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Objective: To investigate whether the course of depression changes when (a) follow-up duration is longer and (b) in addition to depression other mood and anxiety disorders are considered as outcome measures., Design: Longitudinal observational cohort study., Method: We selected patients from the Netherlands Study of Depression and Anxiety (NESDA) who had active depression at baseline (n=903) and for whom data from the 2, 4 and/or 6 year measurements were available. Using DSM-IV diagnoses and data from the 'Life chart interview', we divided participants in one of the following four course categories: (1) recovered (no diagnosis at 2-year measurement or later), (2) recurring without chronic episodes, (3) recurring with chronic episodes or (4) consistent chronic depression since baseline. We looked at the distribution of patients over the course categories from a short, diagnostically narrow perspective (over 2 years, only looking at depression) to a long, diagnostically broad perspective (over 6 years, looking at depression, dysthymia, hypomania, mania and anxiety)., Results: In the short, diagnostically narrow perspective, 58% of participants had recovered and 21% met the criteria for a chronic episode. In the long, diagnostically broad perspective however, only 17% had recovered while 55% had chronic episodes., Conclusion: Monitoring patients with depression over a longer period and with broader outcome measures (depression and related psychiatric disorders belonging to the mood disorder spectrum) shows that the course of depression is unfavourable and chronic for the majority. Conceptualising depression as a defined episodic disorder underestimates the severity of the prognosis for many patients and, as a consequence, the type of care indicated.

Background: Depressive and anxiety disorders are associated with shorter leukocyte telomere length (LTL), an indicator of cellular aging. It is, however, unknown which pathways underlie this association. This study examined the extent to which lifestyle factors and physiological changes such as inflammatory or metabolic alterations mediate the relationship., Method: We applied mediation analysis techniques to data from 2750 participants of the Netherlands Study of Depression and Anxiety. LTL was assessed using quantitative polymerase chain reaction. Independent variables were current depressive (30-item Inventory of Depressive Symptoms - Self Report) and anxiety (21-item Beck's Anxiety Inventory) symptoms and presence of a depressive or anxiety disorder diagnosis based on DSM-IV; mediator variables included physiological stress systems, metabolic syndrome components and lifestyle factors., Results: Short LTL was associated with higher symptom severity (B = -2.4, p = 0.002) and current psychiatric diagnosis (B = -63.3, p = 0.024). C-reactive protein, interleukin-6, waist circumference, triglycerides, high-density lipoprotein cholesterol and cigarette smoking were significant mediators in the relationship between psychopathology and LTL. When all significant mediators were included in one model, the effect sizes of the relationships between LTL and symptom severity and current diagnosis were reduced by 36.7 and 32.7%, respectively, and the remaining direct effects were no longer significant., Conclusions: Pro-inflammatory cytokines, metabolic alterations and cigarette smoking are important mediators of the association between depressive and anxiety disorders and LTL. This calls for future research on intervention programs that take into account lifestyle changes in mental health care settings.

Objective: Several cross-sectional studies have related depressive and anxiety disorders to shorter leukocyte telomere length (LTL) as an indicator of cellular aging. However, these studies have left many unresolved questions about underlying causality and ordering of associations. The objective of the present large, longitudinal study was to examine the relationship between depressive and anxiety disorders and LTL over a 6-year time period., Method: Data are from the Netherlands Study of Depression and Anxiety, including 2,292 patients with remitted and current diagnoses of depressive or anxiety disorders and 644 healthy control subjects. LTL was assessed using quantitative PCR and measured at baseline and after 6 years; depressive and anxiety disorder diagnoses and characteristics (course, duration, and severity) were determined at baseline and after 2, 4, and 6 years., Results: Results showed that persons with remitted (B=-52.6) and current (B=-60.8) depressive or anxiety disorder had consistently shorter LTL compared with healthy control subjects across baseline and at the 6-year follow-up, remaining significant when controlling for lifestyle and somatic health variables. Changes in the course of depressive or anxiety disorder characteristics over 6 years, however, were not associated with different LTL attrition rates., Conclusions: This study confirmed robust associations of depressive and anxiety disorders with shorter telomeres, but interestingly, it did not demonstrate that depressive and anxiety disorders and LTL change together over time, suggesting the absence of a direct within-person relationship. Short LTL is suggested to be either a long-term consequence or an underlying vulnerability factor for depressive or anxiety disorders.

Objective: Depressive disorders have been associated with increased risk for aging-related diseases, possibly as a consequence of accelerated cellular aging. Cellular aging, indexed by telomere length (TL) shortening, has been linked to depression in adults younger than 60 years; however, it remains unclear whether this is the case in late-life depression (age >60 years). The objective of this study was to assess differences in TL between persons with current late-life depression and never-depressed comparisons and to examine the association between characteristics of late-life depression and TL., Methods: In this cross-sectional study using the Netherlands Study of Depression in Older Persons, 355 persons with current late-life depression and 128 never-depressed comparisons, aged 60-93 years (mean age [SD]: 70.5 [7.4] years, 65% women), were recruited through primary care and mental healthcare. Late-life depression was established using a Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition-based structured psychiatric interview. Leukocyte TL, expressed in base pairs (bp), was determined in fasting blood samples by performing quantitative polymerase chain reaction., Results: Mean TL did not differ between depressed persons (bp [SD]: 5,035 [431]) and never-depressed (bp [SD]: 5,057 [729]) comparisons. Further, TL was not associated with severity, duration, and age at onset of depression; comorbid anxiety disorders; anxiety symptoms; apathy severity; antidepressant use; benzodiazepine use; cognitive functioning; and childhood trauma., Conclusion: Late-life depression was not associated with increased cellular aging. This absent association, which contradicts observations in younger adults, may be due to the potential larger heterogenic nature of late-life depression and lifetime cumulative exposure to other TL-damaging factors, possibly overruling effects of late-life depression., (Copyright © 2015 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.)