Household energy poverty and trajectories of emotional and behavioural difficulties in children and adolescents: findings from two prospective cohort studies.

PURPOSE: The aim of this study is to examine the association between household energy poverty (EP) and trajectories of emotional and behavioural difficulties during childhood. METHODS: The Growing up in Ireland study is two nationally representative prospective cohorts of children. The Infant Cohort (n = 11,134) were recruited at age 9 months (9 m) and followed up at 3, 5, 7 and 9 years (y). The Child Cohort (n = 8,538) were recruited at age 9 y and followed up at 13 y and 17/18 y. EP was a composite of two relative measures of EP. Emotional and behavioural difficulties were repeatedly measured using the strengths and difficulties questionnaire (SDQ). Linear spline multilevel models were used, adjusted for confounders to examine the association between (1) EP (9 m or 3 y) and trajectories of emotional and behavioural difficulties from 3 to 9 y in the Infant Cohort and (2) EP at 9 y and the same trajectories from 9 to 18 y in the Child Cohort. RESULTS: In adjusted analyses, EP at 9 m or 3 y of age was associated with higher total difficulties score at 3 y (0.66, 95% CI 0.41, 0.91) and 5 y (0.77, 95% CI 0.48, 1.05) but not at 7 y or 9 y. EP at 9 y was associated with higher total difficulties score at 9 y (1.73, 95% CI 1.28, 2.18), with this difference reducing over time leading to 0.68 (95% CI 0.19, 1.17) at 17/18 y. CONCLUSIONS: Our study demonstrates a potential association between early life EP and emotional and behavioural difficulties that may be transient and attenuate over time during childhood. Further studies are required to replicate these findings and to better understand if these associations are causal.

Dietary intakes of iron, folate, and vitamin B12 during pregnancy and correlation with maternal hemoglobin and fetal growth: findings from the ROLO longitudinal birth cohort study.

PURPOSE: Dietary micronutrient intakes of iron, folate and vitamin B12 are known to influence hemoglobin. Low maternal hemoglobin (maternal anemia) has been linked to low birthweight and other adverse health outcomes in the fetus and infant. Our primary aim was to explore relationships between maternal dietary micronutrient intakes, maternal full blood count (FBC) parameters and fetal abdominal circumference (AC) and estimated fetal weight (EFW) growth trajectories. Secondarily, we aimed to assess relationships between maternal dietary micronutrient intakes, maternal hemoglobin values and placental weight and birthweight. METHODS: Mother-child pairs (n = 759) recruited for the ROLO study were included in this analysis. Maternal dietary micronutrient intakes were calculated from food diaries completed during each trimester of pregnancy. FBC samples were collected at 13- and 28-weeks' gestation. Fetal ultrasound measurements were recorded at 20- and 34-weeks' gestation. Growth trajectories for AC and EFW were estimated using latent class trajectory mixture models. RESULTS: Dietary intakes of iron and folate were deficient for all trimesters. Mean maternal hemoglobin levels were replete at 13- and 28-weeks' gestation. Dietary iron, folate and vitamin B12 intakes showed no associations with fetal growth trajectories, placental weight or birthweight. Lower maternal hemoglobin concentrations at 28 weeks' gestation were associated with faster rates of fetal growth and larger placental weights and birthweights. CONCLUSION: The negative association between maternal hemoglobin at 28 weeks' gestation and accelerated fetal and placental growth may be due to greater consumption of maternal iron and hemoglobin by fetuses' on faster growth trajectories in addition to placental biochemical responses to lower oxygen states.

Sex-specific associations of adiposity with cardiometabolic traits in the UK: A multi-life stage cohort study with repeat metabolomics.

