Calculators, Algorithms, Drug Interaction CheckersTools
Back To Search Results

Seasonal Affective Disorder

Author: Sadaf Munir Author: Sasidhar Gunturu Editor: Muhammad Abbas Updated: 4/20/2024 3:39:12 PM

Introduction

Seasonal affective disorder (SAD) is a mood disorder subtype characterized by recurrent depressive episodes with a seasonal pattern.[1] It typically presents with major depressive episodes starting in late autumn or winter and remitting by spring or summer. Conceptualized by Rosenthal et al in 1984, SAD symptoms include atypical features such as hypersomnia, overeating, carbohydrate craving, and significant fatigue, in addition to typical depressive symptoms.[2] Despite its distinct seasonal pattern, it is not classified separately in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR)  but as a specifier for major depressive disorder and bipolar disorder.[3] There is an ongoing debate about its classification within DSM-5 TR, highlighting the need for continuing vigorous research.[4]

Understanding SAD's symptomatology and biological basis is critical for developing effective treatments as it causes significant psychiatric morbidity.[1] Research shows its prevalence varies globally, higher in regions farther from the equator, highlighting daylight exposure's role in the disorder's onset. Prevalence rates range from 1% to 10%, influenced by latitude and assessment methods, with variations observed between countries such as the US and Australia.[5][6][7][8] The etiology of SAD involves complex factors like circadian rhythm disruptions, changes in melatonin and serotonin levels, and photoperiod sensitivity.[9] These factors underscore the need for further investigation into SAD's biological and neurological underpinnings.[10][11] 

Etiology

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Etiology

SAD is believed to have a multifaceted etiology, with various hypotheses suggesting that sunlight deficiency and hormonal changes play significant roles. SAD is associated with a seasonal pattern, typically starting in the fall and continuing into the winter months when daylight hours are shorter. The condition is linked to neurotransmitters like dopamine, norepinephrine, and glutamate, although the exact pathophysiology is unclear.[1][12] Disruptions in the body's circadian rhythm due to reduced sunlight exposure during fall and winter are thought to be involved in the onset of winter-onset SAD.[13]  Additionally, alterations in melatonin levels due to seasonal changes can impact sleep patterns and mood regulation.[14][15]

Epidemiology

SAD affects a significant portion of the population, with varying prevalence rates based on geographic location and individual susceptibility. The prevalence of the disorder increases in regions situated further from the equator, characterized by more significant variations in daylight hours across different seasons.[5] Women are more likely to experience SAD than men, with onset typically occurring in early adulthood. The disparity in the population seems to center around young adults with peak hormone production.[16] Young adults are more reactive to mild environmental changes, including sunlight, than older adults.[6] Winter depression is more commonly studied than summer depression, with prevalence rates of 3% percent and 0.1%, respectively.[17] SAD is more common among those with a family history of depression and those who have a history of bipolar disorder.[9]

Research conducted in the US reveals varying prevalence rates of SAD, ranging from 9.7% in New Hampshire to 1.4% in Florida.[18] Although the prevalence increases with rising latitudes within North America, this association lacks statistical significance in other parts of the world.[19] However, the data on global prevalence, including that of the United States, is 2 decades old and needs further study.

Pathophysiology

While the underlying causes of SAD remain unclear,  several hypotheses are proposed. These include disturbances in circadian rhythms, reduced retinal sensitivity, genetic factors, and dysregulation of neurotransmitters such as serotonin.[18] One model suggests 2 contributing factors: a seasonal element and a depressive component, each driven by different mechanisms. For instance, seasonal changes in circadian rhythms, influenced by the length of daylight, may contribute to symptoms of SAD.

Two main theories based on circadian rhythms have been proposed: the photoperiod hypothesis, which suggests that shorter daylight hours in winter may trigger depression in vulnerable individuals due to prolonged melatonin secretion, and the phase shift hypothesis, which proposes that misalignment between circadian rhythms and sleep may lead to symptoms of SAD.[20][21] The suprachiasmatic nucleus in the hypothalamus is crucial in regulating circadian rhythms.[22]

Furthermore, light exposure can affect mood directly, with certain retinal cells sensitive to light, particularly blue light, influencing mood-regulating brain areas.[23][24] Additionally, the retinal subsensitivity hypothesis posits that impaired retinal response to decreased light levels during winter may affect circadian function and contribute to SAD.[25] 

Genetic factors may also play a role, with the results of some studies suggesting associations between SAD and variants of genes involved in dopamine, G protein, and serotonin synthesis. However, results have been inconsistent.[26] The results of family history studies indicate higher rates of mood disorders among relatives of patients with SAD, suggesting genetic predisposition.[27][28]

The results of studies on seasonality and gene activity have variations in gene expression across seasons, with certain genes more active in summer or winter.[29][30] Abnormal serotonin functioning in the central nervous system has also been implicated in SAD, with studies suggesting decreased serotonergic activity and altered serotonin transporter protein levels in affected individuals.[31] Experimental studies have demonstrated the role of tryptophan depletion in triggering depressive symptoms in patients with SAD who had previously responded to bright light therapy, highlighting the involvement of serotonin in the pathogenesis.[32]

History and Physical

Given its clinical diagnosis basis, a comprehensive history is essential for accurately diagnosing and managing SAD. As SAD manifests as a variant of major depressive disorder and bipolar disorder, the historical evaluation should prioritize identifying these disorders and subsequently associating the episodes with seasonal variations. SAD often coexists with other psychiatric conditions like alcohol use disorders, anxiety disorders, and personality disorders, which may complicate diagnosis and treatment and should be documented during the detailed evaluation.[6]This in-depth clinical history forms the bedrock for developing a personalized treatment strategy.

