Frailty In Late Life Research Articles

Diet quality from mid to late life and its association with physical frailty in late life in a cohort of Chinese adults

BackgroundIt is unclear if improving diet quality after midlife could reduce the risk of physical frailty at late life. We aimed to associate changes in diet quality after midlife with physical frailty at late life.MethodsDiet quality in 12,580 participants from the Singapore Chinese Health Study was assessed with the Dietary Approaches to Stop Hypertension (DASH) scores at baseline (1993–1998; mean age 53 years) and follow-up 3 (2014–2016; mean age 73 years). Physical frailty was assessed using the modified Cardiovascular Health Study phenotype at follow-up 3. Multivariable logistic regressions examined associations between DASH scores and physical frailty.ResultsComparing participants in extreme quartiles of DASH scores, the odds ratios (OR) [95% confidence interval (CI)] for physical frailty were 0.85 (0.73,0.99) at baseline and 0.49 (0.41, 0.58) at follow-up 3. Compared to participants with consistently low DASH scores, participants with consistently high scores (OR 0.74, 95% CI: 0.59, 0.94) and those with > 10% increase in scores (OR 0.78, 95% CI: 0.64, 0.95) had lower odds of frailty. Compared to those in the lowest DASH tertiles at both time-points, significantly lower odds of physical frailty were observed in those who were in the highest DASH tertiles at both time points [0.59 (0.48, 0.73)], and in those who improved their scores from the lowest [0.68 (0.51, 0.91)] or second tertile at baseline [0.61 (0.48, 0.76)] to the highest tertile at follow-up 3.ConclusionsMaintaining a high diet quality or a substantial improvement in diet quality after midlife could lower the risk of physical frailty at late life.

High Throughput Plasma Proteomics and Risk of Heart Failure and Frailty in Late Life

ImportanceHeart failure (HF) and frailty frequently coexist and may share a common pathobiology, although the underlying mechanisms remain unclear. Understanding these mechanisms may provide guidance for preventing and treating both conditions.ObjectiveTo identify shared pathways between incident HF and frailty in late life using large-scale proteomics.Design, Setting, and ParticipantsIn this cohort study, 4877 aptamers (Somascan v4) were measured among participants in the community-based longitudinal Atherosclerosis Risk In Communities (ARIC) cohort study at visit 3 (V3; 1993-1995; n = 10 638) and at visit 5 (V5; 2011-2013; n = 3908). Analyses were externally replicated among 3189 participants in the Cardiovascular Health Study (CHS). Data analysis was conducted from February 2022 to June 2023.ExposuresProtein aptamers, measured at study V3 and V5.Main Outcomes and MeasuresOutcomes assessed included incident HF hospitalization after V3 and after V5, prevalent frailty at V5, and incident frailty between V5 and visit 6 (V6; 2016-2017; n = 4131). Frailty was assessed using the Fried criteria. Analyses were adjusted for age, gender, race, field center, hypertension, diabetes, smoking status, body mass index, estimated glomerular filtration rate, prevalent coronary heart disease, prevalent atrial fibrillation, and history of myocardial infarction. Mendelian randomization (MR) analysis was performed to assess potential causal effects of candidate proteins on HF and frailty.ResultsA total of 4877 protein aptamers were measured among 10 638 participants at V3 (mean [SD] age, 60 [6] years; 4886 [46%] men). Overall, 286 proteins were associated with incident HF after V3 (822 events; P < 1.0 × 10−5), 83 of which were also associated with incident after V5 (336 events; P < 1.7 × 10−4). Among HF-free participants at V5 (n = 3908; mean [SD] age, 75 [5] years; 1861 [42%] men), 48 of 83 HF-associated proteins were associated with prevalent frailty (223 cases; P < 6.0 × 10−4), 18 of which were also associated with incident frailty at V6 (152 cases; P < 1.0 × 10−3). These proteins enriched fibrosis and inflammation pathways and demonstrated stronger associations with incident HF with preserved ejection fraction (HFpEF) than HF with reduced ejection fraction. All 18 proteins were associated with both prevalent frailty and incident HF in CHS. MR identified potential causal effects of several proteins on frailty and HF.Conclusions and RelevanceIn this study, the proteins associated with risk of HF and frailty enrich for pathways related to inflammation and fibrosis as well as risk of HFpEF. Several of these proteins could potentially contribute to the shared pathophysiology of frailty and HF.

