scholarly journals Association of early- and adult-life socioeconomic circumstances with muscle strength in older age

2018 ◽  
Vol 47 (3) ◽  
pp. 398-407 ◽  
Author(s):  
Boris Cheval ◽  
Matthieu P Boisgontier ◽  
Dan Orsholits ◽  
Stefan Sieber ◽  
Idris Guessous ◽  
...  

Abstract Background socioeconomic circumstances (SEC) during a person’s lifespan influence a wide range of health outcomes. However, solid evidence of the association of early- and adult-life SEC with health trajectories in ageing is still lacking. This study assessed whether early-life SEC are associated with muscle strength in later life—a biomarker of health—and whether this relationship is caused by adult-life SEC and health behaviours. Methods we used data from the Survey of Health Ageing and Retirement in Europe, a 12-year population-based cohort study with repeated measurement in six waves (2004–15) and retrospective collection of life-course data. Participants’ grip strength was assessed by using a handheld dynamometer. Confounder-adjusted logistic mixed-effect models were used to examine the associations of early- and adult-life SEC with the risk of low muscle strength (LMS) in older age. Results a total of 24,179 participants (96,375 observations) aged 50–96 living in 14 European countries were included in the analyses. Risk of LMS was increased with disadvantaged relative to advantaged early-life SEC. The association between risk of LMS and disadvantaged early-life SEC gradually decreased when adjusting for adult-life SEC for both sexes and with unhealthy behaviours for women. After adjusting for these factors, all associations between risk of LMS and early-life SEC remained significant for women. Conclusion early-life SEC are associated with muscle strength after adjusting for adult-life SEC and behavioural lifestyle factors, especially in women, which suggests that early life may represent a sensitive period for future health.

2018 ◽  
Vol 74 (7) ◽  
pp. 1134-1140 ◽  
Author(s):  
Boris Cheval ◽  
Clovis Chabert ◽  
Dan Orsholits ◽  
Stefan Sieber ◽  
Idris Guessous ◽  
...  

Abstract Background Poor lung function in late life may stem from early-life risk factors, but the epidemiological evidence is inconsistent. We investigated whether individuals who experienced disadvantageous socioeconomic circumstances (SEC) in early life showed lower levels of respiratory function in older age, a steeper decline over time, and whether these relationships were explained by adult-life SEC, body mass index, and physical inactivity in older age. Methods We used data from the Survey of Health Ageing and Retirement in Europe (2004–2015). Participants’ peak expiratory flow (PEF) was assessed with a mini-Wright peak flow meter at second, fourth, and sixth waves. Confounder-adjusted linear mixed-effect models were used to examine the associations between early-life SEC and PEF in older age. A total of 21,734 adults aged 50–96 years (46,264 observations) were included in the analyses. Results Older adults with disadvantaged early-life SEC showed lower levels of PEF compared with those with advantaged early-life SEC. The association between early-life SEC and late-life PEF persisted after adjusting for adult-life SEC, smoking, physical inactivity, and body mass index. PEF declined with age, but the effect of early-life SEC on this decline was not consistent across robustness and sensitivity analyses. Conclusions Early life is a sensitive period for respiratory health. Further considering the effect of SEC arising during this period may improve the prevention of chronic respiratory diseases.


2020 ◽  
Vol 375 (1802) ◽  
pp. 20190468 ◽  
Author(s):  
Federico Cappa ◽  
Alessandro Cini ◽  
Lisa Signorotti ◽  
Rita Cervo

Social recognition represents the foundation of social living. To what extent social recognition is hard-wired by early-life experience or flexible and influenced by social context of later life stages is a crucial question in animal behaviour studies. Social insects have represented classic models to investigate the subject, and the acknowledged idea is that relevant information to create the referent template for nest-mate recognition (NMR) is usually acquired during an early sensitive period in adult life. Experimental evidence, however, highlighted that other processes may also be at work in creating the template and that such a template may be updated during adult life according to social requirements. However, currently, we lack an ad hoc experiment testing the alternative hypotheses at the basis of NMR ontogeny in social insects. Thus, to investigate the mechanisms underlying the ontogeny of NMR in Polistes wasps, a model genus in recognition studies, and their different role in determining recognition abilities, we subjected Polistes dominula workers to different olfactory experiences in different phases of their life before inserting them into the social environment of a novel colony and testing them in recognition bioassays. Our results show that workers develop their NMR abilities based on their social context rather than through pre-imaginal and early learning or self-referencing. Our study demonstrates that the social context represents the major component shaping recognition abilities in a social wasp, therefore shedding new light on the ontogeny of recognition in paper wasps and prompting the reader to rethink about the traditional knowledge at the basis of the recognition in social insects. This article is part of the theme issue ‘Signal detection theory in recognition systems: from evolving models to experimental tests'.


