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Meta-analysis is used to test a variant of a Developmental Origins of Adult Health and Disease (DOHaD)'s conjecture known as predictive adaptive response (PAR). According to it, individuals who are exposed to mismatches between adverse or constrained in utero conditions, on the one hand, and postnatal obesogenic environments, on the other, are at higher risk of developing adult chronic conditions, including obesity, type 2 diabetes (T2D), hypertension and cardiovascular disease. We argue that migrant populations from low and middle to high-income countries offer a unique opportunity to test the conjecture. A database was constructed from an exhaustive literature search of peer-reviewed papers published prior to May 2021 contained in PUBMED and SCOPUS using keywords related to migrants, DOHaD, and associated health outcomes. Random effects meta-regression models were estimated to assess the magnitude of effects associated with migrant groups on the prevalence rate of T2D and hypertension in adults and overweight/obesity in adults and children. Overall, we used 38 distinct studies and 78 estimates of diabetes, 59 estimates of hypertension, 102 estimates of overweight/obesity in adults, and 23 estimates of overweight/obesity in children. Our results show that adult migrants experience higher prevalence of T2D than populations at destination (PR 1.48; 95% CI 1.35–1.65) and origin (PR 1.80; 95% CI 1.40–2.34). Similarly, there is a significant excess of obesity prevalence in children migrants (PR 1.22; 95% CI 1.04–1.43) but not among adult migrants (PR 0.89; 95% CI 0.80–1.01). Although the total effect of migrant status on prevalence of hypertension is centered on zero, some migrant groups show increased risks. Finally, the size of estimated effects varies significantly by migrant groups according to place of destination. Despite limitations inherent to all meta-analyses and admitting that some of our findings may be accounted for alternative explanations, the present study shows empirical evidence consistent with selected PAR-like conjectures. [ABSTRACT FROM AUTHOR]

The conditions animals experience during the early developmental stages of their lives can have critical ongoing effects on their future health, welfare, and proper development. In this paper we draw on evolutionary theory to improve our understanding of the processes of developmental programming, particularly Predictive Adaptive Responses (PAR) that serve to match offspring phenotype with predicted future environmental conditions. When these predictions fail, a mismatch occurs between offspring phenotype and the environment, which can have long-lasting health and welfare effects. Examples include metabolic diseases resulting from maternal nutrition and behavioral changes from maternal stress. An understanding of these processes and their evolutionary origins will help in identifying and providing appropriate developmental conditions to optimize offspring welfare. This serves as an example of the benefits of using evolutionary thinking within veterinary science and we suggest that in the same way that evolutionary medicine has helped our understanding of human health, the implementation of evolutionary veterinary science (EvoVetSci) could be a useful way forward for research in animal health and welfare. [ABSTRACT FROM AUTHOR]

In this article, we examine the relations between extreme environmental harshness during childhood and personal fertility ideals in African students. The study is informed by biological models of predictive adaptive responses (PAR) for individual reproductive schedules in the context of life history theory (LHT). Following theoretical models of external and internal environmental cues, we tested whether war and starvation during childhood differentially predict African students' personal fertility ideals in terms of their desired number of children and their desired age of first parenthood. The data were collected in eight different countries from sub-Saharan Africa with an overall sample size of N  = 392. Standardized effect estimates were obtained using a Bayesian approach. The results suggest that war and starvation are predictive of the desired number of children, but not of the desired age of first parenthood. Moreover, the effect estimates varied considerably between females and males, indicating possible interactions between the two independent variables depending on the students' sex. Furthermore, we found a small negative correlation between the desired number of children and the desired age of first parenthood, providing only weak support for a clustering of the two variables on a slow-fast continuum. The results are discussed in light of current models of individual life histories in humans., Competing Interests: Declaration of Conflicting InterestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Evolutionary-minded developmentalists studying predictive-adaptive-response processes linking childhood adversity with accelerated female reproductive development and health scientists investigating the developmental origins of health and disease (DOoHaD) may be tapping the same process, whereby longer-term health costs are traded off for increased probability of reproducing before dying via a process of accelerated reproductive maturation. Using data from 73 females, we test the following propositions using path analysis: (a) greater exposure to prenatal stress predicts greater maternal depression and negative parenting in infancy, (b) which predicts elevated basal cortisol at 4.5 years, (c) which predicts accelerated adrenarcheal development, (d) which predicts more physical and mental health problems at age 18. Results prove generally consistent with these propositions, including a direct link from cortisol to mental health problems. DOoHaD investigators should consider including early sexual maturation as a core component linking early adversity and stress physiology with poor health later in life in females.