BACKGROUND: Sex differences in cardiometabolic disease risk are commonly observed across the life course but are poorly understood and may be due to different associations of adiposity with cardiometabolic risk in females and males. We examined whether adiposity is differently associated with cardiometabolic trait levels in females and males at 3 different life stages. METHODS AND FINDINGS: Data were from 2 generations (offspring, Generation 1 [G1] born in 1991/1992 and their parents, Generation 0 [G0]) of a United Kingdom population-based birth cohort study, the Avon Longitudinal Study of Parents and Children (ALSPAC). Follow-up continues on the cohort; data up to 25 y after recruitment to the study are included in this analysis. Body mass index (BMI) and total fat mass from dual-energy X-ray absorptiometry (DXA) were measured at mean age 9 y, 15 y, and 18 y in G1. Waist circumference was measured at 9 y and 15 y in G1. Concentrations of 148 cardiometabolic traits quantified using nuclear magnetic resonance spectroscopy were measured at 15 y, 18 y, and 25 y in G1. In G0, all 3 adiposity measures and the same 148 traits were available at 50 y. Using linear regression models, sex-specific associations of adiposity measures at each time point (9 y, 15 y, and 18 y) with cardiometabolic traits 3 to 6 y later were examined in G1. In G0, sex-specific associations of adiposity measures and cardiometabolic traits were examined cross-sectionally at 50 y. A total of 3,081 G1 and 4,887 G0 participants contributed to analyses. BMI was more strongly associated with key atherogenic traits in males compared with females at younger ages (15 y to 25 y), and associations were more similar between the sexes or stronger in females at 50 y, particularly for apolipoprotein B-containing lipoprotein particles and lipid concentrations. For example, a 1 standard deviation (SD) (3.8 kg/m2) higher BMI at 18 y was associated with 0.36 SD (95% confidence interval [CI] = 0.20, 0.52) higher concentrations of extremely large very-low-density lipoprotein (VLDL) particles at 25 y in males compared with 0.15 SD (95% CI = 0.09, 0.21) in females, P value for sex difference = 0.02. By contrast, at 50 y, a 1 SD (4.8 kg/m2) higher BMI was associated with 0.33 SD (95% CI = 0.25, 0.42) and 0.30 SD (95% CI = 0.26, 0.33) higher concentrations of extremely large VLDL particles in males and females, respectively, P value for sex difference = 0.42. Sex-specific associations of DXA-measured fat mass and waist circumference with cardiometabolic traits were similar to findings for BMI and cardiometabolic traits at each age. The main limitation of this work is its observational nature, and replication in independent cohorts using methods that can infer causality is required. CONCLUSIONS: The results of this study suggest that associations of adiposity with adverse cardiometabolic risk begin earlier in the life course among males compared with females and are stronger until midlife, particularly for key atherogenic lipids. Adolescent and young adult males may therefore be high priority targets for obesity prevention efforts.

Sleep duration and eating behaviours are associated with body composition in 5-year-old children: findings from the ROLO longitudinal birth cohort study.

Inadequate sleep and poor eating behaviours are associated with higher risk of childhood overweight and obesity. Less is known about the influence sleep has on eating behaviours and consequently body composition. Furthermore, whether associations differ in boys and girls has not been investigated extensively. We investigate associations between sleep, eating behaviours and body composition in cross-sectional analysis of 5-year-old children. Weight, height, BMI, mid upper arm circumference (MUAC), abdominal circumference (AC) and skinfold measurements were obtained. Maternal reported information on child's eating behaviour and sleep habits were collected using validated questionnaires. Multiple linear regression examined associations between sleep, eating behaviours and body composition. Sleep duration was negatively associated with BMI, with 1-h greater sleep duration associated with 0·24 kg/m2 (B = 0·24, CI -0·42, -0·03, P = 0·026) lower BMI and 0·21 cm lower (B = -0·21, CI -0·41, -0·02, P = 0·035) MUAC. When stratified by sex, girls showed stronger inverse associations between sleep duration (h) and BMI (kg/m2) (B = -0·32; CI -0·60, -0·04, P = 0·024), MUAC (cm) (B = -0·29; CI -0·58, 0·000, P = 0·05) and AC (cm) (B = -1·10; CI -1·85, -0·21, P = 0·014) than boys. Positive associations for 'Enjoys Food' and 'Food Responsiveness' with BMI, MUAC and AC were observed in girls only. Inverse associations between sleep duration and 'Emotional Undereating' and 'Food Fussiness' were observed in both sexes, although stronger in boys. Sleep duration did not mediate the relationship between eating behaviours and BMI. Further exploration is required to understand how sleep impacts eating behaviours and consequently body composition and how sex influences this relationship.

Ecological factors and childhood eating behaviours at 5 years of age: findings from the ROLO longitudinal birth cohort study.

BACKGROUND: Individual differences in children eating behaviours have been linked with childhood overweight and obesity. The determinants of childhood eating behaviours are influenced by a complex combination of hereditary and ecological factors. This study examines if key ecological predictors of childhood overweight; maternal socio-economic status (SES), children's screen time, and childcare arrangements, are associated with eating behaviours in children aged 5-years-old. METHODS: This is secondary, cross-sectional analysis of the ROLO (Randomized COntrol Trial of LOw glycemic diet in pregnancy) study, using data from the 5-year follow-up (n = 306). Weight, height, and body mass index (BMI) were obtained from mothers and children at the 5-year follow-up. Children's BMI z-scores were calculated. SES was determined using maternal education level and neighborhood deprivation score. Information on children's screen time and childcare arrangements were collected using lifestyle questionnaires. Children's eating behaviours were measured using the Children's Eating Behaviour Questionnaire (CEBQ). Multiple linear regression, adjusted for potential confounders, assessed associations between maternal SES, screen time and children's eating behaviours. One-way ANOVA, independent sample t-tests and Spearman's correlation examined childcare exposure and children's eating behaviour. RESULTS: Mothers in the lowest SES group had higher BMI and were younger than those in the highest SES group (p = < 0.001, p = 0.03 respectively). In adjusted analysis, the lowest SES group was associated with a 0.463-point higher mean score for 'Desire to Drink' (95% CI = 0.054,0.870, p = 0.027) and higher 'Slowness to Eat' (B = 0.388, 95% CI = 0.044,0.733, p = 0.027) when compared with the highest SES group. Screen time (hours) was associated with higher 'Food Fussiness' (B = 0.032, 95% CI = 0.014,0.051, p = 0.001). Those who attended childcare had higher scores for 'Desire to Drink'(p = 0.046). No relationship was observed between longer duration (years) spent in childcare and eating behaviours. CONCLUSIONS: In this cohort, the ecological factors examined had an influence on children's eating behaviours aged 5-years-old. Our results illustrate the complexity of the relationship between the child's environment, eating behaviour and children's body composition. Being aware of the ecological factors that impact the development of eating behaviours, in the pre-school years is vital to promote optimal childhood appetitive traits, thus reducing the risk of issues with excess adiposity long-term.

