Are Glycans the Holy Grail for Biomarkers of Aging? (Comment On: Glycans Are a Novel Biomarker of Chronological and Biological Age by Kristic Et Al.)

Total Page:16

File Type:pdf, Size:1020Kb

Are Glycans the Holy Grail for Biomarkers of Aging? (Comment On: Glycans Are a Novel Biomarker of Chronological and Biological Age by Kristic Et Al.) Journals of Gerontology: BIOLOGICAL SCIENCES © The Author 2013. Published by Oxford University Press on behalf of The Gerontological Society of America. Cite journal as: J Gerontol A Biol Sci Med Sci 2014 July;69(7):777–778 All rights reserved. For permissions, please e-mail: [email protected]. doi:10.1093/gerona/glt202 Advance Access publication December 10, 2013 Guest Editorial Are Glycans the Holy Grail for Biomarkers of Aging? (Comment on: Glycans Are a Novel Biomarker of Chronological and Biological Age by Kristic et al.) David G. Le Couteur,1,2,3 Stephen J. Simpson,3,4 and Rafael de Cabo5 Downloaded from https://academic.oup.com/biomedgerontology/article/69/7/777/662886 by guest on 24 September 2021 1Centre for Education and Research on Ageing and 2ANZAC Research Institute, University of Sydney and Concord Repatriation General Hospital, New South Wales, Australia. 3The Charles Perkins Centre and 4School of Biological Sciences, University of Sydney, Australia. 5Translational Gerontology Branch, National Institute on Ageing, Baltimore. Address correspondence to David Le Couteur, PhD, Centre for Education and Research on Ageing, University of Sydney and Concord Repatriation General Hospital, Hospital Rd, Concord, Sydney, NSW 2139, Australia. Email: [email protected] Posttranslational modifications of circulating proteins such as immunoglobulins may prove to be important biomarkers of aging. Key Words: Biomarkers of aging—Glycans. Received November 11, 2013; Accepted November 12, 2013 Decision Editor: Rafael de Cabo, PhD Valuating the effect of any intervention that influ- •• It must monitor a basic process that underlies the aging Eences aging requires some sort of endpoint to be meas- process, not the effects of disease ured, ideally life span. Maximum life span is the key outcome •• It must be able to be tested repeatedly without harming influenced primarily by interventions that act on aging and the person or animal is the gold standard. Median life span can also be influenced •• It must be something that works in human and in labora- by interventions that prevent disease, thereby squaring popu- tory animals (3) lation survival curves without necessarily extending maxi- From a pragmatic perspective, biomarkers of aging mum life span. Measurement of either median or maximum should also be easy to measure (eg, blood tests) and change life span requires the study of large populations over their over a relatively short period of time (4). lifetime, which, in long-lived species, is an insurmountable In human clinical trials of diseases, surrogate mark- barrier. Thus clinical trials in humans are unlikely to use life ers and composite outcomes are well-established, if span as an initial primary outcome, and some sort of surrogate sometimes controversial, endpoints that are used to outcome or biomarker of aging is essential. Consequently, facilitate and speed up the development and testing of the discovery of robust and accurate biomarkers of aging has new pharmaceutical agents. Surrogate outcomes such as become a holy grail for aging research. As yet, there is no blood pressure, lipids, and hemoglobin A1c are accepted established set of biological or clinical biomarkers of aging in outcomes for vascular disease and diabetes mellitus, animals or humans, although many have been proposed (1–6). whereas composite outcomes combining death, hospi- Various criteria for biomarkers of aging have been put talization, acute coronary syndrome, and angioplasty forward (4,6). The underlying assumption is that any inter- are frequent in cardiovascular prevention trials. We vention that alters a biomarker of aging will, by extrapola- need similar approaches to study aging interventions, tion, also alter the aging process and maximum life span. although this will be much more complex than for For example the American Federation for Aging Research disease-based interventions (4). In 1988, the National concluded that any useful biomarker of aging should fulfill Institute of Aging established an extensive program to a variety of criteria, including the following: develop biomarkers of aging based on studies of mice, •• It must predict the rate of aging and be a better predictor but biomarkers of aging that could be used as surrogates of life span than chronological age alone for aging were not forthcoming (4). 