Key areas of focus when compiling a patient's history with SAD include the following:

  • Symptom chronology and seasonality: Detailing symptoms' onset, duration, and remission with an emphasis on their seasonal pattern is essential. It is crucial to differentiate SAD from non-seasonal major depressive disorder and bipolar disorder, which may also exhibit seasonal variations.                                            
  • Specific symptoms: Typically, SAD presents with atypical vegetative symptoms like oversleeping, overeating, weight gain, and carbohydrate craving during winter months. Summer depression, though less common, may include symptoms such as insomnia, decreased appetite, and weight loss.[33][9][1]                                                                  
  • Impact on daily life: It is important to document how symptoms affect the patient's daily activities, work, relationships, and overall quality of life.[23]                                                                                                         
  • Past episodes and treatments: It is valuable to record any past mood disturbances, treatments received, and their outcomes, including pharmacological and nonpharmacological interventions like light therapy. 
  • Family history: A family history of mood disorders, especially SAD and other forms of depression, should be noted, as SAD has a higher occurrence in individuals with a familial predisposition to mood disorders.                                                              
  • Medical history: It is vital to gather a comprehensive medical history, including any ophthalmologic conditions that may be a contraindication to using bright light therapy in treatment.                                                                                        
  • Substance use: The use of alcohol, drugs, or medication should be documented since these can affect mood and complicate the diagnosis and treatment of SAD.                                                                                                         
  • Suicidal ideation or behavior: Assessing for suicidal thoughts, plans, or attempts is critical, as SAD can heighten suicidality risk, particularly during peak depressive episodes.                                                                                                        
  • Lifestyle and coping mechanisms: Insights into the patient's lifestyle, such as physical activity, diet, and natural light exposure, as well as stress and depression coping strategies, can inform potential adjunctive treatment options.
  • Psychosocial factors: Exploring seasonal stressors, like significant changes in routine or work status during the winter, can reveal precipitating factors for depressive episodes not necessarily classified as SAD.

The mental status examination (MSE) for a patient with SAD includes a structured evaluation of their current mental condition. Given that SAD frequently manifests as depression during the winter months, the following MSE is tailored to capture this common presentation. Nonetheless, it is essential to recognize that patients may also experience seasonal manic episodes, necessitating a comprehensive approach to assess the full spectrum of possible mood states. Patients with SAD often present with comorbid conditions that can lead to variations in their MSE findings from the typical presentation described here.

  • Appearance and behavior: Patients with SAD exhibit changes in their appearance, reflecting decreased energy or interest in personal care, especially during depressive episodes, psychomotor retardation, or agitation. 
  • Speech: Patients with SAD might speak slowly, reflecting lethargy or decreased energy levels.                                                 
  • Mood and affect: Patients with SAD may report feeling depressed, sad, or hopeless. Their affect is typically congruent with their mood, showing limited range and appearing sad or tearful.                                                                     
  • Thought process and content: Patients with SAD typically exhibit depressive thought content, including pessimism, hopelessness, or thoughts of worthlessness.                                                                                                       
  • Perceptual disturbance: Any reports of hallucinations or other perceptual disturbances should be noted. While less common in SAD, it is essential to rule out these symptoms.                                                                                                    
  • Cognitive function: Cognitive impairments, such as difficulty concentrating or making decisions, are common in depressive disorders, including SAD.                                                                                                                      
  • Insight and judgment: Patients with SAD may vary in their insight into their condition, and depressive symptoms may impair their judgment.                                                                                                                
  • Risk assessment: Assessment of risk to self or others, focusing on suicidal ideation, intent, plans, and means, should be conducted.

The course of SAD varies, with symptoms typically improving on bright sunny days and sometimes persisting into summer. Recurrence rates from 1 winter to the next range from 50% to 70%, and the seasonal pattern of recurrent unipolar major depression tends not to be a long-term phenomenon in many patients.[34] Longitudinal studies indicate that less than half of patients continue to experience recurrent depression with a seasonal pattern over several years, with a significant proportion recovering without further episodes of major depression.[35] 

Among bipolar disorder, the seasonal subtype impacts 15% to 25% of individuals.[36] This subtype is identified by a consistent seasonal occurrence of mood episodes (mania, hypomania, or depression) over the last 2 years. Typically, depressive episodes emerging in the autumn or winter are the most common. This seasonal pattern is more prevalent among women, individuals with bipolar II disorder, and those with a familial history of bipolar disorder.[37][38] Patients with a seasonal subtype of bipolar disorder have higher rates of obesity as well as suicidality.[37]

Evaluation

Two commonly used screening instruments for identifying SAD are the following:

  • Seasonal Pattern Assessment Questionnaire (SPAQ): This tool comprises a 6-item scale evaluating seasonal variations in areas such as sleep, social activity, mood, weight, appetite, and energy levels. Responses are graded on a Likert scale from 0 (indicating no change) to 4 (the most significant change). However, it has faced criticism for potentially being too broad in its inclusivity.[39]                                                                                                
  • The Seasonal Health Questionnaire: This questionnaire is considered a more reliable and valid tool for screening patients with SAD.[40]

Diagnosing SAD involves a comprehensive clinical evaluation, including a detailed patient history and mental status examination, adhering to standardized diagnostic criteria. According to the DSM-5-TR, published by the American Psychiatric Association in 2022, SAD is classified as a subtype of major depressive disorder (MDD) and bipolar disorder, characterized by a "with seasonal pattern" specifier.

For a diagnosis of MDD with a seasonal pattern, the patient must satisfy the established criteria of MDD and demonstrate the characteristics defined by the "with seasonal pattern" specifier. For bipolar disorder with a seasonal pattern, the diagnostic criteria require that the patient first meets the criteria for bipolar disorder, followed by establishing that the individual experiences at least 1 mood episode (which may be depressive, manic, or hypomanic) that exhibits a seasonal pattern. 

