University at Albany, State University of New York Thyroid Function and Perfluoroalkyl Acids in Children Living Near a Chemical PlantMaria-Jose Lopez-Espinosa Debapriya MondalUniversity of Salford, firstname.lastname@example.org Ben ArmstrongLondon School of Hygiene & Tropical Science, email@example.com Michael S. BloomUniversity at Albany, State University of New York, firstname.lastname@example.org
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Ubcmood.caAnnals of Clinical Psychiatry, 19:239–246, 2007
Copyright American Academy of Clinical Psychiatrists
ISSN: 1040-1237 print / 1547-3325 online
Seasonal Affective Disorder:
A Clinical Update
Seasonal Affective Disorder: A Clinical Update ÅSA WESTRIN, MD, PHD
Department of Clinical Sciences, Division of Psychiatry, Lund University Hospital, Lund, Sweden RAYMOND W. LAM, MD, FRCPC
Division of Clinical Neuroscience, Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada Background. Seasonal affective disorder (SAD) consists of recurrent major depressive episodes in the fall/winter with
remissions in spring/summer.
Method. A Medline search was conducted to identify studies relating to clinical management of SAD using the Medical
Subject Heading, seasonal affective disorder, and key words, depress* and season*, focusing on studies published in the
past 10 years. The Cochrane library of systematic reviews was also searched for relevant studies.
Results. A careful history is important to make the diagnosis and differentiate SAD from other similar conditions such as
subsyndromal SAD and atypical depression. Seasonal patterns with winter worsening are also recognized in "nonseasonal"
depression as well as many other psychiatric conditions, and comorbidity with SAD is common. The pathophysiology of SAD
seems to be heterogeneous as research on circadian, neurotransmitter function and genetic hypotheses have shown discrepant
results. A dual vulnerability model with differential loading on separate seasonal and depression factors has been proposed to
explain these findings. Recent systematic reviews have shown that light therapy is an efficacious and well-tolerated treatment for
SAD. There is also evidence for efficacy of pharmacotherapy to treat and prevent SAD. Clinical studies show equal effectiveness
with light and antidepressants, so patient preference should be considered in the selection of initial treatment. Dawn stimulation,
negative air ions, exercise and cognitve behaviour therapy are under investigation and may also be helpful treatments for SAD.
Conclusions. SAD is a common condition with significant psychosocial impairment. Clinicians should be vigilant in
recognizing seasonal patterns of depressive episodes because there are effective, evidence-based treatments for SAD.
Seasonal affective disorder, Depression, Light, Seasons, Diagnosis depression, but advances in chronobiology and genetics have Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 suggested that the pathophysiology of SAD and the mechanism The identification of seasonal patterns for mood disturbances of light therapy may be more complex than previously thought.
dates back to ancient times, with astute medical observers such as For this review, we identified relevant clinical studies of Hippocrates, Pinel, and Kraepelin reporting clear recurrent winter SAD by conducting an electronic search on Medline using depressive episodes in some of their patients (1). The first sys- the Medical Subject Heading, seasonal affective disorder, and tematic description of seasonal affective disorder (SAD) in 1984 the key words, depress* and season*. We also searched the (2) led to the development of bright, artificial light, or light ther- Cochrane library of systematic reviews for relevant studies. In apy, as a treatment. In the past two decades, the concept of SAD this article, we focus on recent findings within the past 10 has captured media and public interest, while at the same time years and their importance to the clinical management of SAD.
provoking some skepticism amongst some in the medical com-munity. Recent systematic reviews have demonstrated that lighttherapy is a safe, well-tolerated and effective treatment for winter The first criteria for the diagnosis of winter SAD were described Address correspondence to Dr. Raymond W. Lam, Department of Psychiatry, University of British Columbia, 2255 Wesbrook Mall, Vancouver, by Rosenthal and colleagues (2). The diagnostic criteria have since B.C., Canada V6T 2A1. E-mail: email@example.com been revised and narrowed but they have basically remained the Å. WESTRIN AND R.W. LAM DSM-IV Criteria for Seasonal Pattern of Major Depressive Disorder One of the difficulties in making the diagnosis of SAD is (Recurrent Major Depressive Disorder, Bipolar I Disorder or Bipolar II Disorder) that the diagnosis rests on the patient's retrospective history.
Despite the presence of physical symptoms, medical examina- A. There has been a regular temporal relationship between the onset of major tion and laboratory studies are routinely normal in SAD.
depressive episodes and a particular time of the year.
