Early-life maltreatment predicts adult stress response in a long-lived wild bird.
Ontology highlight
ABSTRACT:
SUBMITTER: Grace JK
PROVIDER: S-EPMC5803595 | biostudies-literature | 2018 Jan
REPOSITORIES: biostudies-literature
Publications
Early-life maltreatment predicts adult stress response in a long-lived wild bird.
Grace Jacquelyn K JK Anderson David J DJ
Biology letters 20180101 1
Persistent phenotypic changes due to early-life stressors are widely acknowledged, but their relevance for wild, free-living animals is poorly understood. We evaluated effects of two natural stressors experienced when young (maltreatment by adults and nutritional stress) on stress physiology in wild Nazca boobies (<i>Sula granti</i>) 6-8 years later, an exceptionally long interval for such studies. Maltreatment as a nestling, but not nutritional stress, was associated years later with depressed ...[more]
Similar Datasets
Project description:Stress in early life has been associated with insufficient glucocorticoid signaling in adulthood, possibly affecting inflammation processes. Childhood maltreatment has been linked to increased risk of adult disease with potential inflammatory origin. However, the impact of early life stress on adult inflammation is not known in humans. We tested the life-course association between childhood maltreatment and adult inflammation in a birth cohort followed to age 32 years as part of the Dunedin Multidisciplinary Health and Development Study. Regression models were used to estimate the effect of maltreatment on inflammation, adjusting for co-occurring risk factors and potential mediating variables. Maltreated children showed a significant and graded increase in the risk for clinically relevant C-reactive protein levels 20 years later, in adulthood [risk ratio (RR)=1.80, 95% confidence interval (CI)=1.26-2.58]. The effect of childhood maltreatment on adult inflammation was independent of the influence of co-occurring early life risks (RR=1.58, 95% CI=1.08-2.31), stress in adulthood (RR=1.64, 95% CI=1.12-2.39), and adult health and health behavior (RR=1.76, 95% CI=1.23-2.51). More than 10% of cases of low-grade inflammation in the population, as indexed by high C-reactive protein, may be attributable to childhood maltreatment. The association between maltreatment and adult inflammation also generalizes to fibrinogen and white blood cell count. Childhood maltreatment is a previously undescribed, independent, and preventable risk factor for inflammation in adulthood. Inflammation may be an important developmental mediator linking adverse experiences in early life to poor adult health.
| S-EPMC1783123 | biostudies-literature
Project description:Conditions experienced during early life can have profound consequences for both short- and long-term fitness. Variation in the natal environment has been shown to influence survival and reproductive performance of entire cohorts in wild vertebrate populations. Telomere dynamics potentially provide a link between the early environment and long-term fitness outcomes, yet we know little about how the environment can influence telomere dynamics in early life. We found that environmental conditions during growth have an important influence on early-life telomere length (TL) and attrition in nestlings of a long-lived bird, the European storm petrel Hydrobates pelagicus. Nestlings reared under unfavourable environmental conditions experienced significantly greater telomere loss during postnatal development compared with nestlings reared under more favourable natal conditions, which displayed a negligible change in TL. There was, however, no significant difference in pre-fledging TL between cohorts. The results suggest that early-life telomere dynamics could contribute to the marked differences in life-history traits that can arise among cohorts reared under different environmental conditions. Early-life TL was also found to be a significant predictor of survival during the nestling phase, providing further evidence for a link between variation in TL and individual fitness. To what extent the relationship between early-life TL and mortality during the nestling phase is a consequence of genetic, parental and environmental factors is currently unknown, but it is an interesting area for future research. Accelerated telomere attrition under unfavourable conditions, as observed in this study, might play a role in mediating the effects of the early-life environment on later-life performance.
| S-EPMC4376192 | biostudies-literature
Project description:Conditions during early life, including maternal cohort effects, can influence the future fitness of individuals. This may be particularly true for long-distance migrating birds, because, apart from conditions experienced by cohorts during rearing, conditions during early life in regions far from breeding grounds may also influence their population dynamics. Very little is known about the fitness consequences of those conditions experienced by juveniles after independence, especially in wild populations and for long-lived birds. We used multi-event capture-recapture-recovery models and a unique 26-year dataset for the Audouin's gull (Larus audouinii) to assess for the first time whether survival was influenced by early conditions, both during the rearing period (i.e. a maternal cohort effect potentially affected by density dependence) and the first winter (i.e. a cohort effect driven by climate when birds disperse to wintering grounds). Our results show that juvenile survival was highly sensitive to early-life conditions and that survival decreased with stronger density dependence and harsh climate. The two consecutive cohort effects were of similar magnitude and they may represent a selection filter. Thus, early-life conditions had a strong impact on survival, and neglecting this complexity may hinder our understanding on how populations of long-lived animals fluctuate and respond to perturbations.