The DSM-5-TR specifies criteria for the "with seasonal pattern" specifier, which includes the following:

  • There is a temporal pattern of occurrence of major depressive episodes in MDD or mood episodes in bipolar disorder during a particular season.                                                                                                                 
  • Complete remission or a significant reduction in the severity of the symptoms occurs at a characteristic time of year (eg, depressive episodes diminish in the spring).                                                                                  
  • Over the preceding 2 years, seasonal mood episodes must clearly exhibit a temporal relationship to specific seasons, with no non-seasonal episodes of the same polarity occurring within this timeframe.                         
  • Throughout the individual's lifetime, mood episodes with a seasonal pattern must predominate over those without such a pattern.

Treatment / Management

Managing SAD involves a comprehensive approach to alleviate symptoms and improve overall well-being. Patients generally require a combination of the following treatment approaches.

Bright light therapy: A systematic approach to managing SAD emphasizes the initial use of Bright Light Therapy (BLT) as a primary intervention. The standard protocol suggests administering BLT at an intensity of 10,000 lux for 30 minutes daily, with treatments preferably conducted during the early morning hours.[41][39][42]                                                                                                                                                       The optimal distance between the patient and the light source is 60 to 80 cm, or as per the device manufacturer's recommendations. Alternative regimens utilizing lower light intensities (eg, 2500 lux for 2 hours per day or 5000 lux for 1 hour per day) have also been proven effective, albeit necessitating prolonged exposure durations. The response is generally observable after 2 to 3 weeks, with the course of treatment extending until the natural resolution of symptoms in the spring or summer months, reflecting the transient efficacy of BLT. Research further indicates the comparability of blue-enriched light sources to standard BLT in terms of effectiveness. At the same time, the treatment overall maintains a favorable safety profile, predominantly eliciting only minor and temporary adverse effects such as headache and eyestrain. However, individuals with preexisting eye conditions or those at elevated risk should seek comprehensive ophthalmological assessment before initiating BLT therapy.[43]                                                                                                                                                                                        Moreover, based on the synthesis of evidence from 3 Cochrane Library reviews, light therapy has been delineated as ineffective in the prophylaxis of seasonal depression. In contrast, the use of bupropion XL has demonstrated efficacy in the prevention of seasonal onset depression and is FDA-approved for this indication.[39][44] Additionally, BLT's utility in treating seasonal mania remains unsupported by the current evidence base.[45][37] Dawn simulation, a different therapeutic option from bright light therapy, employs a significantly lower-intensity light (around 250 lux), which is progressively introduced towards the end of the patient's sleep cycle and during their awakening period.[9](A1)

Psychotherapy: Psychotherapy, including cognitive-behavioral therapy (CBT), provides support in managing symptoms of SAD by addressing maladaptive thought patterns and behaviors contributing to depression. Specifically adapted for individuals with SAD (CBT-SAD), this therapeutic modality focuses on challenging negative seasonal-related thoughts and implementing behavioral activation techniques.[46] One randomized controlled trial found CBT—SAD to be equally efficacious but more durable than light therapy over 2 years.[47] Another found it equally efficacious but with slower symptom resolution.[46]                     

Antidepressant medication: Selective serotonin reuptake inhibitors (SSRIs) are considered suitable primary treatments for SAD, whether used as stand-alone therapies or in conjunction with light therapy. However, bupropion holds the distinct status as the sole pharmacological agent explicitly approved for the prevention of SAD. A Cochrane review from 2019 provided evidence that initiating bupropion treatment in the period from September to November—prior to the typical onset of depressive symptoms—resulted in a lower incidence of recurrent major depressive episodes during the winter months.[48]                                              (A1)

Vitamin D supplementation: Given the prevalence of vitamin D deficiency among individuals with winter-pattern SAD, supplementation with vitamin D may complement other treatment modalities. However, the efficacy of vitamin D as a stand-alone treatment for SAD remains inconclusive, with mixed findings from research studies. Patients with SAD may benefit from optimizing their vitamin D levels, particularly in regions with limited sunlight exposure during colder months.[43][46][49][50](A1)

Differential Diagnosis

Differential diagnoses for SAD include the following:

  • Major depressive disorder (MDD): SAD shares many symptoms with non-seasonal MDD, such as persistent sadness, loss of interest or pleasure in activities, changes in appetite or weight, sleep disturbances, fatigue, feelings of worthlessness or guilt, difficulty concentrating, and suicidal ideation. A comprehensive assessment is necessary to differentiate between SAD and MDD.                                                    
  • Bipolar disorder: Some patients with bipolar disorder may experience seasonal mood changes, which can mimic SAD. However, bipolar disorder is characterized by distinct manic or hypomanic episodes alternating with depressive episodes, whereas SAD typically lacks manic or hypomanic features.                                                                                  
  • Adjustment disorder with depressed mood: Stressors related to seasonal changes, such as weather alterations or holiday events, can trigger depressive symptoms resembling those of SAD. However, the onset and duration of symptoms in adjustment disorder are directly related to identifiable stressors and usually resolve when the stressor is removed or the individual adapts.                                                                                                              
  • Persistent depressive disorder (dysthymia): Similar to MDD, persistent depressive disorder involves chronic depressive symptoms. However, the symptoms are typically less severe than those seen in MDD and may not exhibit a clear seasonal pattern.                                                                                                         
  • Generalized anxiety disorder (GAD): While anxiety disorders primarily manifest with symptoms of excessive worry, patients with GAD may also experience symptoms of depression, such as sleep disturbances, fatigue, and difficulty concentrating. Distinguishing between SAD and GAD requires a thorough assessment of mood and anxiety symptoms.                                                                                                   
  • Substance use disorders: Substance abuse, particularly alcohol and sedative-hypnotic medications, can lead to symptoms resembling depression, including changes in mood, sleep disturbances, and decreased energy. Substance-induced depressive symptoms should be considered, especially if a history of substance use or dependence is documented.                                                                                                                                                        
  • Other medical conditions: Certain medical conditions, such as hypothyroidism, vitamin deficiencies, or chronic illnesses, can present with depressive symptoms that fluctuate seasonally. A comprehensive medical evaluation is essential to rule out underlying medical causes of mood disturbances.                                                      
  • Other psychiatric disorders: Various psychiatric disorders, including eating disorders, psychotic disorders, and personality disorders, may present with depressive symptoms. A comprehensive psychiatric assessment is necessary to identify and differentiate these conditions from SAD.[51][52][53][54][55]

