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Lewy AJ, Emens JS, Songer JB, et al. Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model. Sleep Med Clin. 2009;4(2):285-299doi: 10.1016/j.jsmc.2009.02.003.
Lewy, A. J., Emens, J. S., Songer, J. B., Sims, N., Laurie, A. L., Fiala, S. C., & Buti, A. L. (2009). Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model. Sleep medicine clinics, 4(2), 285-299. https://doi.org/10.1016/j.jsmc.2009.02.003
Lewy, Alfred J, et al. "Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model." Sleep medicine clinics vol. 4,2 (2009): 285-299. doi: https://doi.org/10.1016/j.jsmc.2009.02.003
Lewy AJ, Emens JS, Songer JB, Sims N, Laurie AL, Fiala SC, Buti AL. Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model. Sleep Med Clin. 2009 Jun 01;4(2):285-299. doi: 10.1016/j.jsmc.2009.02.003. PMID: 20160896; PMCID: PMC2768314.
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Sleep Med Clin. 2009 Jun 01;4(2):285-299. doi: 10.1016/j.jsmc.2009.02.003.

Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model.

Sleep medicine clinics

Alfred J Lewy, Jonathan S Emens, Jeannie B Songer, Neelam Sims, Amber L Laurie, Steven C Fiala, Allie L Buti

Affiliations

  1. Oregon Health & Science University, Portland, OR; phone: 503-494-7746, fax: 503-494-5329, [email protected].

PMID: 20160896 PMCID: PMC2768314 DOI: 10.1016/j.jsmc.2009.02.003

Abstract

The phase shift hypothesis (PSH) states that most patients with SAD become depressed in the winter because of a delay in circadian rhythms with respect to the sleep/wake cycle: According to the PSH, these patients should preferentially respond to the antidepressant effects of bright light exposure when it is scheduled in the morning so as to provide a corrective phase advance and restore optimum alignment between the circadian rhythms tightly coupled to the endogenous circadian pacemaker and those rhythms that are related to the sleep/wake cycle. Recent support for the PSH has come from studies in which symptom severity was shown to correlate with the degree of circadian misalignment: it appears that a subgroup of patients are phase advanced, not phase delayed; however, the phase-delayed type is predominant in SAD and perhaps in other disorders as well, such as non-seasonal unipolar depression. It is expected that during the next few years the PSH will be tested in these and other conditions, particularly since healthy subjects appear to have more severe symptoms of sub-clinical dysphoria correlating with phase-delayed circadian misalignment; critically important will be the undertaking of treatment trials to investigate the therapeutic efficacy of morning bright light or afternoon/evening low-dose melatonin in these disorders in which symptoms are more severe as the dim light melatonin onset (DLMO) is delayed with respect to the sleep/wake cycle (non-restorative sleep should also be evaluated, as well as bipolar disorder). The possibility that some individuals (and disorders) will be of the phase-advanced type should be considered, taking into account that the correct timing of phase-resetting agents for them will be bright light scheduled in the evening and/or low-dose melatonin taken in the morning. While sleep researchers and clinicians are accustomed to phase-typing patients with circadian-rhythm sleep disorders according to the timing of sleep, phase typing based on the DLMO with respect to the sleep/wake cycle may lead to quite different recommendations for the optimal scheduling of phase-resetting agents, particularly for the above disorders and conditions.

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