---l
~---u••-•-
!I
I
1
;
CALIFORNIA STATE UNIVERSITY, NORTHRIDGE
THE CAUSES
OF AGING:
r
~
AN ANTHROPOLOGICAL PERSPECTIVE
• !
A thesis submitted in partial satisfaction of the
requirements for the degree of Master of Arts in
Anthropology
by
Janice Arlene Nadeau
~
July, 1976
The thesis
;:l Janice Arlene
Na~deau is approved:
California State University, Northridge
July, 1976
ii
ACKNOWLEDGMENTS
I am grateful for the helpful suggestions and encouragement
of Gail Kennedy and Bruce Gelvin, and C?f my committee chairman,
Lynn Mason.
I also wish to thank Ronald J. Grant for his editorial
assistance and patience with me during this project.
iii
!
l
TABLE OF CONTENTS
l
Page
iii
ACKNOWLEDGMENTS
v
ABSTRACT.
CHAPTER
I
DEFINITION AND EVOLUTION OF
SEN ESC ENG E . . . . . . . . . . .
1
GENETIC THEORIES OF SENESCENCE
12
m
ENVIRONMENTAL THEORIES OF SENESC.ENCE
34
IV
CONCLUSIONS
53
II
60
A SELECTED BIBLIOGRAPHY.
i
I
I
I
iv
I!
'
ABSTRACT
THE CAUSES OF AGING:
AN ANTHROPOLOGICAL PERSPECTIVE
by
Janice Arlene Nadeau
Master of Arts in Anthropology
July, 1976
One of the prime concerns of the modern field of gerontology
is the cause of the degeneration which accompanies the aging
process.
Most theories attempt to answer this question either from
the perspective of the geneticist, who primarily studies internal
processes, or the environmentalist, who is concerned with external
forces.
Anthropologists have had little -impact on the resolution of
the problem.
The primary purpose of this thesis is to demonstrate that
most of the modern gerontological studies do not synthesize the
genetic and environmental data; as a result, their conclusions
appear to be very deterministic.
The synthetic approach of the
v
ranthrop~~:;~:~.
however, would stimulate broader new interpreta-
~
I tions of presently-known facts and focus attention on the study of
I man, rather than on lahoratory rodents.
This thesis will also organize the various theories into
related units.
This. organization will of course reflect the author's
anthropological orientation.
As the gerontological theories are
described, they will be discussed in terms of evolutionary, genetic,
and environmental (both cultural and physical) theories and in line
with the recent synthetic approach, their mutual interdependence
will be proposed.
Due to the fact that the causes of aging have never been
interpreted from an anthropological viewpoint to my knowledge, I
cannot cite specific studies which will confirm or deny my point of
view.
Information presented here, therefore, is speculative and
should be regarded as a proposal for future research.
vi
I
Chapter I
DEFINITION AND EVOLUTION OF SENESCENCE
I
The primary purpose of this thesis is to show that the causes
of aging have been inadequately
studi~d
by most gerontologists up to
the present, and that an anthropological orientation might overcome
many of these past insufficiencies.
In this chapter, senescence,
the manifestation of the aging process will be defined, followed by
a discussion of the evolution of senescence.
The second chapter
will outline the many genetic theories of senescence such as the
metabolic waste, the cellular death, and the free radical theories.
The third chapter will analyze evidence for an environmentallydetermined aging process.
Because no single theory is universally
accepted today, the merits of each will be analyzed, particularly
from an anthropological perspective.
The thesis will be concluded
with suggested guidelines for human senescence research which
anthropologists might follow.
A.
Definition of Senescence
Normal senescence is the gradual and irreversible breakdown
of the body's homeostatic mechanisms which eventually results in
death.
In humans this occurs during the postreproductive period
of the female and during the equivalent chronological date of the
male.
Comfort (1965: 45)
stated that"· .. ageing depends on
1
2
I pa~~-~ng,.
II
expenditure, accumulation, or happening of 'something'--,
.
other than time ....
11
It is the determination of that "something" to
I which gerontology devotes itself.
Abnormal senescence includes such diseases as senile
dementia, which may or may not occur after the onset of senescence
and is characterized by lesions on the cerebral cortex, and
Alzheimer's syndrome, which has the same symptoms as senile
dementia but occurs at a younger age and causes earlier death
(Shelahskj
1975: 113}.
Such conditionsas these are not considered
to be normal senescent processes, hence they will not be discussed
here.
They are disease states rather than processes.
Nervous system changes indicative of mammalian advancing
age include reduced motor speed, increased variability in motor
response timing, increased stimulus threshold, and a reduction in
the amount of data that can be held in the mind and used simultaneously (Brozek
1961: 184).
(~Jsiological
changes brought about with the onset of sen-
escence are, following Koller (1968: 43-47):
1.
cellular - fatty cholesterol accumulation, scarred
fibrotic tissue, pigment granules inside
cells
2.
cardiovascular - muscles dehydrated, reduced flexibility
of heart tissue and valves
3.
central nervous system - irreplaceable loss of neural
cells and fluids
;
!
3
I
----------------
----~--.
4.
reprodu<;:tive - male climacteric, female menopause
5.
endocrine - change in production of hormones by
pituitary, thyroid, adrenal, pancreas,
II
I
gonads
6.
cosmetic - depigmentation of hair, reduced skin
j
elasticity
7.
cancer - risk due to virus, injury, radiation, carcinogenic chemicals, heredity
8.
psychological - social role change accompanied by neural
cell loss often causes personality changes
The cultural definitions of senescence are as complex as the
physical definitions.
Many industrial societies define "old 11 as
"retired," using the formal marker of chronological years to define
cultural roles.
At that point the culture defines the subculture as a
dependent and nonproductive group.
Many senescent members of
industrial nations perceive themselves as ill and exhibit sick role
behavior such as lengthened bedrest and increased use of medication (Clark and Anderson
1967: 9; Fry
1976).
Many nonwestern societies define old age in functional terms.
Members of a culture who are no longer physically capable of
perfornring certain econonric tasks are reassigned to less demanding tasks.
Frequently this involves care and education of children.
In this circumstance the accumulated knowledge of the elderly plays
an important role in the enculturation of the young.
Other duties
relegated to the old may include household tasks such as cooking
an_d cleaning (Clark and Anderson
1967: 6).
.,
4
~i:~-~ge ac-~~-~ded
1
l
t.o
t~;·old
varies
considerabl;~g~
cultures; for example, nonindustrial societies honor their senescent
l,.
members with esteemed possessions and ceremonies more often
than do industrial societies (Simmons
1946: 93).
Senescence, therefore, is both a physically and culturally
defined state.
While the biological symptoms of aging are rela-
tively uniform, the cultural definition of senescence varies considerably among the numerous kinds of societal organizations and
economies.
B.
Evolution of Senescence
Clearly one of the most important questions the anthropolo-
gist would ask about senescence is how it evolved.
Few gerontolo-
gists consider this question; it is ignored when genetic and
environmental theories are being discussed.
The anthropologist,
however, distinguishes between the mechanisms of a process, which
many biologists mistakenly identify as the cause of a process (see
Comfort
1957a; Strehler
1971; Verzar
forces which caused its existence.
1957a), and the selective
In the following pages, I will
describe the selective forces and the relative importance of the
numerous mechanisms of aging and how they relate to anthropology.
Many biologists have made the mistake of confusing senility
and senescence and have concluded that only man truly ages.
Senility is a neural diseas'e unique to man and domesticated
5
r
----.
·-·
l animals and is a product of domestication and civilization.
~~
~
It is
l
almost nonexistent in wild populations which die when their ability
I
to defend themselves causes quick death {Bourliere
1962).
I However, wild animals do senesce, although few members of such
I
species attain full maturity.
The process of senescence in these
cases is usually exemplified by a reduction in reproductivity with
time (Suntzeff et al.
1962).
Senescence, then, is a natural process
which occurs in mammalian and many nonmammalian species
although its proportion to the total life- span is largest in man.
Senescence has thus evolved as one of many processes of living
systems.
For decades theorists have attempted to explain why
senescence has changed in character in advanced and evolving
species, though by definition it reduces their population size.
Is
aging adaptive?
At the turn of the century, Weismann (translated from German
by Comfort
1957a) proposed that the selective advantage of
senescence lies in ridding a species of burdensome members who
are no longer efficiently reproductive.
Intrapopulation numbers
are sacrificed in order to promote total population growth.
Brues
and Sacher (1965) have recently reiterated this argument.
Medawar (1957:20) disagrees with Weismann, Brues, and
Sacher.
He has stated that senescent members of a population may
6
Erd;;,;;;-~retain
a social function.
Dobzhansky
1 (1958) along with Medawar (1957:68) revise Weismann's theory.
I_,
I. They state that selection only operates on the members of the
l
I
reproductive age bracket of a species.
Selectively, the postpone-
' ment of deleterious traits until the end 9f the reproductive cycle
equals their elinlination altogether.
Hence, senescence is the
result of the delayed appearance of these traits.
The difference
between Weismann's theory and that of Medawar and Dobzhansky is
that Weismann has concluded that senescence was favorable for the
survival of the species, while Medawar and Dobzhansky theorize that
senescence may not be favorable, but that nature has no means by
which it can be elinlinated.
Williams (1957:402) has modified Medawar's argument by
stating that senescence is not a selective "accident." He postulates
the existence of pleiotropic genes which programmatically delay
senescence until the postreproductive period, which is indirectly
i demonstrated by the fact that appearance of senescence occurs
almost simultaneously in many systems of the body.
Williams'
theory, like those above, has not yet been directly valid;;tted.
A problem with each of the theories mentioned is that none
ask why the reproductive period itself is linlited in time.
One is
left to assume that a selective advantage for life-long reproductivity
does not exist.
This is a particularly interesting question for the
7
f"anthropologist to s~udy.
For example, how might e~~~~~
l
l been affected if the human generational span was increased to fifty
l
l; years,
or if each female was capable of producing thirty offspring?
Has selection only recently begun to operate on the last decade of
the years of human reproductivity?
If prehistoric man died before
his repr-oductive years were completed and Medawar' s theory is
acceptable, then senescence may begin at the age of thirty and cause
the end of the reproductive cycle, along with all other physical
changes.
The anthropologist might also consider how evolution will
be affected by the increasing chance for selection to operate upon
aging populations as the numbers of old persons proportionately
increase.
And finally, the traditional definition of selective
advantage (total number of surviving offspring) will have to be
modified to apply to entire cultures, rather than to individuals.
term
11
The
selection 11 can have no meaning when applied to postrepro-
ductive populations unless their existence enhances or jeopardizes
the fertility of the culture's youthful population.
Fortunately for the anthropologist, several theorists have
attempted to explain the evolution of aging in terms of factors which
are specifically applicable to man rather than to all animals.
Man
is unique in that certain cultures are ''aging 11 ; the elderly population
is growing in numbers more rapidly than the youth.
This rise is
actually due to the simultaneous control of infant mortality and
8
r Hen~e,
I
until old age (Leaf
I
l
------~-~-------,
;;;_ost children at birth in some cultures cart expect to live
1973).
Man is also unique because the mean length of life has been
extended without a distinguishable genetic adjustment.
Less than
five percentof the prehistoric men lived past forty years (Vallois
1961).
Dublin (1939) found that the average Roman lived 25 years,
a seventeenth century Englishman lived 33. 5 years, a nineteenth
century Swede lived 41. 5 years, and today' s modernized populations have an expected life-span of 63 to 69 years.
Since pan-
human genetic changes do not occur this: rapidly, factors other than
heredity must be involved.
The generally-accepted explanation for this extension of the
human life expectancy is that prehistoric human populations were
benefitted rather than burdened by old members (Williams
1957).
In fact,· delayed maturation necessitated the presence of experienced
individuals who cared for the young, while increased brain size
made advanced learning possible.
The elderly actually performed
two very important functions; first, their accumulated body of
knowledge was drawn upon by the population at large and second,.
they cared for and educated the young.
Furthermore, many
historic populations were able to accommodate increased numbers
of dependent members (McCance and Widdowson
1957; Williams
1957).
1955; Verzar
9
____,_
r
This explanation also extends into the animal world.
-
One
...
j interesting nonhuman study of infant care and life- span was made by
II
!{
Maurizo (1959) on bees.
She found that the need to care for the
young was the most influential variable in the life- span of the adult
'
nursing bee.
Harlow (1962) obtained similar results on maturing
infants, as opposed to adults, when he tested mother-reared and
mechanically- reared monkey infants.
More studies such as these
should be conducted in order to determine the relative importance
of infant care in relation to maximal life- span.
The above-mentioned explanation of human culture and life
expectation was actually preceded by an early mathematical equation,
known as the Gompertz equation, which predicted the mortality
curve of a species.
The Gompertz equation (in Clark
1964: 213)
was devised during the nineteenth century to explain why the human
species was multiplying more rapidly than other species.
Gompertz
hypothesized that protective devices kept humans and advanced
mammals alive until close to the biological life-span limit, so that
the
mortality rate was not random (as it is in species which die
'accidentally,
1
i.e., due to predation or starvation).
The mortality
rate of man and a few other species is a logarithmically-increasing
curve.