MID-LIFE PLASMA PROTEINS ASSOCIATE WITH PREFRAILTY AND FRAILTY: A PROTEOMIC ANALYSIS

Abstract Physical frailty is a syndrome that typically manifests in later life, although the pathogenic process causing physical frailty likely begins decades earlier. To date, few studies have examined the biological signatures in mid-life associated with frailty in late life. We evaluated 4955 plasma proteins (log 2-transformed and standardized) measured using the SomaScan platform among 3810 participants (57.8+/-5.0 years, 58.2% women) at Visit 3 of the Atherosclerosis Risk in Community (ARIC) study, and their frailty status across up to 3 study visits in late-life (median follow-up 19 years). We used multinomial logistic regression models to examine the associations between the protein levels and the frailty status, adjusting for demographics, health indicators, comorbidities, and follow-up time. Two sets of 2 proteins were identified to be associated with prefrailty and frailty, respectively, after Bonferroni correction (p&amp;lt; 1.01×10-5). Higher concentration of hydroxymethylglutaryl-CoA synthase (HMGCS1; OR=1.22), a regulator of cholesterol synthesis, and lower concentration of dual specificity protein phosphatase 13 isoform A (DUSP13A; OR=0.82), a protein involved in cell apoptosis, were associated with higher odds of prefrailty. Higher concentration of growth differentiation factor 15 (GDF15; OR=1.39), a protein related to inflammation and cell senescence, and lower concentration of contactin-1 (CNTN1; OR=0.72), a protein involved in nervous system development and signalling, were associated with higher odds of frailty. The pathway and upstream regulator analyses of the physical frailty- or prefrailty-associated proteins (p&amp;lt; 0.01) revealed the dysregulation of apoptosis, inflammation, and neuromuscular communication in mid-life. Our findings provides new insights into frailty etiology earlier in the life course.

4 The Effect of Age on the Relationship Between Adverse Childhood Experiences and Frailty in Late Life: A Moderation Model

Objective:Although relationships between Fried frailty criteria (i.e., weakness, slowness, weight loss, exhaustion and low physical activity), cognitive decline, and adverse childhood experiences (ACEs) have been examined (Brigalo et al., 2015, Brown et al., 2022, Fabricio et al., 2020, &amp; Tani et al., 2021), the moderating effect of age on the relationship between ACEs and frailty has yet to be explored. The present study examined whether age moderates the relationship between total number of ACEs and number of frailty criteria in older age.Participants and Methods:137 older adults were recruited from University of Miami clinics and surrounding community care centers. Collected data included demographic information, number of frailty criteria met, and number of ACEs endorsed. Participants were primarily Hispanic-White (64.2%) and female (56.9%), with a mean age of 73.62 years (SD=6.252). Data were initially analyzed using descriptive statistics. A hierarchical linear regression was run to test the effect of ACE score on number of frailty criteria met. A simple moderation analysis using the PROCESS macro was then performed with total number of medical conditions included as a covariate to address any potentially confounding effects. To avoid multicollinearity issues, number of ACEs endorsed and age were mean centered and an interaction term between the two was produced.Results:Scores on the ACE did substantially effect the total number of frailty criteria met by participants in this study (f=2.37, p=0.028, ΔR2=0.023), independent of number of medical conditions. The overall moderation model was significant (f=2.99, p=0.022, R2=0.103), and the addition of the interaction effect resulted in a statistically significant change to the model (f=4.08, p=0.045, ΔR2=0.035). Taken together, support for a moderating effect was found, specifically within the lower age group (65 - 71years), but not older (greater than 72 years) with ACE score positively predicting the number of frailty criteria met (b =0.230, t=2.62, p=0.010).Conclusions:Results largely support the positive effect of ACE endorsement on the number of frailty criteria met in later life. Age acted as a moderating effect, for the younger old population, such that as number of ACEs endorsed increased, so too did the number of frailty criteria met. This finding highlights the importance of early intervention among those in younger late life who have experienced trauma. Given the positive relationship between frailty and cognitive decline in late life (Brigalo et al., 2015 &amp; Fabricio et al., 2020), these findings also support the need for a better understanding of how childhood adversity impacts physical well-being over the life course.

