treated with red or white light. The results of this study suggest that the phototherapy light visor may function as an elaborate placebo. Alternative explanations, however, are considered.

Nine patients with rapid cycling bipolar disorder were treated with a total of 13 trials of bright light therapy in the morning (n = 5), evening (n = 3), or midday (n = 5). In each instance, the patient's mood ratings during 3 months of light therapy (added to a stable medication regimen) were compared to his or her mood ratings during 3 months on the same medication but without light treatment. Of the 3 light therapy schedules, only midday lights appeared to have beneficial clinical effects, improving mood ratings in 3 patients. In contrast, the morning light therapy trial was terminated prematurely in 3 patients because of clinical instability. Light treatment was better tolerated if patients discontinued it on days when they were hypomanic. The clinical and theoretical implications of these preliminary findings are discussed.

1,25 (OH)2 vitamin D3 levels were assessed in nine females and six males with winter seasonal affective disorder and in 15 age- and gender-matched controls in winter during periods with and without treatment with light therapy. No difference was found between groups or across conditions, though wide variations within each group make the presence of a type II error possible.

Disturbances of sleep are a hallmark of seasonal affective disorders (SAD), as they are of other mood disorders. Fall/winter SAD patients most often report hypersomnia. Among responses of 293 SAD patients on a symptom questionnaire, complaints of winter hypersomnia (80%) greatly exceeded insomnia (10%), hypersomnia plus insomnia (5%), or no sleep difficulty (5%). Increased sleep length in fall/winter is not unique to SAD. Among 1571 individuals across four latitudes surveyed at random from the general population, winter sleep increases of < or = 2 hr/day relative to summer were reported by nearly half. However, hypersomnia had a low correlation (r = 0.29) with the total number of other SAD symptoms that were reported in this sample. Ten SAD patients kept daily sleep logs across 1 yr that showed increases in fall and winter (sleeping most in October; least in May) whose maximum averaged 2.7 hr per day more weekend sleep than in spring and summer. These winter increases might have been somewhat attenuated since most received light therapy during part of the winter. Nocturnal EEG recordings of depressed SAD patients in winter showed decreased sleep efficiency, decreased delta sleep percentage, and increased REM density (but normal REM latency) in comparison with recordings: (1) from themselves in summer; (2) from themselves after > or = 9 days of light therapy; or (3) from age- and gender-matched healthy controls. Thus, the extent of fall/winter oversleeping recorded by our SAD patients did not differ dramatically from that reported by the general population, but sleep complaints of our SAD patients have been accompanied by features of sleep architecture that are different from healthy controls and are reversed by summer or by bright-light therapy.

A comparison of the baseline and post-infusion effects of the serotonin agonist meta-chlorophenylpiperazine (m-CPP) in 10 patients with seasonal affective disorder (SAD) and 11 healthy control subjects revealed significantly different subjective response profiles between the groups. Several baseline and m-CPP-stimulated responses in symptoms putatively related to serotonergic function changed significantly after a week's exposure to phototherapy in the SAD patients but not the control subjects. Before phototherapy, depressed patients with SAD reported activation-euphoria responses to m-CPP and significant decreases in carbohydrate hunger, but insignificant changes in feeling slowed or sleepy, while control subjects reported no mood or appetite changes but significant increases in feeling slowed down following m-CPP. After phototherapy, which led to a significant reduction in baseline depressive symptom rating to near-euthymic levels in the SAD patients, almost all of the patients' responses to m-CPP were normalized and no longer differed from the control subjects' responses. These results provide evidence of a possible dysregulation in serotonergic neurotransmission in depressed SAD patients that normalizes following treatment with phototherapy.

In order to evaluate the effect of light on helper- and suppressor-T-cell counts in HIV-infected individuals, with and without a history of seasonal affective disorder (SAD), we treated 35 subjects with 45 min of light therapy in the morning, in a crossover design involving two 2 week treatment conditions: visible white light (half-peak band width, 530-620 nm; 10,000 lux) and visible red light (half-peak band width, 615-685 nm; 175 lux). We found small but significant differences between the two treatment conditions, with higher CD4 and CD8 levels during the white, as compared with the red, condition. There were no differences between baseline and treatment conditions. Both light treatment conditions were associated with significant mood improvements in the SAD, but not the non-SAD, subjects. There was no evidence that the higher cell counts seen under the bright light conditions were mediated by the effects of light on mood or on plasma cortisol levels. While the size of the light effect on T-cells renders questionable the potential therapeutic value of this treatment modality for HIV, the finding is of theoretical interest and is reassuring for those HIV-infected individuals who require light treatment for other reasons.