B. Full remissions (or change from depression to mania or hypomania) also A helpful clinical characteristic of SAD is a positive mood occur at a characteristic time of the year.
response to increased (usually outdoor) light exposure and to C. In the last two years, two major depressive episodes have occurred that winter travel to more southerly latitudes. Collateral informa- demonstrate the temporal seasonal relationships defined in criteria A and B, tion from family and/or friends may also help with diagnosis.
and no nonseasonal major depressive episodes have occurred during the A prospective spring/summer evaluation for hypomania is very same period.
D. Seasonal major depressive episodes (as described above) substantially informative in supporting a bipolar diagnosis.
outnumber the nonseasonal major depressive episodes that may have occurred over the individual's lifetime.
same: a regular temporal relationship between the onset of major Patients with SAD may suffer from general symptoms of depressive episodes during the fall/winter period, and an occur- depression including diminished pleasure or interest, psycho- rence of full remission (or change from depression to mania or motor agitation or retardation, loss of energy, feelings of hypomania) of symptoms during the spring/summer period.
worthlessness or excessive or inappropriate guilt, diminished In DSM-IV, SAD is defined as a specifier of recurrent major ability to think or concentrate, indecisiveness, or recurrent depressive episodes (Table 1). This seasonal pattern specifier thoughts of death. A somatic symptom such as pain is often the can be applied to recurrent major depressive disorder (MDD) or presenting complaint at visits to general practice.
to bipolar I or II disorder. Some patients with SAD may experi- The majority of SAD patients report at least one of the ence nonseasonal depressive episodes (e.g., a winter episode "atypical" depressive symptoms associated with SAD such as that extends into the summer months) during their lifetime, but fatigue, hypersomnia, increased appetite and weight gain, these must be substantially less common than the seasonal although some patients report reduced appetite, insomnia and episodes. The DSM-IV criteria also require that the last two weight loss. The increased appetite is typified by carbohydrate seasonal depressive episodes occur in consecutive winters, but craving for sugars and starches that is often described as this criterion is controversial because it is not evidence-based.
uncontrollable. Binge type eating can occur, although purging Other explanations for seasonal patterns of depressive episodes, behaviors are uncommon. The increased eating and reduced such as regularly recurring psychosocial stressors such as win- activity usually leads to significant weight gain. With initial ter unemployment and holidays, must be ruled out.
winter episodes patients lose the weight during the summer To diagnose SAD, it is important to carefully determine the months when their appetite returns to normal and they are more time of onset and offset of previous depressive episodes, and to active. However, with increasing age it becomes more difficult ensure that patients have full remission in summer. Many patients to shed the winter weight gain and there is a gradual year round with nonseasonal depressions (including dysthymia and chronic increase in weight.
MDD) may experience winter worsening of their symptoms, but The presence of these atypical features has led some investi- they can be differentiated from those with SAD because they are gators to suggest that SAD may be a form of atypical depres- still symptomatic in the summer. Up to 20% of patients with SAD sion, another episode specifier that is characterized by mood Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 will have bipolar I or II disorder (3), so it is also important to iden- reactivity, a marked but temporary improvement in mood in tify spring or summer hypomania/mania. A follow-up reassess- response to favorable external circumstances. However, stud- ment in summer can help to identify these bipolar patients, as they ies have shown that patients with SAD do not have higher rates may not retrospectively recognize hypomanic symptoms.
of mood reactivity, leaden paralysis or rejection sensitivitythan do nonseasonal depressed patients (7). Therefore the over-lap between the two subtypes appears to be limited to the atyp- SAD versus Seasonality
ical vegetative symptoms. Of interest is that these atypicalsymptoms, particularly the overeating, predict good response There is some debate as to whether SAD is a categorical to light therapy (8).
diagnosis or an extreme form of a dimensional seasonalitytrait. Some people have marked symptoms (especially the veg-etative symptoms described below) during the winter, but not to the point where they meet criteria for MDD, or what istermed "subsyndromal" SAD (4). People with subsyndromal The differential diagnosis of SAD is similar to that of MDD SAD may still experience significant distress and impairment in general. Physical illnesses such as hypothyroidism need to of function (5), and they may also respond to the same treat- be ruled out, as do other conditions such as phase delayed sleep ments as SAD (6).