Consumption of Coffee, Tea, and Caffeine at Midlife, and the Risk of Physical Frailty in Late Life

ObjectivesOur study evaluated the prospective association between the consumption of caffeine-containing beverages at midlife and the risk of physical frailty at late life within a population-based cohort of Chinese adults living in Singapore over a follow-up period of 20 years. DesignProspective cohort study. Setting and ParticipantsWe used data from 12,583 participants from the baseline and third follow-up interviews of the Singapore Chinese Health Study (SCHS). Participants had a mean age of 53 years at baseline (1993–1998), and a mean age of 73 years during the third follow-up (2014–2017). MethodsAt baseline, habitual consumption of caffeine-containing beverages was evaluated using a validated semi-quantitative food-frequency questionnaire. During the third follow-up, physical frailty was assessed using the modified Cardiovascular Health Study phenotype. ResultsCompared with non-daily drinkers, those who drank 4 or more cups of coffee daily had reduced odds of physical frailty [odds ratio (OR), 0.54; 95% CI, 0.38–0.76]. Similarly, compared with those who hardly drank tea, participants who drank tea everyday also had reduced odds (OR, 0.82; 95% CI, 0.71–0.95). Total daily caffeine intake at midlife was associated with reduced likelihood of frailty at late life in a dose-response relationship (Ptrend < .001). Relative to their counterparts in the lowest quartile of daily caffeine intake (0–67.6 mg/d), participants in the highest quartile (223.0–910.4 mg/d) had an OR of 0.77 (95% CI, 0.66–0.91). Higher caffeine consumption was associated with lower likelihood of being in the slowest quintile for timed up-and-go (TUG) and weakest quintile for handgrip strength. Conclusions and ImplicationsIn this cohort of Chinese adults, higher consumption of caffeine at midlife, via coffee and tea, was associated with a reduced likelihood of physical frailty in late life.

Proteomic biomarkers associated with incident heart failure and frailty in late life

Abstract Background Heart failure (HF) and frailty are highly prevalent in late life and commonly co-exist, but the mechanisms underlying their bi-directional relationship are incompletely understood. This study aimed to identify shared molecular pathways associated with incident HF and frailty in late life. Methods Among participants in the Atherosclerosis Risk in Communities (ARIC) study, a communit-based cohort study in the United States, 4,877 plasma proteins were measured using an aptamer-affinity assay (Somascan v4) at study Visit 3 (V3; 1993–1994; n=10,368, age 60±6 years; 822 incident HF events) and at study Visit 5 (V5; 2011–2013; n=3,908, age 75±5 years; 336 incident HF events). Frailty was assessed at V5 using Fried criteria, which incorporates gait speed, grip strength, low energy expenditure, weight loss, and exhaustion. We examined the association of proteins at V3 with incident HF after V3 with Bonferroni corrected P&amp;lt;0.05 using multivariable Cox proportional hazard regression models. For HF-associated proteins at V3, we assessed the association of V5 protein levels with incident HF after V5. For the resulting HF-associated proteins, multivariable logistic regression was used to assess associations of V5 protein values with prevalent frailty at V5 (n=223 cases) and with incident frailty by study Visit 6 (2016–2018; n=152 incident cases). All models adjusted for age, sex, race, hypertension, diabetes, cardiovascular disease, BMI, atrial fibrillation, and stroke. The set of HF-related proteins that associated with incident frailty at FDR &amp;lt;0.05 using Benjamini-Hochberg correction was tested for pathway enrichment using the Reactome database. Results Of 289 proteins associated with incident HF post-V3 at p&amp;lt;1.0x10–5 (0.05/4,877), 84 were significantly associated with incident HF post-V5 at p&amp;lt;1.7x10–4 (0.05/289). Among 4,131 HF-free participants at V5, 48 of these 84 HF-associated proteins associated with prevalent frailty at p&amp;lt;5.9x10–4 (0.05/84). Among Visit 5 participants who completed a frailty assessment and were free of both prevalent HF and frailty (n=3,908), 31of 48 candidate proteins were also significantly associated with incident frailty at FDR 0.05, 18 of which were significantly associated with incident frailty at p&amp;lt;1.0x10–3 (0.05/48; Figure 1). The 31 proteins associated with incident frailty at FDR 0.05 enriched for collagen biosynthesis, formation, and trimerization (COL28A1, COL6A3, EFEMP1), and cytokine immune pathways and TNF receptor binding (TNFRSF1A and B, VEGFA, B2M, and HAVCR2) in pathway enrichment analysis. Conclusions Collagen metabolism and immune pathways may be shared biologic pathways between HF and frailty in late-life. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services.

