ReviewInsomnia as a predictor of depression: A meta-analytic evaluation of longitudinal epidemiological studies
Introduction
Depression is the leading cause of disability in both women and men in the United States and worldwide and one of the 10 leading disorders for global disease burden (Lopez et al., 2006). In the United States, it has been reported that each year more than 19 million adult Americans suffer from a depressive illness and the direct and indirect costs of the disorder are more than $30 billion (Lopez et al., 2006). However, consensus reports show that individuals with depression are being underdiagnosed and undertreated (Hirschfeld et al., 1997). Although a substantial increase in the prescription of antidepressants has been observed over the past twenty years, data suggest that this increase is mainly due to increased long-term prescribing, rather than to changes in the recognition or case definition of depression (Moore et al., 2009). In order to narrowing the gap between prevalence and primary care assistance, the recognition of clinical early predictors of depression seems of utmost relevance.
Major depression commonly co-occurs with symptoms of insomnia (Riemann and Voderholzer, 2003, Tsuno et al., 2005), defined in the DSM-IV-TR as difficulties in initiating/maintaining sleep or non-restorative sleep, accompanied by decreased daytime functioning, persisting for at least four weeks. Already 40 years ago, Winokur et al. (1969) described in a sample of 1257 individuals with depression that all of them had insomniac symptoms. Although this relationship between depression and insomnia is well known and its description dates back to the founder of modern psychiatry (Kraepelin, 1909), its conceptualization has radically changed during the last decade. Insomnia has been traditionally conceptualized as a symptom of psychopathology, especially depression (overview see Riemann et al., 2001, Staner, 2010). More recently, insomnia has been considered as a primary disorder if it is present without the co-existence of other clinically relevant psychiatric or medical diseases, and as a secondary disorder if otherwise. Nevertheless, with respect to the link to depression, chronic insomnia can also exist years before the first onset of a depressive episode. Consequently, it has been suggested that “comorbid” insomnia may be a more appropriate term than “secondary” insomnia (McCrae and Lichstein, 2001, NIH, 2005, Lichstein, 2006). This new approach identifies insomnia and depression as two independent diagnostic entities with different clinical courses and characteristics (Staner, 2010). The next edition of DSM, DSM-V, will probably abandon the primary/secondary concept and instead introduce “insomnia disorder” as the main diagnostic category for insomnia, allowing specification whether or not it is co-morbid with another mental or medical disorder (Reynolds and Redline, 2010).
The close link between insomnia and depression suggests that the conditions are not just randomly associated. Insomnia is now considered not only a symptom of but also a possible predictor of depression. Ford and Kamerow (1989) were the first to note that such a relationship exists based on data from a longitudinal epidemiological study. Since then more than 40 studies have been published evaluating the predictor question (overview see Riemann, 2009, Baglioni et al., 2010a). However, despite the large amount of data collected up to now, no systematic meta-analytic evaluation of longitudinal studies has been performed about this type of relationship. Such an analysis might have strong clinical implications. If insomnia is indeed a predictor for depression, early and adequate treatment of insomnia might contribute to the prevention of the future development of depression. This view seems to be supported by some studies showing that adding cognitive-behavior treatment for insomnia (CBT-I) is efficacious also in patients with both symptoms of insomnia and depression and guarantees a better treatment outcome in this population than standard antidepressive treatment alone (Taylor et al., 2007, Manber et al., 2008).
The aim of the current review was to quantitatively summarize the results of studies which have longitudinally investigated the role of insomnia as a predictor for depression with a meta-analytic strategy. We hypothesized that symptoms of insomnia predict depression in different age-samples.
Section snippets
Methods
The meta-analysis was performed according to the MOOSE (Stroup et al., 2000) and the PRISMA (Liberati et al., 2009) guidelines. The first and second authors independently conducted the literature search, screened the titles and the abstracts of potentially eligible studies identified, examined the full text and extracted the data for the analyses from the selected studies.
Results
Fig. 1 illustrates the search flow. The literature search yielded 46 longitudinal studies considering both sleep difficulties and major depression. Five studies were excluded as they focussed on the effect of depression predicting sleep difficulties (Morgan et al., 1989, Hohagen et al., 1993, Foley et al., 1999a, Patten et al., 2000, Jansson and Linton, 2006). Two studies were excluded because the follow-up assessment was conducted after less than 12 months (Hohagen et al., 1994, Schramm et al.,
Discussion
The results of the present analysis indicate that non-depressed subjects with insomnia have a twofold risk to develop depression, compared to people with no sleep difficulties. The pooled estimates were high despite the wide variability in study populations, design and measures, and persisted to be high after exclusion of the outliers (OR = 2.10; 95%; and CI: 1.86–2.38). More specifically, the incidence of depression in the group with insomnia (and no depression) at baseline was significantly
Role of funding source
Dr. Baglioni and Prof. Dr. Riemann have received funding from the European Community's Seventh Framework Programme (People, Marie Curie Actions, Intra-European Fellowship, FP7-PEOPLE-IEF-2008) under grant agreement n. 235321 and from OPTIMI (FP7-JCT-2009-4; 248544) for this work. The sources of funding had no role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.
Conflict of interest
The corresponding author, Dr. Baglioni, confirms that she had full access to all the data in the study and had final responsibility for the decision to submit for publication.
Dr. Nissen has received speaker honoraria from Sanofi-Aventis and Lundbeck. Dr. Voderholzer has received speaker honoraria from Sanofi-Aventis, Lundbeck, Pfizer, Cephalon, and Lilly. He has been principal investigator of an investigator initiated trial sponsored by Lundbeck. Dr. Riemann received research support from
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