Body muscle gain and markers of cardiovascular disease susceptibility in young adulthood: A cohort study.

BACKGROUND: The potential benefits of gaining body muscle for cardiovascular disease (CVD) susceptibility, and how these compare with the potential harms of gaining body fat, are unknown. We compared associations of early life changes in body lean mass and handgrip strength versus body fat mass with atherogenic traits measured in young adulthood. METHODS AND FINDINGS: Data were from 3,227 offspring of the Avon Longitudinal Study of Parents and Children (39% male; recruited in 1991-1992). Limb lean and total fat mass indices (kg/m2) were measured using dual-energy X-ray absorptiometry scans performed at age 10, 13, 18, and 25 y (across clinics occurring from 2001-2003 to 2015-2017). Handgrip strength was measured at 12 and 25 y, expressed as maximum grip (kg or lb/in2) and relative grip (maximum grip/weight in kilograms). Linear regression models were used to examine associations of change in standardised measures of these exposures across different stages of body development with 228 cardiometabolic traits measured at age 25 y including blood pressure, fasting insulin, and metabolomics-derived apolipoprotein B lipids. SD-unit gain in limb lean mass index from 10 to 25 y was positively associated with atherogenic traits including very-low-density lipoprotein (VLDL) triglycerides. This pattern was limited to lean gain in legs, whereas lean gain in arms was inversely associated with traits including VLDL triglycerides, insulin, and glycoprotein acetyls, and was also positively associated with creatinine (a muscle product and positive control). Furthermore, this pattern for arm lean mass index was specific to SD-unit gains occurring between 13 and 18 y, e.g., -0.13 SD (95% CI -0.22, -0.04) for VLDL triglycerides. Changes in maximum and relative grip from 12 to 25 y were both positively associated with creatinine, but only change in relative grip was also inversely associated with atherogenic traits, e.g., -0.12 SD (95% CI -0.18, -0.06) for VLDL triglycerides per SD-unit gain. Change in fat mass index from 10 to 25 y was more strongly associated with atherogenic traits including VLDL triglycerides, at 0.45 SD (95% CI 0.39, 0.52); these estimates were directionally consistent across sub-periods, with larger effect sizes with more recent gains. Associations of lean, grip, and fat measures with traits were more pronounced among males. Study limitations include potential residual confounding of observational estimates, including by ectopic fat within muscle, and the absence of grip measures in adolescence for estimates of grip change over sub-periods. CONCLUSIONS: In this study, we found that muscle strengthening, as indicated by grip strength gain, was weakly associated with lower atherogenic trait levels in young adulthood, at a smaller magnitude than unfavourable associations of fat mass gain. Associations of muscle mass gain with such traits appear to be smaller and limited to gains occurring in adolescence. These results suggest that body muscle is less robustly associated with markers of CVD susceptibility than body fat and may therefore be a lower-priority intervention target.

Puberty timing and markers of cardiovascular structure and function at 25 years: a prospective cohort study.

BACKGROUND: Whether earlier onset of puberty is associated with higher cardiovascular risk in early adulthood is not well understood. Our objective was to examine the association between puberty timing and markers of cardiovascular structure and function at age 25 years. METHODS: We conducted a prospective birth cohort study using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants were born between April 1, 1991, and December 31, 1992. Exposure of interest was age at peak height velocity (aPHV), an objective and validated growth-based measure of puberty onset. Outcome measures included cardiovascular structure and function at age 25 years: carotid intima-media thickness (CIMT), left ventricular mass index (LVMI) and relative wall thickness (RWT), pulse wave velocity (PWV) and systolic blood pressure (SBP). Multiple imputation was used to impute missing data on covariates and outcomes. Linear regression was used to examine the association between aPHV and each measure of cardiac structure and function, adjusting for maternal age, gestational age, household social class, maternal education, mother's partner's education, breastfeeding, parity, birthweight, maternal body mass index, maternal marital status, maternal prenatal smoking status and height and fat mass at age 9. All analyses were stratified by sex. RESULTS: A total of 2752-4571 participants were included in the imputed analyses. A 1-year older aPHV was not strongly associated with markers of cardiac structure and function in males and females at 25 years and most results spanned the null value. In adjusted analyses, a 1-year older aPHV was associated with 0.003 mm (95% confidence interval (CI) 0.00001, 0.006) and 0.0008 mm (95% CI - 0.002, 0.003) higher CIMT; 0.02 m/s (95% CI - 0.05, 0.09) and 0.02 m/s (95% CI - 0.04, 0.09) higher PWV; and 0.003 mmHg (95% CI - 0.60, 0.60) and 0.13 mmHg (95% CI - 0.44, 0.70) higher SBP, among males and females, respectively. A 1-year older aPHV was associated with - 0.55 g/m2.7 (95% CI - 0.03, - 1.08) and - 0.89 g/m2.7 (95% CI - 0.45, - 1.34) lower LVMI and - 0.001 (95% CI - 0.006, 0.002) and - 0.002 (95% CI - 0.006, 0.002) lower RWT among males and females. CONCLUSIONS: Earlier puberty is unlikely to have a major impact on pre-clinical cardiovascular risk in early adulthood.