Genetic and Environmental Influences on Longitudinal Frailty Trajectories From Adulthood into Old Age.

Frailty is a complex, dynamic geriatric condition, but limited evidence has shown how genes and environment may contribute to its longitudinal changes. We sought to investigate sources of individual differences in the longitudinal trajectories of frailty, considering potential selection bias when including a sample of oldest-old twins. Data were from 2 Swedish twin cohort studies: a younger cohort comprising 1 842 adults aged 29-96 years followed up to 15 waves, and an older cohort comprising 654 adults aged ≥79 years followed up to 5 waves. Frailty was measured using the frailty index (FI). Age-based latent growth curve models were used to examine longitudinal trajectories, and extended to a biometric analysis to decompose variability into genetic and environmental etiologies. A bilinear model with an inflection point at age 75 best described the data, indicating a fourfold to fivefold faster FI increase after 75 years. Twins from the older cohort had significantly higher mean FI at baseline but slower rate of increase afterward. FI level at age 75 was moderately heritable in both men (42%) and women (55%). Genetic influences were relatively stable across age for men and increasing for women, although the most salient amplification in FI variability after age 75 was due to individual-specific environmental influences for both men and women; conclusions were largely consistent when excluding the older cohort. Increased heterogeneity of frailty in late life is mainly attributable to environmental influences, highlighting the importance of targeting environmental risk factors to mitigate frailty in older adults.

Associations between loneliness and frailty among older adults: Evidence from the China Health and Retirement Longitudinal Study

BackgroundPrevious studies have demonstrated the associations between loneliness and frailty in late life. However, there is a lack of consensus on the direction of the relationship. The present study aimed to examine the interdependencies between loneliness and frailty over time.MethodsData on participants aged 60 years old and above were collected from the 2011, 2013, and 2015 samples of the China Health and Retirement Longitudinal Study (CHARLS). Loneliness was measured by a single question from the Centre for Epidemiological Studies Depression scale, and frailty was assessed by the Physical Frailty Phenotype (PFP) scale. Cross-lagged panel models were utilized to examine the potential bidirectional relationship between loneliness and frailty.ResultsReciprocal associations were found between loneliness and frailty. Furthermore, we found that baseline frailty and early change in frailty had a significant predictive effect on late change in loneliness. Higher baseline loneliness in older adults may create a potentially vicious cycle that influenced early change in frailty and continued to cause late change in loneliness.ConclusionA bidirectional relationship may exist between loneliness and frailty among older Chinese adults over 60 years old. Lonely older adults should be alerted to the potential self-reinforcing cycle of loneliness that affects their health.

Lifelong Disadvantage and Late Adulthood Frailty

Frailty is a complex state of objective and subjective vulnerability. It tends to increase with age, but the process is influenced by previous life course, especially previous disadvantages. The aim of this paper is to examine how the disadvantages suffered in adulthood (25 to 59 years) in four domains (unemployment, financial hardship, stress, and bad health) affect frailty in late adulthood (60 to 79 years). Using linear regression models on data from the Survey of Health, Ageing, and Retirement in Europe (2004–2017), we estimate frailty levels for several age groups (60–64, 65–69, 70–74, 75–79) accounting for both the persistence of these disadvantages over time and their coexistence, i.e., the number of years when they were simultaneously experienced. Results show that while frailty increases with age, as expected, there is also evidence of an accumulation of risks: the longer the periods of adult life affected by unemployment, stress, financial hardship or, most importantly, bad health, the frailer individuals are in their late years. Furthermore, periods of coexisting disadvantages in adulthood translate into additional frailty in late life. Our findings highlight the importance of fighting disadvantages early in life: long-term improvements in terms of reduced frailty (a concept interrelated with health) may be substantial.

