Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Is aging programed?

Steven N Austad1

  • 1Department of Cellular & Structural Biology, University of Texas Health Science Center, STCBM Bldg., Room 3.100, Barshop Center for Longevity & Aging Studies, 15355 Lambda Drive, San Antonio, TX 78245, USA. austad@uthscsa.edu

Aging Cell
|September 24, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Introduction to the special issue on the impact of climate change and air quality on human aging.

The journals of gerontology. Series A, Biological sciences and medical sciences·2026
Same author

A need for pragmatism in preclinical aging and longevity research.

Nature aging·2026
Same author

In memoriam: Thomas Eugene Johnson.

GeroScience·2026
Same author

Sex-Specific Regulation of the Turandot Gene Family Modulates Temperature-Dependent Lifespan in Drosophila melanogaster.

Aging cell·2026
Same author

Regulation of survival, growth, and metabolism by neuronal mTOR.

GeroScience·2026
Same author

Examining widely held propositions on human dietary protein needs and benefits: a critical review of the science that shapes both the data and our understanding of an essential macronutrient.

Critical reviews in food science and nutrition·2026
Same journal

Bidirectional Relationship and Shared Mechanisms Between Sarcopenia and Osteoporosis: An Observational Study Integrating Genomic, Proteomic, and Metabolomic Data.

Aging cell·2026
Same journal

Clonal Analyses Reveal the Impact of Hematopoietic Stem and Progenitor Cell Aging on T Cell Development.

Aging cell·2026
Same journal

A Gut-Centric View of Ageing: A Pilot Analysis Mapping Age-Associated Immune and Molecular Alterations in Colonic Mucosa Using Spatial Proteomics.

Aging cell·2026
Same journal

Correction to "Environmental Enrofloxacin Exposure as a Modifiable Driver of Mitochondria-Mediated Intestinal Aging and Barrier Dysfunction".

Aging cell·2026
Same journal

Correction to "Social Stress Shortens Lifespan in Mice".

Aging cell·2026
Same journal

A Primate-Specific lncRNA LINC01021 Contributes to Cellular and Organismal Aging via DAZAP1-Dependent Destabilization of RBMX.

Aging cell·2026
See all related articles

Aging is decay, not a programmed process, unlike development. Natural selection shapes adult phenotypes, not senescence, highlighting the absence of evolutionary design in aging. This distinction is crucial for understanding aging research.

Area of Science:

  • Evolutionary biology
  • Gerontology
  • Developmental biology

Background:

  • Development and morphogenesis are viewed as programmed processes driven by natural selection to achieve specific adult phenotypes.
  • Aging, conversely, is generally considered a process of decay rather than a designed outcome, except in specific cases like Pacific salmon.

Purpose of the Study:

  • To differentiate between programmed development and non-programmed senescence.
  • To emphasize that natural selection acts on adult phenotypes, not on the process of aging itself.
  • To guide research by focusing on the phenotypic performance of adults and potential side-effects of aging interventions.

Main Methods:

  • Comparative analysis of aging processes in different organisms (e.g., Pacific salmon vs. humans/mice).

Related Experiment Videos

  • Conceptual distinction between evolutionary "design" and "decay" in biological processes.
  • Main Results:

    • Senescence is characterized by decay due to the absence of natural selection's direct influence, unlike programmed development.
    • The lack of stereotyped aging pathways in most organisms (humans, mice) contrasts with the predictable death sequence in organisms like salmon.
    • Understanding this distinction is key to focusing on adult phenotypic performance and potential pleiotropic effects of interventions.

    Conclusions:

    • Aging is a consequence of evolutionary neglect (decay), not a selected trait.
    • Focusing on adult phenotype is essential for understanding natural selection's role and the implications of aging research.
    • Awareness of non-programmed senescence is vital for evaluating treatments that aim to retard aging.