Seasonal Affective Disorder

Results of a MEDLINE Search by Ivan Goldberg, M.D.

Am J Psychiatry. 2006 Dec;163(12):2126-33.

Controlled trial of naturalistic dawn simulation and negative air ionization for
seasonal affective disorder.

Terman M, Terman JS.

Department of Biopsychology, New York State Psychiatric Institute, New York, NY
10032, USA.

OBJECTIVE: This trial assessed two novel nonpharmaceutical treatments for winter
depression-naturalistic dawn simulation and high-density negative air
ionization-delivered during the final hours of sleep. METHOD: The patients were
99 adults (77 women and 22 men) with the winter seasonal pattern of major
depressive disorder (94 cases) and bipolar II disorder (five cases). Five
parallel groups received 1) dawn simulation (0.0003-250 lux in the pattern of
May 5 at 45 degrees north latitude); 2) a dawn light pulse (13 minutes, 250 lux,
with an illuminant dose of 3.25×10(3) lux-minutes matched to the simulated
dawn); 3) postawakening bright light (30 minutes, 10,000 lux); 4) negative air
ionization at high flow rate (93 minutes, 4.5×10(14 )ions/second); or 5)
ionization at low flow rate (93 minutes, 1.7×10(11) ions/second). The symptoms
were assessed over 3 weeks with the Structured Interview Guide for the Hamilton
Depression Rating Scale-Seasonal Affective Disorder Version. RESULTS:
Posttreatment improvement results were bright light, 57.1%; dawn simulation,
49.5%; dawn pulse, 42.7%; high-density ions, 47.9%; and low-density ions, 22.7%
(significantly lower than the others). Contrary to the authors’ hypothesis,
analysis of variance failed to find superiority of dawn simulation to the dawn
pulse or bright light. However, the dawn pulse led to a pattern of residual or
exacerbated depressive symptoms similar to those seen in low-density ion
nonresponders. CONCLUSIONS: Naturalistic dawn simulation and high-density
ionization are active antidepressants that do not require the effort of
postawakening bright light therapy. They can be considered candidate
alternatives to bright light or medication.
Am Fam Physician. 2006 Nov 1;74(9):1521-4.

Seasonal affective disorder.

Lurie SJ, Gawinski B, Pierce D, Rousseau SJ.

University of Rochester School of Medicine and Dentistry, Rochester, New York,
14620, USA.

Patients with seasonal affective disorder have episodes of major depression that
tend to recur during specific times of the year, usually in winter. Like major
depression, seasonal affective disorder probably is underdiagnosed in primary
care settings. Although several screening instruments are available, such
screening is unlikely to lead to improved outcomes without personalized and
detailed attention to individual symptoms. Physicians should be aware of
comorbid factors that could signal a need for further assessment. Specifically,
some emerging evidence suggests that seasonal affective disorder may be
associated with alcoholism and attention-deficit/hyperactivity disorder.
Seasonal affective disorder often can be treated with light therapy, which
appears to have a low risk of adverse effects. Light therapy is more effective
if administered in the morning. It remains unclear whether light is equivalent
to drug therapy, whether drug therapy can augment the effects of light therapy,
or whether cognitive behavior therapy is a better treatment choice.
Acta Psychiatr Scand. 2006 Sep;114(3):216-8; discussion 218-9.

Bright light therapy for seasonal affective disorder in Israel (latitude 32.6
degrees N): a single case placebo-controlled study.

Moscovici L.

Department of Psychiatry, Tel Aviv Sourasky Medical Center, Sackler Faculty of
Medicine, Tel Aviv University, Tel Aviv, Israel.

INTRODUCTION: We describe a patient diagnosed as having seasonal affective
disorder (SAD, winter depression), an unlikely condition in Israel (latitude
32.6 degrees N), a country with relatively minor daylight photoperiodic changes
between seasons. METHOD: Case report. RESULTS: A 46-year-old woman with a
clinical picture of depression (Diagnostic and Statistical Manual of Mental
Disorders diagnostic criteria for ‘major depression with seasonal pattern’)
reacted positively to 3 weeks of daily bright light therapy of 10,000 lux/wide
spectrum. She was asked to wear dark sunglasses during placebo sessions to
accommodate an A-B-C single-case-design. The intervention resulted in an
improvement of 74-80% in the Hamilton anxiety and depression scales
(clinician-rated) and the Beck depression inventory, similar to results obtained
in high latitude regions. The depression and anxiety levels returned close to
baseline levels following 1 week of the placebo intervention. CONCLUSION:
Seasonal affective disorder is apparently not limited to certain latitudes. The
effect of light therapy was short-lived after discontinuation of the treatment,
with rapid relapse occurring in the placebo phase.
Expert Rev Neurother. 2006 Jul;6(7):1039-48.

Treatment of seasonal affective disorder.

Winkler D, Pjrek E, Iwaki R, Kasper S.

Medical University of Vienna, Department of General Psychiatry Wahringer Gurtel
18-20 A-1090 Vienna, Austria.

Seasonal affective disorder (SAD), winter type, is characterized by the regular
annual onset of major depressive episodes during fall or winter, followed by
spontaneous remission and sometimes hypomanic or manic episodes during spring
and summer. SAD is clinically important, since approximately 2-5% of the general
population in temperate climates are affected. Since the first description of
the syndrome, researchers have made attempts to elucidate the pathophysiological
background of SAD. Bright light therapy has been proposed as the treatment of
choice for this disorder. However, numerous studies have also investigated
suitable psychopharmacological treatments for SAD. This report is aimed to
provide an overview on the clinical management and current therapeutic options
for SAD.
Am J Psychiatry. 2006 May;163(5):805-12.

Comment in:
Evid Based Ment Health. 2007 Feb;10(1):26.

The Can-SAD study: a randomized controlled trial of the effectiveness of light
therapy and fluoxetine in patients with winter seasonal affective disorder.

Lam RW, Levitt AJ, Levitan RD, Enns MW, Morehouse R, Michalak EE, Tam EM.

Mood Disorders Centre, UBC Hospital, 2255 Wesbrook Mall, Vancouver, BC V6T 2A1.