Depression as a determinant of frailty in late life

Objectives Accumulating evidence shows depression as a risk factor for frailty, but studies are mainly population-based and widely differ in their assessment of either depression or frailty. We investigated the association between depression and frailty among geriatric outpatients using different assessment instruments for both conditions. Method Among 315 geriatric outpatients (mean age 72.1 years, 68.3% female sex) participating the MiMiCS-FRAIL cohort study, major and subthreshold depression were measured with psychiatric diagnostic interview according to DSM-5 criteria (SCID-5) as well as with instruments to screen and measure severity of depressive symptoms (GDS-15 and PHQ-9). Frailty was assessed according to a screening instrument (FRAIL-BR) and a multidimensional Frailty Index (FI-36 items). Multiple logistic and linear regression were performed to assess the association between depression (independent variable) and frailty (dependent variable) adjusted for confounders. Results Frailty prevalence in patients with no, subthreshold or major depressive disorder increases from either 14.5%, 46.5% to 65.1% when using the FRAIL-BR questionnaire, and from 10.2%, 20.9%, to 30.2% when using the FI-36 index. These association remain nearly the same when adjusted for covariates. Both the FRAIL-BR and the FI-36 were strongly associated with major depressive disorder, subthreshold depression, and depressive symptoms by PHQ-9 and GDS-15. Conclusion Late life depression and frailty are associated in a dose-dependent manner, irrespective of the used definitions. Nonetheless, to avoid residual confounding, future research on underlying biological mechanisms should preferably be based on formal psychiatric diagnoses and objectively assessment frailty status.

Effects of comorbid physical frailty and low muscle mass on incident disability in community-dwelling older adults: A 24-month follow-up longitudinal study

ObjectivesLow muscle mass frequently precedes or coexists with physical frailty in late life. This study aimed to examine whether comorbid physical frailty and low muscle mass increase the risk of incident disability in community-dwelling older adults. Study designA prospective cohort study. MethodsParticipants were 9229 community-dwelling older Japanese adults (≥65 years). Longitudinal data on incident disability were collected for up to a maximum of 24 months from baseline. Physical frailty was defined as experiencing three or more of the following five symptoms: slowness, weakness, exhaustion, low activity, and weight loss. Low muscle mass was identified based on the AWGS definition (<7.0 kg/m2 for men and <5.7 kg/m2 for women). ResultsDuring the follow-up period, 460 (5.0%) individuals had incident disability. The prevalence rates of low muscle mass, physical frailty, and comorbid physical frailty and low muscle mass were 12.0% (n = 1104), 6.8 % (n = 624), and 1.8 % (n = 167), respectively. Compared with non-physical frailty/normal muscle mass, physical frailty (hazard ratio (HR) 2.50, 95% confidential interval (CI) 1.97−3.18) and comorbid physical frailty and low muscle mass (HR 4.03, 95% CI 2.85−5.70) were significantly associated with incident disability after adjusting for the covariates. ConclusionsAlthough low muscle mass alone may not be associated with an increased risk of incident disability in community-dwelling older adults, comorbid physical frailty and low muscle mass had a significant impact on disability. Low muscle mass was a risk factor for disability in older adults with physical frailty.

Association Between Life-Course Obesity and Frailty in Older Adults: Findings in the GAZEL Cohort.

This study aimed to assess the relationship between weight history during adulthood and frailty in late life in men and women participating in the GAZEL(GAZ and ELectricité) cohort. This cohort study included 8,751 men and 3,033 women (aged 61 to 76 years) followed up since 1989. Modified Fried's frailty criteria (weakness, fatigue, unintentional weight loss, low physical activity, and impaired mobility) were assessed in 2015. Reported BMI was determined each year to characterize: obesity status in 2015, obesity duration over the 1990to2015 period, and trajectories of BMI. Associations between frailty and weight history were assessed using multinomial regression. In 2015, 12% of men had obesity, 1.8% severe obesity, and 0.4% morbid obesity;for women, these percentages were 11%, 2.2%, and 0.8%, respectively. Individuals with obesity were more likely to be frail than those with normal BMI and the risk of frailty increased with each additional year of obesity (adjusted odds ratio1.04 [1.00-1.08] for men and 1.07 [1.02-1.13] for women). Trajectories of BMI revealed that both long-term obesity and onset of obesity in late adulthood were associated with frailty. Current and past obesity appear to be important determinants of frailty. Early weight management may be beneficial in old age.

