The contribution of longevity to population death rates

The magnitude of a population's per capita death rate depends on the maximum age at death and the intensity or schedule of mortality of its members. Knowing the maximum possible lifespan that an animal can achieve when raised under defined conditions makes it possible to calculate the component of per capita death rate due to longevity alone. This component is most important to slow-growing populations of animals with relatively short lifespans. Life-table experiments with two rotifer species and a cladoceran indicate that the short lifespans of these animals account for moderate proportions (up to 37.2%) of their population death rates. Decomposing per capita death rates into two components, one due to maximum length of life and another due to differential mortality of animals of different ages, may therefore be a useful way to examine how deleterious processes, such as predation and starvation, limit growth of zooplankton populations.     

Is sociality associated with high longevity in North American birds?

Sociality, as a life-history trait, should be associated with high longevity because complex sociality is characterized by reproductive suppression, delayed breeding, increased care and survival, and some of these traits select for high longevity. We studied the relationship between cooperative parental care (a proxy of complex sociality) and relative maximum lifespan in 257 North American bird species. After controlling for variation in maximum lifespan explained by body mass, sampling effort, latitude, mortality rate, migration distance and age at first reproduction, we found no significant effect of cooperative care on longevity in analyses of species-specific data or phylogenetically independent standardized linear contrasts. Thus, sociality itself is not associated with high longevity. Rather, longevity is correlated with increased body size, survival rate and age of first reproduction.     

Having it all: historical energy intakes do not generate the anticipated trade-offs in fecundity

An axiom of life-history theory, and fundamental to our understanding of ageing, is that animals must trade-off their allocation of resources since energy and nutrients are limited. Therefore, animals cannot "have it all"--combine high rates of fecundity with extended lifespans. The idea of life-history trade-offs was recently challenged by the discovery that ageing may be governed by a small subset of molecular processes independent of fitness. We tested the "trade-off" and "having it all" theories by examining the fecundities of C57BL/6J mice placed onto four different dietary treatments that generated caloric intakes from -21 to +8.6% of controls. We predicted body fat would be deposited in relation to caloric intake. Excessive body fat is known to cause co-morbidities that shorten lifespan, while caloric restriction enhances somatic protection and increases longevity. The trade-off model predicts that increased fat would be tolerated because reproductive gain offsets shortened longevity, while animals on a restricted intake would sacrifice reproduction for lifespan extension. The responses of body fat to treatments followed our expectations, however, there was a negative relationship between reproductive performance (fecundity, litter mass) and historical intake/body fat. Our dietary restricted animals had lower protein oxidative damage and appeared able to combine life-history traits in a manner contrary to traditional expectations by having increased fecundity with the potential to have extended lifespans.     

Density dependence, lifespan and the evolutionary dynamics of longevity

Longevity is a life-history trait that is shaped by natural selection. Evolution will shape mortality trajectories and lifespans, but until now the evolutionary analysis of longevity is based principally on a density-independent (Euler-Lotka) framework. The effects of density dependence on the evolution of lifespan and mortality remain largely unexplored. We investigate the influence of different population demographies on the evolution of longevity, and show how these can be linked to adaptive radiations. We present a range of models to explore the intraspecific and interspecific density effects on longevity and, consequently, diversification. We show how the magnitude, type, and timing of mutation can also affect fitness, invasion and diversification. We argue that fitness of alternative strategies under a range of different demographic structures leads to flat, as opposed to rugged, landscapes and that these flat fitness surfaces are important in the evolution of lifespan and senescence.     

