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Low social participation is a potentially modifiable risk factor for cognitive deterioration in the general population and related to lower quality of life (QoL). We aimed to find out whether social participation is linked to cognitive deterioration and QoL for people with borderline intellectual functioning and mild intellectual disability. We used data from the National Child Development Study, consisting of people born during one week in 1958, to compare midlife social participation in people with mild intellectual disability, borderline intellectual functioning, and without intellectual impairment. We defined social participation as 1. confiding/emotional support from the closest person and social network contact frequency at age 44, and 2. confiding relationships with anyone at age 50. We then assessed the extent to which social participation mediated the association between childhood intellectual functioning and cognition and QoL at age 50. 14,094 participants completed cognitive tests at age 11. People with borderline intellectual functioning and mild intellectual disability had more social contact with relatives and confiding/emotional support from their closest person, but fewer social contacts with friends and confiding relationships with anyone than those without intellectual disability. Having a confiding relationship partially mediated the association at age 50 between IQ and cognition (6.4%) and QoL (27.4%) for people with borderline intellectual functioning. We found adults with intellectual disability have positive family relationships but fewer other relationships. Even at the age of 50, confiding relationships may protect cognition for people with borderline intellectual functioning and are important for QoL.

We tested the association between APOE-ε4 and processing speed and memory between ages 43 and 69 in a population-based birth cohort. Analyses of processing speed (using a timed letter search task) and episodic memory (a 15-item word learning test) were conducted at ages 43, 53, 60–64 and 69 years using linear and multivariable regression, adjusting for gender and childhood cognition. Linear mixed models, with random intercepts and slopes, were conducted to test the association between APOE and the rate of decline in these cognitive scores from age 43 to 69. Model fit was assessed with the Bayesian Information Criterion. A cross-sectional association between APOE-ε4 and memory scores was detected at age 69 for both heterozygotes and homozygotes (β = −0.68 and β = −1.38, respectively, p = 0.03) with stronger associations in homozygotes; no associations were observed before this age. Homozygous carriers of APOE-ε4 had a faster rate of decline in memory between ages 43 and 69, when compared to non-carriers, after adjusting for gender and childhood cognition (β = −0.05, p = 0.04). There were no cross-sectional or longitudinal associations between APOE-ε4 and processing speed. We conclude that APOE-ε4 is associated with a subtly faster rate of memory decline from midlife to early old age; this may be due to effects of APOE-ε4 becoming manifest around the latter stage of life. Continuing follow-up will determine what proportion of this increase will become clinically significant.

Midlife hypertension confers increased risk for cognitive impairment in late life. The sensitive period for risk exposure and extent that risk is mediated through amyloid or vascular-related mechanisms are poorly understood. We aimed to identify if, and when, blood pressure or change in blood pressure during adulthood were associated with late-life brain structure, pathology, and cognition. Participants were from Insight 46, a neuroscience substudy of the ongoing longitudinal Medical Research Council National Survey of Health and Development, a birth cohort that initially comprised 5362 individuals born throughout mainland Britain in one week in 1946. Participants aged 69–71 years received T1 and FLAIR volumetric MRI, florbetapir amyloid-PET imaging, and cognitive assessment at University College London (London, UK); all participants were dementia-free. Blood pressure measurements had been collected at ages 36, 43, 53, 60–64, and 69 years. We also calculated blood pressure change variables between ages. Primary outcome measures were white matter hyperintensity volume (WMHV) quantified from multimodal MRI using an automated method, amyloid-β positivity or negativity using a standardised uptake value ratio approach, whole-brain and hippocampal volumes quantified from 3D-T1 MRI, and a composite cognitive score—the Preclinical Alzheimer Cognitive Composite (PACC). We investigated associations between blood pressure and blood pressure changes at and between 36, 43, 53, 60–64, and 69 years of age with WMHV using generalised linear models with a gamma distribution and log link function, amyloid-β status using logistic regression, whole-brain volume and hippocampal volumes using linear regression, and PACC score using linear regression, with adjustment for potential confounders. Between May 28, 2015, and Jan 10, 2018, 502 individuals were assessed as part of Insight 46. 465 participants (238 [51%] men; mean age 70·7 years [SD 0·7]; 83 [18%] amyloid-β-positive) were included in imaging analyses. Higher systolic blood pressure (SBP) and diastolic blood pressure (DBP) at age 53 years and greater increases in SBP and DBP between 43 and 53 years were positively associated with WMHV at 69–71 years of age (increase in mean WMHV per 10 mm Hg greater SBP 7%, 95% CI 1–14, p=0·024; increase in mean WMHV per 10 mm Hg greater DBP 15%, 4–27, p=0·0057; increase in mean WMHV per one SD change in SBP 15%, 3–29, p=0·012; increase in mean WMHV per 1 SD change in DBP 15%, 3–30, p=0·017). Higher DBP at 43 years of age was associated with smaller whole-brain volume at 69–71 years of age (−6·9 mL per 10 mm Hg greater DBP, −11·9 to −1·9, p=0·0068), as were greater increases in DBP between 36 and 43 years of age (−6·5 mL per 1 SD change, −11·1 to −1·9, p=0·0054). Greater increases in SBP between 36 and 43 years of age were associated with smaller hippocampal volumes at 69–71 years of age (−0·03 mL per 1 SD change, −0·06 to −0·001, p=0·043). Neither absolute blood pressure nor change in blood pressure predicted amyloid-β status or PACC score at 69–71 years of age. High and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69–71 years of age. We found no evidence that blood pressure affected cognition or cerebral amyloid-β load at this age. Blood pressure monitoring and interventions might need to start around 40 years of age to maximise late-life brain health. Alzheimer's Research UK, Medical Research Council, Dementias Platform UK, Wellcome Trust, Brain Research UK, Wolfson Foundation, Weston Brain Institute, Avid Radiopharmaceuticals.

