scholarly journals The Danaid Theory of Aging

Author(s):  
Maarten J. Wensink ◽  
Alan A. Cohen

The classical evolutionary theories of aging suggest that aging evolves due to insufficient selective pressure against it. In these theories, declining selection pressure with age leads to aging through genes or resource allocations, implying that aging could potentially be stalled were genes, resource allocation, or selection pressure somewhat different. While these classical evolutionary theories are undeniably part of a description of the evolution of aging, they do not explain the diversity of aging patterns, and they do not constitute the only possible evolutionary explanation. Without denying selection pressure a role in the evolution of aging, we argue that the origin and diversity of aging should also be sought in the nature and evolution of organisms that are, from their very physiological make up, unmaintainable. Drawing on advances in developmental biology, genetics, biochemistry, and complex systems theory since the classical theories emerged, we propose a fresh evolutionary-mechanistic theory of aging, the Danaid theory. We argue that, in complex forms of life like humans, various restrictions on maintenance and repair may be inherent, and we show how such restrictions are laid out during development. We further argue that there is systematic variation in these constraints across taxa, and that this is a crucial factor determining variation in aging and lifespan across the tree of life. Accordingly, the core challenge for the field going forward is to map and understand the mosaic of constraints, trade-offs, chance events, and selective pressures that shape aging in diverse ways across diverse taxa.

2018 ◽  
Author(s):  
Peter Lenart ◽  
Julie Bienertová-Vašků ◽  
Luděk Berec

AbstractSince at first sight aging seems to be omnipresent, many authors to this very day regard it as an inevitable consequence of the laws of physics. However, studies published in the past two decades have conclusively shown that a number of organisms do not age, or at least do not age on a scale comparable with other aging organisms. This disparity leads us to question why aging evolved in some organisms and not in others. We thus present a mathematical model which simulates evolution in a sexually reproducing population composed of aging and non-aging individuals. We have observed that aging individuals may outcompete non-aging individuals if they have a higher starting fertility or if the main mating pattern in the population is assortative mating. Furthermore, stronger pathogen pressure was found to help the aging phenotype when compared to the non-aging phenotype. Last but not least, the aging phenotype was found to more easily outcompete the non-aging one or to resist the dominance of the latter for a longer period of time in populations composed of dimorphic sexually reproducing individuals compared to populations of hermaphrodites. Our findings are consistent with both classical evolutionary theories of aging and with evolutionary theories of aging which assume the existence of an aging program. They can thus potentially work as a bridge between these two opposing views, suggesting that the truth in fact lies somewhere in between.Significance StatementThis study presents the first mathematical model which simulates the evolution of aging in a population of sexually reproducing organisms. Our model shows that aging individuals may outcompete non-aging individuals in several scenarios known to occur in nature. Our work thus provides important insight into the question why aging has evolved in most, but not all, organisms.


2002 ◽  
Vol 2 ◽  
pp. 339-356 ◽  
Author(s):  
Leonid A. Gavrilov ◽  
Natalia S. Gavrilova

The purpose of this article is to provide students and researchers entering the field of aging studies with an introduction to the evolutionary theories of aging, as well as to orient them in the abundant modern scientific literature on evolutionary gerontology. The following three major evolutionary theories of aging are discussed: 1) the theory of programmed death suggested by August Weismann, 2) the mutation accumulation theory of aging suggested by Peter Medawar, and 3) the antagonistic pleiotropy theory of aging suggested by George Williams. We also discuss a special case of the antagonistic pleiotropy theory, the disposable soma theory developed by Tom Kirkwood and Robin Holliday. The theories are compared with each other as well as with recent experimental findings. At present the most viable evolutionary theories are the mutation accumulation theory and the antagonistic pleiotropy theory; these theories are not mutually exclusive, and they both may become a part of a future unifying theory of aging.Evolutionary theories of aging are useful because they open new oppor-tunities for further research by suggesting testable predictions, but they have also been harmful in the past when they were used to impose limitations on aging studies. At this time, the evolutionary theories of aging are not ultimate completed theories, but rather a set of ideas that themselves require further elaboration and validation. This theoretical review article is written for a wide readership.


BMC Biology ◽  
2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Martin I. Brengdahl ◽  
Christopher M. Kimber ◽  
Phoebe Elias ◽  
Josephine Thompson ◽  
Urban Friberg

Abstract Background In order for aging to evolve in response to a declining strength of selection with age, a genetic architecture that allows for mutations with age-specific effects on organismal performance is required. Our understanding of how selective effects of individual mutations are distributed across ages is however poor. Established evolutionary theories assume that mutations causing aging have negative late-life effects, coupled to either positive or neutral effects early in life. New theory now suggests evolution of aging may also result from deleterious mutations with increasing negative effects with age, a possibility that has not yet been empirically explored. Results To directly test how the effects of deleterious mutations are distributed across ages, we separately measure age-specific effects on fecundity for each of 20 mutations in Drosophila melanogaster. We find that deleterious mutations in general have a negative effect that increases with age and that the rate of increase depends on how deleterious a mutation is early in life. Conclusions Our findings suggest that aging does not exclusively depend on genetic variants assumed by the established evolutionary theories of aging. Instead, aging can result from deleterious mutations with negative effects that amplify with age. If increasing negative effect with age is a general property of deleterious mutations, the proportion of mutations with the capacity to contribute towards aging may be considerably larger than previously believed.


Gerontology ◽  
2009 ◽  
Vol 55 (2) ◽  
pp. 205-216 ◽  
Author(s):  
Predrag Ljubuncic ◽  
Abraham Z. Reznick

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Stephen Cutie ◽  
Guo N. Huang

AbstractCardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury – as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.