Accurate diagnosis of SAD requires a thorough evaluation of the patient's clinical history, symptomatology, seasonal patterns, and response to environmental factors. Collaboration between allied mental health professionals and clinicians is essential to ensure comprehensive assessment and appropriate management.

Prognosis

The prognosis for SAD varies depending on several factors, including the severity of symptoms, the effectiveness of treatment, and the patient's individual characteristics. Generally, the prognosis for SAD is favorable with appropriate interventions.

Key considerations regarding prognosis are as follows:

  • Treatment response: Many individuals with SAD experience significant improvement in symptoms with treatment, particularly with interventions such as light therapy, psychotherapy, and medication. The majority of patients respond well to these treatments, leading to a reduction in depressive symptoms and an improvement in overall functioning.                                                                                                                                                              
  • Seasonal variation: Symptoms of SAD typically remit with the onset of spring or summer when increased daylight exposure occurs. Therefore, patients can expect their symptoms to improve naturally as the seasons change, especially for those with winter-pattern SAD. However, symptoms may recur without consistent management and with the onset of subsequent fall or winter seasons.                                                                                                           
  • Relapse prevention: Patients who have experienced SAD in the past are at an increased risk of recurrence in subsequent years. Proactive measures such as continuing maintenance treatments, implementing lifestyle modifications, and practicing self-care strategies during high-risk seasons can help prevent relapse and maintain long-term wellness.                                                                                                                                                                                                       
  • Comorbid conditions: The presence of comorbid psychiatric or medical conditions may influence the prognosis of SAD. Patients with underlying mood disorders, anxiety disorders, or chronic medical illnesses may require a more comprehensive treatment approach and monitoring to address their complex needs.                                                               
  • Individual factors: The prognosis may be influenced by factors such as coping skills, social support, adherence to treatment recommendations, and access to resources. Patients who actively engage in treatment, make lifestyle changes, and seek support from healthcare professionals and loved ones are more likely to experience favorable outcomes.[6][33]

Complications

Complications associated with SAD can arise from untreated or inadequately managed symptoms.

Potential complications include the following:

  • Impaired functioning: SAD can significantly impact daily functioning, including work or school performance, interpersonal relationships, and overall quality of life. Persistent sadness, fatigue, and lethargy may hinder productivity and social engagement.                                                                                         
  • Social isolation: Patients with SAD may withdraw from social activities and relationships due to low mood and lack of interest. Social isolation can exacerbate feelings of loneliness, exacerbating depressive symptoms and increasing the risk of developing additional mental health issues.                                                                                                                   
  • Substance abuse: Some individuals may turn to alcohol or drugs as a means of self-medication to cope with symptoms of SAD. Substance abuse can worsen mood disturbances, impair judgment, and lead to addiction or substance use disorders.                                                                                                                                    
  • Suicidal ideation: In severe cases, untreated SAD may be associated with suicidal thoughts or behaviors. Feelings of hopelessness, worthlessness, and despair can escalate to suicidal ideation without appropriate intervention and support.                                                                                                                                                                                           
  • Interference with relationships: Symptoms of SAD, particularly irritability, mood swings, and social withdrawal, can strain relationships with family members, friends, and romantic partners. Communication breakdowns and conflict may arise, exacerbating feelings of isolation and distress.                                                                                                                                                          
  • Work or academic challenges: Decreased energy, concentration difficulties, and absenteeism resulting from SAD can impact performance at work or school. Persistent absenteeism or underperformance may jeopardize employment or academic success.                                                                                                                                                            
  • Physical health complications: SAD may contribute to changes in appetite, sleep disturbances, and decreased physical activity, increasing the risk of developing obesity, cardiovascular diseases, and other physical health problems over time.                                                                                                                                                           
  • Worsening mental health: Untreated SAD can predispose individuals to recurrent depressive episodes or the development of other mood disorders, such as major depressive disorder or bipolar disorder.[6][33][56]

Deterrence and Patient Education

Deterrence and prevention strategies for SAD encompass both lifestyle modifications and targeted interventions. Advising lifestyle modifications, such as increasing exposure to natural sunlight, adopting a healthy diet, engaging in regular physical activity, and ensuring adequate sleep, can mitigate symptoms. Simple strategies like taking daily walks during daylight and optimizing living spaces for sunlight exposure can be beneficial. Such proactive measures, combined with awareness, can help prevent severe episodes and improve overall well-being for individuals with SAD. 

Educating patients about SAD's symptoms and seasonal patterns empowers them to recognize early signs and seek treatment. Implementing light therapy during the fall and winter months, even before symptoms manifest, may preemptively address the disorder's onset. Psychological interventions such as CBT may also play a preventive role by equipping individuals with coping mechanisms to manage seasonal fluctuations in mood. By emphasizing proactive measures and fostering resilience, deterrence and prevention efforts promise to reduce the burden of SAD and improve overall mental well-being. 