2016 ◽  
Vol 30 (5) ◽  
pp. 438-455 ◽  
Author(s):  
Mathew A. Harris ◽  
Caroline E. Brett ◽  
John M. Starr ◽  
Ian J. Deary ◽  
Wendy Johnson

Recent observations that personality traits are related to later–life health and wellbeing have inspired considerable interest in exploring the mechanisms involved. Other factors, such as cognitive ability and education, also show longitudinal influences on health and wellbeing, but it is not yet clear how all these early–life factors together contribute to later–life health and wellbeing. In this preliminary study, we assessed hypothesised relations among these variables across the life course, using structural equation modelling in a sample assessed on dependability (a personality trait related to conscientiousness) in childhood, cognitive ability and social class in childhood and older age, education, and health and subjective wellbeing in older age. Our models indicated that both health and subjective wellbeing in older age were influenced by childhood IQ and social class, via education. Some older–age personality traits mediated the effects of early–life variables, on subjective wellbeing in particular, but childhood dependability did not show significant associations. Our results therefore did not provide evidence that childhood dependability promotes older–age health and wellbeing, but did highlight the importance of other early–life factors, particularly characteristics that contribute to educational attainment. Further, personality in later life may mediate the effects of early–life factors on health and subjective wellbeing. © 2016 The Authors. European Journal of Personality published by John Wiley & Sons Ltd on behalf of European Association of Personality Psychology


2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.


2019 ◽  
Vol 78 (3) ◽  
pp. 305-312 ◽  
Author(s):  
Mark A. Burton ◽  
Karen A. Lillycrop

Non-communicable diseases (NCD) such as type-2 diabetes and CVD are now highly prevalent in both developed and developing countries. Evidence from both human and animal studies shows that early-life nutrition is an important determinant of NCD risk in later life. The mechanism by which the early-life environment influences future disease risk has been suggested to include the altered epigenetic regulation of gene expression. Epigenetic processes regulate the accessibility of genes to the cellular proteins that control gene transcription, determining where and when a gene is switched on and its level of activity. Epigenetic processes not only play a central role in regulating gene expression but also allow an organism to adapt to the environment. In this review, we will focus on how both maternal and paternal nutrition can alter the epigenome and the evidence that these changes are causally involved in determining future disease risk.


2019 ◽  
Vol 374 (1785) ◽  
pp. 20190283 ◽  
Author(s):  
S. M. Géranton

Animal behaviours are affected not only by inherited genes but also by environmental experiences. For example, in both rats and humans, stressful early-life events such as being reared by an inattentive mother can leave a lasting trace and affect later stress response in adult life. This is owing to a chemical trace left on the chromatin attributed to so-called epigenetic mechanisms. Such an epigenetic trace often has consequences, sometimes long-lasting, on the functioning of our genes, thereby allowing individuals to rapidly adapt to a new environment. One gene under such epigenetic control is FKBP5 , the gene that encodes the protein FKPB51, a crucial regulator of the stress axis and a significant driver of chronic pain states. In this article, we will discuss the possibility that exposure to stress could drive the susceptibly to chronic pain via epigenetic modifications of genes within the stress axis such as FKBP5 . The possibility that such modifications, and therefore, the susceptibility to chronic pain, could be transmitted across generations in mammals and whether such mechanisms may be evolutionarily conserved across phyla will also be debated. This article is part of the Theo Murphy meeting issue ‘Evolution of mechanisms and behaviour important for pain’.