For example, at age ten (the lowest point in the curve) a
human might have a two percent chance of dying that year.
At age
sixty-five a human might have a thirty percent chance of dying that
1
10
~year. l:h~~-;,_-;;;lture's Go~m-.;-;w-ity ;;-,;rv~!
used as a measure of life expectancy analysis.
1
I
Of course, this
equation does not explain what those protective devices are.
·
A
century passed before gerontologists spoke of the beneficial effects
of an elderly human population.
The Gompertz mortality curve of modern human populations
1
varies greatly (Rosen
until old age.
1961), along with the chance for survival
The difference, however, is not due to variable
selective forces nor to cultural differences in physical conditions of
senescence.
The physical manifestations of senescence are pan-
human; the selective forces for longevity do not influence only
western nations.
.,
The difference in achieved life- span is due to the
cultural means of disease prevention attributed to western
populations.
Because gerontology is a medical field of industrial nations,
the majority of modern gerontological research ignores nonwestern
peoples.
This is unfortunate because human studies should include
all cultures.
This western-oriented approach will be evident in
many examples provided in this thesis; senescence is not, however,
unique to industrialized societies.
In conclusion, it has been shown that not only has senescence
i
l
evolved along with man, but that studying senescence itself discloses'
much about man.
Aging is both a cause and an effect of delayed
11
,--.....--,------~
II
~
-·--
--·"')
anthropologist, un,like the gerontologist who studies all species, is
.
I primarily concerned with how the aging process developed in man.
I
Death is now delayed until long after the period of reproductive
I
fitness because aging is functional and specialized to an advanced
!
degree only inman.
The next chapter will deal with the specific mechanisms which ·
initiate senescence.
Gerontologists usually label these mechanisms
as the causes of aging.
In this thesis, however, genetically-
programmed senescence mechanisms are regarded as the result of
a selective process.
The following chapter will discuss environ-
mental factors which influence the aging process.
In this thesis,
the influence of the environment is regarded as evidence of the
selective process at work.
I
Chapter II
l
GENETIC THEORIES OF SENESCENCE
I
It is extremely difficult to categorize and describe the
.
numerous theories which revolve around the general theme that
aging occurs as a result of internal, or genetic, forces.
difficulty is certainly not due to a lack of evidence.
This
To the contrary,
'
1
there exists an abundance of data available today that points to a
genetic source for the aging process.
The problem which plagues
gerontologists is that the data never conclusively prove that one
theory is more correct than another.
In fact, identical pieces of
data are often cited by opposing gerontologists as evidence for their
respective theories.
The result of this ambiguity is that many
schools of thought have arisen, often utilizing the same laboratory
tests.
What is more, established theories are often restated with
a single additional feature and a new school of thought is formed.
Therefore, many of the theories are interrelated and overlapping.
In this chapter, I will attempt to categorize theories which
do reflect different assumptions and distinct kinds of evidence.
theories will be presented in the following sequence:
The
(1) metabolic
waste theory, (2) endocrine theory, .(3) metabolic rate theory,
(4) cellular death theory, (5) homeostatic failure theory, (6) collagen theory, (7) somatic mutation theory, (8) inl.munologic theory,
12
13
r-and (9) free radical theory.
1,
chronological formation.
This order loosely conforms to their
An anthropological analysis of the
theories will conclude the chapter.
I
;
A.
Metabolic Waste Theory
One of the earliest theories of aging proposed by a gerontolo-
gist was Metchnikoff' s metabolic waste theory (interpreted from
Russian by Medawar
1957:24; Birren
1959:130).
In 1908
Metchnikoff stated that toxins accumulated in the intestines; bacterial decomposition in the intestines then poisoned the host.
To
prevent his own intoxication, he consumed yogurt cultures which
supposedly prevent bacterial accumulation.
Metchnikoff later died
in his sixties.
Despite Metchnikoff' s failure to prove the validity of his
theory by preventing his own death, the metabolic waste theory
persisted in the field of gerontology in updated forms.
In 1923
wastes in the blood were located which interfere with cell respiration (explained by Curtis
1966:20).
Unfortunately, juvenile blood
was contrasted with normal adult blood, rather than senescent ·.
blood; therefore, the results do not establish waste products in the
blood as a cause of the senescent-years aging process.
Today waste theorists center their arguments around the
presence of pigment waste granules (called lipofuscin) inside the
cell walls.
Newborn humans and dogs have no such pigment inside
14
~alar
spinal cord cells.
Senescent cells, however, have
II an increasingly larger percentage of lipofuscin which,
I
according to
l
proponents of this theory, interferes with cellul.ar function (Brody
Muscular tis sue also accumulat~s lipofuscin.
1960).
Although the
young heart contains almost no lipofuscin,, by age eighty up to
thirty percent of the heart weight is pigment (Curtis
1966:20).
Other evidence supports the metabolic waste theory in an
indirect manner.
Ammonia, a waste by-product of normal cell
· function, has a three-and-one-hal£ times higher concentration in
old rats than in young rats (Oeriu
1964:54).
Ammonia is toxic to
the central nervous system, and may play a part in its gradual
decline.
Andrew (1964:92) proposed that accumulation of lipofuscin
in the cell's cytoplasm is not the crucial waste product involved,
but that the intrusion of portions of the cytoplasm into the nucleus
plays the key role.
He found that remnants of cytoplasm remained
in the nucleus of old rat and old human cells.
The nucleus, then,
grows in relative size to the cytoplasm and the added cytoplasmic
material detracts from nuclear regulation of the cell.
One last
piece of evidence is that the human kidney filtration rate is reduced
to an average of 69 percent of the youthful function in senescent
adults (Leaf
1973).
Waste accumulation may then be an element
in the aging process.
Although waste accumulation is one aspect of the aging
15
~----------·--~----·------------------------~---------------------------~,
process, there is no reason to assume that it is the cause of aging.
Curtis (1966:20) noted that some humans die at an old age with little
accumulated lipofuscin and that rodents can function well although
their cell lipofuscin content may be high.
Moreover, gerontologists
have failed to find a direct link between waste accumulation and the
numerous physical changes which occur during senescence.
Because
of these exceptions, and because of the simplicity of the metabolic
waste theory, waste accumulation is generally considered to be a
symptom, rather than a cause, of the degenerative aging process
(Kimmel
. B.
1974: 354) .
Endocrine Theory
Senescence has always been conceptually linked to the end of
the reproductive cycle in the female and to the male climacteric.
In the medieval past, testicular extracts were administered in order
to protect patients from early aging, despite the fact that eunuchs
live as long as other men (Curtis
1966:21).
Modern hormone experiments have yielded direct evidence
that the length of the life- span is related to reproductivity in some
species.
For example, when the flowering of plants is delayed, the
plant lives longer; salmon die after a single mating; the May fly
emerges as an adult without an eating apparatus, hence has evolved
only to mate and die (Hyndman
1952:551).
It is well-documented
that human widows have a higher mortality rate than married
16
r wo~n
[
l
of the same age, although the cause
nonhormona1 factors (Comfort
1964:181).
i;-~~:w~lly ..attributed
to--·;
But facts such as these
. do not establish reproduction as the only factor involved.
Because
human reproductivity varies considerably, while the aging process
j
is relatively uniform, the amount of re:production is not acceptable
as a cause of aging.
Both the aging process and the end of the
reproductive cycle may have a common cause.
Because gerontological studies of reproduction are inconclu·j
sive, endocrine theorists usually state that the gonadal hormones
'
themselves are guided by another hormone system, the pituitary
gland.
Although experiments have not shown specifically that the
pituitary gland causes aging, hormone production which is indirectly
regulated by the pituitary does change through time.
For example,
the content of elastase in elastic tissue, produced by the pancreas,
is reduced at the same time arteriosclerosis, or hardening of the
arteries, occurs.
When the hormone elastase is injected into old
rabbits, their elastic tissue regains its youthful properties (Lansing
1955).
The same result has been demonstrated in humans (Strehler
1964).
Other hormones which are regulated by the pituitary gland
have shown similar experimental results (Curtis
1966:21).
Thomson and Forfar (1950) also claimed that childhood progeria, or
infantile aging, is the result of a pituitary malfunction.
Some evidence supports the endocrine theory without
17
ji;;;ii~i~-;iliepituit~ry ~l~;d~ s
ultim;te
c~:;t~cl.. Old ~~-gan~· can~-~
l
l
be transplanted into young animals and, within a youthful hormonal
l'
environment, former function revives (Parkes
l
1955).
Rat ovaries
j
l
regained reproductive capability in that experiment.
Another
convincing argument concerns Simmond's disease, a degeneration
of the endocrine system due to a sudden shock.
The symptoms of
this disease are baldness, weakness, impotence, and white hair
(Comfort
1965 :72).
Hence, if an endocrine "shut-down" causes
the sy:m.ptoms of aging, then the true cause of senescence may lie
somewhere within the endocrine system.:
Is senescence then the absence of something?
ogists say no.
Most gerontal-
When hormone supplements .are given, the subject
1964:236).
still ages (Comfort
When attempts were made to
prevent pituitary aging, "monster" laboratory rodents were
created· (Comfort
1965:86).
Although some symptoms of aging
may be caused by endocrine breakdown, something changes or is
added to the system which causes the hormonal imbalance.
The endocrine theory, like the metabolic waste theory, suffers
from a restrictive view of the organism.
Changes which occur
during senescence are so extensive that unicausal
theories cannot
explain the process.
Genetic theories which are discus sed in the following sections
involve many systems of the body, cells, or even molecules.
If a
18
genetic mechanism has evolved which initiates the aging process,
then the following theories may even~ually reveal the cause of
senescence.
C.
Metabolic Rate Theory
Another early theory of the. aging process is the metabolic
rate theory, or rate of living theory.
Metabolic theorists assume
that each individual is born with a finite amount of energy common
to its species.
Because smaller animals burn energy faster in order
i to maintain homeostasis, they use this supply and die more rapidly
than larger animals (Verzar
of 1908 (explained in Comfort
1963:9).
Hence, ·Max Rubner's "law"
1965:47) states that length of life is
inversely proportional to metabolic rate, and thereby body size.
Pearl (1922) tested calorie use as a function of energy
expenditure.
When Drosophila lived at 10° Centigrade, their
metabolic rates were lower and their life-spans longer than at 30°
Centigrade.
This test was also applicable to invertebrates, fish,
and amphibia: the poikilotherms, or cold-blooded animals.
Therefore, when calorie consumption dinrinishes: the body energy
reserves are used at a slower rate and the subject lives longer.
Recently, Sacher (1959) tested assorted variables as possible
predictors of life-span on mammals.
He found that body weight
accounts for 60 percent of the regression line variance.
weight accounts for 79 percent of the variance.
Brain
When both factors
19
are combined, 84. 4 percent of the variance is· explained.
So Sacher
added another feature to the energy consumption theory: the brain's
energy use.
Curtis (1966:28) noted another experiment with a homoiotherm,
or warm- blooded animal.
Rats died earlier when kept at cold
temperatures because homoiotherms, unlike poikilotherms, increase
metabolic rate in order to maintain body heat.
Another rat experiment was conducted by Bourlier·e (1957},
who retarded rat metabolic rates by underfeeding one group.
The
slow-growing hungry rats recovered quickly from stress while the
fast-growing control group did not.
It is possible, then, to slow
the metabolic rate of warm- blooded animals, although the advantage
of the hungry group was probably due to the disadvantage of obesity
in the control group.
1
In the last two decades, metabolic rate studies have
to the cellular level.
~xtended
For example, tissues which are kept frozen
retain their youthful properties longer than the animal from which
they originate (Parkes
·;
1955}.
The preceding arguments point out that it is possible to retard ·
or accelerate the aging process, but again they do not explain aging.
Based on energy expenditure and body size alone, man could not
1
Nutrition will be discussed in detail in the following chapter.
20
l
,....._p_o_s-~--~-~--1-;·-1-iv~e-to_o_n_e_h_un_d_r_e_d_y_e_a_r_s_n,_o_r_p_a_r_r_o_t_s_t_o_s_lX-._t_y_y_e_a_r_s___
(Kimmel
I
1974:345).
And according to this theory, athletes should
die sooner than sedentary men, which is not the rule (Skinner
This theory of the aging process, then, is not applicable
1969).
to man.
The metabolic rate theory, like the endocrine theory, is no
longer accepted because it relies on the expenditure of something
. !
rather than on a basic change in the system.
Whatever ultimately
lies at the basis of aging also causes accelerated or delayed aging
when the metabolic rate changes.
D.
Cellular Death Theory
The internal mechanism which undoubtedly causes many of
the physiological and psychological changes of old age is the
eventual death of neural cells.
These cells do not have the ability
to replicate after maturity (Hyndman
1952:547), hence the brain
weight is reduced by eight percent during senescence (Leaf
1973:
52).
A few gerontologists have suggested that cellular death could
provide the answer to the cause of aging.
Comfort (1957a; 1965:95)
observed that creatures such as the sea anemone which continually
replicate do not "age"; they die due to accidents such as predation.
On the other hand, mammals which have certain nonreplicating
cells,· such as the neural and muscle cells, do senesce before dying.