OBJECTIVE: Light therapy and antidepressants have shown comparable efficacy in
separate studies of seasonal affective disorder treatment, but few studies have
directly compared the two treatments. This study compared the effectiveness of
light therapy and an antidepressant within a single trial. METHOD: This
double-blind, randomized, controlled trial was conducted in four Canadian
centers over three winter seasons. Patients met DSM-IV criteria for major
depressive disorder with a seasonal (winter) pattern and had scores > or = 23 on
the 24-item Hamilton Depression Rating Scale. After a baseline observation week,
eligible patients were randomly assigned to 8 weeks of double-blind treatment
with either 1) 10,000-lux light treatment and a placebo capsule, or 2) 100-lux
light treatment (placebo light) and fluoxetine, 20 mg/day. Light treatment was
applied for 30 minutes/day in the morning with a fluorescent white-light box;
placebo light boxes used neutral density filters. RESULTS: A total of 96
patients were randomly assigned to a treatment condition. Intent-to-treat
analysis showed overall improvement with time, with no differences between
treatments. There were also no differences between the light and fluoxetine
treatment groups in clinical response rates (67% for each group) or remission
rates (50% and 54%, respectively). Post hoc testing found that light-treated
patients had greater improvement at 1 week but not at other time points.
Fluoxetine was associated with greater treatment-emergent adverse events
(agitation, sleep disturbance, palpitations), but both treatments were generally
well-tolerated with no differences in overall number of adverse effects.
CONCLUSIONS: Light treatment showed earlier response onset and lower rate of
some adverse events relative to fluoxetine, but there were no other significant
differences in outcome between light therapy and antidepressant medication.
Although limited by lack of a double-placebo condition, this study supports the
effectiveness and tolerability of both treatments for seasonal affective
disorder and suggests that other clinical factors, including patient preference,
should guide selection of first-line treatment.
Appetite. 2006 Jul;47(1):119-22. Epub 2006 May 2.

Night eating syndrome and winter seasonal affective disorder.

Friedman S, Even C, Thuile J, Rouillon F, Guelfi JD.

Clinique des Maladies Mentales et de l’Encephale (CMME), Centre Hospitalier
Sainte-Anne, Universite Paris V, Rene Descartes, France.

Night eating syndrome (NES) and winter seasonal affective disorder (SAD) share
some features such as snacking for high-carbohydrate/high-fat food with
increased weight, emotional distress, circadian disturbances, good response to
serotoninergic antidepressants (SSRIs) and bright-light therapy. This study
assessed the prevalence and socio-demographical and clinical correlates of the
NES in a sample of 62 consecutive depressed outpatients with winter seasonal
features (DSM-IV criteria). Depression was assessed with the 29 item-HDRS and
Sigh-SAD version and with the 7-item depression subscale of the Hospital Anxiety
and Depression scale. The prevalence of NES was low (4.8%). Patients suffering
from NES were significantly older with a greater duration of the illness. NES
was not related to depression and to Body Mass Index. NES and winter SAD are not
overlapping disorders.
Tidsskr Nor Laegeforen. 2006 Apr 6;126(8):1044-7.

Comment in:
Tidsskr Nor Laegeforen. 2006 Jun 22;126(13):1768-9; author reply 1769.

[Rhythms, depressions and light] [Article in Norwegian]

Johnsson A, Moan J.

Institutt for fysikk, Norges teknisk-naturvitenskapelige universitet, 7491

Many aspects of life in plants, animals and humans are controlled by light.
Endogenous, so-called circadian rhythms in the body deviate from the exact
24-hour day and have typically a period of around 25.5 hours in man. Normally
these rhythms adapt to the external 24-hour day-and night changes but under
constant conditions the rhythms can free run. Many studies show how important
the interplay between light and the circadian rhythms are for man as well as for
other organisms. The control of these rhythms by light is mediated via the
retina and the melatonin system in man. The adaptation of the rhythms is very
important in shift work, in rapid jet lag travels over time zones, etc.
Organisms often use the circadian rhythm to determine the length of day and of
night, a feature that has given rise to the term biological clocks. A biological
clock provides possibilities to determine the proper time for physiological
processes to start in plants and animals (flowering, hibernation etc). The
importance of light and circadian rhythms for seasonal affective disorders and
manic-depressive disorders is also discussed. For several organisms one has now
been able to specify genes that determine the period of the clocks. The rhythmic
physiologic processes, the light reactions and the general importance of light
for rhythms and for man are now studied at the molecular level.
J Affect Disord. 2006 Apr;91(2-3):251-5. Epub 2006 Feb 2.

Seasonality of mood disorders in adults with lifetime
attention-deficit/hyperactivity disorder (ADHD).

Amons PJ, Kooij JJ, Haffmans PM, Hoffman TO, Hoencamp E.

Parnassia Group, PsyQ, psycho-medical programmes, Programme Adult ADHD, Carel
Reinierszkade 197, 2593 HR Den Haag, The Netherlands.

BACKGROUND: The objective of this study was to estimate the prevalence of
Seasonal Affective Disorder (SAD) in adults with lifetime
Attention-Deficit/Hyperactivity Disorder (ADHD). METHOD: Patients eligible for
this study had lifetime impairing symptoms of ADHD and a current and/or past
co-morbid mood disorder according to their medical record. The Seasonal Pattern
Assessment Questionnaire (SPAQ) was administered by a telephone interview to
assess seasonality. RESULTS: The overall rate of SAD in this clinical population
of adults with ADHD was estimated at 27%. Females were more at risk to develop
SAD than men. LIMITATIONS: The SPAQ is a screening, not a diagnostic instrument.
CONCLUSIONS: SAD symptoms are frequently comorbid with ADHD in adults. These
results have clinical relevance for the recognition and treatment of SAD with
bright light therapy in adults with ADHD.
J Affect Disord. 2006 Feb;90(2-3):227-31. Epub 2005 Dec 7.

O sweet spot where art thou? Light treatment of Seasonal Affective Disorder and
the circadian time of sleep.

Murray G, Michalak EE, Levitt AJ, Levitan RD, Enns MW, Morehouse R, Lam RW.

Faculty of Life and Social Sciences, Swinburne University of Technology, PO Box
218 John St., Hawthorn 3122 Melbourne, Victoria, Australia.

