Long-lived Individuals Research Articles

Similar burden of pathogenic coding variants in exceptionally long-lived individuals and individuals without exceptional longevity.

Centenarians (exceptionally long‐lived individuals—ELLI) are a unique segment of the population, exhibiting long human lifespan and healthspan, despite generally practicing similar lifestyle habits as their peers. We tested disease‐associated mutation burden in ELLI genomes by determining the burden of pathogenic variants reported in the ClinVar and HGMD databases using data from whole exome sequencing (WES) conducted in a cohort of ELLI, their offspring, and control individuals without antecedents of familial longevity (n = 1879), all descendent from the founder population of Ashkenazi Jews. The burden of pathogenic variants did not differ between the three groups. Additional analyses of variants subtypes and variant effect predictor (VEP) biotype frequencies did not reveal a decrease of pathogenic or loss‐of‐function (LoF) variants in ELLI and offspring compared to the control group. Case–control pathogenic variants enrichment analyses conducted in ELLI and controls also did not identify significant differences in any of the variants between the groups and polygenic risk scores failed to provide a predictive model. Interestingly, cancer and Alzheimer's disease‐associated variants were significantly depleted in ELLI compared to controls, suggesting slower accumulation of mutation. That said, polygenic risk score analysis failed to find any predictive variants among the functional variants tested. The high similarity in the burden of pathogenic variation between ELLI and individuals without familial longevity supports the notion that extension of lifespan and healthspan in ELLI is not a consequence of pathogenic variant depletion but rather a result of other genomic, epigenomic, or potentially nongenomic properties.

A 25-y longitudinal dolphin cohort supports that long-lived individuals in same environment exhibit variation in aging rates

While it is believed that humans age at different rates, a lack of robust longitudinal human studies using consensus biomarkers meant to capture aging rates has hindered an understanding of the degree to which individuals vary in their rates of aging. Because bottlenose dolphins are long-lived mammals that develop comorbidities of aging similar to humans, we analyzed data from a well-controlled, 25-y longitudinal cohort of 144 US Navy dolphins housed in the same oceanic environment. Our analysis focused on 44 clinically relevant hematologic and clinical chemistry measures recorded during routine blood draws throughout the dolphins' lifetimes. Using stepwise regression and general linear models that accommodate correlations between measures obtained on individual dolphins, we demonstrate that, in a manner similar to humans, dolphins exhibit independent and linear age-related declines in four of these measures: hemoglobin, alkaline phosphatase, platelets, and lymphocytes. Using linear regressions and analyses of covariance with post hoc Tukey-Kramer tests to compare slopes (i.e., linear age-related rates) of our four aging rate biomarkers among 34 individual dolphins aging from 10 y to up to 40 y old, we could identify slow and accelerated agers and differentiate subgroups that were more or less likely to develop anemia and lymphopenia. This study successfully documents aging rate differences over the lifetime of long-lived individuals in a controlled environment. Our study suggests that nonenvironmental factors influencing aging rate biomarkers, including declining hemoglobin and anemia, may be targeted to delay the effects of aging in a compelling model of human biology.

Genetics of extreme human longevity to guide drug discovery for healthy ageing.

Ageing is the greatest risk factor for most common chronic human diseases, and it therefore is a logical target for developing interventions to prevent, mitigate or reverse multiple age-related morbidities. Over the past two decades, genetic and pharmacologic interventions targeting conserved pathways of growth and metabolism have consistently led to substantial extension of the lifespan and healthspan in model organisms as diverse as nematodes, flies and mice. Recent genetic analysis of long-lived individuals is revealing common and rare variants enriched in these same conserved pathways that significantly correlate with longevity. In this Perspective, we summarize recent insights into the genetics of extreme human longevity and propose the use of this rare phenotype to identify genetic variants as molecular targets for gaining insight into the physiology of healthy ageing and the development of new therapies to extend the human healthspan.

The Role of microRNAs in Organismal and Skin Aging.

