Is Old Age or Aging a Disease, in a Literal or a Metaphorical Sense?
In: Public policy & aging report, Band 29, Heft 4, S. 123-125
ISSN: 2053-4892
6 Ergebnisse
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In: Public policy & aging report, Band 29, Heft 4, S. 123-125
ISSN: 2053-4892
In: American journal of health promotion, Band 19, Heft 5, S. 376-382
ISSN: 2168-6602
Purpose.This study describes the prevalence and characteristics of physician health promotion referrals and patient adherence to referrals in a community-based primary care clinic and associated wellness facility. The role of reimbursement for attendance to the wellness facility was specifically examined.Design.Retrospective cohort study.Setting.The Church Health Center of Memphis, Tennessee: a low-income urban clinic and its affiliated wellness center.Subjects.Patients were primarily African-American, lower-income, urban residents of Shelby County, Tennessee.Measures.All study data came from existing medical clinic and wellness facility records of utilization, patient history, and diagnoses.Results.Of 6321 clinic patients, 16.7% (n = 1069) received a provider health promotion referral. Logistic regression analyses identified that physician referral was related to patient factors of access to free wellness-facility membership, employment status, receiving a behavior-related diagnosis, and being African-American and female. Of patients receiving a referral, 17.2% (n = 184) adhered to this advice and visited the wellness facility. New patients were more likely to adhere to a referral than established patients.Conclusion.Demographic, financial, and patient characteristics influenced whether health behavior change referrals were made by primary care physicians in a community clinic. Removing financial barriers did not influence patient adherence, but new patients were more likely to follow the recommendation than those previously seen at the clinic.
In: The journals of gerontology. Series A, Biological sciences, medical sciences, Band 74, Heft 8, S. 1303-1309
ISSN: 1758-535X
Abstract
Background
Observational research has identified several mortality biomarkers; however, their responsiveness to change is unknown. We tested whether the Healthy Aging Index (HAI) and other mortality biomarkers were responsive to intentional weight loss (WL), which is associated with lower mortality risk in recent meta-analyses.
Methods
Older adults (70.3 ± 3.7 years) with obesity were randomized into a 6-month WL (n = 47) or weight stability (WS: ±5% baseline weight; n = 48) program. Baseline and 6-month HAI score (0–10) was calculated from component sum (each 0–2: systolic blood pressure, forced vital capacity [FVC], creatinine, fasting blood glucose [FBG], Montreal Cognitive Assessment), and gait speed, grip strength, Digit Symbol Substitution Test, FEV1, Interleukin-6, C-Reactive Protein, and Cystatin-C were assessed at baseline and 6 months.
Results
Mean baseline HAI was 3.2 ± 1.6. By 6 months, WL participants lost 8.87 (95% CI: −10.40, −7.34) kg, whereas WS participants remained weight stable. WL group reduced HAI score (WL: −0.75 [95% CI: −1.11, −0.39] vs WS: −0.22 [95% CI: −0.60, 0.15]; p = .04), and components changing the most were FBG (WL: −3.89 [95% CI: −7.78, 0.00] mg/dL vs WS: 1.45 [95% CI: −2.61, 5.50] mg/dL; p = .047) and FVC (WL: 0.11 [95% CI: −0.01, 0.23] L vs WS: −0.05 [95% CI: −0.17, 0.08] L; p = .06). Among other biomarkers, only Cystatin-C significantly changed (WL: −2.53 [95% CI: −4.38, −0.68] ng/mL vs WS: 0.07 [95% CI: −1.85, 1.98] ng/mL; p = .04). Combining treatment groups, 1 kg WL was associated with a 0.07 (95% CI: 0.03, 0.12) HAI reduction (p < .01).
Conclusion
Intentional WL via caloric restriction reduced HAI score by 0.53 points, largely attributable to metabolic and pulmonary improvements.