Adolescent mental health difficulties are increasing over time. However, it is not known whether their adulthood health and socio-economic sequelae are changing over time. Participants ( = 31 349) are from two prospective national birth cohort studies: 1958 National Child Development Study ( = 16 091) and the 1970 British Cohort Study ( = 15 258). Adolescent mental health was operationalised both as traditional internalising and externalising factors and a hierarchical bi-factor. Associations between adolescent psychopathology and age 42 health and wellbeing (mental health, general health, life satisfaction), social (cohabitation, voting behaviour) and economic (education and employment) outcomes are estimated using linear and logistic multivariable regressions across cohorts, controlling for a wide range of early life potential confounding factors. The prevalence of adolescent mental health difficulties increased and their associations with midlife health, wellbeing, social and economic outcomes became more severe or remained similar between those born in 1958 and 1970. For instance, a stronger association with adolescent mental health difficulties was found for those born in 1970 for midlife psychological distress [odds ratio (OR) 1970 = 1.82 (1.65-1.99), OR 1958 = 1.60 (1.43-1.79)], cohabitation [OR 1970 = 0.64 (0.59-0.70), OR 1958 = 0.79 (0.72-0.87)], and professional occupations [OR 1970 = 0.75 (0.67-0.84), OR 1958 = 1.05 (0.88-1.24)]. The associations of externalising symptoms with later outcomes were mainly explained by their shared variance with internalising symptoms. The widening of mental health-based inequalities in midlife outcomes further supports the need to recognise that secular increases in adolescent mental health symptoms is a public health challenge with measurable negative consequences through the life-course. Increased public health efforts to minimise adverse outcomes are needed.

We aimed to estimate multimorbidity trajectories and quantify socioeconomic inequalities based on childhood and adulthood socioeconomic position (SEP) in the risks and rates of multimorbidity accumulation across adulthood. Participants from the UK 1946 National Survey of Health and Development (NSHD) birth cohort study who attended the age 36 years assessment in 1982 and any one of the follow-up assessments at ages 43, 53, 63, and 69 years (N = 3,723, 51% males). Information on 18 health conditions was based on a combination of self-report, biomarkers, health records, and prescribed medications. We estimated multimorbidity trajectories and delineated socioeconomic inequalities (based on childhood and adulthood social class and highest education) in multimorbidity at each age and in longitudinal trajectories. Multimorbidity increased with age (0.7 conditions at 36 years to 3.7 at 69 years). Multimorbidity accumulation was nonlinear, accelerating with age at the rate of 0.08 conditions/year (95% CI 0.07 to 0.09, p < 0.001) at 36 to 43 years to 0.19 conditions/year (95% CI 0.18 to 0.20, p < 0.001) at 63 to 69 years. At all ages, the most socioeconomically disadvantaged had 1.2 to 1.4 times greater number of conditions on average compared to the most advantaged. The most disadvantaged by each socioeconomic indicator experienced an additional 0.39 conditions (childhood social class), 0.83 (adult social class), and 1.08 conditions (adult education) at age 69 years, independent of all other socioeconomic indicators. Adverse adulthood SEP was associated with more rapid accumulation of multimorbidity, resulting in 0.49 excess conditions in partly/unskilled compared to professional/intermediate individuals between 63 and 69 years. Disadvantaged childhood social class, independently of adulthood SEP, was associated with accelerated multimorbidity trajectories from age 53 years onwards. Study limitations include that the NSHD cohort is composed of individuals of white European heritage only, and findings may not be generalizable to the non-white British population of the same generation and did not account for other important dimensions of SEP such as income and wealth. In this study, we found that socioeconomically disadvantaged individuals have earlier onset and more rapid accumulation of multimorbidity resulting in widening inequalities into old age, with independent contributions from both childhood and adulthood SEP.