777 778 LE COUTEUR ET AL. Some of the biomarkers of aging based on our under- age could be predicted by a combination of glycans, sys- standing of aging biology include inflammatory mark- tolic blood pressure, and FEV1. ers (interleukin 6, tumor necrosis factor alpha, C-reactive As well as being a strong statistical marker of aging, gly- protein), DNA changes (mitochondrial DNA, telomeres), cans are of particular interest because they regulate pro- and and markers of oxidative stress and advanced glycation anti-inflammatory IgG responses by influencing the bind- endproducts (4,6,7). Panels of clinical biomarkers (com- ing of IgG to its various receptors. For example, the age- posite outcomes) that predict age and risk of death have related reduction in IgG galactosylation will increase the been developed from longitudinal human studies, includ- proinflammatory function of IgG. This is of importance, ing anthropometry, muscle strength, serum albumin, blood given the key association of inflammation with aging, a pressure, forced expiratory volume (FEV1), lipoproteins, process termed inflammaging by Franceschi and colleagues Downloaded from https://academic.oup.com/biomedgerontology/article/69/7/777/662886 by guest on 24 September 2021 and cognitive and functional status. Such parameters might (13). The authors conclude with the appropriate epidemio- predict chronological age and risk of death, but many over- logical caveat that the direction of causality between aging lap with typical definitions of disease or disease risk factors. and altered IgG glycosylation is uncertain. Even so, IgG The -omics technologies are promising to generate novel glycans might prove to be significant biomarkers of aging but complicated biomarkers based on patterns of change because of both their strong statistical link with age and in tissue or blood transcriptome, proteasome, metabolome, their plausible mechanistic link with age-related changes in microRNAs, and DNA methylation (7,8). Detailed profiling inflammatory responses. of posttranslational modification of circulating proteins (eg, N-glycans on circulating glycoproteins such as immuno- References globulins) has also generated new biomarkers of aging (9), 1. Ingram DK, Nakamura E, Smucny D, Roth GS, Lane MA. Strategy for and this approach has been promoted for future research on identifying biomarkers of aging in long-lived species. Exp Gerontol. aging and biomarkers (8,10). 2001;36:1025–1034. In this issue of the Journal of Gerontology, a new study 2. Le Couteur DG, McLachlan AJ, Quinn RJ, Simpson SJ, de Cabo R. Aging biology and novel targets for drug discovery. J Gerontol A Biol of the relationship between aging and posttranslational Sci Med Sci. 2012;67:169–174. glycosylation of IgG is reported (11). This study might 3. Johnson TE. Recent results: biomarkers of aging. Exp Gerontol. prove to be a significant advance because of the strong 2006;41:1243–1246. statistical association with chronological age and plau- 4. Sprott RL. Biomarkers of aging and disease: introduction and defini- sible mechanistic contribution to age-related changes in tions. Exp Gerontol. 2010;45:2–4. 5. Butler RN, Sprott RL. Biomarkers of aging: From primitive organisms inflammation. Krištić and colleagues (11) studied 5,117 to man. New York: International Longevity Center; 2000. participants ranging in age from 16 to 100 years from four 6. Simm A, Johnson TE. Biomarkers of ageing: A challenge for the different European cohorts—the Croatian island of Vis, the future. Exp Gerontol. 2010;45:731–732. Croatian island of Korcula, Scottish Orkney Islands, and 7. Holly AC, Melzer D, Pilling LC, et al. Towards a gene expression bio- the TwinsUK cohort. There were complicated but strong marker set for human biological age. Aging Cell. 2013;12:324–326. 8. Valdes AM, Glass D, Spector TD. Omics technologies and the study relationships between changes in IgG glycosylation and of human ageing. Nat Rev Genet. 2013;14:601–607. age. The greatest impact of age was a reduction of about 9. Vanhooren V, Dewaele S, Libert C, et al. Serum N-glycan profile shift 50% in galactosylation. This finding had stood the test of during human ageing. Exp Gerontol. 