I. Theories of Aging
 Biological
Theories of Aging
 Psychological Theories of Aging
 Psychosocial Factors and Aging
Theories of Aging (cont.)
Aging process along with biological and
psychological change and social interaction. There
are many theories of aging which describe and
interpret the aging process.
 However, Bengtson and associates (1999) pointed
out two reasons of the lack of integration in
theories of gerontology.
 1) three different aspects of age (page 43)
 2) models and theories are not clearly
distinguished.

Biological Theories of Aging

Genetic Theories
Programmed cell death
2. Stochastic process
3. DNA repair mechanisms
1.

Molecular/Cellular Theories of Aging
Oxidation
2. Lipofuscin
3. Heat shock proteins
1.

System-Level Theories
Homeostasis
2. Wear-and-tear theories
3. Stress
1.
Biological Theories of Aging (cont.)
Genetic Theories
1. Programmed cell death (PCD) - the process
of PCD that may occur in multicellular
organisms. Biochemical events lead to
characteristic cell changes and death. These
changes include blebbing, loss of cell
membrane asymmetry and attachment, cell
shrinkage, nuclear fragmentation, chromatin
condensation, and chromosomal DNA
fragmentation.

Biological Theories of Aging (cont.)
Apoptosis is one mechanism for the
destruction of cells that have proliferated for
specific purposes, such as T-cells in the immune
system, and need to destroyed after
accomplishing their tasks.
 In humans, the number of times somatic cells
can replicate is partially regulated by the
telomere length.
 Apoptosis may be a necessary process to get
rid of damaged and cancerous cells (Campisise,
2001)

Biological Theories of Aging (cont.)
2. Stochastic Processes (replication error)
 Hayflick (1996) stated that there may be a
limited times a cell can replicate without error.
This function of random (or stochastic) error is
a part of aging process.
 DNA is susceptible to damage by a host of
environmental factors, such as chemical agents
(air pollution, smoking), and radiation, and
internal processes such as oxidation.

Biological Theories of Aging (cont.)
3. DNA repair mechanisms
 In the process of replication, the are several
different checkpoints through which the cell
checks the integrity of the DNA strands. If an
error is caught, replication is stopped so that
repairs can made.

Biological Theories of Aging (cont.)
Molecular/Cellular Theories of Aging
1. Oxidation – Free radicals or reactive oxygen
species (ROS) are molecules that are
generated during the oxidation process in cell.
They are unstable and may interfere with the
function of other molecular in the cell.
• The concentration of free radicals increases
with age (Sohal & Weindruch, 1996) on page
49.

Biological Theories of Aging (cont.)
2. Lipofuscin – accumulated waster products in aging
cells. These waster products normally are disposed
via liposomal enzymes, but impaired in aging cells.
Lipofuscin blocks cell proliferation and induces cell
death, and may be associated with Alzeimer’s disease.
3. Heat shock proteins (HSPs) – having cellular repair
mechanism and decelerating aging process. HSPs
protect cells from stress and oxidative process by
regulating enzymatic processes necessary for repair
and apoptosis; others refold damaged proteins into
their configuration; they play a major roles in the
inflammatory and immune process.
Biological Theories of Aging (cont.)
System-level theories
1. Homeostasis – stability in intra- and extracellular
environmental conditions, such as pH balance, blood,
pressure, heart rate, temperature, and fluid balance.
Homeostasis is a dynamic balance and requires
communication among the various organ systems
and is largely regulated by the autonomic nervous
system via the neuroendocrine system.
 It becomes harder to maintain homeostasis as we
age: 1) a decline in the production of hormones; 2)
the target organs become less responsive; 3) the
target organs synthesize less than optimal amount of
its product.
•
Biological Theories of Aging (cont.)
2. Wear-and-tear theory – this theory may not hold
for most organ systems. A phrase in gerontology is
“Use it or lose it”. Many systems such as
cardiovascular system, need regular and moderate
exercise to maintain function, and intellectual
stimulation may be necessary to the maintenance
of cognitive function. However, skeleton joints may
be an exception.
3. Stress – is a feeling that's created when we react to
particular events. It's the body's way of rising to a
challenge and preparing to meet a tough situation.
It could be a over-stress or moderate stress.
Psychological Theories of Aging
 The flowchart in Fig. 3.1 (next slide)
presents the intellectual history of
the major theories of adult
development and traces the origins
of the major schools and their
development from classical to
modern theories.
Psychological Theories of Aging
 Classic Theories
1. Ontogenetic models
2. Sociogenic models
Current Theories
1. Life course theory
2. Goal-oriented models
3. Postformal operations
4. Conscious development
Psychological Theories of Aging (cont.)
Classic Theories
1. Ontogenetic models – posit that development stems
from internal forces and consists of stages that are
universal, sequential, and irreversible. In these
models, change is discontinuous, and characterized
by qualitative changes.
a. Erikson (1950) modified Freud’s psychosexual
theory of early childhood to a psychosocial model
that extended from birth through late life.
b. Jung (1933) focused on adult development, believing
that adolescents and young adults develop a
persona.