disorder and anniversary grief reactions. Mixed conditions and annals of clinical psychiatry vol. 19 no. 4 2007 SEASONAL AFFECTIVE DISORDER: A CLINICAL UPDATE comorbidity should be considered, especially since seasonal and hypothalamic serotonin transporter sites are lower in win- patterns are becoming increasingly recognized in other psychi- ter than in summer (27,28). Several studies show that tryp- atric conditions including bulimia nervosa, premenstrual tophan depletion can reverse the antidepressant effect of light depressive disorder, panic disorder, obsessive compulsive therapy, suggesting that the therapeutic effect of light involves disorder, post traumatic stress disorder and attention deficit a serotonergic mechanism (29,30). However, other reports hyperactivity disorder (9–11). The lifetime prevalence of anxi- implicate catecholamines in the pathogeneses of SAD, e.g., ret- ety disorder (generalized anxiety disorder, simple phobia, inal light sensitivity (which is dependent on retinal dopamine social phobia) in patients with SAD is also high, though per- function) is lower in SAD patients than in healthy controls (31) haps not different from that seen in nonseasonal MDD (12).
and catecholamine depletion can also reverse the effects of Furthermore, premenstrual depressive disorder has been light therapy (32).
reported to be much more common in SAD patients than in Genetic studies have also focused on monoamine-related comparison subjects (13).
genes in SAD and seasonality. Promising candidate genesinclude 5 HT2A (33–35), 5-HT2C (36) and the dopamine-4receptor (DRD4) (37). G protein (38,39) and clock-related genes (40) have also been investigated. However, these small-sample association studies are at risk for false-positive results, Many epidemiological studies have reported prevalence and as yet there are few replicated findings in the field.
rates for SAD as high as 10% (14), but most of these studies These discrepant results are likely related to heterogeneity in were not conducted in general population samples and were the pathophysiology of SAD and may be explained by a dual based on the Seasonal Pattern Assessment Questionnaire vulnerability model that was first proposed by Young et al. (41) (SPAQ), a retrospective self-report questionnaire that assesses and subsequently expanded upon by Lam et al. (6). According to seasonality rather than the diagnosis of SAD (15). The more this hypothesis, seasonality and SAD may be phenotypically rigorous studies of large community samples using diagnostic expressed via differential loading on separate seasonal and interviews and DSM criteria have found prevalence rates for depression factors with different mechanisms. For example, the SAD of 0.4% in the United States (16) and 1.7% to 2.9% in seasonal factor may have a circadian mechanism while the Canada (17;18). SAD appears linked to photoperiod (the light/ depression factor may be related to monoamine dysregulation.
dark cycle) since the prevalence of SAD is correlated with lati- Alternatively, the depression factor may reflect psychological tude (i.e., more northerly latitudes have shorter winter days) vulnerability (41), such as neuroticism. A recent study (42) sug- (19) but not to other environmental factors such as tempera- gested that vulnerability to distress symptoms in response to sea- ture, sunshine hours, cloud cover, snowfall, etc., especially in sonal physiological changes is associated with neuroticism, so North American studies (for reviews, see (14,20)) that individuals with high levels of seasonality but too high of aloading on the depression factor (neuroticism) may not show apattern of SAD because their higher level of vulnerability to dis- tress may manifest as non-seasonal depressive episodes.
The major theories explaining the pathophysiology of SAD have recently been reviewed (21,22) and include circadian, neurotransmitter function, and genetic hypotheses. The most Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 prominent of the circadian rhythm hypotheses is the phase shift hypothesis (23), which suggests that SAD is associated with anabnormal phase delay of the internal circadian rhythms relative Although light treatment for SAD is closely intertwined to the external clock. In this hypothesis, light therapy timed in with the original description of the syndrome, its efficacy has the morning would exert a corrective phase-advance of circa- been questioned. There have been dozens of positive efficacy dian rhythms. Support for the phase-shift hypothesis includes studies of light therapy, but the results are clouded by method- recent studies suggesting an optimal circadian timing for light ological weaknesses in study designs. For example, there has therapy (24) and beneficial effects of circadian phase-shifting been a lack of an accepted standard for adequate dosing of light doses of melatonin in patients with SAD (25). However, stud- treatment and for credible placebo conditions.
ies using rigorous methodologies for examining circadian However, two recent systematic reviews have rigorously rhythms have not found evidence for circadian dysregulation in addressed the efficacy question. The first used Cochrane Col- patients with SAD (22) and many treatment studies have not laboration methodology to review 14 randomized controlled tri- found correlation of therapeutic response with circadian phase- als (RCTs) of light therapy versus control conditions (43). The shifts following treatment (e.g., (26)).