Growing evidence suggests that population mental health outcomes have worsened since the pandemic started. The extent that these changes have altered common age-related trends in psychological distress, where distress typically rises until midlife and then falls after midlife in both sexes, is unknown. We aimed to analyse whether long-term pre-pandemic psychological distress trajectories were disrupted during the pandemic, and whether these changes have been different across cohorts and by sex. We used data from three nationally representative birth cohorts comprising all people born in Great Britain in a single week of 1946 (National Survey of Health and Development, NSHD), 1958 (National Child Development Study, NCDS), or 1970 (British Cohort Study, BCS70). The follow-up data used spanned 39 years in NSHD (1982 to 2021), 40 years in NCDS (1981 to 2001), and 25 years in BCS70 (1996 to 2021). We used psychological distress factor scores, as measured by validated self-reported questionnaires (NSHD: Present State Examination, Psychiatric Symptoms Frequency, and 28- and 12-item versions of General Health Questionnaire; NCDS and BCS70: Malaise Inventory; all: 2-item versions of Generalized Anxiety Disorder scale and Patient Health Questionnaire). We used a multilevel growth curve modelling approach to model the trajectories of distress across cohorts and sexes and obtained estimates of the differences between the distress levels observed during the pandemic and those observed at the most recent pre-pandemic assessment and at the peak in the cohort-specific pre-pandemic distress trajectory, located at midlife. We further analysed whether pre-existing cohort and sex inequalities had changed with the pandemic onset using a difference-in-differences (DiD) approach. The analytic sample included 16,389 participants. By September/October 2020, distress levels had reached or exceeded the levels of the peak in the pre-pandemic life-course trajectories, with larger increases in younger cohorts (standardised mean differences [SMD] and 95% confidence intervals of SMDNSHD,pre-peak = -0.02 [-0.07, 0.04], SMDNCDS,pre-peak = 0.05 [0.02, 0.07], and SMDBCS70,pre-peak = 0.09 [0.07, 0.12] for the 1946, 1958, and 1970 birth cohorts, respectively). Increases in distress were larger among women than men, widening pre-existing sex inequalities (DiD and 95% confidence intervals of DiDNSHD,sex,pre-peak = 0.17 [0.06, 0.28], DiDNCDS,sex,pre-peak = 0.11 [0.07, 0.16], and DiDBCS70,sex,pre-peak = 0.11 [0.05, 0.16] when comparing sex inequalities in the pre-pandemic peak in midlife to those observed by September/October 2020). As expected in cohort designs, our study suffered from high proportions of attrition with respect to the original samples. Although we used non-response weights to restore sample representativeness to the target populations (those born in the United Kingdom in 1946, 1958, and 1970, alive and residing in the UK), results may not be generalisable to other sections within the UK population (e.g., migrants and ethnic minority groups) and countries different than the UK. Pre-existing long-term psychological distress trajectories of adults born between 1946 and 1970 were disrupted during the COVID-19 pandemic, particularly among women, who reached the highest levels ever recorded in up to 40 years of follow-up data. This may impact future trends of morbidity, disability, and mortality due to common mental health problems.

Objectives. We examined the relationship between childhood and adult socioeconomic position (SEP) and objectively assessed, later-life functioning. Methods. We used the Medical Research Council’s National Survey of Health and Development data to examine performance at 60 to 64 years (obtained in 2006–2011) for a representative UK sample. We compared 9 physical and cognitive performance measures (forced expiratory volume, forced vital capacity, handgrip strength, chair rise time, standing balance time, timed get up and go speed, verbal memory score, processing speed, and simple reaction time) over the SEP distribution. Results. Each performance measure was socially graded. Those at the top of the childhood SEP distribution had between 7% and 20% better performance than those at the bottom. Inequalities generally persisted after adjustment for adult SEP. When we combined the 9 performance measures, the relative difference was 66% (95% confidence interval = 53%, 78%). Conclusions. Public health practice should monitor and target inequalities in functional performance, as well as risk of disease and death. Effective strategies will need to affect the social determinants of health in early life to influence inequalities into old age.