Psychological Theories of Aging (cont.)
2. Sociogenic models – focus on life course with
reference to gender, social class, culture, and
cohort, and focus on change in adulthood that
varies as a function of social roles and historical
context or timing events.
a. Disengagement theory – posits a mutual
withdrawal between the individuals and society
as one ages.
b. Active theory – argues that more active the
older person is, the greater life satisfaction.
Psychological Theories of Aging (cont.)
Current Theories:
Most current theories take some sort of middle
ground between strict sociogenic and
ontogenetic stands, but they do so with varying
emphases on the context, individual goals, and
the individual’s choice or ability.
1. Life course theory – Elder (1998) has
developed a life course theory which examines
the ways in which cohort and historical periods
affect the life course structure of individuals (Ex
on page 58).
Psychological Theories of Aging (cont.)
2. Goal-oriented models – assume that older
individuals have fewer resources, they must
select the goals or activities the wish to pursue
and optimize their performance by devoting
resources to those particular goals.
3. Postformal operations – more complex
cognitive development in adulthood. Not only do
people become more cognitively complex with
age, but they also may become more emotionally
complex. However, the emotional complexity
may decrease in late life. Why?
Psychological Theories of Aging (cont.)
4. Conscious development – a growing sense
that adult development is something that
individuals do, not something that simply
occurs. The development in adulthood
consists of increasing mindfulness with
three characteristics: 1) the continuous
creation of new categories; 2) openness to
new information; and 3) an implicit
awareness of more than one perspective.
Psychological Theories of Aging (cont.)
Interrelationships among theories:

Early theories of adult development tended
to focus on one aspect of adult development,
such as personality or social, whereas
contemporary theories tend to emphasize
multiple influences.

Most current theories emphasize some sort
of conscious choice in developmental process.
Some theories posit the opportunity for
conscious choice as an outcome of
developmental processes.
Psychosocial Factors and Aging
Factors affecting health in late-life:
1. Genetic factors may have 0 – 40%
contributions to health.
2. Other factors may have 60 – 100%
contributions to health. However,
psychological, social and physical health are
tightly intertwined.
3. Psychological factors:
1) Personality A and B.
2) How and what we think affect our health.

II. Understanding Change
in Aging Research
 Basic
Definitions
 Age-Related Designs
 Statistics for Assessing Change
 Statistics That Predict Change
Basic Definitions





Two basic questions in research with statistical
analysis:
a. Is there a difference between two or more
groups on a given (dependent) variable?
b. Is there an association between two or more
variables?
However, these two types of questions may be
asked in different way (page 66).
Different statistical methods may be used to
answer these two types of research questions.
Basic Definitions (cont)


Continuous variables:
Interval (numbers) – numbers that share the characteristics of
ordinal and nominal measures but also have the characteristics
of equal spacing between categories, such as temperature
scales.
Ratio (numbers) – numbers that have all the characteristics of
interval numbers but also have an absolute 0 point, such as
incomes.
Categorical variables:
Nominal (numbers) – numbers used to name attributes of a
variable in category, such as male and female.
Ordinal (numbers) – numerical values that assign an order to a
set of observation, such as health condition ranked from 1 =
very poor to 5 = excellent.
Basic Definitions (cont)
Bivariate – two variables.
 Multivariate – more than two variables.
 Partial correlation – controls for one variable a,
when correlating two other variables (b with c),
example on page 68 (education, a, income, b, and
health, c)
 Regression equation – cause and effect relationship
between dependent variable and independent
variable(s).
 Structural equation modeling (SEM) –
simultaneously estimates the relationships among
several variables.

