Between Zeus and the Salmon The Biodemography of Longevity (1997) / Chapter Skim
Currently Skimming:
13 Comparative Perspectives on Plasticity in Human Aging and Life Spans
13 Comparative Perspectives on Plasticity in Human Aging and Life Spans
Pages 245-268
The Chapter Skim interface presents what we've algorithmically identified as the most significant single chunk of text within every page in the chapter.
Select key terms on the right to highlight them within pages of the chapter.
From page 245... ...
The life history of multicellular organisms is built on the scheduling of functions during the life span. In sexually reproducing organisms, life history may be considered to begin with the gametes produced in the prior parental generation, which may exist for many decades before fertilization.
|
From page 246... ...
The plasticity of life histories is generally consistent with an evolutionary basis for the numeric life span as a life-history trait. The vast range of schedules shown by multicellular organisms, as described next, implies that the plasticity in life-history schedules and phenotypes is itself a general outcome of evolution by allowing multiple alternative adaptive schedules.
|
From page 247... ...
Indirectly, these parameters of the reproductive schedule are statistical determinants of the life span. While the evolution of senescence in nonsexually reproducing organisms has been given less attention, clonal reproduction is well documented to coexist with senescence of the individual organism e.g., two species of annelid worms (Martinez and Levinton, 1992~.
|
From page 248... ...
Schema of the range of intensities of senescence on a spectrum from rapid to gradual to negligible, as indicated by thickness of the wedge. Durations of total life spans, embryo-toadult life phase, are shown on the vertical scale as days in powers of 10.
|
From page 249... ...
The fruit fly Drosophila and the nematode Cacnorhabditis are valuable laboratory invertebrate models for senescence, with life spans of up to several months that show extensive pathophysiological changes. Unlike the hyperadrenocorticism of Pacific salmon, however, no single pathophysiological trigger has been identified in the senescence of Drosophila or Cacnorhabditis.
|
From page 250... ...
Several cohorts at the Jackson Laboratory showed progressive improvement in adult survival between 1948 and 1962, when the mean life span increased from about 560 days to 700 days, and maximum life spans increased from 800 to 900 days. Another cohort of this strain obtained from Jackson Laboratory by this author a few years later had markedly greater life spans, with a mean of 900 days and a maximum of 1460 days (Finch, 1971; Finch et al., 1969~.
|
From page 251... ...
Ongoing studies of food-restricted rodents may lead to even greater life spans. It might be informative to analyze historical trends for mortality rates and life spans of laboratory rodents since the beginnings of modern small animal husbandry.
|
From page 252... ...
The preservation of natural age-structured populations with multiple coexisting generations should be considered as a crucial aspect of the efforts to protect endangered species and biodiversity (Finch and Ricklefs, l991~. Investigators will encounter special statistical problems of sampling the few individuals of advanced ages to obtain estimates of the distribution of life spans and of age-related diseases.
|
From page 253... ...
These striking experiments demonstrate that somatic cells have a great deal more potential for function than available in the usual life span. In fact, the evolutionary theory of senescence does not require that the leading causes of death during senescence be synchronized with other aging processes (Rose, 1991:167~.
|
From page 254... ...
The ad libitum food intake of laboratory rodents may be atypical, because food resources are subject to seasonal and other fluctuations in natural populations. This plasticity in the reproductive schedule is hypothesized to be adaptive, because it would coordinate reproduction with food availability (Holliday, 1989; Harrison and Archer, 1989; Graves, 1993~.
|
From page 255... ...
CELL PROLIFERATION AND LIFE-HISTORY PLASTICITY Against the above examples, we must also consider if there are changes at cellular and molecular levels that may not be readily reversible or open to intervention. The Hayflick phenomenon, or the limited proliferative life span of diploid human fibroblasts in serial culture, is often cited as an example of a builtin aging clock (Hayflick, 1977, 1994; Fries, 1980~.
|
From page 256... ...
Vegetative reproduction includes reproduction from somatic cells by budding or segmentation. In many examples, vegetative reproduction can prevail for many successive generations, without a required intermediate cycle of sexual reproduction.
|
From page 257... ...
From a comparative perspective, the plasticity of the human life span should not depend as much on the proliferative capacity of somatic cells as on changes in hormones and growth factors that modify cell functions. The huge proliferative capacity of mouse cells when obtained from blasto
|
From page 258... ...
MOLECULAR AGE CHANGES AND PLASTICITY At a molecular level, long-lived proteins and DNA are subject to diverse changes that may ultimately limit the plasticity of the life span. Proteins such as collagen and elastin slowly accumulate oxidative damage from a variety of chemical processes, including the formation of oxidation productions from glucose.
|
From page 259... ...
Correspondingly, food restriction, which lowers blood glucose, has been shown to decrease oxidative damage to proteins in rats (Reiser, 1994; Youngman et al., 1992~. This finding points to the potential impact of nutrition across the life span on amount of damage that may accumulate in slowly replaced molecules.
|
From page 260... ...
The present findings point to an utterly different form of plasticity in molecular aging processes, which suggest that physiological manipulations could be used to intervene and reduce mutational changes in DNA. PROSPECTS FOR A GENETICS OF LONGEVITY Many laboratories are actively pursuing genes that influence life spans in short-lived animal models of aging, particularly nematodes (Johnson and Shook, in this volume)
|
From page 261... ...
Increased population size is certainly another factor. Although population size does not have a major effect on maximum life span during the Gompertz acceleration of mortality, when mortality accelerations slow at very advanced ages, population size will be a greater determinant of maximum life span (Finch and Pike, 1996)
|
From page 262... ...
Pike 1996 Maximum lifespan predictions from the Gompertz mortality model. Journal of Gerontology B183-B194.
|
From page 263... ...
1988 Life history variation within a population of the colonial ascidian Botryllus schlosseri I: The genetic and environmental control of seasonal variation. Evolution 42:900-920.
|
From page 264... ...
1989 Natural selection for extended longevity from food restriction. Growth Development and Aging 53:3-6.
|
From page 265... ...
Liu, R.K., and R.L. Walford 1969 Laboratory studies on life span, growth, aging, and pathology of the annual fish, Cynolebiasbellottii Steindachner.
|
From page 266... ...
1995 Senescence in organisms with clonal reproduction and complex life histories. American Naturalist 145:90-108.
|
From page 267... ...
Ingram, and A D'Costa 1995 Moderate caloric restriction alters the subcellular distribution of somatostatin mRNA and increases growth hormone pulse amplitude in aged animals.
|
From page 268... ...
Park, and B.N. Ames 1992 Protein oxidation associated with aging is reduced by dietary restriction of protein or calories.
|
Key Terms
This material may be derived from roughly machine-read images, and so is provided only to facilitate research.
More
information on Chapter Skim is available.