By William R. Clark
Why can we age? Is getting older inevitable? Will advances in scientific wisdom let us expand the human lifespan past its current limits? simply because growing older has lengthy been the single irreducible fact of human life, those exciting questions come up extra usually within the context of technological know-how fiction than technology truth. yet contemporary discoveries within the fields of phone biology and molecular genetics are heavily demanding the belief that human lifespans are past our keep watch over. With such discoveries in brain, famous phone biologist William R. Clark basically and elegantly describes how senescence starts off 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 indications of getting older. Clark additionally explains how aid in caloric consumption may very well aid elevate lifespan, and the way the harmful results of oxidative components within the physique can be restricted through the intake of antioxidants present in fruit and veggies. In a last bankruptcy, Clark considers the social and financial elements of residing longer, the consequences of gene remedy on senescence, and what we'd know about getting older from experiments in cloning. it is a hugely readable, provocative account of a few of the main far-reaching and debatable 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
Rather, a collection of senescence-inducing mechanisms, based on cellular senescence and leading to the eventual extinction of the somatic organism, has become part of the eukaryotic heritage. A very large proportion of these mechanisms were in fact already in place in the earliest single-cell eukaryotic organisms. Nonreplicative Senescence in Eukaryotic Cells Not all cells divide; in fact, aside from cells lining the intestines, skin cells, bone marrow cells, and a few other examples, most cells in adult organisms do not divide most of the time.
13 A M E A N S TO AN END both basic scientists and demographers, maximum lifespan is a bit of a slippery concept. 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.
It seems quite likely that senescence, accompanied by obligatory death, appeared in evolution very close to the time that eukaryotes first emerged from prokaryotes. None of the protists in existence today expresses senescence exactly as we find it in more advanced multicellular animals, but there can be no question that aging was a normal part of the protist life cycle. One trend in the evolution of early eukaryotes was simply to get larger; the freshwater ciliated protozoan called Paramecium is an excellent example of this trend.
A Means to an End: The Biological Basis of Aging and Death by William R. Clark