Neuroticism as a Predictor of Frailty in Old Age: A Genetically Informative Approach.

Neuroticism is associated with poor health outcomes, but its contribution to the accumulation of health deficits in old age, that is, the frailty index, is largely unknown. We aimed to explore associations between neuroticism and frailty cross-sectionally and longitudinally, and to investigate the contribution of shared genetic influences. Data were derived from the UK Biobank (UKB; n = 274,951), the Australian Over 50's Study (AO50; n = 2849), and the Swedish Twin Registry (Screening Across the Lifespan of Twins Study [SALT], n = 18,960; The Swedish Adoption/Twin Study of Aging [SATSA], n = 1365). Associations between neuroticism and the frailty index were investigated using regression analysis cross-sectionally in UKB, AO50, and SATSA and longitudinally in SALT (25-29 years of follow-up) and SATSA (6 and 23 years of follow-up). The co-twin control method was applied to explore the contribution of underlying shared familial factors (SALT, SATSA, AO50). Genome-wide polygenic risk scores for neuroticism were used in all samples to further assess whether common genetic variants associated with neuroticism predict frailty. High neuroticism was consistently associated with greater frailty cross-sectionally (adjusted β [95% confidence intervals] in UKB = 0.32 [0.32-0.33]; AO50 = 0.35 [0.31-0.39]; SATSA = 0.33 [0.27-0.39]) and longitudinally up to 29 years (SALT = 0.24 [0.22-0.25]; SATSA 6 years = 0.31 [0.24-0.38]; SATSA 23 years = 0.16 [0.07-0.25]). When adjusting for underlying shared genetic and environmental factors, the neuroticism-frailty association remained significant, although decreased. Polygenic risk scores for neuroticism significantly predicted frailty in the two larger samples (meta-analyzed total β = 0.059 [0.055-0.062]). Neuroticism in midlife predicts frailty in late life. Neuroticism may have a causal influence on frailty, whereas both environmental and genetic influences, including neuroticism-associated common genetic variants, contribute to this relationship.

Psychosocial Correlates of Frailty in Older Adults.

Background: The aim of this study was to investigate psychosocial variables associated with frailty status. Moreover, gender differences in the psychosocial variables associated with frailty were examined. Methods: This cross-sectional study examined a community-dwelling sample of N = 210 older adults (M = 75.31 years). Frailty was measured with the Tilburg Frailty Indicator. Quality of life, depression, resilience, social support, self-efficacy, traumata experienced, and trauma severity were assessed as psychosocial variables. Logistic regression analyses were performed. Results: In total, 41.4% of the participants were frail (49.6% women, 27.8% men). Main correlates of frailty were depressive symptoms, quality of life, and resilience. Gender differences for frailty correlates were found. Depressive symptoms and perceived social support were mainly associated with frailty in women. Furthermore, age was only significantly associated with frailty in women. Quality of life was significantly associated with frailty being a protective factor in both women and men. Trauma count and trauma severity were associated with an elevated risk for frailty in men. Conclusions: The results show that the psychosocial variables depressive symptoms, quality of life, and resilience are associated with frailty. Gender-specific differences in psychosocial correlates of frailty were revealed. Results suggest that gender-specific assessments and interventions should be developed to prevent frailty in late life.

Tall stature in coronary heart disease patients is associated with decreased risk of frailty in late life.

