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The tapertail anchovy Coilia brachygnathus, a commercially important species mainly distributed along the mid‐lower Chang‐Jiang basin, is by far the most dominant species in Lake Honghu. To figure out its success in this semiclosed lake, some basic biological parameters of this anchovy were analysed based on samples seasonally collected from October 2020 to December 2021. The results demonstrated that the age classes of fished individuals varied from 0.5 to 3.5, with the majority (97.36%) being between 0.5 and 3 years old. The size at 50% maturity of 17.2 cm total length (TL) for females and 19.0 cm TL for males corresponded to 1 and 1.6 years, respectively. Coilia brachygnathus has a short life span, early sexual maturity and a relatively fast growth rate. The flourishing of the fish in the lake is mainly attributed to its short life span, early maturity, fast growth rate, closed fishing, pelagic spawners, the availability of plenty of food and low predation effect on it. Age 3.5 year occurs in an extremely small percentage of the total (<3%), indicating that a large number of larger‐sized or older fish died after spawning, which is probably one of the major sources of water pollution if the closed fishing measure is adopted in Lake Honghu. Thus, individuals older than 2 years or more than 20.0 cm TL should be harvested. These findings have important management implications for the fish resources in Lake Honghu and beyond. [ABSTRACT FROM AUTHOR]

The influential Whitehall studies found that top‐ranking civil servants in Britain experienced lower mortality than civil servants below them in the organizational hierarchy due to differential exposure to workplace stress. I test for a Whitehall effect in the United States using a 1930 cohort of white‐collar employees at a leading firm – General Electric (GE). All had access to a corporate health and welfare program during a critical period associated with the health transition. I measure status using position in the managerial hierarchy, attendance at prestigious management training camps and promotions, none of which is associated with a Whitehall‐like rank‐mortality gradient. Instead, senior managers and executives experienced a 3–5‐year decrease in lifespan relative to those in lower levels, with the largest mortality penalty experienced by individuals in the second level of the hierarchy. I discuss generalizability and potential explanations for this reversal of the Whitehall phenomenon using additional data on the status and lifespan of top business executives and US senators. [ABSTRACT FROM AUTHOR]

Several studies demonstrate genetic variation in response to dietary restriction (DR) by replicating treatments across isogenic lines/strains from genetic reference panels. These studies typically quantify the response to DR as an effect size, estimated for each strain separately (eg, the difference in mean life span between groups). Such "no-pooling" analyses are expected to systematically overestimate variation in response DR, principally by overlooking sampling variance. In contrast, "partial-pooling" analyses using mixed-effects models are less prone to this bias. I demonstrate these issues using simulations, which also show that partial-pooling analyses can improve replicability among studies. Regardless of the analyses used, estimates of among-strain variation will have low precision when sample sizes are small. A worked example using survival data in mice is given. Life-span studies using genetic reference panels always have to trade-off within- and among-strain replication owing to logistical challenges. The simulation presented can also be used to help design such studies through power analysis. [ABSTRACT FROM AUTHOR]

Although individual estimates of life expectancy are readily available, analogous couple-based estimates are not. The dearth of such estimates can be detrimental for couples undertaking important decisions together, such as retirement, savings, and other later-life considerations. Moreover, relying on available individual measures can be misleading because it results in overestimating the number of years the couple should expect to live together (joint life expectancy) and underestimating the number of years the widowed spouse expects to live (survivor life expectancy). In this article, we use data from the Longitudinal Administrative Database to provide benchmark estimates for joint and survivor life expectancy for Canadian couples and show how these estimates vary with the income and employment status of couples approaching retirement. [ABSTRACT FROM AUTHOR]

It is a classical argument that how parties are born affects how they die. Nevertheless, few studies theorize and rigorously estimate the impact of formative features on the risk of organizational death. Using a life cycle perspective, we theorize how and when party mortality is shaped by four formative features constituting parties' heritage: insider status, societal rootedness, ideological novelty, and roots in preexisting parties. To assess the dynamic influence of these formative features on party death, we fit a state-space duration model to a data set covering 204 party trajectories in 22 consolidated democracies. Our modeling approach outperforms conventional methods and yields results that contradict the notion that formative features lose relevance as parties age. Our findings indicate that insider status affects mortality risk toward parties' midlife, societal rootedness matters early and late in parties' trajectories, while the combination of ideological novelty and roots in preexisting parties matters throughout parties' life spans. [ABSTRACT FROM AUTHOR]

Small vertebrates on islands are expected to attain a larger body size, and a greater survival than their mainland counterparts. Comparative studies have questioned whether lizards exhibit this set of adaptations, referred to as the 'island syndrome'.We collected data on 730 individuals the endemic Lilford's lizard Podarcis lilfordi throughout a 10‐year period on a small island of the Balearic archipelago (Spain). We coupled a growth function with a capture–mark–recapture model to simultaneously estimate size‐ and sex‐dependent growth rate and survival. To put our results into a wider context, we conducted a systematic review of growth, life span and age at maturity in different Podarcis species comparing insular and mainland populations.We found a low average growth coefficient (0.56 and 0.41 year−1 for males and females to reach an asymptotic size of 72.3 and 65.6 mm respectively), a high annual survival probability of 0.81 and 0.79 in males and females, and a large variability between individuals in growth parameters.Survival probability decreased with body size in both sexes, indicating a senescence pattern typical of long‐lived species or in populations with a low extrinsic mortality. Assuming a constant survival after sexual maturity, at about 2 years old, the average life span was 6.18 years in males and 8.99 in females. The oldest animal was a male last captured at an estimated age of ≥13 years and still alive at the end of the study.Our results agree with the predictions of the 'island syndrome' for survival, life span and growth parameters. A comparative analysis of these values across 29 populations of 16 different species of Podarcis indicated that insular lizards grow slower and live longer than their mainland counterparts. However, our data differed from other island populations of the same species, suggesting that island‐specific characteristics play an additional role to isolation.Within this study we developed an analytical approach to study the body size‐dependent survival of small reptiles. We discuss its applicability to contrast hypotheses on senescence in different sexes of this species, and provide the code used to integrate the growth and capture–mark–recapture models. [ABSTRACT FROM AUTHOR]

Body size influences many life‐history traits, with small‐bodied animals tending to have short life spans, high mortality and greater reproductive effort early in life. In this study, the authors investigated the life‐history traits and reproductive strategies of three small‐bodied coral reef gobies of the genus Trimma: Trimma benjamini, Trimma capostriatum and Trimma yanoi. The authors found all Trimma species studied attained a small body size of <25 mm, had a short life span of <140 days and experienced high estimated daily mortality of 3.0%–6.7%. Furthermore, the pelagic larval phase accounted for 25.3%–28.5% of the maximum life span, and maturation occurred between 74.1 and 82.1 days at 15.2–15.8 mm, leaving only 35%–43% of the total life span as a reproductively viable adult. All mature individuals had gonad structures consistent with bidirectional sex change, with bisexual gonads including both ovarian and testicular portions separated by a thin wall of connective tissue. In the female and male phases, only ovaries or testes were mature, whereas gonadal tissue of the non‐active sex remained. One T. benjamini individual and one T. yanoi individual had ovarian and testicular tissue active simultaneously. The results of this study highlight the life‐history challenges small CRFs face on their path to reproduction and reproductive strategies that could be beneficial in fishes with high and unpredictable mortality and short reproductive life spans. [ABSTRACT FROM AUTHOR]