The aging process starts directly after birth and lasts for the entire lifespan; it manifests itself with a decline in an organism’s ability to adapt and is linked to the development of age-related diseases that eventually lead to premature death. This review aims to explore how microRNAs (miRNAs) are involved in skin functioning and aging. Recent evidence has suggested that miRNAs regulate all aspects of cutaneous biogenesis, functionality, and aging. It has been noted that some miRNAs were down-regulated in long-lived individuals, such as let-7, miR-17, and miR-34 (known as longevity-related miRNAs). They are conserved in humans and presumably promote lifespan prolongation; conversely, they are up-regulated in age-related diseases, like cancers. The analysis of the age-associated cutaneous miRNAs revealed the increased expression of miR-130, miR-138, and miR-181a/b in keratinocytes during replicative senescence. These miRNAs affected cell proliferation pathways via targeting the p63 and Sirtuin 1 mRNAs. Notably, miR-181a was also implicated in skin immunosenescence, represented by the Langerhans cells. Dermal fibroblasts also expressed increased the levels of the biomarkers of aging that affect telomere maintenance and all phases of the cellular life cycle, such as let-7, miR-23a-3p, 34a-5p, miR-125a, miR-181a-5p, and miR-221/222-3p. Among them, the miR-34 family, stimulated by ultraviolet B irradiation, deteriorates collagen in the extracellular matrix due to the activation of the matrix metalloproteinases and thereby potentiates wrinkle formation. In addition to the pro-aging effects of miRNAs, the plausible antiaging activity of miR-146a that antagonized the UVA-induced inhibition of proliferation and suppressed aging-related genes (e.g., p21WAF-1, p16, and p53) through targeting Smad4 has also been noticed. Nevertheless, the role of miRNAs in skin aging is still not fully elucidated and needs to be further discovered and explained.

Physical robustness and resilience among long-lived female siblings: a comparison with sporadic long-livers.

Long-lived individuals are central in studies of healthy longevity. However, few pro-longevity factors have been identified, presumably because of “phenocopies”, i.e. individuals that live long by chance. Familial longevity cases may include less phenocopies than sporadic cases and provide better insights into longevity mechanisms. Here we examined whether long-lived female siblings have a better ability to avoid diseases at ages 65+ (proxy for “robustness”) and/or survive to extreme ages (proxy for “resilience”) compared to sporadic long-livers. A total of 1,156 long-lived female siblings were selected from three nationwide Danish studies and age-matched with sporadic long-lived female controls. Outcomes included cumulative incidence of common health disorders from age 65 and overall survival. Long-lived female siblings had lower risks of some but not all health conditions, most significantly, depression (OR=0.74; 95%CI=0.62-0.88), and less significantly hypertensive (OR=0.84; 95%CI=0.71-0.99) and cerebrovascular (OR=0.73; 95%CI=0.55-0.96) diseases. They also had consistently better survival to extreme ages (HR=0.71; 95%CI= 0.63-0.81) compared to sporadic long-livers. After adjustment for the diseases, the association with mortality changed only marginally suggesting central role of better physiological resilience in familial longevity. Due to their consistently better resilience, familial longevity cases could be more informative than sporadic cases for studying mechanisms of healthy longevity.

Epidemics as an adaptive driving force determining lifespan setpoints

Species-specific limits to lifespan (lifespan setpoint) determine the life expectancy of any given organism. Whether limiting lifespan provides an evolutionary benefit or is the result of an inevitable decline in fitness remains controversial. The identification of mutations extending lifespan suggests that aging is under genetic control, but the evolutionary driving forces limiting lifespan have not been defined. By examining the impact of lifespan on pathogen spread in a population, we propose that epidemics drive lifespan setpoints' evolution. Shorter lifespan limits infection spread and accelerates pathogen clearance when compared to populations with longer-lived individuals. Limiting longevity is particularly beneficial in the context of zoonotic transmissions, where pathogens must undergo adaptation to a new host. Strikingly, in populations exposed to pathogens, shorter-living variants outcompete individuals with longer lifespans. We submit that infection outbreaks can contribute to control the evolution of species' lifespan setpoints.