This study investigated Lewy’s Phase Shift Hypothesis (PSH) for winter Seasonal
Affective Disorder, which asserts that the phase angle difference (PAD) between
circadian and sleep rhythms is critical in the mechanism of light’s therapeutic
action. Specifically, we sought to test whether a euthymic “sweet spot” could be
identified at a PAD (between temperature minimum and wake time) of circa 3 h.
After a baseline week, symptomatic SAD patients (N = 43) received 8 weeks of
morning light treatment. Analyses were based on SIGH-SAD ratings made at
baseline and posttreatment. Also estimated pre- and posttreatment were T(min)
(calculated from an algorithm based on Morningness-Eveningness self-report
scores), and the phase of the sleep-wake rhythm (as assessed by daily sleep
logs). It was predicted that a quadratic relationship would exist between PAD
and depression ratings at baseline and posttreatment, with lowest levels around
PAD = 3 h. It was further predicted that shift towards PAD = 3 h with treatment
would be associated with decreases in depression with treatment. Although trends
were in the expected direction, none of the three predictions were supported.
Findings are discussed in terms of the study’s limitations and the experimental
challenge of parsing independent and interacting contributions of sleep and
circadian phase.
Chronobiol Int. 2005;22(5):937-43.

Therapeutic mechanism in seasonal affective disorder: do fluoxetine and light
operate through advancing circadian phase?

Murray G, Michalak EE, Levitt AJ, Levitan RD, Enns MW, Morehouse R, Lam RW.

Faculty of Life and Social Sciences, Swinburne University of Technology,
Melbourne, Victoria, Australia.

In the context of Lewy’s phase delay hypothesis, the present study tested
whether effective treatment of winter Seasonal Affective Disorder (SAD) is
mediated by advancing of circadian phase. Following a baseline week, 78
outpatients with SAD were randomized into 8 weeks of treatment with either
fluoxetine and placebo light treatment or light treatment and placebo pill.
Depression levels were measured on the Ham17+7 and the BDI-II, and circadian
phase was estimated on the basis of daily sleep logs and self-reported
morningness-eveningness. Among the 61 outpatients with complete data, both
treatments were associated with significant antidepressant effect and phase
advance. However, pre- and post-treatment comparisons found that the degree of
symptom change did not correlate with the degree of phase change associated with
treatment. The study therefore provides no evidence that circadian phase advance
mediates the therapeutic mechanism in patients with SAD. Findings are discussed
in terms of the limitations of the circadian measures employed.
Biol Psychiatry. 2006 Mar 15;59(6):502-7. Epub 2005 Sep 13.

Light therapy for seasonal affective disorder with blue narrow-band
light-emitting diodes (LEDs).

Glickman G, Byrne B, Pineda C, Hauck WW, Brainard GC.

Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania
19107, USA.

BACKGROUND: While light has proven an effective treatment for Seasonal Affective
Disorder (SAD), an optimal wavelength combination has not been determined. Short
wavelength light (blue) has demonstrated potency as a stimulus for acute
melatonin suppression and circadian phase shifting. METHODS: This study tested
the efficacy of short wavelength light therapy for SAD. Blue light emitting
diode (LED) units produced 468 nm light at 607 microW/cm2 (27 nm half-peak
bandwidth); dim red LED units provided 654 nm at 34 microW/cm2 (21 nm half-peak
bandwidth). Patients with major depression with a seasonal pattern, a score of >
or =20 on the Structured Interview Guide for the Hamilton Depression Rating
Scale-SAD version (SIGH-SAD) and normal sleeping patterns (routine bedtimes
between 10:00 pm and midnight) received 45 minutes of morning light treatment
daily for 3 weeks. Twenty-four patients completed treatment following random
assignment of condition (blue vs. red light). The SIGH-SAD was administered
weekly. RESULTS: Mixed-effects analyses of covariance determined that the short
wavelength light treatment decreased SIGH-SAD scores significantly more than the
dimmer red light condition (F = 6.45, p = .019 for average over the
post-treatment times). CONCLUSIONS: Narrow bandwidth blue light at 607
microW/cm2 outperforms dimmer red light in reversing symptoms of major
depression with a seasonal pattern.
Psychiatr Pol. 2005 May-Jun;39(3):459-68.

[Platelet serotonin transport in the group of outpatients with seasonal
affective disorder before and after light treatment, and in remission (in the
summer)] [Article in Polish]

Swiecicki L, Bidzinski A, Tonderska A.

II Klinika Psychiatryczna IPiN, Warszawie.

STUDY AIM: To asses the results of phototherapy on platelet serotonin transport
in the group of patients with seasonal affective disorder (SAD), DSM-IV
criteria, with complete clinical remission during the summer period. METHODS: It
was a 3 year prospective study. 33 patients were qualified, 20 participated in
at least two assessments (before and after light treatment) and were included in
the final analysis. During the study, the patients were not using psychotropic
drugs. The intensity of depression was measured with the Hamilton Depression
Rating Scale (HAMD21), Beck Depression Inventory (BDI) and Clinical Global
Impression Scale. We measured Bmax and Kd of [3H] citalopram in the platelets of
the patients. RESULTS: 13 patients dropped out from the study. There was a
significant reduction in the Hamilton Depression Rating Scale (HAMD21) score
after therapy vs. before treatment. Further reduction during the summer was also
observed. Kd for citalopram binding was significantly higher after phototherapy
than before treatment, the same was true for the Bmax value, but only in the
subgroup of patients with depression with atypical symptoms. CONCLUSIONS:
Phototherapy is an effective method of treatment for SAD patients, although
during the summer period the intensity of depression falls significantly vs. the
period after light treatment. Phototherapy had a significant influence on both
the measured serotonin transport parameters (Bmax and Kd). One may suggest that
an influence of light treatment on the psychomotor drive is greater than on
depressive mood.
Psychiatr Pol. 2005 May-Jun;39(3):449-58.

[Observations of tolerance of bright light treatment in psychiatry] [Article in Polish]

Krzystanek M, Krupka-Matuszczyk I, Bargiel-Matusiewicz K.

