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Accepted manuscript

Exploring the Association between Sarcopenic Obesity and Cardiovascular Risk: A Summary of Findings from Longitudinal Studies and Potential Mechanisms

Published online by Cambridge University Press:  18 November 2024

Zhongyang Guan
Affiliation:
Dementia Centre of Excellence, enAble Institute, Faculty of Health Sciences, Curtin University, Bentley, WA, Australia Curtin School of Population Health, Faculty of Health Science, Curtin University, Bentley, WA, Australia
Blossom CM Stephan
Affiliation:
Dementia Centre of Excellence, enAble Institute, Faculty of Health Sciences, Curtin University, Bentley, WA, Australia
Lorenzo Maria Donini
Affiliation:
Department of Experimental Medicine, Sapienza University, Rome, Italy
Carla M. Prado
Affiliation:
Department of Agricultural, Food & Nutritional Science, University of Alberta, Edmonton, AB, Canada
Marc Sim
Affiliation:
Nutrition and Health Innovation Research Institute, School of Health and Medical Science, Edith Cowan University, Perth, WA, Australia Medical School, The University of Western Australia, Perth, WA, Australia
Mario Siervo*
Affiliation:
Dementia Centre of Excellence, enAble Institute, Faculty of Health Sciences, Curtin University, Bentley, WA, Australia Curtin School of Population Health, Faculty of Health Science, Curtin University, Bentley, WA, Australia Vascular and Metabolic Disorder Group, Curtin Health Innovation Research Institute (CHIRI), Curtin University, Bentley, WA, Australia
*
Corresponding Author: Prof. Mario Siervo, Curtin University, Email: [email protected]
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Abstract

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It is estimated that more than one-tenth of adults aged ≥60 years are now classified as having sarcopenic obesity (SO), a clinical condition characterized by the concurrent presence of sarcopenia (low muscle mass and weakness) and obesity (excessive fat mass). Independently, sarcopenia and obesity are associated with a high risk of numerous adverse health outcomes including cardiovascular diseases (CVDs) and neurological conditions (e.g. dementia), but SO may confer a greater risk, exceeding either condition alone. This imposes a substantial burden on individuals, healthcare systems and society. In recent years, an increasing number of observational studies have explored the association between SO and the risk of CVDs; however, results are mixed. Moreover, the pathophysiology of SO is governed by a complex interplay of multiple mechanisms including insulin resistance, inflammation, oxidative stress, hormonal shifts and alteration of energy balance, which may also play a role in the occurrence of various CVDs. Yet, the exact mechanisms underlying the pathological connection between these two complex conditions remain largely unexplored. The aim of this review is to examine the association between SO and CVDs. Specifically, we seek to: (1) discuss the definition, epidemiology and diagnosis of SO; (2) reconcile previously inconsistent findings by synthesizing evidence from longitudinal studies on the epidemiological link between SO and CVDs; and (3) discuss critical mechanisms that may elucidate the complex and potentially bidirectional relationships between SO and CVDs.

Type
Review Article
Copyright
© The Authors 2024. Published by Cambridge University Press on behalf of The Nutrition Society