Pearls and Other Issues

The essence of managing SAD lies in acknowledging its unique seasonality, where symptoms predominantly exacerbate during the fall and winter months due to decreased sunlight. Early recognition and intervention, which can significantly mitigate symptoms before they fully develop, is critical. Understanding the potential pitfalls, such as misdiagnosis or overlooking SAD in patients with non-seasonal mood disorders, is essential for healthcare professionals. 

Clinical pearls for SAD encompass several key points for effective management as follows:

  • Light therapy optimization: Advise patients to use light therapy as it can help regulate circadian rhythms and improve mood.

  • Regular exercise: Encourage regular physical activity, which has been shown to alleviate symptoms of depression and boost serotonin levels, helping counteract the effects of SAD.

  • Nutritional considerations: Emphasize a balanced diet rich in omega-3 fatty acids and complex carbohydrates, as these nutrients may positively influence mood and energy levels.

  • Psychoeducation: Educate patients about the importance of recognizing early symptoms of SAD and seeking timely treatment to prevent exacerbation of depressive episodes.

  • Medication adjustment: Consider adjusting the dosage or timing of antidepressant medications for patients with SAD, particularly during seasonal exacerbations.

  • Mindfulness and stress reduction techniques: Encourage the practice of mindfulness-based stress reduction techniques or relaxation exercises to help manage stress and improve coping skills.

  • Regular follow-up: Schedule regular follow-up appointments to monitor symptom severity, treatment response, and potential adverse effects of interventions, ensuring comprehensive care throughout the seasonal cycle.

By integrating these clinical pearls into practice, clinicians can optimize the management of SAD and enhance patient outcomes. 

Enhancing Healthcare Team Outcomes

The care of patients with SAD requires a collaborative effort among healthcare professionals to ensure a holistic, patient-centered approach that enhances overall outcomes. This team may include psychiatrists, primary care physicians, psychologists, advanced care practitioners, nurses, pharmacists, and other health professionals, who must thoroughly understand SAD's clinical manifestations and treatment options. This includes proficiency in applying therapeutic strategies such as BLT, CBT, and pharmacological interventions.

Developing a comprehensive strategy for managing SAD involves tailoring treatment plans to each patient's individual needs and preferences while minimizing potential adverse effects. This may include a combination of pharmacological and nonpharmacological interventions, lifestyle modifications, and ongoing monitoring of symptom severity and treatment response. Respecting patient autonomy in selecting treatment modalities is imperative in managing SAD. Educating patients and caregivers about the importance of recognizing early symptoms, environmental modifications to increase sunlight exposure, and adherence to treatment plans is essential in preventing the exacerbation of SAD symptoms. 

Each healthcare professional must acknowledge their role and contribute their specialized knowledge to the care continuum, fostering a multidisciplinary strategy. Effective communication among team members is crucial for coordinating care and making informed, collaborative decisions. This may involve coordinating appointments with primary care clinicians, mental health specialists, and other allied health professionals, as well as facilitating referrals to community resources and support groups. By prioritizing these principles of early identification, patient and caregiver education, interprofessional collaboration, and care coordination, healthcare teams can significantly improve the management of SAD, leading to better patient outcomes and optimal team performance in the care of individuals affected by this seasonal mood disorder.

References

[1]

Fonte A, Coutinho B. Seasonal sensitivity and psychiatric morbidity: study about seasonal affective disorder. BMC psychiatry. 2021 Jun 29:21(1):317. doi: 10.1186/s12888-021-03313-z. Epub 2021 Jun 29     [PubMed PMID: 34187417]

[2]

Theódórsdóttir D, Höller Y. Emotional Bias among Individuals at Risk for Seasonal Affective Disorder-An EEG Study during Remission in Summer. Brain sciences. 2023 Dec 20:14(1):. doi: 10.3390/brainsci14010002. Epub 2023 Dec 20     [PubMed PMID: 38275507]

[3]

Chakrabarti S. Bipolar disorder in the International Classification of Diseases-Eleventh version: A review of the changes, their basis, and usefulness. World journal of psychiatry. 2022 Dec 19:12(12):1335-1355. doi: 10.5498/wjp.v12.i12.1335. Epub 2022 Dec 19     [PubMed PMID: 36579354]

[4]

Rosenthal NE. Issues for DSM-V: seasonal affective disorder and seasonality. The American journal of psychiatry. 2009 Aug:166(8):852-3. doi: 10.1176/appi.ajp.2009.09020188. Epub     [PubMed PMID: 19651748]

[5]

Rosen LN, Targum SD, Terman M, Bryant MJ, Hoffman H, Kasper SF, Hamovit JR, Docherty JP, Welch B, Rosenthal NE. Prevalence of seasonal affective disorder at four latitudes. Psychiatry research. 1990 Feb:31(2):131-44     [PubMed PMID: 2326393]

[6]

Melrose S, Seasonal Affective Disorder: An Overview of Assessment and Treatment Approaches. Depression research and treatment. 2015;     [PubMed PMID: 26688752]

Level 3 (low-level) evidence

[7]

Wirz-Justice A, Benedetti F. Perspectives in affective disorders: Clocks and sleep. The European journal of neuroscience. 2020 Jan:51(1):346-365. doi: 10.1111/ejn.14362. Epub 2019 Mar 1     [PubMed PMID: 30702783]

Level 3 (low-level) evidence

[8]

Murray G. How common is seasonal affective disorder in temperate Australia? A comparison of BDI and SPAQ estimates. Journal of affective disorders. 2004 Jul:81(1):23-8     [PubMed PMID: 15183596]

[9]

Galima SV,Vogel SR,Kowalski AW, Seasonal Affective Disorder: Common Questions and Answers. American family physician. 2020 Dec 1;     [PubMed PMID: 33252911]

[10]