21
f Bi~(l960) add~d that this~ptibility to gradual aging is the
I "counterpart" to learning ability,
benefits of reliance on the brain.
memory retention, and
othe:~;
Hence, that which makes man
neurologically human also makes man more likely to senesce than
other animal!'>.
If the counterpart theory is correct, one would expect that
men with more total brain cells than average (but not. necessarily
larger brains) would be less likely to become early victims of
senile-dementia.
A Stanford study of intellectually gifted individuals
(Muller and Ciompi 1968:23) tends to confirm this.
The study
showed that a high Intelligence Quotient positively correlates with
a delayed onset of senile psychoses.
Of course, one must assume
that the Intelligence Quotient measures the total number of learning
cells and that other factors, such as medical care and proper
nutrition, are not involved.
.,
The dubious evidence which supports the counterpart theory
is contradicted by other studies.
When nerve cells were
deliberately destroyed in rats, early aging did not occ'!lr (Comfort
1965:105).
Isolated rat studies, of course, do not necessarily apply
to other mammals or man, but Albert (translated from German by
Muller and Ciompi
1968:66) found that brain damage caused early
senility in men only if a familial predisposition existed.
In conclusion, it is widely accepted that neural cell loss is
22
~-respo~:;;;-;e for
I
1.:1
1
'
senile dementia, higher
stim~-;;~;:sholds,
decreased sensory sensitivity, and decreased reaction speed
(Kimmel
1974:373).
These are only a few of the extensive
symptoms of aging, however.
Most gerontologists conclude that
senescence involves not only a reduced number of cells but also
changing functions in remaining cells.
E.
Homeostatic Failure Theory
A very generalized theory of aging is the homeostatic failure
theory.
Yapp and Bourne (1957:25) and Medawar (1957:40) state that
; because natural selection no·longer assures fitness of senescent
individuals, then logically the first body mechanisms to falter would
be adaptability-regulation devices.
These include temperature
regulation, aerobic capacity, anabolic-catabolic processes, and
blood sugar levels (Lee
1969).
In actuality, old persons do show evidence of declining
homeostatic control mechanisms.
Because of reduced circulation,
the brain receives less oxygen than when the body was younger,
which may account for some of the neural loss discussed in the
previous section (Strehler
1969; Arnoff
1961).
Old workers also
sweat less during labor in a hot climate, thereby accumulating
excess body heat (Lind and Hellon
1962).
In addition, the aged do
not efficiently retain heat, as evidenced by their lack of shivering
in cold climates.
( Verzar 1963:27).
There are more
23
r
temperature-related occupational accidents of
l
young workers (Birren
o~:~-1
1959:429) . . Blood chemistry also becomes
variable; albumin protein in blood decreased by 16 percent by age
65 (Oeriu
1964:30).
Rat studies confirm the homeostatic theory.
Aged rats do not
efficiently maintain body temperature during heat, cold, and low
pressure (Verzar
1963:27).
Blood serum regulation of various
vitamins changes without dietary change, especially pantothenic
acid, riboflavin (Bz), ascorbic acid (C), and nicotinamide (PP)
(Oeriu
1964:55).
Clearly, this generalized homeostatic failure theory of aging
better explains why individuals .die than age.
It is also self-
verifying; homeostatic failure always causes death in the end.
Because of these arguments, the homeostatic failure theory is
almost universally dismissed as one aspect of the other theories of
aging (Curtis
1966:17) and is rarely even discussed.
On the other hand, the great benefit of this theory is that it
provides a multicausal model composed of
select~on
environmental effects, and biological mechanisms.
forces,
Unfortunately,
it appears tfiat its proponents have not argued its validity as an
independent theory.
F.
Collagen Theory
The collagen (or colloid) theory, unlike the homeostatic theory,
Z4
Fs highl; specific.
I
Collagen is the most abundant protein in
mammals; it is contained in skin, b<;>ne, cartilage, tendons, and
! blood vessel walls and is responsible for their elastic properties
~..: (Sinex 1964). With time, collagen becomes increasingly organized,
causing tissues to become rigid (Casarett
1964).
This rigidity.
results in such conditions as elastosis, or wrinkled skin (Verzar
1963:43), and arteriosclerosis, or hardening of arterial walls
' (Hershey
1974:144).
It is the cumulative effect of collagen change
that initiates the aging process according to the colloid theory.
During the last two decades this theory has been called the
cross-linkage theory because it has been found that chemical crosslinking in large molecules is responsible for the increased rigidity
of collagen (Comfort
1965:110). ·One of the specific chemicals
involved is the calcium ion (Verzar
1963:43).
Cross-linkages are
held by some gerontologists to be responsible for the aging process
because their effects are symptomatic of aging: reduced tissue
elasticity, increased brittleness of bone, and cellular dehydration
(Bjorksten
1958).
On the other hand, more is involved in aging than 'Cosmetic
changes of the skin and hardening of the arteries.
Collagen changes
are indeed responsible for some symptoms of aging, but other
regulatory devices are also involved.
If this were not the case, a
rat and an elephant, each born with life's supply of collagen, would
l
)
25
f
age-:nd die at the ·same time.
Therefore, the collagen theory of
I aging does not adequately explain the numerous effects of aging.
G.
Somatic,Mutation Theory
The recently proposed somatic mutation theory purports to
explain many of the changes which occur during senescence.
This
theory arose out of the studies of atonric warfare victims after
World War II (Curtis
1966:43).
The radiation damage which
occurred (sexual decline, balding, arthritis, and so forth)
resembled the aging process itself.
In addition, it was
demonstrated that by age 75, 15 percent of body cells do not have
.~
·the normal 46 chromosomes (Jarv:ik
1969) and that there is at least
one mutated characteristic in every cell by the age of 90 (Hershey
1974:54).
The fact that anincrease in the mutation rate and aging
occur together, therefore, has led many current gerontologists to
conclude that somatic mutations cause the many effects of the aging
process (Clark
1964:230).
2
Gerontologists are divided,· though, on the question of the
location of these mutations.
Rose and Bell (1971 :35}, Strehler
(1971:45), Danielli (1957), and Curtis (1966:64) agree that somatic
mutations accumulate in the DNA of nonreplicating cells because
2 Some theorists claim that radiation itself is the cause of
aging. This topic will be discussed in the following chapter.
26
--~-·--...,
only dividing cells have the opportunity to "select out" mutant cells,
only higher animals with many nondividing cells senesce, and
nondividing human oocytes (ova) from old mothers accumulate
chromosomal errors and cause birth defects such as mongolism
while dividing spermatogonia from old fathers do not.
This implies
that old cells are defective.
Other somatic mutation theorists state that senescence
' originates in the replicating cells.
Hayflick (1970) first demon-
strated the Phase Three phenomenon which underlies this
hypothesis.
He found that human fibroblasts, in vivo and in vitro,
survived for only 50 doublings before dying.
At some point,
accumulated changes in the cells pas sed a critical level and caused
cell disorganization.
The aging process, therefore, is determined
by the speed of the replication process (Failla
1958).
Two examples of mutations of dividing cells are as follows:
Szilard (1959) proposes that "hits" of ionizing radiation on the
chromosome accumulate until a critical value is reached when the
replicating cell dies; Blumenthal and Berns (1964:303) theorize that
a point mutation, or single molecular change, causes a substitution
of the purine or pyrimidine base and cellular information changes.
Both proposals deal specifically with clonal replication _of cellular
errors.
1
Hayflick' s phenomenon is not undisputed.
Curtis and Tilley
27
r·
I
(1971) and ~550)'~dd tha;;he
l~mit in number
cellular doublings is beyond the li£e 0 span of the animal.
of
Hence,
I the end of cell replication could not be the cause of death.
Their
remarks are not conclusive, however, because their results were
obtained from mice and artificially-grown cultures.
Despite whatever flaws exist in the somatic mutation theory,
it receives the majority of research grants and is well-respected
by gerontologists who subscribe to genetic theories of aging
(Comfort
1965:106).
This acceptance is due to the fact that the
theory is generalized enough that it can be stretched to meet many
explanatory requirements of an aging theory.
For example, the
cellular deatl). theory relates to the somatic mutation theory if one
explains nerve cell loss as the result of accumulated mutations
(Comfort
1965:97).
It also relates to metabolic rate theory; the
chromosomes of mice mutate thirty times faster than do those of
man (Sacher· 1959:136) because their metabolic rates and cell
replication rates are proportionately quicker.
Even though the mutation theory is
compre~ensive,
it relies
upon the random mutation of genes throughout the body, while the
aging process affects body systems selectively (Maynard Smith
1962:121).
Other, highly regular, external factors mitigate
internal factors such as cellular mutations.
These external factors
will be discussed in the environmental chapter of this thesis.
;
>>•~--"~~----·
.. ··~ ....,.,, ....~--->'>O'"'_.,-""'<•'V_.~...~ .. ~ .. ,..,.,-
..... ,, ..... ~-· ..r~~----~-A•--
--~~..._.,,_._,_,.,,~
. . . . ,.. _. . _. . . .
,....~--~--~-~~·M<--~___.,.......,.,..._.,<.>,....,_,.,..,_,_
..,.......... _,
..
·--·-~- ·-~~··•"""'"'"~
28
The following two theories which deal with immunology and
Walford (1969:11) criticized the somatic mutation theory for
being untestable and unmeasurable and proposed instead the more
specific auto-immunity mutation theory.
He noted that lymphoid
cells are altered at the same time the mortality curve rises and
that circulating antibody levels decrease with advancing age;
moreover, the proportion of self-destructive antibodies increases
·with age (1969:44-46).
Walford (1969:15) reasoned that mutations
in the lymphatic system produce mutant cells which mistakenly
recognize the host as a foreign body.
This auto-immune reaction
might cause the diabetes which begins during old age, elastosis,
arthritis, arterial lesions (Walford
and Bell
1969:80), and cancer (Rose·
1971 :36).
The advantage of the immunologic theory over many other
genetic theories is that it correlates with environmental data
(Walford
1969:154-186).
For example, Walford theorizes that
the antigen systems of poikilotherms are temperature-dependent
and undernourishment slows the replication of lymphatic cells.
3
3 undernourishment delays senescence; this will be discussed
in the following chapter.
29
~Th~~-;,logic theory, however, better explains the diseases of-·•
l
I
I
;
senescence# such as the diabetes and arthritis which first appear
during senescence, than the cause of the process itse.lf.
I.
Free Radical Theory
The most recent of the genetic theoi-ies of aging is the free
radical theory.
Harman (1956) proposed that two by-products of
normal metabolic oxidation# hydroxide (OH) and hydrogen dioxide
(HOz)# are the cause of senescent decline.
These electrically-
charged free radicals produce molecular microlesions and alter
cellular function when they chemically bond with tissues undergoing
metabolic processes.
Any outside influences that change the rate
of oxidation# then, should affect the average life- span, which does
occur.
The highest human cancer rates occur where the diet is
high in unsaturated fats, which are oxidants (Harman
1969).
When
antioxidants such as BHT, vitamin A, vitamin C, and vitamin E are
added to the young mouse's diet above the average rodent intake,
the mouse's life-span is lengthened (Hershey
1974:87).
Moreover,
high metabolic rates correlate with both increased oxidation and a
reduced life- span (Harman
1961). · Therefore# Harman has shown
that when free radical-producing operations are slowed, the
average life- span is increased; the opposite occurs when oxidation
is increased.
Clearly, the free radical's fundamental nature makes it a
30
Etial
cau~~~p~o~s-:£ ~gi~~-:-Agi;; is
: pan-mammalian, so a basic process such as oxidation could be
j involved in the initiation of aging. Oxidation by-prodUcts might
I
then be responsible for accumulated wastes, the correlation of body
!
;
size to life- span, cellular death, homeostatic system failure,
colloid changes, somatic mutations, and immunologic reactions.
Because oxidation can also be influenced by environmental factors,
it provides the gerontologist with the most comprehensive of genetic
theories of aging.
The direct causal link of free radicals to
senescence, however, remains to be demonstrated.
Other evidence supports an internal basis of aging exclusive
of the environment ·without favoring any particular theory more _
than the others.
1.
This evidence is:
familial- Beeton and Pearson (1901) observed that
some lineages contain more unusually long-lived
members than other lineages.
Moreover, siblings
often live to approximately the same age.
Longevity
may then be an inherited trait (Pearl and Pearl
1934:
53).
2.
heterozygotic - Hybrids live longer than inbred strains
of tested animals; the heterozygote is more fit.
Length
of life is therefore not an "additive" trait (Maynard
Smith
1 9 57 and C hai
19 59).
31
3.
sex-related - There is an almost pan-mammalian
female advantage in life-span (Kallman and Jarvik
1959:230).
One might then speculate that aging is a
sex-linked trait.
4.
species-related - The range of .life- span variation among
the species is greater than the range within any single
species (Shock
1960); life-span limits are determined
by the genetic code of each species.
In conclusion, each of the proponents of the various genetic
theories of senescence has presented a great deal of evidence
upholding a particular inborn mechanism as the cause of senescence:
Further evidence endorses a generalized genetic theory, but not
any one mechanism.
