Article

Vitamin and carotenoid status in older women: associations with the frailty syndrome.

The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
The Journals of Gerontology Series A Biological Sciences and Medical Sciences (Impact Factor: 4.98). 07/2006; 61(6):600-7. DOI: 10.1093/gerona/61.6.600
Source: PubMed

ABSTRACT We investigated the relationship of micronutrient deficiencies with the frailty syndrome in older women living in the community.
Frailty status and serum micronutrients were assessed in a cross-sectional study of 754 women, 70-80 years old, from the Women's Health and Aging Studies I and II.
Among nonfrail, prefrail, and frail women, respectively, geometric mean serum concentrations were 1.842, 1.593, and 1.376 micromol/L for total carotenoids (p <.001); 2.66, 2.51, and 2.43 micromol/L for retinol (p =.04); 50.9, 47.4, and 43.8 nmol/L for 25-hydroxyvitamin D (p =.019); 43.0, 35.8, and 30.9 nmol/L for vitamin B(6) (p =.002); and 10.2, 9.3, and 8.7 ng/mL for folate (p =.03). Frail women were more likely to have at least two or more micronutrient deficiencies (p =.05). The age-adjusted odds ratios of being frail were significantly higher for those participants whose micronutrient concentrations were in the lowest quartile compared to the top three quartiles for total carotenoids, alpha-tocopherol, 25-hydroxyvitamin D, and vitamin B(6). The association between nutrients and frailty was strongest for beta-carotene, lutein/zeaxanthin, and total carotenoids (odds ratio ranging from 1.82 to 2.45, p =.05), after adjusting for age, sociodemographic status, smoking status, and body mass index.
Frail women are more likely to have relatively low serum carotenoid and micronutrient concentrations and are more likely to have multiple micronutrient deficiencies. Future longitudinal studies are needed to examine the relationships between micronutrient concentrations and frailty in older women.

