RESUMEN

Empirical studies of aging in primates show that local selective forces rather than phylogenetic history determine the exceptional nature of human longevity (Bronikowski et al., Science 331:1325-1328, 2011). This article proposes an evolutionary rationale for this pattern of primate mortality by invoking the parameter, Life-Table Entropy, a measure of the uncertainty in the life span of a randomly chosen newborn. Life-table entropy is positively correlated with maximal life span, that is, the mean life span of a species living under favourable conditions.The logic which underlies the exceptional nature of human longevity derives from the terrestrial life-history of humans - a singularity within the primate lineage; and the concomitant ecological constraints-the hunter-gatherer, agricultural, and industrial modes of subsistence, that have defined human evolutionary history. The effect of these ecological constraints on the evolution of life span is encoded in the Entropic Principle of Longevity: life-table entropy increases in equilibrium species, populations evolving in environments with stable, renewable resources; and decreases in opportunistic species, populations subject to fluctuating resource endowments.The Entropic Principle of Longevity is a derivative of Directionality Theory, an analytic study of the evolutionary process of variation and selection based on Evolutionary Entropy, a statistical measure of the uncertainty in the age of the mother of a randomly chosen newborn. Evolutionary entropy is the organizing concept of The Entropic Principle of Evolution: Evolutionary Entropy increases in equilibrium species and decreases in opportunistic species.

RESUMEN

Retirement is a critical life event for older people. Health scholars have scrutinized the health effects of retirement, but its consequences on age-related diseases and mortality are unclear. We extend this body of research by integrating measurements of biological age, representing the physiological decline preceding disease onset. Using data from the UK Biobank and a fuzzy regression discontinuity design, we estimated the effects of retirement on two biomarker-based biological age measures. Results showed that retirement significantly increases biological age for those induced to retire by the State Pension eligibility by 0.871-2.503 years, depending on sex and specific biological age measurement. Given the emerging scientific discussion about direct interventions to biological age to achieve additional improvements in population health, the positive effect of retirement on biological age has important implications for an increase in the State Pension eligibility age and its potential consequences on population health, public health care policy, and older people's labor force participation. Overall, this study provides novel empirical evidence contributing to the question of what social factors make people old.

Asunto(s)

RESUMEN

Causal life course research examining consequences of early-life exposures has largely relied on associations between early-life environments and later-life outcomes using exogenous environmental shocks. Nonetheless, even with (quasi-)randomized early-life exposures, these associations may reflect not only causation ("scarring") but also selection (i.e., which members are included in data assessing later life). Investigating this selection and its impacts on estimated effects of early-life conditions has, however, often been ignored because of a lack of pre-exposure data. This study proposes an approach for assessing and correcting selection, separately from scarring, using genetic measurements. Because genetic measurements are determined at the time of conception, any associations with early-life exposures should be interpreted as selection. Using data from the UK Biobank, we find that in utero exposure to a higher area-level infant mortality rate is associated with genetic predispositions correlated with better educational attainment and health. These findings point to the direction and magnitude of selection from this exposure. Corrections for this selection in examinations of effects of exposure on later educational attainment suggest underestimates of 26-74%; effects on other life course outcomes also vary across selection correction methods.

Asunto(s)

RESUMEN

This research note reinvestigates Abdellaoui et al.'s (2019) findings that genetically selective migration may lead to persistent and accumulating socioeconomic and health inequalities between types (coal mining or non-coal mining) of places in the United Kingdom. Their migration measure classified migrants who moved to the same type of place (coal mining to coal mining or non-coal mining to non-coal mining) into "stay" categories, preventing them from distinguishing migrants from nonmigrants. We reinvestigate the question of genetically selective migration by examining migration patterns between places rather than place types and find genetic selectivity in whether people migrate and where. For example, we find evidence of positive selection: people with genetic variants correlated with better education moved from non-coal mining to coal mining places with our measure of migration. Such findings were obscured in earlier work that could not distinguish nonmigrants from migrants.

