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Background: Adults who were born prematurely (<37 weeks' gestation) are at increased cardiovascular disease risk, but it is unclear when in the life course this risk emerges. Our aim was to compare trajectories of multiple cardiometabolic risk factors from childhood to early adulthood between those who had and had not been born preterm., Methods and Results: Multilevel models were used to compare trajectories from early childhood (<9 years) to age 25 years of body mass index, fat and lean mass, systolic and diastolic blood pressure, lipids, glucose, and insulin, between individuals born preterm (N=311-676; range, 25-36 weeks' gestation) and term (N=4973-10 534) in a UK birth cohort study. We also investigated gestational age as a continuum. In children born preterm (versus term), systolic and diastolic blood pressures were higher at age 7 years (mean predicted differences, 0.7 [95% CI, -0.2 to 1.6] mm Hg and 0.6 [95% CI, -0.04 to 1.3] mm Hg, respectively). By age 18 years, the difference in systolic blood pressure persisted (1.9 [95% CI, 0.8-3.1] mm Hg) and in diastolic blood pressure (0.1 [95% CI, -0.7 to 1.0 mm Hg]) disappeared. By age 25 years, this difference in systolic blood pressure began to attenuate towards the null (0.9 [95% CI, -0.5 to 2.3] mm Hg). Participants born preterm (versus term) had lower body mass index between ages 7 and 18 years, but by age 25 years, there was no difference. Fat and lean mass trajectories were consistent with body mass index. High-density lipoprotein cholesterol was higher and triglycerides lower at birth, in those born preterm, but this difference also disappeared by age 25 years. There was no evidence of differences in glucose and insulin., Conclusions: Few, modest differences in cardiometabolic health were found in those born preterm versus term. All disappeared by age 25 years, except the small difference in systolic blood pressure. Longer follow-up is needed to establish if and when cardiometabolic health trajectories diverge between these 2 groups.

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., Competing Interests: MVH has collaborated with Boehringer Ingelheim in research, and in adherence to the University of Oxford’s Clinical Trial Service Unit & Epidemiological Studies Unit (CSTU) staff policy, did not accept personal honoraria or other payments from pharmaceutical companies. GDS is a PLOS Medicine editorial board member. No others to declare.

Background and Aims: Sex differences in measures of cardiovascular health in adults are well documented. However, the sex-specific aetiology of cardiovascular health across childhood and adolescence is poorly understood., Methods: We examined sex differences in trajectories of 11 measures of cardiovascular health from birth to 18 years, in a contemporary birth cohort study in England (N participants per outcomes: 662-13,985, N repeated measures per outcome: 1,831-112,768). Outcomes were measured over varying time spans from birth or mid-childhood to age 18 and with different numbers of repeated measures per outcome. Analyses were performed using fractional polynomial and linear spline multilevel models., Results: Females had higher mean BMI, height-adjusted fat mass, pulse rate, insulin, triglycerides, and non-high-density lipoprotein cholesterol (HDL-c) and lower mean height-adjusted lean mass from birth or from mid-childhood to age 18. For example, mean non-HDL-c was 0.07 mmol/l (95% confidence interval (CI), 0.04, 0.10) higher in females compared with males at birth. By age 18, this difference persisted and widened to 0.19 mmol/l (95% CI, 0.16, 0.23) higher non-HDL-c in females compared with males. Females had lower levels of glucose from mid-childhood and developed lower systolic blood pressure and higher HDL-c from mid-adolescence onward. For example, females had 0.08 mmol/l (95% CI, 0.05, 0.10) lower mean glucose compared with males at age seven which widened to a difference of 0.22 mmol/l (95% CI, 0.25, 0.19) at age 18., Conclusions: Sex differences in measures of cardiovascular health are apparent from birth or mid-childhood and change during early life. These differences may have implications for sex-specific disease risk in future adult populations., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background and Aims: Males have greater cardiometabolic risk than females, though the reasons for this are poorly understood. The aim of this study was to examine the association between common Y chromosomal haplogroups and cardiometabolic risk during early life., Methods: In a British birth cohort, we examined the association of Y chromosomal haplogroups with trajectories of cardiometabolic risk factors from birth to 18 years and with carotid-femoral pulse wave velocity, carotid intima media thickness and left ventricular mass index at age 18. Haplogroups were grouped according to their phylogenetic relatedness into categories of R, I, E, J, G and all other haplogroups combined (T, Q, H, L, C, N and O). Risk factors included BMI, fat and lean mass, systolic blood pressure (SBP), diastolic blood pressure, pulse rate, triglycerides, high density lipoprotein cholesterol (HDL-c), non-HDL-c and c-reactive protein. Analyses were performed using multilevel models and linear regression, as appropriate., Results: Y chromosomal haplogroups were not associated with any cardiometabolic risk factors from birth to 18 years. For example, at age 18, the difference in SBP comparing each haplogroup with haplogroup R was -0.39 mmHg (95% Confidence Interval (CI): -0.75, 1.54) for haplogroup I, 2.56 mmHg (95% CI: -0.76, 5.89) for haplogroup E, -0.02 mmHg (95% CI: -2.87, 2.83) for haplogroup J, 1.28 mmHg (95% CI: -4.70, 2.13) for haplogroup G and -2.75 mmHg (95% CI: -6.38, 0.88) for all other haplogroups combined., Conclusions: Common Y chromosomal haplogroups are not associated with cardiometabolic risk factors during childhood and adolescence or with subclinical cardiovascular measures at age 18., (Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.)