Katedra i Klinika Psychiatrii i Psychoterapii Slaskiej AM, Katowicach.

Bright light (BL) treatment is a new biological treatment used in psychiatry.
The probable mechanisms of action of BL treatment are synchronisation of
biological rhythms and increase of serotonin transmission in the human brain.
The main indication for BL treatment is seasonal affective disorder (SAD).
Indications, tolerance and mechanism of action of BL treatment are still under
exploration. AIM OF THE STUDY: To present 3 years of experience from the
treatment of different psychiatric disorders with BL. METHOD: The examined group
consisted of 104 out-patients with different diagnoses. The mean age was 41.1
and the mean number of sessions of BL treatment was 17.2. Besides-of BL
treatment (1 hour, 5000 lux) the patients were treated with psychotropic drugs.
Side effects and BL tolerance were observed. RESULTS: Side effects were present
in 34 (32.6%) patients. They were: tearsing (11.5%), headaches (6.7%),
restlessness and agitation (5.7%), eyeball pain (3.8%) and eye burning (4.8%).
Tearsing and eyeball pain subsided in the first 15 minutes, the other symptoms
subsided by 1 hour after a session. Six patients discontinued the BL treatment
due to intolerance of a side effect. CONCLUSIONS: BL treatment is a safe and
well-tolerated form of biological treatment in psychiatry. The absence of a
control group limits the specificity of these side effects. New indications for
BL treatment may include psychiatric disorders with brain serotoninergic system
or biological rhythms disturbances.
J Affect Disord. 2005 Oct;88(2):163-6.

Psychic and somatic anxiety differentially predict response to light therapy in
women with seasonal affective disorder.

MacKenzie B, Levitan RD.

Centre for Addiction and Mental Health and the Department of Psychiatry,
University of Toronto, Toronto, Ontario, Canada.

OBJECTIVE: To examine whether psychic and/or somatic anxiety predict
responsiveness to light therapy in women with winter Seasonal Affective Disorder
(SAD). DESIGN: Eighty-one women with SAD were administered a standard 10-day
trial of light therapy administered for one-half hour in the early morning.
Using a multiple regression model, baseline somatic and psychic anxiety item
scores were used to predict percentage change scores on the 29-item SIGH-SAD
post treatment. Baseline scores for weight gain, hypersomnia and the total
SIGH-SAD were also included as predictor variables. RESULTS: The regression
model was highly significant (F=4.63, df=5,75; p=.001; model R(2)=.236), with
both psychic anxiety and somatic anxiety contributing significantly to the
model. Consistent with prior work using anti-depressant medication in
non-seasonal depression, psychic anxiety was positively correlated with outcome,
while somatic anxiety negatively predicted outcome. CONCLUSIONS: In SAD, psychic
and somatic anxiety scores at baseline appear to be independent and opposite
predictors of light therapy response. These effects were independent of baseline
scores for weight gain and hypersomnia, two previously established predictors of
response to light. These findings may be an important consideration in the
design and interpretation of light therapy studies of SAD.
CNS Spectr. 2005 Aug;10(8):664-9.

Pharmacotherapy of seasonal affective disorder.

Pjrek E, Winkler D, Kasper S.

Department of General Psychiatry at the Medical University of Vienna, Vienna,

Seasonal affective disorder is a common variant of recurrent major depressive
disorder or bipolar disorder. Treatment with bright artificial light has been
found to be effective in this condition. However, for patients who do not
respond to light therapy or those who lack compliance, conventional drug
treatment with antidepressants also has been proposed. Substances with selective
serotonergic or noradrenergic mechanisms should be preferred over older
antidepressants. Although there are a number of open and controlled studies
evaluating different compounds, these studies were often limited by relatively
small sample sizes. Furthermore, there are no studies specifically addressing
bipolar seasonal depression. This article will review the published literature
on pharmacotherapy of seasonal affective disorder.
CNS Spectr. 2005 Aug;10(8):647-63.

Light therapy for seasonal and nonseasonal depression: efficacy, protocol,
safety, and side effects.

Terman M, Terman JS.

Clinical Chronobiology, New York State Psychiatric Institute, New York, NY
10032, USA.

Bright light therapy for seasonal affective disorder (SAD) has been investigated
and applied for over 20 years. Physicians and clinicians are increasingly
confident that bright light therapy is a potent, specifically active,
nonpharmaceutical treatment modality. Indeed, the domain of light treatment is
moving beyond SAD, to nonseasonal depression (unipolar and bipolar), seasonal
flare-ups of bulimia nervosa, circadian sleep phase disorders, and more. Light
therapy is simple to deliver to outpatients and inpatients alike, although the
optimum dosing of light and treatment time of day requires individual
adjustment. The side-effect profile is favorable in comparison with medications,
although the clinician must remain vigilant about emergent hypomania and
autonomic hyperactivation, especially during the first few days of treatment.
Importantly, light therapy provides a compatible adjunct to antidepressant
medication, which can result in accelerated improvement and fewer residual
CNS Spectr. 2005 Aug;10(8):635-46.

Update on the biology of seasonal affective disorder.

Sohn CH, Lam RW.

Mood Disorders Centre, University of British Columbia Hospital, Vancouver,
British Columbia, Canada.

The etiology and pathophysiology of seasonal affective disorder (SAD) has been
linked to the seasons and to light since its first conceptualization. Aspects of
SAD that make it particularly amenable to biological investigation include the
predictable recurrent episodes, the rapid response to a nonpharmacologic
treatment, the specific neurovegetative features, and the availability of rich
animal models of seasonality. This paper reviews new findings for the major
biological hypotheses for SAD, focusing on circadian rhythms, neurotransmitters,
and molecular genetics. Integrative issues and future directions for the study
of SAD, including the heuristic value of a dual-vulnerability hypothesis that
conceptualizes seasonality as a dimensional construct and the importance of
studying endophenotypes, will be discussed.
CNS Spectr. 2005 Aug;10(8):625-34.

The diagnosis, symptomatology, and epidemiology of seasonal affective disorder.

Magnusson A, Partonen T.

Department of Psychiatry, Aker University Hospital, Oslo, Norway.