Ciarleglio CM, Axley JC, Strauss BR, Gamble KL, McMahon DG. Perinatal photoperiod imprints the circadian clock. Nature neuroscience. 2011 Jan:14(1):25-7. doi: 10.1038/nn.2699. Epub 2010 Dec 5     [PubMed PMID: 21131951]

[11]

Oldham MA, Ciraulo DA. Bright light therapy for depression: a review of its effects on chronobiology and the autonomic nervous system. Chronobiology international. 2014 Apr:31(3):305-19. doi: 10.3109/07420528.2013.833935. Epub 2014 Jan 7     [PubMed PMID: 24397276]

[12]

Sandman N, Merikanto I, Määttänen H, Valli K, Kronholm E, Laatikainen T, Partonen T, Paunio T. Winter is coming: nightmares and sleep problems during seasonal affective disorder. Journal of sleep research. 2016 Oct:25(5):612-619. doi: 10.1111/jsr.12416. Epub 2016 May 13     [PubMed PMID: 27174375]

[13]

Dollish HK, Tsyglakova M, McClung CA. Circadian rhythms and mood disorders: Time to see the light. Neuron. 2024 Jan 3:112(1):25-40. doi: 10.1016/j.neuron.2023.09.023. Epub 2023 Oct 18     [PubMed PMID: 37858331]

[14]

Praschak-Rieder N, Willeit M. Imaging of seasonal affective disorder and seasonality effects on serotonin and dopamine function in the human brain. Current topics in behavioral neurosciences. 2012:11():149-67. doi: 10.1007/7854_2011_174. Epub     [PubMed PMID: 22218931]

[15]

Nakayama T,Okimura K,Shen J,Guh YJ,Tamai TK,Shimada A,Minou S,Okushi Y,Shimmura T,Furukawa Y,Kadofusa N,Sato A,Nishimura T,Tanaka M,Nakayama K,Shiina N,Yamamoto N,Loudon AS,Nishiwaki-Ohkawa T,Shinomiya A,Nabeshima T,Nakane Y,Yoshimura T, Seasonal changes in NRF2 antioxidant pathway regulates winter depression-like behavior. Proceedings of the National Academy of Sciences of the United States of America. 2020 Apr 28;     [PubMed PMID: 32277035]

[16]

Salk RH, Hyde JS, Abramson LY. Gender differences in depression in representative national samples: Meta-analyses of diagnoses and symptoms. Psychological bulletin. 2017 Aug:143(8):783-822. doi: 10.1037/bul0000102. Epub 2017 Apr 27     [PubMed PMID: 28447828]

[17]

Øverland S, Woicik W, Sikora L, Whittaker K, Heli H, Skjelkvåle FS, Sivertsen B, Colman I. Seasonality and symptoms of depression: A systematic review of the literature. Epidemiology and psychiatric sciences. 2019 Apr 22:29():e31. doi: 10.1017/S2045796019000209. Epub 2019 Apr 22     [PubMed PMID: 31006406]

Level 1 (high-level) evidence

[18]

Roecklein KA, Rohan KJ. Seasonal affective disorder: an overview and update. Psychiatry (Edgmont (Pa. : Township)). 2005 Jan:2(1):20-6     [PubMed PMID: 21179639]

Level 3 (low-level) evidence

[19]

Kious BM, Bakian A, Zhao J, Mickey B, Guille C, Renshaw P, Sen S. Altitude and risk of depression and anxiety: findings from the intern health study. International review of psychiatry (Abingdon, England). 2019 Nov-Dec:31(7-8):637-645. doi: 10.1080/09540261.2019.1586324. Epub 2019 May 14     [PubMed PMID: 31084447]

[20]

Lewy AJ, Emens JS, Songer JB, Sims N, Laurie AL, Fiala SC, Buti AL. Winter Depression: Integrating mood, circadian rhythms, and the sleep/wake and light/dark cycles into a bio-psycho-social-environmental model. Sleep medicine clinics. 2009 Jun 1:4(2):285-299     [PubMed PMID: 20160896]

[21]

Kripke DF, Elliott JA, Welsh DK, Youngstedt SD. Photoperiodic and circadian bifurcation theories of depression and mania. F1000Research. 2015:4():107. doi: 10.12688/f1000research.6444.1. Epub 2015 May 6     [PubMed PMID: 26180634]

[22]

Pandi-Perumal SR, Cardinali DP, Zaki NFW, Karthikeyan R, Spence DW, Reiter RJ, Brown GM. Timing is everything: Circadian rhythms and their role in the control of sleep. Frontiers in neuroendocrinology. 2022 Jul:66():100978. doi: 10.1016/j.yfrne.2022.100978. Epub 2022 Jan 14     [PubMed PMID: 35033557]

[23]

Rohan KJ, Franzen PL, Roeckelin KA, Siegle GJ, Kolko DJ, Postolache TT, Vacek PM. Elucidating treatment targets and mediators within a confirmatory efficacy trial: study protocol for a randomized controlled trial of cognitive-behavioral therapy vs. light therapy for winter depression. Trials. 2022 May 12:23(1):383. doi: 10.1186/s13063-022-06330-9. Epub 2022 May 12     [PubMed PMID: 35550645]

Level 1 (high-level) evidence

[24]

Alkozei A, Dailey NS, Bajaj S, Vanuk JR, Raikes AC, Killgore WDS. Exposure to Blue Wavelength Light Is Associated With Increases in Bidirectional Amygdala-DLPFC Connectivity at Rest. Frontiers in neurology. 2021:12():625443. doi: 10.3389/fneur.2021.625443. Epub 2021 Mar 26     [PubMed PMID: 33841300]

[25]

