44 E
VIDENCE
-B
ASED
T
HEORY
& Gavrilova, 1994). However, Weismann’s foreshadowing of the discovery of lim-
its to cell divisions did nothing to support his theory of programmed death.
When the cells stopped dividing, no programmed cell death occurred. In fact, the
cessation of cell division actually seems to benefit organism survival as a means
of cancer protection.
Gavrilov and Gavrilova (2002) report that Weismann’s perspective on the evo-
lution of aging itself evolved as he aged. In his own old age he considered old or-
ganisms “neutral,” not “harmful” for the biological species. This significant
change in his own theory went unnoticed by the majority of scientists. His re-
vised theory never received the attention that his earlier theory did.
Experimental tests of the theory of programmed death were performed. Re-
sulting evolutionary theories of aging were then tested on fruit flies (Drosophila
melanogaster) in the laboratory (Luckinbill & Clare, 1985) and on guppy popula-
tions (Poecilia reticulosa) in nature (Reznick, Buckwalter, Groff, & Elder, 2001).
Findings were that life spans evolve in subsequent generations of species in a the-
oretically predictable way as a function of specific conditions of nature. Off-
spring born later in life to mothers artificially selected for breeding predictably
produced fruit flies with longer life spans in the laboratory. However, animals in
the natural environment with a greater number of surrounding mortality sources
had a shorter offspring life span. If death is programmed, the differences in life
span between these two populations should not significantly vary, so Weismann’s
theory was not supported. This same experiment was repeated with chaffinches
(Comfort, 1964; Paevsky, 1985), field voles (Fenyuk & Sheikina, 1940), and chim-
panzees (Hill et al., 2001), with similar results. The same conclusion is reached in
analysis of data regarding human life span when comparing developed and un-
derdeveloped countries.
Another way to test the validity of the theory of programmed death is to study
age as the independent variable that affects the dependent variable, death. If this
theory is correct, age-dependence of death rate should demonstrate a dramatic
change at some critical age in later life when this programmed death phenomenon
is activated. A group of genetically identical animals in a species could be studied
in the laboratory to determine if and where this dramatic change occurred. Hun-
dreds of published life tables were analyzed for dramatic age-dependent death
changes. However, all plots of death as a function of age were very smooth curves,
with no dramatic changes. Finally, a programmed death would have no benefit to
an individual’s survival or the survival of his or her offspring via parental protec-
tion (Gavrilov & Gavrilova, 2002).
M
UTATION
A
CCUMULATION
T
HEORY OF
A
GING
Mutation accumulation theory,
originally proposed by Peter Medawar (1952), sees aging as a side effect of natu-
ral selection. This theory considers aging a nonadaptive trait endorsed by natural
selection because beyond a certain age, increased life span does not promote re-
production probability. Detrimental mutations that occur at a young age are se-
lected against in a forceful way because they have a deleterious effect on
reproduction. However, detrimental mutations occurring after the age of repro-
duction do not have this profound negative response from natural selection be-
cause they do not affect reproduction of individuals or their offspring.
In relation to humans, people with many detrimental mutations have less
probability of reproducing the earlier in human development these mutations are
expressed. An example is people with progeria, having a life span of about 14