0 Bookmarks
 · 
62 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sokołowski Remigiusz, Ciesielska Natalia, Czajkowska Agnieszka, Bentryn Dominika, Węgrzyn Edyta, Oleksy Patrick, Zukow Walery. Patogeneza zespołu kruchości = Patogenesis of Frailty Syndrome. Journal of Health Sciences. 2014;4(9):197-204. ISSN 1429-9623 / 2300-665X. Retrieved from http://journal.rsw.edu.pl/index.php/JHS/article/view/2014%3B4%289%29%3A197-204. DOI: 10.13140/2.1.4322.4327 http://dx.doi.org/10.13140/2.1.4322.4327 The journal has had 5 points in Ministry of Science and Higher Education of Poland parametric evaluation. Part B item 1107. (17.12.2013). © The Author (s) 2014; This article is published with open access at Licensee Open Journal Systems of Radom University in Radom, Poland Open Access. This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. This is an open access article licensed under the terms of the Creative Commons Attribution Non Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non commercial use, distribution and reproduction in any medium, provided the work is properly cited. Conflict of interest: None declared. Received: 10.06.2014. Revised 07.08.2014. Accepted: 05.09.2014. Patogeneza zespołu kruchości Patogenesis of Frailty Syndrome Remigiusz Sokołowski1, Natalia Ciesielska1, Agnieszka Czajkowska1, Dominika Bentryn1, Edyta Węgrzyn1, Patrick Oleksy1, Walery Zukow2 1Department and Clinic of Geriatrics, Nicolaus Copernicus University Collegium Medicum, Bydgoszcz, Poland 2 Wydział Kultury Fizycznej, Zdrowia i Turystyki, Uniwersytet Kazimierza Wielkiego w Bydgoszczy, Polska Słowa klucze: zespół kruchości, słabość, patogeneza, stan zapalny, IL-6, starzenie. Key words: frailty syndrom, weakness, patogenesis, inflammation, IL-6, aging. Streszczenie Wstęp. Zespół kruchości (Frailty Syndrome – FS) jest szeroko występującym zespołem geriatrycznym charakteryzującym się fizjologicznym obniżeniem odporności na czynniki stresogenne. W ostatnich latach poczyniono znaczny postęp w rozumieniu patogenezy FS. Prawdopodobnie kluczowym procesem patogenetycznym jest stan przewlekłego zapalenia, które wpływa na układy: mięśniowo- szkieletowy, dokrewny, sercowo-naczyniowy i krwiotwórczy. Cel. Przedstawienie najnowszych doniesień dotyczących patogenezy FS i szersze omówienie najbardziej istotnych mechanizmów patogenetycznych. Materiał i metody. Posługując się słowami kluczowymi: zespół kruchości (frailty syndrom), słabość (weakness), patogeneza (patogenesis), stan zapalny (inflammation), IL-6, starzenie (aging), przeszukano elektroniczne polskie oraz zagraniczne pełnotekstowe bazy bibliograficzne: Polska Bibliografia Lekarska, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct oraz Medline oraz przeanalizowano 40 publikacji nawiązujących do patogenezy FS. Wyniki. Badania wykazały, że podłożem zespołu kruchości jest proces zapalny różnych układów i narządów. U pacjentów z zespołem kruchości odnotowano zwiększony poziom prozapalnych cytokin, takich jak IL- 6, IL- 1 oraz zwiększony poziom leukocytów, głównie limfocytów T oraz monocytów i neutrofili. Zauważono obniżanie się poziomu hormonów steroidowych i IGF-1 prowadzące do sarkopenii oraz osteopenii. Wpływa to w sposób znaczący na objawy FS u starszego pacjenta. Wnioski. Patogeneza zespołu kruchości jest wieloczynnikowa. Jej podłożem jest przewlekle toczący się proces zapalny, który dotykając poszczególnych układów i narządów organizmu, prowadzi do dysfunkcji, takich jak sarkopenia, osteopenia, zaburzenia funkcji poznawczych, anoreksja, zaburzenia endokrynologiczne. Należy zwiększyć skuteczności diagnostyki oraz opracować programy leczenia wczesnych zaburzeń FS. Abstract Introduction. Frailty Syndrome (FS) is a widely common geriatric syndrome characterized by a decrease in resistance to physiological stressors. In recent years there has been considerable progress in understanding the pathogenesis of FS. Probably the key pathogenetic process is a state of chronic inflammation that affects the systems: musculoskeletal, endocrine, cardiovascular and hematopoietic. Purpose. Presentation of the latest reports on the pathogenesis of FS and wider discussion of the most important pathogenetic mechanisms. Material and methods. Using the key words: frailty syndrome, weakness, pathogenesis, inflammation, IL-6, and aging, searched Polish and foreign electronic full-text bibliographic databases: Polish Medical Bibliography, EBSCO host Web, Wiley Online Library, Springer Link, Science Direct and Medline and analyzed 40 publications referring to the pathogenesis of FS. Results. Studies have shown that the basis of FS is inflammation of various systems and organs. In patients with FS reported an increase of proinflammatory cytokines such as IL-6, IL-1, and increased levels of leukocytes, especially T lymphocytes as well as monocytes and neutrophils. It was observed the decrease of the steroid hormone and IGF-1 leads to sarcopenia and osteopenia. This effects in a significant way the symptoms of FS an elderly patient. Conclusions. Pathogenesis of fragility is multifactorial. The basis is a chronic ongoing inflammatory process that effects various systems and organs of the body, leading to dysfunction, such as sarcopenia, osteopenia, cognitive disorders, anorexia, endocrine disorders. Increasing the efficiency of diagnosis and developing treatment programs for early disorders of FS is required.
    Journal of Health Sciences 09/2014; 4(9):197-204.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The need for preventing or postponing the onset of Alzheimer’s disease (AD) and delaying or slowing its progression is a direct consequence of the current symptomatic approach of existing drugs for the treatment of AD. Dietary factors may affect the risk of AD and dementia, with a substantial body of evidence suggesting that certain diets have been associated with a lower incidence of AD and late-life cognitive disorders. Among healthy diets, higher adherence to a Mediterranean-type diet and to the Dietary Approaches to Stop Hypertension diet was associated with decreased cognitive decline, although the Mediterranean diet (MeDi) combines several foods, micro-, and macronutrients already separately proposed as potential protective factors against dementia. Higher adherence to the MeDi was associated with a reduced risk of cognitive impairment, MCI, and AD, as well as the transition from MCI to AD, and decreased all-causes mortality in AD patients. Influencing some age-related conditions, such as frailty, may have an impact on the prevention of late-life cognitive decline. Frailty reflects a nonspecific state of vulnerability and a multisystem physiological change and it is a widely recognized risk factor for adverse health outcomes in older persons. At present, no operational definition has been established, although nutritional status, cognition, and mood have been proposed as markers of frailty. Physical frailty may be associated with late-life cognitive impairment/decline, incidence of AD, vascular dementia, non-AD dementias, and AD pathology in older persons with and without dementia, also suggesting the definition of cognitive frailty as a new clinical condition. The reviewed evidence supports the hypothesis that frailty could be important in the prevention of late-life cognitive disorders, and nutritional influences may be of major relevance. Nutritional interventions might be able to address the impaired nutrition and weight loss of frailty. There is a critical need for randomized, controlled trials investigating the role of nutrition on late-life cognitive disorders and frailty that might open new routes for the prevention and management of cognitive decline and AD, supplementing existing symptomatic approaches, also through the nutritional prevention of frailty.
    Current Nutrition Reports. 06/2014; 3(2).
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Frailty is a common and important geriatric syndrome characterized by age-associated declines in physiologic reserve and function across multiorgan systems, leading to increased vulnerability for adverse health outcomes. Two major frailty models have been described in the literature. The frailty phenotype defines frailty as a distinct clinical syndrome meeting three or more of five phenotypic criteria: weakness, slowness, low level of physical activity, self-reported exhaustion, and unintentional weight loss. The frailty index defines frailty as cumulative deficits identified in a comprehensive geriatric assessment. Significant progress has recently been made in understanding the pathogenesis of frailty. Chronic inflammation is likely a key pathophysiologic process that contributes to the frailty syndrome directly and indirectly through other intermediate physiologic systems, such as the musculoskeletal, endocrine, and hematologic systems. The complex multifactorial etiologies of frailty also include obesity and specific diseases. Major clinical applications include risk assessment and stratification. This can be applied to the elderly population in the community and in a variety of care settings. Frailty may also be useful for risk assessment in surgical patients and those with cardiovascular diseases, cancer, or human immunodeficiency virus infection, as well as for assessment of vaccine effectiveness in older adults. Currently, exercise and comprehensive geriatric interdisciplinary assessment and treatment are key interventions for frailty. As understanding of the biologic basis and complexity of frailty further improves, more effective and targeted interventional strategies and innovative geriatric-care models will likely be developed.
    Clinical Interventions in Aging 01/2014; 9:433-441. · 2.65 Impact Factor