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D. A. Oren

Bio: D. A. Oren is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Melatonin & Retinal. The author has an hindex of 1, co-authored 1 publications receiving 35 citations.
Topics: Melatonin, Retinal

Papers
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Journal ArticleDOI
TL;DR: This hypothesis offers a framework in which winter-induced retinal dopamine deficiency or retinal melatonin overactivity may cause SAD and by which light reverses this syndrome.
Abstract: The author describes how phototherapy may treat seasonal affective disorder (SAD) by stimulating the production of retinal dopamine and suppressing the production of retinal melatonin. This hypothesis offers a framework in which winter-induced retinal dopamine deficiency or retinal melatonin overactivity may cause SAD and by which light reverses this syndrome. This hypothesis is consistent with recent data indicating that phototherapy in SAD acts specifically through the eyes.

36 citations


Cited by
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Journal ArticleDOI
TL;DR: An understanding of the role of the pineal hormone and of its alterations in psychiatric diseases could help to identify the biological mechanisms underlying such disorders.

227 citations

Journal Article
TL;DR: There is substantial evidence for circadian phase shift and serotonergic hypotheses, but conflicting results may indicate that SAD is a biologically heterogeneous condition.
Abstract: The study of the pathophysiology of seasonal affective disorder (SAD, also known as winter depression) has historically been intimately linked to investigations into the mechanisms of action of light therapy. This paper reviews the studies on the pathophysiology of SAD with emphasis on circadian, neurotransmitter, and genetic hypotheses. There is substantial evidence for circadian phase shift and serotonergic hypotheses, but conflicting results may indicate that SAD is a biologically heterogeneous condition. Recent progress in defining the molecular mechanisms of the human circadian clock and retinal phototransduction of light will provide important new directions for future studies of the etiology and pathophysiology of SAD.

187 citations

Journal ArticleDOI
TL;DR: Bright light treatment is an established treatment for Seasonal Affective Disorder, but in non‐seasonal depression research results have been contrasting.
Abstract: Objective: Bright light treatment is an established treatment for Seasonal Affective Disorder, but in non-seasonal depression research results have been contrasting. Method: This study was designed as a 5-week controlled, double-blind, parallel trial in out-patients with a diagnosis (DSM-IV) of non-seasonal major depression, randomized to either active treatment (white light, 10 000 lux, 1 h daily) or placebo treatment (red light, 50 lux, 30 min daily) and concomitant treatment with sertraline in both groups. Results: One hundred and two patients were included in the study. Analyses showed that on all used scales the reduction in depression scores was larger in the bright light group than in the dim light group, and this reached statistical significance on all observer rating scales and on the SCL-90R self-assessment scale. The HAM-D6 was the most sensitive scale to measure improvement at endpoint. Conclusion: The study results support the use of bright light as an adjunct treatment to antidepressants in non-seasonal depression.

102 citations

Journal Article
TL;DR: It is hypothesized that brain neurotransmitter dysregulation may be at the origin of both the mood disorder and retinal sensitivity change, but the explanation for lower rod photoreceptor sensitivity in SAD is not known.
Abstract: A retinal sensitivity abnormality has been hypothesized in seasonal affective disorder (SAD). To explore this hypothesis, the electroretinogram (ERG) was used to assess retinal sensitivity at the level of the rod photoreceptor system. We examined 27 depressed patients who met DSM-III-R criteria for major depression, recurrent, with a seasonal (winter) pattern and 23 normal control subjects who were age-paired and sex-matched as much as possible with the SAD patients. ERG testing was performed in dark-adapted, dilated eyes in winter between 10:00 and 15:00 h. Retinal sensitivity was based on the light stimulus intensity necessary to reach a 50-μV amplitude threshold. We found that retinal sensitivity was significantly lower (0.21 log units) in SAD patients compared with normal control subjects and that 55% of the patients had a retinal sensitivity value one standard deviation lower than the mean value of the control subjects. These results are consistent with a retinal hyposensitivity hypothesis for SAD, but the explanation for lower rod photoreceptor sensitivity in SAD is not known. We hypothesize that brain neurotransmitter dysregulation may be at the origin of both the mood disorder and retinal sensitivity change.

65 citations

Journal ArticleDOI
TL;DR: The findings showed that for phototherapy of medium light intensity, a combination of morning-evening therapy regime yielded the best therapeutic effect, and the antidepressant effect of the morning- evening light regime was superior to a single pulse of light administered at other times of day.

64 citations