Evidence linking nitrogen dioxide (NO 2) air pollution to life span of high-vulnerability older adults is extensively scarce in low- and middle-income countries. This study seeks to quantify mortality risk, excess deaths, and loss of life expectancy (LLE) associated with long-term exposure to NO 2 among elderly individuals in China. A nationwide dynamic cohort of 20352 respondents ≥65 years old were enrolled from the China Longitudinal Health and Longevity Survey during 2005–2018. Residential exposures to NO 2 and co-pollutants were assessed by well-validated spatiotemporal prediction models. A Cox regression model with time-dependent covariates was utilized to quantify the association of all-cause mortality with NO 2 exposure, controlling for confounders such as demographics, lifestyle, health status, and ambient temperature. NO 2 -attributable deaths and LLE were evaluated for the years 2010 and 2020 based on the pooled NO 2 -mortality relation derived from multi-national cohort investigations. Decomposition analyses were conducted to dissociate net shift in NO 2 -related deaths between 2010 and 2020 into four primary contributing factors. A total of 14313 deaths were recorded during follow-up of approximately 100 hundred person-years (median 3.6 years). We observed an approximately linear relationship (nonlinear P = 0.882) of NO 2 exposure with all-cause death across a broad range from 6.6 to 95.7 μg/m3. Every 10-μg/m3 rise in yearly average NO 2 concentration was linked to a hazard ratio (HR) of 1.045 (95% confidence interval [CI]: 1.031–1.059). In the updated meta-analysis of this study and 9 existing cohorts, we estimated a pooled HR of 1.043 (95% CI: 1.023–1.063) for each 10-μg/m3 growth in NO 2. Reaching a 10-μg/m3 counterfactual target of NO 2 concentration in China could avoid 0.33 (95% empirical CI: 0.19–0.49) million premature deaths and an LLE of 0.40 (95% empirical CI: 0.23–0.59) years in 2010, which greatly dropped to 0.24 (95% empirical CI: 0.14–0.36) million deaths and 0.21 (95% empirical CI: 0.12–0.31) years of LLE in 2020. The net fall in NO 2 -attributable deaths (–26.8%) between 2010 and 2020 was primarily driven by the declines in both NO 2 concentration (–41.6%) and mortality rate (–27.1%) under population growth (+41.0%) and age structure transition (+0.9%). Our findings provide national evidence for increased risk of premature death and loss of life expectancy attributed to later-life NO 2 exposure among the elderly in China. In an accelerated aging society, strengthened clean air actions should be formulated to minimize the health burden and regional inequality in NO 2 -attributable mortality. • Linear NO 2 -mortality association was observed in elders aged 80 years and over. • Meta-analysis estimated a 4.3% excess risk of death for each 10-μg/m3 rise in NO 2. • Reaching NO 2 target of 10 μg/m3 in 2020 could extend life expectancy by 0.21 years. • Decrease in NO 2 -related deaths during 2010–2020 was primarily driven by declined NO 2 concentration. [ABSTRACT FROM AUTHOR]

The Great Plains drought of 1931–1939 was a prolonged socio-ecological disaster with widespread impacts on society, economy, and health. While its immediate impacts are well documented, we know much less about the disaster's effects on distal human outcomes. In particular, the event's effects on later life mortality remain almost entirely unexplored. Closing this gap would contribute to our understanding of the long-term effects of place-based stress. To help fill this gap, I use a new, massive, linked mortality dataset to investigate whether young men's exposure to drought and dust storms in 341 Great Plains counties was linked to a higher risk of death in early-old age. Contrary to expectations, results suggest exposure to drought conditions had no obvious adverse effect among men aged 65 years or older at time of death—rather, the average age at death was slightly higher than for comparable men without exposure. This effect also appears to have been stronger among Plainsmen who stayed in place until the drought ended. A discussion of potential explanations for these counterintuitive results is provided. [ABSTRACT FROM AUTHOR]

The Elongate glass-perchlet Chanda nama Hamilton, 1822 is broadly found in Bangladesh, Myanmar, India, Pakistan, and Nepal. Our study represents a detailed report on stock status such as population structure, growth parameter (asymptotic length, L∞; growth co-efficient, K; age at zero length, t0; growth performance index, Ø'), life span (tmax), mortality (total, Z; natural, M; fishing, F), recruitment pattern, exploitation rate (E) and maximum sustainable yield (MSY) of ray-finned Chanda nama for the first time from the Ganges River of north-western Bangladesh. A sum of 1260 fish was collected during January to December 2017. The total length (TL) was recorded in the range of 3.3 to 9.9 cm. The negative allometric growth pattern was assessed through the b value < 3.0. Further, the L∞ was 10.25 cm as well as K was found 0.55 year-1. The Ø' was calculated as 1.762, t0 was 0.057 years while the tmax was estimated as 2.49 years. In addition, the Z, M, and F were obtained as 3.11, 1.63, and 1.48 year-1, respectively. The trend of recruitment was continual through one peak occurrence in May-July. Length of the first capture (Lc50) observed at TL of 3.32 cm. However, the exploitation rate (E) was assessed as 0.48 whereas the maximum allowable yield (Emax) was 0.46. The maximum sustainable yield was estimated as 4.51 metric tons. Consequently, the information from this study would be beneficial for the implementation of a proper management strategy in the Ganges River and the related ecosystems. [ABSTRACT FROM AUTHOR]

Analysis of demographic data indicates uneven distribution of mortality within a year, month, and even week time period. This is of great practical importance for the operation of medical institutions, including intensive care units, and makes it possible to calculate economic and labor requirements of medical institutions. All the above is especially relevant during the era of the COVID-19 pandemic. Malygin showed the presence of one to two fluctuations per week in the mortality of male patients with type 2 diabetes. The height of the peaks of such fluctuations is determined, as expected, by the regular parameter indicating their position on the axis of lifespan and random parameter reflecting adverse effects of external environmental factors on the body, as well as the extent of the periodically occurring sharp decrease in the nonspecific resistance. This article discusses results of recent research in the field of small (semi-weekly, weekly, monthly, and seasonal) fluctuations of mortality. Based on a large array of accumulated data, it can be concluded that the decrease in seasonal variability of mortality accompanies an increase in the life expectancy. Studying characteristics of mortality fluctuations makes it possible to move from investigating the impact of biorhythms (Master Clock) on the development of acute and chronic phenoptotic processes directly to studying the patterns of mortality rhythms themselves (rhythms of phenoptosis). [ABSTRACT FROM AUTHOR]

