Research suggests that anxiety disorders tend to temporally precede depressive disorders, a finding potentially relevant to understanding comorbidity. The current study used diary methods to determine whether daily anxious mood also temporally precedes daily depressed mood. 55 participants with generalized anxiety disorder (GAD) and history of depressive symptoms completed a 21-day daily diary tracking anxious and depressed mood. Daily anxious and depressed moods were concurrently associated. Daily anxious mood predicted later depressed mood at a variety of time lags, with significance peaking at a two-day lag. Depressed mood generally did not predict later anxious mood. Results suggest that the temporal antecedence of anxiety over depression extends to daily symptoms in GAD. Implications for the refinement of comorbidity models, including causal theories, are discussed.
Research has consistently documented extensive comorbidity between anxiety and depression (Maser & Cloninger, 1990). Major depressive disorder (MDD) co-occurs substantially with each individual anxiety disorder, at much higher rates than with other diagnostic categories, such as impulse-control or substance use disorders (Kessler et al., 2003; Kessler, Chiu, Demler, & Walters, 2005; Kessler, Merikangas, & Wang, 2007). Moreover, co-occurring anxiety and depression have negative implications beyond the impact of each individual disorder, including poorer prognosis, academic difficulties, suicide risk, lower quality of life, and worse treatment outcomes (Kessler, Stang, Wittchen, Stein, & Walters, 1999; Ledley et al., 2005; Lewinsohn, Rohde, & Seeley, 1995; Rush et al., 2005; Young, Mufson, & Davies, 2006). Clearly, a full understanding of the origins of comorbidity has important theoretical and practical implications, and yet many aspects of comorbidity are poorly understood.
Existing comorbidity models have traditionally fallen into two categories: the “lumper” perspective that anxiety and depression and their components cannot be meaningfully distinguished, and the “splitter” standpoint that anxiety and depression are fundamentally separate phenomena, distinguished by disparate risk factors, courses, and phenomenological experiences (see Wittchen, Kessler, Pfister, & Lieb, 2000). Some models, such as the widely-cited tripartite theory (Clark & Watson, 1991; Watson, Clark et al., 1995; Watson, Weber et al., 1995), both split and lump by identifying overlapping factors (negative affectivity) as well as specific components distinct to anxiety (physiological hyperarousal) and depression (anhedonia), but ultimately take the lumper approach of attributing comorbidity to shared substrates.