Asunto(s)

RESUMEN

Migration is selective, resulting in inequalities between migrants and nonmigrants. However, investigating migration selection is empirically challenging because combined pre- and post-migration data are rarely available. We propose an alternative approach to assessing internal migration selection by integrating genetic data, enabling an investigation of migration selection with cross-sectional data collected post-migration. Using data from the UK Biobank, we utilized standard tools from statistical genetics to conduct a genome-wide association study (GWAS) for migration distance. We then calculated genetic correlations to compare GWAS results for migration with those for other characteristics. Given that individual genetics are determined at conception, these analyses allow a unique exploration of the association between pre-migration characteristics and migration. Results are generally consistent with the healthy migrant literature: genetics correlated with longer migration distance are associated with higher socioeconomic status and better health. We also extended the analysis to 53 traits and found novel correlations between migration and several physical health, mental health, personality, and sociodemographic traits.

Asunto(s)

RESUMEN

Several social dimensions including social integration, status, early-life adversity, and their interactions across the life course can predict health, reproduction, and mortality in humans. Accordingly, the social environment plays a fundamental role in the emergence of phenotypes driving the evolution of aging. Recent work placing human social gradients on a biological continuum with other species provides a useful evolutionary context for aging questions, but there is still a need for a unified evolutionary framework linking health and aging within social contexts. Here, we summarize current challenges to understand the role of the social environment in human life courses. Next, we review recent advances in comparative biodemography and propose a biodemographic perspective to address socially driven health phenotype distributions and their evolutionary consequences using a nonhuman primate population. This new comparative approach uses evolutionary demography to address the joint dynamics of populations, social dimensions, phenotypes, and life history parameters. The long-term goal is to advance our understanding of the link between individual social environments, population-level outcomes, and the evolution of aging.

Asunto(s)

RESUMEN

Synthesizing prior gene-by-cohort (G×C) interaction studies, we theorize that changes in genetic effects by social conditions depend on the level of resource constraints, the distribution and use of resources, structural constraints, and constraints on individual choice. Motivated by the theory, we explored several sex-specific G×C trends across a set of outcomes using 30 birth cohorts of UK Biobank data (N = 400,000). We find that genetic coefficients on years of schooling and secondary educational attainment substantially decrease, but genetic coefficients on college attainments only moderately increase. On the other hand, genetic coefficients for education ranks are stable. Genetic coefficients on reproductive behavior increase for younger cohorts. Additional genetic-correlation-by-cohort analysis shows shifting genetic correlations between education and reproductive behavior. Our results suggest that the G×C patterns are highly heterogenous and that social and genetic factors jointly shape the diversity of human phenotypes.

RESUMEN

Diverse manifestations of biological aging often reflect disparities in socioeconomic status (SES). In this paper, we examine associations between indicators of SES and an mRNA-based aging signature during young adulthood, before clinical indications of aging are common. We use data from wave V (2016-2018) of the National Longitudinal Study of Adolescent to Adult Health, a nationally representative study of adults aged 33-43 years, with transcriptomic data from a subset of 2,491 participants. Biological aging is measured using 1) a composite transcriptomic aging signature previously identified by Peters et al.'s out-of-sample meta-analysis (Nat Commun. 2015;6:8570) and 2) 9 subsets that represent functional pathways of coexpressed genes. SES refers to income, education, occupation, subjective social status, and a composite measure combining these 4 dimensions. We examine hypothesized mechanisms through which SES could affect aging: body mass index, smoking, health insurance status, difficulty paying bills, and psychosocial stress. We find that SES-especially the composite measure and income-is associated with transcriptomic aging and immune, mitochondrial, ribosomal, lysosomal, and proteomal pathways. Counterfactual mediational models suggest that the mediators partially account for these associations. The results thus reveal that numerous biological pathways associated with aging are already linked to SES in young adulthood.

Asunto(s)

RESUMEN

Many common chronic diseases of aging are negatively associated with socioeconomic status (SES). This study examines whether inequalities can already be observed in the molecular underpinnings of such diseases in the 30s, before many of them become prevalent. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a large, nationally representative sample of US subjects who were followed for over two decades beginning in adolescence. We now have transcriptomic data (mRNA-seq) from a random subset of 4,543 of these young adults. SES in the household-of-origin and in young adulthood were examined as covariates of a priori-defined mRNA-based disease signatures and of specific gene transcripts identified de novo. An SES composite from young adulthood predicted many disease signatures, as did income and subjective status. Analyses highlighted SES-based inequalities in immune, inflammatory, ribosomal, and metabolic pathways, several of which play central roles in senescence. Many genes are also involved in transcription, translation, and diverse signaling mechanisms. Average causal-mediated effect models suggest that body mass index plays a key role in accounting for these relationships. Overall, the results reveal inequalities in molecular risk factors for chronic diseases often decades before diagnoses and suggest future directions for social signal transduction models that trace how social circumstances regulate the human genome.