Growth rate, longevity, and maturity were estimated for four commonly targeted species of surgeonfish in Hawai'i: ringtail surgeonfish/pualu Acanthurus blochii, eyestripe surgeonfish/palani Acanthurus dussumieri, orange-band surgeonfish/na'ena'e Acanthurus olivaceus, and yellowfin surgeonfish/pualu Acanthurus xanthopterus. All species demonstrated rapid growth with long life spans. The maximum observed ages were 26 years for A. blochii, 30 years for A. dussumieri, 14 years for A. olivaceus, and 29 years for A. xanthopterus. Females reached maturity at a greater size and age for all four species. All species reached maturity within the first 3 years of life and approximately 59–67% of maximum size. All four surgeonfish species demonstrated a biphasic mortality schedule with a higher total mortality rate occurring earlier part of life. This study provides a comprehensive study of the age, growth, and maturity for four large-bodied surgeonfish species which are commonly targeted throughout Hawai'i and the rest of the Indo-Pacific. [ABSTRACT FROM AUTHOR]

Recent work has unearthed many empirical regularities in mortality trends, including the inverse correlation between life expectancy and life span inequality, and the compression of mortality into older age ranges. These regularities have furnished important insights into the dynamics of mortality by describing, in demographic terms, how different attributes of the life table deaths distribution interrelate and change over time. However, though empirical evidence suggests that the demographically-meaningful metrics these regularities involve (e.g., life span disparity and life table entropy) are correlated to the moments of the deaths distribution (e.g., variance), the broader theoretical connections between life span inequality and the moments of the deaths distribution have yet to be elucidated. In this article we establish such connections and leverage them to furnish new insights into mortality dynamics. We prove theoretical results linking life span disparity and life table entropy to the central moments of the deaths distribution, and use these results to empirically link statistical measures of variation of the deaths distribution (e.g., variance, index of dispersion) to life span disparity and life table entropy. We validate these results via empirical analyses using data from the Human Mortality Database and extract from them several new insights into mortality shifting and compression in human populations. [ABSTRACT FROM AUTHOR]

Sweden has made a contribution to mammography screening research considerably disproportionate to its size. With 0.13% of the world's population, Sweden contributed almost half of the randomized trial evidence on mammography screening. In addition to the fundamental efficacy of screening in preventing deaths from breast cancer, Swedish researchers have produced a considerable volume of research evaluating mammography screening in the routine healthcare services setting and illuminating issues of breast cancer progression and natural history. The basic result that screening prevents deaths from breast cancer has informed policy and led to substantial preservation of life internationally. [ABSTRACT FROM AUTHOR]

Background: Wasting is a common complication of kidney failure that leads to weight loss and poor outcomes. Recent experimental data identified parathyroid hormone (PTH) as a driver of adipose tissue browning and wasting, but little is known about the relations among secondary hyperparathyroidism, weight loss, and risk of mortality in dialysis patients. Methods: We included 42,319 chronic in‐centre haemodialysis patients from the Dialysis Outcomes and Practice Patterns Study phases 2–6 (2002–2018). Linear mixed models were used to estimate the association between baseline PTH and percent weight change over 12 months, adjusting for country, demographics, comorbidities, and labs. Accelerated failure time models were used to assess 12 month weight loss as a mediator between baseline high PTH and mortality after 12 months. Results: Baseline PTH was inversely associated with 12 month weight change: 12 month weight loss >5% was observed in 21%, 18%, 18%, 17%, 15%, and 14% of patients for PTH ≥600 pg/mL, 450–600, 300–450, 150–300, 50–150, and <50 pg/mL, respectively. In adjusted analyses, 12 month weight change compared with PTH 150–299 pg/mL was −0.60%, −0.12%, −0.10%, +0.15%, and +0.35% for PTH ≥600, 450–600, 300–450, 50–150, and <50 pg/mL, respectively. This relationship was robust regardless of recent hospitalization and was more pronounced in persons with preserved appetite. During follow‐up after the 12 month weight measure [median, 1.0 (interquartile range, 0.6–1.7) years; 6125 deaths], patients with baseline PTH ≥600 pg/mL had 11% [95% confidence interval (CI), 9–13%] shorter lifespan, and 18% (95% CI, 14–23%) of this effect was mediated through weight loss ≥2.5%. Conclusions: Secondary hyperparathyroidism may be a novel mechanism of wasting, corroborating experimental data, and, among chronic dialysis patients, this pathway may be a mediator between elevated PTH levels and mortality. Future research should determine whether PTH‐lowering therapy can limit weight loss and improve longer term dialysis outcomes. [ABSTRACT FROM AUTHOR]

Dozens of surrogates have been used to reflect the rate of aging in comparative biology. For wild organisms, the maximum reported life span is often considered a key metric. However, the connection between the maximum reported life span for a single individual and the aging rate of that species is far from clear. Our objective was to identify a pragmatic solution to calculate the aging rate from the maximum reported life span of wild birds. We explicitly linked the maximum reported life span to the aging process by employing a Weibull distribution and calculating the shape parameter in this model, which reflects the change in mortality across ages and be used as a surrogate for the aging rate. From simulated data, we demonstrated that the percentile estimator is suitable for calculating the aging rate based on the maximum reported life span. We also calculated the aging rate in 246 bird species based on published information from EURING and tested its relationship with body mass. Our study constitutes a new approach for using maximum reported life span in aging research. The aging rate calculated in the study is based on numerous assumptions/prerequisites and can be improved as more is learned about these assumptions/prerequisites. [ABSTRACT FROM AUTHOR]

This article reviews some key strands of demographic research on past trends in human longevity and explores possible future trends in life expectancy at birth. Demographic data on age-specific mortality are used to estimate life expectancy, and validated data on exceptional life spans are used to study the maximum length of life. In the countries doing best each year, life expectancy started to increase around 1840 at a pace of almost 2.5 y per decade. This trend has continued until the present. Contrary to classical evolutionary theories of senescence and contrary to the predictions of many experts, the frontier of survival is advancing to higher ages. Furthermore, individual life spans are becoming more equal, reducing inequalities, with octogenarians and nonagenarians accounting for most deaths in countries with the highest life expectancy. If the current pace of progress in life expectancy continues, most children born this millennium will celebrate their 100th birthday. Considerable uncertainty, however, clouds forecasts: Life expectancy and maximum life span might increase very little if at all, or longevity might rise much faster than in the past. Substantial progress has been made over the past three decades in deepening understanding of how long humans have lived and how long they might live. The social, economic, health, cultural, and political consequences of further increases in longevity are so significant that the development of more powerful methods of forecasting is a priority. [ABSTRACT FROM AUTHOR]

Older age is a strong shared risk factor for many chronic diseases, and there is increasing interest in identifying aging biomarkers. Here, a proteomic analysis of 1301 plasma proteins was conducted in 997 individuals between 21 and 102 years of age. We identified 651 proteins associated with age (506 over-represented, 145 underrepresented with age). Mediation analysis suggested a role for partial cis-epigenetic control of protein expression with age. Of the age-associated proteins, 33.5% and 45.3%, were associated with mortality and multimorbidity, respectively. There was enrichment of proteins associated with inflammation and extracellular matrix as well as senescence-associated secretory proteins. A 76-protein proteomic age signature predicted accumulation of chronic diseases and all-cause mortality. These data support the use of proteomic biomarkers to monitor aging trajectories and to identify individuals at higher risk of disease to be targeted for in depth diagnostic procedures and early interventions. [ABSTRACT FROM AUTHOR]

