The underexplored presence of seasonal affective disorder in the southern hemisphere: A narrative review of the Australian literature.

BACKGROUND: Seasonal Affective Disorder (SAD) is well documented in the medical literature, particularly in more northern latitudes in agreement with proposed hypotheses for SAD's pathophysiology. However, in the southern latitudes SAD's presence remains underexplored. The second largest country in the southern hemisphere is Australia. Australia has wide ranging geographical and climatic differences that are expected to support SAD's presence. The aim of this study is therefore, to establish an evidence base for SAD in Australia. METHODS: PubMed and Google Scholar were searched for published peer-review studies focussed on, or related to SAD, winter depression or seasonal variation in mood in Australia. There were no time-period restrictions. RESULTS: Thirteen studies were identified. Studies explored the presence/nature of SAD, contributing factors, autonomic activity, treatment, and the validity of the Seasonal Pattern Assessment Questionnaire in the Australian population. An association between changes in mood and behaviour and seasonal occurrence was clearly identified, with SAD's presence varying by location. The highest percentage of study participants with SAD in a single location was observed in Tasmania, Australia's most southern state. The findings and interpretations of the studies included in this review are subject to the number of locations assessed, the number of studies undertaken at each location and individual study limitations. CONCLUSIONS: Ascertaining information on the prevalence and correlates of SAD in the southern hemisphere, particularly in high-risk locations could contribute to clinical literacy into the syndrome, support management practices, and promote the early identification and treatment of the disorder.

Second-generation antidepressants for preventing seasonal affective disorder in adults.

BACKGROUND: Seasonal affective disorder (SAD) is a seasonal pattern of recurrent major depressive episodes that most commonly occurs during autumn or winter and remits in spring. The prevalence of SAD ranges from 1.5% to 9%, depending on latitude. The predictable seasonal aspect of SAD provides a promising opportunity for prevention. This review - one of four reviews on efficacy and safety of interventions to prevent SAD - focuses on second-generation antidepressants (SGAs). OBJECTIVES: To assess the efficacy and safety of SGAs (in comparison with other SGAs, placebo, light therapy, melatonin or agomelatine, psychological therapies or lifestyle interventions) in preventing SAD and improving patient-centred outcomes among adults with a history of SAD. SEARCH METHODS: We searched Ovid MEDLINE (1950- ), Embase (1974- ), PsycINFO (1967- ) and the Cochrane Central Register of Controlled Trials (CENTRAL) to 19 June 2018. An earlier search of these databases was conducted via the Cochrane Common Mental Disorders Controlled Trial Register (CCMD-CTR) (all years to 11 August 2015). Furthermore, we searched the Cumulative Index to Nursing and Allied Health Literature, Web of Science, the Cochrane Library, the Allied and Complementary Medicine Database and international trial registers (to 19 June 2018). We also conducted a grey literature search and handsearched the reference lists of included studies and pertinent review articles. SELECTION CRITERIA: For efficacy, we included randomised controlled trials (RCTs) on adults with a history of winter-type SAD who were free of symptoms at the beginning of the study. For adverse events, we planned to include non-randomised studies. Eligible studies compared a SGA versus another SGA, placebo, light therapy, psychological therapy, melatonin, agomelatine or lifestyle changes. We also intended to compare SGAs in combination with any of the comparator interventions versus placebo or the same comparator intervention as monotherapy. DATA COLLECTION AND ANALYSIS: Two review authors independently screened abstracts and full-text publications, extracted data and assessed risk of bias of included studies. When data were sufficient, we conducted random-effects (Mantel-Haenszel) meta-analyses. We assessed statistical heterogeneity by calculating the Chi2 statistic and the Cochran Q. We used the I2 statistic to estimate the magnitude of heterogeneity. We assessed publication bias by using funnel plots.We rated the strength of the evidence using the system developed by the GRADE Working Group. MAIN RESULTS: We identified 3745 citations after de-duplication of search results and excluded 3619 records during title and abstract reviews. We assessed 126 full-text papers for inclusion in the review, of which four publications (on three RCTs) providing data from 1100 people met eligibility criteria for this review. All three RCTs had methodological limitations due to high attrition rates.Overall, moderate-quality evidence indicates that bupropion XL is an efficacious intervention for prevention of recurrence of depressive episodes in people with a history of SAD (risk ratio (RR) 0.56, 95% confidence interval (CI) 0.44 to 0.72; 3 RCTs, 1100 participants). However, bupropion XL leads to greater risk of headaches (moderate-quality evidence), insomnia and nausea (both low-quality evidence) when compared with placebo. Numbers needed to treat for additional beneficial outcomes (NNTBs) vary by baseline risks. For a population with a yearly recurrence rate of 30%, the NNTB is 8 (95% CI 6 to 12). For populations with yearly recurrence rates of 50% and 60%, NNTBs are 5 (95% CI 4 to 7) and 4 (95% CI 3 to 6), respectively.We could find no studies on other SGAs and no studies comparing SGAs with other interventions of interest, such as light therapy, psychological therapies, melatonin or agomelatine. AUTHORS' CONCLUSIONS: Available evidence indicates that bupropion XL is an effective intervention for prevention of recurrence of SAD. Nevertheless, even in a high-risk population, three out of four people will not benefit from preventive treatment with bupropion XL and will be at risk for harm. Clinicians need to discuss with patients advantages and disadvantages of preventive SGA treatment, and might want to consider offering other potentially efficacious interventions, which might confer a lower risk of adverse events. Given the lack of comparative evidence, the decision for or against initiating preventive treatment of SAD and the treatment selected should be strongly based on patient preferences.Future researchers need to assess the effectiveness and risk of harms of SGAs other than bupropion for prevention of SAD. Investigators also need to compare benefits and harms of pharmacological and non-pharmacological interventions.

