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Träfflista för sökning "WFRF:(Olsson Tommy) ;pers:(Cederholm Tommy)"

Sökning: WFRF:(Olsson Tommy) > Cederholm Tommy

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1.
  • Byberg, Liisa, et al. (författare)
  • Reply to WB Grant
  • 2017
  • Ingår i: The American journal of clinical nutrition. - : Elsevier BV. - 1938-3207 .- 0002-9165. ; 106:2, s. 700-701
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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2.
  • Byberg, Liisa, et al. (författare)
  • Reply to Y Mao and H Yu.
  • 2017
  • Ingår i: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 106:2, s. 698-699
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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3.
  • Karlsson, Mikael, et al. (författare)
  • Ability to predict resting energy expenditure with six equations compared to indirect calorimetry in octogenarian men
  • 2017
  • Ingår i: Experimental Gerontology. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0531-5565 .- 1873-6815. ; 92, s. 52-55
  • Tidskriftsartikel (refereegranskat)abstract
    • The accuracy of predictive equations for calculating resting energy expenditure (REE) in elderly people has been questioned. Aging is associated with progressive declines in REE, which partly is explained by loss of fat free mass (FFM). Against this background we aimed to identify the most accurate predictive equation for REE in octogenarian men, taking body composition into account and using indirect calorimetry as reference value. REE was measured in 22 men (mean age 82.6 +/- 0.3 years) and compared with six predictive equations: two based on FFM and four based on body weight, height and/or age. FFM was derived from Dual-energy X-ray absorptiometry analyses. Spearman's rank correlations showed a moderate to high positive monotonic correlation (r = 0.62 to 0.79) between measured and calculated REE (all p < 0.005).The mean calculated REE was significantly different from measured REE for all equations except Mifflin-St Jeor. A calculated REE within 10% of measured REE was considered acceptable and the equations of Mifflin-St Jeor, WHO and Harris-Benedict captured 64%, 50% and 45% of the participant, respectively. The Mifflin-St Jeor equation had the lowest root mean square error (138 kcal), followed by the equation by Harris-Benedict (189 kcal) and WHO (220 kcal). The equations from Luhrmann, Henry and Cunningham predicted REE rather poorly in our study subjects, with e.g. <40% of the individuals within 10% of measured REE. Our results indicate that the Mifflin-St Jeor equation (using FFM) is the most accurate equation estimating REE in these octogenarian men. Harris-Benedict or WHO equations are potential alternatives if information on FFM is unavailable, although their accuracy on an individual level is limited.
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4.
  • Mak, Jonathan K. L., et al. (författare)
  • Development of an Electronic Frailty Index for Hospitalized Older Adults in Sweden
  • 2022
  • Ingår i: The journals of gerontology. Series A, Biological sciences and medical sciences. - : Oxford University Press. - 1079-5006 .- 1758-535X. ; 77:11, s. 2311-2319
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Frailty assessment in the Swedish health system relies on the Clinical Frailty Scale (CFS), but it requires training, in-person evaluation, and is often missing in medical records. We aimed to develop an electronic frailty index (eFI) from routinely collected electronic health records (EHRs) and assess its association with adverse outcomes in hospitalized older adults. Methods EHRs were extracted for 18 225 patients with unplanned admissions between 1 March 2020 and 17 June 2021 from 9 geriatric clinics in Stockholm, Sweden. A 48-item eFI was constructed using diagnostic codes, functioning and other health indicators, and laboratory data. The CFS, Hospital Frailty Risk Score, and Charlson Comorbidity Index were used for comparative assessment of the eFI. We modeled in-hospital mortality and 30-day readmission using logistic regression; 30-day and 6-month mortality using Cox regression; and length of stay using linear regression. Results Thirteen thousand one hundred and eighty-eight patients were included in analyses (mean age 83.1 years). A 0.03 increment in the eFI was associated with higher risks of in-hospital (odds ratio: 1.65; 95% confidence interval: 1.54-1.78), 30-day (hazard ratio [HR]: 1.43; 1.38-1.48), and 6-month mortality (HR: 1.34; 1.31-1.37) adjusted for age and sex. Of the frailty and comorbidity measures, the eFI had the highest area under receiver operating characteristic curve for in-hospital mortality of 0.813. Higher eFI was associated with longer length of stay, but had a rather poor discrimination for 30-day readmission. Conclusions An EHR-based eFI has robust associations with adverse outcomes, suggesting that it can be used in risk stratification in hospitalized older adults.
