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Background: Electronic frailty indices (eFIs) can expand measurement of frailty in research and practice and have demonstrated predictive validity in associations with clinical outcomes. However, their construct validity is less well studied. We aimed to assess the construct validity of the VA-FI, an eFI developed for use in the U.S. Veterans Affairs Healthcare System., Methods: Veterans who underwent comprehensive geriatric assessments between January 31, 2019 and June 6, 2022 at VA Boston and had sufficient data documented for a comprehensive geriatric assessment-frailty index (CGA-FI) were included. The VA-FI, based on diagnostic and procedural codes, and the CGA-FI, based on geriatrician-measured deficits, were calculated for each patient. Geriatricians also assessed the Clinical Frailty Scale (CFS), functional status (ADLs and IADLs), and 4-meter gait speed (4MGS)., Results: A total of 132 veterans were included, with median age 81.4 years (IQR 75.8-88.7). Across increasing levels of VA-FI (<0.2; 0.2-0.4; >0.4), mean CGA-FI increased (0.24; 0.30; 0.40). The VA-FI was moderately correlated with the CGA-FI (r 0.45, p < 0.001). Every 0.1-unit increase in the VA-FI was associated with an increase in the CGA-FI (linear regression beta 0.05; 95% confidence interval [CI] 0.03-0.06), higher CFS category (ordinal regression OR 1.69; 95% CI 1.24-2.30), higher odds of ADL dependency (logistic regression OR 1.59; 95% CI 1.20-2.11), IADL dependency (logistic regression OR 1.68; 95% CI 1.23-2.30), and a decrease in 4MGS (linear regression beta -0.07, 95% CI -0.12 to -0.02). All models were adjusted for age and race, and associations held after further adjustment for the Charlson Comorbidity Index., Conclusion: Our results demonstrate the construct validity of the VA-FI through its associations with clinical measures of frailty, including summary frailty measures, functional status, and objective physical performance. Our findings complement others' in showing that eFIs can capture functional and mobility domains of frailty beyond just comorbidity and may be useful to measure frailty among populations and individuals., (Published 2023. This article is a U.S. Government work and is in the public domain in the USA.)

Mortality due to COVID-19 has been correlated with laboratory markers of inflammation, such as C-reactive protein (CRP). The lower mortality during Omicron variant infections could be explained by variant-specific immune responses or host factors, such as vaccination status. We hypothesized that infections due to Omicron variant cause less inflammation compared to Alpha and Delta, correlating with lower mortality. This was a retrospective cohort study of veterans hospitalized for COVID-19 at the Veterans Health Administration. We compared inflammatory markers among patients hospitalized during Omicron infection with those of Alpha and Delta. We reported the adjusted odds ratio (aOR) of the first laboratory results during hospitalization and in-hospital mortality, stratified by vaccination status. Of 2,075,564 Veterans tested for COVID-19, 29,075 Veterans met the criteria: Alpha (45.1%), Delta (23.9%), Omicron (31.0%). Odds of abnormal CRP in Delta (aOR = 1.85, 95% CI:1.64-2.09) and Alpha (aOR = 1.94, 95% CI:1.75-2.15) were significantly higher compared to Omicron. The same trend was observed for Ferritin, Alanine aminotransferase, Aspartate aminotransferase, Lactate dehydrogenase, and Albumin. The mortality in Delta (aOR = 1.92, 95% CI:1.73-2.12) and Alpha (aOR = 1.68, 95% CI:1.47-1.91) were higher than Omicron. The results remained significant after stratifying the outcomes based on vaccination status. Veterans infected with Omicron showed milder inflammatory responses and lower mortality than other variants.

Age-associated changes in DNA methylation have been implicated as 1 mechanism to explain the development of frailty; however, previous cross-sectional studies of epigenetic age acceleration (eAA) and frailty have had inconsistent findings. Few longitudinal studies have considered the association of eAA with change in frailty. We sought to determine the association between eAA and change in frailty in the MOBILIZE Boston cohort. Participants were assessed at 2 visits 12-18 months apart. Intrinsic, extrinsic, GrimAge, and PhenoAge eAA were assessed from whole-blood DNA methylation at baseline using the Infinium 450k array. Frailty was assessed by a continuous frailty score based on the frailty phenotype and by frailty index (FI). Analysis was by correlation and linear regression with adjustment for age, sex, smoking status, and body mass index. Three hundred and ninety-five participants with a frailty score and 431 with an FI had epigenetic and follow-up frailty measures. Mean (standard deviation) ages were 77.8 (5.49) and 77.9 (5.47) for the frailty score and the FI cohorts respectively, and 232 (58.7%) and 257 (59.6%) were female. All participants with epigenetic data identified as White. Baseline frailty score was not correlated with intrinsic or extrinsic eAA, but was correlated with PhenoAge and, even after adjustment for covariates, GrimAge. Baseline FI was correlated with extrinsic, GrimAge, and PhenoAge eAA with and without adjustment. No eAA measure was associated with change in frailty, with or without adjustment. Our results suggest that no eAA measure was associated with change in frailty. Further studies should consider longer periods of follow-up and repeated eAA measurement., (Published by Oxford University Press on behalf of The Gerontological Society of America 2022.)

Background: The World Health Organization's Global Burden of Disease (GBD) reports are an important tool for global health policy makers, however the accuracy of estimates for countries undergoing an epidemiologic transition is unclear. We attempted to validate the life table model used to generate estimates for all-cause mortality in developing countries., Methods and Results: Data were obtained for males and females from the Human Mortality Database for all countries with available data every ten years from 1900 to 2000. These provided inputs for the GBD life table model and served as comparison observed data. Above age sixty model estimates of survival for both sexes differed substantially from those observed. Prior to the year 1960 for males and 1930 for females, estimated survival tended to be greater than observed; following 1960 for both males and females estimated survival tended to be less than observed. Viewing observed and estimated survival separately, observed survival past sixty increased over the years considered. For males, the increase was from a mean (sd) probability of 0.22 (0.06) to 0.46 (0.1). For females, the increase was from 0.26 (0.06) to 0.65 (0.08). By contrast, estimated survival past sixty decreased over the same period. Among males, estimated survival probability declined from 0.54 (0.2) to 0.09 (0.06). Among females, the decline was from 0.36 (0.12) to 0.15 (0.08)., Conclusions: These results show that the GBD mortality model did not accurately estimate survival at older ages as developed countries transitioned in the twentieth century and may be similarly flawed in developing countries now undergoing transition. Estimates of the size of older-age populations and their attributable disease burden should be reconsidered.