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BMC Biology

, 2:16

First Online: 08 July 2004Received: 13 February 2004Accepted: 08 July 2004


BackgroundHumans die at an increasing rate until late in life, when mortality rates level off. The causes of the late-life mortality plateau have been debated extensively over the past few years. Here, I examine mortality patterns separately for each of the leading causes of death. The different causes of death show distinct mortality patterns, providing some clues about the varying acceleration of mortality at different ages.

ResultsI examine mortality patterns by first plotting the data of mortality rate versus age on a log-log scale. The slope of the age-specific mortality rate at each age is the age-specific acceleration of mortality. About one-half of total deaths have causes with similar shapes for the age-specific acceleration of mortality: a steady rise in acceleration from midlife until a well-defined peak at 80 years, followed by a nearly linear decline in acceleration. This first group of causes includes heart disease, cerebrovascular disease, and accidental deaths. A second group, accounting for about one-third of all deaths, follows a different pattern of age-specific acceleration. These diseases show an approximately linear rise in acceleration to a peak at 35–45 years of age, followed by a steep and steady decline in acceleration for the remainder of life. This second group includes cancer, chronic respiratory diseases, and liver disease. I develop a multistage model of disease progression to explain the observed patterns of mortality acceleration.

ConclusionsA multistage model of disease progression can explain both the early-life increase and late-life decrease in mortality acceleration. An early-life rise in acceleration may be caused by increasing rates of transition between stages as individuals grow older. The late-life decline in acceleration may be caused by progression through earlier stages, leaving only a few stages remaining for older individuals.

Electronic supplementary materialThe online version of this article doi:10.1186-1741-7007-2-16 contains supplementary material, which is available to authorized users.

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Autor: Steven A Frank

Fuente: https://link.springer.com/article/10.1186/1741-7007-2-16

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