This study examined the relationship between childhood diet quality and arterial stiffness and thickness during adolescence/early adulthood. Participants were from the Avon Longitudinal Study of Parents and Children (ALSPAC) with dietary data at ages 7, 10 and 13 years and pulse wave velocity (PWV) and carotid intima-media thickness (cIMT) at ages 17 and/or 24 years. Diet quality (DQ) was assessed using five scores: a children’s Mediterranean-style diet (C-rMED) Z-score, a children’s Dietary Inflammatory Z-score (C-DIS), a DASH diet Z-score, a children’s Eatwell Guide (C-EWG) Z-score reflecting UK dietary guidelines and a data-driven obesogenic Z-score. Adjusted regression models examined the associations between DQ scores at 7–13 years and PWV and cIMT at 17 and 24 years. In adjusted models, a high v. low Obesogenic Z-score at 7 and 10 years was associated with higher PWV at 17: β 0.07 (95 % CI 0.01, 0.13) and β 0.10 (95 % CI 0.04, 0.16), respectively. A high v. low C-rMED Z-score at 7 years was associated with lower PWV at 17 (β −0.07; 95 % CI −0.14, −0.01). A high (more anti-inflammatory) vs low C-DIS Z-score at 10 years was associated with a lower PWV at 17 years: β −0.06 (95 % CI −0.12, −0.01). No other associations were observed. In conclusion, an Obesogenic dietary pattern in childhood (7–10 years) was related to increased arterial stiffness, while Mediterranean-style and anti-inflammatory diets were related to decreased arterial stiffness in adolescence. This highlights the importance of establishing healthy dietary habits early in life to protect against vascular damage.

Research into how alignment to UK dietary guidelines during childhood affects cardiometabolic health is limited. The association between adherence to UK dietary guidelines during childhood and overall cardiometabolic risk (CMR) in adolescence/early adulthood was explored using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). ALSPAC children with diet diaries completed at 7, 10 and 13 years of age, and data on CMR markers at 17 years (n 1940) and 24 years (n 1957) were included. A children’s Eatwell Guide (C-EWG) score was created by comparing dietary intakes at each age to UK dietary guidelines for nine foods/nutrients. Cardiometabolic health at 17 and 24 years was assessed using a composite CMR score. Multivariable linear regression models examined associations between C-EWG scores at 7, 10 and 13 years and the CMR score at 17 and 24 years, adjusting for confounders. C-EWG scores were generally low. However, a higher score (adherence to more dietary guidelines) at 7 years old was associated with a lower CMR score at 17 and 24 years: β −0·13 (95 % CI −0·25, –0·01) and β −0·25 (95 % CI −0·38, –0·13) for a 1-point increase in C-EWG score, respectively. A higher C-EWG score at 10 years was also associated with a lower CMR z-score at 24 years. No clear associations were evident at other ages. Greater adherence to UK dietary guidelines during mid-childhood was associated with a better overall cardiometabolic profile, suggesting that encouraging children to eat in this way has long-term benefits to health.

Compliance to UK dietary recommendations was assessed in school-aged children from a population-based cohort: the Avon Longitudinal Study of Parents and Children (ALSPAC). A Children’s Eatwell Guide (C-EWG) score was developed to assess socio-demographic predictors of meeting dietary recommendations. ALSPAC children with plausible diet diary data at 7 years (n 5373), 10 years (n 4450) and 13 years (n 2223) were included in the study. Their dietary intakes (recorded between 1998 and 2006) were compared with dietary guidelines for total and saturated fats, free sugars, salt, fibre, protein, carbohydrates, fruit and vegetables, non-oily and oily fish and red/processed meat. The C-EWG score (0–9 points) indicated the number of recommendations met at each age. Cross-sectional associations between socio-demographic characteristics and C-EWG scores were assessed using multivariable regression. The lowest adherence to guidelines at 7 years was for sugar (0·1 % meeting recommendations), followed by fibre (7·7 %), oily fish (9·5 %), saturated fat (9·7 %) and fruit and vegetables (15·2 %). Highest adherence was for limiting red/processed meat (67·3 %) and meeting carbohydrate recommendations (77·3 %). At 7 years, 12·1 % of participants failed to meet any of the nine recommendations, 26·9 % met one and 28·2 % met two. Similar patterns were seen at 10 and 13 years. A lower social class and maternal educational attainment and higher maternal BMI were associated with meeting fewer recommendations. Most school-aged children in this cohort did not meet UK dietary recommendations, particularly children from lower socio-economic backgrounds. Additional public health initiatives are needed to improve the quality of UK children’s diets, particularly targeting lower socio-economic groups.

An adequate intake of PUFA plays a vital role in human health. Therefore, it is important to assess PUFA intakes in different populations and validate them with biomarkers, but only a few small studies are in paediatric populations. We calculated the dietary intake of PUFA and their main food sources in children and assessed associations between PUFA intakes and plasma proportions. Dietary intakes of 7-year-old children (n 8242) enrolled in the Avon Longitudinal Study of Parents and Children were calculated from the parental-completed FFQ. Plasma PUFA were measured in 5571 children 8 months later, and 4380 children had complete dietary and plasma data. The association between dietary and plasma PUFA proportions was estimated using Spearman’s correlation coefficients, quintile cross-classification and Cohen’s κ coefficients. Mean total PUFA intake was 13·2 g/d (sd 4·2), contributing 6·5 % of total energy intake; n-6 PUFA contributed 5·2 % and n-3 PUFA 0·7 %. The n-6:n-3 ratio was 7·9:1. Mean intakes of EPA and DHA were 35·7 mg/d and 49·7 mg/d, respectively. Most n-3 and n-6 PUFA intakes were weakly correlated with their respective plasma lipids (0·07 ≤ r ≤ 0·16, P < 0·001). The correlation between dietary and plasma DHA was stronger though (r = 0·34, P < 0·001), supported by a modest level of agreement between quintiles (k = 0·32). The results indicate that the FFQ was able to reasonably rank the long-chain (LC) PUFA, DHA, in this paediatric population. Public health initiatives need to address the suboptimal ratio of n-6:n-3 PUFA and very low n-3 LC-PUFA intakes in school-age children in the UK.

Fetal supply with long-chain PUFA (LC-PUFA) during pregnancy is important for brain growth and visual and cognitive development and is provided by materno–fetal placental transfer. We recently showed that maternal fatty acid desaturase (FADS) genotypes modulate the amounts of LC-PUFA in maternal blood. Whether FADS genotypes influence the amounts of umbilical cord fatty acids has not been investigated until now. The aim of the present study was to investigate the influence of maternal and child FADS genotypes on the amounts of LC-PUFA in umbilical cord venous plasma as an indicator of fetal fatty acid supply during pregnancy. A total of eleven cord plasma n-6 and n-3 fatty acids were analysed for association with seventeen FADS gene cluster SNP in over 2000 mothers and children from the Avon Longitudinal Study of Parents and Children. In a multivariable analysis, the maternal genotype effect was adjusted for the child genotype and vice versa to estimate which of the two has the stronger influence on cord plasma fatty acids. Both maternal and child FADS genotypes and haplotypes influenced amounts of cord plasma LC-PUFA and fatty acid ratios. Specifically, most analysed maternal SNP were associated with cord plasma levels of the precursor n-6 PUFA, whereas the child genotypes were mainly associated with more highly desaturated n-6 LC-PUFA. This first study on FADS genotypes and cord fatty acids suggests that fetal LC-PUFA status is determined to some extent by fetal fatty acid conversion. Associations of particular haplotypes suggest specific effects of SNP rs498793 and rs968567 on fatty acid metabolism.