Breast milk leptin plays a potential role in preventing childhood obesity. However, the associations of breast milk leptin with maternal metabolism in pregnancy and dietary patterns during lactation are still unclear. We aimed to explore associations of breast milk leptin with maternal metabolic profiles in pregnancy and dietary patterns during lactation. A total of 332 participants were recruited for this retrospective cohort study. Breast milk samples were collected at approximately 6 weeks postpartum. Breast milk leptin and twenty-three metabolic profiles in pregnancy were measured in this study. A semi-quantitative FFQ was used to gather dietary information during lactation. Both principal component analysis and the diet balance index were used to derive dietary patterns. Among twenty-three maternal metabolic profiles, maternal serum glucose (β = 1·61, P = 0·009), γ-glutamyl transferase (β = 0·32, P = 0·047) and albumin (β = −2·96, P = 0·044) in pregnancy were correlated with breast milk leptin. All dietary patterns were associated with breast milk leptin. Given the joint effects of maternal metabolism in pregnancy and dietary patterns during lactation, only diet quality distance was significantly associated with leptin concentrations in breast milk (low level v. almost no diet problem: β = −0·46, P = 0·011; moderate/high level v. almost no diet problem: β = −0·43, P = 0·035). In conclusion, both maternal metabolism in pregnancy and dietary patterns during lactation were associated with breast milk leptin. Maternal diet balance during lactation was helpful to improve breast milk leptin concentration.

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.

In this study, the heavy metal (Al, Mn, Co, Cu, Zn, As, Se, Cd, Sn, Pb and Hg) concentrations were determined in a total of seventy-two infant formula samples manufactured by sixteen different brands in Türkiye. During the analyses, inductively coupled plasma MS was used in evaluating the nutritional profile and the toxicological risk associated with the consumption of these products. Given the analysis results, the highest Pb content was found in milk-based ‘beginner’ formulas (0–6 months, three samples) packed in metal containers. The highest concentration of Mn was found in powdered infant formula (Brand 3) that is suitable for 9–12-month-olds. Mn level was found to be above the limit values in nine samples (12·5 %). Cd level exceeded the limit values in two infant formula samples of Brand 3 (0·038 µg/g) and Brand 15 (0·023 µg/g). Therefore, the mean Cd concentration found here reaches the maximum limit set by the European Union commission legislation. Cu was detected in all infant formulas. The highest concentration was determined in Brand 1 (9–12 months, seven samples) and found to be 2·637 (sd 1·928) µg/g. This value is much higher than the reference values set in the national and international standards. Based on the results achieved here, the estimated daily intake (EDI) and target hazard quotient values for all the metals in infant formulas were found lower than < 1. These findings suggest that the baby foods examined would not pose any health risk. The daily intakes exceeding the baby nutrition values recommended by the WHO would pose health risk since they would exceed the EDI levels.

The aim of the present study is to examine whether overweight or obese people in Taiwan have an inadequate intake of selected micronutrients. A population-based study was conducted using data from the Nutrition and Health Survey in Taiwan (NAHSIT) 2013–2016. We evaluated fourteen nutrient intakes using the 24 h dietary recall method. The dietary reference intake (DRI) adherence was estimated by the prevalence of participants whose intake was lower than the recommended dietary allowance (RDA) or adequate intakes (AIs) for selected micronutrients. Body mass index (BMI) ≥ 27 kg/m2 and waist circumference (WC), with men having WC ≥ 90 cm or women having WC ≥ 80 cm, were defined as obesity. A total of 3075 participants aged 19 years and above were included. After adjusting for confounders, we found that obese women have a lower DRI adherence of vitamin C (odds ratio (OR) 0⋅73, 95 % confidence interval (CI) 0⋅56, 0⋅95) and magnesium (OR 0⋅72, 95 % CI 0⋅54, 0⋅95), compared with normal-weight women. Obese men have a higher DRI adherence of vitamin B3 (OR 1⋅70, 95 % CI 1⋅29, 2⋅23), iron (OR 1⋅46, 95 % CI 1⋅06, 2⋅00) and zinc (OR 1⋅41, 95 % CI 1⋅07, 1⋅85), compared with normal-weight men. Similar findings were found using WC to define obesity. We conclude that obese women may have insufficient intakes of vitamin A, vitamin C and magnesium.

