By William R. Clark
Why will we age? Is getting older inevitable? Will advances in scientific wisdom let us expand the human lifespan past its current limits? simply because getting older has lengthy been the only 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 cellphone biology and molecular genetics are heavily hard the idea that human lifespans are past our regulate. With such discoveries in brain, famous phone biologist William R. Clark sincerely and assuredly describes how senescence starts on the point of person cells and the way mobile replication could be certain up with getting older of the total 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 affliction, and the insights won via learning human genetic disorders--such as Werner's syndrome--that mimic the indicators of getting older. Clark additionally explains how relief in caloric consumption may very well support elevate lifespan, and the way the damaging results of oxidative components within the physique might be constrained by means of the intake of antioxidants present in vegetables and fruit. In a last bankruptcy, Clark considers the social and financial features of residing longer, the consequences of gene remedy on senescence, and what we would find out about getting older from experiments in cloning. it is a hugely readable, provocative account of a few of the main far-reaching and arguable questions we're more likely to ask within the subsequent century.
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Additional resources for A Means to an End: The Biological Basis of Aging and Death
It could be defined as the last documentable point on the survival curve for a species at which an individual has been observed to be alive. It is often defined as the average age of some small proportion—1 percent or so—of the longest living members of a species. We do not know exactly where along the age axis in curves C and D the true maximum lifespan lies for humans; it is certainly closer to the "three-score and ten" of the 90th Psalm than to the 900-plus years attributed to some of the Old Testament patriarchs.
They die from disease or predation long before they become noticeably old; for most species, elderly individuals can be found only in zoos or laboratories. That means that the very thing natural selection is supposed to act upon rarely ever shows up in nature. Yet, if kept in zoos or labs, animals definitely do age. But where did the genes responsible for aging come from? To get around these problems, some of the early evolutionary theorists proposed that certain traits may be selected for in evolution that are contrary to the interests of the individual, as long as they benefit the species to which the individual belongs.
This gradual slide through reduced metabolic activity toward arrested cell division and death represents another expression of replicative senescence. An interesting and fundamentally important feature of replicative senescence in Saccharomyces is that it is a dominant trait. For example, when an older cell gives rise to a daughter by budding, the daughter will actually divide somewhat slowly for one or two cell divisions, at the rate of the mother, before rebounding to the more rapid replication rate of a younger cell.
A Means to an End: The Biological Basis of Aging and Death by William R. Clark