Seasonal Affective Disorder

Seasonal Affective Disorder (SAD) is a form of mood disturbance in which individuals who function with typical mental health for most of the year develop recurring depressive symptoms at specific, predictable times of the year. Although most frequently associated with the darker winter months, seasonal depression can also occur during the spring or summer. The phenomenon reflects complex interactions between environmental light exposure, circadian rhythm regulation and biological vulnerability, contributing to seasonal patterns of mood fluctuation.

Epidemiology and Historical Context

SAD exhibits marked geographical variation. Rates tend to increase in regions with reduced winter daylight, particularly at higher latitudes. In the United States, prevalence ranges from about 1.4% in Florida to nearly 9.9% in Alaska, illustrating a clear relationship between seasonal light availability and depressive symptoms. Early professional scepticism gradually diminished as clinical patterns became more documented, eventually leading to formal recognition of the condition. However, later population analyses have challenged its universality, suggesting that the extent of seasonality may vary among individuals and populations.
SAD was initially described in psychiatric literature as a distinct disorder. In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), it is now classified not as a standalone condition but as a specifier, termed with seasonal pattern, applied to recurrent major depressive disorder or bipolar disorder when seasonal fluctuation is consistently observed.

Clinical Presentation

SAD encompasses the full spectrum of major depressive disorder symptoms, including persistent low mood, feelings of hopelessness or worthlessness, diminished interest in pleasurable activities, impaired concentration, social withdrawal and reduced libido. Thoughts of suicide may occur in severe cases, and some individuals require clinical intervention or hospitalisation.
Winter-pattern SAD characteristically presents with hypersomnia, difficulty waking, early evening sleepiness, overeating—particularly carbohydrate cravings—and subsequent weight gain. Nausea, low energy and pronounced lethargy are common. Conversely, individuals who experience depression in spring or summer often display insomnia, reduced appetite and weight loss, together with heightened agitation or anxiety.
Although strongly associated with unipolar depression, approximately one-fifth of affected individuals may have an underlying bipolar disorder. In bipolar I disorder, manic episodes may also occur, whereas bipolar II disorder presents with hypomania, a less severe elevation of mood without marked functional impairment. Distinguishing between these conditions is clinically essential, as treatment strategies differ significantly. Around a quarter of individuals with bipolar disorder may show a seasonal depressive pattern.
Sex-related differences have been noted. Men with a seasonal pattern may show a higher prevalence of bipolar II disorder and more depressive episodes, while women may experience rapid cycling or additional co-occurring conditions such as eating disorders.

Associated Conditions

Research indicates notable links between SAD and disorders involving circadian rhythm disruption. A significant association has been observed between SAD and Attention-Deficit Hyperactivity Disorder (ADHD). Adults with ADHD have been found to be several times more likely to exhibit SAD or subsyndromal SAD (sSAD). Symptoms such as irritability, withdrawal and sluggishness may overlap between the two conditions, complicating clinical assessment. Women appear more susceptible than men to co-occurring ADHD and SAD.

Causes and Contributing Factors

The development of SAD reflects both evolutionary and biological influences. Many species naturally reduce activity during winter when food availability declines and environmental conditions become harsher. Human mood regulation appears sensitive to similar seasonal variations.
Several biological mechanisms have been proposed:

• Serotonin regulation: Reduced sunlight may lower serotonin activity, a neurotransmitter linked with mood stability. Some genetic variants affecting serotonin metabolism have been investigated, though findings remain inconclusive.
• Melatonin production: Melatonin, secreted by the pineal gland in darkness, increases during long winter nights. Its regulation is closely linked with the retina, the suprachiasmatic nucleus and circadian biological clocks. Excessive melatonin secretion or misalignment with circadian rhythms may contribute to daytime lethargy.
• Circadian rhythm phase shifts: Many individuals with SAD exhibit patterns consistent with delayed sleep phase disorder. Bright-light therapy is believed to correct these circadian delays, leading to symptom improvement.
• Personality traits: Higher levels of neuroticism, openness, agreeableness and avoidance-oriented coping styles appear more common in those with SAD.
• Risk factors: Being female, younger age, a personal or family history of depressive or bipolar conditions, and living far from the equator are considered established risk determinants.

Pathophysiology

Light exposure is central to the underlying mechanisms of SAD. Reduced daylight during winter, often compounded by persistent cloud cover, influences the production and synchronisation of melatonin and serotonin. Prevalence tends to be markedly higher in regions above the Arctic Circle, where extremely short daylight hours occur.
Symptoms may closely resemble those of dysthymia or nonseasonal major depressive disorder. Some individuals experience profound fatigue without overt low mood, yet still fulfil diagnostic criteria for seasonal depression. A subset of patients may also experience suicidal ideation or require hospitalisation during severe episodes.
Subsyndromal SAD (sSAD), a milder variant, is more common than full SAD and affects a significant proportion of the population. Physical exercise, increased outdoor activities and greater exposure to natural light can alleviate symptoms in many cases. Seasonal variations in mood and energy are widely documented even in individuals who do not meet clinical thresholds for SAD.

Diagnosis

In clinical practice, SAD is diagnosed using the seasonal pattern specifier within the broader categories of major depressive disorder or bipolar disorder. The specifier requires:

• Depressive episodes occurring at a particular time of year.
• Remission — or the presence of mania or hypomania in bipolar disorders — at a characteristic annual time.
• A pattern maintained for at least two consecutive years.
• Seasonal depressive episodes outnumbering nonseasonal episodes across the person’s lifetime.

Assessment typically includes a detailed clinical history, evaluation of seasonal patterns and exclusion of alternative medical or psychological causes.

Types of Seasonal Affective Disorder

SAD is commonly described in three forms based on seasonal timing:

• Winter-pattern SAD: The most prevalent form, occurring during late autumn and winter, associated with hypersomnia, carbohydrate cravings and weight gain.
• Summer-pattern SAD: Less common, featuring symptoms such as insomnia, poor appetite, agitation and heightened anxiety.
• Subsyndromal SAD (sSAD): A milder manifestation featuring similar but less intense symptoms, often responsive to lifestyle modification and increased daylight exposure.

Implications and Significance

SAD highlights the profound influence of environmental light on human physiology and emotional regulation. Its links with circadian biological systems have supported the development of targeted treatments such as bright-light therapy and behavioural interventions aimed at increasing exposure to natural light. The condition also underscores the importance of differentiating unipolar and bipolar depressive patterns, as misdiagnosis may lead to inappropriate treatment strategies.