Sex differences in systemic metabolites at four life stages: cohort study with repeated metabolomics.

BACKGROUND: Males experience higher rates of coronary heart disease (CHD) than females, but the circulating traits underpinning this difference are poorly understood. We examined sex differences in systemic metabolites measured at four life stages, spanning childhood to middle adulthood. METHODS: Data were from the Avon Longitudinal Study of Parents and Children (7727 offspring, 49% male; and 6500 parents, 29% male). Proton nuclear magnetic resonance (1H-NMR) spectroscopy from a targeted metabolomics platform was performed on EDTA-plasma or serum samples to quantify 229 systemic metabolites (including lipoprotein-subclass-specific lipids, pre-glycaemic factors, and inflammatory glycoprotein acetyls). Metabolites were measured in the same offspring once in childhood (mean age 8 years), twice in adolescence (16 years and 18 years) and once in early adulthood (25 years), and in their parents once in middle adulthood (50 years). Linear regression models estimated differences in metabolites for males versus females on each occasion (serial cross-sectional associations). RESULTS: At 8 years, total lipids in very-low-density lipoproteins (VLDL) were lower in males; levels were higher in males at 16 years and higher still by 18 years and 50 years (among parents) for medium-or-larger subclasses. Larger sex differences at older ages were most pronounced for VLDL triglycerides-males had 0.19 standard deviations (SD) (95% CI = 0.12, 0.26) higher at 18 years, 0.50 SD (95% CI = 0.42, 0.57) higher at 25 years, and 0.62 SD (95% CI = 0.55, 0.68) higher at 50 years. Low-density lipoprotein (LDL) cholesterol, apolipoprotein-B, and glycoprotein acetyls were generally lower in males across ages. The direction and magnitude of effects were largely unchanged when adjusting for body mass index measured at the time of metabolite assessment on each occasion. CONCLUSIONS: Our results suggest that males begin to have higher VLDL triglyceride levels in adolescence, with larger sex differences at older ages. Sex differences in other CHD-relevant metabolites, including LDL cholesterol, show the opposite pattern with age, with higher levels among females. Such life course trends may inform causal analyses with clinical endpoints in specifying traits which underpin higher age-adjusted CHD rates commonly seen among males.

Puberty timing and adiposity change across childhood and adolescence: disentangling cause and consequence.

STUDY QUESTION: Is earlier puberty more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood? SUMMARY ANSWER: Pre-pubertal fat mass is associated with earlier puberty timing but puberty timing is not associated with post-pubertal fat mass change. WHAT IS KNOWN ALREADY: Age at puberty onset has decreased substantially in the last several decades. Whether reducing childhood adiposity prevents earlier puberty and if early puberty prevention itself also has additional independent benefits for prevention of adult adiposity is not well understood. STUDY DESIGN, SIZE, DURATION: Prospective birth cohort study of 4176 participants born in 1991/1992 with 18 232 repeated measures of fat mass from age 9 to 18 years. PARTICIPANTS/MATERIALS, SETTING, METHODS: We used repeated measures of height from 5 to 20 years to identify puberty timing (age at peak height velocity, aPHV) and repeated measures of directly measured fat mass from age 9 to 18 years, from a contemporary UK birth cohort study to model fat mass trajectories by chronological age and by time before and after puberty onset. We then examined associations of these trajectories with puberty timing separately in females and males. MAIN RESULTS AND THE ROLE OF CHANCE: In models by chronological age, a 1-year later aPHV was associated with 20.5% (95% confidence interval (CI): 18.6-22.4%) and 23.4% (95% (CI): 21.3-25.5%) lower fat mass in females and males, respectively, at 9 years. These differences were smaller at age 18 years: 7.8% (95% (CI): 5.9-9.6%) and 12.4% (95% (CI): 9.6-15.2%) lower fat mass in females and males per year later aPHV. Trajectories of fat mass by time before and after puberty provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal fat mass change. The role of chance is likely to be small in this study given the large sample sizes available. LIMITATIONS, REASONS FOR CAUTION: Participants included in our analyses were more socially advantaged than those excluded. The findings of this work may not apply to non-White populations and further work examining associations of puberty timing and fat mass in other ethnicities is required. WIDER IMPLICATIONS OF THE FINDINGS: Previous research has relied on self-reported measures of puberty timing such as age of voice breaking in males, has lacked data on pre-and post-pubertal adiposity together and relied predominantly on indirect measures of adiposity such as BMI. This has led to conflicting results on the nature and direction of the association between puberty timing and adiposity in females and males. Our work provides important clarity on this, suggesting that prevention of adiposity in childhood is key for prevention of early puberty, adult adiposity and associated cardiovascular risk. In contrast, our findings suggest that prevention of early puberty without prevention of childhood adiposity would have little impact on prevention of adult adiposity. STUDY FUNDING/COMPETING INTEREST(S): The UK Medical Research Council and Wellcome (Grant ref: 102215/2/13/2) and the University of Bristol provide core support for Avon Longitudinal Study of Parents and Children (ALSPAC). L.M.O.K. is supported by a UK Medical Research Council Population Health Scientist fellowship (MR/M014509/1) and a Health Research Board (HRB) of Ireland Emerging Investigator Award (EIA-FA-2019-007 SCaRLeT). J.A.B. is supported by the Elizabeth Blackwell Institute for Health Research, University of Bristol and the Wellcome Trust Institutional Strategic Support Fund (204813/Z/16/Z). L.D.H. and A.F. are supported by Career Development Awards from the UK Medical Research Council (grants MR/M020894/1 and MR/M009351/1, respectively). All authors work in a unit that receives funds from the UK Medical Research Council (grant MC_UU_00011/3, MC_UU_00011/6). No competing interests to declare. TRIAL REGISTRATION NUMBER: N/A.

