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Background: Even before the onset of age-related diseases, obesity might be a contributing factor to the cumulative burden of oxidative stress and chronic inflammation throughout the life course. Obesity may therefore contribute to accelerated shortening of telomeres. Consequently, obese persons are more likely to have shorter telomeres, but the association between body mass index (BMI) and leukocyte telomere length (TL) might differ across the life span and between ethnicities and sexes., Objective: A collaborative cross-sectional meta-analysis of observational studies was conducted to investigate the associations between BMI and TL across the life span., Design: Eighty-seven distinct study samples were included in the meta-analysis capturing data from 146,114 individuals. Study-specific age- and sex-adjusted regression coefficients were combined by using a random-effects model in which absolute [base pairs (bp)] and relative telomere to single-copy gene ratio (T/S ratio) TLs were regressed against BMI. Stratified analysis was performed by 3 age categories ("young": 18-60 y; "middle": 61-75 y; and "old": >75 y), sex, and ethnicity., Results: Each unit increase in BMI corresponded to a -3.99 bp (95% CI: -5.17, -2.81 bp) difference in TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -7.67 bp (95% CI: -10.03, -5.31 bp) difference. Each unit increase in BMI corresponded to a -1.58 × 10(-3) unit T/S ratio (0.16% decrease; 95% CI: -2.14 × 10(-3), -1.01 × 10(-3)) difference in age- and sex-adjusted relative TL in the total pooled sample; among young adults, each unit increase in BMI corresponded to a -2.58 × 10(-3) unit T/S ratio (0.26% decrease; 95% CI: -3.92 × 10(-3), -1.25 × 10(-3)). The associations were predominantly for the white pooled population. No sex differences were observed., Conclusions: A higher BMI is associated with shorter telomeres, especially in younger individuals. The presently observed difference is not negligible. Meta-analyses of longitudinal studies evaluating change in body weight alongside change in TL are warranted.

Objectives: Childhood abuse has been associated with depression in later life. This may be related to hypothalamic-pituitary-adrenal (HPA) axis functioning. Therefore we aimed to examine the impact of childhood abuse and its interaction with depression on cortisol levels in older adults., Methods: Data from 418 participants (mean age 70.8 years) in the Netherlands Study of Depression in Older Persons (NESDO) were used; 187 participants experienced childhood abuse; 309 participants had a diagnosis of depression. Diurnal cortisol levels were determined using six saliva samples from every participant. Multiple regression analyses were performed., Results: Significant negative associations between childhood abuse and morning cortisol levels were found. In nondepressed persons, both psychological and sexual abuse were associated with greater dynamics of the HPA axis in response to awakening., Conclusions: Childhood abuse is associated with lower basal cortisol levels at awakening irrespective of major depressive disorder (MDD). Higher reactivity of the HPA axis during the hour after awakening was found in nondepressed participants only, which might suggest that late-life depression modifies the effect of childhood abuse on the HPA axis. Older adults with a history of childhood abuse may be more negatively affected by stress or stressful events and this is reflected in dysregulation of the HPA axis.

