The worldwide spread of a novel influenza A (H1N1) virus in 2009 showed that influenza remains a significant health threat, even for individuals in the prime of life. This paper focuses on the unusually high young adult mortality observed during the Spanish flu pandemic of 1918. Using historical records from Canada and the U.S., we report a peak of mortality at the exact age of 28 during the pandemic and argue that this increased mortality resulted from an early life exposure to influenza during the previous Russian flu pandemic of 1889–90. We posit that in specific instances, development of immunological memory to an influenza virus strain in early life may lead to a dysregulated immune response to antigenically novel strains encountered in later life, thereby increasing the risk of death. Exposure during critical periods of development could also create holes in the T cell repertoire and impair fetal maturation in general, thereby increasing mortality from infectious diseases later in life. Knowledge of the age-pattern of susceptibility to mortality from influenza could improve crisis management during future influenza pandemics.

References 618Appendix 623 A1 From B-splines to P-splines 623 A2 The penalized likelihood function for P-splines 624 A3 Smoothing mortality data with P-splines 625 A4 Comparison between HMD life table age-at-death distributions and P-spline smoothed density functions for Japan 626Demographic Research: Volume 25, Article 19 Research ArticleChanges in the age-at-death distribution in four low mortality countries: A nonparametric approach Nadine Ouellette 1 Robert Bourbeau 2 AbstractSince the beginning of the twentieth century, important transformations have occurred in the age-at-death distribution within human populations. We propose a flexible nonparametric smoothing approach based on P-splines to refine the monitoring of these changes. Using data from the Human Mortality Database for four low mortality countries, namely Canada (1921Canada ( -2007, France (1920( ), Japan (1947, and the USA , we find that the general scenario of compression of mortality no longer appropriately describes some of the recent adult mortality trends recorded. Indeed, reductions in the variability of age at death above the mode have stopped since the early 1990s in Japan and since the early 2000s for Canadian, US, and French women, while their respective modal age at death continued to increase. These findings provide additional support to the shifting mortality scenario, using an alternative method free from any assumption on the shape of the age-at-death distribution. Ouellette & Bourbeau: Changes in the age-at-death distribution in four low mortality countries IntroductionOver the course of the last century, we have witnessed major improvements in the level of mortality in regions all across the globe. This remarkable mortality decrease has also been characterized by important changes in the age-pattern of mortality, which inevitably led to substantial modifications in the shape of the distribution of age at death and the survival curve over time. Measuring transformations in the age-at-death distribution or in the survival curve quickly became a topic of great interest among researchers, as their implications on societies are profound. For example, with accurate historical trends on average lifespan and lifespan inequality in hand, governments and policymakers are in a better position to ensure sustainability of social security and health-care systems.Efforts to document such trends have indeed been made for several countries and regions: Canada ( Recently, Cheung et al. (2005) listed and reviewed more than 20 indicators used in these studies, each indicator aimed at quantifying either the central tendency or the dispersion (variability) of age at death across individuals. Since the computation of these indicators often involves the use of parametric statistical modelling techniques (e.g., quadratic model, normal model, or logistic model) that impose a predetermined structure on data, an exploration of nonparametric statistical methods, free from assumptions related to the structure of the data, is worth considering. Indeed, concer...

Recent outbreaks of H5, H7, and H9 influenza A viruses in humans have served as a vivid reminder of the potentially devastating effects that a novel pandemic could exert on the modern world. Those who have survived infections with influenza viruses in the past have been protected from subsequent antigenically similar pandemics through adaptive immunity. For example, during the 2009 H1N1 “swine flu” pandemic, those exposed to H1N1 viruses that circulated between 1918 and the 1940s were at a decreased risk for mortality as a result of their previous immunity. It is also generally thought that past exposures to antigenically dissimilar strains of influenza virus may also be beneficial due to cross-reactive cellular immunity. However, cohorts born during prior heterosubtypic pandemics have previously experienced elevated risk of death relative to surrounding cohorts of the same population. Indeed, individuals born during the 1890 H3Nx pandemic experienced the highest levels of excess mortality during the 1918 “Spanish flu.” Applying Serfling models to monthly mortality and influenza circulation data between October 1997 and July 2014 in the United States and Mexico, we show corresponding peaks in excess mortality during the 2009 H1N1 “swine flu” pandemic and during the resurgent 2013–2014 H1N1 outbreak for those born at the time of the 1957 H2N2 “Asian flu” pandemic. We suggest that the phenomenon observed in 1918 is not unique and points to exposure to pandemic influenza early in life as a risk factor for mortality during subsequent heterosubtypic pandemics.

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Longevity runs in families, either through genetic or environmental influences. Using Quebec civil registration and historical

The main purposes of this paper is to evaluate the quality of Canadian data among the oldest-old (80+) over the 1951-1995 period, and to compare estimations of Canadian probabilities of death based on the extinct generation method with those of other developed countries in order to ascertain whether Canada experiences a distinct low mortality profile. The evaluation of the data quality suggests that Canadian data are quite good up to the age of 100, and that the main problems concern the centenarians (overstatement of age at death and errors in census age declarations). International comparisons on the basis of two mortality indicators for the 80-99 age-interval lead to the same conclusion: Canadian mortality is lower than in most European countries. The best match is still with the United States.

This study examines the roles of age, period, and cohort in influenza mortality trends over the years 1959–2016 in the United States. First, we use Lexis surfaces based on Serfling models to highlight influenza mortality patterns as well as to identify lingering effects of early-life exposure to specific influenza virus subtypes (e.g., H1N1, H3N2). Second, we use age-period-cohort (APC) methods to explore APC linear trends and identify changes in the slope of these trends (contrasts). Our analyses reveal a series of breakpoints where the magnitude and direction of birth cohort trends significantly change, mostly corresponding to years in which important antigenic drifts or shifts took place (i.e., 1947, 1957, 1968, and 1978). Whereas child, youth, and adult influenza mortality appear to be influenced by a combination of cohort- and period-specific factors, reflecting the interaction between the antigenic experience of the population and the evolution of the influenza virus itself, mortality patterns of the elderly appear to be molded by broader cohort factors. The latter would reflect the processes of physiological capital improvement in successive birth cohorts through secular changes in early-life conditions. Antigenic imprinting, cohort morbidity phenotype, and other mechanisms that can generate the observed cohort effects, including the baby boom, are discussed.Electronic supplementary materialThe online version of this article (10.1007/s13524-019-00809-y) contains supplementary material, which is available to authorized users.

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