ReviewNature aging2024
The brain-body energy conservation model of aging.
Review in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed.
- Age and loneliness relate to reduced trust learning and alterations in amygdala function.iScience · 2026Article
- Molecular damage associated with ageing drives inflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Inflammaging mediates testosterone declines in men while maintaining high testosterone increases mortality risk.bioRxiv : the preprint server for biology · 2026Article
- Stress is inevitable; recovery is conditional: bioenergetic limits of resilience in aging and disease.Biogerontology · 2026Review
- Unlocking the Functional Properties of Plant Proteins in Designing Food Formulations for Senior Adults.Comprehensive reviews in food science and food safety · 2026Review
- Biomarkers, Cognitive Function, and Mortality in Centenarians.JAMA network open · 2026Article
- Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026Review
- Brain-body interactions in systemic diseases: a survey from an imaging perspective.MedScience · 2026Review
- Saliva cell-free mitochondrial DNA (cf-mtDNA) as a dynamic biomarker of stress and emotion in daily life: Evidence from two independent repeated-measures studies.medRxiv : the preprint server for health sciences · 2026Article
- Evaluating oxidative stress marker FBMC pediatrics · 2026Article
- Ferulic acid promotes hair growth via estrogen receptor alpha activation in cultured human dermal papilla cells.Scientific reports · 2026Article
- Retinal Microvasculature and Emotional, Behavioral, and Cognitive Outcomes at School Age.Journal of the American Heart Association · 2026Article
- Exercise as a multiscale recalibration of stress-related homeostatic balance.Frontiers in neuroscience · 2026Review
- The influence of social physical exercise on the health of middle-aged and older adults: a mediating model of health behavior change mechanisms moderated by age.Frontiers in public health · 2026Article
- Roles of DRP1 and the fission protein interactome as regulators of cellular stability and sarcopenia in skeletal muscle aging.Aging advances · 2025Article
- The allostatic triage model of psychopathology (ATP Model): How reallocation of brain energetic resources under stress elicits psychiatric symptoms.Neuroscience and biobehavioral reviews · 2025Review
- Mitochondrial and psychosocial stress-related regulation of FGF21 in humans.Nature metabolism · 2025Article
- Evidence for an energetic trade-off model linking inflammaging and immunosenescence in the US Health and Retirement Study and UK Biobank.bioRxiv : the preprint server for biology · 2025Article
- Microcirculation-Promoting Effect of Escin on Cutaneous Tissue via Gsk3β Down-Regulation.Current issues in molecular biology · 2025Article
- Astrocytes as Metabolic Sensors Orchestrating Energy-Driven Brain Vulnerability in Alzheimer's Disease.Journal of neurochemistry · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Aging involves seemingly paradoxical changes in energy metabolism. Molecular damage accumulation increases cellular energy expenditure, yet whole-body energy expenditure remains stable or decreases with age. We resolve this apparent contradiction by positioning the brain as the mediator and broker in the organismal energy economy. As somatic tissues accumulate damage over time, costly intracellular stress responses are activated, causing aging or senescent cells to secrete cytokines that convey increased cellular energy demand (hypermetabolism) to the brain. To conserve energy in the face of a shrinking energy budget, the brain deploys energy conservation responses, which suppress low-priority processes, producing fatigue, physical inactivity, blunted sensory capacities, immune alterations and endocrine 'deficits'. We term this cascade the brain-body energy conservation (BEC) model of aging. The BEC outlines (1) the energetic cost of cellular aging, (2) how brain perception of senescence-associated hypermetabolism may drive the phenotypic manifestations of aging and (3) energetic principles underlying the modifiability of aging trajectories by stressors and geroscience interventions.
Indexed as
Identifiers
39379694What OpenQuestion holds
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.