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Background Atherosclerosis develops across the life course, and variation in aortic intima‐media thickness (IMT) is evident from infancy onward, although most early‐life data are cross‐sectional. We investigated whether abdominal aortic IMT at age 6 weeks is associated with vascular measures at 4 years and the relationship of prenatal and perinatal exposures with these measures in early childhood. Methods and Results We analyzed data from 518 participants with 6‐week and 4‐year vascular measures from the Barwon Infant Study. Aortic IMT was measured at 6 weeks (mean, 6.1±SD 1.5 weeks) and aortic and carotid IMT, carotid–femoral pulse wave velocity, and blood pressure at 4 years of age (4.3±0.3 years). Associations of early‐life exposures—maternal enteric microbiome, smoking and low‐density lipoprotein cholesterol during pregnancy, birth weight, and gestational age—were also investigated. In the primary model, 6‐week aortic IMT (649±66 μm) was associated with small differences in 4‐year carotid IMT (453±45 μm) (mean difference in carotid IMT per 100 μm higher 6‐week aortic IMT=7.0 μm [95% CI, 0.7–13.3]; P=0.03), with no evidence for associations with 4‐year aortic IMT, pulse wave velocity, or blood pressure. Higher birth weight was associated with greater 4‐year aortic IMT, and maternal smoking with higher systolic blood pressure. Conclusions Vascular measures do not show strong evidence of tracking between infancy and early childhood. Longitudinal studies with repeated assessment beyond age 4 years would inform optimal timing of early prevention and targets for primordial prevention.

Abstract Hypertensive disorders of pregnancy (HDP) are associated with an increased risk of cardiovascular disorders, with recent evidence linking pre‐eclampsia with vascular dementia. We examined associations of HDP with cognitive performance measured in midlife, in a prospective cohort study, the Avon Longitudinal Study of Parents and Children. Six cognitive function domains were measured 20 years after pregnancy at a mean age of 51 years. The cognition tests were repeated at clinics in the following two years. Cognitive function domains measured were immediate and delayed verbal episodic memory, working memory, processing speed, verbal intelligence, and verbal fluency. Exposures were pre‐eclampsia, gestational hypertension (GH), and a combined category of any HDP, all compared to normotensive pregnancy. Of 3393 pregnancies included in the analysis, GH was experienced by 417 (12.3%) and pre‐eclampsia by 57 (1.7%). GH was associated with lower verbal episodic memory, in the delayed logic memory test (‐0.16 SDs; 95% CI ‐0.30, ‐0.03; p = .015) and there was weak evidence of an association with the immediate logic memory test (‐0.13 SDs; ‐0.27, 0.001; p = .058). However, we did not see steeper declines by age for women with GH and there was no evidence of associations with other cognitive domains or for pre‐eclampsia with any domains. Results were not substantially changed after controlling for midlife blood pressure. Our findings suggest that a history of GH is associated with slightly reduced episodic memory 20 years after pregnancy, but we found no evidence of a quicker age‐related decline compared to women with normotensive pregnancies.

Abstract Background Parental personality may influence the course of offspring depression but epidemiological evidence for associations is lacking. It is also unknown whether associations between parental personality and offspring depression differ by socio‐economic position (SEP). Our aims were to describe the trajectories of depressive symptoms across adolescence of offspring of parents with and without maladaptive personality traits and to test for effect modification by SEP. Methods A longitudinal study in the Avon Longitudinal Study of Parents and Children birth cohort (ns = 3054–7046). Exposures were binary measures of maladaptive maternal and paternal personality traits. The outcome was depressive symptoms measured over nine occasions (ages 11–24) using the short mood and feelings questionnaire (SMFQ; range: 0–26). Effect modifiers were parental education and self‐reported material hardship. Multilevel growth curve models were used to estimate trajectories. Results offspring of mothers with high (vs. low) maladaptive traits showed higher levels of depressive symptoms at multiple ages of adolescence, the greatest of which was observed at age 22 (predicted SMFQ difference age 10 = 0.66, 95% confidence intervals [CIs]: 0.25 to 1.28; age 22 = 1.00, CI: 0.51 to 1.50). There was weaker and inconsistent evidence of an association between paternal maladaptive personality and offspring depressive symptoms (SMFQ difference age 10 = 0.21, CI: −0.58 to 0.99; age 22 = 0.02, CI: −0.94 to 0.90). Lower SEP was also associated with higher offspring depressive symptoms (SMFQ difference material hardship vs. no hardship age 10 = 0.79, 95% CI: 0.46 to 1.13; age 22 = 0.96, CI: 0.56 to 1.36). There was minimal statistical evidence for effect modification. Conclusions The offspring of mothers with high levels of maladaptive personality traits show evidence of greater depressive symptoms throughout adolescence although the absolute increase in symptoms is small. Evidence for the associations with fathers' personality was weaker. Socio‐economic position and maladaptive personality traits appear to be independent risk factors for offspring depressive symptoms.