| S-EPMC4855379 | biostudies-literature
Project description:Evolutionary senescence theory postulates that aging results from the declining force of natural selection with increasing chronological age. A goal of comparative studies in the biology of aging is to identify genetic and biochemical mechanism(s) driving species-specific differences in the aging process that are the end product of life history trade-offs. We hypothesized that cells from long-lived bird species are more resistant to stress agents than are cells from short-lived species, and that cells from birds are more resistant to stress than are cells from relatively short-lived mammals of similar size. We tested primary fibroblast cultures from 35 species of free-living birds for their resistance to multiple forms of cellular stress and found that cell lines from longer-lived species were resistant to death caused by cadmium (R(2)=0.27, P=0.002), paraquat (R(2)=0.13, P=0.03), hydrogen peroxide (R(2)=0.09, P=0.07) and methyl methanesulfonate (R(2)=0.13, P=0.03), as well as to the metabolic inhibition seen in low-glucose medium (R(2)=0.37, P<0.01). They did not differ in their resistance to UV radiation, or to thapsigargin or tunicamycin, inducers of the unfolded protein response. These results were largely consistent even after accounting for the influence of body mass and phylogeny. Cell lines from longer-lived bird species also proliferate more rapidly than cells from short-lived birds, although there was no relationship between proliferation and stress resistance. Finally, avian fibroblasts were significantly more resistant than rodent fibroblasts to each of the tested stressors. These results support the idea that cellular resistance to injury may be an important contributor to the evolution of slow aging and long lifespan among bird species, and may contribute to the relatively long lifespan of birds compared with rodents of the same body size.
| S-EPMC3092728 | biostudies-literature
Project description:Stressful life events increase vulnerability to problematic alcohol use, and they may do this by disrupting reward-related neural circuitry. This is particularly relevant for adolescents because alcohol use rises sharply after mid-adolescence and alcohol abuse peaks at age 20. Adolescents also report more stressors compared with children, and neural reward circuitry may be especially vulnerable to stressors during adolescence because of prefrontal cortex remodeling. Using a large sample of male participants in a longitudinal functional magnetic resonance imaging study (N = 157), we evaluated whether cumulative stressful life events between the ages of 15 and 18 were associated with reward-related brain function and problematic alcohol use at age 20 years. Higher cumulative stressful life events during adolescence were associated with decreased response in the medial prefrontal cortex (mPFC) during monetary reward anticipation and following the receipt of monetary rewards. Stress-related decreases in mPFC response during reward anticipation and following rewarding outcomes were associated with the severity of alcohol dependence. Furthermore, mPFC response mediated the association between stressful life events and later symptoms of alcohol dependence. These data are consistent with neurobiological models of addiction that propose that stressors during adolescence increase risk for problematic alcohol use by disrupting reward circuit function.
| S-EPMC4350480 | biostudies-literature
Project description:In humans and other animals, harsh circumstances in early life predict morbidity and mortality in adulthood. Multiple adverse conditions are thought to be especially toxic, but this hypothesis has rarely been tested in a prospective, longitudinal framework, especially in long-lived mammals. Here we use prospective data on 196 wild female baboons to show that cumulative early adversity predicts natural adult lifespan. Females who experience ?3 sources of early adversity die a median of 10 years earlier than females who experience ?1 adverse circumstances (median lifespan is 18.5 years). Females who experience the most adversity are also socially isolated in adulthood, suggesting that social processes partially explain the link between early adversity and adult survival. Our results provide powerful evidence for the developmental origins of health and disease and indicate that close ties between early adversity and survival arise even in the absence of health habit and health care-related explanations.