The essential fault with most of the theories is their
genetically deterministic nature; internal forces appear to be
independent of external forces.
This is not a realistic image of
living organisms.
Anthropo~ists, unlike the majority of the gerontological
geneticists or biologists, deal with multiple causal factors.
This
is the proper approach to a problem such as the cause of aging
because both internal and external factors influence senescence.
An anthropologist would study senescence differently in several
ways than a geneticist.
First, most genetic theories treat all
32
, accept that different factors, suc.h as social organization, may
influence each species.
And culture is one factor that applies only
to man.
Second, most genetically-oriented gerontologists discard
environments as incidental to the study of senescence.
To the
anthropologist, the cultural, physical, and psychological environment act as selective forces which affect the genetic code.
And last, anthropologists distinguish between capability and
attainment.
In the gerontological sense, this means that the
genetic basis of the species determines the maximal number of
functioning years before senescence must begin, while the real
expectation of each individual is usually considerably less than the
maximum.
Because so few people live to the human potential of
110 years (Kimmel
1974:344), environmental fa<7tors and genetic
variability must greatly influence the attainment of the species'
potential.
Consider further that the forces of selection only act
upon those traits that have been tested in a given environment.
Nothing else is "real" in the course of evolution; natural selection
operates only on phenotypes (the physical expression of the genotype
I
'
33
r
interacting with the environment), not on
'
potentials).
genotype~~
Because physical anthropology concerns itself with
selection, then the anthropologist must study se?-escence as a
human process undergoing selective evolution.
The following chapter will discuss v:,:-hy some recent
gerontological studies have begun to evaluate the environment and
how it influences the aging process.
Among the environmental
factors which will be listed are stress, the physical environment,
the cultural environment, and the psychological state of the
individual.
..
Chapter III
rI
ENVIRONMENTAL THEORIES OF SENESCENCE
Gerontologists have tended to accept the fact of
aging as an inescapable process, built-in obsolescence, if you please .. ~ Yet, such a conclusion is
by no means warranted by whatever evidence we
have at hand ... Living systems must interact with
-an environment. (Brauer 1962:197)
i
A recent trend of some gerontological studies has been to
examine senescence as it occurs within the environmental setting
of a given species.
The purpose of this chapter of the thesis is to
examine the theories of gerontologists who hypothesize that the
environment is a key variable in the aging process.
These
gerontologists are primarily concerned with life expectancy rather
than an abstract potential life- span.
Many envi"ronmentalists have
come to the conclusion that environmental variables are more
important than biological variables in determining how and when the
individual senesces (Clark and Anderson
1967:4; Jones
1959).
One of the reasons that environmental factors are being
studied more frequently is that population demographics are
changing.
Some western societies are "aging"; that is, the
relative proportions of elderly members are growing at the expense
..
of the younger groups (Darling
1955:132).
Another aspect of this
demographic change is that life expectancy is increasing; the white
American born in 1969 could expect to live an average of 23 years
34
35
,--------------:
longer than the white American born in 1900 (Leaf 1973).
I
1,1
I
j
These
changes are occurring too rapidly to be the result of a change in the
genetic structure of senescence.
l altered,
It is the envirorunent that has
enabling some societies to
genetic potential (Jones
1959).
mor~
closely approach the
It is impprtant to realize the
significance of this interpretation; humans may never have
approached their biological maximum in nature because of environmental stress.
A cultural advancement, which is itself an aspect
of the envirorunent, was needed in order to relieve stress due to
disease or malnutrition.
Another reason that environmental factors are being
examined by gerontologists· is that the envirorunent determines the
genetic potential of a spec_ies to some extent.
An example of this
is early man's probable loss of body hair associated with colder
climates and the use of clothing, according to Muller (1959).
A very
interesting example was provided by McCracken (1971), who found
that some human populations have evolved an adult lactose tolerance
in response to milk-drinking habits.
An ability for adults to
consume milk is an evolved trait which is not evident in societies
which do not drink milk, such as hunters and gatherers.
If cultural
and physical envirorunents alter the genetic endowment of man in
cases like these, then the environment may also have ultimately
4
created the "programed" biological decline known as senescence.
36
---------
Although enyironmental gerontologists may agree that the
Unlike the biological gerontologists
Selye (1960; 1970) and Jones (1956;1959) hypothesize that aging is
totally due to environmental stress and the resultant injuries.
The
internal process, therefore, is triggered only by external forces.
The second school of thought, or rather collection of many
suggestions, states that outside forces strongly influence an
inherent process.
This chapter of the thesis is organized in accordance with
these two schools.
The first section deals exclusively with Selye's
and Jones' stress theory.
The next three sections treat aspects
of the modified stress theory, as I will call it, separately: the
physical environment, the cultural environment, and the individual
psychological environment.
I will conclude this chapter with an
anthropological interpretation of the environmental approach.
A.
Stress Theory
Selye (1960; 1970) has stated that each individual is born with ,
I
a finite amount of adaptation energy.
Stressful events which occur
after conception reduce the supply of adaptation energy.
The
severity and onset o£ senescence are then determined by two
j
j
37
r·.r~c;ors:
the genetic endowment at conception and the rate at
,;hl:;-h .. ,
I the adaptability is ·expended.
I
l
!j
Jones (1956; 1959) emphasizes that childhood disease is an
important stressful agent.
He observed that populations with the
lowest mortality rates also controlled
diseases.
The inversewas also true.
~any
of the childhood
Jones (1956) concluded that
early damage related directly to later stress resistance; adaptation
energy is retained if early injuries are reduced.
Other evidence which supports the stress theory is provided
by radiation studies.
Although most radiologists claim that
radiation damage only mimics aging, a few theorists hypothesize
that aging is the result of life-long background radiation injuries.
For example, Lindop and Rotblat (1962) demonstrated that there is
a straight-line curve between graded doses of radiation and the
reduction in life- span of mice.
If laboratory life- span and
radiation dose are proportional,. then natural life- span may relate
to the continual background radiation of the planet.
Hollingsworth
et al. (1965) proposed that the same results occur in man.
In
another study, Upton (1960) outlined the effects which resemble
aging on radiologists who have a high occupational radiation danger:
atrophy of the iris, atrophy of the epidermis and collagen, hair
graying, degeneration of the elastic arteries, and atrophy of the
kidney, adrenal cortex, and ovary.
38
jN~ ;;.di~tion..effects
I
l.l
l
replicate normal aging.
resemble aging, they do not
The contractility of tendon collagen
remains normal, there is not a neural.cellloss, and other nonreplicating tissues remain functional during radiation (Upton 1960}.
These tissues do not retain normal func.tion during senescence.
Casarett (1964:129), Comfort (1964:254}, and Demoise and Conrad
(1972) concur that radiation damage increases the disease level and
mortality risk, but that senescence and disease are separate.
Senescence occurs without radiation-induced disease.
Moreover, Curtis (1966:30} argues that the fundamental
weakness of the stress theory is that Selye (1960} has not dis tinguished between disease and senescence.
For example, if stress
is artificially removed, the individual still ages.
Selye has not
shown whether the absence of stress imparts eternal youth or
disease-free aging.
Furthermore, if an individual dies at age 25
after a long illness, has he aged?
Clearly, not all progressive
degeneration is senescence.
Curtis (1966:34} also criticized Jones (1956} for his
conclusions regarding childhood disease and aging.
When past
medical histories of aged Swedes were compared, no pattern of
disease-free youth was found.
In fact, a normal recovery from a
l
childhood disease left the patient without any longevity disadvantage. ·
Hence, Jones did not satisfactorily prove his hypothesis that the
39
llogical result of a healthy
I
~hildhood
!
is a longer life.
Because there is no evidence that aging occurs due to
II
environmental effects only, this theory suffers from an overly
deterministic simplicity, much like many of the genetic theories of
senescence .. While the individual cannot operate in an environmentfree existence, neither is he without a biological basis.
The
broader studies of anthropology cause me to reject environmental
determinism and consider instead both the environmental and
genetic variables which influence a genetic system.
B.
Physical Environment Influences
There are a few puzzling ethnic enclaves of remarkably
long-lived individuals.
These groups have several environmental
factors in common which might begin to explain the longevity of
their members.
Vileabamba, Ecuador, Hunza, near Pakistan, and
the Soviet Caucasus are inhabited by genetic isolates located at high
altitudes.
The members of each culture also eat less meat in their
diets than members of Western societies and engage in strenuous
physical activity.
The combination of these factors results in a
reduced incidence of arteriosclerosis and its effects (Leaf
1973).
Except for diet and exercise which will be considered in the
following section, high altitude is the single physical environmental
variable that these cultures share.
Along with this, of course, is
the clean air enjoyed by high altitude dwellers (Medvedev
1974) and
!
40
than those of radiation.
Climate is another environmental variable that relates to
longevity.
The subtropical zone that extends around the globe
through Nigeria, Ghana, and Mexico promotes longevity when
economic variables are held constant; temperate climate is less
beneficial than subtropical but more than cold climate (Ciuca
1972).
The disease-related mortality rate increases during winter in those
areas which have severe climates in northern temperate zones
(Collins
1955).
Rural regions have lower mortality rates than urban areas in
the United States and Europe because of the cleaner environment
and a lower level of emotional stress.
The highest United States
mortality rates are in the urban east coast (Rose and Bell
1971 :38).
The highest longevity in the United States is achieved in South
Dakota, Nebraska, Minnesota, Iowa, and Kansas (Anonymous
1955), which are rural middle-class areas.
Hotcin and Sikora (1970) found .that the presence of debilitating
viruses reduced the life expectancy of mice.
itself appeared earlier in time.
Moreover, senescence·
Whether or not the same effect
41
f. occ~rs in man is d,isputable because a pathogen-free environment·-·-...)
I1
II
has not been tested nor been shown to occur naturally.
Countless physical environment factors could be listed.
An
;
l
example of how detailed this list might be is Schroeder's (1960) study
of water hardness.
He found that hard water is positively correlated
with reduced mortality and lessened risk of cardiovascular system
disease.
He neglected to consider other factors involved.
I have listed a few of the less-detrimental physical environments: high altitude, warm or temperate climate, rural setting,
and hard water.
Unfortunately, the list of potentially detrimental
environments, including highly changeable regional climate
patterns (Kleemeier
1959), smog (Ciuca
and abnormal radiation (Lindop and Rotblat
1972; Leonard, 1976),
1962), is endless.
Moreover, the physical environment is always linked to a cultural
environment.
For example, cultural and social factors determine
where a group lives and thereby its physical environment.
Therefore, I will discuss cultural factors in greater detail than
physical factors.
C.
Cultural Environment Influences
Naturally, human life expectancy is affected by cultural and
social variables.
Among these variables are: diet, exercise level,
medicine, marital status, smoking and drinking habits, occupation,
educat.ion, and economic status.
Because they are unique to man
42
r-and
l
I
!
~ce
aging, it is
rel~vant
that they be analyzed in an
anthropological interpretation of sen.escence.
None of these factors
"causes" aging, but each of them influences the aging process.
Therefore, culture and personal behavior themselves influence
; senescence.
1.
is diet.
One longevity variable that has been studied for decades
This is of particular interest to the anthropologist for three ·
!
reasons.
First, each culture defines a suitable diet according to
-I its regional accessibility, its social or prestige value, its physical
'
appearance and smell, and its economic practicality (Howell and
Loeb
1969; Queen
1957).
Second, the diet choice is also
determined by its practicality within a given physical environment.
And third, diet has played an important role in the evolution of man.
During the hunting phase of human evolution, man evolved the
exceptional fat-storage capability of mammalian hunters due to
feast-or-famine conditions.
animal proteins.
He also became dependent upon certain
With the population growth of the Neolithic period,
it became necessary to develop agrarian
starches.
econom~es
which cultivated
The result of this dietary change is that man is now
either overnourished, because of excess fat storage capability, or
malnourished, because of amino acid and vitamin deficiencies.
Obesity, the disease of overnutrition, and scurvy, rickets,
kwashiorkor, beriberi, pellagra, goiter, and anemia, the diseases
43
r
o:f
maln~t~ition,
l
1
are now pandemic
<N~-~~a~·"7975>.
.
Chronic malnutrition reduces the life-span and causes
senescence to begin earlier in life than might otherwise occur.
Shank (1975) and Aykroyd et al. (1949) studied Newfoundlanders who
were malnourished during World War II. They were short, prema-
; turely gray and wrinkled during their twenties and thirties, and died
1
at an early age.
Malnutrition caused early aging.
Moreover,
malnourishment may be more prevalent than is usually thought
; becaus.e nutrition needs vary greatly.
There is a five-fold range
I.
!
in human calcium requirements (from 3.:5 mg to 16.2 mg per day),
a ten- to thirty-fold range in vitamin A requirements, and at least
a five-fold ¥ariability in requirements of vitamin D, vitamin C,
thiamine
(B 1 ), amino acids, potassium, iodine, and other
B-vita:n:iins (Williams
1956; 1969), depending on individual
constitution and activity.
Therefore, it is possible that everyone
is deficient in at least one of the 40 requl.red nutrients of man
(Williams
1969).
There is a medical school dictum which states, "There are
old people and there are fat people but there are no old fat people"
(Ostfeld
1975:217).