Basic Definitions (cont)


Research designs (experiment)
1. Experimental design – randomization, control and
manipulation.
2. Quasi-experimental design – control and
manipulation.
3. Non-experimental – has none of these three
characteristics, naturalistic.
Research designs (subjects)
1. Between subject designs (between groups)
2. Within subject designs (within groups)
Research question
What design to employ?
Quasiexperimental
Experimental
What entities,
phenomena, or
variables to study
From whom (or what)
to collect data?
In what setting to
collect data
Controlled
Nonexperimental
Naturalistic
What type of data Under what condition to
to collect?
collect data?
At what time points to
collect data
Cross-sectional
Single instance
Group study
Prospective
Qualitative
Longitudinal
Retrospective
Quantitative
Comparative
Manipulation
Control
Noncomparative
Randomization
Figure 7.4 Principal design features (shaded elements) of the Low Back Pain Study (from Sim,
J. & Wright, C. (2000). Research in Health Care: Concepts, Designs and Methods. Nelson
Thomes Ltd., Cheltenham, United Kingdom)
Research question
What design to employ?
Experimental
What entities,
phenomena, or
variables to study
Quasiexperimental
From whom (or what)
to collect data?
In what setting to
collect data
Controlled
Nonexperimental
Naturalistic
What type of data Under what condition to
to collect?
collect data?
At what time points to
collect data
Cross-sectional
Single instance
Group study
Prospective
Qualitative
Longitudinal
Retrospective
Quantitative
Comparative
Manipulation
Control
Noncomparative
Randomization
Figure 7.4 Principal design features (shaded elements) for quasi-experimental Study (same source).
Research question
What design to employ?
Experimental
What entities,
phenomena, or
variables to study
Quasiexperimental
From whom (or what)
to collect data?
In what setting to
collect data
Controlled
Nonexperimental
Naturalistic
What type of data Under what condition to
to collect?
collect data?
At what time points to
collect data
Cross-sectional
Single instance
Group study
Prospective
Qualitative
Longitudinal
Retrospective
Quantitative
Comparative
Manipulation
Control
Noncomparative
Randomization
Figure 6.5 The Rheumatoid Arthritis Study (shaded). It is debatable whether or not the setting for a study
such as this should be classed as ‘naturalistic’. Although the situation in which a questionnaire is completed
may be a natural one. The process of responding to items on a questionnaire is somewhat unnatural one
(same source).
Age-Related Design

Many studies of the effects of aging use quasiexperimental design. Because it is nor possible to
randomly assign people to different ages.
1. Cross-sectional designs – which compare
different age groups at one point in time for the
studies of age difference. Example?
2. Longitudinal designs – which follow people over
a certain period (years or decades) of time for
the studies of age-related changes. Examples?
Age-Related Design (cont.)

Sequential designs in Table 4.2 (next slide):
1. Cohort-sequential designs – can examine
age and cohort effects, but confound period.
2. Cross-sequential designs – can examine
cohort and period effects, bout confound age.
3. Time-sequential designs – can examine age
and period effects, but confound cohort.
Age-Related Design (cont.)

In summary, in two of three sequential designs,
Parker and Aldwin (1997) had significant age
effects but no cohort and period effects. They
concluded that the increase in mastery in
early adulthood is an age or developmental
effect not restrict to a particular cohort or
time period.
Statistics That Predict Change (cont.)
Two point designs – researchers want to use
baselines data at time 1 to predict some
outcome at time 2.
 Multiple regression equation:
y1 = a + b1x1 + b2x2
 Residualized regression equation:
y2 - y1 = a + b1x1 + b2x2

Statistics That Predict Change (cont.)

Relative risk is a ratio of the probability of the event occurring in
the exposed group versus a non-exposed group.
exposedratio
RelativeRisk (RR) 
nonexposedratio

Consider an example where the probability of developing lung
cancer among smokers was 20% and among non-smokers 1%. This
situation is expressed in the 2 × 2 table to the right.
Here, a = 20, b = 80, c = 1, and d = 99. Then the relative risk of
cancer associated with smoking would be

a /(a  b) 20 /(20  80)
RR 

 20
c /(c  d )
1 /(1  99)
Risk
Disease status
Present
Absent
Smoking
a = 20
b = 80
Nonsmoking
c=1
d = 99
Statistics That Predict Change (cont)
Analyzing multiple-point longitudinal data
 1. Fixed effect model in Figure 4.6


2. Random effect model in Figure 4.7