2002 ◽  
Vol 99 (22) ◽  
pp. 14286-14291 ◽  
Author(s):  
K. A. Hughes ◽  
J. A. Alipaz ◽  
J. M. Drnevich ◽  
R. M. Reynolds

The Condor ◽  
2007 ◽  
Vol 109 (1) ◽  
pp. 132-141
Author(s):  
Diego Santiago-Alarcon ◽  
Patricia G. Parker

Abstract Abstract Sexual size dimorphism is a conspicuous trait of many wild bird species. Differences in body size between the sexes might reflect selective pressures and trade-offs to optimize performance. Here, we analyze the size dimorphism of the Galápagos Dove (Zenaida galapagoensis) using principal component and discriminant analyses with samples obtained from six islands: Santiago, Santa Fe, Santa Cruz, Española, Genovesa, and Wolf. We also reanalyze published morphological data but also including additional samples from Wolf Island to account for morphological differences among islands. Males were significantly larger than females. Discriminant analyses correctly classified 98% of males and 100% of females, and cross-validation of the model correctly classified 97% of males and 98% of females. We created two sexual size dimorphism indices using wing chord and tarsus as body-size surrogates. Significant differences were found in the sexual size dimorphism index for both measurements among islands. Significant differences in sexual size dimorphism among islands might indicate the role of different selective pressures acting on individual islands (e.g., competition, predation, resources, sexual selection), which might result in life history variation of the species among islands. For the first time, we provide significant morphological evidence supporting the classification of the Galápagos Dove into two subspecies: Z. g. galapagoensis and Z. g. exsul.


Author(s):  
Kevin S. Shah ◽  
Kalyanam Shivkumar ◽  
Mehdi Nojoumi ◽  
Barbara Natterson-Horowitz

Cardiovascular (CV) disease is the leading killer of our species. Various evolutionary lenses can be applied to better understand human vulnerability to CV disorders. The evolutionary origins of a healthy human heart—its myocardial, electrophysiologic, valvular and vascular systems—offers a history of the selective pressures, trade-offs and adaptations leading to the normal mammalian CV systems. Beyond these evolutionary-developmental perspectives, the application of a framework based on Tinbergen’s four questions offers a novel evolutionary lens for understanding our species’ vulnerability to CV pathology. This is done by a consideration of comparative information about non-human animals who spontaneously develop the same CV diseases. This phylogenetic information can then be used to develop trade-off-based adaptive hypotheses to explain the nature and origins of vulnerability to a range of CV pathologies including atherosclerosis, heart failure, valvular heart disease and arrhythmias.


2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Tomoyoshi Komiyama ◽  
Mengjie Lin ◽  
Atsushi Ogura

Chickens have been familiar to humans since ancient times and have been used not only for culinary purposes but also for cultural purposes including ritual ceremonies and traditional entertainment. The various chicken breeds developed for these purposes often display distinct morphological and/or behavioural traits. For example, the JapaneseShamois larger and more aggressive than other domesticated chickens, reflecting its role as a fighting cock breed, whereas JapaneseNaganakidoribreeds, which have long-crowing behaviour, were bred instead for their entertaining and aesthetic qualities. However, the genetic backgrounds of these distinct morphological and behavioural traits remain unclear. Therefore, the question arises as to which genomic regions in these chickens were acted upon by selective pressures through breeding. We compared the entire genomes of six chicken breeds domesticated for various cultural purposes by utilizing array comparative genomic hybridization. From these analyses, we identified 782 regions that underwent insertions, deletions, or mutations, representing man-made selection pressure in these chickens. Furthermore, we found that a number of genes diversified in domesticated chickens bred for cultural or entertainment purposes were different from those diversified in chickens bred for food, such as broilers and layers.


2015 ◽  
Author(s):  
Maja Slijepčević ◽  
Frietson F Galis ◽  
Jan W Arntzen ◽  
Ana Ivanović

We explored intraspecific variation in vertebral formulae, more specifically the variation in the number of thoracic vertebrae and frequencies of transitional sacral vertebrae in Triturus newts (Caudata: Salamandridae). Within salamandrid salamanders this monophyletic group shows the highest disparity in the number of thoracic vertebrae and considerable intraspecific variation in the number of thoracic vertebrae. Triturus species also differ in their ecological preferences, from predominantly terrestrial to largely aquatic. Following Geoffroy St. Hilaire’s and Darwin’s rule which states that structures with a large number of serially homologous repetitive elements are more variable than structures with smaller numbers, we hypothesized that the variation in vertebral formulae increases in more elongated species with a larger number of thoracic vertebrae. We furthermore hypothesized that the frequency of transitional vertebrae will be correlated with the variation in the number of thoracic vertebrae within the species. We also investigated potential effects of species hybridization on the vertebral formula. The proportion of individuals with a number of thoracic vertebrae different from the modal number and the range of variation in number of vertebrae significantly increased in species with a larger number of thoracic vertebrae. Contrary to our expectation, the frequencies of transitional vertebrae were not correlated with frequencies of change in the complete vertebrae number. The frequency of transitional sacral vertebra in hybrids did not significantly differ from that of the parental species. Such a pattern could be a result of selection pressure against transitional vertebrae and/or a bias towards the development of full vertebrae numbers. Although our data indicate relaxed selection for vertebral count changes in more elongated, aquatic species, more data on different selective pressures in species with different numbers of vertebrae in the two contrasting, terrestrial and aquatic environments are needed to test for causality.


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