Abstract
The longstanding debate about whether aging may have evolved for some adaptive reason is generally considered to pit evolutionary theory against empirical observations consistent with aging as a programmed aspect of organismal biology, in particular conserved aging genes. Here I argue that the empirical evidence on aging mechanisms does not support a view of aging as a programmed phenomenon, but rather supports a view of aging as the dysregulation of complex networks that maintain organismal homeostasis. The appearance of programming is due largely to the inadvertent activation of existing pathways during the process of dysregulation. It is argued that aging differs markedly from known programmed biological phenomena such as apoptosis in that it is (a) very heterogeneous in how it proceeds, and (b) much slower than it would need to be. Furthermore, the taxonomic distribution of aging across species does not support any proposed adaptive theories of aging, which would predict that aging rate would vary on a finer taxonomic scale depending on factors such as population density. Thus, while there are problems with the longstanding non-adaptive paradigm, current evidence does not support the notion that aging is programmed or that it may have evolved for adaptive reasons.
Keywords: Adaptation, aging, comparative, disposable soma, physiological dysregulation, programmed.
Current Aging Science
Title:Physiological and Comparative Evidence Fails to Confirm an Adaptive Role for Aging in Evolution
Volume: 8 Issue: 1
Author(s): Alan A. Cohen
Affiliation:
Keywords: Adaptation, aging, comparative, disposable soma, physiological dysregulation, programmed.
Abstract: The longstanding debate about whether aging may have evolved for some adaptive reason is generally considered to pit evolutionary theory against empirical observations consistent with aging as a programmed aspect of organismal biology, in particular conserved aging genes. Here I argue that the empirical evidence on aging mechanisms does not support a view of aging as a programmed phenomenon, but rather supports a view of aging as the dysregulation of complex networks that maintain organismal homeostasis. The appearance of programming is due largely to the inadvertent activation of existing pathways during the process of dysregulation. It is argued that aging differs markedly from known programmed biological phenomena such as apoptosis in that it is (a) very heterogeneous in how it proceeds, and (b) much slower than it would need to be. Furthermore, the taxonomic distribution of aging across species does not support any proposed adaptive theories of aging, which would predict that aging rate would vary on a finer taxonomic scale depending on factors such as population density. Thus, while there are problems with the longstanding non-adaptive paradigm, current evidence does not support the notion that aging is programmed or that it may have evolved for adaptive reasons.
Export Options
About this article
Cite this article as:
Cohen A. Alan, Physiological and Comparative Evidence Fails to Confirm an Adaptive Role for Aging in Evolution, Current Aging Science 2015; 8 (1) . https://dx.doi.org/10.2174/1874609808666150422124332
DOI https://dx.doi.org/10.2174/1874609808666150422124332 |
Print ISSN 1874-6098 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-6128 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Small Molecule Inhibitors of NF-κB and JAK/STAT Signal Transduction Pathways as Promising Anti-Inflammatory Therapeutics
Mini-Reviews in Medicinal Chemistry Low Lymphocyte Count and Cardiovascular Diseases
Current Medicinal Chemistry Midlife Modifiable Risk Factors for Dementia: A Systematic Review and Meta-analysis of 34 Prospective Cohort Studies
Current Alzheimer Research Coffee: A Selected Overview of Beneficial or Harmful Effects on the Cardiovascular System?
Current Vascular Pharmacology Fast Food Versus Slow Food and Hypertension Control
Current Hypertension Reviews Hyperglycaemia and Vitamin D: A Systematic Overview
Current Diabetes Reviews Efficacy and Safety of Evacetrapib for Modifying Plasma Lipids: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
Current Pharmaceutical Design The Pathway Less Traveled: Moving from Candidate Genes to Candidate Pathways in the Analysis of Genome-Wide Data from Large Scale Pharmacogenetic Association Studies
Current Pharmacogenomics and Personalized Medicine The Heart and Brain Imaging in Lone Atrial Fibrillation – Are We Surprised?
Current Pharmaceutical Design Lipoprotein-associated Phospholipase A2: A Potential Therapeutic Target for Atherosclerosis
Current Drug Targets - Cardiovascular & Hematological Disorders Contribution of ALDH2 Polymorphism to Alcoholism-Associated Hypertension
Recent Patents on Endocrine, Metabolic & Immune Drug Discovery Analysis of QTc Interval during Levofloxacin Prescription in Cardiac Patients with Pneumonia
Current Drug Safety Oxidized-LDL and Paraoxonase-1 As Biomarkers of Coronary Artery Disease in Patients with Sleep-Disordered Breathing
Current Medicinal Chemistry The Potential Impact of Sirtuin 1 Protein on Premature Ovarian Insufficiency
Current Proteomics Arterial Stiffness and Hypertension: A Review of Mechanism and Clinical Relevance
Current Hypertension Reviews Rhodanine as a Privileged Scaffold in Drug Discovery
Current Medicinal Chemistry Lock Stock and Barrel of Wound Healing
Current Pharmaceutical Design Effect of Immunoglobulin Therapy on Blood Viscosity and potential concerns of Thromboembolism, Especially in Patients with Acute Kawasaki Disease
Recent Patents on Cardiovascular Drug Discovery Dietary Phytochemicals in Chemoprevention of Cancer: An Update
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) The Development of Preventives and Therapeutics for Alzheimers Disease that Inhibit the Formation of β-Amyloid Fibrils (fAβ), as Well as Destabilize Preformed fAβ
Current Pharmaceutical Design