HLTB01H3 Health, aging and the lifecycle
Monday, September 27, 2010
Chapter 3- Theories of Aging
Sometime in literature, theories and models are not distinguished among themselves very well, which makes it harder to
understand. In a way, theories are more specifications of the process involved for a particular phenomenon. It’s a set of ideas to
explain something. Models on the other hand specify categories of variables that should be related/ representing the theory.
• Aging is usually defined as:
•death is the final event
Theories of aging
• Since the beginning, the aging process happens at the biological, psychological and social levels. No one knows for sure why
we age, but there has been some outlooks on processes as to why we age and coming up with theories.
•Bengtson, Rice and Johnson (1999): these 3 argues that there is a lack of connection between theories of gerontology.
- explains 2 reasons for this lack
1. There are 3 different aspects of age that theories can look upon: characteristics of aging population, the developmental or
aging process, and the way age is incorporated into the aging structure.
2. Gerontology is a bottom-up discipline. They start with getting facts and try to group them into models and hardly achieve
the status of theory. Model and theory often not carefully distinguished.
Gender is one of the strongest predictors of life expectancy with women living the longest.
Deviation Amplification Mechanisms: developed by Maruyama in 1963
argued that systems (Homeostasis: heart rate, blood pressure, respiratory rate) can and do
change over time.
Once a system is out of homeostasis, deviation amplification mechanisms take over and speed up the change or imbalance.
This theory kinda represents the chaos theory= a way of specifying a Nondeteminate process, a process where it doesn’t follow a
simple cause and effect, there are many variables to this acting out onto this imbalance. Chaos theory shows us how small
changes can result in very large differences.
The biological theories of aging
Genetic Theory, Molecular/ cellular theories of aging and system level theories.
When it comes to aging, in a biological process, 2 things can happen. 1. A process where homeostasis is maintained and
decelerates the aging process. (Heat shock proteins and DNA repair mechanisms) and 2. Deviations that accelerate the aging
process (free radicals).
Programmed cell death: •There’s a death gene
• regulates sudden cell death
• this process is called Apoptosis
•Damage to cell regulators may be a mechanism to cancer, but cells can also be turned off, failing to
produce needed substances.
• Apoptosis= a mechanism for the destruction of cells like T-Cells in the immune system. And destroyed
after completing their task
• some cells have a programmed cell death.
Telomeres: they are certain sequences at the end of a DNA strand. They are specialized ends of the DNA strand that helps hold
DNA strand together during mitosis. DNA doesn’t completely unwind during mitosis because they are held together by caps at
their ends which don’t replicate and are lost.
About 100 are lost and when they are lost, the cell stops replicating. But Telomeres can be restored by an enzyme called
In cancer cells however, it has a longer telomeres and a more active telomerase than normal cells. But it’s like this in the
intestine, but this is needed.
The number of times cell replicate can be controlled by genes. There can also be immortality genes that control cell senescence
Mutations in genes may also invoke immortality =genes replicate rapidly.
Stochastic (random) processes: Hayflick Theory (1996)-geneticists
• states that aging may be a function of RANDOM ERROR
• why? : There may simply be a limited # of times a cell can replicate without error
•replication error = leading theories for aging.
DNA for example can get damaged in many ways, Due to chemicals, toxins, radiation, etc. this can impair a DNA’s ability to
create proteins and other substances. Therefore, due to these problems, there are multiple backups.
That’s where DNA REPAIR MECHANISMS come in: cells can turn off these damaged segment and tuning on identical back up
segments or by using DNA REPAIR MECHANISMS, which
But the cells can run out of backup and can no longer function adequately.
ALSO: DNA in Mitochondria can get damaged also. Oxidation process is carried out in the Mitochondria and the close proximity
of mitochondrial DNA to reactive oxygen is part of the reason why they are susceptible to damage. And its repair system seems to
be less efficient. Cells in highly oxidative organs have the most damaged, then the functioning of the whole cell is impaired and it
becomes susceptible to Apoptosis.
DNA that is repaired is considered a deviation countering mechanism for aging.
What can damage DNA? UV light, chemical, oxidation, etc…
The 4 things that repair DNA: Base excision repair, nucleotide excision repair, mismatch repair and repair of strands
Sometimes error can be missed and it’s ok, it’s not that severe, but if it’s really severe this can lead to apoptosis.
Molecular/cellular theories of aging.
Oxidation : Free radicals is also known as reactive oxygen species (ROS).
• it’s a molecule that is created during the oxidative process in cells.
• why are they dangerous: they have an unpaired electron and they are unstable and highly chemically reactive and they
could interfere with other functions of other molecules in the cell like DNA replication, protein synthesis, etc…
•can cause proteins to unfold and also interferes with DNA and its transcription process.
But the cells also produce antioxidants like superoxide dismutase (SOD)
The concentration of free radicals (cell damage) increases with age because : more free radicals in aging cells, decrease
ability for cell to create antioxidents, and repair mechanisms in cells are less efficient.
SOD IS HIGHER IN CELLS OF CENTENARIANS.
Lipofuscin : when cells that are aging produces waste.
• A dark mixture.
•disposed through Liposomal enzymes , but in older people, this processes is impaired (damaged)
•increases with ages, can be found in many cell types
•reduce caloric restriction appears to decrease the rate of production of lipofusion
Heat Shock protein (HSP)s: a cellular repair mechanism=aging decelerator
•First identified in plant cells undergoing heat-related stress. That’s why they are called this
•protect cells from STERSSORS (radiation, oxidation, infection)
•Found in every organism and cells (bacteria and humans)
• promotes healthy cell growth and proliferation.
•Also called MOLECULAR CHAPERONS (assist in protein synthesis and repair)
Different types of HSP’s that has different functions.
Small HSP’s: protect cells from stress
other refold damaged proteins
Sometime in literature, theories and models are not distinguished among themselves very well, which makes it harder to understand. In a way, theories are more specifications of the process involved for a particular phenomenon. It"s a set of ideas to explain something. Models on the other hand specify categories of variables that should be related/ representing the theory: aging is usually defined as, death is the final event. Theories of aging: since the beginning, the aging process happens at the biological, psychological and social levels. They start with getting facts and try to group them into models and hardly achieve the status of theory. Gender is one of the strongest predictors of life expectancy with women living the longest. Deviation amplification mechanisms: developed by maruyama in 1963 argued that systems (homeostasis: heart rate, blood pressure, respiratory rate) can and do change over time.