Preventive health counselling during antenatal care using the pregnancy risk assessment monitoring system (PRAMS) in Ireland.

BACKGROUND: Maternal behaviours during pregnancy have short- and long-term consequences for maternal and infant health. Pregnancy is an ideal opportunity to encourage positive behaviour change. Despite this, limited information exists about the nature and content of lifestyle advice provided by healthcare professionals during antenatal care. Pregnancy Risk Assessment Monitoring System (PRAMS) Ireland is based on the Centers for Disease Control and Prevention (CDC) developed PRAMS that monitors maternal behaviours and experiences before, during and after pregnancy. The aim of the study was to assess the prevalence of preventive health counselling during pregnancy. METHODS: Secondary data analysis of the PRAMS Ireland study. Using hospital discharge records, a sampling frame of 2424 mother-infant pairs was used to alternately sample 1212 women whom had recently given birth. Preventive health counselling was defined as advice during antenatal care on smoking, alcohol, infant feeding and weight gain. Self-reported maternal behaviours (smoking/alcohol cessation, gestational weight gain, infant feeding). Univariate and multivariable analyses were conducted, adjusting for maternal characteristics. RESULTS: Among 718 women (61% response rate), the reported counselling rates were 84.8% for breastfeeding (n = 592), 48.4% for alcohol (n = 338), 47.6% for smoking (n = 333) and 31.5% for weight gain (n = 218). Women who smoked pre-pregnancy (23.7%, n = 170) were more likely to receive counselling on its effects compared to non-smokers (Adjusted Odds Ratio (AOR) 2.72 (95% Confidence Interval (CI), 1.84-4.02)). In contrast, women who did not breastfeed (AOR 0.74, 95%CI 0.44-1.26) and those who reported alcohol consumption pre-pregnancy (AOR 0.94, 95%CI 0.64-1.37) were not more likely to receive counselling on these topics. CONCLUSION: Pregnancy is an ideal opportunity to encourage positive behaviour change. Preventive health counselling during pregnancy is not routinely provided and rates vary widely depending on the health behaviour. This study suggests that additional strategies are needed to promote positive behaviour before and during the unique opportunity provided by pregnancy.

The Association Between Preeclampsia and Childhood Development and Behavioural Outcomes.

OBJECTIVES: To examine the associations between preeclampsia and longitudinal child developmental and behavioural outcomes using data from a nationally representative study of children living in Ireland. METHODS: We used maternal-reported data from the Growing Up in Ireland longitudinal study of children. Data on preeclampsia and preeclampsia + small for gestational age (SGA) were collected when children were 9-months old. Data on child development and behavioural outcomes were collected at 9-months using the Ages and Stages Questionnaire (ASQ), and at 3 years, 5 years and 7-8 years using the Strengths and Difficulties Questionnaire (SDQ). Multivariate logistic regression analysis was used to examine the association between preeclampsia exposure and failure of ASQ domains, and abnormal SDQ domains. Linear spline multilevel models were used to examine the association between preeclampsia and preeclampsia + SGA and repeated measures of SDQ. All models controlled for several perinatal and sociodemographic factors. RESULTS: A total of 10,692 children were included in the study at baseline, representing a weighted total of 70,791. Multivariate logistic regression suggested that preeclampsia was not associated with failing any ASQ domain. Preeclampsia was associated with abnormal SDQ cut-off of emotional (≥ 5) and hyperactivity (≥ 7) domains at age 5 years only. In the linear spline model, mean SDQ score was higher at each time point in exposed groups. CONCLUSIONS FOR PRACTICE: While we did not find strong evidence of associations between preeclampsia and child developmental and behavioural outcomes overall, some associations between preeclampsia-exposure and subtle behavioural issues did persist. Further research is needed to replicate these findings, and determine the clinical significance of changes in SDQ scores.

