Life course psychological distress and cardiovascular disease risk factors in middle age: birth cohort study.
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ABSTRACT:
SUBMITTER: Batty GD
PROVIDER: S-EPMC8632781 | biostudies-literature | 2021 Jan
REPOSITORIES: biostudies-literature
Publications
Life course psychological distress and cardiovascular disease risk factors in middle age: birth cohort study.
Batty G D GD Hamer Mark M Gale Catharine R CR
Cardiovascular research 20210101 2
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Project description:Early life factors, like intelligence and socioeconomic status (SES), are associated with health outcomes in adulthood. Fitting comprehensive life-course models, we tested (1) the effect of childhood intelligence and SES, education and adulthood SES on psychological distress at midlife, and (2) compared alternative measurement specifications (reflective and formative) of SES. Prospective cohort study (the Aberdeen Children of the 1950s). Aberdeen, Scotland. 12 500 live-births (6282 boys) between 1950 and 1956, who were followed up in the years 2001-2003 at age 46-51 with a postal questionnaire achieving a response rate of 64% (7183). Psychological distress at age 46-51 (questionnaire). Childhood intelligence and SES and education had indirect effects on psychological distress at midlife, mediated by adult SES. Adult SES was the only variable to have a significant direct effect on psychological distress at midlife; the effect was stronger in men than in women. Alternative measurement specifications of SES (reflective and formative) resulted in greatly different model parameters and fits. Even though formative operationalisations of SES are theoretically appropriate, SES is better specified as reflective than as a formative latent variable in the context of life-course modelling.
| S-EPMC3651977 | biostudies-literature
Project description:BackgroundExposure to prenatal maternal psychological distress may contribute to the development of childhood atopic disorders. Little is known about the importance of distress severity and its duration for the risk. Our aim was to investigate how chronic maternal depressive and anxiety symptoms across gestation influence the risk of wheezing and eczema at child age 24 months.MethodsThe study population was drawn from the FinnBrain Birth Cohort Study, including 1305 mother-infant dyads followed across gestation until the child age of 24 months when the outcomes were mother-reported wheezing ever and doctor-diagnosed eczema. To investigate the risk of wheezing phenotypes, wheezing with and without eczema was separated. Maternal distress was assessed with the Edinburgh Postnatal Depression Scale for depressive and the Symptom Checklist-90 for anxiety symptoms three times during pregnancy, and the chronicity was demonstrated using symptom trajectories composed by latent growth mixture modeling.ResultsOf the children, 219/1305 (17%) had wheezing ever and 285/1276 (22%) had eczema. Risk of wheezing ever was elevated with maternal consistently high depressive symptoms (adjusted odds ratio 2.74; 95% confidence interval 1.37-5.50) or moderate and increasing anxiety symptoms (1.94; 1.06-3.54, respectively). Similarly, wheezing without eczema was associated with consistently high depressive (3.60; 1.63-7.94, respectively) and moderate and increasing anxiety symptoms (2.43; 1.21-4.91, respectively).ConclusionsMaternal chronic psychological distress across gestation was associated with toddler wheezing and especially wheezing without other atopic features (eczema). This finding supports the theory of intrauterine programming effect by maternal psychological distress on offspring immune system and respiratory morbidity.
| S-EPMC9299775 | biostudies-literature
Project description:BackgroundStudies of body mass index and semen quality have reported mixed results, but almost all were cross-sectional and many were conducted in selected populations. Longitudinal studies in population-based cohorts are necessary to identify how timing and duration of excess adiposity may affect semen quality.MethodsIn 193 members of the Child Health and Development Studies birth cohort, we examined associations of birth weight and adiposity at six time points spanning early childhood and adulthood with sperm concentration, motility, and morphology at mean age 44 years, as well as with corresponding 2010 World Health Organization (WHO) subfertility reference levels.ResultsBirth weight for gestational age percentile was positively associated with square-root sperm concentration (regression coefficient B [95% confidence interval] = 0.02 × 103 sperm/ml [0.004, 0.04]). Overweight/obesity in men's 20s was associated with lower percent progressive motility (B =-5.2 [-9.9, -0.63]), higher odds of low motility (odds ratio (OR) = 2.4 [1.3, 4.4]), and higher odds of poor morphology (OR = 1.9 [0.94, 3.8]). Those who were overweight/obese in their 20s were also more likely to meet two or three WHO subfertility criteria (OR = 3.9 [1.6, 9.4]) compared with normal-weight men. Each additional adult decade in which a participant was overweight/obese was associated with higher odds of low motility (OR = 1.3 [0.96, 1.6]) and higher odds of meeting two or three WHO subfertility criteria (OR = 1.5 [1.0, 2.2]).ConclusionsIn our data, associations among adiposity and sperm concentration, motility, and morphology varied according to timing and duration of exposure, potentially reflecting different biological mechanisms that influence these semen parameters.