Bedrosian TA, Nelson RJ. Timing of light exposure affects mood and brain circuits. Translational psychiatry. 2017 Jan 31:7(1):e1017. doi: 10.1038/tp.2016.262. Epub 2017 Jan 31     [PubMed PMID: 28140399]

[26]

Gao X, Liu J, Gong P, Wang J, Fang W, Yan H, Zhu L, Zhou X. Identifying new susceptibility genes on dopaminergic and serotonergic pathways for the framing effect in decision-making. Social cognitive and affective neuroscience. 2017 Sep 1:12(9):1534-1544. doi: 10.1093/scan/nsx062. Epub     [PubMed PMID: 28431168]

[27]

Shadrina M, Bondarenko EA, Slominsky PA. Genetics Factors in Major Depression Disease. Frontiers in psychiatry. 2018:9():334. doi: 10.3389/fpsyt.2018.00334. Epub 2018 Jul 23     [PubMed PMID: 30083112]

[28]

Ho KWD,Han S,Nielsen JV,Jancic D,Hing B,Fiedorowicz J,Weissman MM,Levinson DF,Potash JB, Genome-wide association study of seasonal affective disorder. Translational psychiatry. 2018 Sep 14;     [PubMed PMID: 30217971]

[29]

Zhang R, Volkow ND. Seasonality of brain function: role in psychiatric disorders. Translational psychiatry. 2023 Feb 22:13(1):65. doi: 10.1038/s41398-023-02365-x. Epub 2023 Feb 22     [PubMed PMID: 36813773]

[30]

Wucher V, Sodaei R, Amador R, Irimia M, Guigó R. Day-night and seasonal variation of human gene expression across tissues. PLoS biology. 2023 Feb:21(2):e3001986. doi: 10.1371/journal.pbio.3001986. Epub 2023 Feb 6     [PubMed PMID: 36745672]

[31]

Margoob MA, Mushtaq D. Serotonin transporter gene polymorphism and psychiatric disorders: is there a link? Indian journal of psychiatry. 2011 Oct:53(4):289-99. doi: 10.4103/0019-5545.91901. Epub     [PubMed PMID: 22303036]

[32]

Lam RW, Bowering TA, Tam EM, Grewal A, Yatham LN, Shiah IS, Zis AP. Effects of rapid tryptophan depletion in patients with seasonal affective disorder in natural summer remission. Psychological medicine. 2000 Jan:30(1):79-87     [PubMed PMID: 10722178]

[33]

Cléry-Melin ML, Gorwood P, Friedman S, Even C. Stability of the diagnosis of seasonal affective disorder in a long-term prospective study. Journal of affective disorders. 2018 Feb:227():353-357. doi: 10.1016/j.jad.2017.11.014. Epub 2017 Nov 7     [PubMed PMID: 29145077]

[34]

Cobb BS, Coryell WH, Cavanaugh J, Keller M, Solomon DA, Endicott J, Potash JB, Fiedorowicz JG. Seasonal variation of depressive symptoms in unipolar major depressive disorder. Comprehensive psychiatry. 2014 Nov:55(8):1891-9. doi: 10.1016/j.comppsych.2014.07.021. Epub 2014 Aug 4     [PubMed PMID: 25176622]

[35]

Leonhardt G, Wirz-Justice A, Kräuchi K, Graw P, Wunder D, Haug HJ. Long-term follow-up of depression in seasonal affective disorder. Comprehensive psychiatry. 1994 Nov-Dec:35(6):457-64     [PubMed PMID: 7867319]

[36]

Fico G, de Toffol M, Anmella G, Sagué-Vilavella M, Dellink A, Verdolini N, Pacchiarotti I, Goikolea JM, Solmi M, Vieta E, Murru A. Clinical correlates of seasonality in bipolar disorder: A specifier that needs specification? Acta psychiatrica Scandinavica. 2021 Feb:143(2):162-171. doi: 10.1111/acps.13251. Epub 2020 Dec 25     [PubMed PMID: 33140436]

[37]

McIntyre RS, Alda M, Baldessarini RJ, Bauer M, Berk M, Correll CU, Fagiolini A, Fountoulakis K, Frye MA, Grunze H, Kessing LV, Miklowitz DJ, Parker G, Post RM, Swann AC, Suppes T, Vieta E, Young A, Maj M. The clinical characterization of the adult patient with bipolar disorder aimed at personalization of management. World psychiatry : official journal of the World Psychiatric Association (WPA). 2022 Oct:21(3):364-387. doi: 10.1002/wps.20997. Epub     [PubMed PMID: 36073706]

[38]

Yeom JW, Cho CH, Jeon S, Seo JY, Son S, Ahn YM, Kim SJ, Ha TH, Cha B, Moon E, Park DY, Baek JH, Kang HJ, An H, Lee HJ. Bipolar II disorder has the highest prevalence of seasonal affective disorder in early-onset mood disorders: Results from a prospective observational cohort study. Depression and anxiety. 2021 Jun:38(6):661-670. doi: 10.1002/da.23153. Epub 2021 Apr 5     [PubMed PMID: 33818866]

[39]

Maj M, Stein DJ, Parker G, Zimmerman M, Fava GA, De Hert M, Demyttenaere K, McIntyre RS, Widiger T, Wittchen HU. The clinical characterization of the adult patient with depression aimed at personalization of management. World psychiatry : official journal of the World Psychiatric Association (WPA). 2020 Oct:19(3):269-293. doi: 10.1002/wps.20771. Epub     [PubMed PMID: 32931110]

[40]

Thompson C, Cowan A. The Seasonal Health Questionnaire: a preliminary validation of a new instrument to screen for seasonal affective disorder. Journal of affective disorders. 2001 Apr:64(1):89-98     [PubMed PMID: 11292523]

Level 1 (high-level) evidence

[41]