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5.
  • Mak, Jonathan K. L., et al. (författare)
  • Two Years with COVID-19 : The Electronic Frailty Index Identifies High-Risk Patients in the Stockholm GeroCovid Study
  • 2023
  • Ingår i: Gerontology. - : S. Karger. - 0304-324X .- 1423-0003. ; 69:4, s. 396-405
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Frailty, a measure of biological aging, has been linked to worse COVID-19 outcomes. However, as the mortality differs across the COVID-19 waves, it is less clear whether a medical record-based electronic frailty index (eFI) that we have previously developed for older adults could be used for risk stratification in hospitalized COVID-19 patients. Objectives: The aim of the study was to examine the association of frailty with mortality, readmission, and length of stay in older COVID-19 patients and to compare the predictive accuracy of the eFI to other frailty and comorbidity measures. Methods: This was a retrospective cohort study using electronic health records (EHRs) from nine geriatric clinics in Stockholm, Sweden, comprising 3,980 COVID-19 patients (mean age 81.6 years) admitted between March 2020 and March 2022. Frailty was assessed using a 48-item eFI developed for Swedish geriatric patients, the Clinical Frailty Scale, and the Hospital Frailty Risk Score. Comorbidity was measured using the Charlson Comorbidity Index. We analyzed in-hospital mortality and 30-day readmission using logistic regression, 30-day and 6-month mortality using Cox regression, and the length of stay using linear regression. Predictive accuracy of the logistic regression and Cox models was evaluated by area under the receiver operating characteristic curve (AUC) and Harrell's C-statistic, respectively. Results: Across the study period, the in-hospital mortality rate decreased from 13.9% in the first wave to 3.6% in the latest (Omicron) wave. Controlling for age and sex, a 10% increment in the eFI was significantly associated with higher risks of in-hospital mortality (odds ratio = 2.95; 95% confidence interval = 2.42-3.62), 30-day mortality (hazard ratio [HR] = 2.39; 2.08-2.74), 6-month mortality (HR = 2.29; 2.04-2.56), and a longer length of stay (beta-coefficient = 2.00; 1.65-2.34) but not with 30-day readmission. The association between the eFI and in-hospital mortality remained robust across the waves, even after the vaccination rollout. Among all measures, the eFI had the best discrimination for in-hospital (AUC = 0.780), 30-day (Harrell's C = 0.733), and 6-month mortality (Harrell's C = 0.719). Conclusion: An eFI based on routinely collected EHRs can be applied in identifying high-risk older COVID-19 patients during the continuing pandemic.
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6.