There are few studies on man which confirm
this, but many studies have been completed using rats.
For
example, in Berg's experiment (1960; 1962) rats fed ad libitum
became obese.
Young rats fed 33 or 46 percent less than the
44
.· .
~
r
des~-:mount :·~d b:tter
o;er-all health, increased fertility,
cance~ lesion incidence,
j
reduced
l
life expectation.
!
received adequate nutrition while calorie intake was reduced.
1
i
and a 25 to 30 percent increase in
The restricted group was not malnourished; they
1
;
Therefore, overnutrition also reduces life expectancy.
Not only do malnourishment and overnourishment decrease
life expectancy, but the proportions of specific types of food also
influence longevity.
The ratio of saturated to polyunsaturated fats
positively correlates with increased risk of cardiovascular system
disease in human westernized populations (Walker
1969).
Life
expectancy and reproductivity of rats and mice are also reduced
when the sucrose to protein ratio is increased (Ross
et al.
1952).
1961; Visscher
Nutrition, therefore, is a factor that influences life
expectancy in several ways.
2.
Continual exercise is one aspect of the cultural environ-
ment that the three most long-lived peoples share (Leaf
Outside of those groups, the evidence is unclear.
1973).
While it is
physically detrimental to lead an unusually sedentary life (Leaf
1973), it is also hazardous to begin strenuous activity during the
fifth decade of life (Edington et al.
1972).
There have been too
few studies on humans to demonstrate what comprises the most
beneficial level of activity for a long life.
3.
Naturally, the presence of a "modern11 medicine in a
45
It does this by reducing the risk of
heart-vessel·disease, and brain-vessel disease, life expectancy
from age 65 onward would increase by only two years (Comfort
1969a).
Modern medicine treats diseases, not processes.
The female advantage in life- span is at least partly due to
; medical intervention.
For example, in regions such as Ceylon and
Pakistan where "modern" medical care is not available, women
have a shorter life expectancy than men because of death during
childbirth (Rose
1971).
The opposite presumably occurs when
prenatal medical care is practiced.
The use of oral contraceptives may further lengthen the
female life expectancy.
HUngarian women with several children
lived longer than other women because of gonadal hormonal
stimulation; the use of oral contraceptives artificially duplicates
that same hormonal protection (Rose and Bell
1971 :49).
Individuals
who take the medical conception preventative may live longer,
l therefore, than women who use other methods or none at all. Of
!
I
I
course, this hypothesis will not be demonstrated until the first oral
contraceptive users reach the normal period of senescence and
increased cancer and cardiovascular disease risks can be evaluated.
46
I
!
In conclusion, medicine's role in the aging process is to
insure that a greater proportion of a population reaches senescence
and later dies of degenerative disease.
Because modern medicine
is not a cultural universal, the proportion of aged individuals in
western societies is higher than in cultures where many young
persons die of acute infectious diseases.
4.
It is well-documented in western societies that married
individuals live longer than widows and widowers (Sheps
and Bell
1971 :46).
This is the result of social selection.
1961; Rose
Socially
unfit and unhealthy individuals are less likely to remarry than active
and healthy individuals.
Moreover, never-married men are more
subject to a violent early death due to suicide and murder than
married men (Rose and Bell
1971:46).
Never-married women
have the same life expectancy as married women, however (Beard
1962).
One would expect that the continuous presence of a spouse
would improve the life expectancy in nonwestern societies as well.
Unfortunately, I have been unable to locate data to substantiate this
i
hypothesis.
Birth order and child-rearing are important variables which
also influence life expectancy.
For example, children born very
early or very late during a mother's reproductive period are
oftentimes deprived physically, economically, and socially (Rose
47
r·an~
I
I
I
I1
l
-------,
Bell
1971:33).
Each culture defines a suitable age for women
to bear children, and thereby influences the health of offspring.
Another example of child care and its relation to longevity is birth
order.
If a cultural law of primogeniture or esteem for the eldest
child exists, .then the .oldest child will receive more attentive care
than his siblings (Rose and Bell
1971:34).
This may also result in
a greater chance for him to survive childhood.
Also, cultural
esteem for male children enhances their survival (for instance
among-Eskimos).
Marital status and child-rearing practices, then,
are another aspect of life expectancy estimation.
5.
Both heavy cigarette smoking and alcoholism greatly
reduce life expectancy.
Alcoholics have two-and-one-half times
the mortality risk of nonalcoholics, especially due to violent causes
(Tashiro and Lipscomb
1963).
Moderate cigarette smoking causes
the same increased mortality risk as alcoholism (Walker
1969) and
appears to accelerate the aging process (Auerbach et al.
1965).
6.
variable.
In many studies occupation was shown to be an important
Despite the fact that mid-level managerial workers have
a high risk of coronary disease (Reeder
1959), white-collar
workers are longer-lived than physically-stressed manual laborers
(Pfeiffer
1971).
Quint (1970) completed a study of men listed in
Who's Who in America.
Of these men, those in emotionally stress-
ful jobs had a reduced life expectancy. Journalists had the highest
48
lowest mortality rates.
Therefore, the emotional stress and
physical difficulty of an occupation relate to the longevity of the
worker.
7.
Educational level corresponds to occupation and this is
reflected in longevity studies.
College graduates live longer than
the white population as a whole, and of these, the honor graduates
live longer than college graduates as a group.
The lowest mortality
rate of' men listed in Who's Who belonged to the scientists, one of
the most highly educated groups (Rose
8.
1971).
Because social class and income level are usually
determined by occupation and education, the same results are
shown again: low income and a high mortality rate occur together
(Patno
1960; Stockwell
evaluated income.
1960).
Pfeiffer (1971) tested for self-
The short-lived individuals listed themselves
as economically uncertain.
Long-lived individuals, however, listed
themselves as comfortable.
Cause of death also relates to social class.
For example, the
social and ethnic practices of groups influence the types of diseases
that nright occur.
Abstinence from breast feeding is associated with
a high rate of breast cancer in upper income mothers; male circum- I'
cision reduces the risk of cervical cancer in women (Graham
l
1963). ·
The factors that have been listed in this section of the thesis
49
rare .biase.d toward western civilization.
!,:
This reflects the socio-
logical nature of the data that are available. An anthropological
exanrination of longevity data might reveal cross-cultural patterns
which supply more information than specific single-culture studies.
Unfortunately, the number of anthropological publications dealing
with this subject is small (see Barrows
1968; Hershey
1974;
Palmore 1971 b).
D.
Psychological Influences
In addition to environmental and cultural influences, the
individual's psychological profile affects expected life- span.
Of
working men, those who express job satisfaction live several years
longer than those who are displeased with their jobs; women live
longer if they consider themselves to be "happy" (Eisdorfer
1975).
In fact, .the female life expectancy advantage may be due to the
low-stress mode of life of women in many cultures (Palmore
197la; Walker
11
1969).
Hope 11 is often cited as the source of alleged recovery from
degenerative disease (Eisdorfer
1975):
Furthermore, self-
evaluated health is a more accurate predictor of life expectancy
than is a medical diagnosis (Palmore and Luikart
1974; Pfeiffer
1971).
Lastly, the Intelligence Quotient, often studied by psycho!ogists, predicts life expectancy, long-lived persons having.
50
~~ghe~~n-average
l
I
!'
I. Q.
s~~r-es
test measures, it positively
(Pfeiffer
1971).
Whatever the
-l
correla~es with educational attainment,
and thereby social class and income level.
Therefore, the I. Q.
score is, in reality, a measure of the potential for success in a
, western civilization (Cohen
i'
1973).
Its. relation to the psychological
background of an individual is remote.
The primary source of psychological influence on life
·j
1
expectancy, then, is the individual's sense of contentment and
self-evaluated well- being.
In conclusion, many of the environmental, cultural, and
psychological variables that were listed in this chapter are unique
to or most fully developed in man.
And each of them also jeopar-
dizes or contributes to the attainment of the biologically-determined
life .. span.
Therefore, it is important that they be included in a
study of the cause of senescence in man.
While geneticists often ignore environmental data altogether,
the theories of environmental gerontologists range from almost total
environmental determinism (Selye
1960; 1970) to those who state
that environmental factors are more important than genetic factors
(Palmore
1971:285; Eisdorfer
1975) to those who claim that the
environment merely alters the timing of programed events (Barrows
1968).
Because anthropologists analyze all factors involved in the
environment of man, and because the genetic basis is regarded as
51
... although it will probably be conclusively demonstrated some day that maximum possible life span
is determined by genetic inheritance, at the present
time it seems that the many intervening environmental factors such as nutrition, disease, stress,
psychological attitudes, social roles, and life-styles
probably outweigh the genetic factors in accounting
for longevity.
Although environmental variables that influence life expectancy
should be of interest to anthropologists, very little work has been
accomplished in this field.
To my
studies have not been conducted.
know~edge,
cross-cultural
Most of the literature available
is written by sociologists and psychologists, who are oriented
toward western cultures and individuals, respectively.
Although
life expectancy figures are available, cross-cultural patterns of
variables caused by other life-styles are not presently testable.
Furthermore, the interrelatedness of many variables might be
shown by anthropological studies.
For example, the physical
environment and economic exploitation variables are often parallel.
Out of this, certain economies, diets, and social class systems are
possible, along with certain medical, educational, and occupational
systems.
Hence, a single variable which influences life expectancy
is part of the wider cultural mode of living, which is the ultimate
unit of study for the anthropologist.
The field of environmental
52
r
gerontology, therefore, should expand in order to include anthro-
l
j pological analysis.
Chapter IV
CONCLUSIONS
Some of the variables that have been shown to be factors in
the aging process are metabolic .rate, cellular death and mutation,
radiation, climate, diet, smoking habits, and a sense of contentment.
These and numerous other factors which have been discussed·
in Chapters II and Ill reflect the biological, sociological, and
psychological orientation of gerontology.
dissertations in gerontology which were
Of the 547 doctoral
writte~
from 1934 to 1969,
one-quarter were in the field of psychology, one-fifth were
sociological, and one-fifth were written in the biological sciences-.
The remainder were in the fields of economics, education, public
welfare, health sciences, and social work.
an anthropologist (Moore and Birren
Not one was written by
1971).
As Scotch (1963:32) stated, "· .. what comes out of research
is not dependent on the nature of the problem to be studied but
rather on the way the problem is studied." This .is clearly
demonstrated in gerontology to date.
Biologists, sociologists,
and psychologists have written very descriptive gerontological_
research.
They have not, however, synthesized their results.
Hence, research results appear to be biologically, socially, or
psychologically deterministic.
Comments such as Strehler' s (1960)
53
54
r~·that ~gin~·~~es
l
1,
not occur in living tissues
environment are commonplace.
whic~ conta~t the --~,
Each field, therefore, seems to
operate independently of other fields which deal with gerontology.
111
I
The study of senescence, however, clearly requires a
systemic approach because of the multifactoral nature of the ca-q.ses
of aging.
approach.
Anthropology is one field which is amenable to that
The anthropologist would first ask how and why
senescence evolved (how it became selectively advantageous).
He
would then bring together the biological basis of senescence and the
various environmental and cultural variables which relate to that
biological basis and to each other.
Such a broad examination might
yield a more comprehensive explanation of the aging process.
The answer to the question of how senescence evolved and its
function in relation to man is that senescence is a preadapted
condition.
In other words, senescence evolved in mammals because
of one of many possible reasons: to insure a rapid span of
generational turnover, because selection could not eliminate
postreproductive flaws, or because postreproductive individuals
are burdensome; and was therefore a preexisting
hominids emerged.
trait when
How aging evolved to its present form in man
is the result of other factors which are most fully developed in man.
Among these factors are delayed maturation of offspring, dependence upon learned information for survival, and a greatly enlarged
55
r
I
--·----·---
memory.
..---•-•-,
---·-~-----~·---u---··-
Because lessons learned by experience accumulate,
.
i
i those persons with the most experiences are also most able to
1
i educate and protect the young.
adults.
These persons are also the oldest
Hence, man is faced with an evolutionary dilemma: the
individuals who produce the most young may not be most fit if their
young are not able to efficiently exploit the environment.
Fitness
for longevity assures reproductive fitness by preserving learned
means of survival in multigenerational populations.
The problem is more complicated today, however.
It is
questionable whether the elderly serve their former function in
societies which educate the young by written materials, mass
communication, and specialized learning centers.
Furthermore,
the learned information itself changes so rapidly that the information
which was accumulated 30 years before is no longer considered to
be accurate or relevant.
The means of economic and social
survival may no longer exist from one generation to another.
l
'
Because this trend is not yet characteristic of all peoples,
divergent selection is occurring.
Only in nonindustrial nations is
it still advantageous to combine longevity with reproductive fitness
in order to educate offspring.
factors in western societies.
There is no relation between these
One can only speculate that a function
for the elderly will develop which will resolve this situation.
Given the evolutionary background of the cause of senescence,
56
r·t;~ ·~n~
fc:-;m.ula~~- a multidimert~a~~~
1
would then
I assimilating both genetic and environmental data.
For example,
the basal metabolic rate is greatly influenced by factors such as
climate and diet; senescence is therefore affected by environmental
and biological variables interacting with each other in a feedback
system.