Mid- and Long-Term Health Risks in Living Kidney Donors: A Systematic Review and Meta-analysis.

Background: Long-term health risks for adults who donate kidneys are unclear. Purpose: To summarize evidence about mid- and long-term health risks associated with living kidney donation in adults. Data Sources: PubMed, Embase, Scopus, and PsycINFO without language restriction from April 1964 to July 2017. Study Selection: Observational studies with at least 1 year of follow-up that compared health outcomes in adult living kidney donors versus nondonor populations. Data Extraction: Two investigators independently extracted study data and assessed study quality. Data Synthesis: 52 studies, comprising 118 426 living kidney donors and 117 656 nondonors, were included. Average follow-up was 1 to 24 years. No evidence suggested higher risk for all-cause mortality, cardiovascular disease, hypertension, type 2 diabetes, or adverse psychosocial health outcomes in living kidney donors than in nondonor populations. Donors had higher diastolic blood pressure, lower estimated glomerular filtration rates, and higher risk for end-stage renal disease (ESRD) (relative risk [RR], 8.83 [95% CI, 1.02 to 20.93]) and preeclampsia in female donors (RR, 2.12 [CI, 1.06 to 4.27]). Despite the increased RR, donors had low absolute risk for ESRD (incidence rate, 0.5 event [CI, 0.1 to 4.9 events] per 1000 person-years) and preeclampsia (incidence rate, 5.9 events [CI, 2.9 to 8.9 events] per 100 pregnancies). Limitation: Generalizability was limited by selected control populations, few studies reported pregnancy-related outcomes, and few studies were from low- and middle-income countries. Conclusion: Although living kidney donation is associated with higher RRs for ESRD and preeclampsia, the absolute risk for these outcomes remains low. Compared with nondonor populations, living kidney donors have no increased risk for other major chronic diseases, such as type 2 diabetes, or for adverse psychosocial outcomes. Primary Funding Source: National Health Service Blood and Transplant and National Institute for Health Research. (PROSPERO: CRD42017072284).

The impact of obstetric mode of delivery on childhood behavior.

PURPOSE: We investigated the hypothesis that mode of delivery affects childhood behavior and motor development and examined whether there are sex-specific associations, i.e., whether males and females have different risk estimates. METHODS: Families with infants born between December 2007 and May 2008 (N = 11,134) were randomly selected and recruited to the Growing Up in Ireland study. Mode of delivery was classified into spontaneous vaginal delivery; instrumental vaginal delivery; emergency Cesarean section (CS); and elective CS. The 'Ages and Stages Questionnaire' was completed at age 9-months and the 'Strengths and Difficulties Questionnaire' at 3 years. Data were weighted to represent the national sample (N = 73,662) and multivariate logistic regression was used for the statistical analyses. RESULTS: At age 9 months, elective CS was associated with a delay in personal social skills [adjusted odds ratio, aOR 1.24; (95% confidence interval, CI 1.04, 1.48)] and gross motor function [aOR 1.62, (95% CI 1.34, 1.96)], whereas emergency CS was associated with delayed gross motor function [aOR 1.30, (95% CI 1.06, 1.59)]. At age 3 years there was no significantly increased risk of an abnormal total SDQ score across all modes of delivery. CONCLUSIONS: Children born by elective CS may face a delay in cognitive and motor development at age 9 months. No increase in total SDQ score was found across all modes of delivery. Further investigation is needed to replicate these findings in other populations and explore the potential biological mechanisms.

Pregnancy Risk Assessment Monitoring System in Ireland: methods and response rates.

To describe response rates and characteristics associated with response to the Pregnancy Risk Assessment Monitoring System study in Ireland (PRAMS Ireland). Using hospital discharge records of live births at a large, urban, obstetric hospital, a sampling frame of approximately 2,400 mother-infant pairs were used to alternately sample 1,200 women. Mothers' information including name, address, parity, age and infant characteristics such as sex and gestational age at delivery were extracted from records. Modes of contact included an invitation letter with option to opt out of the study, three mail surveys, a reminder letter and text message reminder for remaining non-respondents. Sixty-one per cent of women responded to the PRAMS Ireland survey over a 133 day response period. Women aged <30, single women, multiparous women and women with a preterm delivery were less likely to respond. Women participating in PRAMS Ireland were similar to the national birth profile in 2011 which had a mean age of 32, were 40 % primiparous, 33 % single or never married and had a 28 % caesarean section rate. Survey and protocol changes are required to increase response rates above recommended Centers for Disease Control and Prevention (CDC) thresholds of 65 % within the recommended 90 day data collection cycle. Additional efforts such as stratification and over-sampling are required to increase representativeness among hard to reach groups such as younger, single and multiparous women before expanding the project to an ongoing, national surveillance system in Ireland.

Association of Cardiometabolic Multimorbidity With Mortality.