Second-generation antidepressants for preventing seasonal affective disorder in adults.

BACKGROUND: Seasonal affective disorder (SAD) is a seasonal pattern of recurrent major depressive episodes that most commonly occurs during autumn or winter and remits in spring. The prevalence of SAD ranges from 1.5% to 9%, depending on latitude. The predictable seasonal aspect of SAD provides a promising opportunity for prevention. This review - one of four reviews on efficacy and safety of interventions to prevent SAD - focuses on second-generation antidepressants (SGAs). OBJECTIVES: To assess the efficacy and safety of second-generation antidepressants (in comparison with other SGAs, placebo, light therapy, melatonin or agomelatine, psychological therapies or lifestyle interventions) in preventing SAD and improving patient-centred outcomes among adults with a history of SAD. SEARCH METHODS: A search of the Specialised Register of the Cochrane Depression, Anxiety and Neuorosis Review Group (CCDANCTR) included all years to 11 August 2015. The CCDANCTR contains reports of randomised controlled trials derived from EMBASE (1974 to date), MEDLINE (1950 to date), PsycINFO (1967 to date) and the Cochrane Central Register of Controlled Trials (CENTRAL). Furthermore, we searched the Cumulative Index to Nursing and Allied Health Literature, Web of Knowledge, The Cochrane Library and the Allied and Complementary Medicine Database (to 26 May 2014). We also conducted a grey literature search and handsearched the reference lists of included studies and pertinent review articles. SELECTION CRITERIA: For efficacy, we included randomised controlled trials on adults with a history of winter-type SAD who were free of symptoms at the beginning of the study. For adverse events, we planned to include non-randomised studies. Eligible studies compared an SGA versus another SGA, placebo, light therapy, psychological therapy, melatonin, agomelatine or lifestyle changes. We also intended to compare SGAs in combination with any of the comparator interventions versus the same comparator intervention as monotherapy. DATA COLLECTION AND ANALYSIS: Two review authors screened abstracts and full-text publications and assigned risk of bias ratings based on the Cochrane 'Risk of bias' tool. We resolved disagreements by consensus or by consultation with a third party. Two review authors independently extracted data and assessed risk of bias of included studies. When data were sufficient, we conducted random-effects (Mantel-Haenszel) meta-analyses. We assessed statistical heterogeneity by calculating the Chi(2) statistic and the Cochran Q. We used the I(2) statistic to estimate the magnitude of heterogeneity and examined potential sources of heterogeneity using sensitivity analysis or analysis of subgroups. We assessed publication bias by using funnel plots. However, given the small number of component studies in our meta-analyses, these tests have low sensitivity to detect publication bias. We rated the strength of the evidence using the system developed by the GRADE (Grading of Recommendations Assessment, Development and Evaluation) Working Group. MAIN RESULTS: We identified 2986 citations after de-duplication of search results and excluded 2895 records during title and abstract reviews. We assessed 91 full-text papers for inclusion in the review, of which four publications (on three RCTs) providing data from 1100 people met eligibility criteria for this review. All three RCTs had methodological limitations due to high attrition rates.Overall moderate-quality evidence indicates that bupropion XL is an efficacious intervention for prevention of recurrence of depressive episodes in patients with a history of SAD (risk ratio (RR) 0.56, 95% confidence interval (CI) 0.44 to 0.72; three RCTs, 1100 participants). However, bupropion XL leads to greater risk of headaches (moderate-quality evidence), insomnia and nausea (both low-quality evidence) when compared with placebo. Numbers needed to treat for additional beneficial outcomes (NNTBs) vary by baseline risks. For a population with a yearly recurrence rate of 30%, the NNTB is 8 (95% CI 6 to 12). For populations with yearly recurrence rates of 40% and 50%, NNTBs are 6 (95% CI 5 to 9) and 5 (95% CI 4 to 7), respectively.We could find no studies on other SGAs and no studies comparing SGAs with other interventions of interest such as light therapy, psychological therapies, melatonin or agomelatine. AUTHORS' CONCLUSIONS: Available evidence indicates that bupropion XL is an effective intervention for prevention of recurrence of SAD. Nevertheless, even in a high-risk population, four of five patients will not benefit from preventive treatment with bupropion XL and will be at risk for harm. Clinicians need to discuss with patients advantages and disadvantages of preventive SGA treatment and might want to consider offering other potentially efficacious interventions, which might confer lower risk of adverse events. Given the lack of comparative evidence, the decision for or against initiating preventive treatment of SAD and the treatment selected should be strongly based on patient preferences.Future researchers need to assess the effectiveness and risk of harms of SGAs other than bupropion for prevention of SAD. Investigators also need to compare benefits and harms of pharmacological and non-pharmacological interventions.