Another case is the relationship between contractility of
collagen and nutrition; undernutrition positively correlates with
retention of
11
yoling" collagen (Chvapil and Hruza
1959).
The close
relationship between choice of dietary starches, culture, and
cardiovascular disease is well-known (Sinclair
1956).
Even the
human mode of locomotion, bipedality, causes early arthritic aging
of the spinal column in comparison to the quadrupeds (Medawar
1957:129).
The causes of senescence, then, form a network of
relationships which are incomplete when analyzed out of context or
only from a biological or an environmental perspective.
A very important aspect of the environment is the cultural
milieu, including sets of attitudes toward the world which each
culture possesses.
Included in these belief systems are notions of
a suitable diet, medicine, religious practices, occupations, and
proper outlets of psychological dysfunction.
Hence, not only does
man adjust his cultural values in response to environmental
changes, but he also alters his own environment and thereby his
biological condition.
This fact has been too often ignored by
57
~-biologists,
sociologists, and psychologists who portray
~l
I changing in response to the environment and his genetic make-up.
Once the interrelationship of the evolutionary past, biological
mechanisms, environment, and culture
~ave
been clearly
established, the process of senescence wi,U be explained.
A
hypothetical model can now be theorized and is presented diagrammatically in Figure 1.
Mter ecological deaths are discounted, the
cause of senescence is seen in a combination of two processes.
The first process operates independently, but can be influenced by
the environment.
This is the eventual death of nonreplicating cells
and the errors which accumulate in replicating cells.
This aging
process is universal in the organic world, from the seemingly
ageless replicating amoebas to the primates.
The underlying
assumption to this premise is that errors will eventually occur at
the cellular level which cause either the death of the organism or a
change leading to speciation.
Simple one-celled organisms which
replicate by fission, therefore, are not ageless.
From one point
to another in the future, some change will occur.
Multicellular
animals which contain nonreplicating cells also
11
age 11 ; as each
nonreplicating cell dies, a small portion of the organism's function
is reduced.
When the functional capability drops below a minimum
acceptable level, the organism dies.
Environmental stress can
accelerate this rudimentary aging process.
58
r
Living
!•-...;....---------Organism-------------
First Aging Process
necrosis
,
Ecological
Second Aging Process
D~ath
Physical and Social
environment influences
cultural and
psychological
influences
..____-L------~• Death +------------......1
Figure 1.
Processes of Senescence
59
The second process which causes aging consists of the
interaction of the cultural and physi~al environments with the
metabolic and mutation rates.
This process is unique to animals,
and the influence of the cultural environment is unique to hominids.
The activity level which is required in a given environment either
accelerates or retards the metabolic rate, which in turn effects the
production of free radicals during oxidation.
The effects of the
environment can also act directly on the mutation rate.
For
example, occupational radiation exposure can cause a greater
mutation risk than the exposure due to normal background radiation.
Many of the possible environmental influences on the aging process
affect all animals: i.e., the accessibility of adequate nutrition,
extremes of climate, altitude, and so forth.
Other influences are
experienced only by man: i.e., the psychological environment,
urban stress, medical practices, and many more.
With increasing
control of the physical environment in some societies, the role of
these last mechanisms may become more apparent (Washburn
1964).
While all species "age" as defined by the lirst process,
members of a species senesce only if their metabolic and mutation
rates are influenced by the environment.
This two-part theory of
senescence is not inconsistent with presently known facts; it is
unique in its attempted synthetic approach to aging.
60
r-----------------------------~----------------------~---------------·~
l
l
l
I
1
:
I
·A SELECTED BIBLIOGRAPHY
Andrew, Warren
1964 Changes in the Nucleus with Advancing Age of the
Organism. Advances in Gerontological Research 1:87-107.
J
-j
Anonymous
1955 State Variations in Longevity. Statistical Bulletin of
the Metropolitan Life Insurance Company 36(10):3-5.
Arnoff, Franklin N.
1961 Concepts of Aging. In Psychopathology of Aging. Paul
H. Hoch and Joseph Zubin, eds. Pp. 136-148 .. New York:
Grune and Stratton.
Auerbach, Oscar, E. Cuyler Hammond, and Lawrence Garfinkel
1965 Smoking in Relation to Atherosclerosis of the Coronary
Arteries. New England Journal of Medicine 273:775-779.
Aykroyd, W. R. , et al.
1949 Medical Resurvey of Nutrition in Newfoundland, 1948.
·Canadian Medical Association Journal 60:329-352.
Barat, George
1970 Rejuvenation.
Center.
Beverly Hills: Neuroendocrine Research
Baker, Paul T.
197 5 The Place of Physiological Studies in Anthropology.
In Physiological Anthropology. Albert Damon, ed. Pp. 3-12.
New York: Oxford University Press.
Barrows, Charles H.
1968 Ecology of Aging and of the Aging Process - Biological
Parameters. Gerontologist 8(2):84-87.
Beard, Belle Boone
1962 Longevity and the Never-Married. In Aging Around
the World: Social and Psychological Aspects of Aging.
Clark Tibbitts and Wilma Donahue, eds. Pp. 36-50. New
York: Columbia Univer.sity Press.
I!
Il
61
r Bee~~ry a~K:;IPe~~I
1901 On .the Inheritance of the Duration of Life, and on the
Intensity of Natural
Selection in Man. Biometrika 1:50-89.
.
I
j
I, Berg,
j
l
!
l
·-·-u
Benjamin
1957 Growth, Disease, and Aging in the Rat.
Gerontology 12:370-377.
Journal of
~
i
·j
1960 Nutrition and Longevity in tpe Rat.
71:242-263.
Journal of Nutrition
Berg, Benjamin N. and HenryS. Simms
1962 Relation of Nutrition to Longevity and Onset of Disease
in Rats. In Aging Around the World: Biological Aspects of
Aging. Nathan W. Shock, ed. Pp. 35-37. New York:
Columbia University Press.
Birren, James
1960 Behavioral Theories of Aging. In Aging - Some Social
and Biological Aspects. Nathan W. Shock, ed. pp. 305332. American Association for the Advancement of Science,
Pub. 65. Washington, D. C.
Bjorksten, Johan
1958 A Common Molecular Basis for the Aging Syndrome.
Journal of the American Geriatrics Society 6:740-748.
Blumenthal, Herman T. and Aline W. Berns
1964 Autoimmunity and Aging. Advances in Gerontological
Research 1:289-342.
Bogomolets, Alexander A.
1946 The Prolongation of Life.
Pearce.
New York: Duell, Sloan and
Bourliere, Francois
1957 The Comparative Biology of Ageing: A Physiological
Approach. In Ciba Foundation Colloquia on Ageing, Vol. III.
·G. E. W. Wolstenholme and Cecilia M. O'Connor, eds.
Pp. 20-30. London:. J. andA. Churchill.
1962 Introduction. In Aging Around the World: Biological
Aspects of Aging. Nathan W. Shock, ed. Pp. 3-10. New
'York: Columbia University Press.
~l
l
1
62
~;5·~
l
FrancQis, Norman R. Joseph, and Robert Molimard
Ageing of Skin. Gerontologia 1:163-173.
Brauer, R. W.
1962 Introductory Remarks: Biological Memory, Aging, and
Environment. In Aging Around the World: Biological
Aspects of Aging, Nathan W. Shock, ed. Pp. 197-199. New
York: Columbia University Pre·ss.
Briggs, John C.
1960 The Deposition of Aging Pigment in the Human Cerebral
Cortex. Journal of Gerontology 15:258-261.
Brozek, Josef
1961 Aging: Some. Contributions of Physiological Anthropology. In Psychopathology of Aging. Paul H. Hoch and
Joseph Zubin, eds. Pp. 182-202. New York: Grune and
Stratton.
Brues, Austin M .. and George A. Sache·r, eds.
1965 Aging and Levels of Biological Organization.
University of Chicago Press.
Chicago:
Burgess, Ernest W.
1962 A Comparison of Interdisciplinary Findings of the Study
of Objective Criteria of Aging. In Aging Around the World:
Social and Psychological Aspects of Aging. Clark Tibbitts
and Wilma Donahue, eds. Pp. 671-677. New York:
Columbia University Press.
Cannon, Walter B.
1939 Ageing of Homeostatic Mechanisms. In Problems of
Ageing. E. V. Cowdry, ed. Pp. 624-641. Baltimore:
Williams and Wilkins.
Cassarett, George W.
1964 Similarities and Contrasts between Radiation and Time
Pathology. Advances in Gerontological Research 1: 109163.
Chai, C. K.
1959 Life Span in Inbred Hybrid Mice.
50:203-208.
Journal of Heredity
I
r!
63
l
lchoe~
•
.
1
.
Byung-Kil and Noel R. ·Rose
1976 In Vitro Senescence of Mammalian Cells.
22:89-108 ..
Gerontology
Chvapil, M. and Z. Hruza
1959 The Influence of Aging and Undernutrition on Chemical
I
Contractility and Relaxation of Collagen Fibres in Rats.
I
Gerontologia
3:241-252.
'
Ciuca~
Alexandru
1972 The Geography of Longevity. Proceedings of IX
International Cong1;:ess of Gerontology~ Vol. I. Pp. 199-200.
)'
Clark, Arnold M.
1964 Genetic Factors Associated with Aging.
Gerontological Research 1:207-255.
1
I
Advances in
Clark, Margaret and Barbara Gallatin Anderson
1967 Culture and Aging. Springfield, Illinois: Charles C.
Thomas.
Cohen, Rosalie A.
1973 Conceptual Styles, Culture Conflict, and Nonverbal
Tests of Intelligence. In Cultural Relevance and Educational Is sues. Francis A. J. Ianni and Edward Storey, eds.
Pp. 495-517.
Collins, Selwyn D.
1955 A Review of Illness from Chronic Disease and its
Variation with Age, Sex, and Season, with Some Trends.
Journal of Chronic Diseases 1:412-441.
Comfort~
Alex
1957a Ageing in Animals. In The Biology of Ageing. W. B.
Yapp and G. H. Bourne, eds. Pp. 23-25. Symposia of the
Institute of Biology, No. 6. London.
1957a The Biological Approach in the Comparative Study of
Ageing. In Ciba Foundation Colloquia on Ageing, Vol. III.
G. E. W. Wolstenholme and Cecilia M. O'Connor, eds.
Pp. 2-19. London: J. and A. Churchill.
1964 Ageing: The Biology of Senescence.
and Kegal Paul.
London: Routledge
64
r
I
1968 Physiology, Homeostasis and Ageing.
14:224-234.
I
1969a Longer Life by 1990?
j
l
1965 The Process of Ageing.
Nicholson.
London: Weidenfeld and
Gerontologia
New Scientist 44(679):549-551.
1969b Test- battery to Measure Ageing-rate in Man.
ii: 1411-1415.
Lancet
Cowgill, Donald 0.
1974 Aging and Modernization: A Revision of the Theory.
In Late Life. Jaber F. Gubrium, ed. Pp. 123-146.
Springfield, Illinois: Charles C. Thomas.
Cristofalo, Vincent J.
1972 Animal Cell Cultures as a Model System for the Study
of Aging. Advances in Gerontological Research 4:45-79.
Curtis, Howard J.
1966 Biological Mechanisms of Aging.
Charles C. Thomas.
Springfield, Illinois:
Curtis, Howard J. and John Tilley
1971 The Life-Span of Dividing Mammalian Cells In Vivo.
Journal of Gerontology Z6:1-7.
·
--Danielli, J. F.
1957 The Study of the Ageing of Cells. In Ciba Foundation
Colloquia on Ageing, Vol. III. G. E. W. Wolstenholme and
Cecilia M. O'Connor, eds. Pp. 39-44. London: J. and
A. Churchill.
Darling, F. Fraser
1955 West Highland Survey.
Press.
London: Oxford University
Demoise, Charles F. and Robert A. Conrad
1972 Effects of Age and Radiation Exposure on Chromosomes
in a Marshall Island Population. Journal of Gerontology
27:197-201.
Dobzhansky, Theodosius
1958 Genetics of Homeostasis and of Senility. Annals of the
New York Academy of Sciences 71:1234-1241.
65
r
1
Dublin, Louis I.
1939 Longevity in Retrospect and in Prospect. In Problems
of Ageing. E. V. Cowdry, ed. Pp. 100-119. Baltimore:
Williams and Wilkins.
:!
j
Dubos, Rene
1965 Man Adapting.
New Haven: Yale University Press.
l
i
I
!
Dunn, John E., George Linden, and Lester Brewlow
1960 Lung Cancer Mortality Experience of Men in Certain
Occupations in California.. American Journal of Public
Health 50:1475-1487.
Edington, Dee W., Arthur C. Cosmas, and William B. McCafferty
1972 Exercise and Longevity: Evidence for a Threshold Age.
Journal of Gerontology 27:341-343.
Eisdorfer, Carl
1975 Some Variables Relating to Longevity in Humans. In
Epidemiology of Aging. Adrian M. Ostfeld and Don C.
Gibson, eds. Pp. 97-108. DHEW Pub. NIH 75-7111.
Bethesda.
i
Failla, G.