Publisher's version (útgefin grein) ; Importance: Dual decline in both memory and gait speed may characterize a group of older individuals at high risk for future dementia. Objective: To assess the risk of dementia in older persons who experience parallel declines in memory and gait speed compared with those who experience no decline or decline in either memory or gait speed only. Design, Setting, and Participants: A multicohort meta-analysis was performed of 6 prospective cohort studies conducted between 1997 and 2018 in the United States and Europe. Participants were 60 years or older, had an initial gait speed of more than 0.6 m/s (ie, free of overt dismobility), with repeated measures of memory and gait speed before dementia diagnosis during a mean follow-up of 6.6 to 14.5 years. Within each study, participants were divided into 4 groups: memory decline only, gait speed decline only, dual decline, or no decline (hereafter referred to as usual agers). Gait decline was defined as a loss of 0.05 m/s or more per year; memory decline was defined as being in the cohort-specific lowest tertile of annualized change. Main Outcomes and Measures: Risk of incident dementia according to group membership was examined by Cox proportional hazards regression with usual agers as the reference, adjusted for baseline age, sex, race/ethnicity, educational level, study site, and baseline gait speed and memory. Results: Across the 6 studies of 8699 participants, mean age ranged between 70 and 74 years and mean gait speed ranged between 1.05 and 1.26 m/s. Incident dementia ranged from 5 to 21 per 1000 person-years. Compared with usual agers, participants with only memory decline had 2.2 to 4.6 times higher risk for developing dementia (pooled hazard ratio, 3.45 [95% CI, 2.45-4.86]). Those with only gait decline had 2.1 to 3.6 times higher risk (pooled hazard ratio, 2.24 [95% CI, 1.62-3.09]). Those with dual decline had 5.2 to 11.7 times the risk (pooled hazard ratio, 6.28 [95% CI, 4.56-8.64]). Conclusions and Relevance: In this study, dual decline of memory and gait speed was associated with increased risk of developing dementia among older individuals, which might be a potentially valuable group for preventive or therapeutic interventions. Why dual decline is associated with an elevated risk of dementia and whether these individuals progress to dementia through specific mechanisms should be investigated by future studies. ; This research work was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging (Drs Tian, Resnick, Launer, Simonsick, Studenski, and Ferrucci). The BLSA was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging. The AGES-Reykjavik Study was funded by contract N01-AG-12100 from the National Institutes of Health; by the Intramural Research Program of the National Institute on Aging; and by the Icelandic Heart Association and the Icelandic Parliament. The Health ABC study was supported by National Institute on Aging contracts N01-AG-6-2101, N01-AG-6-2103, and N01-AG-6-2106; National Institute on Aging grant R01-AG028050; and National Institute of Nursing Research grant R01-NR012459, and was funded in part by the Intramural Research Program of the National Institutes of Health, National Institute on Aging. The MCSA was supported by funding from the National Institutes of Health, National Institute on Aging (U01 AG006786), the Gerald and Henrietta Rauenhorst Foundation, and the Mayo Foundation for Medical Education and Research; and was made possible by the Rochester Epidemiology Project (R01 AG034676). The SNAC-K was supported by the funders of the Swedish National Study on Aging and Care; the Ministry of Health and Social Affairs, Sweden; the participating County Councils and Municipalities; and the Swedish Research Council. The InCHIANTI study was supported by National Institute on Aging contracts 263MD9164 (Dr Ferrucci) and 263 MD 821336, N01-AG-1-1, N01-AG-10211, and N01-AG-5-0002 (Dr Bandinelli), and partially supported by grant n PE 2011 02350413 of the Italian Ministry of Health (Dr Cherubini). ; Peer Reviewed
