A life course approach for understanding later life sustainability

Author(s):  
Holly Syddall ◽  
Avan Aihie Sayer

This chapter describes a life course approach for understanding later life sustainability, focusing on grip strength as a marker of physical sustainability, and explaining how a life course approach recognizes that muscle strength in later life reflects not only rate of loss in later life, but also the peak attained earlier in life. We present evidence that risk factors operating throughout the life course have an impact on physical sustainability in later life with particular consideration of the effects of body size, socioeconomic position, physical activity, diet, and smoking. We have shown that low birth weight is associated with weaker grip strength across the life course and that there is considerable evidence for developmental influences on ageing skeletal muscle. Finally, a life course approach suggests opportunities for early intervention to promote later life physical sustainability; but optimal strategies and timings for intervention are yet to be identified.

Author(s):  
Richard Dodds ◽  
Holly Syddall ◽  
Avan Aihie Sayer

This chapter describes a life course approach for understanding later life sustainability, focusing on grip strength as a marker of physical sustainability, and explaining how a life course approach recognizes that muscle strength in later life reflects not only rate of loss in later life, but also the peak attained earlier in life. We present evidence that risk factors operating throughout the life course have an impact on physical sustainability in later life with particular consideration of the effects of body size, socioeconomic position, long-term conditions, physical activity, diet, and smoking. We have shown that low birth weight is associated with weaker grip strength across the life course and that there is considerable evidence for developmental influences on ageing skeletal muscle. Finally, a life course approach suggests opportunities for early intervention to promote later life physical sustainability; but optimal strategies and timings for intervention are yet to be identified.


Author(s):  
Ruth Bell ◽  
Michael Marmot

A long and healthy life is universally valued. The starkest inequalities in later life are how many years of life remain at an older age such as 65 years, and how many years of life that remain free from disabilities that impede physical, cognitive, and social functioning to the extent that they limit the sense of valuing one’s life. In this chapter we apply the frame of social determinants of health, using the life course approach to understand inequalities in health in later life. Healthy ageing is patterned by degrees of social advantage. Biological ageing, as revealed by physical and cognitive changes, is slower in people in better socioeconomic circumstances. These inequalities in health in later life need to be understood in terms of current social, economic, environmental conditions of living, as well as previous experiences and living conditions across the life course that affect the biological processes of ageing.


Author(s):  
Yoav Ben-Shlomo

The demographic changes experienced globally mean that the 21st century faces the challenge of caring for an ageing population. Without preventative measures, this will be further aggravated by the successes of medical technologies which continue to reduce case fatality and hence add to the multi-morbid nature of older populations. A life-course approach to ageing conceptualizes the different trajectories by which traits may decline before leading to clinical disease or disability. It highlights gaps in our current understanding of the drivers of such trajectories and periods where the timing of adverse exposures may have a disproportionate negative or positive impact on later life outcomes. This is illustrated with a wide variety of examples and applied to neurodegenerative disorders such as dementia. Future primary and secondary preventative measures must consider interventions across the whole of the life course.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Yiyi Zhang ◽  
Eric Vittinghoff ◽  
Mark J Pletcher ◽  
Norrina B Allen ◽  
Adina Zeki Al Hazzouri ◽  
...  

Introduction: Cumulative exposure to cardiovascular disease (CVD) risk factors during young adulthood is associated with later life CVD risk. Few prospective cohort studies measured exposures in young adulthood. We sought to develop and validate a method to impute trajectories of CVD risk factors across the life course. Methods: 36,546 participants (55% women, 25% black, average exams 5.1/participant) from 6 studies (ARIC, CARDIA, CHS, Framingham Offspring, Health ABC, and MESA) were included. Demographics and CVD risk factors (BMI, smoking, BP, lipids, glucose, medications for BP, lipids and glucose) were collected at each exam and harmonized across cohorts. We multiply imputed complete risk factor trajectories from age 18 to 99 years for each participant using an extension of linear mixed modeling (for continuous variables) and interval-censored survival modeling (for categorical variables), taking into account the multilevel structure of data. For validation, we randomly selected 25% of all participants and deleted their observed data for exam age 20-35, 50-65, or 80-95 years. We then imputed risk factor values for deleted age periods and compared imputed values with directly observed values. Results: Imputed values were relatively consistent with observed values for BMI, SBP, LDL, and glucose, particularly in young and middle ages ( Figure ). The mean (standard deviation) of the difference between imputed vs. observed values for BMI, SBP, LDL, and glucose were 0.1 (2.7) kg/m 2 , 0.9 (16.3) mm Hg, -1.1 (30.2) mg/dL, and -0.6 (23.0) mg/dL. The prevalence of imputed smoking, diabetes, and medications were also consistent with observed data. Conclusions: We demonstrated a validated method for estimating CVD risk factor trajectories across the life course. This approach may advance understanding of potential impact of cumulative early risk factor exposures on later life CVD risk, and inform primary prevention strategies over the life course. Figure. Mean and prevalence of observed vs. imputed risk factors by age periods 2