| S-EPMC7055633 | biostudies-literature
Project description:ObjectiveCardiovascular risk factors (CVRFs) are associated with increased risk of cognitive decline, but little is known about how early adult CVRFs and those across the life course might influence late-life cognition. To test the hypothesis that CVRFs across the adult life course are associated with late-life cognitive changes, we pooled data from 4 prospective cohorts (n = 15,001, ages 18-95).MethodsWe imputed trajectories of body mass index (BMI), fasting glucose (FG), systolic blood pressure (SBP), and total cholesterol (TC) for older adults. We used linear mixed models to determine the association of early adult, midlife, and late-life CVRFs with late-life decline on global cognition (Modified Mini-Mental State Examination [3MS]) and processing speed (Digit Symbol Substitution Test [DSST]), adjusting for demographics, education, and cohort.ResultsElevated BMI, FG, and SBP (but not TC) at each time period were associated with greater late-life decline. Early life CVRFs were associated with the greatest change, an approximate doubling of mean 10-year decline (an additional 3-4 points for 3MS or DSST). Late-life CVRFs were associated with declines in early late life (<80 years) but with gains in very late life (≥80 years). After adjusting for CVRF exposures at all time periods, the associations for early adult and late-life CVRFs persisted.ConclusionsWe found that imputed CVRFs across the life course, especially in early adulthood, were associated with greater late-life cognitive decline. Our results suggest that CVRF treatment in early adulthood could benefit late-life cognition, but that treatment in very late life may not be as helpful for these outcomes.
| S-EPMC8166431 | biostudies-literature
Project description:OBJECTIVE:To evaluate the association between growth trajectories from birth to adolescence and cardiovascular risk marker levels at age 18 years in a population-based cohort. In order to disentangle the effect of weight gain from that of height gain, growth was analysed using conditional weight relative to linear growth (CWh) and conditional length/height (CH). DESIGN:Prospective study. SETTING:1993 Pelotas birth cohort, Southern Brazil. PARTICIPANTS:Individuals who have been followed up from birth to adolescence (at birth, 1, 4, 11, 15 and 18 years). PRIMARY OUTCOME MEASURES:C-reactive protein (CRP), total cholesterol (TC), LDL cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides (TGL), systolic and diastolic blood pressure (SBP and DBP), body mass index (BMI) and waist circumference (WC). RESULTS:In both sexes, greater CWh at 1 year was positively associated with BMI and WC, whereas greater CWh at most age periods in childhood and adolescence predicted higher CRP, TC, LDL-C, TGL, SBP, DBP, BMI and WC levels, as well as lower HDL-C level. Higher CH during infancy and childhood was positively related with SBP in boys and girls, and with BMI and WC only in boys. CONCLUSION:Our study shows that rapid weight gain from 1 year onwards is positively associated with several markers of cardiovascular risk at 18 years. Overall, our results for the first year of life add evidence to the 'first 1000 days initiative' suggesting that prevention of excessive weight gain in childhood might be important in reducing subsequent cardiovascular risk.
| S-EPMC5786082 | biostudies-literature
Project description:BackgroundIn designing prevention strategies, it may be useful to understand how early and midlife cardiovascular disease risk factor (CVDRF) exposures affect outcomes that primarily occur in mid to late life. Few single US cohorts have followed participants from early adulthood to late life.MethodsWe pooled four prospective cohorts that represent segments of the adult life course, and studied 15 001 White and Black adults aged 18 to 95 years at enrollment. We imputed early and midlife exposure to body mass index (BMI), glucose, lipids and blood pressure (BP). CVDRF trajectories were estimated using linear mixed models. Using the best linear unbiased predictions, we obtained person-specific estimates of CVDRF trajectories beginning at age 20 until each participant's end of follow-up. We then calculated for each CVDRF, summary measures of early and midlife exposure as time-weighted averages (TWAs).ResultsIn the pooled cohort, 33.7% were Black and 54.8% were female. CVDRF summary measures worsened in midlife compared with early life and varied by sex and race. In particular, systolic and diastolic BP were consistently higher over the adult life course among men, and BMI was higher among Blacks, particularly Black women. Simulation studies suggested acceptable imputation accuracy, especially for the younger cohorts. Correlations of true and imputed CVDRF summary measures ranged from 0.53 to 0.99, and agreement ranged from 67% to 99%.ConclusionsThese results suggest that imputed CVDRFs may be accurate enough to be useful in assessing the effects of early and midlife exposures on later life outcomes.
