Sleep in fall/winter seasonal affective disorder: effects of light and changing seasons.

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.

Biogenic amines in seasonal affective disorder: effects of light therapy.

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.

Effects of different wavelengths in seasonal affective disorder.

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.

Effects of bright light on resting metabolic rate in patients with seasonal affective disorder and control subjects.

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.

Measurement of cortisol and lymphocyte subpopulations in depressed and conduct-disordered adolescents.

Lymphocyte subpopulations were analyzed in 11 adolescents with major depressive disorder, 11 with conduct disorder, and eight normal age-matched subjects. No significant differences were noted on any T or B cell measure between the groups. Further, no significant correlations were found between any cortisol measure (baseline cortisol, post-dexamethasone cortisol, urinary free cortisol) and any lymphocyte measure in either depressed or conduct-disordered adolescents. The negative findings in this small sample contrast with those reported in adult patients and suggest that an aging effect may be associated with the immunological changes reported in older depressed patients.

Effects of light treatment on core body temperature in seasonal affective disorder.

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.

Seasonal affective disorder and visual impairment: two case studies.

Winter depressive episodes in patients with seasonal affective disorder are induced by light deficiency and are successfully treated by enhancing environmental light. The authors investigated the role of abnormal visual information processing in the genesis of seasonal affective disorder symptoms by examining two patients with impaired vision and recurrent winter depressions. The first patient developed winter depressions after developing a traumatic cataract in one eye, and was helped by light therapy. The second patient, fully blind since she was 1 year old, nonetheless suffered as an adult from winter depressions, which responded to bright--but not to dim--light treatment. The authors discuss the implications of these findings.

Phototherapy in individuals with and without subsyndromal seasonal affective disorder.

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.

Psychobiological effects of carbohydrate- and protein-rich meals in patients with seasonal affective disorder and normal controls.

Patients with seasonal affective disorder (SAD) frequently report carbohydrate craving and note that carbohydrate ingestion energizes them. Bright artificial light has been shown to reverse the symptoms of SAD, including carbohydrate craving. In this study, 16 depressed SAD patients and 16 matched controls were fed two different isocaloric meals, one rich in protein and one rich in carbohydrates, in a crossover design. Although their biochemical response in terms of plasma large neutral amino acid concentrations was identical, SAD patients reported activation following carbohydrate ingestion, whereas normal controls reported sedation. Marked ordering effects on psychological parameters were noted, suggesting that order should be taken into account as a methodological consideration in meal studies.

Phototherapy in subsyndromal seasonal affective disorder (S-SAD) and "diagnosed" controls.

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.

Differential response of rat splenic lymphocytes to short-term and long-term neuroendocrine challenges: possible desensitization of the cellular immune response to corticosteroids.

The effects of acute or chronic in vivo or in vitro exposures to supra-physiologic doses of isoproterenol, insulin or dexamethasone on rat splenic lymphocyte proliferation were investigated. Acutely, all in vivo challenges inhibited mitogen-induced lymphocyte proliferation, and correlated to increased corticosterone levels. However, chronic in vivo exposure to dexamethasone resulted in lymphocyte activity which was equivalent to controls, while chronic isoproterenol treatment enhanced the lymphocyte response to mitogen. These data suggest that chronic stress may result in a desensitization of the immune system to corticosteroids as well as a direct in vivo modulation by isoproterenol to enhance lymphocyte proliferation.

No mood-altering effects found after treatment of normal subjects with bright light in the morning.

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.

Eye versus skin phototherapy 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.

Depression, immunocompetence, and prostaglandins of the E series.

Plasma prostaglandin E1 and E2, and quantitative and qualitative measures of immune function, were determined in depressed patients and healthy controls. Prostaglandin E2 was significantly elevated in the depressed group, and prostaglandin E1 showed a trend in the same direction. Lymphocyte stimulation responses, as measured by phytohemagglutinin, concanavalin A, and pokeweed mitogen, were significantly lower in the depressed group. Helper and suppressor T cell percentages did not significantly differ in the two populations. In the depressed group, prostaglandin E1 showed a significant inverse correlation with concanavalin A, and prostaglandin E2 showed a similar trend. These preliminary data suggest prostaglandins of the E series may be related to abnormalities of cellular immunity previously documented in depression.