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Background: The number of patients with dementia who are granted euthanasia or assisted suicide (EAS) increases yearly in the Netherlands. By law, patients need to be decisionally competent or have an advance directive. Assessment of decisional capacity is challenging as dementia progressively affects cognitive performance. We aimed to assess qualitatively which factors, and how, influence the judgment of decisional capacity in EAS cases with dementia., Methods: We performed a qualitative study of 60 dementia EAS case summaries published by the Dutch regional euthanasia review committees between 2012 and 2021. Included reports were evaluated using the grounded theory approach. All quotes related to decisional capacity were coded independently by two researchers and compared in an iterative process to formulate an overarching framework on the assessment of decisional capacity. We selected 20 patients who had an advance directive and were judged to be decisionally compromised, as well as a selection of 40 EAS cases judged to be decisionally competent, half of which also had an advance directive (purposive sampling)., Results: Decisional capacity was present in every case report. Predefined, external criteria were rarely described explicitly, but physicians indirectly referred to the (cognitive) criteria set by Appelbaum and Grisso. Whether the thresholds for these dimensional criteria were met was influenced by six supporting factors (level of communication, psychiatric comorbidity, personality, presence of an advance directive, consistency of the request, and, finally, the patient-physician relationship) that also directly contributed to the judgment of capacity. The involved physicians and executed investigations were the two contextual factors providing a background., Conclusions: Decisional capacity regarding euthanasia is a multidimensional construct, often implicitly assessed and influenced by supporting and contextual factors. The subjectivity of the final judgment poses ethical and legal issues and argues for continuous quality improvement processes., (© 2024 The Author(s). Journal of the American Geriatrics Society published by Wiley Periodicals LLC on behalf of The American Geriatrics Society.)

Background: Frailty is an important concept for risk stratification in clinical practice, but it is hardly acknowledged at all in mental healthcare settings. This paper aims to assess the impact of frailty on the course of depression and anxiety, and the impact of these affective disorders on the course of frailty., Methods: Lifelines, a prospective population-based cohort study, evaluated 167,729 people living in the northern Netherlands. Frailty was based on the deficit accumulation model, which resulted in a 60-item frailty index (FI) at baseline and a 35-item FI at baseline and 5-year follow-up. Current depressive and anxiety disorders were assessed with the Mini International Neuropsychiatric Interview according to DSM-IV criteria. Bidirectional associations between frailty and affective disorders were investigated using separate multivariable regression analyses in younger (<60 years) and older adults (≥60 years)., Results: The FI was associated with the onset of a depressive disorder (younger adults: odds ratio [OR] = 1.12; 95% confidence interval [CI] 1.11-1.13; older adults: OR = 1.13; 95% CI 1.09-1.16) as well as any anxiety disorder (younger adults: OR = 1.10; 95% CI 1.09-1.10; older adults: OR = 1.07; 95% CI 1.04-1.09). The other way around, depressive disorder and anxiety disorders were associated with an accelerated increase of frailty over time (depressive disorder: younger adults: beta [β] = 0.03, p < 0.001; older adults: β = 0.04, p < 0.001; and any anxiety disorder: younger adults: β = 0.02, p < 0.001; older adults: β = 0.01, p < 0.142), although the effect of anxiety disorders was less equivocal among older adults., Conclusions: Affective disorders are reciprocally related to frailty. Results with respect to the impact of anxiety disorders on frailty suggest most impact at lower levels of frailty. Our results might imply that interventions to slow biological aging should be broadened towards younger and middle-aged people as well as non-frail older patients. To develop targeted treatment, future clinical and epidemiologic studies on the underlying pathways of this bidirectional association are needed., (© 2022 The Authors. Journal of the American Geriatrics Society published by Wiley Periodicals LLC on behalf of The American Geriatrics Society.)

Objectives: To determine whether physical frailty is associated with low-grade inflammation in older adults with depression, because late-life depression is associated with physical frailty and low-grade inflammation., Design: Baseline data of a cohort study., Setting: Primary care and specialized mental health care., Participants: Individuals aged 60 and older with depression according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria (N = 366)., Measurements: The physical frailty phenotype, defined as three out of five criteria (weight loss, weakness, exhaustion, slowness, low physical activity level), and three inflammatory markers (C-reactive protein (CRP), interleukin-6 (IL-6), and neutrophil gelatinase-associated lipocalin (NGAL)) were assessed., Results: The physical frailty phenotype was not associated with inflammatory markers in linear regression models adjusted for sociodemographic characteristics, lifestyle characteristics, and somatic morbidity. Of the individual criteria, handgrip strength was associated with CRP (β = -0.21, P = .002) and IL-6 (β = -0.25, P < .001), and gait speed was associated with NGAL (β = 0.15, P = .02). Principal component analysis identified two dimensions within the physical frailty phenotype: performance-based physical frailty (encompassing gait speed, handgrip strength, and low physical activity) and vitality-based physical frailty (encompassing weight loss and exhaustion). Only performance-based physical frailty was associated with higher levels of inflammatory markers (CRP: β = 0.14, P = .03; IL-6: β = 0.13, P = .06; NGAL: β = 0.14, P = .03)., Conclusion: The physical frailty phenotype is not a unidimensional construct in individuals with depression. Only performance-based physical frailty is associated with low-grade inflammation in late-life depression, which might point to a specific depressive subtype., (© 2015, Copyright the Authors Journal compilation © 2015, The American Geriatrics Society.)

