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Biological Aging Is No Longer an Unsolved Problem
Abstract
Abstract: The belief that aging is still an unsolved problem in biology is no longer true. Of the two major classes of theories, the one class that is tenable is derivative of a single common denominator that results in only one fundamental theory of aging. In order to address this complex subject, it is necessary to first define the four phenomena that characterize the finitude of life. These phenomena are aging, the determinants of longevity, age‐associated diseases, and death. There are only two fundamental ways in which age changes can occur. Aging occurs either as the result of a purposeful program driven by genes or by events that are not guided by a program but are stochastic or random, accidental events. The weight of evidence indicates that genes do not drive the aging process but the general loss of molecular fidelity does. Potential longevity is determined by the energetics of all molecules present at and after the time of reproductive maturation. Thus, every molecule, including those that compose the machinery involved in turnover, replacement, and repair, becomes the substrate that experiences the thermodynamic instability characteristic of the aging process. However, the determinants of the fidelity of all molecules produced before and after reproductive maturity are the determinants of longevity. This process is governed by the genome. Aging does not happen in a vacuum. Aging must be the result of changes that occur in molecules that have existed at one time with no age changes. It is the state of these pre‐existing molecules that governs longevity determination. The distinction between the aging process and age‐associated disease is not only based on the molecular definition of aging described above but it is also rooted in several practical observations. Unlike any disease, age changes (a) occur in every multicellular animal that reaches a fixed size at reproductive maturity, (b) cross virtually all species barriers, (c) occur in all members of a species only after the age of reproductive maturation, (d) occur in all animals removed from the wild and protected by humans even when that species probably has not experienced aging for thousands or even millions of years, (e) occur in virtually all animate and inanimate matter, and (f) have the same universal molecular etiology, that is, thermodynamic instability. Unlike aging, there is no disease or pathology that shares these six qualities. Because this critical distinction is poorly understood, there is a continuing belief that the resolution of age‐associated diseases will advance our understanding of the fundamental aging process. It will not. The distinction between disease and aging is also critical for establishing science policy because although policy makers understand that the funding of research on age‐associated diseases is an unquestioned good, they also must understand that the resolution of age‐associated diseases will not provide insights into understanding the fundamental biology of age changes. They often believe that it will and base decisions on that misunderstanding. The impact has been to fund research on age‐associated diseases at several orders of magnitude greater than what is available for research on the biology of aging. There is an almost universal belief by geriatricians and others that the greatest risk factor for all of the leading causes of death is old age. Why then are we not devoting significantly greater resources to understanding more about the greatest risk factor for every age‐associated pathology by attempting to answer this fundamental question—“What changes occur in biomolecules that lead to the manifestations of aging at higher orders of complexity and then increase vulnerability to all age‐associated pathology?”
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“Although aging is not a disease, it is a significant risk factor for functional decline, affective impairments, exaggerated response to illnesses, dementia, and overall vulnerability for diseases (Hayflick, 2007;Seals and Melov, 2014).”
From Microglia Priming with Aging and Stress (2017) · cites this paper as Hayflick, 2007
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Metadata
- Authors
- HAYFLICK, L.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- HAYFLICK, LEONARD
- ORCID
- HAYFLICK, LEONARD
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2007-04
- Volume
- 1100
- Issue
- 1
- Pages
- 1-13
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- OpenAlex
- W2156815362
- Cited by
- 418
- References
- 14
- Citations by year
- 2026: 16 · 2025: 19 · 2024: 18 · 2023: 16 · 2022: 33 · 2021: 25 · 2020: 20 · 2019: 21 · 2018: 27 · 2017: 27 · 2016: 18 · 2015: 25 · 2014: 18 · 2013: 23 · 2012: 19
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Keywords
- aging, thermodynamic instability, age-related diseases, programmed aging, stochastic aging, reproductive maturation, science policy, death
- MeSH terms
- Adult, Aged, Aging, Animals, Humans, Life Expectancy, Longevity, Middle Aged, Models, Biological
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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