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      Chronobiology and mood disorders Translated title: Cronobiología y trastornos afectivos Translated title: Chronobiologie et troubles de l'humeur

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          Abstract

          The clinical observations of diurnal variation of mood and early morning awakening in depression have been incorporated into established diagnostic systems, as has the seasonal modifier defining winter depression (seasonal affective disorder, SAD). Many circadian rhythms measured in depressive patients are abnormal: earlier in timing, diminished in amplitude, or of greater variability. Whether these disturbances are of etiological significance for the role of circadian rhythms in mood disorders, or a consequence of altered behavior can only be dissected out with stringent protocols (eg, constant routine or forced desynchrony). These protocols quantify contributions of the circadian pacemaker and a homeostatic sleep process impacting on mood, energy, appetite, and sleep. Future studies will elucidate any allelic mutations in “circadian clock” –related or “sleep”-related genes in depression. With respect to treatment, antidepressants and mood stabilizers have no consistent effect on circadian rhythmicity. The most rapid antidepressant modality known so far is nonpharmacological: total or partial sleep deprivation in the second half of the night. The disadvantage of sleep deprivation, that most patients relapse after recovery sleep, can be prevented by coadministration of lithium, pindolol, serotonin (5-HT) reuptake inhibitors, bright light, or a subsequent phase-advance procedure. Phase advance of the sleep-wake cycle alone also has rapid effects on depressed mood, which lasts longer than sleep deprivation. Light is the treatment of choice for SAD and may prove to be useful for nonseasonal depression, alone or as an adjunct to medication. Chronobiological concepts emphasize the important role of zeitgebers to stabilize phase, light being the most important, but dark (and rest) periods, regularity of social schedules and meal times, and use of melatonin or its analogues should also be considered. Advances in chronobiology continue to contribute novel treatments for affective disorders.

          Translated abstract

          Las observaciones clínicas de la variatión diurna del ánimo y el despertar precoz en la depresión se han incorporado a sistemas diagnósticos establecidos, como es el caso de la modificatión estacional que define la depresión invernal (trastorno afectivo estacional, TAE). Muchos ritmos circadianos medidos en pacientes depresivos son anormales: por ocurrir antes del tiempo que corresponde, tener una amplitud disminuida o una mayor variabilidad. Para precisar si estas alteraciones tienen un significado etiológico en el rol que cumplen los ritmos circadianos en los trastornos afectivos o si son una consecuencia de conductas alteradas se requiere de un análisis minucioso con protocolos muy estrictos (por ejemplo, rutina constante o desincronía forzada). Estos protocolos cuaniifican las contribuciones del marcapaso circadiano y del proceso de sueño homeostático que influyen en el ánimo, la energía, el apetito y el sueño. Estudios futuros aclararán algunas mutaciones alélicas de genes relacionados con el “reloj circadiano” o el “sueño” en la depresión. Respecto al tratamiento, los antidepresivos y los estabilizadores del ánimo no tienen efectos consistentes en la ritmicidad circadiana. La esirategia antidepresiva más rápida conocida hasta la fecha es de tipo no farmacológico: la privatión total o parcial de sueño durante la segunda mitad de la noche. La desventaja de la privatión de sueño es que la mayoría de los patientes recaen después de recuperar el sueño; esto puede prevenirse mediante la coadministratión de litio, pindolol, inhibidores de la recaptatión de serotonina (5-HT), luz brillante, o a través de un procedimiento posterior de avance de fase. El avance de fase del ciclo sueño vigilia en forma exclusiva tiene también rápidos efectos en el ánimo depresivo, lo que dura mayor tiempo que la privation de sueño. La luz es el tratamiento de electión para el TAE y puede resulter útil en la depresión no estacional al administrarla sola o en combinatión con medicamentos. Los conceptos cronobiológicos enfatizan el importante papel de los “zeitgebers” para estabilizar la fase, siendo la luz el más importante, pero también se deben considerar los períodos de oscuridad (y reposo), la regularidad de los horarios sociales y de las comidas y el empleo de melatonina o de sus análogos. Los avances en la cronobiologia continúan para contribuir a nuevos tratamientos para los trastornos afectivos.