Objectives: To systematically compare and pool the prevalence of frailty, including prefrailty, reported in community-dwelling older people overall and according to sex, age, and definition of frailty used., Design: Systematic review of the literature using the key words elderly, aged, frailty, prevalence, and epidemiology., Setting: Cross-sectional data from community-based cohorts., Participants: Community-dwelling adults aged 65 and older., Measurements: In the studies that were found, frailty and prefrailty were measured according to physical phenotype and broad phenotype, the first defining frailty as a purely physical condition and the second also including psychosocial aspects., Results: Reported prevalence in the community varies enormously (range 4.0-59.1%). The overall weighted prevalence of frailty was 10.7% (95% confidence interval (CI) = 10.5-10.9; 21 studies; 61,500 participants). The weighted prevalence was 9.9% for physical frailty (95% CI = 9.6-10.2; 15 studies; 44,894 participants) and 13.6% for the broad phenotype of frailty (95% CI = 13.2-14.0; 8 studies; 24,072 participants) (chi-square (χ(2) ) = 217.7, degrees of freedom (df)=1, P < .001). Prevalence increased with age (χ(2) = 6067, df = 1, P < .001) and was higher in women (9.6%, 95% CI = 9.2-10.0%) than in men (5.2%, 95% CI = 4.9-5.5%; χ(2) = 298.9 df = 1, P < .001)., Conclusion: Frailty is common in later life, but different operationalization of frailty status results in widely differing prevalence between studies. Improving the comparability of epidemiological and clinical studies constitutes an important step forward., (© 2012, Copyright the Authors Journal compilation © 2012, The American Geriatrics Society.)

Objectives: To examine the relationship between obesity and depressive symptoms taking into account different measures for obesity (body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR)) and different depressive symptom clusters., Design: Cross-sectional population-based survey., Setting: Baseline data of the Nijmegen Biomedical Study., Participants: One thousand two hundred eighty-four persons aged 50 to 70., Measurements: Obesity (BMI, WC, and WHR) and depressive symptoms were measured, the latter using the Beck Depression Inventory (BDI). Principal components analysis of the BDI items yielded two factors, one representing a cognitive-affective symptom cluster and the other a somatic-affective symptom cluster. Multiple regression analyses corrected for confounders were conducted for each measure of obesity, with separate models testing the BDI sum score and the depression symptom clusters., Results: BMI was significantly associated with BDI sum score (β=0.12, P<.001) and the cognitive- (β=0.08, P=.008) and somatic-affective symptom clusters (β=0.10, P=.001). WC (β=0.11, P<.001) and WHR (β=0.07, P=.004) were specifically associated with the somatic-affective symptom cluster., Conclusion: Visceral obesity, which is more indicative of vascular risk than BMI, is specifically associated with somatic-affective depressive symptom cluster, which might suggest that these symptoms are primarily due to a (subclinical) somatic condition., (© 2011, Copyright the Authors. Journal compilation © 2011, The American Geriatrics Society.)

Objectives: To examine the association between the angiotensin-converting enzyme (ACE) deletion/insertion (D/I) polymorphism and white matter hyperintensities (WMHs) in patients with dementia., Design: Observational pilot study with adjustment for potential confounders using analysis of covariance., Setting: Secondary care old-age psychiatry services in greater Manchester, United Kingdom., Participants: Ninety-seven patients with dementia: 49 with Alzheimer's disease (AD, National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association criteria) and 48 with vascular dementia (VaD, National Institute of Neurological Disorders and Stroke/Association Internationale pour la Recherche et l'Enseignement en Neurosciences criteria)., Measurements: The ACE D/I polymorphism, WMHs (deep WMHs (DWMHs) and periventricular hyperintensities (PVHs)) on T2-weighted magnetic resonance imaging, and potential cardiovascular confounders., Results: The D/D polymorphism of the ACE genotype was associated with severity of DWMH (P = .005) but not PVH (P = .34), corrected for age, cardiovascular risk factors, and type of dementia. Post hoc analyses were limited by statistical power but suggested an interaction with the apolipoprotein E epsilon4 allele., Conclusion: The results support previous observations that genetic factors influence the development of WMHs in dementia. The involvement of the ACE D/I polymorphism in the pathogenesis of DWMHs in dementia (AD and VaD), by a mechanism that is independent of its association with cardiovascular risk factors, should be confirmed in a large population-based sample.