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Paradoxes of aging
1Cancer Center, Ordway Research Institute, 150 New Scotland Ave., Albany, New York 12208, USA. blagosklonny@oncotarget
Abstract:
Insightful articles by Kirkwood and other outstanding scientists reveal paradoxes of aging. The source of paradoxes is an assumption that aging is caused by random, cumulative molecular damage. Here I demonstrate that a concept of TOR-driven program-like aging almost automatically resolves eleven paradoxes of aging. This article discusses why the accumulation of molecular damage does not limit life span, why calorie restriction and inhibition of protein synthesis extend life span, why the non-existing 'program' for aging is nevertheless robust, why a key gene for aging cannot be found by knocking it out, why low insulin is associated with good health but low insulin response with bad health, why aging is not a disease but can be treated as a disease, why 'healthy' aging is slow aging, and how we know that calorie restriction actually slows aging in humans.
Insights
Aging is a programmed process driven by TOR, not random damage. This TOR-driven aging concept resolves key paradoxes, explaining lifespan, calorie restriction benefits, and aging
Area of Science:
- Gerontology
- Molecular Biology
- Genetics
Background:
- The prevailing theory attributes aging to random molecular damage.
- This perspective presents several paradoxes that challenge current understanding.
- Notable scientists like Kirkwood have highlighted these paradoxes.
Purpose of the Study:
- To propose a new framework for understanding aging.
- To demonstrate how a TOR-driven, program-like aging concept resolves existing paradoxes.
- To explain the mechanisms behind lifespan regulation and age-related health outcomes.
Main Methods:
- Theoretical analysis of existing aging research and data.
- Conceptual integration of the TOR pathway's role in aging.
- Re-evaluation of established findings in light of the proposed model.
Main Results:
- The TOR-driven aging model resolves eleven major paradoxes of aging.
- It explains why molecular damage accumulation doesn't limit lifespan.
- It clarifies the effects of calorie restriction and protein synthesis inhibition on longevity.
Conclusions:
- Aging is best understood as a program-like process driven by the TOR pathway.
- This model provides a unified explanation for diverse aging phenomena.
- It reframes our approach to understanding and potentially treating aging.
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