| S-EPMC6659365 | biostudies-literature
Project description:While the associations of mid-life cardiovascular risk factors with late-life white matter lesions (WMH) and cognitive decline have been established, the role of cerebral haemodynamics is unclear. We investigated the relation of late-life (69-71 years) arterial spin labelling (ASL) MRI-derived cerebral blood flow (CBF) with life-course cardiovascular risk factors (36-71 years) and late-life white matter hyperintensity (WMH) load in 282 cognitively healthy participants (52.8% female). Late-life (69-71 years) high systolic (B = -0.15) and diastolic (B = -0.25) blood pressure, and mean arterial pressure (B = -0.25) were associated with low grey matter (GM) CBF (p < 0.03), and white matter CBF (B = -0.25; B = -0.15; B = -0.13, p < 0.03, respectively). The association between systolic blood pressure and GM CBF differed between sexes (male/female B = -0.15/0.02, p = 0.04). No associations were found with early- or mid-life cardiovascular risk factors. Furthermore, WMHs were associated with cerebral haemodynamics but not cardiovascular risk factors. These findings suggest that cerebral blood flow autoregulation is able to maintain stable global cerebral haemodynamics until later in life. Future studies are encouraged to investigate why cardiovascular risk factors have differential effects on haemodynamics and WMH, and their implications for cognitive decline.
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Project description: Not available
| S-EPMC6208281 | biostudies-literature
Project description:BackgroundA neuroimaging-based biomarker termed the brain age is thought to reflect variability in the brain's ageing process and predict longevity. Using Insight 46, a unique narrow-age birth cohort, we aimed to examine potential drivers and correlates of brain age.MethodsParticipants, born in a single week in 1946 in mainland Britain, have had 24 prospective waves of data collection to date, including MRI and amyloid PET imaging at approximately 70 years old. Using MRI data from a previously defined selection of this cohort, we derived brain-predicted age from an established machine-learning model (trained on 2001 healthy adults aged 18-90 years); subtracting this from chronological age (at time of assessment) gave the brain-predicted age difference (brain-PAD). We tested associations with data from early life, midlife, and late life, as well as rates of MRI-derived brain atrophy.FindingsBetween May 28, 2015, and Jan 10, 2018, 502 individuals were assessed as part of Insight 46. We included 456 participants (225 female), with a mean chronological age of 70·7 years (SD 0·7; range 69·2 to 71·9). The mean brain-predicted age was 67·9 years (8·2, 46·3 to 94·3). Female sex was associated with a 5·4-year (95% CI 4·1 to 6·8) younger brain-PAD than male sex. An increase in brain-PAD was associated with increased cardiovascular risk at age 36 years (β=2·3 [95% CI 1·5 to 3·0]) and 69 years (β=2·6 [1·9 to 3·3]); increased cerebrovascular disease burden (1·9 [1·3 to 2·6]); lower cognitive performance (-1·3 [-2·4 to -0·2]); and increased serum neurofilament light concentration (1·2 [0·6 to 1·9]). Higher brain-PAD was associated with future hippocampal atrophy over the subsequent 2 years (0·003 mL/year [0·000 to 0·006] per 5-year increment in brain-PAD). Early-life factors did not relate to brain-PAD. Combining 12 metrics in a hierarchical partitioning model explained 33% of the variance in brain-PAD.InterpretationBrain-PAD was associated with cardiovascular risk, and imaging and biochemical markers of neurodegeneration. These findings support brain-PAD as an integrative summary metric of brain health, reflecting multiple contributions to pathological brain ageing, and which might have prognostic utility.FundingAlzheimer's Research UK, Medical Research Council Dementia Platforms UK, Selfridges Group Foundation, Wolfson Foundation, Wellcome Trust, Brain Research UK, Alzheimer's Association.
| S-EPMC10499760 | biostudies-literature
Project description:ObjectiveWith there being an apparent impact of experience of out-of-home care in childhood on chronic disease and mortality, we examined how such adversity might be embodied such that it has a measurable impact on human biology, so mediating this relationship.MethodsWe used data from the UK National Child Development Study in which exposure to public care was prospectively gathered on three occasions up to age 16. Study members also participated in a social survey at age 42 and a clinical examination at age 44/45 when cardiovascular, inflammatory, neuroendocrine, and respiratory risk markers for mortality were collected, 19 of which were included as endpoints in the present analyses.ResultsOf the 8012 participants in the biomedical survey, 4% (n = 322) had been in care at some point in childhood and/or adolescence. We found the expected marked differences in the early life characteristics of poverty, health, and disability in children with experience of public care relative to their unexposed counterparts. After controlling for these confounding factors, however, care in childhood was essentially unrelated to biomarkers in middle-age. We also found no consistent links between these biomarkers and the duration, timing, or type of care.ConclusionsOur results suggest that the biomarkers captured in the present study are unlikely to mediate the link between public care in childhood and later chronic disease or mortality. Processes involving mental health, socioeconomic position, and health behaviors would seem to be a potential alternative pathway warranting investigation.
| S-EPMC7317568 | biostudies-literature