2017 ◽  
Vol 5 (2) ◽  
pp. 107-119
Author(s):  
Hollie Nyseth Brehm ◽  
Christopher Uggen ◽  
Suzy McElrath

We argue in this article that the study of genocide would benefit from the application and use of theoretical tools that criminologists have long had at their disposal, specifically, conception and theorization surrounding the life course. Using the 1994 Genocide Against the Tutsi as a case study, we detail how the building blocks of life-course criminology can be effectively used in analyses of (1) risk factors for the onset of genocide, (2) trajectories and duration of genocidal violence, and (3) desistance from genocidal crime and transitions after genocide. We conclude by highlighting the conceptual gains for research on genocide and political conflict by briefly discussing the analytic implications for future genocide research.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C.C Topriceanu ◽  
J.C Moon ◽  
R Hardy ◽  
A.D Hughes ◽  
N Chaturvedi ◽  
...  

Abstract Background Cardiovascular diseases are an important component of the multi-morbidity syndrome which is associated with negative health outcomes resulting in a major societal economic burden. An objective way to assess multi-morbidity is to calculate a frailty index based on medical deficit accumulation. Late-life frailty has been validated to predict mortality, but little is known about the association between life-course frailty and cardiovascular health in later-life. Purpose To study the association between life-course frailty and later-life heart size and function using data from the world's longest running birth cohort with continuous follow-up. Methods A 45-deficit frailty index (FI) was calculated at 4 age-intervals across the life-course (0 to 16 years old, 19 to 44 years old, 45 to 54 years old and 60 to 64 years old) in participants from the UK 1946 Medical Research Council (MRC) National Survey of Heath and Development (NSHD) birth cohort. The life-course frailty indices (FI0_16, FI19_44, FI45_54 and FI60_64) reflect the cumulative medical deficits at the corresponding age-intervals. They were used to derive FImean and FIsum reflecting overall-life frailty. The step change in deficit accumulation between age-intervals was also calculated (FI2-1, FI3-1, FI4-1, FI3-2, FI4-2, FI4-3). Echocardiographic data at 60–64 years provided: E/e' ratio, ejection fraction (EF), myocardial contraction fraction index (MCFi) and left ventricular mass index (LVmassi). Generalized linear mixed models with gamma distribution and log link assessed the association between FIs and echo parameters after adjustment for sex, socio-economic position and body mass index. Results 1.805 NSHD participants were included (834 male). Accumulation of a single deficit had a significant impact (p<0.0001 to p<0.049) on LVmassi and MCFi in all the life-course FIs and overall FIs. LVmassi increased by 0.89% to 1.42% for the life-course FIs and by 0.36%/1.82% for FIsum and FImean respectively. MCFi decreased by 0.62% to 1.02% for the life-course FIs and by 0.33%/ 1.04%. for FIsum and FImean respectively. One accumulated deficit translated into higher multiplicative odds (13.2 for FI60-64, 2.1 for FI4-1, 75.4 for FI4-2 and 78.5 for FI4-3) of elevated filling pressure (defined as E/e' ratio >13, p<0.0.005 to p<0.02).A unit increase in frailty decreased LV EF (%) by 11%/12% for FI45-54 and FI60-64 respectively, by 10% to 12% for FI2-1, FI3-1, FI4-1 and FI4-2, and 4%/15% for FIsum and FImean respectively (p<0.0014 to p<0.044). Conclusion Frailty during the life-course, overall life-frailty and the step change in deficit accumulation is associated with later-life cardiac dysfunction. Frailty strain appears to have its greatest impact on pathological myocardial hypertrophy (high LVmassi and low MCFi) potentially paving the way to later-life systolic or diastolic dysfunction in susceptible individuals. Funding Acknowledgement Type of funding source: None


BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Saira Khan ◽  
K. Y. Wolin ◽  
R. Pakpahan ◽  
R. L. Grubb ◽  
G. A. Colditz ◽  
...  

Abstract Background Existing evidence suggests that there is an association between body size and prevalent Benign Prostatic Hyperplasia (BPH)-related outcomes and nocturia. However, there is limited evidence on the association between body size throughout the life-course and incident BPH-related outcomes. Methods Our study population consisted of men without histories of prostate cancer, BPH-related outcomes, or nocturia in the intervention arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) (n = 4710). Associations for body size in early- (age 20), mid- (age 50) and late-life (age ≥ 55, mean age 60.7 years) and weight change with incident BPH-related outcomes (including self-reported nocturia and physician diagnosis of BPH, digital rectal examination-estimated prostate volume ≥ 30 cc, and prostate-specific antigen [PSA] concentration > 1.4 ng/mL) were examined using Poisson regression with robust variance estimation. Results Men who were obese in late-life were 25% more likely to report nocturia (Relative Risk (RR): 1.25, 95% Confidence Interval (CI): 1.11–1.40; p-trendfor continuous BMI < 0.0001) and men who were either overweight or obese in late-life were more likely to report a prostate volume ≥ 30 cc (RRoverweight: 1.13, 95% CI 1.07–1.21; RRobese: 1.10, 95% CI 1.02–1.19; p-trendfor continuous BMI = 0.017) as compared to normal weight men. Obesity at ages 20 and 50 was similarly associated with both nocturia and prostate volume ≥ 30 cc. Considering trajectories of body size, men who were normal weight at age 20 and became overweight or obese by later-life had increased risks of nocturia (RRnormal to overweight: 1.09, 95% CI 0.98–1.22; RRnormal to obese: 1.28, 95% CI 1.10–1.47) and a prostate volume ≥ 30 cc (RRnormal to overweight: 1.12, 95% CI 1.05–1.20). Too few men were obese early in life to examine the independent effect of early-life body size. Later-life body size modified the association between physical activity and nocturia. Conclusions We found that later-life body size, independent of early-life body size, was associated with adverse BPH outcomes, suggesting that interventions to reduce body size even late in life can potentially reduce the burden of BPH-related outcomes and nocturia.


2015 ◽  
Vol 25 (3) ◽  
pp. 313 ◽  
Author(s):  
Taylor W. Hargrove, MA ◽  
Tyson H. Brown, PhD

<br clear="all" /><p> </p><p> <strong>Objective: </strong>Previous research has docu­mented a relationship between childhood socioeconomic conditions and adult health, but less is known about racial/ethnic dif­ferences in this relationship, particularly among men. This study utilizes a life course approach to investigate racial/ethnic differ­ences in the relationships among early and later life socioeconomic circumstances and health in adulthood among men.</p><p><strong>Design: </strong>Panel data from the Health and Retirement Study and growth curve models are used to examine group differences in the relationships among childhood and adult socioeconomic factors and age-tra­jectories of self-rated health among White, Black and Mexican American men aged 51-77 years (<em>N</em>=4147).</p><p><strong>Results: </strong>Multiple measures of childhood socioeconomic status (SES) predict health in adulthood for White men, while significant­ly fewer measures of childhood SES predict health for Black and Mexican American men. Moreover, the health consequences of childhood SES diminish with age for Black and Mexican American men. The child­hood SES-adult health relationship is largely explained by measures of adult SES for White men.</p><p><strong>Conclusion: </strong>The life course pathways link­ing childhood SES and adult health differ by race/ethnicity among men. Similar to argu­ments that the universality of the adult SES-health relationship should not be assumed, results from our study suggest that scholars should not assume that the significance and nature of the association between child­hood SES and health in adulthood is similar across race/ethnicity among men.<em> Ethn Dis.</em>2015;25(3):313-320.</p>


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