Circadian phase-shifting effects of a laboratory environment: a clinical trial with bright and dim light

BACKGROUND: Our aims were to examine the influence of different bright light schedules on mood, sleep, and circadian organization in older adults (n = 60, ages 60–79 years) with insomnia and/or depression, contrasting with responses of young, healthy controls (n = 30, ages 20–40 years). METHODS: Volunteers were assessed for one week in their home environments. Urine was collected over two 24-hour periods to establish baseline acrophase of 6-sulphatoxymelatonin (aMT6s) excretion. Immediately following home recording, volunteers spent five nights and four days in the laboratory. Sleep periods were fixed at eight hours in darkness, consistent with the volunteers' usual sleep periods. Volunteers were randomly assigned to one of three light treatments (four hours per day) within the wake period: (A) two hours of 3,000 lux at 1–3 hours and 13–15 hours after arising; (B) four hours of 3,000 lux at 6–10 hours after arising; (C) four hours of dim placebo light at 6–10 hours after arising. Lighting was 50 lux during the remainder of wakefulness. The resulting aMT6s acrophase was determined during the final 30 hours in the laboratory. RESULTS: Neither mood nor total melatonin excretion differed significantly by treatment. For the three light treatments, significant and similar phase-response plots were found, indicating that the shift in aMT6s acrophase was dependent upon the circadian time of treatment. The changes in circadian timing were not significantly correlated to changes in sleep or mood. CONCLUSION: The trial failed to demonstrate photoperiodic effects. The results suggest that even low levels of illumination and/or fixed timing of behavior had significant phase-shifting effects

Circadian phase response curves to light in older and young women and men

<p>Abstract</p> <p>Background</p> <p>The phase of a circadian rhythm reflects where the peak and the trough occur, for example, the peak and trough of performance within the 24 h. Light exposure can shift this phase. More extensive knowledge of the human circadian phase response to light is needed to guide light treatment for shiftworkers, air travelers, and people with circadian rhythm phase disorders. This study tested the hypotheses that older adults have absent or weaker phase-shift responses to light (3000 lux), and that women's responses might differ from those of men.</p> <p>Methods</p> <p>After preliminary health screening and home actigraphic recording baselines, 50 young adults (ages 18–31 years) and 56 older adults (ages 59–75 years) remained in light-controlled laboratory surroundings for 4.7 to 5.6 days, while experiencing a 90-min ultra-short sleep-wake cycle. Following at least 30 h in-lab baseline, over the next 51 h, participants were given 3 treatments with 3000 lux white light, each treatment for 3 h, centered at one of 8 clock times. The circadian rhythms of urinary aMT6s (a melatonin metabolite), free cortisol, oral temperature, and wrist activity were assessed at baseline and after treatment.</p> <p>Results</p> <p>Light (3000 lux for 3 h on 3 days) induced maximal phase shifts of about 3 h. Phase shifts did not differ significantly in amplitude among older and young groups or among women and men. At home and at baseline, compared to the young, the older adults were significantly phase-advanced in sleep, cortisol, and aMT6s onset, but not advanced in aMT6s acrophase or the temperature rhythm. The inflection from delays to advances was approximately 1.8 h earlier among older compared to young participants in reference to their aMT6s rhythm peaks, and it was earlier in clock time.</p> <p>Conclusion</p> <p>In these experimental conditions, 3000 lux light could shift the phase of circadian rhythms to about the same extent among older and young adults, but the optimal light timing for phase shifting differed. For an interval near 4 PM, bright light produced only negligible phase shifts for either age group.</p

Delayed sleep phase cases and controls

This is an Open Access article distributed under the terms of the Creative Commons Attribution Licens

Weak evidence of bright light effects on human LH and FSH

<p>Abstract</p> <p>Background</p> <p>Most mammals are seasonal breeders whose gonads grow to anticipate reproduction in the spring and summer. As day length increases, secretion increases for two gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH). This response is largely controlled by light. Light effects on gonadotropins are mediated through effects on the suprachiasmatic nucleus and responses of the circadian system. There is some evidence that seasonal breeding in humans is regulated by similar mechanisms, and that light stimulates LH secretion, but primate responses seem complex.</p> <p>Methods</p> <p>To gain further information on effects of bright light on LH and FSH secretion in humans, we analyzed urine samples collected in three experiments conducted for other goals. First, volunteers ages 18-30 years and 60-75 commenced an ultra-short 90-min sleep-wake cycle, during which they were exposed to 3000 lux light for 3 hours at balanced times of day, repeated for 3 days. Urine samples were assayed to explore any LH phase response curve. Second, depressed participants 60-79 years of age were treated with bright light or dim placebo light for 28 days, with measurements of urinary LH and FSH before and after treatment. Third, women of ages 20-45 years with premenstrual dysphoric disorder (PMDD) were treated to one 3-hour exposure of morning light, measuring LH and FSH in urine before and after the treatments.</p> <p>Results</p> <p>Two of the three studies showed significant increases in LH after light treatment, and FSH also tended to increase, but there were no significant contrasts with parallel placebo treatments and no significant time-of-day treatment effects.</p> <p>Conclusions</p> <p>These results gave some support for the hypothesis that bright light may augment LH secretion. Longer-duration studies may be needed to clarify the effects of light on human LH and FSH.</p

