X-Message-Number: 29467
Date: Fri, 27 Apr 2007 00:27:38 -0400
From: Keith Henson <>
Subject: Hayflick on aging

Part I. Aging, Longevity, and Evolution
Biological Aging Is No Longer an Unsolved Problem

LEONARD HAYFLICK

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?"

http://www.annalsnyas.org/cgi/content/abstract/1100/1/1?etoc

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