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Obesity and biological aging across the life course: A geroscience framework for metabolic health.

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Title: Obesity and biological aging across the life course: A geroscience framework for metabolic health.
Authors: Correa-Burrows P; Human Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Geroscience Center for Brain Health and Metabolism (GERO), Santiago, Chile., Burrows R; Public Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Childhood and Adolescent Obesity Clinic, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile., Kennedy BK; Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Departments of Biochemistry and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore., Gonzalez-Billault C; Public Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Department of Biology, Faculty of Sciences, Universidad de Chile, Chile; Department of Neuroscience, Faculty of Medicine, Universidad de Chile, Chile; The Buck Institute for Research on Aging, USA; Geroscience Center for Brain Health and Metabolism (GERO), Santiago, Chile. Electronic address: chrgonza@uchile.cl.
Source: Metabolism: clinical and experimental [Metabolism] 2026 Aug; Vol. 181, pp. 156634. Date of Electronic Publication: 2026 May 16.
Publication Type: Journal Article; Review; Research Support, Non-U.S. Gov't
Language: English
Journal Info: Publisher: Elsevier Inc Country of Publication: United States NLM ID: 0375267 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1532-8600 (Electronic) Linking ISSN: 00260495 NLM ISO Abbreviation: Metabolism Subsets: MEDLINE
Imprint Name(s): Publication: New York, NY : Elsevier Inc.
Original Publication: New York, Grune & Stratton.
MeSH Terms: Obesity*/metabolism , Obesity*/physiopathology , Aging*/metabolism , Aging*/physiology , Geroscience*, Humans ; Animals
Abstract: In this narrative translational review, we propose that obesity and aging are not merely parallel epidemics, but biologically convergent processes with shared metabolic and molecular substrates. We introduce the Obesity-Accelerated Aging (ObAGE) framework, arguing that excess adiposity functions as a clinically relevant accelerator of biological aging trajectories. Because much of the supporting human evidence is observational, we use acceleration to indicate earlier appearance or increases in aging-related biological signatures and clinical phenotypes, while recognizing that causal strength varies across aging pathways and study designs. By prematurely engaging core aging hallmarks, including dysregulated nutrient sensing, chronic low-grade inflammation, cellular senescence, and epigenetic drift, obesity may intensify aging-related decline without replacing the underlying aging process, progressively eroding physiological resilience before overt cardiometabolic disease becomes clinically manifest. This convergence helps explain why obesity does not simply increase risk for isolated non-communicable diseases but is associated with earlier multimorbidity and functional impairment. Importantly, this biological embedding begins during sensitive life-course windows. Yet, converging evidence from human studies (from lifestyle interventions to incretin-based pharmacotherapy) suggests that several aging-related signatures remain at least partially modifiable through metabolic optimization. Framing obesity within a geroscience paradigm positions metabolic treatment not only as disease management but also as a strategy to preserve physiological capacity and delay aging-related decline.
(Copyright © 2026 Elsevier Inc. All rights reserved.)
Competing Interests: Declaration of competing interest The authors declare no competing interests.
Contributed Indexing: Keywords: Biological aging; Cellular senescence; Epigenetic clocks; Geroscience; Healthspan; Life-course epidemiology; Multimorbidity; Obesity
Entry Date(s): Date Created: 20260517 Date Completed: 20260612 Latest Revision: 20260810
Update Code: 20260810
DOI: 10.1016/j.metabol.2026.156634
PMID: 42144183
Database: MEDLINE
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  Data: Obesity and biological aging across the life course: A geroscience framework for metabolic health.
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  Data: <searchLink fieldCode="AU" term="%22Correa-Burrows+P%22">Correa-Burrows P</searchLink>; Human Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Geroscience Center for Brain Health and Metabolism (GERO), Santiago, Chile.<br /><searchLink fieldCode="AU" term="%22Burrows+R%22">Burrows R</searchLink>; Public Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Childhood and Adolescent Obesity Clinic, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile.<br /><searchLink fieldCode="AU" term="%22Kennedy+BK%22">Kennedy BK</searchLink>; Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; Departments of Biochemistry and Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.<br /><searchLink fieldCode="AU" term="%22Gonzalez-Billault+C%22">Gonzalez-Billault C</searchLink>; Public Nutrition Unit, Institute of Nutrition and Food Technologies (INTA), Universidad de Chile, Chile; Department of Biology, Faculty of Sciences, Universidad de Chile, Chile; Department of Neuroscience, Faculty of Medicine, Universidad de Chile, Chile; The Buck Institute for Research on Aging, USA; Geroscience Center for Brain Health and Metabolism (GERO), Santiago, Chile. Electronic address: chrgonza@uchile.cl.
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  Data: In this narrative translational review, we propose that obesity and aging are not merely parallel epidemics, but biologically convergent processes with shared metabolic and molecular substrates. We introduce the Obesity-Accelerated Aging (ObAGE) framework, arguing that excess adiposity functions as a clinically relevant accelerator of biological aging trajectories. Because much of the supporting human evidence is observational, we use acceleration to indicate earlier appearance or increases in aging-related biological signatures and clinical phenotypes, while recognizing that causal strength varies across aging pathways and study designs. By prematurely engaging core aging hallmarks, including dysregulated nutrient sensing, chronic low-grade inflammation, cellular senescence, and epigenetic drift, obesity may intensify aging-related decline without replacing the underlying aging process, progressively eroding physiological resilience before overt cardiometabolic disease becomes clinically manifest. This convergence helps explain why obesity does not simply increase risk for isolated non-communicable diseases but is associated with earlier multimorbidity and functional impairment. Importantly, this biological embedding begins during sensitive life-course windows. Yet, converging evidence from human studies (from lifestyle interventions to incretin-based pharmacotherapy) suggests that several aging-related signatures remain at least partially modifiable through metabolic optimization. Framing obesity within a geroscience paradigm positions metabolic treatment not only as disease management but also as a strategy to preserve physiological capacity and delay aging-related decline.<br /> (Copyright © 2026 Elsevier Inc. All rights reserved.)
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  Data: Declaration of competing interest The authors declare no competing interests.
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        Text: English
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      – SubjectFull: Obesity metabolism
        Type: general
      – SubjectFull: Obesity physiopathology
        Type: general
      – SubjectFull: Aging metabolism
        Type: general
      – SubjectFull: Aging physiology
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      – SubjectFull: Geroscience
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      – TitleFull: Obesity and biological aging across the life course: A geroscience framework for metabolic health.
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              Text: 2026 Aug
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