Ethnicity, sleep, mood, and illumination in postmenopausal women

BACKGROUND: This study examined how ethnic differences in sleep and depression were related to environmental illumination and circadian rhythms. METHODS: In an ancillary study to the Women's Health Initiative, 459 postmenopausal women were recorded for one week in their homes, using wrist monitors. Sleep and illumination experience were estimated. Depression was self-rated with a brief adjective check list. Affective diagnoses were made using the SCID interview. Sleep disordered breathing was monitored with home pulse oximetry. RESULTS: Hispanic and African-American women slept less than European-American women, according to both objective recordings and their own sleep logs. Non-European-American women had more blood oxygen desaturations during sleep, which accounted for 26% of sleep duration variance associated with ethnicity. Hispanic women were much more depressed. Hispanic, African-American and Native-American women experienced less daily illumination. Less daily illumination experience was associated with poorer global functioning, longer but more disturbed sleep, and more depression. CONCLUSIONS: Curtailed sleep and poor mood were related to ethnicity. Sleep disordered breathing was a factor in the curtailed sleep of minority women. Less illumination was experienced by non-European-American women, but illumination accounted for little of the contrasts between ethnic groups in sleep and mood. Social factors may be involved

Evaluation of two circadian rhythm questionnaires for screening for the delayed sleep phase disorder.

ObjectiveDelayed sleep phase disorder (DSPD) is a condition in which patients often fall asleep some hours after midnight and have difficulty waking up in the morning. Circadian chronotype questionnaires such as Horne-Östberg Morningness-Eveningness Questionnaire (MEQ) and Basic Language Morningness (BALM) scale have been used for screening for DSPD. This study was to evaluate these two chronotype questionnaires for screening of DSPD.MethodsThe study samples were 444 DSPD and 438 controls. Cronbach's alpha coefficient was calculated to evaluate for internal consistency. An exploratory factor analysis was conducted using principal-axis factoring. The diagnostic performance of a test was evaluated using Receiver Operating Characteristic (ROC) curve analysis. A discriminant function analysis was also performed.ResultsFor internal consistency, Cronbach's alpha of 0.898 for BALM was higher than the 0.837 for MEQ, though both have acceptable internal consistency. BALM has better construct validity than the MEQ because some MEQ items measure different dimensions. However, when we evaluated the efficiency of two questionnaires for DSPD diagnosis by using the ROC curve, the BALM was similar to the MEQ. In a discriminant analysis with the BALM to classify the two groups (DSPD vs. normal), 6 items were identified that resulted in good classification accuracy. Upon examination of the classification procedure, 94.2% of the originally grouped cases were classified correctly.ConclusionThese findings suggest that the BALM has better psychometric properties than the MEQ in screening and discriminating DSPS

Delayed sleep phase syndrome is related to seasonal affective disorder.

BackgroundBoth delayed sleep phase syndrome (DSPS) and seasonal affective disorder (SAD) may manifest similar delayed circadian phase problems. However, the relationships and co-morbidity between the two conditions have not been fully studied. The authors examined the comorbidity between DSPS and SAD.MethodsWe recruited a case series of 327 DSPS and 331 controls with normal sleep, roughly matched for age, gender, and ancestry. Both DSPS and controls completed extensive questionnaires about sleep, the morningness-eveningness trait, depression, mania, seasonality of symptoms, etc.ResultsThe prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ(2)=12.65, p=0.002). DSPS were 3.3 times more likely to report SAD (odds ratio, 3.34; 95% CI, 1.41-7.93) compared to controls as defined by the Seasonal Pattern Assessment Questionnaire (SPAQ). Correspondingly, DSPS showed significantly higher seasonality scores compared to controls in mood, appetite, and energy level subscores and the global seasonality score (t=3.12, t=0.002; t=2.04, p=0.041; t=2.64, p=0.008; and t=2.15, p=0.032, respectively). Weight fluctuation during seasons and winter-summer sleep length differences were also significantly higher in DSPS than controls (t=5.16, p&lt;0.001 and t=2.64, p=0.009, respectively). SAD and S-SAD reported significantly higher eveningness, higher depression self-ratings, and more previous mania symptoms compared to non-seasonal subjects regardless of whether they were DSPS or controls.ConclusionsThese cases suggested that DSPS is partially comorbid with SAD. These data support the hypothesis that DSPS and SAD may share a pathophysiological mechanism causing delayed circadian phase

Delayed sleep phase syndrome is related to seasonal affective disorder.

BackgroundBoth delayed sleep phase syndrome (DSPS) and seasonal affective disorder (SAD) may manifest similar delayed circadian phase problems. However, the relationships and co-morbidity between the two conditions have not been fully studied. The authors examined the comorbidity between DSPS and SAD.MethodsWe recruited a case series of 327 DSPS and 331 controls with normal sleep, roughly matched for age, gender, and ancestry. Both DSPS and controls completed extensive questionnaires about sleep, the morningness-eveningness trait, depression, mania, seasonality of symptoms, etc.ResultsThe prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ(2)=12.65, p=0.002). DSPS were 3.3 times more likely to report SAD (odds ratio, 3.34; 95% CI, 1.41-7.93) compared to controls as defined by the Seasonal Pattern Assessment Questionnaire (SPAQ). Correspondingly, DSPS showed significantly higher seasonality scores compared to controls in mood, appetite, and energy level subscores and the global seasonality score (t=3.12, t=0.002; t=2.04, p=0.041; t=2.64, p=0.008; and t=2.15, p=0.032, respectively). Weight fluctuation during seasons and winter-summer sleep length differences were also significantly higher in DSPS than controls (t=5.16, p&lt;0.001 and t=2.64, p=0.009, respectively). SAD and S-SAD reported significantly higher eveningness, higher depression self-ratings, and more previous mania symptoms compared to non-seasonal subjects regardless of whether they were DSPS or controls.ConclusionsThese cases suggested that DSPS is partially comorbid with SAD. These data support the hypothesis that DSPS and SAD may share a pathophysiological mechanism causing delayed circadian phase