| S-EPMC4838827 | biostudies-literature
Project description:Hypopituitary Ames dwarf mice were injected either with growth hormone (GH) or thyroxine for a 6-wk period to see whether this intervention would reverse their long life span or the resistance of their cells to lethal stresses. Ames dwarf mice survived 987 ± 24 d (median), longer than nonmutant control mice (664 ± 48), but GH-injected dwarf mice did not differ from controls (707 ± 9). Fibroblast cells from Ames dwarf mice were more resistant to cadmium than cells from nonmutant controls (LD(50) values of 9.98 ± 1.7 and 3.9 ± 0.8, respectively), but GH injections into Ames dwarf mice restored the normal level of cadmium resistance (LD(50)=5.8 ± 0.9). Similar restoration of normal resistance was observed for fibroblasts exposed to paraquat, methyl methanesulfonate, and rotenone (P<0.05 in each case for contrast of GH-treated vs. untreated dwarf mice; P<0.05 for dwarf vs. nonmutant control mice.) T4 injections into Ames dwarf mice, in contrast, did not restore normal life span. We conclude that the remarkable life-span extension of Ames dwarf mice, and the stress resistance of cells from these mice, depends on low levels of GH exposure in juvenile and very young adult mice.
| S-EPMC2992365 | biostudies-literature
Project description:Heterogeneity within a population is a pervasive challenge for studies of individual life-histories. Population-level patterns in age-specific reproductive success can be broken down into relative contributions from selective disappearance, selective appearance of individuals into the study population, and average change in performance for survivors (average ontogenetic development). In this article, we provide an exact decomposition. We apply our formula to data on the reproductive performance of a well characterized population of common terns (Sterna hirundo). We show that improvements with age over most of adult life and senescence at old ages are primarily due to a genuine change in the mean among surviving individuals rather than selective disappearance or selective appearance of individuals. Average ontogenetic development accounts for approximately 87% of the overall age-specific population change.
| S-EPMC2867923 | biostudies-literature
Project description:Although population studies have long assumed that all individuals of a given sex and age are identical, ignoring among-individual differences may strongly bias our perception of eco-evolutionary processes. Individual heterogeneity, often referred to as individual quality, has received increasing research attention in the last decades. However, there are still substantial gaps in our current knowledge. For example, there is little information on how individual heterogeneity influences various life-history traits simultaneously, and studies describing individual heterogeneity in wild populations are generally not able to jointly identify possible sources of this variation. Here, based on a mark-recapture data set of 9,685 known-aged Wandering Albatrosses (Diomedea exulans), we investigated the existence of individual quality over the entire life cycle of this species, from early life to senescence. Using finite mixture models, we investigated the expression of individual heterogeneity in various demographic traits, and examined the origin of these among-individual differences by considering the natal environmental conditions. We found that some individuals consistently outperformed others during most of their life. In old age, however, the senescence rate was stronger in males that showed high demographic performance at younger ages. Variation in individual quality seemed strongly affected by extrinsic factors experienced during the ontogenetic period. We found that individuals born in years with high population density tended to have lower performances during their lifespan, suggesting delayed density dependence effects through individual quality. Our study showed that among-individual differences could be important in structuring individual life history trajectories, with substantial consequences at higher ecological levels such as population dynamics.
| S-EPMC6084314 | biostudies-literature
Project description:BACKGROUND: Theories of ageing predict a trade-off between metabolism, reproduction, and maintenance. Species with low investment in early reproduction are thus expected to be able to evolve more efficient maintenance and repair mechanisms, allowing for a longer potential life span (intrinsic longevity). The erosion of telomeres, the protective caps at the ends of linear chromosomes, plays an important role in cellular and organismal senescence, signalling the onset of age-related disease due to accumulation of unrepaired somatic damage. Using extensive longitudinal data from a long-term study of a natural population of barnacle geese Branta leucopsis, we investigated individual rates of telomere length changes over two years in 34 birds between 0 and 22 years of age, covering almost 80% of the species' lifespan. RESULTS: We show that telomeres in this long-lived bird are very well maintained, as theoretically expected, with an average loss rate of only 5 base pairs per year among adults. We thus found no significant relationship between change in telomere length and age. However, telomeres tended to shorten at a faster pace in juveniles compared to adults. For the first time, we demonstrate a faster telomere attrition rate in females compared to males. We found no correlation between telomere loss rate and adult survival or change in body mass. CONCLUSIONS: Our results add further support for a link between longevity and telomere maintenance, and highlight the complexities of telomere dynamics in natural populations.
| S-EPMC3546850 | biostudies-other