By William R. Clark
Why will we age? Is getting older inevitable? Will advances in clinical wisdom let us expand the human lifespan past its current limits? simply because getting old has lengthy been the single irreducible truth of human lifestyles, those exciting questions come up extra usually within the context of technological know-how fiction than technological know-how truth. yet fresh discoveries within the fields of phone biology and molecular genetics are heavily difficult the belief that human lifespans are past our keep watch over. With such discoveries in brain, famous cellphone biologist William R. Clark essentially and assuredly describes how senescence starts on the point of person cells and the way mobile replication could be sure up with getting older of the complete organism. He explores the evolutionary foundation and serve as of getting older, the mobile connections among getting older and melanoma, the parallels among mobile senescence and Alzheimer's illness, and the insights won via learning human genetic disorders--such as Werner's syndrome--that mimic the indications of getting older. Clark additionally explains how aid in caloric consumption may very well support bring up lifespan, and the way the harmful results of oxidative components within the physique could be restricted through the intake of antioxidants present in fruit and veggies. In a last bankruptcy, Clark considers the social and monetary elements of dwelling longer, the consequences of gene treatment on senescence, and what we would know about getting older from experiments in cloning. this can be a hugely readable, provocative account of a few of the main far-reaching and arguable questions we're prone to ask within the subsequent century.
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Additional info for A Means to an End: The Biological Basis of Aging and Death
This parameter, too, correlates roughly with size, in that smaller animals must consume much more food per unit time and per unit body weight than larger animals. This means that they also must deal with a higher level of metabolic waste products per unit time and body weight. As we will see in a later chapter, some of these by-products—especially of oxygen—are toxic, and are a major contributing factor in cellular senescence. Although relatively constant for a species living in its natural environment, for many single-cell and even multicellular organisms, maximum lifespan can be shortened or lengthened in the laboratory by manipulations as simple as changing the growth temperature.
The challenge for the biogerontologist is not only to untangle the causes of organismal senescence from one another, but to try to understand how they relate to underlying causes of cellular senescence. And at the cellular level, where senescence is still multifaceted, the task will be to determine which causes of senescence are truly primary, and to understand their genetic and molecular basis. Then, and only then, will we truly understand the aging process. This investigation is well under way, and what we have learned so far is described in the remainder of this book.
Although relatively constant for a species living in its natural environment, for many single-cell and even multicellular organisms, maximum lifespan can be shortened or lengthened in the laboratory by manipulations as simple as changing the growth temperature. This is presumably due to alterations in metabolic rates, reinforcing the notion that maximum lifespan is governed at least in part by metabolic processes. Maximum lifespan can also be altered by dietary manipulation, mainly by restricting the intake of calories.