Besides immediate effects, early nutritional conditions also have an impact on the entire life history of individuals. We tracked a cohort of captive fire salamanders that experienced only during their early larval phase, either rich or poor nutritional conditions, and thereafter intermediate standard conditions for almost 10 years. We measured on a regular basis, their morphometric variables, noted behavioural and colouration developments, and monitored their survival. While deficits in body mass and colouration from initially poorly raised individuals vanished in adults, differences in size in comparison to initially richly raised larvae remained throughout life. Behaviour at adulthood did not differ any further from that during early conditions, nevertheless it tended to be consistent in certain exploratory traits over several years. After almost ten years, the overall survival rate was about 50%, but so far, no effect of early living conditions on subsequent survival became apparent. Taken together, our long-term study on the effects of early nutritional conditions on fire salamanders revealed interesting insights into the life trajectory of these animals. Immediate effects from early nutritional conditions were found in almost all aspects of behaviour and physiology. The majority of effects are compensated within the lifetimes of individuals, apparently without detectable costs. [ABSTRACT FROM AUTHOR]

Rickard and associates (2014, this issue) challenge the theoretical claim that early developmental experiences influence sexual development and behavior as a result of the continuity of early- and later-life environments over the course of human history (Belsky, Steinberg, & Draper, 1991). Instead, they contend that sexual development, health, and longevity are regulated by internal (bodily) state reflective of morbidity and mortality risk. By highlighting the importance of internal state-and thereby underscoring the value of focusing on it and on the external environment early in life-these theoreticians continue the tradition of extending a line of human evolutionary-developmental ("evo-devo") theorizing in important ways. In fact, what they make clear is that what was originally conceived as an evolutionary theory of socialization by Belsky et al. (1991) can and should develop into an evolutionary-developmental life-course theory of reproductive strategy, health, and longevity.

External predictive adaptive response (PAR) models assume that developmental exposures to stress carry predictive information about the future state of the environment, and that development of a faster life history (LH) strategy in this context functions to match the individual to this expected harsh state. More recently internal PAR models have proposed that early somatic condition (i.e., physical health) critically regulates development of LH strategies to match expected future somatic condition. Here we test the integrative hypothesis that poor physical health mediates the relation between early adversity and faster LH strategies. Data were drawn from a longitudinal study (birth to age 16; N = 1,388) of mostly African American participants with prenatal substance exposure. Results demonstrated that both external environmental conditions early in life (prenatal substance exposure, socioeconomic adversity, caregiver distress/depression, and adverse family functioning) and internal somatic condition during preadolescence (birthweight/gestational age, physical illness) uniquely predicted the development of faster LH strategies in adolescence (as indicated by more risky sexual and aggressive behavior). Consistent with the integrative hypothesis, the effect of caregiver distress/depression on LH strategy was mostly mediated by worse physical health. Discussion highlights the implications of these findings for theory and research on stress, development, and health. [ABSTRACT FROM AUTHOR]

The developmental origins of disease or fetal programming model predict that early exposures to threat or adverse conditions have lifelong consequences that result in harmful outcomes for health. The maternal endocrine 'fight or flight' system is a source of programming information for the human fetus to detect threats and adjust their developmental trajectory for survival. Fetal exposures to intrauterine conditions including elevated stress hormones increase the risk for a spectrum of health outcomes depending on the timing of exposure, the timetable of organogenesis and the developmental milestones assessed. Recent prospective studies, reviewed here, have documented the neurodevelopmental consequences of fetal exposures to the trajectory of stress hormones over the course of gestation. These studies have shown that fetal exposures to biological markers of adversity have significant and largely negative consequences for fetal, infant and child emotional and cognitive regulation and reduced volume in specific brain structures.

Fetal detection of adversity is a conserved trait that allows many species to adapt their early developmental trajectories to ensure survival. According to the fetal-programming model, exposure to stressful or hostile conditions in utero is associated with compromised development and a lifelong risk of adverse health outcomes. In a longitudinal study, we examined the consequences of prenatal and postnatal exposure to adversity for infant development. We found increased motor and mental development during the 1st year of life among infants whose mothers experienced congruent levels of depressive symptoms during and after pregnancy, even when the levels of symptoms were relatively high and the prenatal and postnatal environments were unfavorable. Congruence between prenatal and postnatal environments prepares the fetus for postnatal life and confers an adaptive advantage for critical survival functions during early development.

Across mammals, cues of developmental support, such as touching, licking or attentiveness, stimulate neural development, behavioural exploration and even overall body growth. Why should such fitness-related traits be so sensitive to developmental conditions? Here, we review what we term the ‘developmental support hypothesis’, a potential adaptive explanation of this plasticity. Neural development can be a costly process, in terms of time, energy and exposure. However, environmental variability may sometimes compromise parental care during this costly developmental period. We propose this environmental variation has led to the evolution of adaptive plasticity of neural and behavioural development in response to cues of developmental support, where neural development is stimulated in conditions that support associated costs. When parental care is compromised, offspring grow less and adopt a more resilient and stress-responsive strategy, improving their chances of survival in difficult conditions, similar to existing ideas on the adaptive value of early-life programming of stress. The developmental support hypothesis suggests new research directions, such as testing the adaptive value of reduced neural growth and metabolism in stressful conditions, and expanding the range of potential cues animals may attend to as indicators of developmental support. Considering evolutionary and ecologically appropriate cues of social support also has implications for promoting healthy neural development in humans. This article is part of the theme issue ‘Life history and learning: how childhood, caregiving and old age shape cognition and culture in humans and other animals’. [ABSTRACT FROM AUTHOR]