Silencing and Silence: Language and Specialized Listening in a Long-Term Institution for the Elderly

This article presents the result of research developed with the language of elderly residents at the Long Term Care Facility for the Elderly - ILPI, in Vitória da Conquista, Bahia, Brazil. In response to the initial questions as to whether institutionalization affects the language of the elderly, whether the re-signification of verbal by non-verbal speech occurs, and whether silence, as language is part of an alternative system of possible meaning for the elderly, it was perceived that language in institutionalized long-lived individuals it reveals that in response to diversified processes of silencing, they have instituted silence as a possibility of reframing, and structuring of meaning. We collected data through the filming and recording of the elderly in enunciative-discursive situations, considering the uniqueness of each subject's history and their respective crossings as well as the condition of production of the narratives based on the concept of data-finding by Maria HadlerCoudry (1), aligned with notions relevant to Linguistics in the theoretical-methodological perspective of Discursive Neurolinguistics.

Intergenerational transmission of longevity is not affected by other familial factors: evidence from 16,905 Dutch families from Zeeland, 1812-1962

ABSTRACT Studies have shown that long-lived individuals seem to pass their survival advantage on to their offspring. Offspring of long-lived parents had a lifelong survival advantage over individuals without long-lived parents, making them more likely to become long-lived themselves. We test whether the survival advantage enjoyed by offspring of long-lived individuals is explained by environmental factors. 101,577 individuals from 16,905 families in the 1812–1886 Zeeland cohort were followed over time. To prevent that certain families were overrepresented in our data, disjoint family trees were selected. Offspring was included if the age at death of both parents was known. Our analyses show that multiple familial resources are associated with survival within the first 5 years of life, with stronger maternal than paternal effects. However, between ages 5 and 100 both parents contribute equally to offspring’s survival chances. After age 5, offspring of long-lived fathers and long-lived mothers had a 16-19% lower chance of dying at any given point in time than individuals without long-lived parents. This survival advantage is most likely genetic in nature, as it could not be explained by other, tested familial resources and is transmitted equally by fathers and mothers.

The longevity-associated variant of BPIFB4 improves a CXCR4-mediated striatum\u2013microglia crosstalk preventing disease progression in a mouse model of Huntington\u2019s disease

The longevity-associated variant (LAV) of the bactericidal/permeability-increasing fold-containing family B member 4 (BPIFB4) has been found significantly enriched in long-living individuals. Neuroinflammation is a key player in Huntington’s disease (HD), a neurodegenerative disorder caused by neural death due to expanded CAG repeats encoding a long polyglutamine tract in the huntingtin protein (Htt). Herein, we showed that striatal-derived cell lines with expanded Htt (STHdh Q111/111) expressed and secreted lower levels of BPIFB4, when compared with Htt expressing cells (STHdh Q7/7), which correlated with a defective stress response to proteasome inhibition. Overexpression of LAV-BPIFB4 in STHdh Q111/111 cells was able to rescue both the BPIFB4 secretory profile and the proliferative/survival response. According to a well-established immunomodulatory role of LAV-BPIFB4, conditioned media from LAV-BPIFB4-overexpressing STHdh Q111/111 cells were able to educate Immortalized Human Microglia—SV40 microglial cells. While STHdh Q111/111 dying cells were ineffective to induce a CD163 + IL-10high pro-resolving microglia compared to normal STHdh Q7/7, LAV-BPIFB4 transduction promptly restored the central immune control through a mechanism involving the stromal cell-derived factor-1. In line with the in vitro results, adeno-associated viral-mediated administration of LAV-BPIFB4 exerted a CXCR4-dependent neuroprotective action in vivo in the R6/2 HD mouse model by preventing important hallmarks of the disease including motor dysfunction, body weight loss, and mutant huntingtin protein aggregation. In this view, LAV-BPIFB4, due to its pleiotropic ability in both immune compartment and cellular homeostasis, may represent a candidate for developing new treatment for HD.

