Abstract review: hyperfunction theory of aging, from caloric restriction to rapamycin
This abstract reviews the history of programmatic theories of aging, including the hyperfunction theory, and cites single-gene manipulations in animal models and rapamycin's lifespan extension as empirical support. [1]
Automatic summary · not editorially reviewed
The key findings
The abstract contrasts damage-focused theories of aging with the idea that aging may be primarily a programmatic process. [1]
The author reviews programmatic theories from early caloric restriction experiments to frameworks including Blagosklonny's hyperfunction theory. [1]
Single-gene manipulations in animal models and evidence that rapamycin extends lifespan are cited as empirical support. [1]
The source at a glance
- Study type / format
- Review abstract
- Population / context
- Animal models cited in a review of aging theories; no human population described.
- Summary based on
- Study abstract
- Original publication
- July 24, 2026
Programmatic theories versus damage theories
The abstract contrasts two views. Many proposed theories of aging focus on errors and the gradual accumulation of molecular damage. By contrast, aging may be primarily a programmatic process: developmental programs that continue to run later in life and, as a form of antagonistic pleiotropy, become detrimental. The author reviews the history of such programmatic theories, from early caloric restriction experiments to more recent conceptual frameworks to which Mikhail Blagosklonny made key contributions, particularly the hyperfunction theory.
Supporting source [1]
Animal gene manipulations and rapamycin as cited support
According to the abstract, two lines of evidence provide empirical support for the hyperfunction theory: the discovery that single-gene manipulations can modulate aging in animal models, and evidence that rapamycin extends lifespan. The abstract does not report which genes, which animal models, how large the effects were, or whether rapamycin's lifespan effect was shown in humans.
Supporting source [1]
Prospects discussed, no results reported
The abstract states that the author discusses the prospects of the hyperfunction theory and its implications for the future of aging biology. It reports no new experiments, no sample sizes and no outcome data of its own. The text is an abstract only; the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. No genes, animal models, effect sizes, sample sizes or human data are reported, and the cited support is preclinical or experimental, not evidence of human lifespan benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Magalhães JP. · europepmc.org · July 24, 2026