IMPORTANCE: The prevalence of cardiometabolic multimorbidity is increasing. OBJECTIVE: To estimate reductions in life expectancy associated with cardiometabolic multimorbidity. DESIGN, SETTING, AND PARTICIPANTS: Age- and sex-adjusted mortality rates and hazard ratios (HRs) were calculated using individual participant data from the Emerging Risk Factors Collaboration (689,300 participants; 91 cohorts; years of baseline surveys: 1960-2007; latest mortality follow-up: April 2013; 128,843 deaths). The HRs from the Emerging Risk Factors Collaboration were compared with those from the UK Biobank (499,808 participants; years of baseline surveys: 2006-2010; latest mortality follow-up: November 2013; 7995 deaths). Cumulative survival was estimated by applying calculated age-specific HRs for mortality to contemporary US age-specific death rates. EXPOSURES: A history of 2 or more of the following: diabetes mellitus, stroke, myocardial infarction (MI). MAIN OUTCOMES AND MEASURES: All-cause mortality and estimated reductions in life expectancy. RESULTS: In participants in the Emerging Risk Factors Collaboration without a history of diabetes, stroke, or MI at baseline (reference group), the all-cause mortality rate adjusted to the age of 60 years was 6.8 per 1000 person-years. Mortality rates per 1000 person-years were 15.6 in participants with a history of diabetes, 16.1 in those with stroke, 16.8 in those with MI, 32.0 in those with both diabetes and MI, 32.5 in those with both diabetes and stroke, 32.8 in those with both stroke and MI, and 59.5 in those with diabetes, stroke, and MI. Compared with the reference group, the HRs for all-cause mortality were 1.9 (95% CI, 1.8-2.0) in participants with a history of diabetes, 2.1 (95% CI, 2.0-2.2) in those with stroke, 2.0 (95% CI, 1.9-2.2) in those with MI, 3.7 (95% CI, 3.3-4.1) in those with both diabetes and MI, 3.8 (95% CI, 3.5-4.2) in those with both diabetes and stroke, 3.5 (95% CI, 3.1-4.0) in those with both stroke and MI, and 6.9 (95% CI, 5.7-8.3) in those with diabetes, stroke, and MI. The HRs from the Emerging Risk Factors Collaboration were similar to those from the more recently recruited UK Biobank. The HRs were little changed after further adjustment for markers of established intermediate pathways (eg, levels of lipids and blood pressure) and lifestyle factors (eg, smoking, diet). At the age of 60 years, a history of any 2 of these conditions was associated with 12 years of reduced life expectancy and a history of all 3 of these conditions was associated with 15 years of reduced life expectancy. CONCLUSIONS AND RELEVANCE: Mortality associated with a history of diabetes, stroke, or MI was similar for each condition. Because any combination of these conditions was associated with multiplicative mortality risk, life expectancy was substantially lower in people with multimorbidity.

Poverty trajectories and child and mother well-being outcomes in Ireland: findings from an Irish prospective cohort.

BACKGROUND: Poverty is associated with poor outcomes, yet exposure to distinct poverty trajectories in early childhood is not well understood. OBJECTIVE: To understand the prevalence of different trajectories of household poverty and their association with mid-childhood and mother indicators of physical health and psychopathology in Ireland. METHODS: We used a nationally representative, prospective cohort (Growing Up in Ireland-Infant Cohort). Household poverty included lowest third income decile, subjective poverty and material deprivation when children were aged 9 months, and 3, 5, 9 years. We used group-based multitrajectory cluster modelling to classify trajectories of poverty. Using multivariable logistic regression, adjusted with separate child and mother confounders, we assessed the association of poverty trajectories from 9 months to 9 years with child outcomes (overweight, any longstanding illness and psychopathology) at age 9 years and the same poverty trajectories over the same 9-year period with mother outcomes (overweight, any longstanding illness and depression). RESULTS: Of 11 134 participants, 4 trajectories were identified: never in poverty (43.1%), material/subjective>monetary poverty (16.1%), monetary>material poverty (25.6%) and persistent poverty (15.2%). Children in persistent poverty compared with those in never in poverty experienced higher odds of being overweight at 9 years (adjusted OR (aOR) 1.70, 95% CI 1.34, 2.16), having a longstanding illness (aOR 1.51, 95% CI 1.20, 1.91), and psychopathology (aOR 2.06, 95% CI 1.42, 2.99). The outcomes for primary parents (99.7% were mothers) were as follows: having higher odds of being overweight (aOR 1.49, 95% CI 1.16, 1.92), having a longstanding illness (aOR 2.13, 95% CI 1.63, 2.79), and depression (aOR 3.54, 95% CI 2.54, 4.94). CONCLUSIONS: Any poverty trajectory was associated with poorer psychopathology and physical well-being in late childhood for children and their mothers in Ireland.

Health care utilization and the associated costs attributable to cardiovascular disease in Ireland: a cross-sectional study.