1958 The Aging Process and Cancerogenesis. Annals of the
New York Academy of Sciences 71:1124-1140.
'·
Fathauer, G. H.
1960 Food Habits - An Anthropologist's View. Journal of
the American Dietary Association 37:335-338.
Fikry, M. Essam
1969 The Ageing Cell: Ageing and Death as Aspects of Growth
and Development; Natural Phenomena Controlled by Genetic
Factors. Journal of the American Geriatrics Society
17:1044-1054.
l
I
I
Fluckiger, E. and F. Verzar
1955 Lack of Adaptation to Low Oxygen Pres sure in Aged
Animals. Journal of Gerontology 10:306-311.
Fry, Christine L.
1976 The Ages of Adulthood: A Question of Numbers.
Journal of Gerontology 31:170-177.
.
},<~P">"•~·~··•""'""'-.-.~---·-·,___.....,,.,.,_.-,.....,._,_,¢-.'"<I'~-.. •• ._..,_...,..,.•.._..,~ ........ -~-~,U~----"-"•-•-.......~ .. -
......-..........~...........-------~--~ ...-
--A---.. .
....
.
-.-.a~-0---,o.~, ... ;,_,...~o~~-- ••• ~- . . . ••,.._,.,-... ,_,,....,.,~.'
66
j Gelfant, Seymour and J. Graham Smith
r--~
j
l
I
1972 Aging: Noncycling Cells and Explanation.
178(4059) :357-361.
Science
Glass, Bentley
1957 The Genetic Hazards of Nuclear Radiations.
126:241-246.
Science
1960 Genetics of Aging. In Aging - Some Social and Biological Aspects. Nathan W. Shock, ed. Pp. 67-100. American
Association for the Advancement of Science, Pub. 65.
Washington, D. C.
Graham, S.
1963 Social Factors in Relation to the Chronic Illnesses. In
Handbook of Medical Sociology. Howard E. Freeman, Sol
- Levine, and Leo G. Reede;r, eds. Pp. 65-98. Englewood
Cliffs, New Jersey: Prentice-Hall.
Gus seck, David J.
1972 Endocrine Mechanisms and Aging.· Advances in
Gerontological Research 4:105-166.
Haldane., J. B.S.
1949 Parental and Fraternal Correlations for Fitness.
of Eugenics 14:288-292.
Harlow, Harry F.
1962 Social Deprivation in Mon~.
206:1-10.
Annals
Scientific American
Harman., Denham
1956 Aging: A Theory Based on Free Radical and Radiation
Chemistry. Journal of Gerontology 11:298-300.
1961 Mutation, Cancer, and Ageing.
Lancet i:200-201.
1962 Free Radical Theory of Aging: Prolongation of the
Normal Life Span by Free Radical Inhibitors. In Aging
Around the World: Biological Aspects of Aging. Nathan W.
Shock., ed. P. 267. New York: Columbia University Press.
1969 Prolongation of Life: Role of Free Radical Reactions
in Aging. Journal of the American Geriatrics Society
17:721-735.
67
I
I
---·~----------~--·-·----·-~·"
1971 F.ree ~adical Theory of Aging: Effect of the Amount
and Degree of Unsaturation of Dietary Fat on Mortality
Rate. Journal of Gerontology 26:451-457.
1972 The Biological Clock: the Mitochondria?· Journal of
the American Geriatrics Society .20:145·-14 7.
Hayflick, L.
1970 Aging under Glass.
303.
Experimental Gerontology 5:291-
Heroux, 0. and J. S. Campbell
1962 A Study of the Pathology and Life Span of 6 °C. - and
30°C. -Acclimated Rats. In Aging Around the World:
Biological Aspects of Aging. Nathan W. Shock, ed. P. 200.
New York: Columbia University Press.
Hershey, Daniel
1974 Lifespan - and Factors Affecting It.
Illinois: Charles C. Thomas .
Springfield,
. Hollingsworth, J. W., A. Hashizume, and Seymour Jablon
1965 Correlations Between Tests of Aging in Hiroshima
Subjects - An Attempt to Define 'Physiological Age.'
Yale Journal of Biology and Medicine 38:11-26.
Hollingsworth, M. J.
1967 Genetic Studies on Longevity. In Social and Genetic
Influences on Life and Death. Robert Plat~ and A. S. Parkes,
eds. Pp. 194-214. Edinburgh: Oliver and Boyd.
Hotcin, John and Edward Sikora
1970 Long-term Effects of Virus Infection on Behavior and
Aging in Mice. Proceedings of the Society for Experimental Biology and Medicine 134:204-209.
Howell, Sandra C. and Martin B. Loeb
1969 Culture, Myths, and Food Preferences Among Aged.
Gerontologist 9(3):31-37.
Hyndman, Olan R.
1952 The Origin of Life and the Evolution of Living Things.
New York: Hallmark-Hubner.
i
!
68
r-;::lavisto, Eeva
I
l
l
i
-·..·-·
.
1959 Parental Age Effects on Man. In Ciba Foundation
Colloquia on Ageing, Vol. V. G. E. W. Wolstenholme and
Maeve O'Connor, eds. Pp. 21-31. London: J. and A.
Churchill.
Jarvik, Lissy F.
1969 Human Genetics and Aging. In Duke University Council
on Aging and Human Development. Center for the Study of
Aging and Human Development. Pp. 266-278. Durham,
North Carolina.
Jones, Hardin B.
1956 A Special Consideration of the Aging Process, Disease,
and Life Expectancy. Advances in Biological and Medical
Physics 4:281-337.
1959 Relation of Human Health to Age, Place, and Time. In
Handbook of Aging and the Individual. James E. Birren,
ed. Pp. 336-363. Chicago: University of Chicago.
Kallmann, Franz J.
1957 Twin Data on the Genetics of Ageing. In Ciba Foundation Colloquia on Ageing, Vol. ill. G. E. W. Wolstenholme
and Cecilia M. O'Connor, eds. Pp. 131-143. London:
J. and A. Churchill.
1961 Genetic Factors in Aging: Comparative and Longitudinal Observations on a Senescent Twin Population. In Psychopathology of Aging. Paul H. Hoch and Joseph Zubin,
eds. Pp. 227-247. New York: Grune and Stratton.
Kallmann, Franz J. and Lissy F. Jarvik
1959 Individual Differences in Constitution and Genetic
Background. In Handbook of Aging and the Individual.
James E. Birren, ed. Pp. 216-263. Chicago: University
of Chicago.
Kannel, William B.
1971 Habits and Heart Disease. In Prediction of Life Span.
Erdman Palmore and Frances C. Jeffers, eds. Pp. 61-70.
Lexington: Heath Lexington.
69
Kannel, William B., William P. Castelli, Tavia Gordon, and
Patricia M. McNamara
1971 Serum Cholesterol, Lipoproteins, and the Risk of ·
Coronary Heart Disease. Annals of Internal Medicine
74:1-12.
Kimmel, Douglas C.
1974 Adulthood and Aging.
New York: John Wiley.
Kiser, Clyde V.
1962 The Aging of Human Populations: Mechanisms of
Change. In Aging Around the World: Social and
Psychological Aspects of Aging. Clark Tibbitts and Wilma
Donahue, eds. Pp. 18-35. New York: Columbia University
Press.
Kleem€der, Robert W.
1959 Behavior and the Organization of the Bodily and the
External Environment. In Handbook of Aging and the
Individual. James E. Birren, ed. Pp. 400-451. Chicago:
University of Chicago.
Koller, Marvin R.
1968 Social Gerontology.
New York: Random House.
Lansing, Albert I.
.
1947 A Transmissible, Cumulative, and Reversible Factor
.in Aging. Journal of Gerontology 2:228-239.
1955 Ageing of Elastic Tis sue and the Systematic Effects of
Elastase. In Ciba Foundation Colloquia on Ageing, Vol. I.
G. E. W. Wolstenholme and Margaret P. Cameron, eds.
Pp. 8'8-103. London: J. and A. Churchill.
1959 General Biology of Senescence. In Handbook of Aging
and the Individual. James E. Birren, ed. Pp. 119-135.
Chicago: University of Chicago.
Lawton, Alfred H. and Thomas A. Rich
1968 Ecology and Gerontology: An Introduction.
Gerontologist 8(2):76-77.
Leaf, Alexander
1973 Getting Old.
Scientific American 229(3):44-52.
70
,.
·-·
j Lee, Douglas H.K.
I
I
l
1969 Significance of Aging in Response to Environmental
Stress. In Duke University Council on Aging and Human
Development. Center for the Study of Aging p.nd Human
Development. Pp. 177-183. Durham,. North Carolina.
Lederman, J. M., A. C. Wallace, and J. A. Hildes
1962 Arteriosclerosis and Neoplasms in Canadian Eskimos.
In Aging Around the World: Biological Aspects of Aging.
Nathan W. Shock, ed. Pp. 201-207. New York: Columbia
University Press.
LeGros Clark, F. and N. W. Pirie·
1957 Introduction. In The Biology of Ageing. W. B. Yapp
and G. H. Bourne, eds . . Pp. ix-xiv. Symposia of the
Institute of Biology, No. 6. London.
Leonard, George
1976 The Holistic Health Revolution.
New West 1 (2):40-49.
Lind, A. R. and R. F. Hellon
1962 Change•s in Thermoregulatory Processes in Man Due to
Aging. In Aging Around the World: Biological Aspects of
Aging. Nathan W. Shock, ed. P. 208. New York:
Columbia University Press.
Lindop, Patricia J. and J. Rotblat
1962 Induction of Aging by Radiation. In Aging Around the
World: Biological Aspects of Aging. Nathan W. Shock,
ed. Pp. 216-221. New York: Columbia University Press.
Lovelock, J. E.
1956 The Physical Instability of Human Red Blood Cells and
Its Possible Importance in their Senescence. In Ciba
Foundation Co~loquia on Ageing, Vol. II. G. E. W.
Wolstenholme and Elaine C. P. Millar, eds. Pp. 215-232.
London: J. and A. Churchill.
Lowenberg, Miriam E., et al.
1974 Food and Man. New York: John Wiley.
Maurizo, Anna
1959 Factors Influencing the Lifespan of Bees. In Ciba
Foundation Colloquia of Ageing, Vol. V. G. E. W.
Wolstenholme and Maeve O'Connor, eds. Pp. 231-243.
London: J. and A. Churchill.
71
r-~-~-·-a-r_d__
S_na--it-h~,--J-;---------------------------~-------------~-------~--------~
I
!
I
1957 Genetic Variations in Ageing. In The· Biology of Ageing, '
W. B. Yapp and G. H. Bourne, eds. Pp. llS-122.
·
Synaposia of the Institute of Biology, No. 6. .London.
1
I
I
1959 The Rate of Ageing in Drosphila subobscura. In Ciba
Foundation Colloquia on Ageing._ Vol. V. G. E. W.
Wolstenholnae and Maeve O'Connor, eds. · Pp. 269-281.
London: J. and A. Churchill.
1962 The Causes of Ageing. Proceedings of the Royal
Society of London 157{B):115-127.
McCance, R. A. and E. M. Widdowson
1955. A Fantasy on Ageing and the Bearing of Nutrition upon
It. In Ciba Foundation Colloquia on Ageing, Vol. I.
G. E. W. Wolstenholnae and Margaret P. Canaeron, eds.
Pp. 186-198. London: J. and A. Churchill.
McCay, C. M.
1939 Chenaical Aspects of Ageing. In Problenas of Ageing.
E. V. Cowdry,- ed. Pp. 572-623. Baltinaore: Willianas
and Wilkins.
1949 Diet and Aging.
Vitanains and Hornaones 7:147-170.
McCracken, Robert D.
1971 Lactase Deficiency: an Exanaple of Dietary Evolution.
Current Anthropology 12:479.-517.
McFarland, Ross A. and Brian M. O'Doherty
1959 Work and Occupational Skills. In Handbook of Aging
and the Individual. Janaes E. Birren, ed. Pp. 452-502.
Chicago: University of Chicago.
Medawar, P. B.
1955 The Definition and Measurenaent of Senescence. In
Ciba Foundation Colloquia on Ageing, Vol. I. G. E. W.
Wolstenholnae and Margaret P. Canrreron, eds. Pp. 4-15.
London: J. and A. Churchill.
1957 The Uniqueness of the Individual.
London: Methuen.
Medvedev, Zhores A.
'?
1974 Doctoral DissertatioifJh Gerontology.
Gerontology 26:249-257.
Journal of
72
~ulie~.
i
[ Moore,
and James E. Birren
I
1971 no·ctoral Dissertations in Gerontology.
I
!
Gerontology 26:249-257.
ll
Journal of
I Muller,
Ch. and L. Ciompi, eds.
1968 Senile Dementia. Bern, Germany: Hans Huber.
Muller, Hermann J.
1959 The Guidance of Human Evolqtion.
Biology and Medicine 3:1-43.
Perspectives in
1
Murakami, M.
1969 Carbohydrates and Arteriosclerosis. Proceedings of
VIII International Congress of Gerontology, Vol. I.
