Effects of bright light on sleepiness, melatonin, and 25-hydroxyvitamin D3in winter seasonal affective disorder

doi:10.1016/0006-3223(95)00294-4

Biological Psychiatry

Volume 39, Issue 10, 15 May 1996, Pages 865-872

https://doi.org/10.1016/0006-3223(95)00294-4 Get rights and content

Sixteen patients with winter seasonal affective disorder and 13 healthy controls were exposed to 3300 lx of cool-white fluorescent light for either 1 hour or 15 min in the morning for 2 weeks during the winter. Subjective sleepiness, melatonin concentration in saliva, and serum 25-hydroxyvitamin D₃ concentration were measured before and after the 2-week trial as well as the following summer when the patients were well. There were no significant differences in the baseline values between the patients and healthy subjects. No significant differences in the outcome measures were observed in the patients or the controls in the two groups of each after the trial. The exposure to bright light resulted in a significant decrease in subjective sleepiness early in the evening in the patients but not in the control subjects. The reduction of depressive symptoms was associated with the decrease in subjective sleepiness but not with the changes in the melatonin or vitamin D concentrations.

References (23)

HarrisS et al.
Seasonal mood changes in 250 normal women
Psychiatry Res
(1993)
PartonenT
Effects of morning light treatment on subjective sleepiness and mood in winter depression
J Affective Disord
(1994)
ThompsonC et al.
Seasonal affective disorder and season-dependent abnormalities of melatonin suppression by light
Lancet
(1990)
YoungMA et al.
The temporal onset of individual symptoms in winter depression: Differentiating underlying mechanisms
J Affective Disord
(1991)
American Psychiatric Association
Diagnostic and Statistical Manual of Mental Disorders
(1987)
American Psychiatric Association
Practice guidelines for major depressive disorder in adults
Am J Psychiatry
(1993)
DahlK et al.
Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression
Acta Psychiatr Scand
(1993)
EastmanCI et al.
A placebo-controlled trial of light treatment for winter depression
J Affective Disord
(1992)
FeinsteinAR
Clinical Epidemiology: The Architecture of Clinical Research
(1985)
HoddesE et al.
Quantification of sleepiness: A new approach
Psychophysiology
(1973)

LewyAJ et al.

Antidepressant and circadian phase-shifting effects of light

Science

(1987)

Cited by (32)