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of mortality and disability globally. We examined healthcare service utilization and costs attributable to CVD in Ireland in the period before the introduction of a major healthcare reform in 2016. METHODS: Secondary analysis of data from 8 113 participants of the first wave of The Irish Longitudinal Study on Ageing. CVD was defined as having a self-reported doctor's diagnosis of myocardial infarction, angina, heart failure, stroke, atrial fibrillation or transient ischaemic attack. Participants self-reported the utilization of healthcare services in the year preceding the interview. Negative binomial regression with average marginal effects (AME) was used to estimate the incremental number of general practitioner (GP) and outpatient department (OPD) visits, accident and emergency department attendances and hospitalisations in population with CVD relative to population without CVD. We calculated the corresponding costs at individual and population levels, by gender and age groups. RESULTS: The prevalence of CVD was 18.2% (95% CI: 17.3, 19.0) Participants with CVD reported higher utilization of all healthcare services. In adjusted models, having CVD was associated with incremental 1.19 (95% CI: 0.99, 1.39) GP and 0.79 (95% CI: 0.65, 0.93) OPD visits. There were twice as many incremental hospitalisations in males with CVD compared to females with CVD (AME (95% CI): 0.20 (0.16, 0.23) vs 0.10 (0.07, 0.14)). The incremental cost of healthcare service use in population with CVD was an estimated €352.2 million (95% CI: €272.8, €431.7), 93% of which was due to use of secondary care services. CONCLUSION: We identified substantially increased use of healthcare services attributable to CVD in Ireland. Continued efforts aimed at CVD primary prevention and management are required.

Surveillance during pregnancy: methods and response rates from a hospital based pilot study of the Pregnancy Risk Assessment Monitoring System in Ireland.

BACKGROUND: Many European countries including Ireland lack high quality, on-going, population based estimates of maternal behaviours and experiences during pregnancy. PRAMS is a CDC surveillance program which was established in the United States in 1987 to generate high quality, population based data to reduce infant mortality rates and improve maternal and infant health. PRAMS is the only on-going population based surveillance system of maternal behaviours and experiences that occur before, during and after pregnancy worldwide. METHODS: The objective of this study was to adapt, test and evaluate a modified CDC PRAMS methodology in Ireland. The birth certificate file which is the standard approach to sampling for PRAMS in the United States was not available for the PRAMS Ireland study. Consequently, delivery record books for the period between 3 and 5 months before the study start date at a large urban obstetric hospital [8,900 births per year] were used to randomly sample 124 women. Name, address, maternal age, infant sex, gestational age at delivery, delivery method, APGAR score and birth weight were manually extracted from records. Stillbirths and early neonatal deaths were excluded using APGAR scores and hospital records. Women were sent a letter of invitation to participate including option to opt out, followed by a modified PRAMS survey, a reminder letter and a final survey. RESULTS: The response rate for the pilot was 67%. Two per cent of women refused the survey, 7% opted out of the study and 24% did not respond. Survey items were at least 88% complete for all 82 respondents. Prevalence estimates of socially undesirable behaviours such as alcohol consumption during pregnancy were high [>50%] and comparable with international estimates. CONCLUSION: PRAMS is a feasible and valid method of collecting information on maternal experiences and behaviours during pregnancy in Ireland. PRAMS may offer a potential solution to data deficits in maternal health behaviour indicators in Ireland with further work. This study is important to researchers in Europe and elsewhere who may be interested in new ways of tailoring an established CDC methodology to their unique settings to resolve data deficits in maternal health.

Life course effects of genetic susceptibility to higher body size on body fat and lean mass: prospective cohort study.

BACKGROUND/OBJECTIVES: Different genetic variants are associated with larger body size in childhood vs adulthood. Whether and when these variants predominantly influence adiposity are unknown. We examined how genetic variants influence total body fat and total lean mass trajectories. METHODS: Data were from the Avon Longitudinal Study of Parents and Children birth cohort (N = 6926). Sex-specific genetic risk scores (GRS) for childhood and adulthood body size were generated, and dual-energy X-ray absorptiometry scans measured body fat and lean mass six times between the ages of 9 and 25 years. Multilevel linear spline models examined associations of GRS with fat and lean mass trajectories. RESULTS: In males, the sex-specific childhood and adulthood GRS were associated with similar differences in fat mass from 9 to 18 years; 8.3% [95% confidence interval (CI) 5.1, 11.6] and 7.5% (95% CI 4.3, 10.8) higher fat mass at 18 years per standard deviation (SD) higher childhood and adulthood GRS, respectively. In males, the sex-combined childhood GRS had stronger effects at ages 9 to 15 than the sex-combined adulthood GRS. In females, associations for the sex-specific childhood GRS were almost 2-fold stronger than the adulthood GRS from 9 to 18 years: 10.5% (95% CI 8.5, 12.4) higher fat mass at 9 years per SD higher childhood GRS compared with 5.1% (95% CI 3.2, 6.9) per-SD higher adulthood GRS. In females, the sex-combined GRS had similar effects, with slightly larger effect estimates. Lean mass effect sizes were much smaller. CONCLUSIONS: Genetic variants for body size are more strongly associated with adiposity than with lean mass. Sex-combined childhood variants are more strongly associated with increased adiposity until early adulthood. This may inform future studies that use genetics to investigate the causes and impact of adiposity at different life stages.