Terman M, Terman JS, Ross DC. A controlled trial of timed bright light and negative air ionization for treatment of winter depression. Archives of general psychiatry. 1998 Oct:55(10):875-82     [PubMed PMID: 9783557]

[42]

Chen ZW, Zhang XF, Tu ZM. Treatment measures for seasonal affective disorder: A network meta-analysis. Journal of affective disorders. 2024 Apr 1:350():531-536. doi: 10.1016/j.jad.2024.01.028. Epub 2024 Jan 12     [PubMed PMID: 38220102]

Level 1 (high-level) evidence

[43]

Praschak-Rieder N, Willeit M. Treatment of seasonal affective disorders. Dialogues in clinical neuroscience. 2003 Dec:5(4):389-98     [PubMed PMID: 22033639]

[44]

Park LT, Zarate CA Jr. Depression in the Primary Care Setting. The New England journal of medicine. 2019 Feb 7:380(6):559-568. doi: 10.1056/NEJMcp1712493. Epub     [PubMed PMID: 30726688]

[45]

Yatham LN, Kennedy SH, Parikh SV, Schaffer A, Bond DJ, Frey BN, Sharma V, Goldstein BI, Rej S, Beaulieu S, Alda M, MacQueen G, Milev RV, Ravindran A, O'Donovan C, McIntosh D, Lam RW, Vazquez G, Kapczinski F, McIntyre RS, Kozicky J, Kanba S, Lafer B, Suppes T, Calabrese JR, Vieta E, Malhi G, Post RM, Berk M. Canadian Network for Mood and Anxiety Treatments (CANMAT) and International Society for Bipolar Disorders (ISBD) 2018 guidelines for the management of patients with bipolar disorder. Bipolar disorders. 2018 Mar:20(2):97-170. doi: 10.1111/bdi.12609. Epub 2018 Mar 14     [PubMed PMID: 29536616]

[46]

Meyerhoff J, Young MA, Rohan KJ. Patterns of depressive symptom remission during the treatment of seasonal affective disorder with cognitive-behavioral therapy or light therapy. Depression and anxiety. 2018 May:35(5):457-467. doi: 10.1002/da.22739. Epub 2018 Apr 16     [PubMed PMID: 29659120]

[47]

Rohan KJ, Meyerhoff J, Ho SY, Evans M, Postolache TT, Vacek PM. Outcomes One and Two Winters Following Cognitive-Behavioral Therapy or Light Therapy for Seasonal Affective Disorder. The American journal of psychiatry. 2016 Mar 1:173(3):244-51. doi: 10.1176/appi.ajp.2015.15060773. Epub 2015 Nov 5     [PubMed PMID: 26539881]

[48]

Gartlehner G, Nussbaumer-Streit B, Gaynes BN, Forneris CA, Morgan LC, Greenblatt A, Wipplinger J, Lux LJ, Van Noord MG, Winkler D. Second-generation antidepressants for preventing seasonal affective disorder in adults. The Cochrane database of systematic reviews. 2019 Mar 18:3(3):CD011268. doi: 10.1002/14651858.CD011268.pub3. Epub 2019 Mar 18     [PubMed PMID: 30883669]

Level 1 (high-level) evidence

[49]

Howland RH. An overview of seasonal affective disorder and its treatment options. The Physician and sportsmedicine. 2009 Dec:37(4):104-15. doi: 10.3810/psm.2009.12.1748. Epub     [PubMed PMID: 20048547]

Level 3 (low-level) evidence

[50]

Frandsen TB, Pareek M, Hansen JP, Nielsen CT. Vitamin D supplementation for treatment of seasonal affective symptoms in healthcare professionals: a double-blind randomised placebo-controlled trial. BMC research notes. 2014 Aug 14:7():528. doi: 10.1186/1756-0500-7-528. Epub 2014 Aug 14     [PubMed PMID: 25125215]

Level 1 (high-level) evidence

[51]

Kennedy SH. Core symptoms of major depressive disorder: relevance to diagnosis and treatment. Dialogues in clinical neuroscience. 2008:10(3):271-7     [PubMed PMID: 18979940]

[52]

Solé B, Jiménez E, Torrent C, Reinares M, Bonnin CDM, Torres I, Varo C, Grande I, Valls E, Salagre E, Sanchez-Moreno J, Martinez-Aran A, Carvalho AF, Vieta E. Cognitive Impairment in Bipolar Disorder: Treatment and Prevention Strategies. The international journal of neuropsychopharmacology. 2017 Aug 1:20(8):670-680. doi: 10.1093/ijnp/pyx032. Epub     [PubMed PMID: 28498954]

[53]

O'Donnell ML, Agathos JA, Metcalf O, Gibson K, Lau W. Adjustment Disorder: Current Developments and Future Directions. International journal of environmental research and public health. 2019 Jul 16:16(14):. doi: 10.3390/ijerph16142537. Epub 2019 Jul 16     [PubMed PMID: 31315203]

Level 3 (low-level) evidence

[54]

DeMartini J, Patel G, Fancher TL. Generalized Anxiety Disorder. Annals of internal medicine. 2019 Apr 2:170(7):ITC49-ITC64. doi: 10.7326/AITC201904020. Epub     [PubMed PMID: 30934083]

[55]

Quello SB, Brady KT, Sonne SC. Mood disorders and substance use disorder: a complex comorbidity. Science & practice perspectives. 2005 Dec:3(1):13-21     [PubMed PMID: 18552741]

[56]

Tan O, Metin B, Ünsalver BÖ, Sayar GH. Seasonal mood changes in patients with obsessive-compulsive disorder. Psychiatry research. 2017 Dec:258():166-170. doi: 10.1016/j.psychres.2016.04.088. Epub 2016 Jun 16     [PubMed PMID: 27979316]