The operational criteria for seasonal affective disorder (SAD) have undergone
several changes since first proposed in 1984. SAD is currently included as a
specifier of either bipolar or recurrent major depressive disorder in the
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The
International Classification of Diseases, Tenth Edition has provisional
diagnostic criteria for SAD. The most characteristic quality of SAD is that the
symptoms usually present during winter and remit in the spring. Furthermore, the
symptoms tend to remit when the patients are exposed to daylight or bright light
therapy. The cognitive and emotional symptoms are as in other types of
depression but the vegetative symptoms are the reverse of classic depressive
vegetative symptoms, namely increased sleep and increased appetite. SAD is a
common condition, but the exact prevalence rates vary between different studies
and countries and is consistently found to be more common in women and in youth.
SAD probably possibly occurs in children although not as commonly as in young
adults. Some studies have found that certain ethnic groups who live at high
northern latitudes may have adapted to the long arctic winter.
Am J Psychiatry. 2005 Apr;162(4):656-62.

Comment in:
ACP J Club. 2005 Sep-Oct;143(2):48.

The efficacy of light therapy in the treatment of mood disorders: a review and
meta-analysis of the evidence.

Golden RN, Gaynes BN, Ekstrom RD, Hamer RM, Jacobsen FM, Suppes T, Wisner KL,
Nemeroff CB.

Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel
Hill, NC 27599-7160, USA.

OBJECTIVE: The purpose of this study was to assess the evidence base for the
efficacy of light therapy in treating mood disorders. METHOD: The authors
systematically searched PubMed (January 1975 to July 2003) to identify
randomized, controlled trials of light therapy for mood disorders that fulfilled
predefined criteria. These articles were abstracted, and data were synthesized
by disease and intervention category. RESULTS: Only 13% of the studies met the
inclusion criteria. Meta-analyses revealed that a significant reduction in
depression symptom severity was associated with bright light treatment (eight
studies, having an effect size of 0.84 and 95% confidence interval [CI] of 0.60
to 1.08) and dawn simulation in seasonal affective disorder (five studies;
effect size=0.73, 95% CI=0.37 to 1.08) and with bright light treatment in
nonseasonal depression (three studies; effect size=0.53, 95% CI=0.18 to 0.89).
Bright light as an adjunct to antidepressant pharmacotherapy for nonseasonal
depression was not effective (five studies; effect size=-0.01, 95% CI=-0.36 to
0.34). CONCLUSIONS: Many reports of the efficacy of light therapy are not based
on rigorous study designs. This analysis of randomized, controlled trials
suggests that bright light treatment and dawn simulation for seasonal affective
disorder and bright light for nonseasonal depression are efficacious, with
effect sizes equivalent to those in most antidepressant pharmacotherapy trials.
Adopting standard approaches to light therapy’s specific issues (e.g., defining
parameters of active versus placebo conditions) and incorporating rigorous
designs (e.g., adequate group sizes, randomized assignment) are necessary to
evaluate light therapy for mood disorders.
Altern Med Rev. 2005 Mar;10(1):5-13.

Epidemiology, etiology, and natural treatment of seasonal affective disorder.

Miller AL.

Thorne Research, Inc., PO Box 25, Dover, ID 83825, USA.

There is much more seasonal difference in higher latitudes than in lower
latitudes. In a significant portion of the population of the northern United
States, the shorter days of fall and winter precipitate a syndrome that can
consist of depression, fatigue, hypersomnolence, hyperphagia, carbohydrate
craving, weight gain, and loss of libido. If these symptoms persist in the
winter, abate as the days grow longer, and disappear in the summer, the
diagnosis of seasonal affective disorder (SAD) can be made. Many hypotheses
exist regarding the biochemical mechanisms behind the predisposition toward this
disease, including circadian phase shifting, abnormal pineal melatonin
secretion, and abnormal serotonin synthesis. Although the mechanism(s) behind
this disease is not fully known, one treatment appears to address each of the
theories. Light therapy is a natural, non-invasive, effective, well-researched
method of treatment for SAD. Various light temperatures and times of
administration of light therapy have been studied, and a combination of morning
and evening exposure appears to offer the best efficacy. Other natural methods
of treatment have been studied, including L-tryptophan, Hypericum perforatum
(St. John’s wort), and melatonin.
Curr Psychiatry Rep. 2004 Dec;6(6):478-85.

Treatment of seasonal affective disorder: unipolar versus bipolar differences.

Sohn CH, Lam RW.

Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall,
Vancouver, BC, Canada V6T 2A1.

Evidence-based treatments for seasonal affective disorder (SAD) include light
therapy and pharmacotherapy. We briefly review the diagnosis and treatment of
SAD, focusing on clinical and treatment differences between patients with
unipolar and bipolar illness. Special considerations for the management of SAD
in patients with bipolar disorder are discussed, including the need to monitor
for emergence of manic and hypomanic mood switches, to use mood stabilizers in
patients with bipolar I disorder, and to be aware of potential interactions
between bright light and medications used in treating bipolar disorder.
Chronobiological treatments such as bright light therapy may be combined with
pharmacotherapy to enhance therapeutic effects, reduce adverse side effects, and
optimize treatment in patients with seasonal and nonseasonal bipolar disorder.
Compr Psychiatry. 2004 Jan-Feb;45(1):51-6.

Alcoholism and seasonal affective disorder.

Sher L.

Division of Neuroscience, Department of Psychiatry, Columbia University, New
York, NY 10032, USA.

Seasonal changes in mood and behavior (seasonality) may be closely related to
alcoholism. Some patients with alcoholism have a seasonal pattern to their
alcohol misuse. They may be self-medicating an underlying seasonal affective
disorder (SAD) with alcohol or manifesting a seasonal pattern to alcohol-induced
depression. Both genetic and environmental factors play a role in the etiology
and pathogenesis of alcoholism and SAD, operating, at least in part, through the
brain serotonergic system. Family and molecular genetic studies suggest that
there may be a genetic link between seasonality and alcoholism. Certain
environmental and social factors may contribute to the development of
seasonality in patients with alcoholism. The fact that SAD and alcoholism may be
comorbid shows the importance of a thorough diagnostic interview. Both mental
health and drug and alcohol professionals should be provided with education to
assist with appropriate identification, management, and referral of patients
presenting with comorbid alcoholism and SAD.
Int J Circumpolar Health. 2003 Sep;62(3):228-41.

