Inflammation is an underlying problem for many disease states and has been implicated in iron deficiency (ID). This study aimed to determine whether iron status is improved by epigallocatechin-3-gallate (EGCG) through reducing inflammation. Thirty-two male Sprague–Dawley rats were fed an iron-deficient diet for 2 weeks and then randomly divided into four groups (n 8 each): positive controls, negative controls, lipopolysaccharide (LPS, 0⋅5 mg/kg body weight), and LPS + EGCG (LPS plus 600 mg EGCG/kg diet) for 3 additional weeks. The study involved testing two control groups, both treated with saline. One group (positive control) was fed a regular diet containing standard iron, while the negative control was fed an iron-deficient diet. Additionally, two treatment groups were tested. The first group was given LPS, while the second group was administered LPS and fed an EGCG diet. Iron status, hepcidin, C-reactive protein (CRP), serum amyloid A (SAA), and interleukin-6 (IL-6) were measured. There were no differences in treatment groups compared with control in CRP, hepcidin, and liver iron concentrations. Serum iron concentrations were significantly lower in the LPS (P = 0⋅02) and the LPS + EGCG (P = 0⋅01) than in the positive control group. Compared to the positive control group, spleen iron concentrations were significantly lower in the negative control (P < 0⋅001) but not with both LPS groups. SAA concentrations were significantly lower in the LPS + EGCG group compared to LPS alone group. EGCG reduced SAA concentrations but did not affect hepcidin or improve serum iron concentration or other iron markers.

Dietary starch contains rapidly (RAG) and slowly available glucose (SAG). To establish the relationships between the RAG:SAG ratio and postprandial glucose, insulin and hunger, we measured postprandial responses elicited by test meals varying in the RAG:SAG ratio in n 160 healthy adults, each of whom participated in one of four randomised cross-over studies (n 40 each): a pilot trial comparing six chews (RAG:SAG ratio 2·4–42·7) and three studies comparing a test granola (TG1-3, RAG:SAG ratio 4·5–5·2) with a control granola (CG1–3, RAG:SAG ratio 54·8–69·3). Within studies, test meals were matched for fat, protein and available carbohydrate. Blood glucose, serum insulin and subjective hunger were measured for 3 h. Data were subjected to repeated-measures analysis of variance (ANOVA). The relationships between the RAG:SAG ratio and postprandial end points were determined by regression analysis. In the pilot trial, 0–2 h glucose incremental areas under the curve (iAUC0–2; primary end point) varied across the six chews (P = 0·014) with each 50 % reduction in the RAG:SAG ratio reducing relative glucose response by 4·0 %. TGs1-3 elicited significantly lower glucose iAUC0–2 than CGs1–3 by 17, 18 and 17 %, respectively (similar to the 15 % reduction predicted by the pilot trial). The combined means ± sem (n 120) for TC and CG were glucose iAUC0–2, 98 ± 4 v. 118 ± 4 mmol × min/l (P < 0·001), and insulin iAUC0–2, 153 ± 9 v. 184 ± 11 nmol × h/l (P < 0·001), respectively. Neither postprandial hunger nor glucose or hunger increments 2 h after eating differed significantly between TG and CG. We concluded that TGs with RAG:SAG ratios <5·5 predictably reduced glycaemic and insulinaemic responses compared with CGs with RAG:SAG ratios >54. However, compared with CG, TG did not reduce postprandial hunger or delay the return of glucose or hunger to baseline.

The objective of the present study was to assess the association between the observed and perceived food environment and food insecurity among households with children <18 years in Lima, Peru. This was a cross-sectional study including an income-stratified random sample of households (n 329) in Villa el Salvador, a low-income district in Lima, Peru. Data were collected with a household questionnaire – including the Household Food Insecurity Access Scale (HFIAS) and the University of Pennsylvania's Perceived Nutrition Environment Survey (NEMS-P) – and a neighbourhood food outlet census, including recording of food outlets’ GPS coordinates. Three-quarters of the households interviewed were food insecure. Compared with food secure households and adjusting for socio-demographic covariates, food insecure households were more likely to disagree to having easy access (OR 5⋅4; 95 % CI 2⋅1, 13⋅4), high quality (OR 3⋅1; 95 % CI 1⋅7, 5⋅5) and variety (OR 2⋅5; 95 % CI 1⋅4, 4⋅6) of fresh fruits and vegetables in their neighbourhood. About 60 % (513 out of 861) of the food outlets identified in participants’ neighbourhoods were classified as fresh, including markets, bodegas, and fruit and vegetable vendors. There was no difference in distance to fresh food outlets by household food insecurity; all households were on average within 52–62 m from a fresh food outlet (~2-min walk). Despite negative perceptions of their neighbourhood food environment, food insecure households had similar physical access to fresh food sources than their food secure counterparts. Thus, changes to the food environment may not alleviate food insecurity in urban poor areas of Peru.

