[Etiopathology and therapy of seasonal affective disorder]

Area of Science:

• Psychiatry
• Neuroscience
• Chronobiology

Background:

• Seasonal Affective Disorder (SAD) etiology is multifactorial, involving biological, psychological, and environmental influences.
• Existing hypotheses on SAD pathophysiology, including circadian rhythm alterations, monoaminergic function, vitamin D3, and cognitive-behavioral models, are insufficient individually.
• The integrative dual vulnerability hypothesis offers a framework for understanding SAD emergence.

Purpose of the Study:

• To review theoretical hypotheses explaining the etiology of Seasonal Affective Disorder (SAD).
• To evaluate therapeutic possibilities derived from these hypotheses.
• To present an integrated view of SAD pathophysiology and treatment.

Main Methods:

• Literature review of theoretical hypotheses for SAD.
• Analysis of biological, psychological, and environmental factors in SAD.
• Evaluation of therapeutic interventions including light therapy, pharmacotherapy, and psychotherapy.

Main Results:

• No single hypothesis fully explains SAD pathophysiology.
• Circadian rhythm disruptions, monoaminergic neurotransmission, vitamin D3 levels, and cognitive factors play roles.
• An integrative dual vulnerability model provides a more comprehensive explanation for SAD.

Conclusions:

• Effective SAD management requires an integrated approach.
• Combination therapy, including light therapy, antidepressants, and psychotherapy, is the most effective treatment strategy for SAD.
• Further research into the integrative dual vulnerability hypothesis is warranted.