The Circadian Basis of Winter Depression

The following test of the circadian phase-shift hypothesis for patients with winter depression (seasonal affective disorder, or SAD) uses low-dose melatonin administration in the morning or afternoon/evening to induce phase delays or phase advances, respectively, without causing sleepiness. Correlat...

Full description

Saved in:
Bibliographic Details
Published inProceedings of the National Academy of Sciences - PNAS Vol. 103; no. 19; pp. 7414 - 7419
Main Authors Lewy, Alfred J., Lefler, Bryan J., Emens, Jonathan S., Bauer, Vance K.
Format Journal Article
LanguageEnglish
Published United States National Academy of Sciences 09.05.2006
Subjects
Adult
Antidepressants
Biological Sciences
Biomarkers
Circadian Rhythm - drug effects
Circadian Rhythm - physiology
Correlations
Depressive disorders
Female
Humans
Male
Medical treatment
Melatonin - metabolism
Melatonin - pharmacology
Middle Aged
Phase shift
Placebos
Pretreatment
Seasonal affective disorder
Seasonal Affective Disorder - drug therapy
Seasonal Affective Disorder - metabolism
Seasonal Affective Disorder - pathology
Seasonal Affective Disorder - physiopathology
Statistical significance
Statistical variance
Online AccessGet full text

Cover

More Information
Summary:The following test of the circadian phase-shift hypothesis for patients with winter depression (seasonal affective disorder, or SAD) uses low-dose melatonin administration in the morning or afternoon/evening to induce phase delays or phase advances, respectively, without causing sleepiness. Correlations between depression ratings and circadian phase revealed a therapeutic window for optimal alignment of circadian rhythms that also appears to be useful for phase-typing SAD patients for the purpose of administering treatment at the correct time. These analyses also provide estimates of the circadian component of SAD that may apply to the antidepressant mechanism of action of appropriately timed bright light exposure, the treatment of choice. SAD may be the first psychiatric disorder in which a physiological marker correlates with symptom severity before, and in the course of, treatment in the same patients. The findings support the phaseshift hypothesis for SAD, as well as suggest a way to assess the circadian component of other psychiatric, sleep, and chronobiologic disorders.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Article-2
ObjectType-Feature-1
Author contributions: A.J.L. designed research; A.J.L. and V.K.B. performed research; A.J.L., B.J.L., J.S.E., and V.K.B. analyzed data; and A.J.L., B.J.L., J.S.E., and V.K.B. wrote the paper.
Communicated by Aaron B. Lerner, Yale University School of Medicine, New Haven, CT, March 27, 2006
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0602425103