The early life environment can have profound, long‐lasting effects on an individual's fitness. For example, early life quality might (a) positively associate with fitness (a silver spoon effect), (b) stimulate a predictive adaptive response (by adjusting the phenotype to the quality of the environment to maximize fitness) or (c) be obscured by subsequent plasticity. Potentially, the effects of the early life environment can persist beyond one generation, though the intergenerational plasticity on fitness traits of a subsequent generation is unclear.To study both intra‐ and intergenerational effects of the early life environment, we exposed a first generation of bank voles to two early life stimuli (variation in food and social environment) in a controlled environment. To assess possible intra‐generational effects, the reproductive success of female individuals was investigated by placing them in large outdoor enclosures in two different, ecologically relevant environments (population densities).Resulting offspring were raised in the same population densities where they were conceived and their growth was recorded. When adult, half of the offspring were transferred to opposite population densities to evaluate their winter survival, a crucial fitness trait for bank voles.Our setup allowed us to assess: (a) do early life population density cues elicit an intra‐generational adaptive response, that is a higher reproductive success when the density matches the early life cues and (b) can early life stimuli of one generation elicit an intergenerational adaptive response in their offspring, that is a higher growth and winter survival when the density matches the early life cues of their mother.Our results show that the early life environment directly affects the phenotype and reproductive success of the focal generation, but adaptive responses are only evident in the offspring. Growth of the offspring is maintained only when the environment matches their mother's early life environment. Furthermore, winter survival of offspring also tended to be higher in high population densities if their mothers experienced an competitive early life. These results show that the early life environment can contribute to maintain high fitness in challenging environments, but not necessarily in the generation experiencing the early life cues. [ABSTRACT FROM AUTHOR]

Telomere length (TL) declines with age in most human tissues, and shorter TL appears to accelerate senescence. By contrast, men’s sperm TL is positively correlated with age. Correspondingly, in humans, older paternal age at conception (PAC) predicts longer offspring TL. We have hypothesized that this PAC effect could persist across multiple generations, and thereby contribute to a transgenerational genetic plasticity that increases expenditures on somatic maintenance as the average age at reproduction is delayed within a lineage. Here, we examine TL data from 3282 humans together with PAC data across four generations. In this sample, the PAC effect is detectable in children and grandchildren. The PAC effect is transmitted through the matriline and patriline with similar strength and is characterized by a generational decay. PACs of more distant male ancestors were not significant predictors, although statistical power was limited in these analyses. Sensitivity analyses suggest that the PAC effect is linear, not moderated by offspring age, or maternal age, and is robust to controls for income, urbanicity and ancestry. These findings show that TL reflects the age at the reproduction of recent male matrilineal and patrilineal ancestors, with an effect that decays across generations. [ABSTRACT FROM AUTHOR]

Environmental conditions during early development, from conception to sexual maturity, can have lasting consequences on fitness components. Although adult life span often accounts for much of the variation in fitness in long‐lived animals, we know little about how early environment affects adult life span in the wild, and even less about whether these effects differ between the sexes.Using data collected over 45 years from wild bighorn sheep (Ovis canadensis), we investigated the effects of early environment on adult mortality in both sexes, distinguishing between natural and anthropogenic sources of mortality.We used the average body mass of yearlings (at about 15 months of age) as a yearly index of environmental quality. We first examined sex differences in natural mortality responses to early environment by censoring harvested males in the year they were shot. We then investigated sex differences in the effects of early environment on overall mortality (natural and hunting mortality combined). Finally, we used path analysis to separate the direct influence of early environment from indirect influences, mediated by age at first reproduction, adult mass and horn length.As early environmental conditions improved, natural adult mortality decreased in both sexes, although for males the effect was not statistically supported. Sex differences in the effects of early environment on adult mortality were detected only when natural and hunting mortality were pooled. Males that experienced favourable early environment had longer horns as adults and died earlier because of trophy hunting, which does not mimic natural mortality. Females that experienced favourable early environment started to reproduce earlier and early primiparity was associated with reduced mortality, suggesting a silver‐spoon effect.Our results show that early conditions affect males and females differently because of trophy hunting. These findings highlight the importance of considering natural and anthropogenic environmental factors across different life stages to understand sex differences in mortality. [ABSTRACT FROM AUTHOR]

Variation in early-life conditions can trigger developmental switches that lead to predictable individual differences in adult behaviour and physiology. Despite evidence for such early-life effects being widespread both in humans and throughout the animal kingdom, the evolutionary causes and consequences of this developmental plasticity remain unclear. The current issue aims to bring together studies of early-life effects from the fields of both evolutionary ecology and biomedicine to synthesise and advance current knowledge of how information is used during development, the mechanisms involved, and how early-life effects evolved. We hope this will stimulate further research into early-life effects, improving our understanding of why individuals differ and how this might influence their susceptibility to disease. [ABSTRACT FROM AUTHOR]

Numerous studies have shown that social adversity in early life can have long-lasting consequences for social behaviour in adulthood, consequences that may in turn be propagated to future generations. Given these intergenerational effects, it is puzzling why natural selection might favour such sensitivity to an individual's early social environment. To address this question, we model the evolution of social sensitivity in the development of helping behaviours, showing that natural selection indeed favours individuals whose tendency to help others is dependent on early-life social experience. In organisms with non-overlapping generations, we find that natural selection can favour positive social feedbacks, in which individuals who received more help in early life are also more likely to help others in adulthood, while individuals who received no early-life help develop low tendencies to help others later in life. This positive social sensitivity is favoured because of an intergenerational relatedness feedback: patches with many helpers tend to be more productive, leading to higher relatedness within the local group, which in turn favours higher levels of help in the next generation. In organisms with overlapping generations, this positive feedback is less likely to occur, and those who received more help may instead be less likely to help others (negative social feedback). We conclude that early-life social influences can lead to strong between-individual differences in helping behaviour, which can take different forms dependent on the life history in question. [ABSTRACT FROM AUTHOR]

A discrepancy between the phenotype of an individual and that which would confer optimal responses in terms of fitness in an environment is termed 'mismatch'. Phenotype results from developmental plasticity, conditioned partly by evolutionary history of the species and partly by aspects of the developmental environment. We discuss two categories of such mismatch with reference primarily to nutrition and in the context of evolutionary medicine. The categories operate over very different timescales. A developmental mismatch occurs when the phenotype induced during development encounters a different environment post-development. This may be the result of wider environmental changes, such as nutritional transition between generations, or because maternal malnutrition or placental dysfunction give inaccurate information about the organism's likely future environment. An evolutionary mismatch occurs when there is an evolutionarily novel environment. Developmental plasticity may involve immediate adaptive responses (IARs) to preserve survival if an environmental challenge is severe, and/or predictive adaptive responses (PARs) if the challenge does not threaten survival, but there is a fitness advantage in developing a phenotype that will be better adapted later. PARs can have long-term adverse health consequences if there is a developmental mismatch. For contemporary humans, maternal constraint of fetal growth makes PARs likely even if there is no obvious IAR, and this, coupled with the pervasive nutritionally dense modern environment, can explain the widespread observations of developmental mismatch, particularly in populations undergoing nutritional transition. Both developmental and evolutionary mismatch have important public health consequences and implications for where policy interventions may be most effective. [ABSTRACT FROM AUTHOR]

Abstract The brain rapidly develops during the prenatal period; therefore, intrauterine conditions can affect neurodevelopment, behavior and health across the lifespan. The developmental origins of health and disease hypothesis posits that physiological alterations are made by the fetus to adapt to prenatal conditions. Research examining links between perinatal adversity and neurodevelopment has focused mainly on the risk for mental health problems. However, these disorders are likely the product of multiple subtle changes in the brain occurring in response to intrauterine stress, alterations that may have important implications for the development of personality. Here, we review the evidence that bears on the question of if and how prenatal conditions influence personality development. We hypothesize that prenatal conditions lead to alterations in systems mediating stress and reward sensitivity and effortful control, changes that may affect personality traits and their stability across time. Understanding how the prenatal environment influences personality development can help to advance theories of personality development and our understanding of normal behavior. [ABSTRACT FROM AUTHOR]

A major problem in the evolution of maternal effects is explaining the origin and persistence of maternally induced phenotypes that lower offspring fitness. Recent work focuses on the relative importance of maternal and offspring selective environments and the mismatch between them. However, an alternative approach is to directly study the origin and performance of offspring phenotypes resulting from mismatch. Here, we capitalize on a detailed understanding of the ecological contexts that provide both the cue and the functional context for expression of maternally induced offspring phenotypes to investigate the consequences of environmental mismatch. In western bluebirds, adaptive integration of offspring dispersal and aggression is induced by maternal competition over nest cavities. When nest cavities are locally abundant, mothers produce nonaggressive offspring that remain in their natal population, and when nest cavities are scarce, mothers produce aggressive dispersers. However, a few offspring neither disperse nor breed locally, instead helping at their parent’s nest, and as a result these offspring have unusually low fitness. Here, we investigate whether females produce helpers to increase their own fitness, or whether helpers result from a mismatch between the cues mothers experience during offspring production and the breeding environment that helpers later encounter. We found that producing helpers does not enhance maternal fitness. Instead, we show that helpers, which were the least aggressive of all returning sons in the population, were most common when population density increased from the time sons were produced to the time of their reproductive maturity, suggesting that the helper phenotype emerges when cues of resource competition during offspring development do not match the actual level of competition that offspring experience. Thus, environmental mismatch might explain the puzzling persistence of maternally induced phenotypes that decrease offspring fitness. [ABSTRACT FROM AUTHOR]

Telomeres are repeating DNA found at the ends of chromosomes that, in the absence of restorative processes, shorten with cell replications and are implicated as a cause of senescence. It appears that sperm telomere length (TL) increases with age in humans, and as a result offspring of older fathers inherit longer telomeres.We reviewpossible mechanisms underlying this paternal age at conception (PAC) effect on TL, including sperm telomere extension due to telomerase activity, age-dependent changes in the spermatogonial stem cell population (possibly driven by 'selfish' spermatogonia) and non-causal confounding. In contrast to the lengthening of TL with PAC, higher maternal age at conception appears to predict shorter offspring TL in humans. We review evidence for heterogeneity across species in the PAC effect on TL, which could relate to differences in statistical power, sperm production rates or testicular telomerase activity. Finally, we review the hypothesis that the PAC effect on TL may allow a gradual multi-generational adaptive calibration of maintenance effort, and reproductive lifespan, to local demographic conditions: descendants of males who reproduced at a later age are likely to find themselves in an environment where increased maintenance effort, allowing later reproduction, represents a fitness improving resource allocation. This article is part of the theme issue 'Understanding diversity in telomere dynamics'. [ABSTRACT FROM AUTHOR]

Predation risk is an important environmental factor for animal populations, expected to trigger maternal effects to prepare offspring for living in an environment with predators. Yet, evidence of adaptive anticipatory maternal effects in wild animals is still weak. Here, we explored this question in a wild colony of yellow-legged gulls, Larus michahellis. To this aim, prior to laying we exposed mothers to either mink decoys or nonpredator rabbit decoys and explored the antipredator behavior of 118 chicks at the age of 2 days. We found that chicks from second-laid eggs by predator-exposed mothers crouched faster after hearing a playback with adult alarm calls than chicks from second-laid eggs by control mothers. Besides, chicks from third-laid eggs by predator-exposed mothers were lighter than control chicks, but this was not due to differences in egg volume. Our results suggest that predator-exposed mothers modified offspring phenotype via eggs to cope with predators, although only in chicks from second-laid eggs. Maternal transference of corticosterone could underlie chick behavioral plasticity. Results support the role of maternal effects as a form of phenotype programming to forewarn offspring about environmental hazards. [ABSTRACT FROM AUTHOR]

The mother is the major interface between the offspring and its prenatal environment. Prenatal toxins and stress-inducing physical agents are important factors programming the developmental trajectory of mammals that likely involve epigenetic modifications. However, prenatal stressors commonly-used in the laboratory (e.g. prenatal restraint stress and prenatal chronic variable stress) are typically administered at high intensities. These exposures typically lead to pathological phenotypes supporting the development origin of health and disease hypothesis. In this review, we compare the phenotypic outcomes of these commonly-used prenatal stressors to an ecologically-relevant, psychogenic stressor that has been present over evolutionary times, predator or predator cues presence. Prenatal stress by predator threat results in behavioral, physiological, endocrine, transcript abundance and epigenetic (DNA methylation) modifications. These phenotypic modifications are consistent with developmental forecasting according to the Predictive Adaptive Response hypothesis, yielding adaptive responses in environments where such predation stress is present. The evidence described in this review suggests that the type of prenatal stress agent and its intensity modifies the phenotype expressed, which can range from adaptive to pathological. Prenatal Bisphenol A exposure studies are presented as an example where graded intensities (concentrations) of prenatal toxin exposure can be compared directly. Finally, we emphasize the importance of studying both sexes in these studies, as sex differences appear to be a common feature of the response to prenatal stress. [ABSTRACT FROM AUTHOR]

Background: Sub-optimal developmental diets often have adverse effects on long-term fitness and health. One hypothesis is that such effects are caused by mismatches between the developmental and adult environment and may be mediated by persistent changes in gene expression. However, there are few experimental tests of this hypothesis. Here we address this using the fruit fly, Drosophila melanogaster. We vary diet during development and adulthood in a fully factorial design and assess the consequences for both adult life history traits and gene expression at middle and old age. Results: We find no evidence that mismatches between developmental and adult diet are detrimental to either lifespan or fecundity. Rather, developmental and adult diet exert largely independent effects on both lifespan and gene expression, with adult diet having considerably more influence on both traits. Furthermore, we find effects of developmental diet on the transcriptome that persist into middle and old-age. Most of the genes affected show no correlation with the observed phenotypic effects of larval diet on lifespan. However, in each sex we identify a cluster of ribosome, transcription and translation-related genes whose expression is altered across the lifespan and negatively correlated with lifespan. Conclusions: As several recent studies have linked decreased expression of ribosomal and transcription related proteins to increased lifespan, these provide promising candidates for mediating the effects of larval diet on lifespan. We place our findings in the context of theories linking developmental conditions to late-life phenotypes and discuss the likelihood that gene expression differences caused by developmental exposure causally relate to adult ageing phenotypes. [ABSTRACT FROM AUTHOR]

Cohort effects can be a major source of heterogeneity and play an important role in population dynamics. Silver-spoon effects, when environmental quality at birth improves future performance regardless of the adult environment, can induce strong lagged responses on population growth. Alternatively, the external predictive adaptive response (PAR) hypothesis predicts that organisms will adjust their developmental trajectory and physiology during early life in anticipation of expected adult conditions but has rarely been assessed in wild species. We used over 40 years of detailed individual monitoring of bighorn ewes (Ovis canadensis) to quantify longterm cohort effects on survival and reproduction. We then tested both the silver-spoon and the PAR hypotheses. Cohort effects involved a strong interaction between birth and current environments: reproduction and survival were lowest for ewes that were born and lived at high population densities. This interaction, however, does not support the PAR hypothesis because individuals with matching high-density birth and adult environments had reduced fitness. Instead, individuals born at high density had overall lower lifetime fitness suggesting a silver-spoon effect. Early-life conditions can induce long-term changes in fitness components, and their effects on cohort fitness vary according to adult environment. [ABSTRACT FROM AUTHOR]

Food availability modulates survival in interaction with (for example) competition, disease and predators, but to what extent food availability in natural populations affects survival independent of these factors is not well known. We tested the effect of food availability on lifespan and actuarial senescence in a large population of captive zebra finches by increasing the effort required to obtain food, reflecting natural contrasts in food availability. Food availability may not affect all individuals equally and we therefore created heterogeneity in phenotypic quality by raising birds with different numbers of siblings. Low food availability had no effect on lifespan for individuals from benign developmental conditions (raised in small broods), but shortened lifespan for individuals from harsh developmental conditions. The lifespan difference arose through higher baseline mortality rate of individuals from harsh developmental conditions, despite a decrease in the rate of actuarial senescence. We found no evidence for sex-specific environmental sensitivity, but females lived shorter than males due to increased actuarial senescence. Thus, low food availability by itself shortens lifespan, but only in individuals from harsh developmental conditions. Our food availability manipulation resembles dietary restriction as applied to invertebrates, where it extends lifespan in model organisms and we discuss possible reasons for the contrasting results. [ABSTRACT FROM AUTHOR]

Human life history (LH) strategies are theoretically regulated by developmental exposure to environmental cues that ancestrally predicted LH-relevant world states (e.g., risk of morbidity–mortality). Recent modeling work has raised the question of whether the association of childhood family factors with adult LH variation arises via (i) direct sampling of external environmental cues during development and/or (ii) calibration of LH strategies to internal somatic condition (i.e., health), which itself reflects exposure to variably favorable environments. The present research tested between these possibilities through three online surveys involving a total of over 26,000 participants. Participants completed questionnaires assessing components of self-reported environmental harshness (i.e., socioeconomic status, family neglect, and neighborhood crime), health status, and various LH-related psychological and behavioral phenotypes (e.g., mating strategies, paranoia, and anxiety), modeled as a unidimensional latent variable. Structural equation models suggested that exposure to harsh ecologies had direct effects on latent LH strategy as well as indirect effects on latent LH strategy mediated via health status. These findings suggest that human LH strategies may be calibrated to both external and internal cues and that such calibrational effects manifest in a wide range of psychological and behavioral phenotypes. [ABSTRACT FROM AUTHOR]

The internal predictive adaptive response (internal PAR) hypothesis predicts that individuals born in poor conditions should start to reproduce earlier if they are likely to have reduced performance in later life. However, whether this is the case remains unexplored in wild populations. Here, we use longitudinal data from a long-term study of Svalbard reindeer to examine age-related changes in adult female life-history responses to environmental conditions experienced in utero as indexed by rain-on-snow (ROSutero). We show that females experiencing high ROSutero had reduced reproductive success only from 7 years of age, independent of early reproduction. These individuals were able to maintain the same annual reproductive success between 2 and 6 years as phenotypically superior conspecifics that experienced low ROSutero. Young females born after high ROSutero engage in reproductive events at lower body mass (about 2.5 kg less) than those born after low ROSutero. The mean fitness of females that experienced poor environmental conditions in early lifewas comparable with that of females exposed to good environmental conditions in early life. These results are consistent with the idea of internal PAR and suggest that the life-history responses to early-life conditions can buffer the delayed effects of weather on population dynamics. [ABSTRACT FROM AUTHOR]

The potential for stressful experiences in early life to cause lasting changes in phenotype is well documented, but the functional and evolutionary context of these changes is not well understood. Many hypotheses have been proposed to explain the role of lasting effects of stress exposure during gestation and early development; the purpose of this review is to discuss these hypotheses in the context of human and non-human animal research in the last three decades in order to (i) further dialogues between those approaching early stress from biomedical and evolutionary/ecological perspectives, (ii) outline strengths and limitations of current hypotheses, with respect to species and context-specific effects of exposure to stress in early development, and (iii) address recent evidence suggesting that stress in early development can have beneficial effects in adulthood. It is suggested that the hypotheses discussed are not mutually exclusive, but the applicability of each hypothesis will depend upon the environmental conditions and stability a species, or perhaps even an individual, experiences in their lifetime. Potential investigations to clarify applications of the current hypotheses are discussed, including longitudinal studies that span multiple developmental stages and investigations of species where measures of fitness are possible. [ABSTRACT FROM AUTHOR]

In the early 2000s, a new component of the cost of reproduction was proposed: oxidative stress. Since then the oxidative cost of reproduction hypothesis has, however, received mixed support. Different arguments have been provided to explain this. Among them, the lack of a life-history perspective on most experimental tests was suggested. We manipulated the levels of a key intracellular antioxidant (glutathione) in captive zebra finches (Taeniopygia guttata) during a short period of early life and subsequently tested the oxidative cost of reproduction. Birds were allowed to mate freely in an outdoor aviary for several months. We repeatedly enlarged or reduced their broods to increase or reduce, respectively, breeding effort. Birds whose glutathione levels were reduced during growth showed higher erythrocyte resistance to free radical-induced haemolysis when forced to rear enlarged broods. This supports the hypothesis predicting the occurrence of developing programmes matching early and adult environmental conditions to improve fitness. Moreover, adult males rearing enlarged broods endured higher plasma levels of lipid oxidative damage than control males, whereas adult females showed the opposite trend. As most previous studies reporting non-significant or opposite results used females only, we also discuss some sex-related particularities that may contribute to explain unexpected results. [ABSTRACT FROM AUTHOR]

Despite classical expectations of a trade-off between immune activity and reproduction, an emergent view suggests that individuals experiencing activation of their immune system actually increase reproductive effort and allocation to offspring as a form of terminal investment in response to reduced survival probability. However, the components and mechanisms of increased parental investment following immunostimulation are currently unknown. We hypothesize that increased glucocorticoid production following immunostimulation modulates the increase in reproductive effort that constitutes terminal investment. We activated the immune system of breeding female house wrens (Troglodytes aedon) with an immunogen and cross-fostered the eggs that they subsequently produced to separate prenatal and postnatal components of maternal investment. Cross-fostering revealed an increase in both pre- and postnatal allocation from immunostimulated females, which was confirmed by quantification of egg constituents and maternal provisioning behavior. The increase in maternal provisioning was mediated, at least in part, by increased corticosterone in these females. Offspring immune responsiveness was also enhanced through transgenerational immune priming via the egg. Thus, our results indicate that maternal immunostimulation induces transgenerational effects on offspring through both pre- and postnatal parental effects and support an important role for corticosterone in mediating parental investment. [ABSTRACT FROM AUTHOR]

Early-life experiences can dramatically affect adult traits. However, the evolutionary origins of such early-life effects are debated. The predictive adaptive response hypothesis argues that adverse early environments prompt adaptive phenotypic adjustments that prepare animals for similar challenges in adulthood. In contrast, the developmental constraints hypothesis argues that early adversity is generally costly. To differentiate between these hypotheses, we studied two sets of wild female baboons: those born during low-rainfall, low-quality years and those born during normal-rainfall, high-quality years. For each female, we measured fertility-related fitness components during years in adulthood that matched and mismatched her early conditions. We found support for the developmental constraints hypothesis: females born in low-quality environments showed greater decreases in fertility during drought years than females born in highquality environments, even though drought years matched the early conditions of females born in low-quality environments. Additionally, we found that females born in low-quality years to high-status mothers did not experience reduced fertility during drought years. These results indicate that early ecological adversity did not prepare individuals to cope with ecological challenges in later life. Instead, individuals that experienced at least one high-quality early environment- either ecological or social-were more resilient to ecological stress in later life. Together, these data suggest that early adversity carries lifelong costs, which is consistent with the developmental constraints hypothesis. [ABSTRACT FROM AUTHOR]

Both developmental nutrition and adult nutrition affect life-history traits; however, little is known about whether the effect of developmental nutrition depends on the adult environment experienced. We used the fruit fly to determine whether life-history traits, particularly life span and fecundity, are affected by developmental nutrition, and whether this depends on the extent to which the adult environment allows females to realize their full reproductive potential. We raised flies on three different developmental food levels containing increasing amounts of yeast and sugar: poor, control, and rich. We found that development on poor or rich larval food resulted in several life-history phenotypes indicative of suboptimal conditions, including increased developmental time, and, for poor food, decreased adult weight. However, development on poor larval food actually increased adult virgin life span. In addition, we manipulated the reproductive potential of the adult environment by adding yeast or yeast and a male. This manipulation interacted with larval food to determine adult fecundity. Specifically, under two adult conditions, flies raised on poor larval food had higher reproduction at certain ages - when singly mated this occurred early in life and when continuously mated with yeast this occurred during midlife. We show that poor larval food is not necessarily detrimental to key adult life-history traits, but does exert an adult environment-dependent effect, especially by affecting virgin life span and altering adult patterns of reproductive investment. Our findings are relevant because (1) they may explain differences between published studies on nutritional effects on life-history traits; (2) they indicate that optimal nutritional conditions are likely to be different for larvae and adults, potentially reflecting evolutionary history; and (3) they urge for the incorporation of developmental nutritional conditions into the central life-history concept of resource acquisition and allocation. [ABSTRACT FROM AUTHOR]

Early-life experience strongly impacts neurodevelopment and stress susceptibility in adulthood. Maternal separation (MS), an established model of early-life adversity, has been shown to negatively impact behavioral and endocrine responses to stress in adulthood. However, the impact of MS in rats with heightened inborn stress susceptibility has not been fully explored. To address this issue we conducted MS in Wistar-Kyoto (WKY) rats, an animal model of comorbid depression and anxiety, and Wistar rats, which share a similar genetic background with WKYs. WKY and Wistar pups experienced either 180-min daily MS or 15-min separation (neonatal handling) during the first two postnatal weeks, and were tested for depressive- and anxiety- like behaviors in adulthood. Exposure to early-life MS in WKY rats decreased anxiety- and depressive- like behaviors, leading to increased exploration on the open field test (OFT), enhanced social interaction, and diminished immobility on the forced swim test. MS had an opposite effect in Wistar offspring, leading to enhanced anxiety-like behaviors, such as reduced OFT exploration and decreased social interaction. These findings are consistent with the match/mismatch theory of disease and the predictive adaptive response, which suggests that early life stress exposure can confer adaptive value in later life within certain individuals. Our data supports this theory, showing that early-life MS has positive and perhaps adaptive effects within stress-vulnerable WKY offspring. Future studies will be required to elucidate the neurobiological underpinnings of contrasting behavioral effects of MS on WKY vs. Wistar offspring. [ABSTRACT FROM AUTHOR]

ABSTRACT This study evaluates two hypotheses that address how Late/Final Jomon period people responded to early-life stress using linear enamel hypoplasia (LEH) and incremental microstructures of enamel. The first hypothesis predicts that Jomon people who experienced early-life stressors had greater physiological competence in responding to future stress events (predictive adaptive response). The second hypothesis predicts that Jomon people traded-off in future growth and maintenance when early investment in growth and survival was required (plasticity/constraint). High resolution tooth impressions were collected from intact, anterior teeth and studied under an engineer's measuring microscope. LEH were identified based on accentuated perikymata and depressions in the enamel surface profile. Age of formation for each LEH was estimated by summing counts of perikymata and constants associated with crown initiation and cuspal enamel formation times. The relationship between age-at-first-defect formation, number of LEH, periodicity between LEH, and mortality was evaluated using multiple regression and hazards analysis. A significant, positive relationship was found between age-at-death relative to age-at-first-defect formation and a significant, negative relationship was found between number of LEH relative to age-at-first-defect formation. Individuals with earlier forming defects were at a significantly greater risk of forming defects at later stages of development and dying at younger ages. These results suggest that Late/Final Jomon period foragers responded to early-life stressors in a manner consistent with the plasticity/constraint hypothesis of human life history. Late/Final Jomon period individuals were able to survive early-life stressors, but this investment weakened responses to future stress events and exacerbated mortality schedules. Am J Phys Anthropol 155:537-545, 2014. © 2014 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Diseases caused by impaired regulation of energy balance, in particular obesity, represent a major global health burden. Although polymorphisms, lifestyle and dietary choices have been associated with differential risk of obesity and related conditions, a substantial proportion of the variation in disease risk remains unexplained. Evidence from epidemiological studies, natural experiments and from studies in animal models has shown that a poor intra-uterine environment is associated causally with increased risk of obesity and metabolic disease in adulthood. Induction of phenotypes that increase disease risk involves the fetus receiving cues from the mother about the environment which, via developmental plasticity, modify the phenotype of the offspring to match her environment. However, inaccurate information may induce an offspring phenotype that is mismatched to the future environment. Such mismatch has been suggested to underlie increased risk of metabolic disease associated with a poor early life environment. Recent studies have shown that induction of modified phenotypes in the offspring involves altered epigenetic regulation of specific genes. Identification of a central role of epigenetics in the aetiology of obesity and metabolic disease may facilitate the development of novel therapeutic interventions and of biomarkers of disease risk. [ABSTRACT FROM AUTHOR]