second was commissioned by the Council on Research of the Research examining the monoamine hypothesis has focused American Psychiatric Association (APA) (44). The authors on serotonin as there is clear seasonal variation in brain and identified 50 RCTs, of which eight studies meeting strict meth- peripheral serotonin in healthy people, e.g., serotonin turnover odological criteria were included in the meta-analysis. Both annals of clinical psychiatry vol. 19 no. 4 2007 Å. WESTRIN AND R.W. LAM meta-analyses found that bright light was superior to credible required to stay well. Thus, they may be able to maintain their control conditions, with an odds ratio of 2.83 (indicating almost response while reducing the daily time of exposure to 15 or 20 3 times better odds of achieving response with light therapy) minutes, or by using the light box on weekdays only. In subse- and an effect size of 0.83 (indicating a medium to large treat- quent years, patients may need to begin light treatments in the ment effect), respectively. These results show that the therapeu- early autumn before the onset of symptoms to avoid any grad- tic effects of light therapy are equal to, or larger than, those ual impairment of function (47).
found in most antidepressant pharmacotherapy trials.
Side effects to light therapy are generally mild and transient In clinical practice the preferred device for light therapy is the and include headache, nausea, eyestrain, blurred vision and fluorescent light box that produces light intensities of greater than agitation (Table 3) (46). Bright light exposure in the later 2,500 lux. Lux is a unit of illumination intensity that corrects for evening may also interrupt onset and maintenance of sleep. As the phototopic spectral sensitivity of the human eye. For compari-son, indoor evening room light is usually less than 100 lux while abrightly lit office is less than 500 lux. In contrast, outdoor light is Reported Adverse Effects of Light Therapy (10,000 Lux Fluorescent much brighter: a cloudy grey winter day is around 4,000 lux and a Light Box, 30 Minutes/Day) for SAD. Only Side Effects Reported in More sunny day can be 50,000 to 100,000 lux or more. Newer light Than 5% of Treated Patients Are Shown devices under investigation use light-emitting diodes (LEDs) thatallow much smaller and more portable fixtures.
Table 2 summarizes a standard protocol for light therapy that is recommended in clinical practice guidelines (45) andthat in naturalistic clinical use has resulted in response rates of Length of treatment 65% or higher (6). Patients should be instructed to properly Emergent Side Effect position themselves and maintain a correct distance to the light source. They have to be awake with their eyes open during light exposure, but they are not required to look directly at the light source, i.e., they can read or eat during the light treatment.
The standard "dose" of light is 10,000 lux for 30 minutes per day. There appears to be a relationship between intensity and Decreased appetite duration of exposure, so that light boxes rated at 2,500 lux Increased appetite require 2 hours of daily exposure for the same response. Light therapy is usually administered in the early morning as soon as possible upon arising, e.g., at 7:00 am or earlier, because most Central nervous systemHeadache studies and meta-analyses have found that early morning exposure is superior to other times of the day (46).
The onset of action of light therapy is usually rapid with sig- nificant clinical improvement found in studies of 1 or 2 weeks' duration. However, individual patients may require 2–3 weeks to show clear responses to light therapy. When light therapy is Decreased sexual interest discontinued, most patients will relapse after a similar period Increased sexual interest Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 of a couple of weeks. Patients are therefore advised to use light Difficulties with orgasm therapy regularly during their symptomatic winter season until Difficulties with erection the time of their usual spring summer remission. Once patients have remitted they can often experiment with individual dosing Eye or vision problem Bright Light Therapy: Summary of Method ChestShortness of breath • 10,000 lux white, fluorescent light; no ultraviolet wavelengths • 30 minutes/day in the early morning, upon arising Breast tenderness • Stay awake, with eyes open; not necessary to stare at the light, so may eat Muscle/bone/joint pain • Determine response after 2–3 weeks • After remission, individualize dosing during the rest of the winter season • Initiate treatment in early autumn in following years to avoid relapses • In patients with retinal risk factors, obtain baseline eye examinations and monitor during treatment *Unlike most clinical trials that depend on spontaneous patient reports, these • In patients with bipolar I disorder, maintain on a mood stabilizer studies used systematic questionnaires to detect treatment-emergent adverseevents.
annals of clinical psychiatry vol. 19 no. 4 2007 SEASONAL AFFECTIVE DISORDER: A CLINICAL UPDATE with any effective antidepressant, light therapy carries a risk other antidepressants are also efficacious for acute treatment.
for precipitating hypomanic or manic episodes in susceptible A large clinical trial also found that citalopram (20–40 mg/day) individuals. Therefore, patients with bipolar I disorder (with was superior to placebo in preventing relapse after one week of manic episodes) should be on mood-stabilizing medications if treatment with light therapy (52).
light therapy is used.