Pp. 244-246.
i
Nahemow, Nina and Bert N. Adams
1974 Old Age among the Baganda: Continuity and Change.
In Late Life. Jaber F. Gubrium, ed. Pp. 147-166.
Springfield, Illinois: Charles C. Thomas.
·f
Neugarten, Bernice L.
1972 Social Implications of a Prolonged Life-Span.
Gerontologist 12(4) :323,438-440.
Newman, Marshall T.
197 5 Nutritional Adaptation in Man. In Physiological
Anthropology. Albert Damon, ed. Pp. 210-259. New
York: Oxford University Press.
Oeriu, Simion
1964 Proteins in Development and Senescence.
in Gerontological Research 1:23-85.
Advances
Osborn, Richard Warren
1971 Social and Economic Factors in Reported Chronic
Morbidity. Journal of Gerontology 26:217-223.
Ostfeld, Adrian M. and Don C. Gibson, eds.
1975 Epidemiology of Aging. DHEW Pub. NIH 75-711.
Bethesda .
. ~ Palmore, Erdman
1971a Conclusions. In Prediction of Life Span. Erdman
Palmore and Frances C. Jeffers, eds. Pp. 283-287.
Lexington: Heath Lexington.
73
r··-··
l
1971b The Promise and Problems of Longevity Studies. In
Prediction of Life Span. Erdman Palmore and Frances C.
Jeffers, eds. Pp. 3-11. Lexington: HeathLexington.
Palmore, Erdman and Clark Luikart
1974 Health and Social Factors Related to Life Satisfaction.
In Normal Aging II. Erdman P~lmore, ed. Pp. 185-201.
Durham, North Carolina: Duke University P:r."ess.
Parkes, A. S.
1955 Preservation of Tissue 'In Vitro. 1 In Ciba Foundation
Colloquia on Ageing, Vol. I. G. E. W. Wolstenholme and
Margaret P. Cameron, eds. Pp. 162-169. London:
J. and A. Churchill.
Parsons, P. A.
1962 Maternal Age and Developmental Variability.
of Experimental Biology 39:251-260.
Journal
Patno, Mary Ellen
1960 Mortality and Economic Level in an Urban Area.
Public Health Reports 75:841-851.
Paul, Benjamin D.
1969 Anthropological Perspectives on Medicine and Public
Health. In Cross-Cultural Approach to Health Behavior.
L. Lynch, ed. Pp. 26-42. Rutherford, New Jersey:
Fairleigh Dickinson University Press.
Pearl, Raymond
1922 The Biology of Death.
Philadelphia: J. B. Lippincott.
Pearl, Raymond and Ruth DeWitt Pearl
1934 The Ancestry of the Long-Lived.
Hopkins.
Baltimore: Johns
Pfeiffer, Eric
1971 Physical, Psychological, and Social Correlates of
Survival in Old Age. In Prediction of Life Span. Erdman
Palmore and Frances C. Jeffers, eds. Pp. 223-236.
Lexington: Heath Lexington.·
Post, Felix
1965 The Clinical Psychiatry of Late Life.
Pergamon.
Oxford:
74
~"ll~~~· A.
j
j
I
-=-- .
1971 Free Radicals in Biological Systems.
American 223(2):70-83.
Scientific
Queen, G. S.
1957 Culture, Economics, and Food Habits. Journal of the
American Dietary Association 33:1044-1052.
Quint, Jules ·V.
1970 Preeminence and Mortality: Longevity of Prominent
Men. American Journal of Public Health 60:1118-1124.
Reeder, Leo G.
1959 Occupation and Socioeconomic Status as Variables in
Heart Disease Research: A Critique. American Journal
of the Medical Sciences 238:297-306.
Reichel, William
1972 Premature Aging. Proceedings of IX International
Congress of Gerontology, Vol. II. Pp. 344-347.
Riley, John W.
1969 Old Age and Death in American Society. In Duke
University Council on Aging and Human Development.
Center for the Study of Aging and Human Development.
Pp. 299-309. Durham, North Carolina.
Rose, Charles L.
1971 Critique of Longevity Studies. In Prediction of Life
Span. Erdman Palmore and Frances C. Jeffers, eds.
Pp. 13-29. Lexington: Heath Lexington.
Rose, Charles L. and Benjamin Bell
1971 Predicting Longevity. Lexington: Heath Lexington.
Rosen, George
1961 Cross-Cultural and Historical Approaches. In
Psychopathology of Aging. Paul H. Hoch and Joseph
Zubin, eds. Pp. 1-20. New York: Grune and Stratton.
Ross, Morris H.
1961 Length of Life and Nutrition in the Rat.
Nutrition 75:197-210.
Journal of
75
r Roth,
i.
I
····-
-
Martin
1967 Psychiatric Aspects of Old Age. In Social and Genetic
Influences on Life and Death. Robert Platt and A. S.
Parkes, eds. Pp. 163-182. Edinburgh: Oliver and Boyd.
Sacher, George A.
1959 Relation of Lifespan to Brain Weight and Body Weight
in Mammals. In Ciba Foundation Colloquia on Ageing,
Vol. V. G. E. W. Wolstenholme and Maeve O'Connor,
eds. Pp. 115-133. London: J. and A. Churchill.
' Schroeder, Henry A.
1960 Relations between Hardness of Water and Death Rates
from certain Chronic and Degenerative Diseases in the
United States. Journal of Chronic Diseases 12:586-591.
Schwartz, Gary
l972 Youth Culture: an Anthropological Approach.
Addison-Wesley Modular Publications 17:1-47.
Scotch, Norman A.
1963 Medical Anthropology.
In Biennial Review of
Anthropology. Bernard J. Siegel, ed. Pp. 30-68.
Stanford: Standard University Press.
Selye, Hans
1970 Stress and Aging.
Society 18:669-680.
Journal of the American Geriatrics
Selye, Hans and P. Prioreschi
1960 Stress Theory of Aging. In Aging - Some Social and
Biological Aspects. Nathan W. Shock, ed. Pp. 261-272.
American Association for the Advancement of Science,
Pub. 65. ·Washington, D. C.
Shanas, Ethel, et al.
1968 Old People in Three Industrial Societies.
Routledge and Kegal Paul.
London:
Shank, Robert E.
1975 Nutrition and Aging. In Epidemiology of Aging. Adrian
M. Ostfeld and Don C. Gibson, eds. Pp. 199-214. DHEW
Pub. NIH 75-711. Bethesda.
76
r-------~-------~-~---··-
l
Shelanski, Michael L.
1
1975 The Aging Brain: Alzheimer's Disease and Senile
Dementia. In Epidemiology· of Aging. Adrian M. Ostfeld
and Don. C. Gibson, eds. Pp. 113-128. DHEW Pub. NIH
75-711. Bethesda.
I
Sheps, Mindel C.
1961 Marriage and Mortality.
Health 51:54 7-555.
American Journal of Public
Shock, Nathan W.
1960 Some of the Facts of Aging. In Aging - Some Social
and Biological Aspects. Nathan W. Shock, ed. Pp. 241260. Washington, D. C.
Siegel, Jacob S.
J. 975 Demographic Aspects of Aging in the United States.
In Epidemiology of Aging. Adrian M. Ostfeld and Don C.
Gibson, eds. Pp. 17-82. DHEW Pub. NIH 75-711.
Bethesda.
Strehler, Bernard L.
1960 Dynamic Theories of Aging. In Aging - Some Social
and Biological Aspects. Nathan W. Shock, ed. Pp. 273304. American Association for the Advancement of Science,
Pub. 65. Washington, D. G.
1969 Turnover in Aging. Proceedings of XIII International
Contress of Gerontology, Vol. I. Pp. 175-178.
1971 Genetic and Cellular Aspects of Life Spim Prediction.
In Prediction of Life Span. Erdman Palmore and Frances
C. Jeffers, eds. Pp. 33-49. Lexington: Heath Lexington.
Strehler, Bernard L. and Albert S. Mildvan
1960 Possible Maternal Influence on Longevity of Offspring.
In Aging Around the World: Biological Aspects of Aging.
Nathan W. Shock, ed. Pp. 26-29. New York: Columbia
University Press.
Szilard, Leo
1959 On the Nature of the Aging Process. Proceedings of
the National Academy of Sciences 45:30-45.
l
77
lTa~hiro, ~ic"~o
1
I
i
and Wendell R. Lipscomb .
1963 Mortal~ty Experience of Alcoholics.
of Studies on Alcohol 24:203.-212.
·~
Quarterly Journal
Thomson, James and John 0. Forfar
1950 Progeria. Archives of Disease in Childhood 25:224234.
Tribe, M.A.
1966 The Effect of Diet on Longevity in Calliphora
erythrocephala Meig. Experimental Gerontology 1:269-284.
Upton, A. C.
1960 Ionizing Radiation and Aging.
·1
Gerontologia 4:162-176.
Vallois, Henri V.
1961 The Social Life of Early Man: the Evidence of
, Skeletons. In Social Life of Early Man. Sherwood L.
Washburn, ed. Fp. 214-235. New York: Viking Fund
Publications in Anthropology 31.
Simmons, Leo W.
1946 Attitudes Toward Aging and the Aged: Primitive
Societies. Journal of Gerontology 1:72-95.
Simmons, Walt R.
1962 The Matrix of Health, Manpower, and Age. In Aging
Around the World: Social and Psychological Aspects of
Aging. Clark Tibbitts and Wilma Donahue, eds. Pp. 208217. New York: Columbia University Press.
Sinclair, H. M.
1955 Too Rapid Maturation in Children as a Cause of Ageing.
In Ciba Foundation Colloquia on Ageing, Vol. I. G. E. W.
Wolstenholme and Margaret P. Cameron, eds. Pp. 194201. London: J. and A. Churchill.
1956 Deficiency of Essential Fatty Acids and Atherosclerosis,
Etcetera. Lancet i:381-383.
1957 Nutrition arid Ageing. In The Biology of Ageing.
W. B. Yapp and G. H. Bourne, eds. Pp. 101-109.
Symposia of the Institute of Biology, No. 6. London.
l.
l
78
rj
'
Sinex~ F. Marott · ~~---~~---------------,
1964 Cross-Lindage and Aging.
Research 1:165-180.
Advances in Gerontological
Skinner, Robert J.
1961 Cultural Differences in the Life Cy~le and the Concept
of Time. In Aging and Leisure .. Robert W. Kleemeier, ed.
Pp. 83-103. New York: Oxford University Press.
Stockwell, Edward G.
1961 Socioeconomic status and mortality in the United States.
Public Health Reports 76:1081-1086.
Stolnitz, George J.
1953 Recent International Differences and Trends in
Expectation of Life. Population Index 19:2-10.
Verza:t:, F.
1957a The Ageing of Connective Tissue.
1:363-378.
Gerontologia
;
1957b Studies on Adaptation as a Method of Gerontological
Research. In Ciba Foundation Colloquia on Ageing, Vol.
III. G. E. W. Wolstenholme and Cecilia M. O'Connor,
eds. Pp. 60-68. London: J. and A. Churchill.
1963 Lectures on Experimental Gerontology.
Illinois: Charles C. Thomas.
Springfield,
Visscher, Maurice B., Joseph T. King, and Y. Chiung Puh Lee
1952 Further Studies of Age and Diet Upon Reproductive
Senescence in Strain A Female Mice. American Journal
of Physiology 170:72-76.
Walford, Roy L.
1969 The Immunologic Theory of Aging.
Williams and Wilkins.
Baltimore:
Walker, A. R. P.
1969 Can Expectation of Life in Western Populations be
Increased by Changes in Diet and Manner of Life? South
African Medical Journal 43:768-775.
'
79
r----·------~-·-·-·~-· ·--~----·
Washburn, Alfred H.
1964 Influences
of Early Development upon Later Life. In
1I
.
!
Relations of Development a:Q.d Aging. James E. Birren,
ed. Pp. 29-37. Springfield, Illinois: Charles C. Thomas.
1
I
l
Weiss, A. Kurt
1974 The Hayflick Hypothesis.
·l
Gerontologist 14:492-493.
Widdowson, Elsie M. and G. C. Kennedy
1962 Rate of Growth, Mature Weight, and Life- span.
Proceedings of the Royal Society of London 156(B):96-108.
Williams, George C.
1957 Pleiotropy, Natural Selection, and the Evolution of
Senescence. Evolution 11:398-411.
Williams, Roger J.
1956 Human Nutrition and Individual Variability.
Review of Nutritional Research 17:11-26.
Borden's
1969 The Individual Approach to Geriatric Nutrition. In
Duke University Council on Aging and Human Development.
Center for the Study of Aging and Human Development.
Pp. 138-150. Durham, North Carolina.
Wissler, Clark
193 9 Human Cultural Levels. In Problems of Ageing.
E. V. Cowdry, ed. Pp. 83-99. Baltimore: Williams
and Wilkins.
Wohl, Michael G. and RobertS. Goodhart
1955 Modern Nutrition in Health and Disease.
Lea and Febiger.
Philadelphia:
Yap, P.M.
1962 Aging in Underdeveloped Asian Countries. In Aging
Around the World: Social and Psychological Aspects of
Aging. Clark Tibbitts and Wilma Donahue, eds. Pp. 442453. New York: Columbia University Press.