Low electrooculographic (EOG) ratios have been reported in patients with seasonal affective disorder (SAD). This study was undertaken to replicate these results and to consider the effects of light therapy on the EOG in SAD patients. Sixteen outpatients with SAD and 16 age-, sex-, and medication-matched control subjects had EOG testing before and after 1 week of light therapy during the winter. The EOG ratios in the SAD patients were only marginally lower than those in the normal control subjects. These differences persisted after light therapy. Although the slightly decreased EOG ratios in SAD patients might have resulted from an artifact of test variability, drowsiness, or other confounding factors, the difference between patients and control subjects raises the possibility of retinal abnormality in SAD.

Reduced light appears to be a key factor in seasonal affective disorder (SAD). This study asks whether the reduced levels of light experienced by elderly persons might result in depression and other SAD symptoms, and how normal elderly persons might respond to bright light interventions similar to those used to treat SAD. In interviews with 140 senior citizens, we found virtually no seasonal variation in mood and behavior and very little depressed affect. Seventeen of these seniors who had good mental and physical health, with no major eye problems, participated in a crossover study of the effects of bright light on both positive and negative affect and sleep. Although sleep did not appear to be affected, the bright light intervention tended to make these normal elderly persons feel worse--more irritable, anxious, and agitated. These findings confirm earlier reports that bright light is not beneficial for normal individuals who are unaffected by seasonal changes.

Fifty-five patients with winter seasonal affective disorder (SAD) were treated with a light visor, a newly developed portable light-delivery system, in a controlled parallel design. A dim (400 lux) visor was compared with a bright (6000 lux) visor for either 30 or 60 minutes in the morning for 1 week. Response rates for these two treatments were 36% and 56%, respectively; the duration of treatment sessions did not affect outcome. There was no evidence that the brighter visor was superior in efficacy to the dimmer one. Significantly greater relapse occurred following withdrawal of the dimmer visor. Alternative explanations for these findings are that the light visor is acting as a placebo or that it is equally effective over a wide range of intensities.

Wintertime measures of central and peripheral monoamine neurotransmitter system activity in 17 medication-free depressed patients with seasonal affective disorder (SAD) were compared with those in eight healthy volunteers. Mean cerebrospinal fluid (CSF) concentrations of the principal metabolites of norepinephrine (NE), serotonin, and dopamine did not differ between the two groups, nor did mean basal or orthostatically stimulated plasma NE levels. Patients' pretreatment depression ratings were inversely correlated with resting plasma NE concentrations. Fourteen SAD patients were clear responders to 2 weeks of full-spectrum bright light treatment. Neither the transmitter measures nor their interrelatedness was affected significantly by phototherapy.

We examined data from 44 women with seasonal affective disorder (SAD) to determine whether any demographic, diagnostic, or symptomatic characteristics would be predictive of a favorable response to phototherapy. Preexistent hypersomnia was particularly associated with lessening of depression after phototherapy. In contrast to a report elsewhere, both "typical" and "atypical" depressive symptoms correlated with improvement after phototherapy.

The authors surveyed 34 patients with obsessive-compulsive disorder for a history of seasonal variations in symptoms and behavior and treated six of these patients with bright light. Overall, the patients with obsessive-compulsive disorder did not report a greater degree of seasonal variations than normal and no response was seen to bright light therapy in the small number of patients treated.

Objective: This study sought to determine whether an equal photon density of green light is superior to red light in treating seasonal affective disorder., Method: After recruitment through the media, 20 outpatients with seasonal affective disorder participated in a balanced-order crossover trial of 1 week of green light therapy compared with 1 week of red light therapy. Each treatment consisted of 2 hours of daily light treatment at home in the early morning. Ultraviolet light was excluded from both treatment conditions. The photon densities of the two treatments (2.3 x 10(15) photons/sec per cm2) were similar to those used in previous studies of therapy with 2500-lux white light. Fourteen patients completed the study. At least 1 week separated each treatment period to allow time for relapse. Effectiveness of treatment was assessed by analysis of variance of changes in ratings on the Hamilton Rating Scale for Depression., Results: Although patients' expectations of the two treatments were similar, green light induced greater antidepressant effects than red light. A Sequence by Color interaction was also demonstrated., Conclusions: Green light provides a treatment effect superior to that of red light and similar to that seen in previous studies with white light. These results are consistent with the hypothesis that retinal photoreceptors mediate the antidepressant response in seasonal affective disorder. Identifying optimal wavelengths for light treatment is important in optimizing phototherapy efficacy.

