ABSTRACT
Introduction: A seasonal affective disorder (SAD) is a subtype of unipolar and bipolar major depressive disorders. It is characterized by its annual recurrence of depressive episodes at a particular season, mostly seen in winter and is responsible for 10–20% of the prevalence of major depressive disorders. Some pathophysiological hypotheses, such as the phase delay and the monoamine depletion hypotheses, have been postulated but the exact cause has not been fully unraveled yet. Studies on treatment for SAD in the last decade are lacking. To tackle this chronic disease, attention needs to be drawn to the gaps in this research field.
Areas covered: In this systematic review, the authors give a broad overview of the pharmacological therapy available for SAD. Also, nutritional substances fitting well with the postulated hypotheses are reviewed for the treatment and prevention of SAD. There is a specific focus on the quality of the currently performed studies.
Expert opinion: Light therapy and fluoxetine are the only proven and effective acute treatment options for SAD, while bupropion is the only registered drug for prevention of SAD. This area of research is in dire need of valid large-scale and sufficiently reproducible randomized control trials.
Article highlights
A final selection of 36 research papers was included in the review. No clear arguments for publication bias were found.
On pharmacological interventions, this review covered trials on SSRIs and other antidepressants; melatonin; beta blockers, benzodiazepines, metergoline, and modafinil; and food supplements.
There are no studies available on the potential effect of mood stabilizers.
Fluoxetine is the best studied drug for acute treatment of SAD. Bupropion is the only approved drug for prevention of SAD.
There is a dire need for research regarding the acute and preventive treatment of SAD with extra attention to the comparison between the different pharmacotherapies and the emerging light therapy.
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Declaration of interest
M Morrens has received grants and personal honoraria from Janssen Pharmaceuticals, AstraZeneca, Lundbeck, Bristol-Myers Squibb and Eli Lilly and Company while B Sabbe has received grants and has acted as a consultant for Takeda, Bristol-Myers Squibb, Janssen Pharmaceuticals and Lundbeck. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose