scholarly journals Effects of early-life competition and maternal nutrition on telomere lengths in wild meerkats

2017 ◽  
Vol 284 (1861) ◽  
pp. 20171383 ◽  
Author(s):  
Dominic L. Cram ◽  
Pat Monaghan ◽  
Robert Gillespie ◽  
Tim Clutton-Brock

Early-life adversity can affect health, survival and fitness later in life, and recent evidence suggests that telomere attrition may link early conditions with their delayed consequences. Here, we investigate the link between early-life competition and telomere length in wild meerkats. Our results show that, when multiple females breed concurrently, increases in the number of pups in the group are associated with shorter telomeres in pups. Given that pups from different litters compete for access to milk, we tested whether this effect is due to nutritional constraints on maternal milk production, by experimentally supplementing females' diets during gestation and lactation. While control pups facing high competition had shorter telomeres, the negative effects of pup number on telomere lengths were absent when maternal nutrition was experimentally improved. Shortened pup telomeres were associated with reduced survival to adulthood, suggesting that early-life competition for nutrition has detrimental fitness consequences that are reflected in telomere lengths. Dominant females commonly kill pups born to subordinates, thereby reducing competition and increasing growth rates of their own pups. Our work suggests that an additional benefit of infanticide may be that it also reduces telomere shortening caused by competition for resources, with associated benefits for offspring ageing profiles and longevity.

2019 ◽  
Author(s):  
Eli D Strauss ◽  
Daizaburo Shizuka ◽  
Kay E Holekamp

AbstractSocial rank has been identified as a significant determinant of fitness in a variety of species. The importance of social rank suggests that the process by which juveniles come to establish their position in the social hierarchy is a critical component of social development. Here, we use the highly predictable process of rank acquisition in spotted hyenas to study the consequences of variation in rank acquisition in early life. In spotted hyenas, rank is ‘inherited’ through a learning process called ‘maternal rank inheritance.’ This pattern is highly predictable: ~80% of juveniles acquire the exact rank predicted by the rules of maternal rank inheritance. This predictable nature of rank acquisition in these societies allows the process of rank acquisition to be studied independently from the ultimate rank that each juvenile attains. In this study, we use a novel application of the Elo-rating method to calculate each juvenile’s deviation from expected pattern of maternal rank inheritance during development. Despite variability in rank acquisition in juveniles, most of these juveniles come to attain the exact rank expected of them according to the rules of maternal rank inheritance. Nevertheless, we find that transient variation in rank acquisition in early life predicts long term fitness consequences for these individuals: juveniles ‘underperforming’ their expected ranks show reduced survival and lower lifetime reproductive success than better-performing peers. Finally, we present evidence that this variability in rank acquisition in early life represents a source of early life adversity, and that multiple sources of early life adversity have cumulative, but not compounding, effects on fitness.


2021 ◽  
Vol 9 ◽  
Author(s):  
Dennis Hasselquist ◽  
Michael Tobler

Mild diseases and moderate stressors are seemingly harmless and are therefore often assumed to have negligible impact on Darwinian fitness. Here we argue that the effects of “benign” parasites and other moderate stressors may have a greater impact on lifespan and other fitness traits than generally thought. We outline the “accumulating costs” hypothesis which proposes that moderate strains on the body caused by mild diseases and other moderate stressors that occur throughout life will result in small irreversible “somatic lesions” that initially are invisible (i.e., induce “hidden” costs). However, over time these somatic lesions accumulate until their summed effect reaches a critical point when cell senescence and malfunction begin to affect organ functionality and lead to the onset of degenerative diseases and aging. We briefly discuss three potential mechanisms through which the effects of moderate strains (e.g., mild diseases) could accumulate: Accelerated telomere shortening, loss of repetitious cell compartments and other uncorrected DNA damage in the genome. We suggest that telomere shortening may be a key candidate for further research with respect to the accumulating costs hypothesis. Telomeres can acquire lesions from moderate strains without immediate negative effects, lesions can be accumulated over time and lead to a critically short telomere length, which may eventually cause severe somatic malfunctioning, including aging. If effects of mild diseases, benign parasites and moderate stressors accrued throughout life can have severe delayed consequences, this might contribute to our understanding of life history strategies and trade-offs, and have important implications for medicine, including consideration of treatment therapies for mild (chronic) infections such as malaria.


2015 ◽  
Vol 282 (1798) ◽  
pp. 20141610 ◽  
Author(s):  
Daniel Nettle ◽  
Pat Monaghan ◽  
Robert Gillespie ◽  
Ben Brilot ◽  
Thomas Bedford ◽  
...  

