Theories of Aging: Why do we age?
Dr Arthur Tjandra
With marked increases anticipated in both life expectancy and life span in the 21st century, anti-aging medicine has emerged in recent times promising
increased longevity with improved quality of life. Anti-aging physicians believe that most illnesses associated with aging can be prevented, or at least slowed,
through optimal cellular health. Their techniques are nutrition, physical fitness and a range of complementary therapies.
They frequently prescribe nutritional supplements, including vitamins, minerals, botanical medicines and natural hormones.
As humans age, all functions and characteristics are modified. However, there is no clear consensus about what aging actually
is—what “naturally” occurs with the passage of time—versus the effects of disuse and disease. Optimal health management requires
not only an understanding of aging processes that are assumed to be natural and inevitable but also knowledge of the most accepted theories
of how and why we age prematurely. This is usually owing to the presence of certain reversible risk factors. Recent advances in medicine has
placed significant emphasis on development of new technologies, especially in the area of human genomics and stem cell research, to provide
greater clarity on genetic and cellular aging mechanisms. Nevertheless, adaptation of both traditional allopathic, complementary and alternative
integrative modalities to reflect current understanding of the effects of aging, and of how to postpone or prevent premature aging, is now possible.
As Thomas Kirkwood correctly points out however, understanding why aging has evolved may help pinpoint factors
(i.e. genes, intrinsic damage, extrinsic damage) are most likely to be causally involved in aging.
Over the years a significant numbers of theories of aging have been proposed:
I. Molecular Theories
- Codon restriction - Fidelity/accuracy of mRNA translation is impaired due to inability to decode codons in mRNA.
- Error catastrophe - Fidelity of gene expression declines with age, resulting in increased fraction of abnormal proteins.
- Somatic mutation - Accumulation of molecular damage, primarily to DNA/genetic material.
- Dysdifferentiation - Gradual accumulation of random molecular damage impairs regulation of gene expression.
- Gene regulation - Aging caused by changes in gene expression regulating both aging and development.
II. Cellular Theories
- Wear and tear - accumulation of normal injury (weak theory).
- Free radical - Oxidative metabolism produces highly reactive free radicals that subsequently damage protein and DNA.
- Apoptosis - Programmed cell death resulting from genetically determined events or genome crisis.
- Senescence - Phenotypes of aging are caused by an increase in frequency of senescent cells. Senescence may be the result of telomere loss (replicative senescence) or cell stress (cellular senescence).