Current Psychiatry Reviews, 2009, 5, 37-47 37 1573-4005/09 $55.00+.00 © 2009 Bentham Science Publishers Ltd. Biological and Psychological Mechanisms of Seasonal Affective Disorder: A Review and Integration Kelly J. Rohan 1 , Kathryn A. Roecklein 2 and David A.F. Haaga* ,3 1 Department of Psychology, University of Vermont, Burlington, VT 05405-0134, USA; 2 Department of Psychology, University of Pittsburgh, Pittsburgh, PA 15260, USA; 3 Department of Psychology, American University, Washington, DC, 20016-8062, USA Abstract: This article: (1) describes and reviews evidence for hypothesized biological and psychological mechanisms of winter seasonal affective disorder (SAD), (2) advocates for an integrative approach to studying SAD etiology that incor- porates both biological and psychological mechanisms, and (3) delineates areas for future research from an integrative perspective. Exciting progress has been made within sub-paradigms testing candidate biological mechanisms (i.e., bio- logical rhythm abnormalities, retinal subsensitivity to light, neurotransmitter alterations, and genetic variations) and psy- chological mechanisms (i.e., maladaptive cognitions and behaviors) of SAD. However, research from an integrative bio- logical/psychological perspective is currently lacking. In contrast to a continued exclusive focus on micro-models, we ar- gue that an integrative approach would maximize the capacity to predict and understand the onset, maintenance, and course of SAD. An integrative approach also provides a comprehensive theoretical framework for developing strategies to effectively treat acute SAD, maintain acute treatment gains throughout the winter, and prevent future episodes of this highly recurrent form of depression. Keywords: Seasonal affective disorder, etiology, integrative approach. 1. INTRODUCTION Winter seasonal affective disorder (SAD) is a subtype of recurrent depression that involves a regular temporal pattern of major depressive episode onset in the fall and/or winter months with full remission in the spring [1]. SAD prevalence increases with latitude in the U. S., ranging from 1.4% in Florida to 9.9% in Alaska [2, 3]. Averaging across latitude, SAD affects an estimated 5% of the U. S. population [4], or over 14.5 million Americans. Population surveys estimating SAD prevalence have consistently reported a gender differ- ence, favoring females over males at least 2:1 [4]. Data on over 600 SAD patients treated at the National Institute of Mental Health Seasonal Studies Program suggest that an untreated fall/winter major depressive episode persists for an average of 4.9±1.4 months before spontaneous springtime remission [5]. Baseline characteristics on a sample of over a thousand SAD patients from a multi-site study included a mean age for onset of 27.2 years and, on average, 13.4 past fall/winter major depressive episodes [6]. Although this number of past episodes is likely an arbitrary function of when participants entered the study, it indicates that the course of untreated SAD is highly recurrent. In addition, SAD is associated with wintertime impairment in overall health, emotional well-being, daily activities, social activi- ties, and pain [7]. Taken cumulatively, these data suggest that SAD patients spend over 40% of the year struggling with substantial depressive symptoms that adversely affect the family and workplace during most years, beginning in *Address correspondence to this author at the Department of Psychology, Asbury Building, American University, 4400 Massachusetts Avenue NW, Washington, DC 20016-8062, USA; Tel: (202) 885-1718; Fax: (202) 885-1023; E-mail: dhaaga@american.edu young adulthood. Given its high prevalence, recurrent course, episode duration, and associated impairment, SAD is a significant mental health problem and an important public health challenge. Since the original publication on SAD [1], several theo- ries of SAD etiology have been proposed, and studies testing proposed mechanisms of SAD have accumulated. This re- view aims to: (1) describe and review evidence for hypothe- sized biological and psychological mechanisms of SAD, (2) propose an integrative approach to studying SAD etiology that incorporates both biological and psychological mecha- nisms, and (3) delineate areas for future research from an integrative perspective. We have limited our review to stud- ies of participants with clinically diagnosed SAD as the out- come of interest as opposed to high seasonality (i.e., the ten- dency to vary across the seasons in mood, energy, sleep, weight, appetite, and social activities; [3]) or subsyndromal SAD (S-SAD; [8]). We conclude that an integrative ap- proach will yield the greatest theoretical and clinical contri- butions. 2. ENVIRONMENTAL STRESS Before reviewing the proposed biological and psycho- logical mechanisms of SAD, a brief discussion of the occa- sion setter or stressor that theoretically causes these mecha- nisms to manifest and annually trigger winter depression onset is in order. Across theories of SAD, the stress is pre- sumed to be a seasonally-linked environmental stressor asso- ciated with a change in the light/dark cycle and/or natural light availability (e.g., short photoperiods, later dawns, less available overall natural luminosity). The few studies that have empirically examined the relation of these stressors to SAD are reviewed below. This small body of research sug- gests that photoperiod is the most salient environmental