Effect of maternal smoking during pregnancy on child blood pressure in a European cohort.

Hypertension is a public health issue that can have its origin in the early phases of development. Maternal smoking during pregnancy (MSDP) could play a role in offspring's cardio-metabolic programming. To assess the relationship between MSDP and later blood pressure (BP) in children we conducted a secondary analysis of a randomized dietary intervention trial (EU-Childhood Obesity Project). Healthy term infants with normal birth weight were recruited during the first 8 weeks of life in 5 European countries and followed until 11 years of age. Data on MSDP was collected at recruitment. BP and anthropometry were assessed at 11 years of age. Children were classified according to AAP guidelines as normal BP: BP < 90th percentile; high BP: ≥ 90th percentile with the subset of children having BP > 95th percentile categorized as hypertensive. Out of 572 children, 20% were exposed to MSDP. At 11 years, 26.8% had BP over the 90th centile. MSDP beyond 12 weeks of gestation was associated with higher systolic BP percentile (adjusted B 6.935; 95% CI 0.454, 13.429; p = 0.036) and over twofold increase likelihood of hypertension (OR 2.195; 95% CI 1.089, 4.423; p = 0.028) in children at 11 years. MSDP was significantly associated with later BP in children.

Usefulness of the waist-to-height ratio for predicting cardiometabolic risk in children and its suggested boundary values.

BACKGROUND & AIMS: Only limited information is available on the usefulness of the waist-to-height ratio (WHtR) as an abdominal obesity marker in children. Our aim was to compare the ability of a WHtR >90th percentile, a WHtR ≥0.50, a WHtR ≥0.55 and a BMI z-score ≥2 SD to predict cardiometabolic risk in children followed-up at different ages. METHODS: We evaluated data from 660 children at 5, 8 and 11 years of age who participated in the Childhood Obesity Project trial in 5 European countries. We classified children with or without cardiometabolic (CMet) risk (yes vs. no) according to the presence of ≥2 parameters (blood pressure, HOMA-IR, triglyceride levels and high-density lipoprotein (HDL) cholesterol levels) ≥90th percentile. RESULTS: The odds ratio for CMet risk in children at all followed-up ages was statistically significant for all measures. The OR for the WHtR≥0.55 cut-off was 29.1 (5.6, 151.7) at 5 years of age, 11.8 (4.1, 33.8) at 8 year of age and 3.6 (1.7, 7.7) at 11 years of age, compared to the WHtR<0.55 cut-off. The WHtR≥0.55 cut-off showed a higher OR at younger ages than the BMI z-score ≥2SD, WHtR ≥90th percentile and WHtR≥0.50 cut-offs and a higher positive predictive value (82% at 5 years of age compared to 55%, 36% and 41%, respectively). CONCLUSION: A WHtR≥0.55 is a suitable cut-off for screening children at high cardiometabolic risk in the general young European population.

Maternal Smoking during Pregnancy and DNA-Methylation in Children at Age 5.5 Years: Epigenome-Wide-Analysis in the European Childhood Obesity Project (CHOP)-Study.

Mounting evidence links prenatal exposure to maternal tobacco smoking with disruption of DNA methylation (DNAm) profile in the blood of infants. However, data on the postnatal stability of such DNAm signatures in childhood, as assessed by Epigenome Wide Association Studies (EWAS), are scarce. Objectives of this study were to investigate DNAm signatures associated with in utero tobacco smoke exposure beyond the 12th week of gestation in whole blood of children at age 5.5 years, to replicate previous findings in young European and American children and to assess their biological role by exploring databases and enrichment analysis. DNA methylation was measured in blood of 366 children of the multicentre European Childhood Obesity Project Study using the Illumina Infinium HM450 Beadchip (HM450K). An EWAS was conducted using linear regression of methylation values at each CpG site against in utero smoke exposure, adjusted for study characteristics, biological and technical effects. Methylation levels at five HM450K probes in MYO1G (cg12803068, cg22132788, cg19089201), CNTNAP2 (cg25949550), and FRMD4A (cg11813497) showed differential methylation that reached epigenome-wide significance according to the false-discovery-rate (FDR) criteria (q-value<0.05). Whereas cg25949550 showed decreased methylation (-2% DNAm ß-value), increased methylation was observed for the other probes (9%: cg12803068; 5%: cg22132788; 4%: cg19089201 and 4%: cg11813497) in exposed relative to non-exposed subjects. This study thus replicates previous findings in children ages 3 to 5, 7 and 17 and confirms the postnatal stability of MYO1G, CNTNAP2 and FRMD4A differential methylation. The role of this differential methylation in mediating childhood phenotypes, previously associated with maternal smoking, requires further investigation.

The introduction of solid food and growth in the first 2 y of life in formula-fed children: analysis of data from a European cohort study.

BACKGROUND: Early introduction of solid food has been suspected to induce excessive infant energy intake and weight gain. OBJECTIVE: The objective of this study was to test whether introduction of solid foods influences energy intake or growth. DESIGN: Healthy, formula-fed infants who were recruited in 5 European countries were eligible for study participation. Anthropometric measurements were taken at recruitment and at 3, 6, 12, and 24 mo. Time of introduction of solid foods and energy intake were determined by questionnaires and 3-d weighed food records at monthly intervals. Age at introduction of solid food was categorized into 4 groups: ≤ 13 wk, 14-17 wk, 18-21 wk, and ≥ 22 wk. RESULTS: Of 1090 recruited infants, 830 (76%) had data available for age at first introduction of solid food, and 671 (61%) completed the study until 24 mo of age. The median age at introduction of solid food was 19 wk. The time of introduction of solid foods was associated with country, sex, birth weight, parental education and marital status, and maternal smoking. Energy intake was higher in the first 8 mo of life in children with solid-food intake. Solid-food introduction did not predict anthropometric measures at 24 mo. Growth trajectories differed significantly: children with solid-food introduction in the first 12 wk experienced early catch-up growth, whereas those introduced to solid food at >22 wk of age grew more slowly and stayed on lower trajectories. CONCLUSIONS: Solid foods do not simply replace infant formula but increase energy intake. Time of introduction of solid food has little influence on infant growth. This trial was registered at clinicaltrials.gov as NCT00338689.