2010;45:738–743. time, having been reported in 1988 by Parekh and col- 10. Dall’Olio F, Vanhooren V, Chen CC, Slagboom PE, Wuhrer M, leagues (12). They developed an index called GlycanAge, Franceschi C. N-glycomic biomarkers of biological aging and longev- ity: a link with inflammaging. Ageing Res Rev. 2013;12:685–698. which combined three of the IgG glycans and explained 11. Krištić J, Vučković F, Menni C, et al. Glycans are a novel biomarker nearly 60% of chronological age. Then they studied the of chronological and biological age. J Gerontol A Biol Sci Med Sci. In relationship between, age, IgG glycans, and other clini- press. cal biomarkers of aging such as anthropometric measure- 12. Parekh R, Roitt I, Isenberg D, Dwek R, Rademacher T. Age-related ments, lipids, blood pressure, and FEV1. Once again, the galactosylation of the N-linked oligosaccharides of human serum IgG. J Exp Med. 1988;167:1731–1736. IgG glycans proved to be strongly associated with age 13. Franceschi C, Capri M, Monti D, et al. Inflammaging and anti-inflam- when these other markers were taken into account. From maging: a systemic perspective on aging and longevity emerged from about 50 years of age, 71% of variance in chronological studies in humans. Mech Ageing Dev. 2007;128:92–105..
Recommended publications
  • Life-Span Trends in Olympians and Supercentenarians Juliana Antero, Geoffroy Berthelot, Adrien Marck, Philippe Noirez, Aurélien Latouche, Jean-François Toussaint
    Learning From Leaders: Life-span Trends in Olympians and Supercentenarians Juliana Antero, Geoffroy Berthelot, Adrien Marck, Philippe Noirez, Aurélien Latouche, Jean-François Toussaint To cite this version: Juliana Antero, Geoffroy Berthelot, Adrien Marck, Philippe Noirez, Aurélien Latouche, et al.. Learn- ing From Leaders: Life-span Trends in Olympians and Supercentenarians. Journals of Gerontology, Series A, Oxford University Press (OUP): Policy B - Oxford Open Option D, 2015, 70 (8), pp.944-949. 10.1093/gerona/glu130. hal-01768388 HAL Id: hal-01768388 https://hal-insep.archives-ouvertes.fr/hal-01768388 Submitted on 17 Apr 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Journals of Gerontology: BIOLOGICAL SCIENCES © The Author 2014. Published by Oxford University Press on behalf of The Gerontological Society of America. Cite journal as: J Gerontol A Biol Sci Med Sci This is an Open Access article distributed under the terms of the Creative Commons Attribution doi:10.1093/gerona/glu130 Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/),
    [Show full text]
  • Living-100-Insights-Challenges.Pdf
    Living to 100 Insights on the Challenges and Opportunities of Longevity Literature Review 2002–2017 April 2019 Living to 100 Insights on the Challenges and Opportunities of Longevity SPONSOR Research Expanding Boundaries Pool AUTHORS Sean She, FSA, MAAA Committee on Life Insurance Research Francisco J. Orduña, FSA, MAAA Product Development Section Peter Carlson, FSA, MAA Committee on Knowledge Extension Research 1 | P a g e This publication has been prepared for general informational purposes only; and is not intended to be relied upon as accounting, tax, financial or other professional advice. It is not intended to be a substitute for detailed research or the exercise of professional judgement. Please refer to your advisors for specific advice. Neither Ernst & Young LLP, the authors, nor any other member of Ernst & Young Global Limited can accept any responsibility or liability for loss occasioned to any person acting or refraining from action as a result of any material in this publication. Neither SOA, the authors nor Ernst & Young LLP recommend, encourage or endorse any particular use of the information provided in this publication. Neither SOA, the authors nor Ernst & Young LLP make any warranty, guarantee or representation whatsoever. None of SOA, the authors nor Ernst & Young LLP assume any responsibility or liability to any person or entity with respect to any losses arising in connection with the use or misuse of this publication. The opinions expressed and conclusions reached by the authors are their own and do not represent any official position or opinion of the Society of Actuaries or its members. The Society of Actuaries makes no representation or warranty to the accuracy of the information.