Longevity in Bovids Is Promoted by Sociality,But Reduced by Sexual Selection

Selection on intrinsic lifespan depends on both external factors affecting mortality and inherent tradeoffs in resource allocation between viability traits and other fitness-related traits. Longevity is therefore likely to vary between species in a sex-specific manner due to interspecific and intersexual differences in behavioural ecology. Here I focus on the bovid family to test two central hypotheses on longevity selection using the comparative method: firstly, that a reduction of extrinsic mortality in social species strengthens selection on intrinsic lifespan, and secondly, that mortality costs associated with intense sexual selection lead to shorter intrinsic lifespan. The results show that longevity (i) increases with sociality in both sexes and (ii) decreases with male-biased sexual size-dimorphism, but in males only. These discoveries suggest that sociality, a key ungulate strategy to reduce predation-related mortality, selects for inherently longer-lived organisms, and that strong sexual selection, which is known to compromise survival rates in the wild, can constrain also intrinsic lifespan. The contrasting results for males and females indicate that selection on longevity in the two sexes is partly uncoupled.     

Measurement of Lifespan in Drosophila melanogaster

Aging is a phenomenon that results in steady physiological deterioration in nearly all organisms in which it has been examined, leading to reduced physical performance and increased risk of disease. Individual aging is manifest at the population level as an increase in age-dependent mortality, which is often measured in the laboratory by observing lifespan in large cohorts of age-matched individuals. Experiments that seek to quantify the extent to which genetic or environmental manipulations impact lifespan in simple model organisms have been remarkably successful for understanding the aspects of aging that are conserved across taxa and for inspiring new strategies for extending lifespan and preventing age-associated disease in mammals.The vinegar fly, Drosophila melanogaster, is an attractive model organism for studying the mechanisms of aging due to its relatively short lifespan, convenient husbandry, and facile genetics. However, demographic measures of aging, including age-specific survival and mortality, are extraordinarily susceptible to even minor variations in experimental design and environment, and the maintenance of strict laboratory practices for the duration of aging experiments is required. These considerations, together with the need to practice careful control of genetic background, are essential for generating robust measurements. Indeed, there are many notable controversies surrounding inference from longevity experiments in yeast, worms, flies and mice that have been traced to environmental or genetic artifacts^1-4. In this protocol, we describe a set of procedures that have been optimized over many years of measuring longevity in Drosophila using laboratory vials. We also describe the use of the dLife software, which was developed by our laboratory and is available for download (http://sitemaker.umich.edu/pletcherlab/software). dLife accelerates throughput and promotes good practices by incorporating optimal experimental design, simplifying fly handling and data collection, and standardizing data analysis. We will also discuss the many potential pitfalls in the design, collection, and interpretation of lifespan data, and we provide steps to avoid these dangers.     

Inferring maximum lifespan from maximum recorded longevity in the wild carries substantial risk of estimation bias

When comparing lifespan (longevity) between species, it is common practice to take the maximum recorded longevity value within each species as a proxy of maximum lifespan. Whether maximum recorded longevity is a reliable proxy of species' maximum longevity remains unclear. Some researchers correct for previously documented life history correlates of maximum recorded longevity before analysing new predictors of lifespan across species in the context of their current, specific hypotheses. At present there is no certainty that all relevant statistical, phenotypic, or ecological biases are accounted for by such corrective measures. Here, we employ Monte Carlo simulation to investigate the effect of differences in recapture numbers, recapture types (the point in life at which individuals are initially captured or recaptured), and actuarial population decay structure of simulated species on their maximum recorded longevities. We show that maximum recorded longevities differ in response to all three of these variables, as well as all of their two‐ and three‐way interactions. We then investigate empirical avian band‐recapture data for evidence of biases caused by recapture number and recapture type, predicted by the Monte Carlo analysis, and confirm the predicted biases as major sources of variance. Finally, we investigate the relationship between recapture type, recapture number, and a selection of ecological and life‐history variables previously documented to correlate with maximum recorded longevity, and find significant correlations between the biasing variables and those published correlates. Our results call into question the validity of using maximum recorded longevity as a proxy for different species' maximum longevities in comparative studies investigating the evolution of lifespan.     

Longevity is associated with relative brain size in birds

Brain size of vertebrates has long been recognized to evolve in close association with basic life‐history traits, including lifespan. According to the cognitive buffer hypothesis, large brains facilitate the construction of behavioral responses against novel socioecological challenges through general cognitive processes, which should reduce mortality and increase lifespan. While the occurrence of brain size–lifespan correlation has been well documented in mammals, much less evidence exists for a robust link between brain size and longevity in birds. The aim of this study was to use phylogenetically controlled comparative approach to test for the relationship between brain size and longevity among 384 avian species from 23 orders. We used maximum lifespan and maximum reproductive lifespan as the measures of longevity and accounted for a set of possible confounding effects, such as allometry, sampling effort, geographic patterns, and life‐history components (clutch size, incubation length, and mode of development). We found that both measures of longevity positively correlated with relative (residual) brain size. We also showed that major diversification of brain size preceded diversification of longevity in avian evolution. In contrast to previous findings, the effect of brain size on longevity was consistent across lineages with different development patterns, although the relatively low strength of this correlation could likely be attributed to the ubiquity of allomaternal care associated with the altricial mode of development. Our study indicates that the positive relationship between brain size and longevity in birds may be more general than previously thought.     

Independent chemical regulation of health and senescent spans in Drosophila

Curcumin feeding of Drosophila larvae or young adults inhibits TOR and other known longevity genes and induces an extended health span in a normal-lived Ra strain adult. Combining larval curcumin feeding with an adult dietary restriction (DR) diet does not yield an additive effect. The age-specific mortality rate is decreased and is comparable with that of genetically selected long-lived La animals. Feeding Ra adults with the drug their whole life, or only during the senescent span, results in a weak negative effect on median longevity with no increase in maximum lifespan. The La strain shows no response to this DR mimetic. Thus, curcumin acts in a life stage-specific manner to extend the health span. Histone deacetylase inhibitors decrease the longevity of Ra animals if administered over the health span only or over the entire adult lifespan, but these inhibitors increase longevity when administered in the transition or senescent spans. Their major effect is a reduction in the mortality rate of older flies, raising the possibility of reducing frailty in older organisms. Their life stage-specific effects are complementary to that of curcumin. Use of stage-specific drugs may enable targeted increases in health or senescent spans, and thus selectively increase the quality of life.     

梵净山自然保护区珙桐天然种群生命表与生存分析

以种群生命表和生存分析理论为基础,采用空间代替时间法和分段匀滑技术,编制梵净山自然保护区珙桐天然种群特定时间生命表,绘制其死亡率曲线、消失率曲线、存活曲线和生存函数曲线,分析种群数量动态变化。结果表明:珙桐种群结构存在波动性,趋于DeeveyⅢ型,其幼年阶段的个体较丰富;珙桐种群死亡率和消失率曲线变化趋势基本一致,在这一发育过程中有两个死亡高峰,一个出现在幼苗向幼树的过渡期(Ⅰ龄级→Ⅱ龄级),另一个出现在从中龄向老龄过渡的阶段(Ⅷ龄级→Ⅸ龄级);种群生存分析表明,珙桐种群的生存率单调下降,累计死亡率单调上升,Ⅷ龄级后,种群生存率小于8%,累计死亡率大于92%,危险率超过生存率;4个生存函数曲线表明,梵净山珙桐有前期锐减、中期稳定和后期衰退的特点。幼苗和中龄级个体的不足是导致珙桐濒危的重要原因。     

Contributions of juvenile and adult diet to the lifetime reproductive success and lifespan of a spider