Asunto(s)

RESUMEN

Despite decades of progress, the future of life expectancy in the United States is uncertain due to widening socioeconomic disparities in mortality, continued disparities in mortality across racial/ethnic groups, and an increase in extrinsic causes of death. These trends prompt us to scrutinize life expectancy in a high-income but enormously unequal society like the United States, where social factors determine who is most able to maximize their biological lifespan. After reviewing evidence for biodemographic perspectives on life expectancy, the uneven diffusion of health-enhancing innovations throughout the population, and the changing nature of threats to population health, we argue that sociology is optimally positioned to lead discourse on the future of life expectancy. Given recent trends, sociologists should emphasize the importance of the social determinants of life expectancy, redirecting research focus away from extending extreme longevity and towards research on social inequality with the goal of improving population health for all.

RESUMEN

Sequence analysis is an established method used to study the complexity of family life courses. Although individual and societal characteristics have been linked with the complexity of family trajectories, social scientists have neglected the potential role of genetic factors in explaining variation in family transitions and events across the life course. We estimate the genetic contribution to sequence complexity and a wide range of family demographic behaviors using genomic relatedness-based, restricted maximum likelihood models with data from the U.S. Health and Retirement Study. This innovative methodological approach allows us to provide the first estimates of the heritability of composite life course outcomes-that is, sequence complexity. We demonstrate that a number of family demographic indicators (e.g., the age at first birth and first marriage) are heritable and provide evidence that composite metrics can be influenced by genetic factors. For example, our results show that 11% of the total variation in the complexity of differentiated family sequences is attributable to genetic influences. Moreover, we test whether this genetic contribution varies by social environment as indexed by birth cohort over a period of rapid changes in family norms during the twentieth century. Interestingly, we find evidence that the complexity of fertility and differentiated family trajectories decreased across cohorts, but we find no evidence that the heritability of the complexity of partnership trajectories changed across cohorts. Therefore, our results do not substantiate claims that lower normative constraints on family demographic behavior increase the role of genes.

Asunto(s)

RESUMEN

Bacteria have been thought to flee senescence by dividing into two identical daughter cells, but this notion of immortality has changed over the last two decades. Asymmetry between the resulting daughter cells after binary fission is revealed in physiological function, cell growth, and survival probabilities and is expected from theoretical understanding. Since the discovery of senescence in morphologically identical but physiologically asymmetric dividing bacteria, the mechanisms of bacteria aging have been explored across levels of biological organization. Quantitative investigations are heavily biased toward Escherichia coli and on the role of inclusion bodies-clusters of misfolded proteins. Despite intensive efforts to date, it is not evident if and how inclusion bodies, a phenotype linked to the loss of proteostasis and one of the consequences of a chain of reactions triggered by reactive oxygen species, contribute to senescence in bacteria. Recent findings in bacteria question that inclusion bodies are only deleterious, illustrated by fitness advantages of cells holding inclusion bodies under varying environmental conditions. The contributions of other hallmarks of aging, identified for metazoans, remain elusive. For instance, genomic instability appears to be age independent, epigenetic alterations might be little age specific, and other hallmarks do not play a major role in bacteria systems. What is surprising is that, on the one hand, classical senescence patterns, such as an early exponential increase in mortality followed by late age mortality plateaus, are found, but, on the other hand, identifying mechanisms that link to these patterns is challenging. Senescence patterns are sensitive to environmental conditions and to genetic background, even within species, which suggests diverse evolutionary selective forces on senescence that go beyond generalized expectations of classical evolutionary theories of aging. Given the molecular tool kits available in bacteria, the high control of experimental conditions, the high-throughput data collection using microfluidic systems, and the ease of life cell imaging of fluorescently marked transcription, translation, and proteomic dynamics, in combination with the simple demographics of growth, division, and mortality of bacteria, make the challenges surprising. The diversity of mechanisms and patterns revealed and their environmental dependencies not only present challenges but also open exciting opportunities for the discovery and deeper understanding of aging and its mechanisms, maybe beyond bacteria and aging.