    [Show full text]
  • Controversy 2
    Controversy 2 WHY DO OUR BODIES GROW OLD? liver Wendell Holmes (1858/1891), in his poem “The Wonderful One-Hoss Shay,” invokes a memorable image of longevity and mortality, the example of a wooden Ohorse cart or shay that was designed to be long-lasting: Have you heard of the wonderful one-hoss shay, That was built in such a logical way, It ran a hundred years to a day . ? This wonderful “one-hoss shay,” we learn, was carefully built so that every part of it “aged” at the same rate and didn’t wear out until the whole thing fell apart all at once. Exactly a century after the carriage was produced, the village parson was driving this marvelous machine down the street, when What do you think the parson found, When he got up and stared around? The poor old chaise in a heap or mound, As if it had been to the mill and ground! You see, of course, if you’re not a dunce, How it went to pieces all at once, All at once, and nothing first, Just as bubbles do when they burst. The wonderful one-horse shay is the perfect image of an optimistic hope about aging: a long, healthy existence followed by an abrupt end of life, with no decline. The one-horse shay image also suggests that life has a built-in “warranty expiration” date. But where does this limit on longevity come from? Is it possible to extend life beyond what we know? The living organism with the longest individual life span is the bristlecone pine tree found in California, more than 4,500 years old, with no end in sight.
    [Show full text]
  • Increase of Human Longevity: Past, Present and Future
    Increase of Human Longevity: Past, Present and Future John R. Wilmoth Department of Demography University of California, Berkeley Instute for Populaon and Social Security Research Tokyo, Japan 22 December 2009 Topics • Historical increase of longevity • Age paerns of mortality • Medical causes of death • Social and historical causes • Limits to the human life span? • Future prospects Historical Increase of Longevity Life Expectancy at Birth, 1950-2009 Data source: United Nations, World Population Prospects: 2008 Revision, 2009 Life Expectancy at Birth, France, 1816-2007 Data source: Human Mortality Database, 2009 (www.mortality.org) Life Expectancy at Birth, France and India, 19th and 20th C. Data sources: HMD, 2009; M. Bhat, 1989, 1998 & 2001; United Nations, 2009 Life Expectancy at Birth, 1950‐2007 W. Europe, USA, Canada, Australia, NZ, Japan Data source: Human Mortality Database, 2009 (www.mortality.org) Historical mortality levels Life expectancy Infant mortality rate at birth (in years) (per 1000 live births) Prehistoric 20-35 200-300 Sweden, 1750s 36 212 India, 1880s 25 230 U.S.A., 1900 48 133 France, 1950 66 52 Japan, 2007 83 <3 Source: J. Wilmoth, Encyclopedia of Population, 2003 (updated) Age Paerns of Mortality Death Rates by Age, U.S., 1900 & 1995 Data source: Social Security Administraon, United States Distribuon of Deaths, U.S., 1900 & 1995 Data source: Social Security Administraon, United States Probability of Survival, U.S., 1900 & 1995 Data source: Social Security Administraon, United States Dispersion of Ages at Death vs. Life Expectancy at Birth, Sweden 1751‐1995 70 80 60 70 Life Expectancy at Birth (in years) 50 Inter-quartile range 60 40 Life expectancy at birth 50 30 40 Inter-quartile Range (in years) 20 Women Men 30 1751-55 1791-95 1831-35 1871-75 1911-15 1951-55 1991-95 Year Source: J.