Background Social networks are associated with better cognitive health in older people, but the role of specific aspects of the social network remains unclear. This is especially the case in Central and Eastern Europe. This study examined associations between three aspects of the social network (network size of friends and relatives, contact frequency with friends and relatives, and social activity participation) with cognitive functions (verbal memory, learning ability, verbal fluency, processing speed, and global cognitive function) in older Czech, Polish, and Russian adults. Methods Linear regression estimated associations between baseline social networks and cognitive domains measured at both baseline and follow-up (mean duration of follow-up, 3.5 ± 0.7 years) in 6691 participants (mean age, 62.2 ± 6.0 years; 53.7% women) from the Health, Alcohol and Psychosocial factors In Eastern Europe (HAPIEE) study. Results Cross-sectional analyses, adjusted for country, age, and sex, showed positive associations of global cognitive function with social activity participation and network size of friends and relatives, but not with contact frequency in either network. Further adjustment for sociodemographic, behavioural, and health characteristics attenuated the associations with network size of relatives (P-trend = 0.074) but not with network size of friends (P-trend = 0.036) or social activities (P-trend< 0.001). In prospective analyses, network size and social activity participation were also linked with better cognition in simple models, but the associations were much stronger for social activities (P-trend< 0.001) than for network size of friends (P-trend = 0.095) and relatives (P-trend = 0.425). Adjustment for baseline cognition largely explained the prospective associations with network size of friends (P-trend = 0.787) and relatives (P-trend = 0.815), but it only slightly attenuated the association with social activities (P-trend< 0.001). The prospective effect of social activities was largely explained by sociodemographic, health behavioural, and health covariates (P-trend = 0.233). Analyses of specific cognitive domains generally replicated the cross-sectional and prospective findings for global cognitive function. Conclusions Older Central and Eastern European adults with larger social networks and greater social activities participation had better cognitive function, but these associations were stronger at baseline than over the short-term follow-up.

Background To describe the development of polypharmacy and its components in a British birth cohort in its seventh decade and to investigate socioeconomic and gender differences independent of disease burden. Methods Data from the MRC National Survey for Health and Development were analysed to determine the prevalence and composition of polypharmacy at age 69 and changes since ages 60 to 64. Multinomial regression was used to test associations between gender, education and occupational social class and total, cardiological and non-cardiological polypharmacy controlling for disease burden. Results At age 69, 22.8% of individuals were taking more than 5 medications. There was an increase in the use of 5 to 8 medications (+ 2.3%) and over 9 medications (+ 0.8%) between ages 60–64 and 69. The greatest increases were found for cardiovascular (+ 13.4%) and gastrointestinal medications (+ 7.3%). Men experienced greater cardiological polypharmacy, women greater non-cardiological polypharmacy. Higher levels of education were associated with lower polypharmacy independent of disease burden, with strongest effects seen for over five cardiological medications (RRR 0.3, 95% CI 0.2–0.5 p  < 0.001 for advanced secondary qualifications compared with no qualification); there was no additional effect of social class. Conclusions Polypharmacy increased over the seventh decade. Those with lower levels of education had more polypharmacy (total, cardiological and non-cardiological), even allowing for disease burden. Further analysis of future outcomes resulting from polypharmacy should take into account educational and gender differences, in an effort to identify at-risk populations who could benefit from medication reviews.

Background Little is known about the prevalence of and risk factors for adolescent mental health problems during the COVID-19 outbreak. We aimed to investigate the prevalence of depressive symptoms, their association with study-relevant problems, and the moderating effect of parent-child relationship among Chinese adolescents during the school closures. Methods We performed a cross-sectional analysis with data collected in middle and high schools in Taizhou, China. Students completed an online survey between April 16 and May 14, 2020. Depressive symptoms were assessed using the Children’s Depression Inventory. Three types of study problems were recorded, including having difficulty in studying at home, dislike of remote learning, and excessive screen entertainment time. Parental relationships were categorized into good or normal relationship and poor relationship. Linear regression and logistic regression analyses were conducted to investigate the associations between study-relevant problems and depressive symptoms. Results Using data from 6435 adolescents, we found that the prevalence of depressive symptoms was 17.7%. All the study problem measures were associated with more severe depressive symptoms. There was a moderating effect of the parental relationship on the associations between study problems and depressive symptoms. The association between number of study problems and depressive symptoms was stronger in adolescents with a poor parent-child relationship (regression coefficient 4.34 [95% CI 2.97, 5.72]) than those with a good or normal relationship (2.55 [2.35, 2.75]), p for interaction 0.002, on multivariable adjustment. Conclusions Study problems due to school closures were particularly problematic for adolescents who had poor parent-child relationships. Public health initiatives could help students to adjust study habits and improve parent-child relationships, thereby protecting against the development of depression.