Key result
Brain-body model proposes aging phenotypes are driven by brain energy conservation responses to cellular hypermetabolism.
Why the study?
Aging involves a contradiction where molecular damage increases cellular energy expenditure while whole-body energy expenditure remains stable or decreases, a paradox the authors aim to resolve.
Introduces a novel conceptual model explaining how brain-mediated energy conservation in response to cellular aging drives phenotypic manifestations of aging.
Does not support changes in aging care; hypothesis-generating model requiring prospective validation.
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/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.
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Shaulson et al. (2023) conducted a review in Aging. The brain-body energy conservation model proposes that aging phenotypes are driven by the brain's adaptive energy conservation responses to systemic signals of cellular hypermetabolism.
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