Food availability can vary widely for animals in nature and can have large effects on growth, reproduction and survival. While the consequences of food limitation for animals have been extensively studied, significant questions still remain including how ontogenetic variation in food availability contributes to lifetime reproductive success. We tested the effects of juvenile and adult food limitation on the lifetime reproductive success and lifespan of bridge spiders, Larinioides sclopetarius. Food availability was manipulated (low or high) over the entire juvenile and adult stage in a full‐factorial design and reproductive output and lifespan were measured. Juvenile and adult food limitation both reduced lifetime egg and hatchling production with effect sizes that were not significantly different from each other. Unlike some other arthropods, where juvenile food limitation reduces fecundity by reducing adult body size, body size was not affected by juvenile diet in bridge spiders. Clutch size was also significantly reduced by both juvenile and adult food limitation. The effect of adult diet on clutch size was stronger than that of juvenile diet. Juvenile and adult food limitation both extended total lifespan, and adult food limitation extended adult longevity (i.e. time from maturation to death). However, juvenile food limitation decreased adult longevity, in contrast to what would be predicted by dietary or caloric restriction. Compensatory feeding and growth are widely recognized mechanisms through which animals can ameliorate some of the negative effects of periods of food limitation. Yet our results combined with studies of a range of other species suggest that there may be lasting consequences of juvenile food limitation on lifetime reproductive success that cannot be compensated for by adult feeding in some species.     

Shuttling between species for pathways of lifespan regulation: A central role for the vitellogenin gene family?

Studies to find genes that affect maximum lifespan aim at identifying important determinants of ageing that may be universal across species. Model organisms show insulin signalling can play an important role in ageing. In view of insulin resistance, such loci can also be important in human ageing and health. The study of long-lived humans and their children points to the relevance of lipoprotein profiles and particle size for longevity. If ageing pathways are conserved, then the genes mediating such pathways may also be conserved. Cross-species sequence comparisons of potential longevity loci may reveal whether the pathways that they represent are central themes in lifespan regulation. Using bioinformatic tools, we performed a sequence comparison of the genes involved in lipid metabolism identified in humans as potential longevity loci. This analysis revealed that lipid storage and transport may be a common theme related to longevity in humans, honeybees and nematodes. Here, the vitellogenin family emerges as a potential key connection between lipid metabolism and the insulin/IGF-1 signalling pathway.     

Mutations in the RAD27 and SGS1 genes differentially affect the chronological and replicative lifespan of yeast cells growing on glucose and glycerol

The Sgs1 protein from Saccharomyces cerevisiae is a member of the RecQ helicases. Defects in RecQ helicases result in premature aging phenotypes in both yeasts and humans, which appear to be promoted by replicative stress. Yeast rad27 mutants also suffer from premature aging. As the human Rad27p and Sgs1p homologs interact, a similar interaction between the yeast proteins could be important for promoting longevity in S. cerevisiae. We tested the contribution of a potential interaction between Rad27p and Sgs1p to longevity by analyzing lifespan and parameters associated with longevity in rad27 and sgs1 mutants. The carbon source supporting growth also modulated longevity as evaluated by replicative and chronological lifespan measurements. Growth on glycerol promoted chronological lifespan, while maximum replicative lifespan was obtained with glucose-supported growth. In comparison to the individual mutants, the sgs1 rad27 double mutant displayed a shortened replicative lifespan and was also more sensitive to DNA-damaging agents. In addition to promoting replicative lifespan, the activity of Rad27p was critical for achieving full chronological lifespan. The rad27 mutants exhibited increased oxidative stress levels along with an elevated spontaneous mutation rate. Removal of Sgs1p activity additionally increased the oxidative stress and spontaneous mutation rate in rad27 mutants without affecting the chronological lifespan.     

A Single Hot Event Stimulates Adult Performance but Reduces Egg Survival in the Oriental Fruit Moth,Grapholitha molesta

Climate warming is expected to increase the exposure of insects to hot events (involving a few hours at extreme high temperatures). These events are unlikely to cause widespread mortality but may modify population dynamics via impacting life history traits such as adult fecundity and egg hatching. These effects and their potential impact on population predictions are still largely unknown. In this study, we simulated a single hot event (maximum of 38°C lasting for 4 h) of a magnitude increasingly found under field conditions and examined its effect in the oriental fruit moth, Grapholitha molesta. This hot event had no impact on the survival of G. molesta adults, copulation periods or male longevity. However, the event increased female lifespan and the length of the oviposition period, leading to a potential increase in lifetime fecundity and suggesting hormesis. In contrast, exposure of males to this event markedly reduced the net reproductive value. Male heat treatment delayed the onset of oviposition in the females they mated with, as well as causing a decrease in the duration of oviposition period and lifetime fecundity. Both male and female stress also reduced egg hatch. Our findings of hormetic effects on female performance but concurrent detrimental effects on egg hatch suggest that hot events have unpredictable consequences on the population dynamics of this pest species with implications for likely effects associated with climate warming.     

Life equations for the senescence process

The Gompertz law of mortality quantitatively describes the mortality rate of humans and almost all multicellular animals. However, its underlying kinetic mechanism is unclear. The Gompertz law cannot explain the mortality plateau at advanced ages and cannot give an explicit relationship between temperature and mortality. In this study a reaction kinetics model with a time dependent rate coefficient is proposed to describe the survival and senescence processes. A temperature-dependent mortality function was derived. The new mortality function becomes the Gompertz mortality function with the same relationship of parameters prescribed by the Strehler–Mildvan correlation when age is smaller than a characteristic value δ, and reaches the mortality plateau when age is greater than δ. A closed-form analytical expression for describing the relationship of average lifespan with temperature and other equations are derived from the new mortality function. The derived equations can be used to estimate the limit of average lifespan, predict the maximal longevity, calculate the temperature coefficient of lifespan, and explain the tendency of the survival curve. This prediction is consistent with the most recently reported mortality trajectories for single-year birth cohorts. This study suggests that the senescence process results from the imbalance between damaging energy and protecting energy for the critical chemical substance in the body. The rate of senescence of the organism increases while the protecting energy decreases. The mortality plateau is reached when the protecting energy decreases to its minimal levels. The decreasing rate of the protecting energy is temperature-dependent. This study is exploring the connection between the biochemical mechanism and demography.     

Carotenoids, oxidative stress and female mating preference for longer lived males

Some of the most spectacular exaggerated sexual ornaments are carotenoid dependent. It has been suggested that such ornaments have evolved because carotenoid pigments are limiting for both signal expression and in their role as antioxidants and immunostimulants. An implicit assumption of this hypothesis is that males which can afford to produce more elaborate carotenoid-dependent displays are signalling their enhanced ability to resist parasites, disease or oxidative stress and hence would be predicted to live longer. Therefore, in species with carotenoid-dependent ornaments where a parent's future longevity is crucial for determining offspring survival, there should be a mating preference for partners that present the lowest risk of mortality during the breeding attempt, as signalled by the ability to allocate carotenoids to sexual displays. In an experimental study using three-spined sticklebacks (Gasterosteus aculeatus), we show that when dietary carotenoid intake is limited, males attempt to maintain their sexual ornament at the expense of body carotenoids and hence suffer from reduced reproductive investment and a shorter lifespan. These males also suffer from an increased susceptibility to oxidative stress, suggesting that this may constitute the mechanism underlying the increased rate of ageing. Furthermore, in pairwise mate-choice trials, females preferred males that had a greater access to carotenoids and chance of surviving the breeding season, suggesting that females can make adaptive mate choice decisions based on a male's carotenoid status and potential future longevity.     

Longevity and skeletal muscle mass: the role of IGF signalling,the sirtuins,dietary restriction and protein intake

Advancing age is associated with a progressive loss of skeletal muscle (SkM) mass and function. Given the worldwide aging demographics, this is a major contributor to morbidity, escalating socio‐economic costs and ultimately mortality. Previously, it has been established that a decrease in regenerative capacity in addition to SkM loss with age coincides with suppression of insulin/insulin‐like growth factor signalling pathways. However, genetic or pharmacological modulations of these highly conserved pathways have been observed to significantly enhance life and healthspan in various species, including mammals. This therefore provides a controversial paradigm in which reduced regenerative capacity of skeletal muscle tissue with age potentially promotes longevity of the organism. This paradox will be assessed and considered in the light of the following: (i) the genetic knockout, overexpression and pharmacological models that induce lifespan extension (e.g. IRS‐1/s6K KO, mTOR inhibition) versus the important role of these signalling pathways in SkM growth and adaptation; (ii) the role of the sirtuins (SIRTs) in longevity versus their emerging role in SkM regeneration and survival under catabolic stress; (iii) the role of dietary restriction and its impact on longevity versus skeletal muscle mass regulation; (iv) the crosstalk between cellular energy metabolism (AMPK/TSC2/SIRT1) and survival (FOXO) versus growth and repair of SkM (e.g. AMPK vs. mTOR); and (v) the impact of protein feeding in combination with dietary restriction will be discussed as a potential intervention to maintain SkM mass while increasing longevity and enabling healthy aging.     