Light therapy for preventing seasonal affective disorder.

BACKGROUND: Seasonal affective disorder (SAD) is a seasonal pattern of recurrent major depressive episodes that most commonly occurs during autumn or winter and remits in spring. The prevalence of SAD ranges from 1.5% to 9%, depending on latitude. The predictable seasonal aspect of SAD provides a promising opportunity for prevention. This review - one of four reviews on efficacy and safety of interventions to prevent SAD - focuses on light therapy as a preventive intervention. Light therapy is a non-pharmacological treatment that exposes people to artificial light. Mode of delivery (e.g. visors, light boxes) and form of light (e.g. bright white light) vary. OBJECTIVES: To assess the efficacy and safety of light therapy (in comparison with no treatment, other types of light therapy, second-generation antidepressants, melatonin, agomelatine, psychological therapies, lifestyle interventions and negative ion generators) in preventing SAD and improving patient-centred outcomes among adults with a history of SAD. SEARCH METHODS: A search of the Specialised Register of the Cochrane Depression, Anxiety and Neuorosis Review Group (CCDANCTR) included all years to 11 August 2015. The CCDANCTR contains reports of relevant randomised controlled trials derived from EMBASE (1974 to date), MEDLINE (1950 to date), PsycINFO (1967 to date) and the Cochrane Central Register of Controlled Trails (CENTRAL). Furthermore, we searched the Cumulative Index to Nursing and Allied Health Literature (CINAHL), Web of Knowledge, The Cochrane Library and the Allied and Complementary Medicine Database (AMED) (to 26 May 2014). We also conducted a grey literature search and handsearched the reference lists of all included studies and pertinent review articles. SELECTION CRITERIA: For efficacy, we included randomised controlled trials on adults with a history of winter-type SAD who were free of symptoms at the beginning of the study. For adverse events, we also intended to include non-randomised studies. We intended to include studies that compared any type of light therapy (e.g. bright white light, administered by visors or light boxes, infrared light, dawn stimulation) versus no treatment/placebo, second-generation antidepressants (SGAs), psychological therapies, melatonin, agomelatine, lifestyle changes, negative ion generators or another of the aforementioned light therapies. We also planned to include studies that looked at light therapy in combination with any comparator intervention and compared this with the same comparator intervention as monotherapy. DATA COLLECTION AND ANALYSIS: Two review authors screened abstracts and full-text publications against the inclusion criteria. Two review authors independently abstracted data and assessed risk of bias of included studies. MAIN RESULTS: We identified 2986 citations after de-duplication of search results. We excluded 2895 records during title and abstract review. We assessed 91 full-text papers for inclusion in the review, but only one study providing data from 46 people met our eligibility criteria. The included randomised controlled trial (RCT) had methodological limitations. We rated it as having high risk of performance and detection bias because of lack of blinding, and as having high risk of attrition bias because study authors did not report reasons for dropouts and did not integrate data from dropouts into the analysis.The included RCT compared preventive use of bright white light (2500 lux via visors), infrared light (0.18 lux via visors) and no light treatment. Overall, both forms of preventive light therapy reduced the incidence of SAD numerically compared with no light therapy. In all, 43% (6/14) of participants in the bright light group developed SAD, as well as 33% (5/15) in the infrared light group and 67% (6/9) in the non-treatment group. Bright light therapy reduced the risk of SAD incidence by 36%; however, the 95% confidence interval (CI) was very broad and included both possible effect sizes in favour of bright light therapy and those in favour of no light therapy (risk ratio (RR) 0.64, 95% CI 0.30 to 1.38). Infrared light reduced the risk of SAD by 50% compared with no light therapy, but in this case also the CI was too broad to allow precise estimations of effect size (RR 0.50, 95% CI 0.21 to 1.17). Comparison of both forms of preventive light therapy versus each other yielded similar rates of incidence of depressive episodes in both groups (RR 1.29, 95% CI 0.50 to 3.28). The quality of evidence for all outcomes was very low. Reasons for downgrading evidence quality included high risk of bias of the included study, imprecision and other limitations, such as self rating of outcomes, lack of checking of compliance throughout the study duration and insufficient reporting of participant characteristics.Investigators provided no information on adverse events. We could find no studies that compared light therapy versus other interventions of interest such as SGA, psychological therapies, melatonin or agomelatine. AUTHORS' CONCLUSIONS: Evidence on light therapy as preventive treatment for patients with a history of SAD is limited. Methodological limitations and the small sample size of the only available study have precluded review author conclusions on effects of light therapy for SAD. Given that comparative evidence for light therapy versus other preventive options is limited, the decision for or against initiating preventive treatment of SAD and the treatment selected should be strongly based on patient preferences.

