What determines longevity: Metabolic rate or stability?
نویسندگان
چکیده
Extract: The conventional wisdom about why species age and live as long as they do is based in part on the modern version of the very old and now discredited "rate of living" (ROL) theory of aging. According to the old ROL theory, aging is caused by the loss of some vital substance such as water or hormones - the more rapid the vital substance is used up the shorter the lifespan. The modern and more plausible version of ROL is based on a hypothesis formulated by Raymond Pearl (1921) in the early 20th century where it was suggested that the primary determinant of how long species live is influenced by the relative speed of their resting metabolism. That is, metabolic rate is thought to be inversely proportional to maximum lifespan, which means that species that live fast will die young while those that have a slower metabolic rate live slower and longer. The evolutionary theory of why aging occurs that arose in the 20th century conceptually supports predictions from the metabolic rate theory, although the evolutionary line of reasoning is silent about the mechanisms involved. According to evolution theory, animals that face high extrinsic mortality such as predation and infectious diseases must develop quickly (i.e., live fast) in order to pass their genes onto the next generation before death occurs, while animals that face low extrinsic mortality delay development and reproduction, and thus live slower and longer.
منابع مشابه
Studies of Caenorhabditis elegans DAF-2/insulin signaling reveal targets for pharmacological manipulation of lifespan
Much excitement has arisen from the observation that decrements in insulin-like signaling can dramatically extend lifespan in the nematode, Caenorhabditis elegans, and fruitfly, Drosophila melanogaster. In addition, there are tantalizing hints that the IGF-I pathway in mice may have similar effects. In addition to dramatic effects on lifespan, invertebrate insulin-like signaling also promotes c...
متن کاملGenetic and environmental conditions that increase longevity in Caenorhabditis elegans decrease metabolic rate.
Mutations that increase the longevity of the soil nematode Caenorhabditis elegans could define genes involved in a process specific for aging. Alternatively, these mutations could reduce animal metabolic rate and increase longevity as a consequence. In ectotherms, longevity is often negatively correlated with metabolic rate. Consistent with these observations, environmental conditions that redu...
متن کاملPii: S0197-4580(99)00095-0
The genetic analysis of the yeast replicative life span has revealed the importance of metabolic control and resistance to stress. It has also illuminated the pivotal role in determining longevity that the RAS genes play by the maintenance of homeostasis. This role appears to be performed by the coordination of a variety of cellular processes. Metabolic control seems to occupy a central positio...
متن کاملTesting the "rate of living" model: further evidence that longevity and metabolic rate are not inversely correlated in Drosophila melanogaster.
In a recent study examining the relationship between longevity and metabolism in a large number of recombinant inbred Drosophila melanogaster lines, we found no indication of the inverse relationship between longevity and metabolic rate that one would expect under the classical "rate of living" model. A potential limitation in generalizing from that study is that it was conducted on experimenta...
متن کاملChapter 15 Oxidative Stress and the Aging Brain: From Theory to Prevention
Aging is characterized by a progressive decline in the efficiency of physiological function and by the increased susceptibility to disease and death. Currently, one of the most plausible and acceptable explanations for the mechanistic basis of aging is the “free radical theory of aging.” This theory postulates that aging and its related diseases are the consequence of free radical-induced damag...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
- Discovery medicine
دوره 5 28 شماره
صفحات -
تاریخ انتشار 2005