Diet and mental health in the Arctic: is diet an important risk factor for
mental health in circumpolar peoples?–a review.

McGrath-Hanna NK, Greene DM, Tavernier RJ, Bult-Ito A.

Department of Psychology, Institute of Arctic Biology, University of Alaska
Fairbanks, 99775-70000, USA.

BACKGROUND: The people living in Arctic and Subarctic environments have adapted
to cold temperatures, short growing seasons, and low precipitation, but their
traditional ways are now changing due to increased contact with Western society.
The rapid alteration of circumpolar cultures has led to generational changes in
diet from traditional foods to the processed groceries common in modern stores.
OBJECTIVES: Develop a link between changing traditional diets and mental health
that may have substantial consequences for circumpolar peoples. METHODS: Review
of English language literature pertaining to the northern circumpolar
environments of the world that consist of the Arctic and Subarctic areas.
Electronic resources such as ISI Web of Science and PubMed were utilized, using
keywords such as arctic, circumpolar, diet, omega-3 fatty acids, mental health,
seasonal affective disorder, and suicide. In addition, we used the cited
references of obtained articles and the extensive University of Alaska Fairbanks
library collections to identify additional publications that were not available
from the electronic resources. The years covered were not restricted to any
particular period, although 83% of the sources were published in the last 16
years. CONCLUSION: The change in traditional diets has already led to increased
health problems, such as obesity, cardiovascular disease, and diabetes, while
the mental health of circumpolar peoples has also declined substantially during
the same time period. The decline in mental health is characterized by increased
rates of depression, seasonal affective disorder, anxiety, and suicide, that now
often occur at higher rates than in lower-latitude populations. Studies in
non-circumpolar peoples have shown that diet can have profound effects on
neuronal and brain development, function, and health. Therefore, we hypothesize
that diet is an important risk factor for mental health in circumpolar peoples.
Chronobiol Int. 2003 Mar;20(2):189-207.

Seasonal affective disorder: an overview.

Magnusson A, Boivin D.

Department of Psychiatry, Ullevaal University Hospital, Oslo, Norway.

Seasonal Affective Disorder (SAD) is a condition of regularly occurring
depressions in winter with a remission the following spring or summer. In
addition to depressed mood, the patients tend to experience increased appetite
and an increased duration of sleep during the winter. SAD is a relatively common
condition, affecting 1-3% of adults in temperate climates, and it is more
prevalent in women. The pathological mechanisms underlying SAD are incompletely
understood. Certain neurotransmitters have been implicated; a dysfunction in the
serotonin system in particular has been demonstrated by a variety of approaches.
The role of circadian rhythms in SAD needs to be clarified. The phase-delay
hypothesis holds that SAD patients’ circadian rhythms are delayed relative to
the sleep/wake or rest/activity cycle. This hypothesis predicts that the
symptoms of SAD will improve if the circadian rhythms can be phase-advanced.
There is some experimental support for this. SAD can be treated successfully
with light therapy. In classical light therapy, the SAD sufferer sits in front
of a light box, exposed to 2000-10,000 lux for 30-120 min daily during the
winter. Other forms of light treatments, pharmacotherapy, and other therapies
are currently being tested for SAD.
Nervenarzt. 2002 Jan;73(1):22-9; quiz 30-1.

[Pharmacotherapy of seasonal depression] [Article in German]

Hilger E, Praschak-Rieder N, Willeit M, Stastny J, Konstandinidis A, Neumeister
A, Kasper S.

Klinische Abteilung fur Allgemeine Psychiatrie, Universitatsklinik fur
Psychiatrie, Wahringer Gurtel 18-20, A-1090 Wien.

Seasonal affective disorder (SAD), first described in 1984, is a condition
characterized by recurring depressive episodes in fall and winter alternating
with nondepressive episodes in spring and summer. Various neurotransmitters have
been implicated in the etiology of SAD, with the strongest evidence for an
involvement of serotonin. Moreover, researchers have focused on the development
of treatment modalities for SAD. Despite the proven efficacy of light therapy in
SAD, some patients do not experience sufficient relief of depressive symptoms
with light, and a number of them feel unable to comply because of logistical
difficulties in administering bright light therapy. Comparatively few studies
have examined the role of pharmacotherapy in the treatment of SAD. So far,
selective serotonin reuptake inhibitors and possibly compounds with a distinct
noradrenergic mechanism of action seem to be the treatment of choice for
seasonal depression. There is, however, a clear need for further
placebo-controlled studies to evaluate pharmacological treatment options for
Int J Neuropsychopharmacol. 2001 Dec;4(4):409-20.

Monoaminergic function in the pathogenesis of seasonal affective disorder.

Neumeister A, Konstantinidis A, Praschak-Rieder N, Willeit M, Hilger E, Stastny
J, Kasper S.

National Institutes of Health, NIMH/Mood and Anxiety Disorders Program,
Bethesda, MD 20892-2670, USA.

Seasonal affective disorder/winter type (SAD) is characterized by recurrent
depressive episodes during autumn and winter alternating with non-depressive
episodes during spring and summer. Light therapy with full-spectrum, bright
white light has been shown to be effective for this condition. Several
hypotheses have been discussed in the literature about the pathogenesis of SAD.
The most prominent includes disturbances in central monoaminergic transmission.
Evidence can be inferred from studies showing a seasonal rhythm of central and
peripheral serotonergic functioning which may be a predisposing factor for SAD.
Some of the symptoms of SAD are believed to represent an attempt to overcome a
putative deficit in brain serotonergic transmission. Moreover, 5-HT receptor
challenge studies suggest altered activity at or downstream to central 5-HT
receptors. Monoamine depletion studies support hypotheses about serotonergic and
catecholaminergic dysfunctions in SAD and suggest that light therapy may well
compensate for this underlying deficit. Further, albeit indirect, support for
the importance of monoaminergic mechanisms in SAD and its involvement in the
mechanism of the action of light therapy comes from studies showing
antidepressant efficacy of serotonergic and noradrenergic antidepressants in the
treatment of SAD. Altogether, disturbances in brain monoaminergic transmission
seem to play a key role in the pathogenesis of SAD; monoaminergic systems may
also play an important role in the mechanisms of the action of light therapy.
Compr Psychiatry. 2001 Mar-Apr;42(2):105-10.

