Early development, stress and depression across the life course: pathways to depression in a national British birth cohort

2014 ◽  
Vol 44 (13) ◽  
pp. 2845-2854 ◽  
Author(s):  
I. Colman ◽  
P. B. Jones ◽  
D. Kuh ◽  
M. Weeks ◽  
K. Naicker ◽  
...  

BackgroundThe aetiology of depression is multifactorial, with biological, cognitive and environmental factors across the life course influencing risk of a depressive episode. There is inconsistent evidence linking early life development and later depression. The aim of this study was to investigate relationships between low birthweight (LBW), infant neurodevelopment, and acute and chronic stress as components in pathways to depression in adulthood.MethodThe sample included 4627 members of the National Survey of Health and Development (NSHD; the 1946 British birth cohort). Weight at birth, age of developmental milestones, economic deprivation in early childhood, acute stressors in childhood and adulthood, and socio-economic status (SES) in adulthood were assessed for their direct and indirect effects on adolescent (ages 13 and 15 years) and adult (ages 36, 43 and 53 years) measures of depressive symptoms in a structural equation modelling (SEM) framework. A structural equation model developed to incorporate all variables exhibited excellent model fit according to several indices.ResultsThe path of prediction from birthweight to age of developmental milestones to adolescent depression/anxiety to adult depression/anxiety was significant (p < 0.001). Notably, direct paths from birthweight (p = 0.25) and age of developmental milestones (p = 0.23) to adult depression were not significant. Childhood deprivation and stressors had important direct and indirect effects on depression. Stressors in adulthood were strongly associated with adult depression.ConclusionsDepression in adulthood is influenced by an accumulation of stressors across the life course, including many that originate in the first years of life. Effects of early-life development on mental health appear by adolescence.

2021 ◽  
pp. 095269512199539
Author(s):  
Penny Tinkler ◽  
Resto Cruz ◽  
Laura Fenton

Birth cohort studies can be used not only to generate population-level quantitative data, but also to recompose persons. The crux is how we understand data and persons. Recomposition entails scavenging for various (including unrecognised) data. It foregrounds the perspective and subjectivity of survey participants, but without forgetting the partiality and incompleteness of the accounts that it may generate. Although interested in the singularity of individuals, it attends to the historical and relational embeddedness of personhood. It examines the multiple and complex temporalities that suffuse people’s lives, hence departing from linear notions of the life course. It implies involvement, as well as reflexivity, on the part of researchers. It embraces the heterogeneity and transformations over time of scientific archives and the interpretive possibilities, as well as incompleteness, of birth cohort studies data. Interested in the unfolding of lives over time, it also shines light on meaningful biographical moments.


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&lt;0.0001 to p&lt;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 &gt;13, p&lt;0.0.005 to p&lt;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&lt;0.0014 to p&lt;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.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Constantin-Cristian Topriceanu ◽  
James C. Moon ◽  
Rebecca Hardy ◽  
Nishi Chaturvedi ◽  
Alun D. Hughes ◽  
...  

AbstractA frailty index (FI) counts health deficit accumulation. Besides traditional risk factors, it is unknown whether the health deficit burden is related to the appearance of cardiovascular disease. In order to answer this question, the same multidimensional FI looking at 45-health deficits was serially calculated per participant at 4 time periods (0–16, 19–44, 45–54 and 60–64 years) using data from the 1946 Medical Research Council (MRC) British National Survey of Health and Development (NSHD)—the world’s longest running longitudinal birth cohort with continuous follow-up. From these the mean and total FI for the life-course, and the step change in deficit accumulation from one time period to another was derived. Echocardiographic data at 60–64 years provided: ejection fraction (EF), left ventricular mass indexed to body surface area (LVmassi, BSA), myocardial contraction fraction indexed to BSA (MCFi) and E/e′. Generalized linear models assessed the association between FIs and echocardiographic parameters after adjustment for relevant covariates. 1375 participants were included. For each single new deficit accumulated at any one of the 4 time periods, LVmassi increased by 0.91–1.44% (p < 0.013), while MCFi decreased by 0.6–1.02% (p < 0.05). A unit increase in FI at age 45–54 and 60–64, decreased EF by 11–12% (p < 0.013). A single health deficit step change occurring between 60 and 64 years and one of the earlier time periods, translated into higher odds (2.1–78.5, p < 0.020) of elevated LV filling pressure. Thus, the accumulation of health deficits at any time period of the life-course associates with a maladaptive cardiac phenotype in older age, dominated by myocardial hypertrophy and poorer function.


Author(s):  
Eric Molin

This paper presents and discusses a structural equation model on hydrogen acceptance. This model unravels the direct and indirect effects among personal characteristics, knowledge about hydrogen, perceptions, attitudes, and willingness to use hydrogen applications. In addition, indicators of differently colored information that can be provided by mass media have been included as explanatory variables. The estimated model indicates that colored information directly influences perceptions of hydrogen and indirectly influences attitudes about hydrogen and willingness to use it. In particular, negatively colored information decreases hydrogen acceptance, which cannot be counterbalanced by providing positively colored information. Furthermore, the model suggests that more factual knowledge about hydrogen increases its acceptance. The paper further discusses the likely development of hydrogen acceptance in the future and how practitioners can influence this.