Adverse experiences in early life can exert powerful delayed effects on adult survival and health. Telomere attrition is a potentially important mechanism in such effects. One source of early-life adversity is the stress caused by competitive disadvantage. Although previous avian experiments suggest that competitive disadvantage may accelerate telomere attrition, they do not clearly isolate the effects of competitive disadvantage from other sources of variation. Here, we present data from an experiment in European starlings ( Sturnus vulgaris ) that used cross-fostering to expose siblings to divergent early experience. Birds were assigned either to competitive advantage (being larger than their brood competitors) or competitive disadvantage (being smaller than their brood competitors) between days 3 and 12 post-hatching. Disadvantage did not affect weight gain, but it increased telomere attrition, leading to shorter telomere length in disadvantaged birds by day 12. There were no effects of disadvantage on oxidative damage as measured by plasma lipid peroxidation. We thus found strong evidence that early-life competitive disadvantage can accelerate telomere loss. This could lead to faster age-related deterioration and poorer health in later life.


2018 ◽  
Vol 373 (1741) ◽  
pp. 20160438 ◽  
Author(s):  
Melissa Bateson ◽  
Daniel Nettle

Individual differences in telomere length are associated with individual differences in behaviour in humans and birds. Within the human epidemiological literature this association is assumed to result from specific behaviour patterns causing changes in telomere dynamics. We argue that selective adoption—the hypothesis that individuals with short telomeres are more likely to adopt specific behaviours—is an alternative worthy of consideration. Selective adoption could occur either because telomere length directly affects behaviour or because behaviour and telomere length are both affected by a third variable, such as exposure to early-life adversity. We present differential predictions of the causation and selective adoption hypotheses and describe how these could be tested with longitudinal data on telomere length. Crucially, if behaviour is causal then it should be associated with differential rates of telomere attrition. Using smoking behaviour as an example, we show that the evidence that smoking accelerates the rate of telomere attrition within individuals is currently weak. We conclude that the selective adoption hypothesis for the association between behaviour and telomere length is both mechanistically plausible and, if anything, more compatible with existing empirical evidence than the hypothesis that behaviour is causal. This article is part of the theme issue ‘Understanding diversity in telomere dynamics’.


2019 ◽  
Author(s):  
Mary Elizabeth Zinn ◽  
Edward Huntley ◽  
Daniel Keating

Introduction. Early life adversity (ELA) can result in negative health-outcomes, including psychopathology. Evidence suggests that adolescence is a critical developmental period for processing ELA. Identity formation, which is crucial to this developmental period, may moderate the effect between ELA and psychopathology. One potential moderating variable associated with identity formation is Prospective Self, a latent construct comprised of future-oriented attitudes and behaviors.Methods. Participants are from the first wave of an ongoing longitudinal study designed to characterize behavioral and cognitive correlates of risk behavior trajectories. A community sample of 10th and 12th grade adolescents (N = 2017, 55% female) were recruited from nine public school districts across eight Southeastern Michigan counties in the United States. Data were collected in schools during school hours or after school via self-report, computer-administered surveys. Structural equation modeling was used in the present study to assess Prospective Self as a latent construct and to evaluate the relationship between ELA, psychopathology, and Prospective Self.Results. Preliminary findings indicated a satisfactory fit for the construct Prospective Self. The predicted negative associations between Prospective Self and psychopathology were found and evidence of moderation was observed for externalizing behavior problems, such that the effects of ELA were lower for individuals with higher levels of Prospective Self. Conclusion. These results support the role of Prospective Self in conferring resilience against externalizing behavior problems associated with ELA among adolescents. Keywords: Adolescence, Adverse Childhood Experiences, Psychopathology, Self-concept, Adolescent Health, Early Life Adversity


Author(s):  
Meg Dennison ◽  
Katie McLaughlin

Early-life adversity is associated with elevated risk for a wide range of mental disorders across the lifespan, including those that involve disruptions in positive emotionality. Although extensive research has evaluated heightened negative emotionality and threat processing as developmental mechanisms linking early-life adversity with mental health problems, emerging evidence suggests that positive emotions play an integral, but complex, role in the association of early-life adversity with psychopathology. This chapter identifies two pathways through which positive emotion influences risk for psychopathology following early-life adversity. First, experiences of early-life adversity may alter the development of the “positive valence system”, which in turn increases risk for psychopathology. Second, the association between adversity and psychopathology may vary as a function of individual differences in positive emotionality. We consider how the development of positive emotionality—measured at psychological, behavioral and neurobiological levels—may be altered by early-life adversity, creating a diathesis for psychopathology. We additionally review evidence for the role of positive emotion, measured at multiple levels, as a protective factor that buffers against the adverse impacts of adversity. In integrating these two roles, it is proposed that characteristics of environmental adversity, including developmental timing, duration, and type of adversity, may differentially impact the development of positive emotionality, leading to a better understanding of risks associated with specific adverse experiences. Methodological issues regarding the measurement of adverse environments as well as implications for early intervention and treatment are discussed.


Sign in / Sign up

Export Citation Format

Share Document