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      The prevalence of inorganic mercury in human cells increases during aging but decreases in the very old

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      Author(s): 1 , 2 ,
      Publication date (Electronic):
      Journal: Scientific Reports
      Publisher: Nature Publishing Group UK
      Keywords: Environmental impact, Cancer, Senescence

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          Abstract

          Successful aging is likely to involve both genetic and environmental factors, but environmental toxicants that accelerate aging are not known. Human exposure to mercury is common, and mercury has genotoxic, autoimmune, and free radical effects which could contribute to age-related disorders. The presence of inorganic mercury was therefore assessed in the organs of 170 people aged 1–104 years to determine the prevalence of mercury in human tissues at different ages. Mercury was found commonly in cells of the brain, kidney, thyroid, anterior pituitary, adrenal medulla and pancreas. The prevalence of mercury in these organs increased during aging but decreased in people aged over 80 years. People with mercury in one organ usually also had mercury in several others. In conclusion, the prevalence of inorganic mercury in human organs increases with age. The relative lack of tissue mercury in the very old could account for the flattened mortality rate and reduced incidence of cancer in this advanced age group. Since mercury may accelerate aging, efforts to reduce atmospheric mercury pollution could improve the chances of future successful aging.

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          Geroscience: linking aging to chronic disease.

          Brian Kennedy, Shelley L Berger, Anne Brunet … (2014)
          Mammalian aging can be delayed with genetic, dietary, and pharmacologic approaches. Given that the elderly population is dramatically increasing and that aging is the greatest risk factor for a majority of chronic diseases driving both morbidity and mortality, it is critical to expand geroscience research directed at extending human healthspan.
          Article 0 comments Cited 669 times – based on 0 reviews     Review now
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            The Continuum of Aging and Age-Related Diseases: Common Mechanisms but Different Rates

            Claudio Franceschi, Paolo Garagnani, Cristina Morsiani … (2018)
            Geroscience, the new interdisciplinary field that aims to understand the relationship between aging and chronic age-related diseases (ARDs) and geriatric syndromes (GSs), is based on epidemiological evidence and experimental data that aging is the major risk factor for such pathologies and assumes that aging and ARDs/GSs share a common set of basic biological mechanisms. A consequence is that the primary target of medicine is to combat aging instead of any single ARD/GSs one by one, as favored by the fragmentation into hundreds of specialties and sub-specialties. If the same molecular and cellular mechanisms underpin both aging and ARDs/GSs, a major question emerges: which is the difference, if any, between aging and ARDs/GSs? The hypothesis that ARDs and GSs such as frailty can be conceptualized as accelerated aging will be discussed by analyzing in particular frailty, sarcopenia, chronic obstructive pulmonary disease, cancer, neurodegenerative diseases such as Alzheimer and Parkinson as well as Down syndrome as an example of progeroid syndrome. According to this integrated view, aging and ARDs/GSs become part of a continuum where precise boundaries do not exist and the two extremes are represented by centenarians, who largely avoided or postponed most ARDs/GSs and are characterized by decelerated aging, and patients who suffered one or more severe ARDs in their 60s, 70s, and 80s and show signs of accelerated aging, respectively. In between these two extremes, there is a continuum of intermediate trajectories representing a sort of gray area. Thus, clinically different, classical ARDs/GSs are, indeed, the result of peculiar combinations of alterations regarding the same, limited set of basic mechanisms shared with the aging process. Whether an individual will follow a trajectory of accelerated or decelerated aging will depend on his/her genetic background interacting lifelong with environmental and lifestyle factors. If ARDs and GSs are manifestations of accelerated aging, it is urgent to identify markers capable of distinguishing between biological and chronological age to identify subjects at higher risk of developing ARDs and GSs. To this aim, we propose the use of DNA methylation, N-glycans profiling, and gut microbiota composition to complement the available disease-specific markers.
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              Measuring population ageing: an analysis of the Global Burden of Disease Study 2017

              Angela Y Chang, Vegard F. Skirbekk, Stefanos Tyrovolas … (2019)
              Summary Background Traditional metrics for population health ageing tend not to differentiate between extending life expectancy and adding healthy years. A population ageing metric that reflects both longevity and health status, incorporates a comprehensive range of diseases, and allows for comparisons across countries and time is required to understand the progression of ageing and to inform policies. Methods Using the Global Burden of Diseases, Injuries, and Risk Factors Study 2017, we developed a metric that reflects age-related morbidity and mortality at the population level. First, we identified a set of age-related diseases, defined as diseases with incidence rates among the adult population increasing quadratically with age, and measured their age-related burden, defined as the sum of disability-adjusted life-years (DALYs) of these diseases among adults. Second, we estimated age-standardised age-related health burden across 195 countries between 1990 and 2017. Using global average 65-year-olds as the reference population, we calculated the equivalent age in terms of age-related disease burden for all countries. Third, we analysed how the changes in age-related burden during the study period relate to different factors with a decomposition analysis. Finally, we describe how countries with similar levels of overall age-related burden experience different onsets of ageing. We represent the uncertainty of our estimates by calculating uncertainty intervals (UI) from 1000 draw-level estimates for each disease, country, year, and age. Findings 92 diseases were identified as age related, accounting for 51·3% (95% UI 48·5–53·9) of all global burden among adults in 2017. Across the Socio-demographic Index (SDI), the rate of age-related burden ranged from 137·8 DALYs (128·9–148·3) per 1000 adults in high SDI countries to 265·9 DALYs (251·0–280·1) in low SDI countries. The equivalent age to average 65-year-olds globally spanned from 76·1 years (75·6–76·7) in Japan to 45·6 years (42·6–48·2) in Papua New Guinea. Age-standardised age-related disease rates have decreased over time across all SDI levels and regions between 1990 and 2017, mainly due to decreases in age-related case fatality and disease severity. Even among countries with similar age-standardised death rates, large differences in the onset and patterns of accumulating age-related burden exist. Interpretation The new metric facilitates the shift from thinking not just about chronological age but the health status and disease severity of ageing populations. Our findings could provide inputs into policymaking by identifying key drivers of variation in the ageing burden and resources required for addressing the burden. Funding National Institute on Aging of the National Institutes of Health.
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                Author and article information

                Contributors
                Roger Pamphlett: roger.pamphlett@sydney.edu.au
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 18 August 2021
                Publication date PMC-release: 18 August 2021
                Publication date Collection: 2021
                Volume: 11
                Electronic Location Identifier: 16714
                Affiliations
                [1 ]GRID grid.1013.3, ISNI 0000 0004 1936 834X, Discipline of Pathology, Sydney Medical School, Brain and Mind Centre, , The University of Sydney, ; Sydney, NSW Australia
                [2 ]GRID grid.413249.9, ISNI 0000 0004 0385 0051, Department of Neuropathology, , Royal Prince Alfred Hospital, ; Sydney, NSW Australia
                Article
                Publisher ID: 96359
                DOI: 10.1038/s41598-021-96359-8
                PMC ID: 8373952
                PubMed ID: 34408264
                SO-VID: ce863676-f161-4135-8947-540504db25cd
                Copyright © © The Author(s) 2021
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 16 June 2021
                Date accepted : 30 July 2021
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Uncategorized
                Keywords: environmental impact,cancer,senescence
                Data availability:
                ScienceOpen disciplines: Uncategorized
                Keywords: environmental impact, cancer, senescence

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