Childhood and puberty can affect metabolism, leading to tissue injury and malfunction later in life. The consumption of high-processed foods rich in salt and sugar is increasing in middle- and high-income countries, especially among young people. It is necessary to evaluate the effects of high salt and sugar levels in the youth on most injured organs during metabolic challenges. We aimed to investigate whether high salt/sucrose intake affects whole-body development and leads to end-organ injury. Weaned Male Wistar rats were divided into two groups: a control group fed a standard diet (CO) and tap water, and an experimental group (SS) fed a standard diet and a beverage containing 1.8% NaCl and 20% sucrose instead of tap water. The animals were treated for 60 days, starting after weaning at 21 days of age, after which the animals were subjected to glucose and insulin tolerance tests, urine collection, and heart rate monitoring, and euthanized for sample collection at 81 days of age. SS showed reduced body weight gain and increased food intake of sodium/sucrose solution. Interestingly, high salt/sucrose intake led to increased body adiposity, liver lipid inclusion, heart rate, and renal dysfunction. SS exhibits increased levels of peroxisome proliferator-activated receptor alpha to counterbalance the hypertrophy of brown adipose tissue. Our findings reveal that the SS rat model exhibits non-obvious obesity with end-organ damage and preserved brown adipose tissue function. This model closely parallels human conditions with normal BMI but elevated visceral adiposity, providing a relevant tool for studying atypical metabolic disorders.

Research into associations between early life nutritional exposures and vulnerability to adult non-communicable disease (NCD) highlights the importance of maternal diet. A booklet outlining evidence-based dietary guidelines for the first 1000 days of life was first published in 2016 by early life nutrition experts for distribution to pregnant women in Australia and New Zealand. First-time New Zealand mothers’ (n=9) perceptions of the booklet and its relevance for the future health of their child were explored via semi-structured focus groups and interviews. Recruitment took place via social media channels and antenatal classes around Auckland. Three major themes were identified using thematic analysis: 1. A difference in the ways mothers related to the booklet depending on their apparent level of health literacy and communication preferences; 2. A tendency for women to outsource decision-making to nutrition ‘rules’, rather than interpreting information to suit personal circumstances; 3. Intense pressure to comply, resulting in feelings of shame or guilt when the ‘rules’ were not followed. In this study, first-time mums expressed feeling under pressure to ‘get it right’ and identified a desire for more support from healthcare providers and society. Nutrition education is essential; however, a booklet should provide a starting point for conversation rather than a stand-alone list of recommendations. Further exploration is needed to develop a resource that can be used by health professionals working alongside women and their partners to support healthy child development.

Gestational diabetes mellitus (GDM) is a major health problem, with increased risks of obesity and diabetes in offspring. However, little is known about the effect of GDM on infant feeding, nutrition and growth, and whether these factors play a role in mediating these risks. We systematically reviewed evidence for the effect of GDM on infant feeding, nutrition and growth. We searched MEDLINE, Web-of-Science, Embase, CINAHL and CENTRAL for studies that reported outcomes in infants <2 years who were and were not exposed to GDM. Studies of pre-gestational diabetes were excluded. Meta-analysis was performed for three epochs (1–6, 7–12, 13–24 months), using inverse-variance, fixed-effects methods. Primary outcomes were energy intake (kJ) and BMI (kg/m2). Twenty-five studies and 308 455 infants were included. Infants exposed to GDM, compared with those not exposed, had similar BMI at age 1–6 months (standardised mean difference (SMD) = 0·01, 95 % CI −0·04, 0·06; P = 0·69) and 7–12 months (SMD = 0·04, 95 % CI −0·01, 0·10; P = 0·09), reduced length at 1–6 and 7–12 months, increased whole-body fat at 1–6 months, higher rates of formula supplementation in hospital, shorter duration of breast-feeding and decreased rates of continued breast-feeding at 12 months. Breast milk of women with GDM had lower protein content. There was no association between GDM and infant weight and skinfold thickness. No data were available for nutritional intake and outcomes at 13–24 months. Low- or very low-quality evidence suggests GDM is not associated with altered BMI in infancy, but is associated with increased fat mass, high rates of formula use and decreased duration of breast-feeding.

There are now significant data to support the hypothesis that early life nutrition in the fetus, infant and young child can have profound effects on long-term health. This review considers some of this evidence with specific reference to the current burden of disease in Australia and New Zealand. As the findings of further research become available, recommendations on optimizing early life nutrition should be formulated and made widely available as part of the preventative health policy agenda in both Australia and New Zealand.