    [Show full text]
  • Position Statement on Human Aging
    PERSPECTIVES Journal of Gerontology: BIOLOGICAL SCIENCES Copyright 2002 by The Gerontological Society of America 2002, Vol. 57A, No. 8, B292–B297 Position Statement on Human Aging S. Jay Olshansky,1 Leonard Hayflick,2 and Bruce A. Carnes3 1School of Public Health, University of Illinois at Chicago. 2University of California, San Francisco. 3 University of Chicago/NORC, Illinois. Downloaded from https://academic.oup.com/biomedgerontology/article/57/8/B292/556758 by guest on 28 September 2021 A large number of products are currently being sold by antiaging entrepreneurs who claim that it is now possible to slow, stop, or reverse human aging. The business of what has become known as antiaging medicine has grown in recent years in the United States and abroad into a multimil- lion-dollar industry. The products being sold have no scientifically demonstrated efficacy, in some cases they may be harmful, and those selling them often misrepresent the science upon which they are based. In the position statement that follows, 52 researchers in the field of aging have collaborated to inform the public of the distinction between the pseudoscientific antiaging industry, and the genuine science of aging that has progressed rapidly in recent years. N the past century, a combination of successful public told of a new highest documented age at death, as in the cel- Ihealth campaigns, changes in living environments, and ebrated case of Madame Jeanne Calment of France, who advances in medicine has led to a dramatic increase in hu- died at the age of 122 (3). Although such an extreme age at man life expectancy.
    [Show full text]
  • Species Selection in Comparative Studies of Aging and Antiaging Research
    2 Species Selection in Comparative Studies of Aging and Antiaging Research Joa˜o Pedro de Magalha˜es A great range of life histories are observed among Despite great differences in lifespan, the aging pheno- mammals. Understanding why different species age at type is remarkably similar across mammals (Finch, 1990; different rates may provide clues about the mechanistic Miller, 1999). For example, aged (8–11 year-old) mouse and genetic basis of aging. This work focuses on animal lemurs (Microcebus murinus) show senile plaques compar- species and their use in comparative studies of aging. able to those witnessed during human cerebral aging Firstly, I debate how to compare aging across different (Bons et al., 1992). Consequently, the principle behind species, including physiological parameters and statis- the comparative biology of aging is that studying why tical analyses. Afterwards, a selection of species for use different species age at different rates may provide clues in the comparative biology of aging is suggested. Taking about the mechanistic basis of aging. Moreover, identify- into account that the ultimate aim of research on aging is ing which genetic factors determine the pace of aging to benefit people, my selection is largely based on in mammals could open the possibility of delaying aging primates. Primates feature such a vast range of aging and/or age-related diseases in people. phenotypes that comparative studies of aging need not The focus of this work is on animal species and employ other more distant species, except perhaps a few their selection for use in comparative studies of aging. rodents. A number of animal species that may serve as Recently, we developed AnAge, an aging-oriented data- models of antiaging strategies are also presented.
    [Show full text]
  • Telomere Shortening Rate Predicts Species Life Span
    Telomere shortening rate predicts species life span Kurt Whittemorea, Elsa Veraa, Eva Martínez-Nevadob, Carola Sanperac,d, and Maria A. Blascoa,1 aTelomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Research Centre, 28029 Madrid, Spain; bVeterinary Department, Madrid-Zoo Aquarium, 28011 Madrid, Spain; cDepartament de Biologia Evolutiva, Ecologia i Ciències Ambientals, Facultat de Biologia, Universitat de Barcelona, 08028 Barcelona, Spain; and dInstitut de Recerca de la Biodiversitat, Universitat de Barcelona, 08028 Barcelona, Spain Edited by Margarita Salas, Consejo Superior de Investigaciones Cientificas, Madrid, Spain, and approved June 11, 2019 (received for review February 13, 2019) Telomere shortening to a critical length can trigger aging and previously shown a rate of telomere shortening of around 7,000 bp shorter life spans in mice and humans by a mechanism that involves per y, which is 100-fold faster than that reported in humans (4). induction of a persistent DNA damage response at chromosome The initial telomere length of the different species under study ends and loss of cellular viability. However, whether telomere was estimated by linear regression (Fig. 1). Note that the initial length is a universal determinant of species longevity is not known. telomere length value is only an estimate and telomere length To determine whether telomere shortening can be a single param- dynamics may not be linear during the early stages of life (19). eter to predict species longevities, here we measured in parallel the First, we confirmed a very high rate of telomere shortening in our telomere length of a wide variety of species (birds and mammals) current mouse cohort of 6,420 bp per y (Fig.
