What is Aging? What are Aging Theories?

Have you ever asked yourself the following questions?


Why do we age?

When do we start aging?

Is there a biomarker for aging?

Is there a limit to how old we can grow?


Many theories have been proposed to explain the process of aging, but neither of them appear to be fully satisfactory.  These theories fall into two main categories:

1.   Programming Theories

2.   Error Theories

All these questions are asked and have been asked by humans in the past couple of hundred years. However, in spite of recent advances in molecular biology and genetics, the mysteries that control human lifespan have not been unraveled yet.


Modern Aging Theories


A.  The programmed theory

1)    Programmed Longevity.

This theory argues that aging is the result of a sequential switching on and off of certain genes. Senescence is being defined as the time when age-associated deficits are manifested.

2)   Endocrine Theory.

This theory assumes that biological clocks act through hormones to control the pace of aging. Several recent studies confirm that aging is hormonally regulated and that the evolutionarily conserved insulin/IGF-1 signaling (IIS) pathway plays a key role in the hormonal regulation of aging.

3)   Immunological Theory.

The notion of this theory is that the immune system is programmed to decline over time. This leads to an increased vulnerability to infectious disease and thus results in aging and death. The immune system peaks at puberty and gradually declines thereafter with advance in age. As a person grows older antibodies lose their effectiveness and fewer new diseases can be combated effectively by the body causing cellular stress and eventual death. Dysregulated immune responses have been linked to cardiovascular disease, inflammation, Alzheimer’s disease (AD), and cancer.

B.   The damage or error theory

1)    Wear and tear theory.

This theory assumes that during aging vital parts of cells and tissues wear out resulting in the aging process and ultimately death. Like components of an aging car, parts of the body eventually wear out from repeated use, killing them and then the body.

2)    Rate of living theory.

It has been noticed that the greater an organism’s rate of oxygen basal metabolism is the shorter is its life span. However, this theory is not completely adequate in explaining the maximum life span of an organism.

3)    Cross-linking theory.

According to this theory, an accumulation of cross-linked proteins damages cells and tissues, slowing down bodily processes which ultimately result in aging. Recent studies have shown that cross-linking reactions are involved in the age related changes in the investigated proteins.

4)    Free radicals theory.

This theory proposes that superoxide and other free radicals cause damage to the macromolecular components of the cell. The accumulated damage causes cells, and eventually organs, to stop functioning ultimately leading to death. When rodents were fed antioxidants they achieved greater mean longevity indicating that this theory may have some merit.

5)    Somatic DNA damage theory.

DNA is continuously damaged in cells of living organisms. Mammals including humans have mechanisms to repair these damages but some accumulate, as the DNA Polymerases and other repair mechanisms cannot correct defects as fast as they are apparently produced. DNA damage appears to accumulate in non-dividing cells of mammals. Genetic mutations occur and accumulate with increasing age, causing cells to deteriorate and malfunction. Further, it is thought that damage to mitochondrial DNA leads to mitochondrial dysfunction. As a result damage to the genetic integrity of the body’s cells leads to aging.


Other proposed molecular models of aging mechanisms

1.   Oxidative Degradation

      a.  Cross-links in proteins

2.   DNA Methylation 

      a.  Hypermethylation  

      b.   Senescence genes

3.    Stem Cell Depletion

4.    Telomere Breakdown


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Carina Frauer and Heinrich Leonhardt; Twists and turns of DNA methylation PNAS 2011 ; published ahead of print May 18, 2011, doi:10.1073/pnas.1105804108.

Jamie A. Hackett, Roopsha Sengupta, Jan J. Zylicz, Kazuhiro Murakami, Caroline Lee, Thomas A. Down, M. Azim Surani;  Germline DNA Demethylation Dynamics and Imprint Erasure Through 5-Hydroxymethylcytosine. Science 25 January 2013: Vol. 339 no. 6118 pp. 448-452. DOI: 10.1126/science.1229277.

A. J. Hulbert, Reinald Pamplona, Rochelle Buffenstein, and W. A. Buttemer; Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals. Physiol Rev October 2007 vol. 87 no. 4 1175-1213.

Hussain Z, Khan MI, Shahid M, Almajhdi FN; S-adenosylmethionine, a methyl donor, up regulates tissue inhibitor of metalloproteinase-2 in colorectal cancer. Genet Mol Res. 2013 Apr 10;12(2):1106-18. doi: 10.4238/2013.April.10.6.

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Categories: Aging, Aging Theories, Cancer, Cancer Risk, Epigenetics, Gene Expression, Gene families, Genetics, Genome, non-coding RNAs

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1 reply

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