Genetic studies of seasonal affective disorder and seasonality.

Sher L.

Section on Biological Rhythms, National Institute of Mental Health, Bethesda,

Genetic studies of seasonal affective disorder (SAD) and seasonality have
received considerable attention over the past several years. Studies of the
prevalence of SAD and nonseasonal mood disorders among relatives of patients
with SAD suggested a familial contribution to the development of SAD. Two twin
studies demonstrated a substantial role of genetic variation in seasonality. Two
genetic variants related to serotonergic transmission, the 5-HTTLPR and the
5-HT(2A)-1438G/A gene promoter polymorphisms, have been found to be associated
with SAD. 5-HTTLPR is also associated with seasonality in SAD patients and in
the general population. It is not clear whether SAD is inherited as a distinct
entity or whether seasonality and depression are separate heritable traits that
happen to coincide in certain individuals. Vulnerability to SAD and disease
pathology may be influenced by many genes, perhaps on several chromosomes.
Copyright 2001 by W.B. Saunders Company
J Psychiatry Neurosci. 2000 Nov;25(5):469-80.

Pathophysiology of seasonal affective disorder: a review

Lam RW, Levitan RD.

Department of Psychiatry, University of British Columbia, Vancouver.

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.
Med Hypotheses. 2000 Jul;55(1):56-9.

The role of brain thyroid hormones in the mechanisms of seasonal changes in mood
and behavior.

Sher L.

Many individuals experience seasonal changes in mood and behavior. Various
theories have been suggested to explain the mechanisms of these changes.
However, the mechanisms of seasonal mood and behavioral changes remain unclear.
The author suggests that brain thyroid hormones may play an important role in
seasonal changes in mood and behavior. This suggestion is based on the facts
that seasonal changes in light and temperature may affect the metabolism of
brain thyroid hormones and that small alterations of the brain thyroid economy,
independent of peripheral changes in thyroid status, may produce significant
behavioral effects. The author further suggests that there may be a fault in the
thyroid metabolism in the brain in seasonal affective disorder patients, and
that fault cannot be identified by studying the peripheral thyroid hormone
metabolism. Seasonal mood and behavioral changes may also be related to the
interaction between thyroid hormones and different neurotransmitter systems in
the brain.
Acta Psychiatr Scand. 2000 Mar;101(3):176-84.

An overview of epidemiological studies on seasonal affective disorder.

Magnusson A.

Department of Psychiatry, Ulleval Hospital, Oslo, Norway.

OBJECTIVE: To review and systematize all epidemiological studies of seasonal
affective disorder (SAD). METHOD: The relevant papers were identified by
searches in Medline, Excerpta Medica, PsychLIT and other databases. The primary
reports were reviewed for additional citations. The studies were classified into
retrospective and prospective population surveys, surveys of patient populations
and studies of seasonal variations in psychiatric illnesses other than mood
disorders. RESULTS: The prevalence estimates of SAD across 20 retrospective
studies varied from 0% to 9.7%. All prospective population studies, except one,
find seasonal variations in mood, depressive symptoms usually peaking in winter.
SAD was more prevalent at higher northern latitudes, but the prevalence varied
across ethnic groups. SAD has also been identified in children and adolescents.
Seasonal exacerbations and remissions are not limited to mood disorders, it has
also been found in bulimia nervosa, anxiety disorders and other psychiatric
illnesses. CONCLUSION: The actuality of seasonal variation in mood has been
documented thoroughly by both retrospective and prospective studies. In the
general population, depressive symptoms peak in winter, and the most extreme
form of this disposition, SAD, appears to be a relatively common disorder.
J Am Pharm Assoc (Wash). 1999 Nov-Dec;39(6):822-9; quiz 880-2.

Current perspectives on the management of seasonal affective disorder.

Jepson TL, Ernst ME, Kelly MW.

University of Iowa Hospitals and Clinics, Iowa City, IA, USA.

OBJECTIVE: To concisely review the etiology and current treatment modalities of
seasonal affective disorder (SAD). DATA SOURCES: A MEDLINE search (1966-1999)
was performed using the search term “seasonal affective disorder.” The search
was subsequently focused to “drug therapy” with limits of human studies and
English-language papers. The search term “light therapy” was combined with
“seasonal affective disorder.” STUDY SELECTION AND DATA EXTRACTION: Articles
discussing the epidemiology and treatment of SAD were independently examined by
each author. Additional literature was reviewed from selected references
identified by the original articles. DATA SYNTHESIS: SAD most likely results
from a deficiency in serotonin. Light therapy remains the therapeutic
intervention with the most experience and success. Selective serotonin reuptake
inhibitors (SSRIs) have also shown benefit in treating the disorder. CONCLUSION:
SAD is an important subtype of major depressive disorder. Clinicians should
remain vigilant for signs and symptoms of the illness. Successful treatment may
include light therapy or antidepressants, particularly SSRIs.
Br J Nurs. 1999 Aug 12-Sep 8;8(15):1004-9.

Seasonal affective disorder: its recognition and treatment.

Birtwistle J, Martin N.

Primary Medical Care, Aldermoor Health Centre, University of Southampton.

This article provides an introduction to seasonal affective disorder (SAD) and
outlines various therapies, including phototherapy (light therapy), used in its
treatment. SAD, colloquially termed ‘winter blues’, is a common condition that
is thought to be caused by reduced levels of daylight in winter. During this
period sufferers generally feel low and may experience clinical depression. The
Department of Psychiatry at the University of Southampton has an established SAD
service as part of its mood disorders clinic, which was developed from a
research-based clinical investigation unit set up in the early 1990s. SAD is
described as a mood disorder with a seasonal pattern and has a greater
prevalence in countries with greater northern latitude. The aetiology of SAD is
unclear, although the most promising theory suggests the role of the
neurotransmitter serotonin. SAD is difficult to treat with conventional
antidepressants although there is evidence that serotonin selective reuptake
inhibitors may be useful for some patients. Phototherapy (light therapy) has
been used successfully by many patients although it remains controversial and
difficult to obtain on the NHS.
J Affect Disord. 1999 Jun;53(3):203-10.