Trastornos afectivos estacionales, 'winter blues' / Seasonal Affective Disorders, 'winter blues'

El Trastorno Afectivo Estacional es una patología frecuente en la práctica clínica habitual, cuya prevalencia se halla entre el 1 y el 10% de la población. Se define como la presencia de episodios depresivos mayores recurrentes en una época determinada del año con remisión total posterior cuando es superada dicha estación. En su fisiopatología están implicados diferentes mecanismos tales como: la alteración del ritmo circadiano, la sensibilidad retiniana a la luz, el metabolismo anormal de la melatonina y la disminución de la secreción de neurotransmisores, sobre todo de la serotonina. El tratamiento se basa en la fototerapia o farmacoterapia, optando por uno u otro según las características clínicas del paciente. El objetivo de este artículo, es hacer una revisión clínica sobre dicho trastorno para su mejor reconocimiento y manejo (AU)

Seasonal Affective Disorder (SAD) is a common condition in clinical practice, the prevalence is 1 to 10% of the population. SAD is defined as the presence of recurrent major depressive episodes at a particular time of the year with total remission when that season has passed. Different mechanisms are involved in the pathophysiology such as alteration of the circadian rhythm, changes in retinal sensitivity to light, abnormal metabolism of melatonin and decreased secretion of neurotransmitters, especially serotonin. The treatment is based on phototherapy or pharmacotherapy, selection depending on the characteristics of the patient. The aim of this article is to review on this disorder clinic for better recognition and management (AU)

Seasonal affective disorder.

Seasonal affective disorder is a combination of biologic and mood disturbances with a seasonal pattern, typically occurring in the autumn and winter with remission in the spring or summer. In a given year, about 5 percent of the U.S. population experiences seasonal affective disorder, with symptoms present for about 40 percent of the year. Although the condition is seasonally limited, patients may have significant impairment from the associated depressive symptoms. Treatment can improve these symptoms and also may be used as prophylaxis before the subsequent autumn and winter seasons. Light therapy is generally well tolerated, with most patients experiencing clinical improvement within one to two weeks after the start of treatment. To avoid relapse, light therapy should continue through the end of the winter season until spontaneous remission of symptoms in the spring or summer. Pharmacotherapy with antidepressants and cognitive behavior therapy are also appropriate treatment options and have been shown to be as effective as light therapy. Because of the comparable effectiveness of treatment options, first-line management should be guided by patient preference.