Effects of pollinia removal and insertion on flower longevity inChloraea alpina (Orchidaceae)

Summary Although it is known that stigmatic pollen deposition may trigger early flower senescence, the existence of a similar plastic response of flower lifespan to pollen removal has been much less studied. Here we report on a factorial, manipulative experiment in which all 2 × 2 flower combinations of pollinia removal and stigmatic pollinia insertion were performed in inflorescences of the Patagonian ground orchidChloraea alpina. This experiment was conducted in the laboratory, in a population of cut inflorescences and in the field. We hypothesized that if expected fitness gains, through both the male and female functions, were weighed against the costs of flower maintenance, then early flower senescence should be triggered by either pollinia removal or insertion. The shortest flower lifespan would be expected in flowers where both processes occurred. Results showed that flower longevity was very strongly affected by pollinia insertion, reducing the flower lifespan by approximately 60%. The response of pollinia removal was much weaker. A significant reduction in flower longevity caused by pollinia removal was only detected in unpollinated flowers (i.e. no pollinia inserted). Within the racemose inflorescences, flowers in basal positions lived longer than flowers in terminal ones, which might be evidence of the importance of resource availability in determining maximum flower longevity. The observed responses of flower lifespan plasticity to pollinia manipulation only partially supported our expectations based on fitness benefit—cost relationships. Other factors that might explain these discrepancies are the different fitness gains that may indeed accrue to the processes of pollinia removal and insertion as they occur in nature, donor manipulation of the recipient flower lifespan associated with the evolution of pollen clustering into pollinia and physiological constraints in terms of the extent to which flower longevity may respond to pollen removal.     

Dauer juvenile longevity and stress tolerance in natural populations of entomopathogenic nematodes: is there a relationship?

Qualitative and quantitative genetic analysis of life span in experimental adult animals predicts that resistance to stress and longevity are positively correlated, but such studies on field populations of animals are rare. We tested this hypothesis using dauer juveniles of 15 natural populations of the entomopathogenic nematode, Heterorhabditis bacteriophora, collected from diverse localities. Dauer juvenile longevity at 25 degrees C in autoclaved tap water and tolerance to major environmental stresses including heat (survival at 40 degrees C for 2 h), ultraviolet (UV) radiation (original virulence remaining after exposure to 302 nm UV for 5 min), hypoxia (survival at approximately 0% dissolved O2 at 25 degrees C for 96 h), and desiccation (survival in 25% glycerol at 25 degrees C for 72 h) differed significantly among populations. Intrinsic dauer juvenile longevity, defined as the number of weeks to 90% mortality (LT90) estimated using probit analysis of nematode survival data at 25 degrees C varied between 6 and 16 weeks among populations. Longevity was most strongly correlated with heat followed by UV and hypoxia tolerance, respectively, but showed no correlation with desiccation tolerance. The strong positive correlation of longevity with heat tolerance was further confirmed through principal components analysis which showed almost identical variance for heat and longevity. Among the stress factors, only UV tolerance was positively correlated with heat and hypoxia tolerance. Differences in longevity and stress tolerance in nematode populations isolated from a single 200 m2 grassland locality further support another hypothesis that population structure of heterorhabditid nematodes is highly fragmented, thus suggesting the existence of metapopulation dynamics.