The recent Covid-19 pandemic highlighted stark social inequalities, notably around access to food, nutrition and to green or blue space (i.e. outdoor spaces with vegetation and water). Consequently, obesity is socio-economically patterned by this inequality; and while the environmental drivers of obesity are widely acknowledged, there is currently little upstream intervention. We know that living with obesity contributes to increasing health inequalities, and places healthcare systems under huge strain. Our environment could broadly be described obesogenic, in the sense of supporting unhealthful eating patterns and sedentary behaviour. Evidence points to the existence of nearly 700 UK obesity policies, all of which have had little success. Obesity prevention and treatment has focused on educational and behavioural interventions targeted at individual consumers. A more sustainable approach would be to try and change the environments that promote less healthy eating and high energy intake as well as sedentary behaviour. Approaches which modify the environment have the potential to assist in the prevention of this complex condition. This review paper focuses on the role of wider food environments or foodscapes. While there is an imperfect evidence base relating to the role of the foodscape in terms of the obesity crisis, policy, practice, civic society and industry must work together and take action now, in areas where current evidence suggests change is required. Despite the current cost-of-living crisis, shaping the foodscape to better support healthful eating decisions has the potential to be a key aspect of a successful obesity prevention intervention.

We prospectively examined the association between low-carbohydrate diet (LCD) score and incidence of type 2 diabetes (T2D) in Japanese adults using Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC Study) data. A total of 19 084 (7052 men and 12 032 women) Japanese non-diabetic participants aged 40–79 years, who enrolled in the JACC study between 1988 and 1990, were included in our analysis. Dietary intake was evaluated using a validated food-frequency questionnaire. The overall, animal and vegetable LCD scores were calculated by dividing the study participants into eleven categories based on the percentages of energy from carbohydrates, protein and fat. The incidence of T2D was assessed using a self-administered questionnaire. We used multivariable logistic regression analysis to estimate the odds ratios (ORs) and 95 % confidence intervals (CIs) of incident T2D across the quintile of each LCD score, with adjustment for potential confounders. During the 5-year study period, 490 adults (247 men and 243 women) developed T2D. The multivariable-adjusted OR of incident T2D for the highest v. lowest quintiles of overall and animal LCD scores, respectively, were 0·64 (95 % CI 0·42, 0·99) and 0·83 (95 % CI 0·55, 1·27) for men, 0·78 (95 % CI 0·51, 1·18) and 0·84 (95 % CI 0·57, 1·24) for women. The vegetable LCD score was associated with a lower risk of T2D in men (OR 0·51; 95 % CI 0·33, 0·77). Our results suggest that diets lower in carbohydrates and higher in fat and protein are unlikely to higher the T2D risk among Japanese individuals.

The iron-regulatory hormone hepcidin is transcriptionally up-regulated by gluconeogenic signals. Recent evidence suggeststhat increases in circulating hepcidin may decrease dietary iron absorption following prolonged exercise, however evidence is limited on whether gluconeogenic signals contribute to post-exercise increases in hepcidin. Mice with genetic knockout of regulated in development and DNA response-1 (REDD1) display greater glycogen depletion following exercise, possibly indicating greater gluconeogenesis. The objective of the present study was to determine liver hepcidin, markers of gluconeogenesis and iron metabolism in REDD1 knockout and wild-type mice following prolonged exercise. Twelve-week-old male REDD1 knockout and wild-type mice were randomised to rest or 60 min treadmill running with 1, 3 or 6 h recovery (n = 5–8/genotype/group). Liver gene expression of hepcidin (Hamp) and gluconeogenic enzymes (Ppargc1a, Creb3l3, Pck1, Pygl) were determined by qRT-PCR. Effects of genotype, exercise and their interaction were assessed by two-way ANOVAs with Tukey's post-hoc tests, and Pearson correlations were used to assess the relationships between Hamp and study outcomes. Liver Hamp increased 1- and 4-fold at 3 and 6 h post-exercise, compared to rest (P-adjusted < 0⋅009 for all), and was 50% greater in REDD1 knockout compared to wild-type mice (P = 0⋅0015). Liver Ppargc1a, Creb3l3 and Pck1 increased with treadmill running (P < 0⋅0001 for all), and liver Ppargc1a, Pck1 and Pygl were greater with REDD1 deletion (P < 0⋅02 for all). Liver Hamp was positively correlated with liver Creb3l3 (R = 0⋅62, P < 0⋅0001) and Pck1 (R = 0⋅44, P = 0⋅0014). In conclusion, REDD1 deletion and prolonged treadmill running increased liver Hamp and gluconeogenic regulators of Hamp, suggesting gluconeogenic signalling of hepcidin with prolonged exercise.