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Chapter 3

Chapter 3 notes


Department
Health Studies
Course Code
HLTC22H3
Professor
Anna Walsh
Chapter
3

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Chapter 3 - Theories of Aging
Lack of integration of theories in gerontology
o3 diff. Aspects of age on whic theories can focus: characteristics of aging pop,
the developmental or aging process, the way in which age is incorporated into
the social structure
oGerontology has been a bottom-up discipline; starts from facts (systematic
observation) that may be grouped loosely into models (which specify
categories of variables that should be related) and only sometimes achieve
status of theory (tries to explain or specify processes involved in a particular
phenomenon)
Rowe & Kahns theory of developmental aging & Ford and Lerners developmental
systems theory are more models than theories
Maruyamas deviation amplification model added component to von Bertalanffys
classis systems theory model, which holds that most systems have deviation-
countering mechanisms to maintain homeostasis
oSo if change occurs, mechanisms typically exist for countering that change
and returning the organism to a steady rate
oE.g blood pressure regualation, heart rate, respiratory rate, glucose
regulation, DNA repair
oMaruyama says that systems do & can change over time
oSimilar to chaos theory (shows how initially small changes can result in very
large differences between systems & individuals) general model for aging
and used to describe cascade effects in Cardiovascular functioning
oBut maruyamas model may be better b/c it includes both positive & negative
changes (maintaining homeostasis & promoting change)
oAdwin & Stokols used this model to describe effects of environmental stress
Biological processes fall into 2 categories
oThose that promote homoestasis & decelerate aging process
oThose that amplify deviations and accelerate aging process (free radicals)
Biological Theories of Aging
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Genetic, molecular/cellular, & system-level theories
Genetic Theories:
Avg life span of humans = 120 yrs
Life span are inversely related to factor such as metabolic rate, length of time to
maturation
Programmed Cell Death (Apoptosis)
Death gene gene that regulates sudden cell death (also called apoptosis)
Genetic material is not static
Damage to regulator proteins may be mechanism for cancer (uncontrolled cell
profileration)
Apoptosis mechanism for destruction of cells that have profilerated for specific
purposes
oE.g T-Cells in immune system, and need to be destroyed after having
accomplished their task
MORF mortality factor which controls the rate of a cells aging
Positive correlation between life span of species, and number of times a cell will
replicate
Humans: number of times somatic cells can replicate is regulated by telomere
length
o Consist of specialized ends of DNA strands that help hold them together
during mitosis
oDont completely unwind during mitosis
oAbout 100 base pairs per cell lost during each replication
oWhen several thousand base pairs are lost, the cell stops replicating and
senesces
oTelomeres can be restored by telomerase
oCancer cells have longer telomeres and ore active telomerese than normal
cells
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Absence of procceses (apoptosis & senescence) may shorten life as they are one way
of getting rid of damaged and cancerous cells
Senescence (Campisise) = major protection against cancer
oAntagonistic pleiotropy process helpful and promotes reproduction in early
life but may have harmful effects later
Stochastic Processes:
Hayflick thinks that there may be specific number of times that cell can replicatie
w/out error
oThus, aging may be function of random (stochastic) errors
oReplication error = one of leading theories of aging
oDamage to dna impairs cells ability to synthesize proteins and other
stubstances and/or respond to regulation
oEventually cells run out of backups (e.g. DNA repair cells to help) and it can
no longer function properly
oIf too many cells in system fail, system can become compromised
oDNA in mitochondria = susceptible to damage
oCells in oxidative organs (heart, brain, skeletal muscles) have most damaged
mitochondrial DNA
oIf cells energy source is damaged, it becomes candidate for apoptosis
oThus, mitochondrial DNA may be cause of significan cell loss in late life
DNA Repair Mechanisms
Deviation countering mechanism for aging
Thigns that can damage DNA = light, radiation, toxic chemicals, or oxidation
process itself
Damage tends to activate replication
Mechanisms of DNA repair
oBase excision repair, nucleotide excision repair, mismatch repair, repair
of strand breaks
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