Age-related epigenetic drift deregulates SIRT6 expression and affects its downstream genes in human peripheral blood mononuclear cells

ABSTRACT Sirtuin 6 (SIRT6) exerts a protective effect on health and extends the lives of model organisms. We, therefore, aimed to clarify whether age-related epigenetic drift is responsible for differences in SIRT6 expression in peripheral blood mononuclear cells (PBMCs) of healthy young (n = 55, mean age 27.5 ± 4.4 years), middle-aged (n = 51, 65.4 ± 3.3 years), and long-lived (n = 51, 93.9 ± 3.6 years) humans. In silico analysis was performed using the STRING network. No age-related differences were observed in the percentage of SIRT6 CpG island methylation. However, the age affected the expression of miR-34a-5p, miR-125a-5p, miR-186-5p, miR-342-5p and miR-766-3p (all p < 0.0001), miR-181-2-3p and Let-7c (both p = 0.0003), and miR-103a-3p (p = 0.0069). A negative association was observed between SIRT6 mRNA and miR-186-5p (rs = −0.25, p = 0.026), and a positive association was observed with miR-34a-5p (rs = 0.31, p = 0.0055) and miR-181a-2-3p (rs = 0.39, p = 0.0002). SIRT6 mRNA also negatively correlated with the expression of TP53 (rs = −0.41, p = 0.0126) and MYC (rs = −0.35, p = 0.0448). Notably, the expression of several miRNAs and genes was similar in young and long-lived groups but different from the middle-aged group. We conclude that age-related epigenetic changes can affect the expression of SIRT6 in PBMCs and, in this way, possibly influence immunosenescence. Moreover, molecular events could differentiate ‘normal’ ageing from that of long-lived individuals.

Resilience in Very Advanced Ages: A Study With Centenarians.

This study intends to assess the relationship between resilience in extremely long-lived individuals and sociodemographic, cognitive and health status variables, and significant life events. A selected sample of 48 centenarians (mean age = 100.8 years, SD = 1.2; 83.3% female) from two centenarian studies was considered. A resilience score covering five items (aging and usefulness, hopefulness, worryness, loneliness, and control) was considered. Multivariable linear regression analyses were conducted in order to identify predictors of resilience. No significant differences in the resilience score regarding sociodemographic variables or typology of significant life events were found. Our findings underscore that health perception (better) and pain (less frequent) were associated with higher levels of resilience. In being present in extremely long-lived individuals, resilience should be object of interest in further research.

Circulating BPIFB4 Levels Associate With and Influence the Abundance of Reparative Monocytes and Macrophages in Long Living Individuals.

Long-Living Individuals (LLIs) delay aging and are less prone to chronic inflammatory reactions. Whether a distinct monocytes and macrophages repertoire is involved in such a characteristic remains unknown. Previous studies from our group have shown high levels of the host defense BPI Fold Containing Family B Member 4 (BPIFB4) protein in the peripheral blood of LLIs. Moreover, a polymorphic variant of the BPIFB4 gene associated with exceptional longevity (LAV-BPIFB4) confers protection from cardiovascular diseases underpinned by low-grade chronic inflammation, such as atherosclerosis. We hypothesize that BPIFB4 may influence monocytes pool and macrophages skewing, shifting the balance toward an anti-inflammatory phenotype. We profiled circulating monocytes in 52 LLIs (median-age 97) and 52 healthy volunteers (median-age 55) using flow cytometry. If the frequency of total monocyte did not change, the intermediate CD14++CD16+ monocytes counts were lower in LLIs compared to control adults. Conversely, non-classical CD14+CD16++ monocyte counts, which are M2 macrophage precursors with an immunomodulatory function, were found significantly associated with the LLIs' state. In a differentiation assay, supplementation of the LLIs' plasma enhanced the capacity of monocytes, either from LLIs or controls, to acquire a paracrine M2 phenotype. A neutralizing antibody against the phosphorylation site (ser 75) of BPIFB4 blunted the M2 skewing effect of the LLIs' plasma. These data indicate that LLIs carry a peculiar anti-inflammatory myeloid profile, which is associated with and possibly sustained by high circulating levels of BPIFB4. Supplementation of recombinant BPIFB4 may represent a novel means to attenuate inflammation-related conditions typical of unhealthy aging.

Multi-Omics Analysis of Diabetic Heart Disease in the db/db Model Reveals Potential Targets for Treatment by a Longevity-Associated Gene.