Aging is a good indicator in demographic and health areas as the lifespan of the elderly population increases. Based on the government's Economic Outlook 2019, it was found that an aging population would increase the government pension payments as the pensioners and their beneficiaries have longer life expectancy. Due to mortality rates decreasing over time, the life expectancy tends to increase in the future. The aims of this study are to forecast the mortality rates in the years 2020 and 2025 using the Heligman-Pollard model and then analyse the effect of mortality improvement on the pension cost (annuity factor) for the Malaysian population. However, this study only focuses on estimating the annuity factor using life annuities through the forecasted mortality rates. The findings indicated that the pension cost is expected to increase if the life expectancy of the Malaysian population increases due to the aging population in the near future. Thus, to reduce pension costs and help the pensioners from insufficient financial income, the government needs to consider an extension of the retirement age in future. [ABSTRACT FROM AUTHOR]

Summary: The invasive red palm weevil (RPW) (Rhynchophorus ferrugineus) (Coleoptera: Curculionidae) is one of the most destructive palm pests in the world. More options are needed for its management, including optimised use of microbial entomopathogens (EP). The sub-lethal effects of an entomopathogenic fungus (EPF) Beauveria bassiana (isolate WG-11) (Ascomycota: Hypocreales) (at 1 × 104 spores ml−1) and two entomopathogenic nematode (EPN) species, Heterorhabditis bacteriophora (at 100 infective juveniles (IJ) ml−1) and Steinernema carpocapsae (at 50 IJ ml−1) were evaluated in various combinations against laboratory-reared 3rd, 5th and 8th instar larvae of RPW in bioassays. Individual and combined effects of both EP were observed after the pre-application of B. bassiana fungus at 0-, 1- and 2-week intervals. Combined treatments were tested for antagonistic, additive and synergistic effects. Additive and synergistic effects were observed in B. bassiana / S. carpocapsae and in B. bassiana / H. bacteriophora combined treatments. Early instar larvae of RPW were more susceptible than older instars. Sole and combined EP treatments decreased pupation, subsequent emergence of RPW adults and hatching. Sub-lethal effects of EP were observed in R. ferrugineus following application at the above-mentioned rates to 3rd, 5th and 8th instar larvae, including reduced larval weights, increased larval, pre-pupal and pupal durations, reduced adult weights and life spans. Simultaneous combined applications of B. bassiana / S. carpocapsae and B. bassiana / H. bacteriophora at the above-mentioned rates against last instar (9th) larvae of R. ferrugineus reduced food consumption, frass production and affected weight gains. [ABSTRACT FROM AUTHOR]

Quantification of biological aging is of interest in gerontology as a means to surveil aging rates in the population and to evaluate the effects of interventions to increase healthy life span. Analysis of proposed methods to quantify biological aging has focused on samples of midlife or mixed-age adults in the West. Research is needed to test whether quantifications of biological aging can differentiate aging rates among older adults and if quantifications of biological aging developed in Western samples can differentiate aging rates in non-Western populations. We conducted analysis of Klemera-Doubal method (KDM) Biological Age and homeostatic dysregulation measures of biological aging developed in the U.S. NHANES and tested in a sample of older Taiwanese adults in the Social Environment and Biomarkers of Aging Study. We conducted analysis of physical and cognitive function and mortality, comparing quantifications of biological aging to a biomarker index based on norms within our analysis sample and to participants' ratings of their own health. Results showed that quantifications of biological aging (a) predicted differences in physical and cognitive function and in mortality risk among Taiwanese older adults and (b) performed as well as a traditional biomarker index and participant self-rated health for prediction of these outcomes. [ABSTRACT FROM AUTHOR]

Disentangling the relationship between age and reproduction is central to understand life‐history evolution, and recent evidence shows that considering condition‐dependent mortality is a crucial piece of this puzzle. For example, nonrandom mortality of 'low‐condition' individuals can lead to an increase in average lifespan. However, selective disappearance of such low‐condition individuals may also affect reproductive senescence at the population level due to trade‐offs between physiological functions related to survival/lifespan and the maintenance of reproductive functions. Here, we address the idea that condition‐dependent extrinsic mortality (i.e. simulated predation) may increase the age‐related decline in male reproductive success and with it the potential for sexual conflict, by comparing reproductive ageing in Drosophila melanogaster male/female cohorts exposed (or not) to condition‐dependent simulated predation across time. Although female reproductive senescence was not affected by predation, male reproductive senescence was considerably higher under predation, due mainly to an accelerated decline in offspring viability of 'surviving' males with age. This sex‐specific effect suggests that condition‐dependent extrinsic mortality can exacerbate survival‐reproduction trade‐offs in males, which are typically under stronger condition‐dependent selection than females. Interestingly, condition‐dependent extrinsic mortality did not affect mating success, hinting that accelerated reproductive senescence is due to a decrease in male post‐copulatory fitness components. Our results support the recent proposal that male ageing can be an important source of sexual conflict, further suggesting this effect could be exacerbated under more natural conditions. [ABSTRACT FROM AUTHOR]

Preclinical studies are important in identifying the underlying mechanisms contributing to frailty. Frailty studies have mainly focused on male rodents with little directed at female rodents. Therefore, the purposes of this study were to identify the onset and prevalence of frailty across the life span in female mice, and to determine if frailty predicts mortality. Female C57BL/6 (n = 27) mice starting at 17 months of age were assessed across the life span using a frailty phenotype, which included body weight, walking speed, strength, endurance, and physical activity. The onset of frailty occurred at approximately 17 months (1/27 mice), with the prevalence of frailty increasing thereafter. At 17 months, 11.1% of the mice were pre-frail and by 26 months peaked at 36.9%. The percentage of frail mice progressively increased up to 66.7% at 32 months. Non-frail mice lived to 29 months whereas frail/pre-frail mice lived only to 26 months (p = .04). In closing, using a mouse frailty phenotype, we are able to identify that the prevalence of frailty in female mice increases across the life span and accurately predicts mortality. Together, this frailty phenotype has the potential to yield information about the underlying mechanisms contributing to frailty. [ABSTRACT FROM AUTHOR]

As people live longer, ages at death are becoming more similar. This dual advance over the last two centuries, a central aim of public health policies, is a major achievement of modern civilization. Some recent exceptions to the joint rise of life expectancy and life span equality, however, make it difficult to determine the underlying causes of this relationship. Here, we develop a unifying framework to study life expectancy and life span equality over time, relying on concepts about the pace and shape of aging. We study the dynamic relationship between life expectancy and life span equality with reliable data from the Human Mortality Database for 49 countries and regions with emphasis on the long time series from Sweden. Our results demonstrate that both changes in life expectancy and life span equality are weighted totals of rates of progress in reducing mortality. This finding holds for three different measures of the variability of life spans. The weights evolve over time and indicate the ages at which reductions in mortality increase life expectancy and life span equality: the more progress at the youngest ages, the tighter the relationship. The link between life expectancy and life span equality is especially strong when life expectancy is less than 70 y. In recent decades, life expectancy and life span equality have occasionally moved in opposite directions due to larger improvements in mortality at older ages or a slowdown in declines in midlife mortality. Saving lives at ages below life expectancy is the key to increasing both life expectancy and life span equality. [ABSTRACT FROM AUTHOR]