          Translated abstract

          Les observations cliniques de variations diurnes de l'humeur et de réveil matinal précoce dans la dépression ont été intégrées dans des systèmes diagnostiques établis tel le facteur saisonnier qui définit la dépression hivernale (trouble affectif saisonnier, TAS). Beaucoup de rythmes circadiens mesurés chez les patients dépressifs sont anormaux: plus précoces, diminués en amplitude ou de plus grande variabilité. Seuls des protocoles rigoureux (par exemple, routine constante ou désynchronisation forcée) sont à même de déterminer si ces perturbations ont une signification étiologique quant au rôle des rythmes circadiens dans les troubles de l'humeur ou si elles sont la conséquence d'une modification comportementale. Ces protocoles quantifient les participations respectives de l'oscillateur circadien et d'un processus homéostatique lié au sommeil ayant des répercussions sur l'humeur, l'énergie, l'appétit et le sommeil. Les études à venir mettront en évidence, si tant est qu'elles existent, les mutations alléliques des gènes qui interviennent dans les phénomènes « d'horloge » ou de « sommeil » au cours de la dépression. En ce qui concerne le traitement, les antidépresseurs et les régulateurs de l'humeur n'ont pas d'effet constant sur le rythme circadien. L'effet antidépresseur le plus rapide connu à ce jour n'est pas pharmacologique: c'est la privation totale ou partielle de sommeil dans la seconde moitié de la nuit. L'inconvénient de la privation de sommeil, constitué par la rechute de la plupart des patients après le sommeil de récupération, peut être prévenu par l'administration concomitante de lithium, de pindolol, d'inhibiteurs de la recapture de la sérotonine (5-HT), de lumière vive ou par une procédure d'avance de phase. L'avance de phase dans les cycles veille-sommeil exerce par elle-même également des effets rapides sur l'humeur dépressive qui se maintiennent plus longtemps que ceux de la privation de sommeil, La photothérapie est le traitement de choix du TAS et pourra s'avérer utile dans la dépression non saisonnière, seule ou en association à un traitement médicamenteux. Les concepts chronobiologiques soulignent le rôle important des synchroniseurs dans la stabilisation de phase, la lumière étant le plus important. Cependant, les périodes d'obscurité (et de repos), la régularité des repas et des rythmes sociaux et l'utilisation de la mélatonine ou de ses analogues doivent être également considérées. Les avancées en chronobiologie continuent à contribuer au développement de médicaments nouveaux dans les troubles affectifs.

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          Most cited references74

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          Timing of human sleep: recovery process gated by a circadian pacemaker.

          A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.
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            Life between clocks: daily temporal patterns of human chronotypes.

            Human behavior shows large interindividual variation in temporal organization. Extreme "larks" wake up when extreme "owls" fall asleep. These chronotypes are attributed to differences in the circadian clock, and in animals, the genetic basis of similar phenotypic differences is well established. To better understand the genetic basis of temporal organization in humans, the authors developed a questionnaire to document individual sleep times, self-reported light exposure, and self-assessed chronotype, considering work and free days separately. This report summarizes the results of 500 questionnaires completed in a pilot study individual sleep times show large differences between work and free days, except for extreme early types. During the workweek, late chronotypes accumulate considerable sleep debt, for which they compensate on free days by lengthening their sleep by several hours. For all chronotypes, the amount of time spent outdoors in broad daylight significantly affects the timing of sleep: Increased self-reported light exposure advances sleep. The timing of self-selected sleep is multifactorial, including genetic disposition, sleep debt accumulated on workdays, and light exposure. Thus, accurate assessment of genetic chronotypes has to incorporate all of these parameters. The dependence of human chronotype on light, that is, on the amplitude of the light:dark signal, follows the known characteristics of circadian systems in all other experimental organisms. Our results predict that the timing of sleep has changed during industrialization and that a majority of humans are sleep deprived during the workweek. The implications are far ranging concerning learning, memory, vigilance, performance, and quality of life.
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              The homeostatic regulation of sleep need is under genetic control.

              Delta power, a measure of EEG activity in the 1-4 Hz range, in slow-wave sleep (SWS) is in a quantitative and predictive relationship with prior wakefulness. Thus, sleep loss evokes a proportional increase in delta power, and excess sleep a decrease. Therefore, delta power is thought to reflect SWS need and its underlying homeostatically regulated recovery process. The neurophysiological substrate of this process is unknown and forward genetics might help elucidate the nature of what is depleted during wakefulness and recovered during SWS. We applied a mathematical method that quantifies the relationship between the sleep-wake distribution and delta power to sleep data of six inbred mouse strains. The results demonstrated that the rate at which SWS need accumulated varied greatly with genotype. This conclusion was confirmed in a "dose-response" study of sleep loss and changes in delta power; delta power strongly depended on both the duration of prior wakefulness and genotype. We followed the segregation of the rebound of delta power after sleep deprivation in 25 BXD recombinant inbred strains by quantitative trait loci (QTL) analysis. One "significant" QTL was identified on chromosome 13 that accounted for 49% of the genetic variance in this trait. Interestingly, the rate at which SWS need decreases did not vary with genotype in any of the 31 inbred strains studied. These results demonstrate, for the first time, that the increase of SWS need is under a strong genetic control, and they provide a basis for identifying genes underlying SWS homeostasis.
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                Author and article information

                Contributors
                Centre for Chronobiology, Psychiatric University Clinic, Basel, Switzerland
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                December 2003
                December 2003
                : 5
                : 4
                : 315-325
                Affiliations
                Centre for Chronobiology, Psychiatric University Clinic, Basel, Switzerland
                Author notes
                Article
                10.31887/DCNS.2003.5.4/awirzjustice
                3181777
                22033593
                5bbbc57e-a304-4691-92f6-823398178642
                Copyright: © 2003 LLS

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                State of the Art

                Neurosciences
                sleep deprivation,major depression,circadian rhythm,melatonin,light therapy,seasonal affective disorder

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