Abstract
This chapter discusses several recent models of frailty and the validation of these models. Despite the ongoing debate on the nature of frailty and whether it is an independent clinical entity or syndrome, some investigators have begun to develop syndromic models to differentiate frail versus nonfrail older adults from further research. Researchers have hypothesized an underlying biology that may be similar to the hypothesized biology that underlies physical or musculoskeletal frailty, including increased levels of inflammatory mediators. Building on existing models of physical frailty, several investigators have tried to identify additional physiologic characteristics of frail, older adults. Using cross-sectional analyses of data generated in large populations of community-dwelling older adults, these investigators have been able to identify frail and intermediate frail subjects, and then compare inflammatory, endocrinologic, hematologic, and metabolic variables hypothesized to underlie declines in multiple other physiologic systems and ultimately frailty. Like the inflammatory system, the endocrine and neuroendocrine systems are composed of several separate, but related organs or tissues that secrete specific hormones and stimulate components of the central and sympathetic nervous system that regulate multiple physiologic processes.
Original language | English (US) |
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Title of host publication | Handbook of Models for Human Aging |
Publisher | Elsevier |
Pages | 697-702 |
Number of pages | 6 |
ISBN (Electronic) | 9780123693914 |
DOIs | |
State | Published - Jan 1 2006 |
ASJC Scopus subject areas
- General Medicine
- General Biochemistry, Genetics and Molecular Biology