Variation in life‐history characteristics is evident within and across animal populations. Such variation is mediated by environmental gradients and reflects metabolic constraints or trade‐offs that enhance reproductive outputs. While generalizations of life‐history relationships across species provide a framework for predicting vulnerability to overexploitation, deciphering patterns of intraspecific variation may also enable recognition of peculiar features of populations that facilitate ecological resilience.This study combines age‐based biological data from geographically disparate populations of bluespine unicornfish (Naso unicornis)—the most commercially valuable reef‐associated species in the insular Indo‐Pacific—to explore the magnitude and drivers of variation in life span and examine the mechanisms enabling peculiar mortality schedules.Longevity and mortality schedules were investigated across eleven locations encompassing a range of latitudes and exploitation levels. The presence of different growth types was examined using back‐calculated growth histories from otoliths. Growth‐type‐dependent mortality (mortality rates associated with particular growth trajectories) was corroborated using population models that incorporated size‐dependent competition.We found a threefold geographic variation in life span that was strongly linked to temperature, but not to anthropogenic pressure or ocean productivity. All populations consistently displayed a two‐phase mortality schedule, with higher than expected natural mortality rates in earlier stages of post‐settlement life. Reconstructed growth histories and population models demonstrated that variable growth types within populations can yield this peculiar biphasic mortality schedule, where fast growers enjoy early reproductive outputs at the expense of greater mortality, and benefits for slow growers derive from extended reproductive outputs over a greater number of annual cycles. This promotes population resilience because individuals can take advantage of cycles of environmental change operating at both short‐ and long‐term scales.Our results highlight a prevailing, fundamental misperception when comparing the life histories of long‐lived tropical ectotherms: the seemingly incongruent combination of extended life spans with high mortality rates was enabled by coexistence of variable growth types in a population. Thus, a demographic profile incorporating contrasting growth and mortality strategies obscures the demographic effects of harvest across space or time in N. unicornis and possibly other ectotherms with the combination of longevity and asymptotic growth. [ABSTRACT FROM AUTHOR]

Nature provides a good opportunity to understand the dynamics of evolution. The country has a huge coastline, which experiences socio-cultural and natural vulnerability. The aim of the paper has been to describe the pattern of selection intensity among the east and west coastal populations of India. Differential fertility and mortality were collected from 2,099 females (mothers) of the western coasts of India, and secondary data were collected from the eastern coast of India for comparison purposes. Selection potential was computed using Crow's index and Johnston & Kensinger's index. The data involved a total of 7,512 pregnancies during their reproductive lifespan and the successful outcomes (live births) were 7,073. The total index (It) for eastern coast varied from 0.221 to 1.078. For the west coast, it varied from 0.262 to 0.617. Among the eastern coastal population groups, the mortality component of selection is comparatively higher than its fertility component, while it is just the reverse among the western coastal population groups. [ABSTRACT FROM AUTHOR]

The aim of this paper is to determine the trends of the main indicators of life expectancy in Russia in the 1950s to 2000s. For this purpose, life tables for Russia (former -- RSFSR) from 1959 to 2014 for one-year age intervals were analyzed. The main indicators under review are the modal age at death and the standard deviation of life expectancy from the modal value for all ages and the mode. As a result, it is concluded that in Russia the modal age at death and the indicator of life expectancy have stagnated over the past 60 years, and definite trends can be traced only in short periods of time, namely after 2009 when all basic life expectancy indicators were steadily increasing. Life expectancy is far behind those of the developed countries by about half a century. [ABSTRACT FROM AUTHOR]

This Viewpoint describes how open innovation has been used by communities to support individual and community health and discusses how scientists and clinicians could apply this idea- and resource-sharing strategy to generate breakthrough advances that may extend the life span of people with serious mental illness (SMI). [ABSTRACT FROM AUTHOR]

Psychosis and/or aggression are common problems in dementia, and when severe or persistent, cause considerable patient distress and disability, caregiver stress, and early institutionalization. In 2005, the Food and Drug Administration (FDA) determined that atypical antipsychotics were associated with a significantly greater mortality risk compared to placebo, which prompted the addition of an FDA black-box warning. The American College of Neuropsychopharmacology (ACNP) White Paper, 2008, reviewed this issue and made clinical and research recommendations regarding the use of antipsychotics in dementia patients with psychosis and/or agitation. Increased mortality risk has also been described in cerebrovascular adverse events in elderly users of antipsychotics. In the present work, at the translational level, we used male 3xTg-AD mice (PS1M146V, APPSwe, tauP301L) at advanced stages of the disease reported to have worse survival than females, to study the behavioral effects of a low chronic dose of risperidone (0.1 mg/kg, s.c., 90 days, from 13 to 16 months of age) and its impact on long-term survival, as compared to mice with normal aging. Animals were behaviorally assessed for cognitive and BPSD (behavioral and psychological symptoms of dementia)-like symptoms in naturalistic and experimental conditions (open-field test, T-maze, social interaction, Morris water maze, and marble test) before and after treatment. Weight, basal glucose levels, and IPGTT (i.p. glucose tolerance test) were also recorded. Neophobia in the corner test was used for behavioral monitoring. Survival curves were recorded throughout the experiment until natural death. The benefits of risperidone were limited, both at cognitive and BPSD-like level, and mostly restricted to burying, agitation/vibrating tail, and other social behaviors. However, the work warns about a clear early mortality risk window during the treatment and long-lasting impact on survival. Reduced life expectancy and life span were observed in the 3xTg-AD mice, but total lifespan (36 months) recorded in C57BL/6 × 129Sv counterparts with normal aging was also truncated to 28 months in those with treatment. Sarcopenia at time of death was found in all groups, but was more severe in wild-type animals treated with risperidone. Therefore, the 3xTg-AD mice and their non-transgenic counterparts can be useful to delimitate critical time windows and for studying the physio-pathogenic factors and underlying causal events involved in this topic of considerable public health significance. [ABSTRACT FROM AUTHOR]

There is great interest among gerontologists, demographers, and actuaries in the question concerning the limits to human longevity. Attempts at getting answers to this important question have stimulated many studies on late-life mortality trajectories, often with opposing conclusions. One group of researchers believes that mortality stops growing with age at extreme old ages, and that hence there is no fixed limit to the human life span. Other studies found that mortality continues to grow with age up to extreme old ages. Our study suggests a possible solution to this controversy. We found that mortality deceleration is best observed when older, less accurate life span data are analyzed, while in the case of more recent and reliable data there is a persistent mortality growth with age. We compared the performance (goodness of fit) of two competing mortality models - the Gompertz model and the Kannisto ("mortality deceleration") model - at ages of 80-105 years using data for 1880-1899 single-year birth cohorts of US men and women. The mortality modeling approach suggests a transition from mortality deceleration to the Gompertzian mortality pattern over time for both men and women. These results are consistent with the hypothesis about disappearing mortality deceleration over time due to improvement in the accuracy of age reporting. In the case of more recent data, mortality continues to grow with age even at very old ages. This observation may lead to more conservative estimates of future human longevity records. [ABSTRACT FROM AUTHOR]