    [Show full text]
  • Biomarkers of the Brain
    DOI: 10.26717/BJSTR.2017.01.000151 Vincent van Ginneken. Biomed J Sci & Tech Res ISSN: 2574-1241 Review Article Open Access Are there any Biomarkers of Aging? Biomarkers of the Brain *Vincent van Ginneken Blue green technologies, Netherlands Received: June 12, 2017; Published: June 27, 2017 *Corresponding author: Vincent van Ginneken, Blue green technologies, Ginkelseweg 2, 6866 DZ Heelsum, The Netherlands, Email Abstract Biomarkers of aging would give the true “biological age”, which may be different from the chronological age. Population perspectives regarding to aging, age-related diseases and life-expectancy of populations are extremely useful for e.g. governments and/or politicians. The damage, telomeres shortage and cellular senescence, apoptosis and genetic predisposition. Although maximum lifespan would be a means of validatingproblem with biomarkers finding biomarkers of aging, it wouldof aging not is thatbe a therepractical are meansseveral for theories long-lived of aging species related such to as research humans areas because like: longitudinal oxidative stress, studies mitochondrial would take far too much time. Ideally, biomarkers of aging should assay the biological process of aging and not a predisposition to disease. Despite the fact that few biomarkers are found for aging some examples are given from Systems Biology: metabolomics, proteomics, potential biomarkers of aging human brain research is underestimated. One target that has been looked at in this manuscript are biomarkers ofgenomics brain aging. and Solipidomics.
    [Show full text]
  • Cybernetic Principles of Aging and Rejuvenation
    Cybernetic Principles of Aging and Rejuvenation: the buffering-challenging strategy for life extension Francis Heylighen Evolution, Complexity and Cognition group Vrije Universiteit Brussel Abstract: Aging is analyzed as the spontaneous loss of adaptivity and increase in fragility that characterizes dynamic systems. Cybernetics defines the general regulatory mechanisms that a system can use to prevent or repair the damage produced by disturbances. According to the law of requisite variety, disturbances can be held in check by maximizing buffering capacity, range of compensatory actions, and knowledge about which action to apply to which disturbance. This suggests a general strategy for rejuvenating the organism by increasing its capabilities of adaptation. Buffering can be optimized by providing sufficient rest together with plenty of nutrients: amino acids, antioxidants, methyl donors, vitamins, minerals, etc. Knowledge and the range of action can be extended by subjecting the organism to an as large as possible variety of challenges. These challenges are ideally brief so as not to deplete resources and produce irreversible damage. However, they should be sufficiently intense and unpredictable to induce an overshoot in the mobilization of resources for damage repair, and to stimulate the organism to build stronger capabilities for tackling future challenges. This allows them to override the trade-offs and limitations that evolution has built into the organism’s repair processes in order to conserve potentially scarce resources. Such acute, “hormetic” stressors strengthen the organism in part via the “order from noise” mechanism that destroys dysfunctional structures by subjecting them to strong, random variations. They include heat and cold, physical exertion, exposure, stretching, vibration, fasting, food toxins, micro-organisms, environmental enrichment and psychological challenges.
