Phase Advance of the Circadian Sleep-Wake Cycle as an Antidepressant

Wehr, T A; Wirz‐Justice, Anna; Goodwin, FK; Duncan, W. Raymond; Gillin, J. Christian

doi:10.1126/science.227056

Cited by 479 publications

(167 citation statements)

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“…In the "internal coincidence model" (Wehr and Wirz-Justice, 1981), a causal link is postulated between a phase advance of circadian rhythms and mood. Evidence consistent with such a causal relationship was obtained in (uncontrolled) experimental studies on the effects of phase-advancing sleep, relative to internal rhythms (Wehr et al, 1979;Sack et al, 1985;Souêtre et al, 1987), with a beneficial effect on mood. Wehr and Goodwin (1983) reviewed evidence for a phase advance of circadian rhythms in depressives compared to healthy controls.…”

Section: Introductionmentioning

confidence: 74%

“…This should be possible by controlling the light-dark cycle while sleep time is changed. As noted earlier, phase shifts of sleep resulted in mood changes in depressed subjects (Wehr et al, 1979;Sack et al, 1985;Souêtre et al, 1987), but in these studies the light-dark cycle was shifted as well. In the present study, we chose the first procedure; that is, subjects were exposed to bright light at particular times of the day to produce phase shifts while sleep time was fixed.…”

Section: Introductionmentioning

confidence: 74%

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Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Gordijn¹,

Beersma²,

Korte³

et al. 1998

J Biol Rhythms

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In a crossover design, 8 nonseasonal depressed subjects, selected on the presence of diurnal mood variations, and 8 sex and age-matched controls were exposed to dim light (< 10 lux) in the evening (18:00-21:00 h) and bright light (2500 lux) in the morning (ML, 6:00-9:00 h), to dim light in the morning and bright light in the evening (EL), or to dim light both in the evening and in the morning (DL) during 3 consecutive days in each of these conditions. There were no initial phase differences between depressed and healthy subjects in the timing of dim light melatonin onset, sleep termination, and body temperature. The phase shifts after EL and ML in both healthy and depressed subjects were as expected on the basis of a human phase response curve. On average, there was no therapeutic effect of the light exposure in the depressed patients. Two patients improved, but these effects do not seem to be related to shifts in the circadian system.

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Section: Introductionmentioning

confidence: 74%

Section: Introductionmentioning

confidence: 74%

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Gordijn¹,

Beersma²,

Korte³

et al. 1998

J Biol Rhythms

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“…Disrupted biological rhythms have been hypothesized to underlie affective dysregulation (Healy, 1987;Ehlers et al, 1988). Phase-advanced temperature profiles and onsets of rapid-eye-movement (REM) sleep relative to sleep schedules in depression prompted treatment trials using a shift of the sleep schedule forward by 6 h to correct the shift in temperature and REM rhythms (Wehr et al, 1979). Alternatively, biological rhythm disruptions and depression after psychosocial losses have also been linked to changes in social zeitgebers resulting from such losses (Ehlers et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Treatment Enhances Ultradian Rhythms of CSF Monoamine Metabolites in Patients with Major Depressive Episodes

