http://precedings.nature.com/tags/longevity Recently posted documents tagged with 'longevity' Nature Publishing Group en Nature Precedings http://precedings.nature.com/images/header_logo.gif http://precedings.nature.com http://precedings.nature.com/documents/3915/version/1 Much literature invokes natural selection to explain the pervasive deficit in the average lifespan of men compared to women.1 The explanation assumes that mothers, not fathers, provisioned children over much of human existence, and that women who lived long enough to help their children and grand children survive to reproductive age had more grandchildren and great-grandchildren than did shorter-lived women.2 Although this argument implies that natural selection would conserve mutations that conferred longevity on mothers but not fathers,3,4 it offers no explanation of the considerable changes over historic time in the male longevity deficit thereby implying that these arise solely from culture.5 I show, however, that natural selection in utero empirically predicts variability over time in the deficit. This mechanism spontaneously aborts less fit fetuses during stressful times and reportedly selects more against males than females. My finding suggests that natural selection interacts with culture to predictably affect both the life span and sex ratio of contemporary human populations. http://precedings.nature.com/documents/3915/version/1 Thu, 29 Oct 2009 13:30:34 UTC Natural Selection In Utero Contributes to the Male Longevity Deficit in Contemporary Human Populations hdl:10101/npre.2009.3915.1 2009-10-29 Ralph Catalano Nature Precedings 2009-10-29T13:30:34Z Manuscript Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2988/version/3 It is now increasingly realized that the underlying mechanisms which govern aging is a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of ‘faults’ on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood 2006. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as ‘damage’ and ‘fault’ are not specified. Therefore we introduce here a specification of the underlying mechanism of aging and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory introduced in the present paper gives explanations for the aging phenotypes, premature aging, and the difference of longevity in different species, and is consistent with the point of view of physical theory of complex adaptive systems. http://precedings.nature.com/documents/2988/version/3 Wed, 17 Jun 2009 20:08:26 UTC Aging as a consequence of misrepair—A novel theory of aging hdl:10101/npre.2009.2988.3 2009-06-17 Thomas Michelitsch Nature Precedings 2009-06-17T20:08:26Z Manuscript Developmental Biology Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://dx.doi.org/10.1038/npre.2009.2988.2 It is now increasingly realized that the underlying mechanisms which govern aging is a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of ‘faults’ on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood 2006. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as ‘damage’ and ‘fault’ are not specified. Therefore we introduce here a specification of the underlying mechanism of aging and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory introduced in the present paper gives explanations for the aging phenotypes, premature aging, and the difference of longevity in different species, and is consistent with the point of view of physical theory of complex systems. http://dx.doi.org/10.1038/npre.2009.2988.2 Mon, 06 Apr 2009 09:27:20 UTC Aging as a consequence of misrepair—A novel theory of aging doi:10.1038/npre.2009.2988.2 2009-04-06 Thomas Michelitsch Nature Precedings 2009-04-06T09:27:20Z Manuscript Developmental Biology Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2988/version/1 It is now increasingly realized that the underlying mechanisms which govern aging is a complex interplay of genetic regulation and damage accumulation. Aging as a result of accumulation of ‘faults’ on cellular and molecular levels, has been proposed in the damage (fault)-accumulation theory by Kirkwood 2006. However, this theory fails to explain some aging phenotypes such as fibrosis and premature aging, since terms such as ‘damage’ and ‘fault’ are not specified. Therefore we introduce here a specification of the underlying mechanism and arrive at a novel theory: aging of the body is a result of the accumulation of Misrepair of tissue. It emphasizes: a) it is Misrepair, not the original damage, that accumulates and leads to aging; and b) aging can occur at different levels, however aging of the body takes place at least on the tissue level, but not necessarily on cellular/molecular level. The novel concept of Misrepair which is introduced here unifies the understanding of the roles of environmental damage, repair, gene regulation, and multicellular structure in the aging process. The Misrepair-accumulation theory which is introduced here gives also explanations for the aging phenotypes, premature aging, and the difference of longevity in different species and is consistent with the point of view of physical theory of complex systems. http://precedings.nature.com/documents/2988/version/1 Mon, 30 Mar 2009 08:51:45 UTC Aging as a consequence of misrepair—A novel theory of aging hdl:10101/npre.2009.2988.1 2009-03-30 Thomas Michelitsch Nature Precedings 2009-03-30T08:51:45Z Manuscript Developmental Biology Evolutionary Biology http://creativecommons.org/licenses/by/3.0/ http://precedings.nature.com/documents/2071/version/1 Aging is one of the most intriguing processes of biology and despite decades of research, many aspects of aging are poorly understood. Aging is known to occur in bacteria and yeast that divide with morphological asymmetry. Morphologically symmetrically dividing bacteria such as Escherichia coli were assumed not to age until they were shown to divide with functional asymmetry leading to aging and death of some of the cells even in exponentially growing cultures. In asymmetrically dividing E. coli the newly synthesized components are presumed to occupy one pole so that after division one of the daughter cells receives newly synthesized components whereas the other retains the older components. Mathematical models predicted that at the population level, asymmetric growth should result in higher growth rate and symmetric growth in higher growth yield. Therefore, arguably symmetric cell division should be selected in low nutrient environments and asymmetric division in nutrient rich environments. A further prediction was that lower substrate concentrations should strengthen repair mechanisms and suppress aging whereas higher substrate concentrations suppress repair and enhance aging. We show here that E. coli divides more symmetrically under caloric restriction, that both genetic selection and phenotypic plasticity are important determinants of cell division symmetry and also that the proportion of cells that stop dividing and therefore are presumably dead is significantly lower in symmetrically dividing cultures. However, contrary to the prediction, symmetry was not always accompanied by reduced growth rate. These results demonstrate that asymmetry of division in E. coli is not hardwired but responsive to the nutritional environment. This provides a new perspective on why caloric restriction increases lifespan in organisms ranging from microbes to mammals. Symmetry of division may be a mechanism spanning across the width of life forms but regulating aging in different ways in different forms. http://precedings.nature.com/documents/2071/version/1 Mon, 28 Jul 2008 14:55:40 UTC Caloric restriction causes symmetric cell division and delays aging in Escherichia coli hdl:10101/npre.2008.2071.1 2008-07-28 Milind G. Watve Nature Precedings 2008-07-28T14:55:40Z Manuscript Microbiology http://creativecommons.org/licenses/by/3.0/