Global Air Pollution in Aging: Reading Smoke Signals is a complete reference connecting environmental pollution research to the human aging process. Since 1800, lifespans have more than doubled as infections declined and medicine improved. But the 20th century introduced a new global scourge of air pollution from fossil fuels with the potential to damage arteries, hearts and lungs that has been related to chronic exposure of air pollution from fossil fuels. Risk areas of study include childhood obesity, brain damage associated with air pollution, increased risk for autism in children and dementia in older adults. In humans and animals, air pollution stimulates chronic inflammation in different organs, and genetic vulnerability to air pollution is being recognized, particularly for carriers of the Alzheimer risk gene ApoE4.

Written by Caleb Finch, one of the leading scientists of our time, The Biology of Human Longevity - Inflammation, Nutrition, and Aging in the Evolution of Lifespans synthesizes several decades of top research on the topic of human aging and longevity particularly on the recent theories of inflammation and its effects on human health. The book expands a number of existing major theories, including the Barker theory of fetal origins of adult disease to consider the role of inflammation and Harmon's free radical theory of aging to include inflammatory damage. Future increases in lifespan are challenged by the obesity epidemic and spreading global infections which may reverse the gains made in lowering inflammatory exposure. This timely and topical book will be of interest to anyone studying aging from any scientific angle.
* Author Caleb Finch is a highly influential and respected scientist, ranked in the top half of the 1% most cited scientists
* Provides a novel synthesis of existing ideas about the biology of longevity and aging
* Incorporates important research findings from several disciplines, including Gerontology, Genomics, Neuroscience, Immunology, Nutrition

Aging is one of those subjects that many biologists feel is largely unknown. Therefore, they often feel comfortable offering extremely facile generalizations that are either unsupported or directly refuted in the experimental literature. Despite this unfortunate precedent, aging is a very broad phenomenon that calls out for integration beyond the mere collecting together of results from disparate laboratory organisms. With this in mind, Part One offers several different synthetic perspectives. The editors, Rose and Finch, provide a verbal synthesis of the field that deliberately attempts to look at aging from both sides, the evolutionary and the molecular. The articles by Charlesworth and Clark both provide population genetic perspectives on aging, the former more mathematical, the latter more experimental. Bell takes a completely different approach, arguing that aging may not be the result of evolutionary forces. Bell's model instead proposes that aging could arise from the progressive deterioration of chronic host pathogen interactions. This is the first detailed publication of this model. It marks something of a return to the type of aging theories that predominated in the 1950's and 1960's, theories like the somatic mutation and error catastrophe theories. We hope that the reader will be interested by the contrast in views between the articles based on evolutionary theory and that of Bell. MR. Rose and C. E. Finch (eds. ), Genetics and Evolution of Aging, 5-12, 1994. (c) 1994 Kluwer Academic Publishers. The J aniform genetics of aging 2 Michael R. Rosel & Caleb E."

In this third volume on longevity Fondation Ipsen has again collected the most recent results in research on genes and diet in the evolution of human longevity, educational level and longevity, cognitive impairment and survival at older age and other contributions. The preponderance of relatively short - compared to long-lived organisms suggests that morphogenesis is easier to accomplish than is maintenace of soma, whereas the broad range of longevities of organisms demonstrates that maintaining soma for extended periods of time is possible. The underlying assumption of "disposable soma" theory of aging is that the expense of maintaining somatic cells depends on their contribution to the welfare of the germ cells.