Background: Although individuals with alcohol use disorder (AUD) have a significantly shorter lifespan than the general population, there is sparse evidence on cause of death when alcohol dependent people die prematurely. Especially the somatic causes of death are shed less light on.Aim: To determine the cause of premature death in individuals with AUD based on recent studies.Methods: This systematic review summarizes evidence from the last 10 years with cohort studies consisting of AUD patients with the subsequent outcome of cause of death and with at least two years of follow-up.Results: Nine studies were included of which only two were assessed to be of good quality. Furthermore, two studies were of moderately good and acceptable quality, respectively. This review found increased mortality in AUD individuals with the main causes of death being malignancy, and problems of the cardiovascular- and the digestive system.Conclusion: Malignancy was the most common cause of death in the included AUD cohorts, but the overall quality of the included studies in this review is low. There is a need for high-quality studies to better understand cause-specific mortality among AUD individuals. [ABSTRACT FROM AUTHOR]

We investigated the toxic effect of visible light on Drosophila life span in both sexes. The toxic effect of ultraviolet light on organisms is well known. However, the effects of illumination with visible light remain unclear. Here, we found that visible light could be toxic to Drosophila survival, depending on the protein content in diet. In addition, further analysis revealed significant interaction between light and sex and showed that strong light shortened life span by causing opposite direction changes in mortality rate parameters in females versus males. Our findings suggest that photoaging may be a general phenomenon and support the theory of sexual antagonistic pleiotropy in aging intervention. The results caution that exposure to visible light could be hazardous to life span and suggest that identification of the underlying mechanism would allow better understanding of aging intervention. [ABSTRACT FROM AUTHOR]

We consider the distributional implications of Social Security policy changes in the context of increases in life expectancy and differential mortality. Using a robust microsimulation model, we examine how several options for raising the retirement age, including a scenario that applies a mortality adjustment in combination with such policies, affect different types of individuals and households. Policy changes are simulated for Social Security beneficiaries in 2030 using the Modeling Income in the Near Term (MINT) microsimulation model. The analysis shows that increasing either the age at which individuals receive their full retirement benefit alone or the early eligibility and full retirement ages together result in across‐the‐board reductions in benefit levels. The policies are projected to result in slightly higher poverty, but the expected rise is sharper among groups known to experience higher rates of mortality, as well as many disadvantaged groups. Analysis of a hypothetical adjustment to offset the historical impacts of differential mortality by lifetime earnings on lifetime benefit receipt, when combined with these retirement age increases, shows varied results. While some groups of individuals experience sharper reductions in median monthly benefits, the adjustment has an offsetting and protective effect for the benefits of disadvantaged groups when combined with options that would raise the retirement age. This combined package of policies, as well as simulations that incorporate a behavioral adjustment in benefit claiming ages, result in an increase of less than one percentage point in the average poverty rate. [ABSTRACT FROM AUTHOR]

Fishing gears are designed to exploit the natural behaviors of fish, and the concern that fishing may cause evolution of behavioral traits has been receiving increasing attention. The first intuitive expectation is that fishing causes evolution toward reduced boldness because it selectively removes actively foraging individuals due to their higher encounter rate and vulnerability to typical gear. However, life‐history theory predicts that fishing, through shortened life span, favors accelerated life histories, potentially leading to increased foraging and its frequent correlate, boldness. Additionally, individuals with accelerated life histories mature younger and at a smaller size and therefore spend more of their life at a smaller size where mortality is higher. This life‐history evolution may prohibit increases in risk‐taking behavior and boldness, thus selecting for reduced risk‐taking and boldness. Here, we aim to clarify which of these three selective patterns ends up being dominant. We study how behavior‐selective fishing affects the optimal behavioral and life‐history traits using a state‐dependent dynamic programming model. Different gear types were modeled as being selective for foraging or hiding/resting individuals along a continuous axis, including unselective fishing. Compared with unselective harvesting, gears targeting hiding/resting individuals led toward evolution of increased foraging rates and elevated natural mortality rate, while targeting foraging individuals led to evolution of decreased foraging rates and lower natural mortality rate. Interestingly, changes were predicted for traits difficult to observe in the wild (natural mortality and behavior) whereas the more regularly observed traits (length‐at‐age, age at maturity, and reproductive investment) showed only little sensitivity to the behavioral selectivity. Using a state‐dependent dynamic programming model, we aimed at clarifying theoretical expectations about how behavior‐selective fishing can shape the evolution of risk‐taking behavior, life‐history traits, and emergent natural mortality. First, our results are in line with earlier findings that an increased fishing mortality leads to increased natural mortality, earlier maturation, reduced size at age, and increased reproductive investment. Second, we found that the intensity of changes in natural mortality, length, and risk‐taking behavior depends on whether fishing is targeting active, foraging ("bold") fish, or passive, sheltering ("timid") fish. [ABSTRACT FROM AUTHOR]

Rectangularization of the survival curve—a key analytical framework in mortality research—relies on assumptions that have become partially obsolete in high-income countries due to mortality reductions among the oldest old. We propose refining the concept to adjust for recent and potential future mortality changes. Our framework, the ‘maximum inner rectangle approach’ (MIRA) considers two types of rectangularization. Outer rectangularization captures progress in mean lifespan relative to progress in maximum lifespan. Inner rectangularization captures progress in lifespan equality relative to progress in mean lifespan. Empirical applications show that both processes have generally increased since 1850. However, inner rectangularization has displayed country-specific patterns since the onset of sustained old-age mortality declines. Results from separating premature and old-age mortality, using the MIRA, suggest there has been a switch from reducing premature deaths to extending the premature age range; a shift potentially signalling a looming limit to the share of premature deaths. [ABSTRACT FROM AUTHOR]

We consider the numerical approximation of the survival probability in the case of an unbounded mortality rate related to a finite life-span in age-structured population models. Our numerical approach is based on the approximation of the integral that characterizes this probability function by means of an appropriate quadrature rule. We demonstrate the convergence of this approximation assuming suitable conditions in relation with the unbounded mortality rate that will be reasonable in the real applications of this model. The numerical experiments carried out with typical mortality rates corroborate the interest of this method. [ABSTRACT FROM AUTHOR]

We analyze human aging-understood as health deficit accumulation-for a panel of European individuals, using four waves of the Survey of Health, Aging and Retirement in Europe (SHARE data set) and constructing a health deficit index. Results from log-linear regressions suggest that, on average, elderly European men and women develop approximately 2.5 % more health deficits from one birthday to the next. In nonlinear regressions (akin to the Gompertz-Makeham model), however, we find much greater rates of aging and large differences between men and women as well as between countries. Interestingly, these differences follow a particular regularity (akin to the compensation effect of mortality) and suggest an age at which average health deficits converge for men and women and across countries. This age, which may be associated with human life span, is estimated as 102 ± 2.6 years. [ABSTRACT FROM AUTHOR]