We investigated the possible inverse association between tall stature and subsequent late-life frailty. A subset of surviving men with coronary heart disease (n = 1232; mean age at baseline 57.0 ± 6.0 years), who previously participated in the Bezafibrate Infarction Prevention clinical trial (1990-1997) were reassessed during 2004-2008 (T1; n = 558) and 2011-2013 (T2; n = 351) at the mean ages of 72.6 ± 6.4 years and 77.2 ± 6.4 years, respectively. Frailty status was measured at T2 according to the physical phenotype developed by Fried, and was categorized into non-frail, prefrail and frail. We estimated the odds ratios of increasing frailty by tertiles of height at baseline. Among 351 patients, 117 (33.3%) were classified as non-frail, 134 (38.2%) as prefrail and 100 (28.5%) as frail. Frailty was found among 21% of participants at the highest tertile, 33% at the middle tertile and 46% at the lowest tertile for height (P for trend = 0.002). Adjusting for age, weight, place of birth, education, blood pressure, New York Heart Association classification functional class and comorbidity score, the estimated OR for increasing frailty for participants in the highest tertile was 0.32 (95% CI 0.17-0.59) and for those at the middle tertile 0.46 (95% CI 0.27-0.79), as compared with the lowest tertile. An increment of 1 SD of height was associated with a 38% (95% CI 18-53%) decrease in frailty odds. Among men with coronary heart disease, tall stature was associated with lower adjusted odds of late-life frailty. Geriatr Gerontol Int 2017; 17: 1270-1277.

Operationalizing Frailty in the Atherosclerosis Risk in Communities Study Cohort.

Factors that may contribute to the development of frailty in late life have not been widely investigated. The Atherosclerosis Risk in Communities (ARIC) Study cohort presents an opportunity to examine relationships of midlife risk factors with frailty in late life. However, we first present findings on the validation of an established frailty phenotype in this predominantly biracial population of older adults. Among 6,080 participants, we defined frailty based upon the Cardiovascular Health Study (CHS) criteria incorporating measures of weight loss, exhaustion, slow walking speed, low physical activity, and low grip strength. Criterion and predictive validity of the frailty phenotype were estimated from associations between frailty status and participants' physical and mental health status, physiologic markers, and incident clinical outcomes. A total of 393 (6.5%) participants were classified as frail and 50.4% pre-frail, similar to CHS (6.9% frail, 46.6% pre-frail). In age-adjusted analyses, frailty was concurrently associated with depressive symptoms, low self-rated health, low medication adherence, and clinical biomarker levels (ie, cholesterol, hemoglobin A1c, white blood cell count, C-reactive protein, and hemoglobin). During 1-year follow-up, frailty was associated with falls, low physical ability, fatigue, and mortality. These findings support the validity of the CHS frailty phenotype in the ARIC Study cohort. Future studies in ARIC may elucidate early-life exposures that contribute to late-life frailty.

Depression and Frailty in Late Life: Evidence for a Common Vulnerability

The study purpose is to estimate the correlation between depression and competing models of frailty, and to determine to what degree the comorbidity of these syndromes is determined by shared symptomology. Data come from the 2010 Health and Retirement Study. Analysis was limited to community-dwelling participants 65 and older (N = 3,453). Depressive symptoms were indexed by the 8-item Centers for Epidemiologic Studies Depression (CESD) scale. Frailty was indexed by 3 alternative conceptual models: (a) biological syndrome, (b) frailty index, and (c) functional domains. Confirmatory factor analysis (CFA) was used to estimate the correlation between depression and each model of frailty. Each of the 3 frailty latent factors was significantly correlated with depression: biological syndrome (ρ = .68, p < .01), functional domains (ρ = .70, p < .01), and frailty index (ρ = .61, p < .01). Substantial correlation remained when accounting for shared symptoms between depression and the biological syndrome (ρ = .45) and frailty index (ρ = .56) models. Results indicate that the correlation of frailty and depression in late life is substantial. The association between the two constructs cannot be fully explained by symptom overlap, suggesting that psychological vulnerability may be an important component of frailty.

Depression and Frailty in Late Life: Evidence for a Common Vulnerability

Depression and Frailty in Late Life: Evidence for a Common Vulnerability

Ethical issues in geriatric psychiatry

The high rates of medical illness in older people, the high prevalence of cognitive disorder in the elderly, and the high prevalence of frailty in late life raise issues that occur infrequently in the care of younger adults. This article discusses the ethical issues that commonly arise in the setting of these medical and psychiatric morbidities, and emphasizes the need for clinicians and researchers to be knowledgeable about the belief systems and values of individual patients, of their carers when relevant, of themselves, and of research participants.