Background Congenital heart diseases (CHDs) are the most common congenital anomaly. The causes of CHDs are largely unknown. Higher prenatal body mass index (BMI), smoking, and alcohol consumption are associated with increased risk of CHDs. Whether these are causal is unclear. Methods and Results Seven European birth cohorts, including 232 390 offspring (2469 CHD cases [1.1%]), were included. We applied negative exposure paternal control analyses to explore the intrauterine effects of maternal BMI, smoking, and alcohol consumption during pregnancy, on offspring CHDs and CHD severity. We used logistic regression, adjusting for confounders and the other parent's exposure and combined estimates using a fixed‐effects meta‐analysis. In adjusted analyses, maternal overweight (odds ratio [OR], 1.15 [95% CI, 1.01–1.31]) and obesity (OR, 1.12 [95% CI, 0.93–1.36]), compared with normal weight, were associated with higher odds of CHD, but there was no clear evidence of a linear increase in odds across the whole BMI distribution. Associations of paternal overweight, obesity, and mean BMI were similar to the maternal associations. Maternal pregnancy smoking was associated with higher odds of CHD (OR, 1.11 [95% CI, 0.97–1.25]) but paternal smoking was not (OR, 0.96 [95% CI, 0.85–1.07]). The positive association with maternal smoking appeared to be driven by nonsevere CHD cases (OR, 1.22 [95% CI, 1.04–1.44]). Associations with maternal moderate/heavy pregnancy alcohol consumption were imprecisely estimated (OR, 1.16 [95% CI, 0.52–2.58]) and similar to those for paternal consumption. Conclusions We found evidence of an intrauterine effect for maternal smoking on offspring CHDs, but no evidence for higher maternal BMI or alcohol consumption. Our findings provide further support for the importance of smoking cessation during pregnancy.

Background We aimed to quantify the role of the plasma metabolic profile in explaining the effect of adiposity on cardiac structure. Methods and Results Body mass index (BMI) was measured at age 11 in the Avon Longitudinal Study of Parents and Children. Left ventricular mass indexed to height2.7 (LVMI) was assessed by echocardiography at age 17. The metabolic profile was quantified via 1H‐nuclear magnetic resonance spectroscopy at age 15. Multivariable confounder (maternal age, parity, highest qualification, maternal smoking, prepregnancy BMI, prepregnancy height, household social class, adolescent birthweight, adolescent smoking, fruit and vegetable consumption, and physical activity)–adjusted linear regression estimated the association of BMI with LVMI and mediation by metabolic traits. We considered 156 metabolomic traits individually and jointly as principal components explaining 95% of the variance in the nuclear magnetic resonance platform and assessed whether the principal components for the metabolic traits added to the proportion of the association explained by putative cardiovascular risk factors (systolic and diastolic blood pressures, insulin, triglycerides, low‐density lipoprotein cholesterol, and glucose). A 1 kg/m2 higher BMI was associated with a 0.70 g/m2.7 (95% CI, 0.53–0.88 g/m2.7) and 0.66 g/m2.7 (95% CI, 0.53–0.79 g/m2.7) higher LVMI in males (n=437) and females (n=536), respectively. Putative risk factors explained 3% (95% CI, 2%–5%) of this association in males, increasing to 10% (95% CI, 8%–13%) when including metabolic principal components. In females, the standard risk factors explained 3% (95% CI, 2%–5%) of the association and did not increase when including the metabolic principal components. Conclusions The addition of the nuclear magnetic resonance‐measured metabolic traits appears to mediate more of the association of BMI on LVMI than the putative risk factors alone in adolescent males, but not females.