Using segmented linear regression to reanalyze the "best-guess" maximum reported age at death data supplied in Aubrey de Grey's editorial, we find compelling evidence for a breakpoint in the mid-1990s, with a positive slope before the breakpoint and a flat or slightly negative slope after it. This confirmation of our earlier results was also modeled using exponential regression. Both the segmented and exponential models were superior to a simple linear regression, providing a better fit for the data even after taking into account their greater number of parameters. These findings are highly robust to the removal of several points from the data and bolster the existing evidence for a limit to human lifespan. Taken in light of both our original analysis and its confirmation by several independent groups, this latest result provides yet more evidence that human lifespan has reached its limit under the current technological paradigm. However, we cannot discount the possibility that novel innovations could propel human lifespan beyond the limit we have identified, if they can overcome the considerable challenges facing them. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to explore the pattern of mortality above the age of 100 years. In particular, we aimed to examine whether Scandinavian data support the theory that mortality reaches a plateau at particularly old ages. Whether the maximum length of life increases with time was also investigated.Methods: The analyses were based on individual level data on all Swedish and Danish centenarians born from 1870 to 1901; in total 3006 men and 10 963 women were included. Birth cohort-specific probabilities of dying were calculated. Exact ages were used for calculations of maximum length of life. Whether maximum age changed over time was analysed taking into account increases in cohort size.Results: The results confirm that there has not been any improvement in mortality amongst centenarians in the past 30 years and that the current rise in life expectancy is driven by reductions in mortality below the age of 100 years. The death risks seem to reach a plateau of around 50% at the age 103 years for men and 107 years for women. Despite the rising life expectancy, the maximum age does not appear to increase, in particular after accounting for the increasing number of individuals of advanced age.Conclusion: Mortality amongst centenarians is not changing despite improvements at younger ages. An extension of the maximum lifespan and a sizeable extension of life expectancy both require reductions in mortality above the age of 100 years. [ABSTRACT FROM AUTHOR]

This study proposes a new decomposition method that permits a difference in an aggregate measure at a final time point to be split into additive components corresponding to the initial differences in the event rates of the measure and differences in trends in these underlying event rates. For instance, when studying divergence in life expectancy, this method allows researchers to more easily contrast age-specific mortality trends between populations by controlling for initial age-specific mortality differences. Two approaches are assessed: (1) an additive change method that uses logic similar to cause-of-death decomposition, and (2) a contour decomposition method that extends the stepwise replacement algorithm along an age-period demographic contour. The two approaches produce similar results, but the contour method is more widely applicable. We provide a full description of the contour replacement method and examples of its application to life expectancy and lifetime disparity differences between the United States and England and Wales in the period 1980-2010. [ABSTRACT FROM AUTHOR]

Evaluating the predictive ability of mortality forecasts is important yet difficult. Death rates and mean lifespan are basic life table functions typically used to analyze to what extent the forecasts deviate from their realized values. Although these parameters are useful for specifying precisely how mortality has been forecasted, they cannot be used to assess whether the underlying mortality developments are plausible. We therefore propose that in addition to looking at average lifespan, we should examine whether the forecasted variability of the age at death is a plausible continuation of past trends. The validation of mortality forecasts for Italy, Japan, and Denmark demonstrates that their predictive performance can be evaluated more comprehensively by analyzing both the average lifespan and lifespan disparity-that is, by jointly analyzing the mean and the dispersion of mortality. Approaches that account for dynamic age shifts in survival improvements appear to perform better than others that enforce relatively invariant patterns. However, because forecasting approaches are designed to capture trends in average mortality, we argue that studying lifespan disparity may also help to improve the methodology and thus the predictive ability of mortality forecasts. [ABSTRACT FROM AUTHOR]

The current molecular understanding of the aging process derives almost exclusively from the study of random or targeted single-gene mutations in highly inbred laboratory species, mostly invertebrates. Little information is available as to the genetic mechanisms responsible for natural lifespan variation and the evolution of lifespan, especially in vertebrates. Here, we investigated the pattern of positive selection in annual (i.e., short-lived) and nonannual (i.e., longer-lived) African killifishes to identify a genomic substrate for evolution of annual life history (and reduced lifespan). We identified genes under positive selection in all steps of mitochondrial biogenesis: mitochondrial (mt) DNA replication, transcription from mt promoters, processing and stabilization of mt RNAs, mt translation, assembly of respiratory chain complexes, and electron transport chain. Signs of paralleled evolution (i.e., evolution in more than one branch of Nothobranchius phylogeny) are observed in four out of five steps. Moreover, some genes under positive selection in Nothobranchius are under positive selection also in long-lived mammals such as bats and mole-rats. Complexes of the respiratory chain are formed in a coordinates multistep process where nuclearly and mitochondrially encoded components are assembled and inserted into the inner mitochondrial membrane. The coordination of this process is named mitonuclear balance, and experimental manipulations of mitonuclear balance can increase longevity of laboratory species. Our data strongly indicate that these genes are also casually linked to evolution lifespan in vertebrates. [ABSTRACT FROM AUTHOR]

Standard evolutionary theories of aging and mortality, implicitly based on assumptions of spatial averaging, hold that natural selection cannot favor shorter lifespan without direct compensating benefit to individual reproductive success. However, a number of empirical observations appear as exceptions to or are difficult to reconcile with this view, suggesting explicit lifespan control or programmed death mechanisms inconsistent with the classic understanding. Moreover, evolutionary models that take into account the spatial distributions of populations have been shown to exhibit a variety of self-limiting behaviors, maintained through environmental feedback. Here we extend recent work on spatial modeling of lifespan evolution, showing that both theory and phenomenology are consistent with programmed death. Spatial models show that self-limited lifespan robustly results in long-term benefit to a lineage; longer-lived variants may have a reproductive advantage for many generations, but shorter lifespan ultimately confers long-term reproductive advantage through environmental feedback acting on much longer time scales. Numerous model variations produce the same qualitative result, demonstrating insensitivity to detailed assumptions; the key conditions under which self-limited lifespan is favored are spatial extent and locally exhaustible resources. Factors including lower resource availability, higher consumption, and lower dispersal range are associated with evolution of shorter lifespan. A variety of empirical observations can parsimoniously be explained in terms of long-term selective advantage for intrinsic mortality. Classically anomalous empirical data on natural lifespans and intrinsic mortality, including observations of longer lifespan associated with increased predation, and evidence of programmed death in both unicellular and multicellular organisms, are consistent with specific model predictions. The generic nature of the spatial model conditions under which intrinsic mortality is favored suggests a firm theoretical basis for the idea that evolution can quite generally select for shorter lifespan directly. [ABSTRACT FROM AUTHOR]