Vitamin D, effects on brain development, adult brain function and the links between low levels of vitamin D and neuropsychiatric disease
2013, Frontiers in Neuroendocrinology
Citation Excerpt :
Stumpf and colleagues first suggested that vitamin D may contribute to the higher prevalence of seasonal affective disorders (i.e. depression associated with winter) at high latitudes (Stumpf and Privette, 1989). However to date, the results of small trials of vitamin D supplements in seasonal affective disorder have been inconclusive (Gloth et al., 1999; Lansdowne and Provost, 1998; Partonen et al., 1996). A number of cross-section studies have reported association between low vitamin D and depression (Hoang et al., 2011; Jorde et al., 2006; Wilkins et al., 2006).
Increasingly vitamin D deficiency is being associated with a number of psychiatric conditions. In particular for disorders with a developmental basis, such as autistic spectrum disorder and schizophrenia the neurobiological plausibility of this association is strengthened by the preclinical data indicating vitamin D deficiency in early life affects neuronal differentiation, axonal connectivity, dopamine ontogeny and brain structure and function. More recently epidemiological associations have been made between low vitamin D and psychiatric disorders not typically associated with abnormalities in brain development such as depression and Alzheimer’s disease. Once again the preclinical findings revealing that vitamin D can regulate catecholamine levels and protect against specific Alzheimer-like pathology increase the plausibility of this link. In this review we have attempted to integrate this clinical epidemiology with potential vitamin D-mediated basic mechanisms. Throughout the review we have highlighted areas where we think future research should focus.
Vitamin D: A neurosteroid affecting brain development and function; Implications for neurological and psychiatric disorders
2011, Vitamin D: Two-Volume Set
This chapter presents a summary of the evidence showing that vitamin D affects not only the function of individual brain cells but also the integrated function of the brain as a whole, i.e. behavior. Vitamin D can affect brain cell differentiation, neurotrophin expression, cytokine regulation, neurotransmitter synthesis, intracellular calcium signaling, antioxidant activity, and the expression of genes/proteins involved in neuronal structural and metabolism. This chapter also presents data from a number of studies that have manipulated vitamin D signaling through either dietary deficiency or by genetically ablating the receptor. Following this, it describes some studies where the active form of the vitamin 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) is administered. Furthermore, it discusses the effects of perturbing vitamin D signaling in both the developing and adult brain. In addition, it provides an understanding of possible mechanisms by which vitamin D is neuroprotective for the brain. Finally it sheds light on how changes in such a diverse array of cellular and molecular events could combine to affect brain function and how this may relate to certain disease states.
Vitamin D: A neurosteroid affecting brain development and function; implications for neurological and psychiatric disorders
2011, Vitamin D
This chapter presents a summary of the evidence showing that vitamin D affects not only the function of individual brain cells but also the integrated function of the brain as a whole, i.e. behavior. Vitamin D can affect brain cell differentiation, neurotrophin expression, cytokine regulation, neurotransmitter synthesis, intracellular calcium signaling, antioxidant activity, and the expression of genes/proteins involved in neuronal structural and metabolism. This chapter also presents data from a number of studies that have manipulated vitamin D signaling through either dietary deficiency or by genetically ablating the receptor. Following this, it describes some studies where the active form of the vitamin 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) is administered. Furthermore, it discusses the effects of perturbing vitamin D signaling in both the developing and adult brain. In addition, it provides an understanding of possible mechanisms by which vitamin D is neuroprotective for the brain. Finally it sheds light on how changes in such a diverse array of cellular and molecular events could combine to affect brain function and how this may relate to certain disease states.
Potential animal models of seasonal affective disorder
2011, Neuroscience and Biobehavioral Reviews
Citation Excerpt :
Vitamin D supplementation elevates mood in healthy individuals (Lansdowne and Provost, 1998), vitamin D deficient individuals (Shipowick et al., 2009), and individuals with SAD in the winter (Gloth et al., 1999). However, in a study with SAD patients, bright light therapy reduced symptoms, but did not alter serum vitamin D concentrations compared with controls (Partonen et al., 1996) indicating that therapeutic relief is achieved independently of vitamin D concentrations. Another alternative possibility is that a reduction in light alters suprachasmatic nuclei (SCN) firing to monoaminergic nuclei to induce a depressive-like phenotype.
Seasonal affective disorder (SAD) is characterized by depressive episodes during winter that are alleviated during summer and by morning bright light treatment. Currently, there is no animal model of SAD. However, it may be possible to use rodents that respond to day length (photoperiod) to understand how photoperiod can shape the brain and behavior in humans. As nights lengthen in the autumn, the duration of the nightly elevation of melatonin increase; seasonally breeding animals use this information to orchestrate seasonal changes in physiology and behavior. SAD may originate from the extended duration of nightly melatonin secretion during fall and winter. These similarities between humans and rodents in melatonin secretion allows for comparisons with rodents that express more depressive-like responses when exposed to short day lengths. For instance, Siberian hamsters, fat sand rats, Nile grass rats, and Wistar rats display a depressive-like phenotype when exposed to short days. Current research in depression and animal models of depression suggests that hippocampal plasticity may underlie the symptoms of depression and depressive-like behaviors, respectively. It is also possible that day length induces structural changes in human brains. Many seasonally breeding rodents undergo changes in whole brain and hippocampal volume in short days. Based on strict validity criteria, there is no animal model of SAD, but rodents that respond to reduced day lengths may be useful to approximate the neurobiological phenomena that occur in people with SAD, leading to greater understanding of the etiology of the disorder as well as novel therapeutic interventions.
Vitamin D, light and mental health
2010, Journal of Photochemistry and Photobiology B: Biology
Citation Excerpt :
The widely held conclusions from these studies have been that UV light does not contribute to efficacy [54] and that vitamin D is not involved [55]. Accordingly, in current phototherapy, UV light is filtered away, the patients may be fully dressed and only negligible amounts of vitamin D are formed [56]. On a closer scrutiny, however, these conclusions may have been drawn prematurely, especially in the light of recent findings from vitamin D research:
Vitamin D receptors and vitamin D metabolizing enzymes are present in the central nervous system. Calcitriol (the active vitamin D hormone) affects numerous neurotransmitters and neurotrophic factors, relevant for mental disorders. In the case of depressive disorders, considerable evidence supports a role of suboptimal vitamin D levels. However, the data are not conclusive and further studies are necessary. Especially, the relative importance of the pineal–melatonin system versus the vitamin D-endocrine system for the pathogenesis of seasonal affective disorders is presently unresolved. Two diagnoses, schizophrenia and autism, have been hypothetically linked to developmental (prenatal) vitamin D deficiency, however, also in adult patients, low levels have been reported, supporting the notion that vitamin D deficiency may not only be a predisposing developmental factor but also relate to the adult patients’ psychiatric state. Two cases are described, whose psychiatric improvement coincided with effective treatment of vitamin D deficiency.
Vitamin D and Mood Disorders Among Women: An Integrative Review
2008, Journal of Midwifery and Women's Health
Citation Excerpt :
Studies were included if the sample consisted of at least 50% women; if the focus was on subjects with major depressive disorder, SAD, PMS, postpartum depression, perinatal depression, or other mood disorders; and if serum 25(OH)D was measured. Of 11 studies initially identified, five were eliminated because they did not meet the inclusion criteria.44–48 The final six studies consist of one focused on SAD3; one on seasonal mood changes (not defined as SAD)49; one on PMS50; one on major depressive disorder51; one on major depression52; and one on mood disorders.53
This integrative review evaluates research studies that investigated the association between vitamin D and mood disorders affecting women to determine whether further research comparing these variables is warranted. A literature search using CINAHL, PsycINFO, MEDLINE, and PubMed databases was conducted to locate peer-reviewed mood disorder research studies that measured serum 25-hydroxyvitamin D (25[OH]D) levels. Four of six studies reviewed imparted significant results, with all four showing an association between low 25(OH)D levels and higher incidences of four mood disorders: premenstrual syndrome, seasonal affective disorder, non-specified mood disorder, and major depressive disorder. This review indicates a possible biochemical mechanism occurring between vitamin D and mood disorders affecting women, warranting further studies of these variables using rigorous methodologies.

View all citing articles on Scopus

View full text

Original articleEffects of bright light on sleepiness, melatonin, and 25-hydroxyvitamin D3in winter seasonal affective disorder

Psychiatry Res

J Affective Disord

Lancet

J Affective Disord

Diagnostic and Statistical Manual of Mental Disorders

Practice guidelines for major depressive disorder in adults

Am J Psychiatry

Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression

Acta Psychiatr Scand

A placebo-controlled trial of light treatment for winter depression

J Affective Disord

Clinical Epidemiology: The Architecture of Clinical Research

Quantification of sleepiness: A new approach

Psychophysiology

Antidepressant and circadian phase-shifting effects of light

Science

Original article
Effects of bright light on sleepiness, melatonin, and 25-hydroxyvitamin D₃in winter seasonal affective disorder