ArticlePsychoneuroendocrinology2023
Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging.
Article in Psychoneuroendocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Allostatic load in female cancer patients: a systematic review.Frontiers in endocrinology · 2026Pooled it
- Monocyte abundance and glycolytic reprogramming associate with motivational impairment in depression.Brain, behavior, and immunity · 2026Article
- Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026Review
- Ultrastructural disturbances of pericapillary microglia, perioligodendrocyte microglia, oligodendrocytes and their interactions in postmortem caudate nucleus in schizophrenia.European archives of psychiatry and clinical neuroscience · 2026Article
- The Energetic Cost of Adrenergic Signaling in Primary Human Fibroblasts.bioRxiv : the preprint server for biology · 2026Article
- Metabolism-weighted brain connectome reveals synaptic integration and vulnerability to neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Evaluating oxidative stress marker FBMC pediatrics · 2026Article
- Epigenome-wide association study of leukocyte telomere length and their effects on smoking-induced lung tumorigenesis: insights from the Dongfeng-Tongji cohort study.Clinical epigenetics · 2026Article
- Spatially convergent functional MRI signatures of diabetes and male sex identify genetic vulnerabilities to accelerated brain ageing.Brain communications · 2026Article
- Computational whole-body-exposome models for global precision brain health.Nature communications · 2025Article
- Integrative DNA methylation and transcriptome analysis reveal cell-type specific patterns in response to elevated allostatic load.Epigenetics · 2025Article
- Mitochondrial respiratory activity and DNA damage in peripheral blood mononuclear cells in borderline personality disorder.Psychological medicine · 2025Article
- Combined association between phenotypic age acceleration and dietary fiber intake with mortality in middle-aged and elderly cancer survivors.Nutrition journal · 2025Article
- Biopsychosocial correlates of resting and stress-reactive salivary GDF15: preliminary findings.Brain, behavior, and immunity · 2025Article
- Mitochondrial and psychosocial stress-related regulation of FGF21 in humans.Nature metabolism · 2025Article
- Brain age gap as a predictive biomarker that links aging, lifestyle, and neuropsychiatric health.Communications medicine · 2025Article
- Disparities in Allostatic Load Among Different Races: A Comprehensive Scoping Review.Journal of racial and ethnic health disparities · 2025Review
- Energetics of whole genome doubling and genomic instability.Cancer letters · 2025Review
- Individual and Comorbid Influences of Chronic Stress and a Western Diet on Allostatic Loads and Cardiac Resilience, Adaptation and Proteome Profiles in Male Mice.Comprehensive Physiology · 2025Article
- Astrocytes as Metabolic Sensors Orchestrating Energy-Driven Brain Vulnerability in Alzheimer's Disease.Journal of neurochemistry · 2025Review
Corrections and comments
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Authors and funding
17 authors at 9 institutions in 2 countries.
Funding
Abstract
Stress triggers anticipatory physiological responses that promote survival, a phenomenon termed allostasis. However, the chronic activation of energy-dependent allostatic responses results in allostatic load, a dysregulated state that predicts functional decline, accelerates aging, and increases mortality in humans. The energetic cost and cellular basis for the damaging effects of allostatic load have not been defined. Here, by longitudinally profiling three unrelated primary human fibroblast lines across their lifespan, we find that chronic glucocorticoid exposure increases cellular energy expenditure by ∼60%, along with a metabolic shift from glycolysis to mitochondrial oxidative phosphorylation (OxPhos). This state of stress-induced hypermetabolism is linked to mtDNA instability, non-linearly affects age-related cytokines secretion, and accelerates cellular aging based on DNA methylation clocks, telomere shortening rate, and reduced lifespan. Pharmacologically normalizing OxPhos activity while further increasing energy expenditure exacerbates the accelerated aging phenotype, pointing to total energy expenditure as a potential driver of aging dynamics. Together, our findings define bioenergetic and multi-omic recalibrations of stress adaptation, underscoring increased energy expenditure and accelerated cellular aging as interrelated features of cellular allostatic load.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.