2020 ◽  

At STIAS, the ‘Health in Transition’ theme includes a programme to address the epidemic rise in the incidence of non-communicable diseases (NCDs) such as Type 2 diabetes, hypertension, obesity, coronary heart disease and stroke in Africa. The aim is to advance awareness, research capacity and knowledge translation of science related to the Developmental Origins of Health and Disease (DOHaD) as a means of preventing NCDs in future generations. Application of DOHaD science is a promising avenue for prevention, as this field is identifying how health and nutrition from conception through the first 1 000 days of life can dramatically impact a developing individual’s future life course, and specifically predicate whether or not they are programmed in infancy to develop NCDs in later life. Prevention of NCDs is an essential strategy as, if unchecked, the burden of caring for a growing and ageing population with these diseases threatens to consume entire health budgets, as well as negatively impact the quality of life of millions. Africa in particular needs specific, focussed endeavors to realize the maximal preventive potential of DOHaD science, and a means of generating governmental and public awareness about the links between health in infancy and disease in adult life. This volume summarizes the expertise and experience of a leading group of international scientists led by Abdallah Daar brought together at STIAS as part of the ‘Health in Transition’ programme.


2021 ◽  
Vol 118 (3) ◽  
pp. e2010211118
Author(s):  
Leah S. Richmond-Rakerd ◽  
Avshalom Caspi ◽  
Antony Ambler ◽  
Tracy d’Arbeloff ◽  
Marieke de Bruine ◽  
...  

The ability to control one’s own emotions, thoughts, and behaviors in early life predicts a range of positive outcomes in later life, including longevity. Does it also predict how well people age? We studied the association between self-control and midlife aging in a population-representative cohort of children followed from birth to age 45 y, the Dunedin Study. We measured children’s self-control across their first decade of life using a multi-occasion/multi-informant strategy. We measured their pace of aging and aging preparedness in midlife using measures derived from biological and physiological assessments, structural brain-imaging scans, observer ratings, self-reports, informant reports, and administrative records. As adults, children with better self-control aged more slowly in their bodies and showed fewer signs of aging in their brains. By midlife, these children were also better equipped to manage a range of later-life health, financial, and social demands. Associations with children’s self-control could be separated from their social class origins and intelligence, indicating that self-control might be an active ingredient in healthy aging. Children also shifted naturally in their level of self-control across adult life, suggesting the possibility that self-control may be a malleable target for intervention. Furthermore, individuals’ self-control in adulthood was associated with their aging outcomes after accounting for their self-control in childhood, indicating that midlife might offer another window of opportunity to promote healthy aging.


2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Xinli Jiang ◽  
Huijie Ma ◽  
Yan Wang ◽  
Yan Liu

Type 2 diabetes mellitus (T2DM) is a multifactorial disease, and its aetiology involves a complex interplay between genetic, epigenetic, and environmental factors. In recent years, evidences from both human and animal experiments have correlated early life factors with programming diabetes risk in adult life. Fetal and neonatal period is crucial for organ development. Many maternal factors during pregnancy may increase the risk of diabetes of offsprings in later life, which include malnutrition, healthy (hyperglycemia and obesity), behavior (smoking, drinking, and junk food diet), hormone administration, and even stress. In neonates, catch-up growth, lactation, glucocorticoids administration, and stress have all been found to increase the risk of insulin resistance or T2DM. Unfavorable environments (socioeconomic situation and famine) or obesity also has long-term negative effects on children by causing increased susceptibility to T2DM in adults. We also address the potential mechanisms that may underlie the developmental programming of T2DM. Therefore, it might be possible to prevent or delay the risk for T2DM by improving pre- and/or postnatal factors.


Author(s):  
Myriam Merz ◽  
Jonathan D. Turner

There are many ‘faces’ of early life adversity (ELA), such as childhood trauma, institutionalization, abuse or exposure to environmental toxins. These have been implicated in the onset and severity of a wide range of chronic non-communicable diseases later in life. The later-life disease risk has a well-established immunological component. This raises the question as to whether accelerated immune-ageing mechanistically links early-life adversity to the lifelong health trajectory resulting in either ‘poor’ or ‘healthy’ ageing. Here we examine observational and mechanistic studies of ELA and inflammageing, highlighting common and distinct features in these two life stages. Many biological processes appear in common including reduction in telomere length, increased immuno-senescence, metabolic distortions and chronic (viral) infections. We propose that ELA shapes the developing immune, endocrine and nervous system in a non-reversible way, creating a distinct phenotype with accelerated immuno-senescence and systemic inflammation. We believe that ELA acts as an accelerator for inflammageing and age-related diseases. Furthermore, we now have the tools and cohorts to be able to dissect the interaction between early life adversity and later life phenotype. This should, in the near future, allow us to identify the ecological and mechanistic processes that are involved in ‘healthy’ or accelerated immune-ageing.


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