In the only antidepressant prevention trial to date, patients There are no absolute contraindications to light therapy with a history of SAD (N = 1042) were randomized to bupro- (although retinopathies are a relative contraindication) and no evi- pion-XL (300 mg/day) or placebo starting early in autumn and dence that light therapy is associated with ocular or retinal damage followed throughout the winter (53). Recurrence of winter with current dosing guidelines (48). However, caution should be depressive episodes was significantly lower in the bupropion applied when treating patients at higher theoretical risk for bright group (15.7% vs. 28%, respectively). However, it should be light-induced eye toxicity (49). This includes patients with pre noted that the recurrence rate of SAD in this study was low existing retinal disease (such as retinitis pigmentosa) or systemic overall, even in the placebo-treated group.
illnesses that involve the retinal (such as diabetes), and those tak- Open-label studies suggest that other medications may also ing photosensitizing medications (such as lithium, phenothiazine be beneficial in SAD. These include antidepressants such as antipsychotics, melatonin, and St. John's wort). For these higher- reboxetine, a selective inhibitor of noradrenaline reuptake (54), risk patients, an ophthalmologic examination is recommended and moclobemide, a reversible inhibitor of monoamine oxidase before starting light therapy as well as regular follow-up exams.
A (55). The wake-promoting agent, modafinil, was also reported Some hospitals and outpatient clinics in Europe have designed to significantly reduce fatigue in patients with SAD (56).
light therapy rooms for patient use, but as most clinical studies usehome treatment, which is much more convenient for patients, thenecessity of light therapy rooms is not clear. Many web sites now Light versus Antidepressants
offer helpful advice and resource materials for the clinical use oflight (e.g., UBCsad.ca, SLTBR.org, CET.org).
One criticism of light therapy research has been the lack of comparisons with antidepressant medications. A recent studydirectly compared the two treatments in a "double-dummy" design, in which patients with SAD (N = 96) were randomlyassigned to 8 weeks of double-blind treatment with either There have been fewer RCTs on pharmacotherapy for SAD 10,000 lux (active) light treatment plus a placebo capsule, or (Table 4). Selective serotonin reuptake inhibitors (SSRIs), 100-lux (placebo) light treatment and fluoxetine, 20 mg/day especially fluoxetine (20 mg/day, (50) and sertraline (50–200 (57). Both groups improved during the 8 weeks with no signif- mg/day, (51)), have the best evidence for efficacy, but likely icant differences between the two in reduction of depression Studies on Pharmacotherapy of SAD. Statistically Significant Differences in Efficacy are Indicated by " > " Study design (N = number of patients) vs. placebo, RCT, 5 weeks, N = 68 • Fluoxetine = placebo in reducing depression scores • Fluoxetine > placebo in response rates vs. moclobemide, RCT, 6 weeks, N = 32 • Fluoxetine = moclobemide in reducing depression Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 scores and in remission rates vs. bright light, RCT, 8 weeks, N = 96 • Fluoxetine = light therapy in reducing depression scores and in response rates vs. bright light, RCT, 5 weeks, N = 40 • Fluoxetine = light therapy in reducing depression scores Ruhrmann et al. (65) • Trend to superiority of fluoxetine in response rates vs. placebo, RCT, 8 weeks, N = 187 • Sertraline > placebo in reducing depression scores and Moscovitch et al. (51) in response rates vs. placebo, RCT, 15 weeks, N = 282 • Following 1 week of successful light therapy, Martiny et al. (52) citalopram > placebo in preventing relapse vs. placebo, prevention RCT, N = 1042 • Bupropion > placebo in preventing seasonal depressive Modell et al (66) Bupropion, desipramine, Case series, open-label treatment, N = 47 • Improvement with all antidepressants Dilsaver et al. (67) Case series, open-label treatment, N = 16 • Improvement with reboxetine Hilger et al. (54) vs. placebo, RCT, 3 weeks, N = 34 • Moclobemide = placebo in reducing depression scores, Lingjaerde et al. (55) but > placebo in reducing atypical symptoms Hypericum (St. John's wort) vs. light therapy, RCT, 4 weeks, N = 20 • Hypericum = hypericum+bright light in reducing Martinez et al. (68) depression scores Case series, open-label treatment, N =13 • Improvement with modafanil annals of clinical psychiatry vol. 19 no. 4 2007 Å. WESTRIN AND R.W. LAM scores, clinical response rates (67% for both groups) or remis- sion rates (50% for light treatment and 54% for fluoxetine).