We mailed a questionnaire to patients affected with seasonal affective disorder (SAD) to determine patterns of self-selected light use and efficacy of treatment. Data obtained from 127 patients who responded indicate that despite, inconvenience and other use-limiting factors, many patients with SAD derive sustained benefit from phototherapy over months. No consistent pattern or duration of effective treatment emerged. Development of a less cumbersome means of delivering phototherapy and reimbursement by insurance companies remain concerns to patients.

Immunological parameters were studied before and after phototherapy, with bright and dim light, in 38 individuals with a range of retrospectively reported seasonal changes in mood and behavior. There was a significant negative correlation between the degree of mood and behavioral difficulties in fall and winter (seasonality) and the total number of circulating natural killer cells. Changes in the numbers of circulating helper T cells correlated significantly with changes in mood following phototherapy. Moreover, mitogen-induced lymphocyte blastogenesis increased significantly after phototherapy, but there was no significant difference between the bright and dim light treatments. The results suggest that cellular immune function is associated with both seasonality and response to phototherapy.

Many of the symptoms of seasonal affective disorder (SAD) could be construed as having an energy-conserving function. We predicted that SAD patients would have abnormally low resting metabolic rates (RMR), which would be increased to normal levels by light therapy. To test this hypothesis we measured RMR in 10 patients on and off light treatment and 9 normal controls. Contrary to our prediction we found that SAD patients had significantly higher RMR values compared with the normal population (p less than 0.02) and these values were significantly lowered by light treatment (p less than 0.05). The possible implications of these findings are discussed.

The aim of this study was to compare the relative therapeutic efficacies of three different light sources for treating winter depression. A balanced incomplete block crossover design was employed, whereby all patients (n = 18) were randomly assigned to two out of the three treatment conditions: white, red and blue light. The degree of depression was assessed by the 21-item Hamilton Depression Rating Scale. The data suggest that at a photon density of 2.3 X 10(15) photons/s/cm2, white light has greater therapeutic benefit than red or blue light. It is clear that a larger sample population should be tested to confirm this result. This preliminary finding indicates that light sources currently in use for phototherapy could not be improved by narrowing the wavelengths provided and shifting them towards either end of the visible spectrum.

Bright light has recently been shown to have phase-shifting effects on human circadian rhythms. In this study we applied this effect to 20 patients with delayed sleep phase syndrome (DSPS) who were unable to fall asleep at conventional clock times and had a problem staying alert in the morning. In a controlled treatment study, we found that 2 h of bright light exposure in the morning together with light restriction in the evening successfully phase advanced circadian rhythms of core body temperature and multiple sleep latencies in these patients. This finding corroborates the importance of light for entraining human circadian rhythms.

Seasonal affective disorder (SAD) has been successfully treated with bright light, and morning exposure has been deemed more effective than exposure at other times. Evening treatment may offer a practical advantage, but the optimal duration of exposure has not been established. Six SAD patients were treated at home for 1 week with 2500 lux of light given either from 6 p.m. to 8 p.m. or from 6 p.m. to 10 p.m. using a counterbalanced crossover design with a minimal withdrawal period of 1 week between conditions. Both treatments were effective in reversing SAD symptoms, but neither treatment was superior. These results suggest that evening phototherapy for as little as 2 hours may be a useful and reasonable alternative for the treatment of SAD.

Patients with recurrent winter depression and its subsyndromal form have been reported to benefit from bright full-spectrum light (phototherapy). In order to determine whether this treatment (2 h in the morning) during winter is effective in a random sample of the general population we investigated the responses of 20 subjects with varying degrees of winter difficulties. A control group (n = 20) matched for the degree of seasonality, age, and sex was treated with dim light. Individuals were selected from a larger survey sample of the Montgomery County population (MD, U.S.A.) and were comparable to the latter in their degree of winter difficulties. Enhancement of environmental light does not, on the basis of the present study, appear to be indicated for the public at large, but rather for a subgroup of individuals with histories of winter difficulties.