    [Show full text]
  • The Genes of Longevity. the Death of Death. February 2018. The
    The genes of longevity. The death of death. February 2018. The real issue is the fight against old age and death, (…) truly increasing human longevity. (...) Life expectancy has been increased thanks to antibiotics, better lifestyles and medical advances. In 1900, for example, the life expectancy of ​ ​ French people was 45. Today, on average it is 82. But we still die more or less at the same time. Basically we still die at around 100. (...) What is the philosophical goal now ? The idea is to create a humanity which would be young and old at the same time. As the saying goes: "If the young only knew, if the old only could” – if we can just bring the two together. Luc Ferry (translation), former French education minister and philosopher (Arte, ​ ​ 8 February, 2017) ​ Theme of the month: Genetics and maximum life span Introduction “In the beginning was the gene”, we could perhaps write, concerning the appearance of life. Even if the first stages remain mysterious. We are probably all the – incredibly ​ lucky – descendants of a common DNA-bearing ancestor which appeared, ​ ​ ​ according to current knowledge, about 3.8 billion years ago. During the first half of the history of life our distant ancestors, who were as yet neither plants nor animals, probably did not die of old age. They simply divided themselves when circumstances were favorable, or died when nutrients were lacking or when the environment changed too much. Then life became more complex; living beings became multicellular. Little by ​ ​ little, the genetic heritage transmitted itself from one generation to the next, no longer by simple division, but by fusion of genetic material.
    [Show full text]
  • Predicting Human Lifespan Limits
    Predicting Human Lifespan Limits Byung Mook Weon1,2 and Jung Ho Je2 1 Department of Physics, School of Engineering and Applied Sciences, Harvard University, Cambridge, Massachusetts 02138, USA. 2 X-ray Imaging Center, Department of Materials Science and Engineering, Pohang University of Science and Technology, Pohang 790-784, Korea. ABSTRACT Recent discoveries show steady improvements in life expectancy during modern decades. Does this support that humans continue to live longer in future? We recently put forward the maximum survival tendency, as found in survival curves of industrialized countries, which is described by extended Weibull model with age-dependent stretched exponent. The maximum survival tendency suggests that human survival dynamics may possess its intrinsic limit, beyond which survival is inevitably forbidden. Based on such tendency, we develop the model and explore the patterns in the maximum lifespan limits from industrialized countries during recent three decades. This analysis strategy is simple and useful to interpret the complicated human survival dynamics. Keywords: Human lifespan; Maximum survival tendency; Lifespan limit E-mail addresses: [email protected], [email protected] To appear in Natural Science by Scientific Research Publishing. 1. INTRODUCTION Humans live longer now. Indeed the life expectancy and the observed maximum age at death have significantly increased during recent decades [1−5]. Such increase is mainly attributable to non-biological aspects such as the intricate interplay of advances in income, nutrition, education, sanitation, and medicine [6,7]. Biologists and gerontologists are hunting for a variety of useful ways to prolong life in animals, including mice and worms [8]. Their research suggests that human lifespan may be remarkably pliable [8].
    [Show full text]
  • BACKGROUND PAPER Longevity
    BACKGROUND PAPER Longevity Dr Hans-Jörg Ehni, Deputy Director, Institute for Ethics and History of Medicine, University of Tübingen, Germany November 2015 Note The author was commissioned by the Nuffield Council on Bioethics to write this paper in order to inform the Council’s discussions about possible future work on this topic. The paper is intended to provide an overview of key clinical, ethical, social, legal and policy issues, but is not intended to offer any conclusions or recommendations regarding future policy and practice. Any views expressed in the paper are the author’s own and not those of the Nuffield Council on Bioethics. 1 Longevity Background paper Hans-Jörg Ehni, Deputy Director, Institute for Ethics and History of Medicine, University of Tübingen Executive summary Subject and approach For the first time, interventions to slow physical ageing are within reach. This background paper examines a possible increase in longevity and its potential ethical implications. The current situation is presented as follows: Several interventions have successfully slowed ageing, prevented or postponed age- associated diseases, and prolonged the life span of animals in laboratory settings. Biogerontologists are confident that their knowledge and methods can be applied to humans. They present these methods as a new paradigm for medicine. Clinical trials of some interventions are already underway. The primary goal would be to prevent age-associated diseases by slowing ageing, but as a corollary, longevity is likely to increase as well. The background paper describes the possible increase of longevity achieved by slowing biological ageing as a ‘second longevity revolution’. The ‘first longevity revolution’ refers to the increase of longevity since the middle of the 19th Century.
    [Show full text]