[More than every tenth person have symptoms of seasonal affective disorder]. / Mere end hver tiende har symptomer på vinterdepression.

Seasonal affective disorder is a syndrome of classical depressive symptoms such as reduced energy, initiative and mood combined with atypical symptoms of increased appetite, weight and sleep duration. The symptoms recur each winter and disappear again in spring or early summer. The prevalence ranges from 1% to 10% in Scandinavian populations. Reduced light exposure, melatonergic and serotonergic disturbances are suggested pathogenetic factors. Light therapy offers convincing effect with minimal adverse effects and remains first-line treatment along with selective serotonin reuptake inhibitors.

Seasonal symptoms in bipolar and primary care patients.

BACKGROUND: There is evidence of seasonality in bipolar affective disorder (BAD) and the preponderance of atypical symptoms in bipolar depressive episodes is also seen in winter type Seasonal Affective Disorder. Differences in seasonal symptoms between BAD and appropriate comparison populations have been scrutinised only in small studies. METHODS: Symptoms described on the Seasonal Pattern Assessment Questionnaire (SPAQ) were compared between 183 patients with BAD and 468 patients consulting their general practitioners. Statistical analyses were adjusted for differing age and gender distributions between the two groups. RESULTS: Compared with the general practice patients, subjects with BAD reported greater seasonal fluctuations in mood (p=0.003). On one measure BAD subjects reported increased seasonal changes in social activity (p<0.001) and greater weight fluctuation over the year (p=0.001). The most striking differences were in sleep patterns; BAD subjects slept significantly more throughout the year, and slept for a mean of 1.8h more in winter than in summer (versus a 1.0h difference in the general practice group, p<0.001). Against 20% of the general practice group, 46% of BAD patients rated seasonal changes in well-being to be at least a moderate problem. LIMITATIONS: The SPAQ was designed as a screening instrument for Seasonal Affective Disorder, not for studies of this nature. Some of the reported differences, notably in social activity and weight changes, may reflect secondary psychosocial effects of BAD. CONCLUSIONS: Seasonal changes, most notably winter hypersomnia, should be identified in patients with BAD. These symptoms may respond to treatments such as light therapy that are used in recurrent winter depression.

Circadian rhythms and depression.

BACKGROUND: Depression is a common disorder in primary care. Disruptions to the circadian rhythms associated with depression have received little attention yet offer new and exciting approaches to treatment. OBJECTIVE: This article discusses circadian rhythms and the disruption to them associated with depression, and reviews nonpharmaceutical and pharmaceutical interventions to shift circadian rhythms. DISCUSSION: Features of depression suggestive of a disturbance to circadian rhythms include early morning waking, diurnal mood changes, changes in sleep architecture, changes in timing of the temperature nadir, and peak cortisol levels. Interpersonal social rhythm therapy involves learning to manage interpersonal relationships more effectively and stabilisation of social cues, such as including sleep and wake times, meal times, and timing of social contact. Bright light therapy is used to treat seasonal affective disorders. Agomelatine is an antidepressant that works in a novel way by targeting melatonergic receptors.

The prevalence of seasonal affective disorder (SAD) in Greenland is related to latitude.

The aim of this study was to determine the prevalence of seasonal affective disorder (SAD) in Greenlanders and Danes living at four different latitudes in Greenland. A Seasonal Pattern Assessment Questionnaire (SPAQ) was mailed to 6021 men and women between the ages of 18 and 59 years living in four different municipalities in Greenland. The recipients were randomly selected from the National Population Register. Approximately 9% of the respondents met the criteria for SAD, and the incidence of SAD varied between a southern municipality and three northern municipalities. The prevalence of SAD was particularly high in northern municipalities. No significant difference was found in the prevalence of SAD between Greenlanders and Danes. The results are comparable with other population studies that have reported a high prevalence of SAD in arctic areas. The clinical implications of our findings and the possibilities for introducing light therapy should be assessed in future studies.

An overview of seasonal affective disorder and its treatment options.