Abnormalities in circadian rhythms of core body temperature have been reported previously in depressed patients. In this study, we compared the temperature rhythms of 10 depressed seasonal affective disorder (SAD) patients with winter depression with those of 12 normal controls and evaluated the effects of bright light on temperature in SAD. Unlike previous studies of depressed patients, the temperature curves of the patients and normal controls during the off-light condition were nearly identical. We found a significant difference in amplitude between the patients in the untreated and light-treated conditions. Although there was no systematic difference in circadian phase across groups or treatment conditions, we present preliminary evidence that suggests that phase-typed subgroups may be present in the population distinguished by their treatment responses.

Sixteen depressed patients with seasonal affective disorder participated in a double-blind crossover study comparing the antidepressant effects of 2 hours of early morning and 2 hours of early afternoon therapy with bright light. They responded equally well to both treatments. These results suggest that the antidepressant effects of phototherapy in seasonal affective disorder do not depend on its capacity to extend day length (photoperiod) and are not likely to be due to a shift in the timing of circadian rhythms. These findings have practical implications for the administration of phototherapy in the treatment of seasonal affective disorder.

In winter, depressed patients with seasonal affective disorder respond to treatment with bright artificial light (phototherapy). The authors found that the antidepressant effects of phototherapy were much greater for 10 patients when light was applied to the eyes than when it was applied to the skin, suggesting that its effects may be mediated by the eyes. The identification of a probable anatomical route of entry is clinically relevant and an important clue for further investigations of the mechanism of phototherapy. However, patients' expectations nearly always predicted the outcome, leaving open the possibility that expectations were responsible for their responses.

A behavioral factor, sleep, and a physical environmental factor, light, can trigger or terminate episodes of affective illness. The authors review the experimental evidence for these effects and discuss recent research on their biological mechanisms. In light of these findings the authors speculate that affective illness could partly be a disorder of systems that mediate the organism's adaptations to changes in the physical environment.

Antidepressant and energizing effects of bright light exposure have been widely reported to occur in patients with seasonal affective disorder (SAD). In order to evaluate whether other segments of the population might also benefit from this treatment, we studied 20 normal individuals with mild SAD-like symptoms (subsyndromal SAD, S-SAD) and 20 with no reported seasonal difficulties (non-S-SAD). Whereas S-SAD individuals benefited from phototherapy, non-S-SAD normals did not. This finding raises the questions of whether a history of seasonal problems might be a marker of vulnerability to affective episodes and if S-SAD individuals might be considered as a high risk population in this regard.

Antidepressant and energizing effects of bright light exposure (phototherapy) have been widely reported to occur in patients with seasonal affective disorder. We have attempted to evaluate whether other segments of the population might benefit from phototherapy, most notably individuals with subsyndromal seasonal affective disorder, as well as healthy individuals with no winter difficulties (controls). We have studied 20 subjects in each of these two categories and have found that bright artificial light did not alter mood and behavior in controls. In contrast, individuals with subsyndromal seasonal affective disorder responded favorably to treatment with bright environmental light. A dose of 5 hours of bright light exposure, divided between morning and evening, was more effective than 2 hours of exposure. This finding may have practical implications for establishing optimal environmental lighting conditions for those individuals whose winter difficulties do not meet criteria for seasonal affective disorder.

Seasonal affective disorder (SAD) is a syndrome characterized by recurrent depressions that occur annually at the same time each year. We describe 29 patients with SAD; most of them had a 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. 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.

The efficacy of phototherapy with bright, fluorescent, full-spectrum light for treatment of seasonal affective disorders (SAD) has now been widely demonstrated in controlled studies. However, treatment with dim light did not reveal a significant therapeutic improvement. Specific parameters of light treatment are necessary or optimal for producing this response and light intensity and duration in contrast to timing and spectrum seem to be a major importance. The mechanism of action of phototherapy is closely linked to the psychobiology of SAD and has not yet been satisfactorily explained. Among the several theories which have been proposed, the melatonin hypothesis and phase shift hypothesis have been the basis for the earlier studies. Newer theories also include the function of further neuroendocrine systems, as well as neurotransmitter and immune function and electrophysiological mechanisms. Until now, the value of phototherapy in the treatment of other non-seasonal syndromes has not yet been explored thoroughly and this line of research seems worth continuing.