Light therapy showed earlier onset of response (at 1 week) and The diagnosis of SAD can be made by taking a careful lower rates of some adverse events (agitation, sleep distur- history of recurrent winter depressive episodes and ruling bance and palpitations) relative to fluoxetine, but both treat- out other diagnoses. Although the etiology and pathogenesis ments were well-tolerated overall. In the subgroup of patients of SAD remain unclear, the high prevalence of SAD (0.4% with greater severity of depression at baseline, there were again to 2.9%) makes it a significant health problem, particularly no differences in the efficacy or response/remission rates in northern countries. Light therapy is an evidence-based, between light and fluoxetine.
effective, well-tolerated treatment for SAD, while antide- These findings suggest that other factors, including patient pressant medications also have demonstrated efficacy. For preference, should be used to guide decisions about light or many patients, the choice of light or drug (or the combina- drugs as first-choice treatment. And, although there are as yet tion) will depend on personal preference. Research in limited data on the combination, many patients with SAD use progress on newer treatments, including smaller and more both light and antidepressant medication for optimal benefit.
efficient light devices, dawn simulation, negative ions,exercise, and CBT, may expand the options for people withwinter depression.
In addition to bright light and pharmacotherapy, other treat- ments under investigation may be beneficial for SAD. Theseinclude dawn simulation, negative air ionization, exercise and 1. Wehr TA: Seasonal affective disorders: A historical overview. In cognitive behaviour therapy (CBT).
Rosenthal NE, Blehar MC (eds): Seasonal Affective Disorders Dawn simulation imitates the natural summer dawn signal and Phototherapy 1989; New York, Guilford Press, 11–32 by gradually increasing ambient bedroom illumination while 2. Rosenthal NE, Sack DA, Gillin JC, Lewy AJ, Goodwin FK, the patient is sleeping. An electronic dawn simulation device Davenport Y, Mueller PS, Newsome DA, Wehr TA: Seasonal controls a bedside lamp that turns on about 90 minutes before affective disorder: A description of the syndrome and preliminaryfindings with light therapy. Arch Gen Psychiatry 1984; 41:72–80 the desired wake time and reaches a final illumination of 250 3. White DM, Lewy AJ, Sack RL, Blood ML, Wesche DL: Is win- lux, which continues until the patient arises. In the systematic ter depression a bipolar disorder? Compr Psychiatry 1990; review by the APA, five dawn simulation studies included in a meta-analysis showed a medium-to-large effect size of 0.73 4. Kasper S, Wehr TA, Bartko JJ, Gaist PA, Rosenthal NE: Epide- favoring dawn simulation over placebo conditions (44). How- miological findings of seasonal changes in mood and behavior. A ever, the total number of patients in the meta-analysis was telephone survey of Montgomery County, Maryland. Arch Gen small and the positive results came from one centre, so these Psychiatry 1989; 46:823–833 results need further replication.
5. Schlager D, Froom J, Jaffe A: Winter depression and functional Negative air ionization is a new treatment and the mecha- impairment among ambulatory primary care patients. Compr Psy- nism of action is still poorly understood. In patients with chiatry 1995; 36:18–24 SAD (N = 158), the antidepressant effects of high-density 6. Lam RW, Tam EM, Yatham LN, Shiah IS, Zis AP: Seasonal depression: The dual vulnerability hypothesis revisited. J Affect negative ions were not significantly different from those of Disord 2001; 63:123–132 Downloaded By: [Canadian Research Knowledge Network] At: 20:59 31 October 2008 bright light (58); therapeutic effects have also been observed 7. Tam EM, Lam RW, Robertson HA, Stewart JN, Yatham LN, Zis in patients with chronic (nonseasonal) depression (59).
AP: Atypical depressive symptoms in seasonal and non-seasonal Another study compared the effects of physical exercise and mood disorders. J Affect Disord 1997; 44:39–44 bright light in age-matched groups of female patients (60).
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