Distinguishing the intrinsic and extrinsic causes of changes in human mortality by examining life-table aging rate (LAR) trajectories through the lens of generalized Gompertz-Makeham law.

IF 4.4 4区 医学 Q1 GERIATRICS & GERONTOLOGY Biogerontology Pub Date : 2025-03-14 DOI:10.1007/s10522-025-10210-5
A Golubev
{"title":"Distinguishing the intrinsic and extrinsic causes of changes in human mortality by examining life-table aging rate (LAR) trajectories through the lens of generalized Gompertz-Makeham law.","authors":"A Golubev","doi":"10.1007/s10522-025-10210-5","DOIUrl":null,"url":null,"abstract":"<p><p>To check whether the reported waves of age-dependent changes in multiomics patterns in humans influence age-specific mortality, life-table aging rate (LAR) trajectories derived from Human Morality Database (HMD) data were modeled based on assumptions inherent in a generalized Gompertz-Makeham Law (gGML). The gGML implies that any changes in resistance to causes of death (CoD) and in exposure to CoD are translated into changes in mortality in an exponential and a linear way, respectively. Modeling suggests that undulations of LAR trajectories derived from HMD data on countries where life expectancy (LE) is above 83 years do not align with the reported waves of multiomics changes and are rather associated with changes in the exposure to CoD. As far as the exposure may be modifiable, it may be inferred from modeling that the contribution of the modifiable CoD to the total mortality is almost 100% at 25 years and reaches zero after ca. 90 years, which is no surprise. Unexpectedly, the contribution may increase by 20% at 55-65 years after the initial decrease, which reaches 30 to 70% at about 40 years. Reasons to revise approaches to attributing mortality to different CoD are discussed. Gains in LE possible upon eliminating all modifiable CoD are estimated. In the countries where LE currently exceeds 83 years, the estimates are 2.9-5.7 years for men and 1.2-2.5 for women. Thus, human LE may approach but hardly can ever exceed 90 years.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"71"},"PeriodicalIF":4.4000,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biogerontology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10522-025-10210-5","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GERIATRICS & GERONTOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

To check whether the reported waves of age-dependent changes in multiomics patterns in humans influence age-specific mortality, life-table aging rate (LAR) trajectories derived from Human Morality Database (HMD) data were modeled based on assumptions inherent in a generalized Gompertz-Makeham Law (gGML). The gGML implies that any changes in resistance to causes of death (CoD) and in exposure to CoD are translated into changes in mortality in an exponential and a linear way, respectively. Modeling suggests that undulations of LAR trajectories derived from HMD data on countries where life expectancy (LE) is above 83 years do not align with the reported waves of multiomics changes and are rather associated with changes in the exposure to CoD. As far as the exposure may be modifiable, it may be inferred from modeling that the contribution of the modifiable CoD to the total mortality is almost 100% at 25 years and reaches zero after ca. 90 years, which is no surprise. Unexpectedly, the contribution may increase by 20% at 55-65 years after the initial decrease, which reaches 30 to 70% at about 40 years. Reasons to revise approaches to attributing mortality to different CoD are discussed. Gains in LE possible upon eliminating all modifiable CoD are estimated. In the countries where LE currently exceeds 83 years, the estimates are 2.9-5.7 years for men and 1.2-2.5 for women. Thus, human LE may approach but hardly can ever exceed 90 years.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
求助全文
约1分钟内获得全文 去求助
来源期刊
Biogerontology
Biogerontology 医学-老年医学
CiteScore
8.00
自引率
4.40%
发文量
54
审稿时长
>12 weeks
期刊介绍: The journal Biogerontology offers a platform for research which aims primarily at achieving healthy old age accompanied by improved longevity. The focus is on efforts to understand, prevent, cure or minimize age-related impairments. Biogerontology provides a peer-reviewed forum for publishing original research data, new ideas and discussions on modulating the aging process by physical, chemical and biological means, including transgenic and knockout organisms; cell culture systems to develop new approaches and health care products for maintaining or recovering the lost biochemical functions; immunology, autoimmunity and infection in aging; vertebrates, invertebrates, micro-organisms and plants for experimental studies on genetic determinants of aging and longevity; biodemography and theoretical models linking aging and survival kinetics.
期刊最新文献
Chrysin alleviates the impeded neurogenesis in accelerated brain aging by D-galactose in rats. Distinguishing the intrinsic and extrinsic causes of changes in human mortality by examining life-table aging rate (LAR) trajectories through the lens of generalized Gompertz-Makeham law. Modelling orexinergic system in ageing in the African turquoise killifish. Neuroinflammation increases in old and oldest-old rats except for dura mater meningeal tissue with significant gender differences: a translational perspective. The crosstalk between CNS resident glial cells and peripheral immune cells is critical for age-dependent demyelination and subsequent remyelination.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1