The role of genetic factors in the etiology of seasonal affective disorder and

Sher L, Goldman D, Ozaki N, Rosenthal NE.

Clinical Psychobiology Branch, National Institute of Mental Health, Bethesda, MD
20892-1390, USA.

The study of the genetic basis of seasonal affective disorder (SAD), a condition
where depressions in fall and winter alternate with nondepressed periods in the
spring and summer, has recently received attention. The data on the genetics of
seasonal affective disorders are of three types: 1. Familiality: Studies on the
prevalence of psychiatric disorders among relatives of patients with SAD
suggested a familial contribution to the development of SAD; 2. Heritability: A
survey of a cohort of twins showed that genetic effects exert a global influence
across a variety of behavioral traits and accounted for at least 29% of the
variance in seasonality in men and women; 3. Molecular genetic research: two
genetic variants related to serotonergic transmission, the 5-HTTLPR and the
5-HT2A-1438G/A gene promoter polymorphisms, are associated with SAD; the former
but not the latter polymorphism is related to seasonality. Future research may
clarify the role of different genes in the development of SAD.
J Affect Disord. 1999 Apr;53(1):35-48.

Seasonal affective disorder and latitude: a review of the literature.

Mersch PP, Middendorp HM, Bouhuys AL, Beersma DG, van den Hoofdakker RH.

Department of Biological Psychiatry, University Hospital Groningen, The

BACKGROUND: The aim of the study is to investigate the relationship between the
prevalence of SAD and latitude. METHODS: An overview of the epidemiological
literature on the prevalence of SAD is given and studies relevant for the
latitudinal dependency of prevalence will be analyzed and discussed. RESULTS:
The mean prevalence of SAD is two times higher in North America compared to
Europe. Over all prevalence studies, the correlation between prevalence and
latitude was not significant. A significant positive correlation was found
between prevalence and latitude in North America. For Europe there was a trend
in the same direction. CONCLUSIONS: The influence of latitude on prevalence
seems to be small and other factors like climate, genetic vulnerability and
social-cultural context can be expected to play a more important role.
Additional controlled studies taking these factors into account are necessary to
identify their influence.
Lancet. 1998 Oct 24;352(9137):1369-74.

Seasonal affective disorder.

Partonen T, Lonnqvist J.

Department of Psychiatry, University of Helsinki, National Public Health
Institute, Finland.

Seasonal affective disorder (SAD) is a form of recurrent depressive or bipolar
disorder, with episodes that vary in severity. Seasonal patterns of depressive
episodes are common, but SAD seems to be less common than such patterns suggest.
SAD was at first believed to be related to abnormal melatonin metabolism, but
later findings did not support this hypothesis. Studies of brain serotonin
function support the hypothesis of disturbed activity. The short-allele
polymorphism for serotonin transporter is more common in patients with SAD than
in healthy people. Atypical depressive symptoms commonly precede impaired
functioning, and somatic symptoms are frequently the presenting complaint at
visits to family physicians. The best treatment regimens include 2500 Ix of
artificial light exposure in the morning. When patients seem to have no response
or to prefer another treatment, antidepressants should be considered.
Br J Clin Psychol. 1996 May;35 ( Pt 2):163-82.

Rhythm and blues: the theory and treatment of seasonal affective disorder.

Dalgleish T, Rosen K, Marks M.

Medical Research Council Applied Psychology Unit, Cambridge, UK.

Seasonal affective disorder (SAD) is a depressive disorder which occurs during
the winter and remits in the spring and summer. It differs from non-seasonal
depression in its seasonal variation and in the presence of neurovegetative
symptoms such as increased appetite and hypersomnia. This review is aimed at
clinical practitioners and presents a detailed description of the syndrome
before discussing the assessment of SAD and the current treatment of choice of
phototherapy. Particular attention is paid to the impotant issue of differential
diagnosis during assessment and the practicalities involved in the
administration of light therapy during treatment.
Encephale. 1996 Jan-Feb;22(1):7-16.

[Seasonal affective syndrome and phototherapy: theoretical concepts and clinical
applications] [Article in French]

Sartori S, Poirrier R.

Universite de Liege, Belgique.

Since 1984, there has been a great interest in the phenomenon of a particular
seasonally recurrent mood disorder called seasonal affective disorder (SAD) or
winter depression and its treatment: the phototherapy. Seasonal affective
disorder is a syndrome described by Rosenthal in 1984. This mood disorder is
characterized by depression with onset recurrent in autumn or winter and
spontaneous spring or summer remission. It is associated with hypersomnia,
anergia, increased appetite, weight gain and carbohydrate craving. The
population prevalence in the north of the USA is estimated between 3 and 5%, but
it changes with sex, age and also latitude. A long time ago, we know that
animals are photoperiod sensitive and that the melatonin secretion in mammals is
suppressed by the light. In 1980, Czeiler reported for the first time that human
melatonin secretion can be suppressed by high light exposure (+/- 1500 lux). In
1982, Rosenthal, Lewy and al. reported an antidepressant effect of light
exposure of a manic-depressive patient. The phototherapy was born. To treat the
SAD, the most common procedure of phototherapy is to expose the subject during 2
hours early in the morning, between 06:00 and 09:00 AM. The subject is sitting
before a light screen, he can work and has to fix the screen one time every
minute. The most common side effects are headache, eyestrain, muscle pain. The
ocular phototoxicity is controversed and it seems to be potentially dangerous if
phototherapy is associated with tricyclic antidepressants, neuroleptics and
other medication containing a tricyclic, heterocyclic or porphyrin ring system.
Since this finding, many questions are asked about photoperiod and its effects
in the human being. Lewy proposes for the winter depression the hypothesis of a
phase delayed circadian rhythm, that can be treated by a morning light exposure.
At the present time, many trials are going on to study the effects of
phototherapy in other problems like insomnia, maladaptation to night work, jet
lag and Alzheimer disease.