Salomon

Kennedy

Johnson

et al. 2005

Neuropsychopharmacol

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Unipolar and bipolar depressions show abnormal behavioral manifestations of ultradian (less than 24 h) rhythms, but abnormal rhythms of the central neurotransmitters thought to be important for depression pathophysiology (eg dopamine (DA) and serotonin (5-HT)) have not been shown in this time frame. Since antidepressant treatments normalize disrupted rhythms in depression (eg rapid-eyemovement sleep and hormonal rhythms), we hypothesized that depression-related changes in ultradian oscillations of DA and 5-HT might be revealed during antidepressant treatment. Cerebrospinal fluid (CSF) samples collected q10 min for 24 h in 13 patients experiencing major depressive episodes (MDE) before and after treatment for 5 weeks with sertraline or bupropion were assayed for levels of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), and their ratio was calculated. Data were analyzed in the frequency domain using Fourier transforms and multivariate permutation testing. Antidepressant treatments were associated with decreased variance for 5-HIAA, increased variance for HVA, and markedly increased variance for the HVA : 5-HIAA ratio (po0.05, po0.02, and po0.003, respectively). With treatment, the correlations between 5-HIAA and HVA weakened (p ¼ 0.06). Power spectral density (PSDFthe Fourier magnitude squared) of the 5-HIAA signals at periods of 1.75 and 3.7 h (both po0.05) decreased, while circadian cycling of HVA levels (po0.05) and of the ratio (po0.005) increased after treatment. The PSD of the full-length HVA : 5-HIAA ratio series after treatment increased in rapid variability (20-103 min periods, po0.05). Spectrographic windowing demonstrated a focal span of enhanced HVA : 5-HIAA ratio variability following antidepressant treatment, in an approximately 84-min period through the evening (po0.05). Periodic neurotransmitter relationships in depressed patients were altered by treatment in this analysis of a small data set. This may represent a baseline abnormality in the regulation of periodic functions involved in the depression pathophysiology, but it could also be due to an unrelated antidepressant effect. Further studies including comparisons with healthy subject data are in progress.

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“…Thus advancing the sleep time by several hours alleviated the clinical condition in some depressives, either as the only therapeutic measure 27 or in combination with preceding partial sleep deprivation. 28 The inter^ pretation of this effect, however, is difficult, as the sleep advance implies a sleep deprivation during the second half of the night, which in itself seems to be of therapeutic value.…”

Section: Phasementioning

confidence: 99%

Circadian Rhythm Disturbances in Affective Disorders: Facts and Fictions

Zerssen¹,

Dirlich²,

Zulley³

1989

New Directions in Affective Disorders

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fjie cycling nature of affective disorders has put these psychopathological con-[tions into the focus of medical chronobiology. However, our knowledge is still tther limited in this respect, and too often casual observations and theoretical eculations are accepted as proving profound disturbances of biological (above |, circadian) rhythms in these disorders. It is our intention to evaluate critically gjfb present State of knowledge in this field in order to disentangle proved facts om mere fictions. Particular reference is made to carefully designed observations laffectively ill patients in a time-cue-free environment, as they provide the only |id basis for conclusions regarding the endogenous component of biological |thms. Only those hypotheses are discussed that have drawn most attention in tronobiological research to affective disorders.jssumed Disturbances of Circadian Rhythms hiod 3id cycling in bipolar affective illness was explained by Halberg 1 as a beat phetenon due to the interaction of circadian rhythms entrained to the 24-h routine Jäily life with a free-running rhythm of, for example, adrenocortical activity. cycle length of psychopathology should then be predictable from the period this nonentrained and the entrained (24-h) rhythm-or vice versa: The period ;the free-running circadian rhythm should be predictable from the 24-h period äntrained circadian rhythms and the period of the cycles of the mental disorder. >This concept was demonstrated rather than validated on the basis of data from gle case study in a rapid cycler. 2 Later it was supported by self-assessed oral gerature data in an outpatient suffering from rapidly cycling bipolar affective |s. 3 The same authors also reported the occurrence of free-running biological s in other outpatients with rapidly cycling manic-depressive disease who Aken the measurements themselves during the illness. Unfortunately, it cannot Huded that the abnormalities were entirely caused by unreliable data due to iental state in which the patients took the measurements. jf| e hght is thrown on this problem by case reports from another group of phers. They had found a 22.5-h component in addition to the 24-h component

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Phase Advance of the Circadian Sleep-Wake Cycle as an Antidepressant

Cited by 479 publications

References 30 publications

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Testing the Hypothesis of a Circadian Phase Disturbance Underlying Depressive Mood in Nonseasonal Depression

Treatment Enhances Ultradian Rhythms of CSF Monoamine Metabolites in Patients with Major Depressive Episodes

Circadian Rhythm Disturbances in Affective Disorders: Facts and Fictions

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