Gompertz empirical law of mortality is often used in practical research to parametrize survival fraction as a function of age with the help of just two quantities: the Initial Mortality Rate (IMR) and the Gompertz exponent, inversely proportional to the Mortality Rate Doubling Time (MRDT). The IMR is often found to be inversely related to the Gompertz exponent, which is the dependence commonly referred to as Strehler-Mildvan (SM) correlation. In this paper, we address fundamental uncertainties of the Gompertz parameters inference from experimental Kaplan-Meier plots and show, that a least squares fit often leads to an ill-defined non-linear optimization problem, which is extremely sensitive to sampling errors and the smallest systematic demographic variations. Therefore, an analysis of consequent repeats of the same experiments in the same biological conditions yields the whole degenerate manifold of possible Gompertz parameters. We find that whenever the average lifespan of species greatly exceeds MRDT, small random variations in the survival records produce large deviations in the identified Gompertz parameters along the line, corresponding to the set of all possible IMR and MRDT values, roughly compatible with the properly determined value of average lifespan in experiment. The best fit parameters in this case turn out to be related by a form of SM correlation. Therefore, we have to conclude that the combined property, such as the average lifespan in the group, rather than IMR and MRDT values separately, may often only be reliably determined via experiments, even in a perfectly homogeneous animal cohort due to its finite size and/or low age-sampling frequency, typical for modern high-throughput settings. We support our findings with careful analysis of experimental survival records obtained in cohorts of C. elegans of different sizes, in control groups and under the influence of experimental therapies or environmental conditions. We argue that since, SM correlation may show up as a consequence of the fitting degeneracy, its appearance is not limited to homogeneous cohorts. In fact, the problem persists even beyond the simple Gompertz mortality law. We show that the same degeneracy occurs exactly in the same way, if a more advanced Gompertz-Makeham aging model is employed to improve the modeling. We explain how SM type of relation between the demographic parameters may still be observed even in extremely large cohorts with immense statistical power, such as in human census datasets, provided that systematic historical changes are weak in nature and lead to a gradual change in the mean lifespan. [ABSTRACT FROM AUTHOR]

Based on the findings from the Radiation Effects Research Foundation's studies of the cohort of Japanese atomic bomb survivors, it has been reported that total-body irradiation at 0.5-1.0 Gy could be responsible for increased rates of mortality from broad-based categories of cardiovascular disease (CVD), i.e., stroke and heart disease. However, CVD consists of various subtypes that have potentially different radiation dose responses, as well as subtype-specific risks that have not been fully evaluated. Potential problems with changes in the coding rules for the International Classification of Diseases (ICD) and the underlying causes and trends in CVD mortality in Japan also need to be considered. The goal of this study was to clarify the radiation risk of subtype-specific heart disease over different time periods. Radiation dose response was examined for mortality from several heart disease subtypes in 86,600 members of the Life Span Study (LSS) cohort during 1950-2008. These subtypes included ischemic heart disease (IHD), valvular heart disease (VHD), hypertensive organ damage (HOD) and heart failure (HF). Individual radiation doses ranged between 0 and 4 Gy. In addition to analyses for the total period, we examined specific periods, 1950-1968, 1969-1980, 1981-1994 and 1995-2008, corresponding to major developments in medical technologies and ICD code revisions. We observed significant positive associations between radiation dose and mortality from heart disease overall in 1950-2008 [excess relative risk or ERR/Gy (95% CI) = 0.14 (0.06, 0.22)]. Subtype-specific ERRs also positively increased with dose: 0.45 (0.13, 0.85) for VHD, 0.36 (0.10, 0.68) for HOD and 0.21 (0.07, 0.37) for HF, respectively. No significant departure from linearity was shown for the dose-response model. Although there was no evidence for a threshold in a model function, the lowest dose ranges with a statistically significant dose response were 0-0.7 Gy for heart disease overall and VHD, 0-1.5 Gy for HOD and 0-0.4 Gy for HF. No significant association between radiation exposure and IHD was observed in any model, although a quadratic model fit the best. The risk of HOD and rheumatic VHD increased significantly in the earliest periods [ERR/Gy = 0.59 (0.07, 1.32) and 1.34 (0.24, 3.16), respectively]. The risk of nonrheumatic VHD increased with calendar time and was significant in the latest period [ERR/Gy = 0.75 (0.02, 1.92)]. The risk of IHD, especially for myocardial infarction, tended to be elevated in the most recent period after 2001, where cautious interpretation is needed due to the uncertain validity of death diagnosis. Radiation risks of heart disease mortality in the LSS appeared to vary substantially among subtypes, indicating possible differences in radiation-induced pathogenesis. Trends in CVD rates in Japan during the long observation period may also impact risk analyses. [ABSTRACT FROM AUTHOR]

Mortality analyses have been performed using underlying causes of death as reported on death certificates; these are uniquely determined for a deceased person according to the World Health Organization coding system. Comorbidities, the disease conditions other than the underlying cause of death from death certificates recording multiple causes of death, have rarely been explored in Life Span Study subjects. The purpose of this study was to clarify associations between atomic bomb radiation exposure and mortality from combinations of the underlying cause of death and comorbidities. The focused follow-up period was 1977-2003, prior to which death certificate accuracy was unreliable. The study cohort was comprised of 10,017 people for whom the category 'all circulatory disease' was listed as the underlying cause of death, of which heart disease (rheumatic, hypertensive and ischemic heart disease) and stroke were major subtypes. Comorbidities considered were pneumonia, renal disease, diabetes mellitus, cancer and the major circulatory disease subtypes listed above. Poisson regression models were used for analyses. Excess relative risks (ERRs) for mortality at 1 Gy were significantly increased when cancer was comorbid with all circulatory disease, heart disease, ischemic heart disease or stroke, ranging from 0.61 [95% confidence interval (CI): 0.13, 1.41; N = 177] for all circulatory diseases to 1.60 (CI: 0.07, 4.86; N = 42) for ischemic heart disease. Among the other comorbidities, only diabetes comorbid with heart disease had a significant radiation dose response (ERR at 1 Gy of 0.62, CI: 0.10, 1.46; N = 128). It remains uncertain if the high ERRs with comorbid cancers were anomalous due to the small number of cases or some dissimilarity in statistical methodologies, or if this might suggest some pathogenetic basis for increased fatality. For this reason, further investigation is required. [ABSTRACT FROM AUTHOR]

Accumulation of various types of lesions in the course of aging increases an organism's vulnerability and results in a monotonous elevation of mortality rate, irrespective of the position of a species on the evolutionary tree. Stroustrup et al. ( Nature, 530, 103-107) [1] showed in 2016 that in the nematode Caenorhabditis elegans, longevity-altering factors (e.g. oxidative stress, temperature, or diet) do not change the shape of the survival curve, but either stretch or shrink it along the time axis, which the authors attributed to the existence of an 'aging program'. Modification of the accelerated failure time model by Stroustrup et al. uses temporal scaling as a basic approach for distinguishing between quantitative and qualitative changes in aging dynamics. Thus we analyzed data on the effects of various longevity-increasing genetic manipulations in flies, worms, and mice and used several models to choose a theory that would best fit the experimental results. The possibility to identify the moment of switch from a mortality-governing pathway to some other pathways might be useful for testing geroprotective drugs. In this work, we discuss this and other aspects of temporal scaling. [ABSTRACT FROM AUTHOR]