Characterisation of animal models of diabetic cardiomyopathy may help unravel new molecular targets for therapy. Long-living individuals are protected from the adverse influence of diabetes on the heart, and the transfer of a longevity-associated variant (LAV) of the human BPIFB4 gene protects cardiac function in the db/db mouse model. This study aimed to determine the effect of LAV-BPIFB4 therapy on the metabolic phenotype (ultra-high-performance liquid chromatography-mass spectrometry, UHPLC-MS) and cardiac transcriptome (next-generation RNAseq) in db/db mice. UHPLC-MS showed that 493 cardiac metabolites were differentially modulated in diabetic compared with non-diabetic mice, mainly related to lipid metabolism. Moreover, only 3 out of 63 metabolites influenced by LAV-BPIFB4 therapy in diabetic hearts showed a reversion from the diabetic towards the non-diabetic phenotype. RNAseq showed 60 genes were differentially expressed in hearts of diabetic and non-diabetic mice. The contrast between LAV-BPIFB4- and vehicle-treated diabetic hearts revealed eight genes differentially expressed, mainly associated with mitochondrial and metabolic function. Bioinformatic analysis indicated that LAV-BPIFB4 re-programmed the heart transcriptome and metabolome rather than reverting it to a non-diabetic phenotype. Beside illustrating global metabolic and expressional changes in diabetic heart, our findings pinpoint subtle changes in mitochondrial-related proteins and lipid metabolism that could contribute to LAV-BPIFB4-induced cardio-protection in a murine model of type-2 diabetes.

The Role of Matrix Metalloproteinases (MMP-2 and MMP-9) in Ageing and Longevity: Focus on Sicilian Long-Living Individuals (LLIs).

Extracellular matrix metalloproteinases (MMPs) are a group of proteins that activate substrates by enzymatic cleavage and, on the basis of their activities, have been demonstrated to play a role in ageing. Thus, in order to gain insight into the pathophysiology of ageing and to identify new markers of longevity, we analysed the activity levels of MMP-2 and MMP-9 in association with some relevant haematochemical parameters in a Sicilian population, including long-living individuals (LLIs, ≥95 years old). A cohort of 154 healthy subjects (72 men and 82 women) of different ages (age range 20-112) was recruited. The cohort was divided into five subgroups: the first group with subjects less than 40 years old, the second group ranging from 40 to 64 years old, the third group ranging from 65 to 89 years old, the fourth group ranging from 90 to 94 years old, and the fifth group with subjects more than 95 years old. A relationship was observed between LLIs and MMP-2, but not between LLIs and MMP-9. However, in the LLI group, MMP-2 and MMP-9 values were significantly correlated. Furthermore, in LLIs, we found a positive correlation of MMP-2 with the antioxidant catabolite uric acid and a negative correlation with the inflammatory marker C-reactive protein. Finally, in LLIs MMP-9 values correlated directly both with cholesterol and with low-density lipoproteins. On the whole, our data suggest that the observed increase of MMP-2 in LLIs might play a positive role in the attainment of longevity. This is the first study that shows that serum activity of MMP-2 is increased in LLIs as compared to younger subjects. As far as we are concerned, it is difficult to make wide-ranging conclusions/assumptions based on these observations in view of the relatively small sample size of LLIs. However, this is an important starting point. Larger-scale future studies will be required to clarify these findings including the link with other systemic inflammatory and antioxidant markers.

Aspectos relevantes do silêncio para a construção do sentido em dados de uma idosa moradora de uma instituição de longa permanência