RESUMEN

The specific objective of this study was to use a logistic regression model for determining the degree to which egg laying patterns of individual females at the end of life (i.e., terminal segments) in each of three different fruit fly species could be distinguished from the egg-laying patterns over a similar period in midlife (i.e., non-terminal segments). Extracting data from large-scale databases for 11-day terminal and 11-day non-terminal segments in the vinegar fly (Drosophila melanogaster), the Mexican fruit fly (Anastrepha ludens) and the Mediterranean fruit fly (Ceratitis capitata) and organizing the model's results in a 2 × 2 contingency table, we found that: (1) daily egg-laying patterns in fruit flies can be used to distinguish terminal from non-terminal periods; (2) the overall performance metrics such as precision, accuracy, false positives and true negatives depended heavily on species; (3) differentiating between terminal and non-terminal segments is more difficult when flies die at younger ages; and (4) among the three species the best performing metrics including accuracy and precision were those produced using data on D. melanogaster. We conclude that, although the reliability of the prediction of whether a segment occurred at the end of life is relatively high for most species, it does not follow precisely predicting remaining life will also be highly reliable since classifying an end of life period is a fundamentally different challenge than is predicting an exact day of death.

Asunto(s)

RESUMEN

Health in later life varies significantly by individual demographic characteristics such as age, sex, and race/ethnicity, as well as by social factors including socioeconomic status and geographic region. This study examined whether sociodemographic variations in the immune and inflammatory molecular underpinnings of chronic disease might emerge decades earlier in young adulthood. Using data from 1,069 young adults from the National Longitudinal Study of Adolescent to Adult Health (Add Health)-the largest nationally representative and ethnically diverse sample with peripheral blood transcriptome profiles-we analyzed variation in the expression of genes involved in inflammation and type I interferon (IFN) response as a function of individual demographic factors, sociodemographic conditions, and biobehavioral factors (smoking, drinking, and body mass index). Differential gene expression was most pronounced by sex, race/ethnicity, and body mass index (BMI), but transcriptome correlates were identified for every demographic dimension analyzed. Inflammation-related gene expression showed the most pronounced variation as a function of biobehavioral factors (BMI and smoking) whereas type I IFN-related transcripts varied most strongly as a function of individual demographic characteristics (sex and race/ethnicity). Bioinformatic analyses of transcription factor and immune-cell activation based on transcriptome-wide empirical differences identified additional effects of family poverty and geographic region. These results identify pervasive sociodemographic differences in immune-cell gene regulation that emerge by young adulthood and may help explain social disparities in the development of chronic illness and premature mortality at older ages.

Asunto(s)

RESUMEN

Individuals differ in their life courses, but how this diversity is generated, how it has evolved and how it is maintained is less understood. However, this understanding is crucial to comprehend evolutionary and ecological population dynamics. In structured populations, individual life courses represent sequences of stages that end in death. These life course trajectories or sequences can be described by a Markov chain and individuals diversify over the course of their lives by transitioning through diverse discrete stages. The rate at which stage sequences diversify with age can be quantified by the population entropy of a Markov chain. Here, we derive sensitivities of the population entropy of a Markov chain to identify which stage transitions generate - or contribute - most to diversification in stage sequences, i.e. life courses. We then use these sensitivities to reveal potential selective forces on the dynamics of life courses. To do so we correlated the sensitivity of each matrix element (stage transition) with respect to the population entropy, to its sensitivity with respect to fitness λ, the population growth rate. Positive correlation between the two sensitivities would suggest that the stage transitions that selection has acted most strongly on (high sensitivities with respect to λ) are also those that contributed most to the diversification of life courses. Using an illustrative example on a seabird population, the Thick-billed Murres on Coats Island, that is structured by reproductive stages, we show that the most influential stage transitions for diversification of life courses are not correlated with the most influential transitions for population growth. Our finding suggests that observed diversification in life courses is neutral rather than adaptive, note this does not imply that the life histories themselves are not adaptive. We are at an early stage of understanding how individual level dynamics shape ecological and evolutionary dynamics, and many discoveries await.