2020 ◽  
Author(s):  
Constantin-Cristian Topriceanu ◽  
James C Moon ◽  
Rebecca Hardy ◽  
Nishi Chaturvedi ◽  
Alun Hughes ◽  
...  

Aim: To study the association between the life course accumulation of health deficits and later life heart size and function using data from the 1946 National Survey of Heath and Development (NSHD) British birth cohort, the longest running birth cohort with continuous follow up in the world. Methods and Results: A multidimensional health deficit index (DI) looking at 45 health deficits was serially calculated at 4 time periods of the life course in NSHD participants (0 to 16, 19 to 44, 45 to 54 and 60 to 64 years), and from these the mean and total DI for the life course was derived (DImean, DIsum). The step change in deficit accumulation from one time period to another was also calculated. Echocardiographic data at 60-64 years provided: ejection fraction (EF), left ventricular mass indexed to body surface area (LVmassi, BSA), myocardial contraction fraction indexed to BSA (MCFi) and E/e. Generalized linear models assessed the association between DIs and echocardiographic parameters after adjustment for sex, socioeconomic position and body mass index. 1,375 NSHD participants were included (46.47% male). For each single new deficit accumulated at any one of the 4 time periods of the life course, LVmassi increased by 0.91 to 1.44% (p<0.013), while MCFi decreased by 0.6 to 1.02% (p<0.05 except at 45 to 54 years). One unit increase in DI at age 45 to 54 and 60 to 64 decreased LV EF by 11 to 12% (p<0.013). A single deficit step change occurring between 60-64 years and one of the earlier time periods, translated into significantly higher odds (2.1 to 78.5, p<0.020) of elevated LV filling pressure defined as E/e>13. Conclusion: The accumulation of health deficits at any time period of the life course associates with a maladaptive cardiac phenotype in older age, dominated by myocardial hypertrophy and poorer function. The burden of health deficits appears to strain the myocardium potentially leading to future cardiac dysfunction. Keywords: frailty; cardiovascular disease; ejection fraction; left ventricular mass index; myocardial contraction fraction; E/e.


2020 ◽  
Vol 11 (1) ◽  
pp. 27-54
Author(s):  
Amy Heshmati ◽  
Gita D Mishra ◽  
Anna Goodman ◽  
Ilona Koupil

Socio-economic position (SEP) is associated with all-cause mortality across all stages of the life course; however, it is valuable to distinguish at what time periods SEP has the most influence on mortality. Our aim was to investigate whether the effect of SEP on all-cause mortality accumulates over the life course or if some periods of the life course are more important. Our study population were from the Uppsala Birth Cohort Multigenerational Study, born 1915–29 at Uppsala University Hospital, Sweden. We followed 3,951 men and 3,601 women who had SEP at birth available, during childhood (at age ten), in adulthood (ages 30–45) and in later life (ages 50–65) from 15 September 1980 until emigration, death or until 31 December 2010. We compared a set of nested Cox proportional regression models, each corresponding to a specific life course model (critical, sensitive and accumulation models), to a fully saturated model, to ascertain which model best describes the relationship between SEP and mortality. Analyses were stratified by gender. For both men and women the effect of SEP across the life course on all-cause mortality is best described by the sensitive period model, whereby being advantaged in later life (ages 50–65 years) provides the largest protective effect. However, the linear accumulation model also provided a good fit of the data for women suggesting that improvements in SEP at any stage of the life course corresponds to a decrease in all-cause mortality.


2020 ◽  
Vol 11 (2) ◽  
pp. 157-180
Author(s):  
Matthew H. Iveson ◽  
Chris Dibben ◽  
Ian J. Deary

Older adults are particularly prone to function-limiting health issues that adversely affect their well-being. Previous work has identified factors from across the life course –childhood socio-economic status, childhood cognitive ability and education – that predict later-life functional outcomes. However, the independence of these contributions is unclear as later-in-the-life-course predictors are themselves affected by earlier ones. The present study capitalised on the recent linkage of the Scottish Mental Survey 1947 with the Scottish Longitudinal Study, using path analyses to examine the direct and indirect associations between life-course predictors and the risk of functional limitation at ages 55 (N = 2,374), 65 (N = 1,971) and 75 (N = 1,534). The odds of reporting a function-limiting long-term condition increased across later life. At age 55, reporting a functional limitation was significantly less likely in those with higher childhood socio-economic status, higher childhood cognitive ability and higher educational attainment; these associations were only partly mediated by other predictors. At age 65, adult socio-economic status emerged as a mediator of several associations, although direct associations with childhood socio-economic status and childhood cognitive ability were still observed. At age 75, only childhood socio-economic status and adult socio-economic status directly predicted the risk of a functional limitation, particularly those associated with disease or illness. A consistent pattern and direction of associations was observed with self-rated health more generally. These results demonstrate that early-life and adult circumstances are associated with functional limitations later in life, but that these associations are partly a product of complex mediation between life-course factors.


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