O objetivo deste artigo é apresentar um recorte da pesquisa desenvolvida com a linguagem de idosos moradores na Instituição de Longa Permanência para Idosos – ILPI, em Vitória da Conquista, Bahia, Brasil. Os dados foram coletados a partir de filmagem e gravação dos idosos em meio a situações enunciativo-discursivas, considerando a história dos sujeitos e seus atravessamentos, bem como a condição de produção desses discursos e o conceito de dado-achado (COUDRY, 1988). Neste artigo, apresentamos a análise de dados referentes ao silêncio que ocorre em sessões com uma das moradoras dessa ILPI. Para tanto, recorremos ao pensamento sobre o silêncio a partir de diferentes áreas, como: da Música, da Filosofia, da Psicanálise e da Análise do Discurso, enquanto disciplina de entremeio da Linguística, com conceitos relevantes para este trabalho. Apesar de serem áreas distintas, observamos que compartilham para o fato que o silêncio não é o zero, vazio, o que nos leva a interpretâ-lo como sentido. Assim, consideramos, por meio das análises, que o silêncio permeia cada signo e se infla de sentido, e que, quando está só, por si só, significa, possibilitando o sujeito institucionalizado rememorar momentos de dependência, (re)elaborar seus desejos, suas respostas.

Cohort Differences in the Associations of Selected Candidate Genes With Risk of All-Cause Mortality at Advanced Ages.

Considerable efforts have been made to identify the genetic basis of human longevity, with only limited progress. One important drawback of current genetic studies is the limited knowledge of gene-environment interaction. Using 2 cohorts of long-lived individuals born in 1905 and 1915 in Denmark, we performed survival analysis to estimate risk of mortality for major candidate genes of aging and longevity and their cohort effects. Through statistical modeling that combines individual genetic and survival information with cohort-specific survival data, we estimated the relative risks of mortality from ages 95 to 103 years associated with genetic variants in apolipoprotein E (APOE), forkhead box class O3a, clusterin, and phosphatidylinositol binding clathrin assembly protein. Our analysis estimated a decreased risk of carrying the APOE$\varepsilon $4 allele (change in risk=-0.403, 95% confidence interval (CI): -0.831, 0.021; P=0.040) in men of the later cohort, although the allele itself was harmful to survival across sexes (relative risk=1.161, 95% CI: 1.027, 1.345; P=0.026). We also estimated a cohort effect of increased risk for the minor allele of rs3851179 in phosphatidylinositol binding clathrin assembly protein with borderline significance (change in risk=0.165, 95% CI: -0.010, 0.331; P=0.052) in women. Our estimated significant cohort effect on APOE$\varepsilon $4 is indicative of the interplay between the gene and the changing environment that modulates survival at extreme ages.

Exceptionally Long-Lived Individuals (ELLI) Demonstrate Slower Aging Rate Calculated by DNA Methylation Clocks as Possible Modulators for Healthy Longevity.

Exceptionally long-lived individuals (ELLI) who are the focus of many healthy longevity studies around the globe are now being studied in Israel. The Israeli Multi-Ethnic Centenarian Study (IMECS) cohort is utilized here for assessment of various DNA methylation clocks. Thorough phenotypic characterization and whole blood samples were obtained from ELLI, offspring of ELLI, and controls aged 53–87 with no familial exceptional longevity. DNA methylation was assessed using Illumina MethylationEPIC Beadchip and applied to DNAm age online tool for age and telomere length predictions. Relative telomere length was assessed using qPCR T/S (Telomere/Single copy gene) ratios. ELLI demonstrated juvenile performance in DNAm age clocks and overall methylation measurement, with preserved cognition and relative telomere length. Our findings suggest a favorable DNA methylation profile in ELLI enabling a slower rate of aging in those individuals in comparison to controls. It is possible that DNA methylation is a key modulator of the rate of aging and thus the ELLI DNAm profile promotes healthy longevity.

Evaluation of the influence of nutritional status, measures of frailty and level of physical activity on the quality of life of long-lived individuals

Abstract Introduction: Aging is a worldwide phenomenon that has favored an increase in people aged 80 years and older. Objective: To assess the influence of nutritional status (NS), measures of frailty, and physical activity level (PAL) on the quality of life (QoL) of long-lived people. Method: The study was carried out from Oct 2016 to Sept 2017 with 103 individuals aged 80 years or more. NS was classified according to the PAHO Health, Well-Being and Aging (SABE) survey; waist circumference (WC) and calf perimeter (CP) was based on the WHO classification; handgrip strength (HGS) and gait speed (GS) used the classification proposed by Lauretani; PAL was classified according to the IPAQ short form; the WHOQoL-bref and WHOQoL-old were applied to measure QOL. Variables were assessed using the Mann-Whitney U and t-tests. Results: 69.2% were women, with an average age of 82.75 (± 2.98) years, and only WC showed a significant association (p &lt;0.001). The older women without dynapenia exhibited better QoL in the physical domain (p = 0.004), social relationships (p = 0.022), self-reported QoL (p = 0.017) of the WHOQoL-bref and social participation facet (p = 0.025) of WHOQOL-old. Comparison of QoL with NS and PAL showed a significant difference in self-reported QoL (p = 0.027) for the former and past, present and future activities for the latter (p = 0.050). Conclusion: Obesity and the absence of dynapenia were positively associated with the QoL of long-lived individuals. PAL was associated with positive QoL in one facet of the WHOQoL-old.