A cross-over comparison study of exposure, in the evenings only, to bright versus dim light was carried out on nine female patients with seasonal affective disorder. A significant antidepressant effect of the bright lights was shown. No consistent observable effects were produced by the dim lights. These results support earlier studies demonstrating the efficacy of bright light given morning and evening. The antidepressant effect of light is not mediated by sleep deprivation, and the early morning hours are not crucial for a response.

In several studies we have found that treatment with bright environmental light, capable of suppressing human melatonin, reverses the winter depressive symptoms of patients with seasonal affective disorder (SAD), whereas light too dim to suppress human melatonin is therapeutically ineffective. This finding, as well as the central importance of melatonin as a hormonal mediator of photoperiodic changes on seasonal rhythms in animals, led us to test the hypothesis that melatonin mediates the effects of shortening days on the winter symptoms of SAD and that the modification of melatonin secretion by bright light mediates its antidepressant effects. We partially reversed the antidepressant effects of phototherapy in 8 SAD patients by oral melatonin administration, but in another study of 19 SAD patients we failed to find any therapeutic difference between the beta-adrenergic blocker, atenolol, which inhibits melatonin secretion, and placebo. In a third study of 7 SAD patients we showed that the anti-depressant effects of phototherapy were not photoperiodic and appeared to be independent of melatonin suppression. There is some preliminary evidence that melatonin secretion may be abnormal in SAD. We conclude that while melatonin may play some role in the symptoms of SAD and the effects of phototherapy, it cannot by itself account for these phenomena.

This report summarizes presentations made at a National Institute of Mental Health-sponsored workshop dealing with recurrent winter depression, or seasonal affective disorder (SAD), and with phototherapy as its treatment. Workshop participants reviewed major issues in the following areas: (1) diagnosis, clinical characteristics, and epidemiology of the disorder; (2) critical issues in phototherapy research; (3) biologic effects of light and mechanism of action of phototherapy; (4) biologic abnormalities in SAD; and (5) animal models and their applicability to the study of SAD. Most research evidence to date supports the efficacy of phototherapy in the treatment of SAD. However, considerable controversy remains concerning its mechanism of action and the underlying pathophysiology of the disorder. These and other unresolved issues are reviewed, and areas of consensus in the field are identified.

Seasonal affective disorder is characterized by recurring cycles of fall-winter depression and spring-summer hypomania (or euthymia). In winter, depressed patients with seasonal affective disorder respond to daily treatments with five to six hours of bright artificial light in two to three days. They relapse two to three days after light is withdrawn. In this study carefully controlled experimental conditions were used to determine whether phototherapy acts via a photoperiodic mechanism in which the timing of light is critical for its therapeutic effect. Photoperiodism is a common regulatory mechanism in animal seasonal rhythms and depends for its effect on light-induced changes in the pattern of nocturnal melatonin secretion. The results reported herein of "skeleton photoperiod" experiments indicate that the efficacy of phototherapy may not depend on its timing or its effect on melatonin secretion.

The authors identified a patient who had premenstrual syndrome (late luteal phase dysphoric disorder) only in the fall and winter and was virtually asymptomatic during the spring and summer. On the basis of previous experience with seasonal affective disorder, they treated the patient with bright artificial light, which reversed her symptoms. On subsequent occasions they reversed this treatment effect with oral melatonin administration and found that propranolol and atenolol, beta-antagonists that inhibit the production of melatonin, had a therapeutic effect similar to that of light. They discuss the implications of these findings in relation to the importance of melatonin as a mediator of seasonal rhythms in biology.

Studies have shown that depressed patients with seasonal affective disorder (SAD) respond to treatment with bright artificial light. In this study 2 hours of bright artificial light administered in the morning for 1 week did not alter mood in 11 normal subjects. This finding suggests that the mood-enhancing effect of light for SAD patients is not necessarily generalizable to other populations.

The authors treated winter depression in 13 patients with typical seasonal affective disorder by extending the length of winter days with bright and dim light in the morning and evening in a balanced-order crossover study. Bright light had a marked antidepressant effect, whereas the dim light did not. This response could not be attributed to sleep deprivation. Subsequent pilot studies indicated that bright evening light alone is probably also effective. Several patients were able to maintain the antidepressant response throughout the winter months by continuing daily light treatments.