Infants born preterm miss out on the peak period of in utero DHA accretion to the brain during the last trimester of pregnancy which is hypothesised to contribute to the increased prevalence of neurodevelopmental deficits in this population. This study aimed to determine whether DHA supplementation in infants born preterm improves attention at 18 months’ corrected age. This is a follow-up of a subset of infants who participated in the N3RO randomised controlled trial. Infants were randomised to receive an enteral emulsion of high-dose DHA (60 mg/kg per d) or no DHA (soya oil – control) from within the first days of birth until 36 weeks’ post-menstrual age. The assessment of attention involved three tasks requiring the child to maintain attention on toy/s in either the presence or absence of competition or a distractor. The primary outcome was the child’s latency of distractibility when attention was focused on a toy. The primary outcome was available for seventy-three of the 120 infants that were eligible to participate. There was no evidence of a difference between groups in the latency of distractibility (adjusted mean difference: 0·08 s, 95 % CI –0·81, 0·97; P = 0·86). Enteral DHA supplementation did not result in improved attention in infants born preterm at 18 months’ corrected age.

There are marked disparities between indigenous and non-indigenous children’s diets and oral health. Both diet and oral health are linked to longer-term health problems. We aimed to investigate whether a culturally appropriate multi-faceted oral health promotion intervention reduced Aboriginal children’s intake of sugars from discretionary foods at 2 years of age. We conducted a single-blind, parallel-arm randomised controlled trial involving women who were pregnant or had given birth to an Aboriginal child in the previous 6 weeks. The treatment group received anticipatory guidance, Motivational Interviewing, health and dental care for mothers during pregnancy and children at 6, 12 and 18 months. The control group received usual care. The key dietary outcome was the percent energy intake from sugars in discretionary foods (%EI), collected from up to three 24-h dietary recalls by trained research officers who were blind to intervention group. Secondary outcomes included intake of macronutrients, food groups, anthropometric z scores (weight, height, BMI and mid-upper arm circumference) and blood pressure. We enrolled 224 children to the treatment group and 230 to the control group. Intention-to-treat analyses showed that the %EI of sugars in discretionary foods was 1·6 % lower in the treatment group compared with control (95 % CI −3·4, 0·2). This culturally appropriate intervention at four time-points from pregnancy to 18 months resulted in small changes to 2-year-old Aboriginal children’s diets, which was insufficient to warrant broader implementation of the intervention. Further consultation with Aboriginal communities is necessary for understanding how to improve the diet and diet-related health outcomes of young Aboriginal children.

There is interest in the degree to which fats in dairy foods contribute to CHD. We undertook a systematic review to investigate the effect of dairy consumption on CHD using prospective cohort studies. A systematic search of electronic databases identified studies relating dairy food intake in adulthood to episodes or death from CHD, IHD and myocardial infarction. Included studies were assessed for quality based on study methodology, validity of dietary assessment, success of follow-up, standardised assessment of CHD, IHD or myocardial infarction end points and appropriateness of statistical adjustment. Data from twelve cohorts involving >280 000 subjects were included. Most studies had follow-up of >80 %, adjusted statistically for three or more confounders and used standard criteria to determine end points. About half the studies used a validated FFQ, administered the FFQ more than once or had follow-up of >20 years. Fewer than half the studies involved subjects representative of the general population. Four of the twelve cohorts found no association between dairy intake and CHD. Eight studies reported varying relationships between different dairy foods and CHD or differential associations based on race, sex or over time. Although dairy foods contribute to the SFA composition of the diet, this systematic review could find no consistent evidence that dairy food consumption is associated with a higher risk of CHD. This could be due to the limited sensitivity of the dietary assessment methods to detect an effect of a single food in a mixed diet on complex clinical outcomes.