Seasonal affective disorder (SAD) is defined as a history of major depressive episodes that recur regularly at a particular time of year. Depending on the diagnostic instruments and criteria available, the reported prevalence (1%-10%) varies. Neurotransmitter abnormalities have been implicated in the pathophysiology, but they do not necessarily explain the seasonal pattern or the known chronobiological abnormalities in SAD compared with nonseasonal depression. Circadian rhythm abnormalies have been hypothesized to account for these aspects of SAD, and they provide a rationale for the therapeutic use of light therapy. Family history, twin, and molecular genetics studies suggest that hereditary factors are also involved. Light therapy and antidepressant medication are effective treatment options, with limited evidence for the efficacy of psychotherapy. Some studies demonstrate that narrow-band short wavelength "blue" light, naturalistic dawn simulation, and high-density negative air ionization are effective. Patients should be informed of the benefits of diet and exercise. Light therapy should be clinically monitored in the same manner, as it is done for other antidepressant treatments.

Seasonal affective disorder: a clinical update.

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.

Mood-worsening with high-pollen-counts and seasonality: a preliminary report.

BACKGROUND: Because aeroallergens produce inflammation in the respiratory airways, and inflammation triggers depression in vulnerable individuals, we hypothesized that mood sensitivity to pollen, the most seasonal aeroallergen, will be associated with a greater seasonality of mood. Since pollen is absent during winter, we specifically predicted that mood sensitivity to tree pollen will predict non-winter SAD but not winter SAD. METHODS: A convenience sample of African and African American college students who lived in the Washington DC metropolitan area for at least the past 3 years completed the Seasonal Pattern Assessment Questionnaire (SPAQ), from which the Global Seasonality Score (GSS) was calculated, a diagnosis of cumulative SAD (syndromal or subsyndromal SAD) was derived, a seasonal pattern (winter vs non-winter) identified, and self-reported mood changes during high pollen counts obtained. A Mann-Whitney test was used to compare GSS between participants with vs without mood worsening during high pollen counts. The capability of mood worsening with high pollen counts, gender, ethnicity, and age to predict non-winter SAD was analyzed with logistic regressions. RESULTS: GSS was greater (z=5.232, p<0.001) in those who reported mood worsening with high pollen counts. Mood sensitivity to pollen predicted non-winter SAD (p=0.017), but not winter SAD. LIMITATIONS: The SPAQ is not a definitive tool to assess seasonality, and self-reported mood worsening with high pollen counts relies on recollection. No direct measures of depression scores or pollen counts were collected. The non-winter SAD concept has not been previously established. CONCLUSIONS: Our study, which should be considered preliminary in light of its limitations, suggests that self-reported mood-worsening with high pollen count is associated with a greater seasonality of mood, and predicts SAD of non-winter type.

Seasonal affective disorder.

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.

An open trial of light therapy in adult attention-deficit/hyperactivity disorder.

OBJECTIVE: In adults with attention-deficit/ hyperactivity disorder (ADHD), a delayed sleep/ activity rhythm and/or seasonal mood symptoms may contribute significantly to core pathology and disability. This study examined whether a chronobiologically based treatment, i.e., morning bright light therapy (LT), might have utility as an adjunctive treatment for adult ADHD in the fall/ winter period. METHOD: Twenty-nine adults with DSM-IV ADHD were administered a standard 3-week open trial of LT during the fall or winter months. Primary outcome measures included percentage reduction on the Brown Adult ADD Scale and the Conners' Adult ADHD Scale. Secondary measures were decrease in depression scores according to the Structured Interview Guide for the Hamilton Depression Rating Scale, Seasonal Affective Disorder version; improvements on various neuropsychological tests; and shift toward an earlier circadian preference as measured by the Horne-Ostberg Morningness-Eveningness questionnaire. Regression analyses determined which variables at baseline best predicted improvement on a given outcome measure and which variables changed in parallel with one another. The study was conducted from November 2003 through February 2004. RESULTS: Morning bright light therapy was associated with a significant decrease in both subjective and objective measures of core ADHD pathology, improved mood symptoms, and a significant phase advance in circadian preference. Multiple regression showed that the shift toward an earlier circadian preference with LT was the strongest predictor of improvement on both subjective and objective ADHD measures. Neither baseline global seasonality scores nor baseline depression scores strongly predicted LT effects on most measures of ADHD. CONCLUSION: These findings suggest that during the fall/winter period, LT may be a useful adjunct in many adults with ADHD. Strikingly, the strongest correlate of improvement in core ADHD pathology was a phase advance in circadian preference rather than alleviation of comorbid seasonal affective disorder, suggesting important clinical benefits of LT beyond the treatment of seasonal affective disorder.

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

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.

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

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.