The Rate of Living Theory Revisited

Lints, F.A.

doi:10.1159/000212998

Cited by 72 publications

(48 citation statements)

References 18 publications

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“…the faster a species lived, the faster it would die. But although life span is not unrelated to metabolism (Economos, 1981), the rate of living theory remains controversial (Burns, 2004) and is generally discounted (Lints, 1989). …”

Section: Model Speciesmentioning

confidence: 99%

Extrapolating brain development from experimental species to humans

et al. 2007

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To better understand the neurotoxic effects of diverse hazards on the developing human nervous system, researchers and clinicians rely on data collected from a number of model species that develop and mature at varying rates. We review the methods commonly used to extrapolate the timing of brain development from experimental mammalian species to humans, including morphological comparisons, "rules of thumb" and "event-based" analyses. Most are unavoidably limited in range or detail, many are necessarily restricted to rat/human comparisons, and few can identify brain regions that develop at different rates. We suggest this issue is best addressed using "neuroinformatics", an analysis that combines neuroscience, evolutionary science, statistical modeling and computer science. A current use of this approach relates numeric values assigned to ten mammalian species and hundreds of empirically derived developing neural events, including specific evolutionary advances in primates. The result is an accessible, online resource (http:// www.translatingtime.net/) that can be used to equate dates in the neurodevelopmental literature across laboratory species to humans, predict neurodevelopmental events for which data are lacking in humans, and help to develop clinically relevant experimental models.

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Section: Model Speciesmentioning

confidence: 99%

Extrapolating brain development from experimental species to humans

et al. 2007

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“…The increased mtDNA stability and longevity could be related to the deficiency in ATP production. Indeed, the idea that a slow rate of living caused by a reduced rate of energy metabolism results in an increased lifespan is currently proposed (48,49). According to this hypothesis, the balance between the rate of molecular damage and that of its repair sets lifespan.…”

Section: Respiratory-dependent Parameters Controlling Mtdna Maintenancementioning

confidence: 99%

A causal link between respiration and senescence in Podospora anserina

Dufour

Boulay

Rincheval

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

160

139

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Senescence, a progressive degenerative process leading to agerelated increase in mortality, is found in most eukaryotes. However, the molecular events underlying aging remain largely unknown. Understanding how longevity is regulated is a fundamental problem. Here we demonstrate that the respiratory function is a key factor that contributes to shortening lifespan of the filamentous fungus Podospora anserina. In this organism, senescence is systematically associated with mitochondrial DNA instabilities. We show that inactivation of the nuclear COX5 gene encoding subunit V of the cytochrome c oxidase complex leads to the exclusive use of the alternative respiratory pathway and to a decrease in production of reactive oxygen species. This inactivation results in a striking increase of longevity associated with stabilization of the mitochondrial chromosome. Moreover, accumulation of several senescence-specific mitochondrial DNA molecules is prevented in this nuclear mutant. These findings provide direct evidence of a causal link between mitochondrial metabolism and longevity in Podospora anserina.

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“…But, of course, that theory has long since been disproved [13,14] and estimating lifetime caloric expenditure makes no such implication. The caloric-age approach does, however, imply that longevity is strongly influenced by the total caloric consumption -in keeping with growing evidence in both animals and humans that caloric reduction promotes longevity [7].…”

Section: Discussionmentioning

confidence: 99%

Measuring Human Age by Estimating Lifetime Caloric Consumption

Gruber

Kalamas²

1999

Gerontology

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Background: This study was prompted by a desire to measure human age by a means other than chronological or biological age. The purpose of the study was to use the total lifetime caloric intake in men as an index of aging. Method: The study was carried out by developing an algorithm to approximate the lifetime caloric intake. The total caloric intake is expressed such that one calorie-age year is defined as the total calories expended by an individual during his/her 20th year. Results: The results indicated that (1) the caloric intake of men progressively decreases with advancing age, that (2) the caloric-age is usually less than chronological age, and that (3) the caloric-age algorithm is a simple although crude method to assess lifetime caloric intake. Conclusion: The most important conclusion is that a person can get a better appreciation of the importance of avoiding excess caloric intake if human age is measured in terms of lifetime caloric intake.

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The Rate of Living Theory Revisited

Cited by 72 publications

References 18 publications

Extrapolating brain development from experimental species to humans

Extrapolating brain development from experimental species to humans

A causal link between respiration and senescence in Podospora anserina

Measuring Human Age by Estimating Lifetime Caloric Consumption

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