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Biomedical subjects

Katharine M Rex

Publications and source records attributed to Katharine M Rex.

5 recordsLinked to original sources

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.

Journal Article↗

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.

Black or African American↗

Melatonin excretion with affect disorders over age 60.

Numerous studies have reported low melatonin secretion in depression, but other studies have suggested no deficit or an increase. Alterations of circadian phase or duration of melatonin secretion have also been described. Since melatonin secretion decreases as we age, it seemed interesting to examine melatonin and depression in an aging sample. Volunteers who complained of mood or sleep problems were recruited for studies in which fractional urine specimens were collected for 24 h, both at home and in the laboratory. The major metabolite, 6-sulfatoxymelatonin (aMT6s), was determined by radioimmunoassay. Of 72 volunteers aged 60-78 years, seven had current major depression and 55% had a lifetime history of an affective disorder. A 55-fold range of home aMT6s excretion rates was observed. A lifetime history of any affective disorder was significantly associated with greater log(10)[mesor] aMT6s excretion in home collections and laboratory collections, but current affective disorders were neither significantly related to melatonin excretion nor to aMT6s acrophase timing, onset, offset or duration. These results are only weakly consistent with a photoperiodic hypothesis of depression.

Aged↗

Age-related changes of circadian rhythms and sleep-wake cycles.

OBJECTIVES: To compare relationships between the sleep-wake cycle and endogenous circadian rhythms in young and older adults and to examine correlates between evening naps and circadian rhythms in older adults. DESIGN: For 1 week of home recording, subjects wore wrist-activity monitors and kept daily sleep logs. After the home monitoring, subjects entered the laboratory on a 90-minute sleep-wake schedule and were monitored on this schedule for at least 30 hours. SETTING: Community living and laboratory. PARTICIPANTS: Sixty-seven young adults, aged 18 to 32, and 56 older adults, aged 60 to 75, who were healthy and had few sleep complaints. MEASUREMENTS: Times of nocturnal sleep, out-of-bed napping, and illumination were obtained at home. Sleep propensity and oral body temperature (OBT) were measured in the laboratory, along with circadian rhythms of cortisol and 6-sulfatoxymelatonin (aMT6s, assayed from urine samples collected every 90 minutes). RESULTS: Home sleep times and illumination acrophases (fitted peak times) were advanced in older adults. The phase angles (time intervals) between onset of aMT6s and sleep onset were not changed in older adults, but sleep offset was more advanced than acrophase and offset of aMT6s with aging. Acrophases of cortisol and sleep propensity were advanced in older adults to the same extent as sleep times, but OBT was less advanced than sleep times. Older adults who took evening naps showed more advanced sleep offset and circadian rhythms of aMT6s, but there were no differences in the phase angles of sleep onset and circadian rhythms of aMT6s and cortisol compared with older adults who did not take evening naps. CONCLUSION: Measuring different circadian markers suggested different phase relationships between the sleep-wake cycle and endogenous circadian rhythms in aging. Early awakening in older adults cannot be explained simply by a relative phase advance of the circadian system. Evening naps and advanced illumination may play a role in the advance of the circadian system in aging.

Adolescent↗

Depression and endogenous melatonin in postmenopausal women.

BACKGROUND: Previous reports on melatonin secretion in depression are numerous but conflicting. There are very few studies relating the duration of the nocturnal melatonin peak to depression, and the results of those studies have been equivocal. METHODS: We studied mood disorders and urinary melatonin excretion in 382 postmenopausal women. Psychiatric diagnoses and global assessment of functioning (GAF) scores were determined based on a Structured Clinical Interview for DSM-IV Axis I Disorders (SCID). Urinary 6-sulfatoxymelatonin (6-SMT) samples were collected for two 24-h periods at home. RESULTS: A positive family history of depression was significantly related to a longer duration of 6-SMT excretion. There were marginally significant associations between current major depression and delayed offset of 6-SMT excretion and between later acrophase and lifetime major depression, even with control for age, ethnicity, season, and several medications. LIMITATIONS: The subjects were studied in their home environments, where light effects were not controlled. Data were restricted to postmenopausal women, including a limited number of subjects with current major depression. CONCLUSIONS: These results suggest that there might be a familial vulnerability in the endogenous melatonin signal in subjects prone to depression, and an abnormality in the duration of the melatonin signal in those with current major depression.

Aged↗