Theories of Aging
What is Aging?
Changes in multiple physiological systems
Increased risk for various diseases:
How we Think about Aging
“accidental” theories of aging (a.k.a. stochastic theories):
aging is caused by a series of adverse events in cells that lead to replicative
programmed-aging theories (a.k.a. non-stochastic theories):
intrinsic & predetermined /programmed changes in cells
Stochastic Theories of Aging
Wear & Tear Theory
Accumulation of normal injury due to continued use
But humans are not like cars!
Our bodies repair themselves, replace lost cells & damaged proteins, make
new mitochondria and molecules, fix DNA, etc....
Somatic Mutation Theory
Mutations occur in cells (soma) due to repeated replication, exposure to
toxins, radiation or ultraviolet light.
The body cannot correct/destroy all mutations, but not all of them, and
eventually the mutated cells accumulate.
Extension of somatic mutation theory
Aging is caused by cumulative errors in DNA/RNA
Free Radical Theory
Cells are damaged by free radicals
Free radicals are chemical byproducts of normal cell metabolism involving
Proteins (e.g., collagen, elastin) become cross-linked and thus less flexible Accumulation Theory
a.k.a waste accumulation theory
Aging is caused by the accumulation of substances in cells
e.g., lipofuscin, a brownish pigment left over from the breakdown and
absorption of damaged blood cells.
Preferential allocation of energy resources for reproduction rather than
maintenance of somatic cells (i.e., cells forming body of organism).
This allocation of energy causes the body to gradually deteriorate with age.
Non-Stochastic Theories of Aging
Programmed Aging theory
States that the aging process is determined by a biological/genetic clock
Every organism has a physiological lifespan that is highly characteristic for
Decreased immune function in older adults results in:
(a) reduced resistance to disease
(b) greater incidence of autoimmune disorders
Evolutionary Theories Of Aging
Alleles with beneficial effects at young ages may have deleterious effects in
e.g., in humans the p53 gene directs damaged cells to stop reproducing or die.
This helps prevent cancer in younger people, but may be partly responsible
for aging by impairing the body’s ability to renew deteriorating tissues.
Thus, altering genes to improve late-life fitness could have a detrimental
effect on health at younger ages.
Over evolutionary time, late-acting mutations accumulate at a much faster
rate than early-acting mutations.
These late-acting mutations will thus lead to declining viability and/or