Background: Although there is some evidence that older people might have a poorer course of major depressive disorder (MDD) than younger or middle-aged people, and that age-related course differences might affect the optimisation of MDD treatment, large-scale studies with a broad age range, including consistent course assessments, are needed to properly address this issue. Therefore, we aimed to longitudinally examine whether older age was associated with a poorer naturalistic course trajectory of MDD than that of younger ages and to establish which prognostic-clinical, social, and health-factors could explain this potentially poorer course., Methods: For this longitudinal cohort study, we used baseline and 2-year follow-up data from the Netherlands Study of Depression and Anxiety (NESDA) and the Netherlands Study of Depression in Older Persons (NESDO) cohorts. People aged between 18 and 88 years, with an MDD diagnosis at baseline, and a valid clinical assessment at 2-year follow-up were included. The primary outcome was the 2-year course of MDD, which was assessed by use of four indicators: having a depression diagnosis (MDD or dysthymia) after 2 years, having a chronic symptom course (depressive symptoms present during 80% or more of the 2-year follow-up period), time to remission, and depression severity change. We used multivariate analyses to examine associations between continuous age and these MDD course indicators. We also examined whether prognostic clinical (eg, comorbid anxiety), social (loneliness and social support), and health (body-mass index, pain, and chronic diseases) factors contributed to the differences in the course of MDD between age groups., Findings: Between 2004-2012, baseline and 2-year follow-up data were obtained for 1042 participants from the NESDA and NESDO cohorts, of whom 690 (66%) were women. Older age was significantly associated with a worse 2-year MDD course for all four indicators (MDD diagnosis: odds ratio [OR] 1·08, 95% CI 1·00-1·17; chronic symptom course: OR 1·24, 1·13-1·35; time to remission: hazard ratio [HR] 0·91, 0·87-0·96; and depression severity change: regression coefficient 1·06, p<0·0001; all per 10-year increase). The course of MDD worsened linearly with age, and people aged 70 years or older had the worst outcomes compared with those of the reference group of people aged 18-29 years (MDD diagnosis: OR 2·02, 95% CI 1·18-3·45; chronic symptom course: OR 3·19, 1·74-5·84; time to remission: HR 0·60, 0·44-0·83; and depression severity change: -12·64 [SD 10·85] in those aged 18-29 years and -5·57 [11·14] in those aged 70 years or older). These results were slightly reduced, but remained mostly significant when adjusting for prognostic clinical, social, and health factors., Interpretation: Older age was found to be a consistent and important risk factor for a poorer MDD course, which could not be explained by a range of well established risk factors. Further investigation of potential underlying mechanisms-including the effect of cognitive impairment, for example-is needed to prevent the negative consequences of a long-term MDD burden in older people., Funding: Netherlands Organisation for Health Research and Development, Fonds NutsOhra, Stichting tot Steun VCVGZ, NARSAD The Brain and Behaviour Research Fund, and European Union's 7th Framework Programme., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Objective: Major depressive disorder (MDD) is common in patients with multiple sclerosis (MS) but may remain unrecognized because of overlapping symptoms and different presentation due to its specific MS-related neurobiological aetiology. We aimed to investigate the clinical profile of MDD in MS., Methods: In a sample of MDD patients with MS (n=83) and without MS (n=782), MDD characteristics, 30 depressive symptoms, and sum scores of cognitive, somatic, atypical and melancholic symptom clusters were compared using logistic regression analyses and analysis of co-variance., Results: MDD in MS was characterized by older age of onset (p<0.001), and fewer comorbid anxiety disorders (37% versus 72%; p<0.001). The symptom 'future pessimism' was more common in MS patients (OR=1.62; 95%CI=1.02-2.59). 'Diminished capacity for pleasure/enjoyment' (OR=0.44; 95%CI=0.24-0.78), 'increased appetite' (OR=0.40; 95%CI=0.19-0.85), 'arousal symptoms' (OR=0.49; 95%CI=0.28-0.84), and 'panic/phobic symptoms' (OR=0.49; 95%CI=0.29-0.84) were less common in MS patients. Twenty-five symptoms (83%) out of 30, including depression's core symptoms (sadness and loss of interest) were not differentially associated with MS and no differences existed for the symptom clusters., Conclusion: Only subtle differences in depressive symptom profiles existed between MDD patients with and without MS. The clinical profile of depression remains valid among MS patients, although it presents with diminished anxiety distress and comorbidity., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Introduction: The occurrence of well-established risk factors for depression differs across the lifespan. Risk factors may be more strongly associated with depression at ages when occurrence, and therefore expectance, is relatively low ("on-time off-time" hypothesis). This large-scale study examined absolute and relative risks of established risk factors for depression across the lifespan., Methods: Participants were 2,215 currently or never depressed adults aged 18 to 93 years from two cohort studies: NESDA and NESDO. The occurrence of 19 established risk factors (absolute risk) was examined in different age groups. In addition, the relative risk of these risk factors for depression was compared across age groups by examining risk factor × age interaction., Results: The occurrence of all risk factors differed significantly across age groups. Although most risk factors had significant associations with depression across the lifespan, for five risk factors the strength of the association was age-dependent. Stronger associations with depression in younger age were found for childhood abuse, pain, higher body mass index (BMI) and number of chronic diseases, whereas low income imposed a stronger risk in older age. Associations with depression were strongest in age groups where occurrence was lowest., Conclusions: Although the exposure to risk factors changes across the lifespan, the relative risk associating them to depression remains similar for most risk factors. Some specific risk factors (low income, and health factors pain, BMI, and number of chronic diseases), however, seem more strongly associated with depression in ages in which occurrence is lowest and least expected., (Copyright © 2017 American Association for Geriatric Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Psychosocial stress has been associated with an increased risk for mental and somatic health problems across the life span. Some studies in younger adults linked this to accelerated cellular aging, indexed by shortened telomere length (TL). In older adults, the impact of psychosocial stress on TL may be different due to the lifetime exposure to competing causes of TL-shortening. This study aims to assess whether early and recent psychosocial stressors (childhood abuse, childhood adverse events, recent negative life events, and loneliness) were associated with TL in older adults., Methods: Data were from the Netherlands Study of Depression in Older Persons (NESDO) in which psychosocial stressors were measured in 496 persons aged 60 and older (mean age 70.6 (SD 7.4) years) during a face-to-face interview. Leukocyte TL was determined using fasting blood samples by performing quantitative polymerase chain reaction (qPCR) and was expressed in base pairs (bp)., Results: Multiple regression analyses, adjusted for age, sex, and chronic diseases, showed that childhood abuse, recent negative life events and loneliness were unrelated to TL. Only having experienced any childhood adverse event was weakly but significantly negatively associated with TL., Conclusions: Our findings did not consistently confirm our hypothesis that psychosocial stress is associated with shorter TL in older adults. Healthy survivorship or other TL-damaging factors such as somatic health problems seem to dominate a potential effect of psychosocial stress on TL in older adults.

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.)