Disentangling environmental from individual factors in isotopic ecology: A 17-year longitudinal study in a long-lived seabird exploiting the Canary Current

Abstract Despite its importance for ecology and conservation, we are still far from understanding how environmental variability interacts with intrinsic factors and individual specialization to determine trophic strategies of long-lived taxa, mostly due to difficulties in studying the same animals over extended periods. Here, by yearly consistently sampling the first primary feather of 99 Cory’s shearwaters (Calonectris borealis) foraging in the Canary Current (CC) upwelling ecosystem, we provide robust evidence on the individual changes of isotopic ratios of carbon (δ13C) and nitrogen (δ15N) over 17 years. We reported a slight longitudinal decline of δ13C values throughout 2001–2017, even after being adjusted for the marine Suess effect (linked to the increasing CO2 emissions). Although CC is often considered to be overexploited by industrial fisheries, we could not detect a decline in Cory’s shearwater trophic level indicating a change in the trophic web structuring, as revealed by δ15N. We found negative correlations of δ13C and δ15N with the CC upwelling intensity, indicating annual variability in baseline isotopic levels propagates through the food chain and it integrates in predators’ tissues. Low individual repeatabilities among years at population level indicates low long-term specialization, suggesting long-lived individuals foraging on highly productive areas can adjust their foraging strategies and diet according to environmental variability. However, individual-level repeatabilities in isotopic values showed a range of individual specialization within the population, indicating most individuals are generalist and a few of them highly specialized. First, although we found a clear influence of the upwelling intensity on the trophic ecology of birds, we could not detect any temporal trend in the trophic level of the Cory’s shearwater population, suggesting a stability in the structure of the pelagic food web of the CC over the last two decades despite the fishing pressure. Second, the existence of individual specialization highlights the importance of considering the repeated sampling of individuals to detect small changes in the trophic ecology of a population. Finally, the coexistence of individuals with different degree of specialization (from extremely flexible [generalists] to highly consistent individuals [specialists]) within a population can have deep implications on the capacity of populations to cope with environmental change.

Differential response to larval crowding of a long- and a short-lived medfly biotype.

Response of endophytic fruit fly species (Tephritidae) to larval crowding is a form of scramble competition that may affect important life history traits of adults, such as survival and reproduction. Recent empirical evidence demonstrates large differences in adult life history traits, especially longevity, among Mediterranean fruit fly (Ceratitis capitata; "medfly") biotypes obtained from different regions of the world. However, whether the evolution of long lifespan is associated with response to stress induced by larval crowding has not been fully elucidated. We investigated, under constant laboratory conditions, the response of a short- and a long-lived medfly biotypes to stress induced by larval crowding. Survival and development of larvae and pupae and the size of resulting pupae were recorded. The lifespan and age-specific egg production patterns of the obtained adults were recorded. Our findings reveal that increased larval density reduced immature survival (larvae and pupae) in the short-lived biotype but had rather neutral effects on the longed-lived one. Only larvae of the long-lived biotype were capable of prolonging their developmental duration under the highest crowding regime to successfully pupate and emerge as adults. Response of emerging adults to larvae crowding conditions was similar in the two medfly biotypes. Those individuals emerging from high larval density regimes had reduced longevity and fecundity. Long-lived biotype individuals, however, appeared to suffer a higher cost in longevity compared with the short-lived one. The importance of our findings to understand the evolution of long lifespan is discussed.