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CONTEXT: Vitamin D inadequacy is common in the adult population of the United States. Although the genetic determinants underlying vitamin D inadequacy have been studied in people of European ancestry, less is known about populations with Hispanic or African ancestry. OBJECTIVE: The Trans-Ethnic Evaluation of Vitamin D (TRANSCEN-D) genomewide association study (GWAS) consortium was assembled to replicate genetic associations with 25-hydroxyvitamin D [25(OH)D] concentrations from the Study of Underlying Genetic Determinants of Vitamin D and Highly Related Traits (SUNLIGHT) meta-analyses of European ancestry and to identify genetic variants related to vitamin D concentrations in African and Hispanic ancestries. DESIGN: Ancestry-specific (Hispanic and African) and transethnic (Hispanic, African, and European) meta-analyses were performed with Meta-Analysis Helper software (METAL). PATIENTS OR OTHER PARTICIPANTS: In total, 8541 African American and 3485 Hispanic American (from North America) participants from 12 cohorts and 16,124 European participants from SUNLIGHT were included in the study. MAIN OUTCOME MEASURES: Blood concentrations of 25(OH)D were measured for all participants. RESULTS: Ancestry-specific analyses in African and Hispanic Americans replicated single nucleotide polymorphisms (SNPs) in GC (2 and 4 SNPs, respectively). An SNP (rs79666294) near the KIF4B gene was identified in the African American cohort. Transethnic evaluation replicated GC and DHCR7 region SNPs. Additionally, the transethnic analyses revealed SNPs rs719700 and rs1410656 near the ANO6/ARID2 and HTR2A genes, respectively. CONCLUSIONS: Ancestry-specific and transethnic GWASs of 25(OH)D confirmed findings in GC and DHCR7 for African and Hispanic American samples and revealed findings near KIF4B, ANO6/ARID2, and HTR2A. The biological mechanisms that link these regions with 25(OH)D metabolism warrant further investigation.
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Publisher's version (útgefin grein). ; Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in ≈131K individuals across several ancestry groups yielded 3, 514 SNVs (245 loci) with suggestive evidence of association (P < 1.0 × 10-5). In Stage 2, these SNVs were tested for independent external replication in ≈440K individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2, 159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 × 10-8). For African ancestry samples, we detected 18 potentially novel BP loci (P < 5.0 × 10-8) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2) have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension. ; The following authors declare commercial private and/or governmental affiliations: Bruce M. Psaty (BMP) serves on the DSMB of a clinical trial funded by Zoll Lifecor and on the Steering Committee of the Yale Open Data Access Project funded by Johnson & Johnson. Barbara V. Howard (BVH) has a contract from National Heart, Lung, and Blood Institute (NHLBI). Brenda W.J.H. Penninx (BWJHP) has received research funding (non-related to the work reported here) from Jansen Research and Boehringer Ingelheim. Mike A. Nalls (MAN) is supported by a consulting contract between Data Tecnica International LLC and the National Institute on Aging (NIA), National Institutes of Health (NIH), Bethesda, MD, USA. MAN also consults for Illumina Inc., the Michael J. Fox Foundation, and the University of California Healthcare. MAN also has commercial affiliation with Data Tecnica International, Glen Echo, MD, USA. Mark J. Caulfield (MJC) has commercial affiliation and is Chief Scientist for Genomics England, a UK government company. Oscar H Franco (OHF) is supported by grants from Metagenics (on women's health and epigenetics) and from Nestlé (on child health). Peter S. Sever (PSS) is financial supported from several pharmaceutical companies which manufacture either blood pressure lowering or lipid lowering agents, or both, and consultancy fees. Paul W. Franks (PWF) has been a paid consultant in the design of a personalized nutrition trial (PREDICT) as part of a private-public partnership at Kings College London, UK, and has received research support from several pharmaceutical companies as part of European Union Innovative Medicines Initiative (IMI) projects. Fimlab LTD provided support in the form of salaries for author Terho Lehtimäki (TL) but did not have any additional role in the study design to publish, or preparation of the manuscript. Gen‐info Ltd provided support in the form of salaries for author Ozren Polašek (OP) but did not have any additional role in the study design to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the 'author contributions' section. There are no patents, products in development, or marked products to declare. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. ; Peer Reviewed
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