Asunto(s)

RESUMEN

Jellyfish blooms are conspicuous demographic events with significant ecological and socio-economic impact. Despite worldwide concern about an increased frequency and intensity of such mass occurrences, predicting their booms and busts remains challenging. Forecasting how jellyfish populations may respond to environmental change requires considering their complex life histories. Metagenic life cycles, which include a benthic polyp stage, can boost jellyfish mass occurrences via asexual recruitment of pelagic medusae. Here we present stage-structured matrix population models with monthly, individual-based demographic rates of all life stages of the moon jellyfish Aurelia aurita L. (sensu stricto). We investigate the life-stage dynamics of these complex populations under low and high food conditions to illustrate how changes in medusa density depend on non-medusa stage dynamics. We show that increased food availability can be an important ecological driver of jellyfish mass occurrences, as it can temporarily shift the population structure from polyp- to medusa-dominated. Projecting populations for a winter warming scenario additionally enhanced the booms and busts of jellyfish blooms. We identify demographic key variables that control the intensity and frequency of jellyfish blooms in response to environmental drivers such as habitat eutrophication and climate change. By contributing to an improved understanding of mass occurrence phenomena, our findings provide perspective for future management of ecosystem health.

Asunto(s)

RESUMEN

Until recently human longevity records continued to grow in history, with no indication of approaching a hypothetical longevity limit. Also, earlier studies found that age-specific death rates cease to increase at advanced ages (mortality plateau) suggesting the absence of fixed limit to longevity too. In this study, we reexamine both claims with more recent and reliable data on supercentenarians (persons aged 110 years and older). We found that despite a dramatic historical increase in the number of supercentenarians, further growth of human longevity records in subsequent birth cohorts slowed down significantly and almost stopped for those born after 1879. We also found an exponential acceleration of age-specific death rates for persons older than 113 years in more recent data. Slowing down the historical progress in maximum reported age at death and accelerated growth of age-specific death rates after age 113 years in recent birth cohorts may indicate the need for more conservative estimates for future longevity records unless a scientific breakthrough in delaying aging would happen. The hypothesis of approaching a biological limit to human longevity has received some empirical support and it deserves further study and testing.

Asunto(s)

RESUMEN

How do early-life conditions affect adult mortality? Research has yielded mixed evidence about the influence of infant and child mortality in birth cohorts on adult health and mortality. Studies rarely consider the specific role of mortality within the family. We estimated how individuals' exposure to mortality as a child is related to their adult mortality risk between ages 18 and 85 in two historical populations, Utah (USA) 1874-2015 and Zeeland (The Netherlands) 1812-1957. We examined these associations for early community-level exposure to infant and early (before sixth birthday) and late (before eighteenth birthday) childhood mortality as well as exposure during these ages to sibling deaths. We find that that exposure in childhood to community mortality and sibling deaths increases adult mortality rates. Effects of sibling mortality on adult all-cause mortality risk were stronger in Utah, where sibling deaths were less common in relation to Zeeland. Exposure to sibling death due to infection was related to the surviving siblings' risk of adult mortality due to cardiovascular disease (relative risk: 1.06) and metabolic disease (relative risk: 1.42), primarily diabetes mellitus, a result consistent with an inflammatory immune response mechanism. We conclude that early-life conditions and exposure to mortality in early life, especially within families of origin, contribute to adult mortality.

RESUMEN

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.

Asunto(s)

RESUMEN

Biodiversity loss is a major challenge. Over the past century, the average rate of vertebrate extinction has been about 100-fold higher than the estimated background rate and population declines continue to increase globally. Birth and death rates determine the pace of population increase or decline, thus driving the expansion or extinction of a species. Design of species conservation policies hence depends on demographic data (e.g., for extinction risk assessments or estimation of harvesting quotas). However, an overview of the accessible data, even for better known taxa, is lacking. Here, we present the Demographic Species Knowledge Index, which classifies the available information for 32,144 (97%) of extant described mammals, birds, reptiles, and amphibians. We show that only 1.3% of the tetrapod species have comprehensive information on birth and death rates. We found no demographic measures, not even crude ones such as maximum life span or typical litter/clutch size, for 65% of threatened tetrapods. More field studies are needed; however, some progress can be made by digitalizing existing knowledge, by imputing data from related species with similar life histories, and by using information from captive populations. We show that data from zoos and aquariums in the Species360 network can significantly improve knowledge for an almost eightfold gain. Assessing the landscape of limited demographic knowledge is essential to prioritize ways to fill data gaps. Such information is urgently needed to implement management strategies to conserve at-risk taxa and to discover new unifying concepts and evolutionary relationships across thousands of tetrapod species.

Asunto(s)