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A Conjecture on Demographic Mortality at High Ages

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The study considers the model of an abstract organism, called Arbitrary Oscillator (ArbO), which is capable of making decisions at each timed step. These decisions are ‘critical’ since, randomly, their outcome can be ‘fatal’ for ArbO, thus bringing its life cycle to an end. If we impose limits on the total number of critical decisions using a fixed parameter TC (Total Cases), we can treat the statistical distribution of fatal events over a large number of ArbOs using statistical mechanics methods. This results in a mathematically definable asymmetric ‘bell’ distribution, which can be compared with demographic mortality curves (dx curves), with an appropriate choice of time scale (one step = five years). The possibility of modeling and therefore predicting the trend of demographic mortality is of great scientific and social interest. Our conjecture assumes that, as demographic longevity improves, i.e., with the lengthening of lifespan, the actual demographic curves will increasingly match the mathematical distribution curve of our ArbO. The statistical distribution of the ArbO was introduced by the author in a previous paper and is here recalled and formalized analytically and its characteristics are detailed. The above said conjecture is based on two case studies: mortality in the United States from 1900 to 2017 and mortality in Italy from 1974 to 2019. The conjecture, applied to both case studies, appears reasonable. Tables and comparison figures are provided to support this. Also, an attempt to predict demographic mortality behavior and limitations for the years to come is provided. Finally, the more general theme of the nature of human aging can also be related to our conjecture, since it can highlight the presence of an absolute limit on the number of ‘critical’ events (the TC parameter). As ‘critical’ events accumulate over time by aging, approaching the final limit value, the probability of death will tend toward one.

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Time-to-event regression is a frequent tool in biomedical research. In clinical trials this time is usually measured from the beginning of the study. The same approach is often adopted in the analysis of longitudinal observational studies. However, in recent years there has appeared literature making a case for the use of the date of birth as a starting point, and thus utilize age as the time-to-event. In this paper, we explore different types of age-scale models and compare them with time-on-study models in terms of the estimated regression coefficients they produce. We consider six proportional hazards regression models that differ in the choice of time scale and in the method of adjusting for the years before the study. By considering the estimating equations of these models as well as numerical simulations we conclude that correct adjustment for the age at entry is crucial in reducing bias of the estimated coefficients. The unadjusted age-scale model is inferior to any of the five other models considered, regardless of their choice of time scale. Additionally, if adjustment for age at entry is made, our analyses show very little to suggest that there exists any practically meaningful difference in the estimated regression coefficients depending on the choice of time scale. These findings are supported by four practical examples from the Framingham Heart Study.

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Comments on 'Choice of time scale and its effect on significance of predictors in longitudinal studies' by Michael J. Pencina, Martin G. Larson and Ralph B. D'Agostino, Statistics in Medicine 2007; 26:1343-1359.
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Statistics in MedicineVolume 28, Issue 8 p. 1315-1317 Letter to the Editor Comments on ‘Choice of time scale and its effect on significance of predictors in longitudinal studies’ by Michael J. Pencina, Martin G. Larson and Ralph B. D'Agostino, Statistics in Medicine 2007; 26:1343–1359 Mitchell H. Gail, Mitchell H. Gail Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, U.S.A.Search for more papers by this authorBarry Graubard, Barry Graubard Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, U.S.A.Search for more papers by this authorDavid F. Williamson, David F. Williamson Rollins School of Public Health, Emory University, Atlanta, GA, U.S.A.Search for more papers by this authorKatherine M. Flegal, Katherine M. Flegal National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, MD, U.S.A.Search for more papers by this author Mitchell H. Gail, Mitchell H. Gail Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, U.S.A.Search for more papers by this authorBarry Graubard, Barry Graubard Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, U.S.A.Search for more papers by this authorDavid F. Williamson, David F. Williamson Rollins School of Public Health, Emory University, Atlanta, GA, U.S.A.Search for more papers by this authorKatherine M. Flegal, Katherine M. Flegal National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, MD, U.S.A.Search for more papers by this author First published: 13 March 2009 https://doi.org/10.1002/sim.3473Citations: 19AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume28, Issue815 April 2009Pages 1315-1317 RelatedInformation

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Eighteen year weight trajectories and metabolic markers of diabetes in modernising China: which timescale is most relevant? Reply to Vistisen D and Færch K [letter
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To the Editor: Vistisen and Faerch [1] make an interesting point regarding the choice of time scale used to fit trajectory models. The authors assert that time since diagnosis would be the appropriate time scale when studying the aetiology of diabetes development or prognosis of diabetes, and we agree that this would be preferred. However, there are some practical issues for defining the appropriate time point of reference relative to diagnosis of disease in a population-based study, such as ours [2]. Examining trajectories up to the time of diagnosis would be ideal. However, it is hard to know the exact timing of diagnosis, since the collection of fasting blood and assays for cardiometabolic biomarkers were completed only in 2009 and therefore we have no data on comparable measures prior to 2009, which would be necessary to establish time of diagnosis. Data from the China Health and Nutrition Survey (CHNS) suggest that in this population the majority of diabetes is undiagnosed (over 50%) [3], and therefore it will be less likely to influence weight trajectories. All that being said, we acknowledge that our method, using time since enrolment could, as the authors suggest, introduce errors that may bias results. This is a testable hypothesis that could be addressed through a simulation study to see what types of inferences one could make using a variety of different approaches to handle time. Indeed, we would welcome the idea of such a future study and are currently investigating related issues using simulation studies. Additionally, future studies involving CHNS data—at which point we will have multiple measurements of fasting blood and assays for cardiometabolic biomarkers—will allow us to additionally investigate this question further.

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