  • Olsson, Erika, et al. (författare)
  • Dietary Patterns and Cognitive Dysfunction in a 12-Year Follow-up Study of 70 Year Old Men
  • 2015
  • Ingår i: Journal of Alzheimer's Disease. - 1387-2877 .- 1875-8908. ; 43:1, s. 109-119
  • Tidskriftsartikel (refereegranskat)abstract
    • Background:Adherence to dietary patterns has been associated with cognitive decline and dementia, but studies are inconsistent.Objective:Dietary patterns, i.e., WHO recommendations (Healthy Diet Indicator), a Mediterranean-like diet (modified Mediterranean Diet Score, mMDS), and a low carbohydrate high protein diet (LCHP), were related to incident cognitive dysfunction, as indicated by Alzheimer's disease (AD), all-type dementia, and all-type cognitive impairment, in a cohort of 1,138 elderly Swedish men.Methods:Dietary patterns were derived from 7-day records. Risk relations were calculated by Cox and logistic regression analyses, adjusted for potential confounders. Sensitivity analysis was performed in a subpopulation (n = 564) with energy intake according to the Goldberg cut-off. Results:During a mean follow-up of 12 years, 84, 143, and 198 men developed AD, all-type dementia, and all-type cognitive impairment, respectively. There was no association between Healthy Diet Indicator and any of the outcomes. Hazard ratios associated with 1 standard deviation (SD) increment in the LCHP score were 1.16 (95% confidence interval [CI]: 0.95, 1.43) for AD and 1.16 (95% CI: 0.99, 1.37) for all-type dementia. mMDS was not associated with dementia diagnosis. Odds ratio (OR)/1 SD increase for mMDS and all-type cognitive impairment was 0.82 (95% CI: 0.65, 1.05). In the subpopulation OR for mMDS and all-type cognitive impairment was 0.32 (95% CI: 0.11, 0.89).Conclusion:We found no strong associations with development of cognitive dysfunction for any of the dietary patterns investigated. However, there was a potentially beneficial association for a Mediterranean-like diet on the development of cognitive dysfunction in the subpopulation.
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9.
  • Olsson, Erika, et al. (författare)
  • Kostmönster och risk för utveckling av demenssjukdom : en 12 års uppföljning av 70 åriga män
  • 2011
  • Ingår i: Svenska läkaresällskapets riksstämma.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Samband mellan kost och demenssjukdom är inte tydligt fastställda. Studiens syfte var att prospektivt undersöka hur tre olika kostmönster relaterar till utvecklingen av demenssjukdom, inkl. Alzheimers sjukdom (AD), eller alla typer av kognitiv störning hos äldre friska män.
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10.
  • Olsson, Erika, et al. (författare)
  • Vitamin D is not associated with incident dementia or cognitive impairment : an 18-y follow-up study in community-living old men
  • 2017
  • Ingår i: American Journal of Clinical Nutrition. - : AMER SOC NUTRITION-ASN. - 0002-9165 .- 1938-3207. ; 105:4, s. 936-943
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Vitamin D has been implicated as being important for maintaining cognitive function in old age. Results from longitudinal studies examining the association of vitamin D with incident dementia and cognitive impairment have been inconsistent. Objective: We investigated the relation between vitamin D, assessed in 3 different ways, and the risk of dementia. Design: We measured plasma 25-hydroxyvitamin D [25(OH) D] with the use of high-performance liquid chromatography-mass spectrometry, assessed dietary vitamin D intake with the use of 7-d dietary records, and created a vitamin D-synthesis genetic risk score (GRS) at baseline (1991-1995) in a cohort of 1182 Swedish men (mean age: 71 y). In a maximum of 18 y (median: 12 y) of follow-up, 116 men developed Alzheimer disease, 64 men developed vascular dementia, and 250 men developed all-cause dementia. An additional 80 men declined in cognitive function as assessed with the use of the Mini-Mental State Examination. Adjusted HRs and ORs were calculated with the use of Cox and logistic regressions. Results: The mean +/- SD plasma 25(OH) D concentration was 68.7 +/- 19.1 nmol/L. Plasma 25(OH) D, dietary vitamin D intake, and vitamin D-synthesis GRS were not associated with any cognitive outcomes (crude and adjusted HRs and ORs were similar to 1.0 for all continuous exposures). The adjusted HR for all-cause dementia was 0.88 (95% CI: 0.59, 1.31) in men with plasma 25(OH) D concentrations <= 50 compared with >75 nmol/L. The adjusted HR for all-cause dementia was 0.92 (95% CI: 0.63, 1.32) for the lowest compared with highest tertiles of vitamin D intake. The adjusted HR for the continuous GRS for all-cause dementia was 1.04 (95% CI: 0.91, 1.19). Conclusion: In this cohort study, we show that there is no association between baseline vitamin D status and long-term risk of dementia or cognitive impairment over an 18-y period of time.
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