By William R. Clark
Why can we age? Is getting older inevitable? Will advances in clinical wisdom let us expand the human lifespan past its current limits? simply because getting older has lengthy been the only irreducible truth of human life, those fascinating questions come up extra usually within the context of technology fiction than technology truth. yet fresh discoveries within the fields of telephone biology and molecular genetics are heavily difficult the idea that human lifespans are past our keep an eye on. With such discoveries in brain, famous cellphone biologist William R. Clark sincerely and assuredly describes how senescence starts on the point of person cells and the way mobile replication will be certain up with getting older of the complete organism. He explores the evolutionary starting place and serve as of getting older, the mobile connections among getting older and melanoma, the parallels among mobile senescence and Alzheimer's ailment, and the insights received via learning human genetic disorders--such as Werner's syndrome--that mimic the indicators of getting older. Clark additionally explains how aid in caloric consumption may very well aid raise lifespan, and the way the damaging results of oxidative components within the physique can be restricted via the intake of antioxidants present in vegetables and fruit. In a last bankruptcy, Clark considers the social and monetary features of dwelling longer, the consequences of gene treatment on senescence, and what we would 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 prone 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
The other copy is retained by the mother cell. Unlike true fission as used by bacteria and paramecia, the two cells resulting from budding are not otherwise equal. Yeast cells are quite large, and the cells emerging from a budding event can be segregated and followed separately. The individual identity of the cell in which budding originates (the mother cell) is preserved when the process is finished; the product of budding is not two identical daughter cells, but a mother and a daughter. And the mother is older than before budding began.
The problem with such "group selectionist" theories is that there is simply no known mechanism whereby they could actually work. As we will discuss in more detail in a moment, variants of existing genes arise within an individual organism. They either allow that individual to breed more effectively, or they don't. If they do, the new variants can, as a result of enhanced breeding efficiency of the "founding" individual and its offspring, over many generations come to be carried by a significant number of other individuals in the species.
This brings up a concept alluded to in our discussion so far, but not fully explained: maximum possible lifespan. Although important to *Because old age is not a single, easily definable stage of life, demographers have found it useful to divide old age into several distinct phases. Throughout this book, we will use the following nomenclature to define stages in the aging of humans. Youngest-old: 50-65 years; old: 65-85 years; oldest-old: 85-99 years; centenarians: 100 years and older. 13 A M E A N S TO AN END both basic scientists and demographers, maximum lifespan is a bit of a slippery concept.