Research suggests that adiponectin, leptin, and genetic polymorphisms such as catechol-O-methyltransferase (COMT) genotype may play an integral role in blood pressure status and thereby cardiovascular health. This is an area especially important for women who are post-menopause; however, the current literature investigating these associations is limited. This study was a cross-sectional secondary analysis of baseline data (N 237) from the Minnesota Green Tea Trial (MGTT). The current study explored the relationships between plasma adiponectin, leptin, and COMT genotype on blood pressure measures. Plasma adiponectin and leptin were obtained after an overnight fast of at least 10 h and were measured by the radioimmunoassay method. The relationships were analysed using multiple linear regression after adjusting for potential confounders. Effect modifications by age, body mass index (BMI) category, blood pressure category, antihypertensive medication use, and COMT genotype were also investigated. The majority of participants were non-Hispanic (97⋅9 %) and Caucasian (94⋅9 %). Mean (sd) age and BMI were 60⋅7 (5⋅0) years and 28⋅2 (2⋅9) kg/m2, respectively. After adjustment for confounding variables, neither plasma adiponectin, plasma leptin nor COMT genotype was associated with systolic or diastolic blood pressure measures. The results of stratified analyses also did not reveal any significant interactions or associations. Based on the findings of this study, which utilised more rigorous statistical methods than previous research, neither adiponectin, leptin nor COMT genotype play a role in blood pressure measures in women who are post-menopause.

Research on children's dietary diversity plays a crucial role in designing effective health interventions. Thus, this study aimed to identify the factors contributing to minimum dietary diversity failure (MDDF) among male and female children aged 6–23 months in Bangladesh. The data for this study was obtained from the Bangladesh Multiple Indicator Cluster Survey, 2019, which included children currently breastfed within a specific age range. Multivariable binary logistic regression was employed to assess the strength and significance of the association. The findings revealed that approximately 59⋅4 % of children in Bangladesh experienced MDDF, with 57⋅8 % of male children and 61 % of female children affected. Proportion test uncovered a significant gender disparity (χ2=6⋅58, P-value = 0⋅01) among children aged 6–23 months. However, the multivariable binary logistic regression analysis revealed that both male and female children shared common risk factors for MDDF, which included child age, maternal educational status, wealth status, number of antenatal care visits, and division. In our study, we observed varied spatial patterns in minimal dietary diversity. Sherpur, Netrokona, Sunamganj, and Sylhet districts showed the highest failure rates. Notably, all are flood-affected areas, impacting food availability and diversity. For targeted regional development programmes, district mapping results may offer valuable insights to policymakers, especially in areas with a high prevalence of dietary diversity failure. By understanding these risk factors, policymakers and stakeholders can implement targeted strategies to improve dietary diversity among children, promoting better health and well-being for the young population in Bangladesh.

Obesity is one of the major contributors to the excess mortality seen in people with severe mental illness (SMI) and in low- and middle-income countries people with SMI may be at an even greater risk. In this study, we aimed to determine the prevalence of obesity and overweight in people with SMI and investigate the association of obesity and overweight with sociodemographic variables, other physical comorbidities, and health-risk behaviours. This was a multi-country cross-sectional survey study where data were collected from 3989 adults with SMI from three specialist mental health institutions in Bangladesh, India, and Pakistan. The prevalence of overweight and obesity was estimated using Asian BMI thresholds. Multinomial regression models were then used to explore associations between overweight and obesity with various potential determinants. There was a high prevalence of overweight (17·3 %) and obesity (46·2 %). The relative risk of having obesity (compared to normal weight) was double in women (RRR = 2·04) compared with men. Participants who met the WHO recommendations for fruit and vegetable intake had 2·53 (95 % CI: 1·65–3·88) times greater risk of having obesity compared to those not meeting them. Also, the relative risk of having obesity in people with hypertension is 69 % higher than in people without hypertension (RRR = 1·69). In conclusion, obesity is highly prevalent in SMI and associated with chronic disease. The complex relationship between diet and risk of obesity was also highlighted. People with SMI and obesity could benefit from screening for non-communicable diseases, better nutritional education, and context-appropriate lifestyle interventions.

Mild-to-moderate iodine deficiency remains a problem worldwide, including in Norway. Of particular, concern is fertile, pregnant and lactating women. The Norwegian Dairy Council developed a digital iodine-specific dietary screener (I-screener) for the assessment of iodine intake levels but has yet to be validated. The aim was thus to investigate the relative validity of the I-screener by comparing estimates of iodine intake from the I-screener against a single 24-hour recall (24HR) and urinary iodine concentration (UIC) in fertile women. Healthy females were recruited in Bergen in August–December 2021. Six spot-urine samples from six consecutive days were collected into a pooled sample to assess UIC. Each participant completed a single administration of the I-screener and the 24HR. The estimated daily iodine intake from the I-screener was compared with the estimations from the 24HR and UIC. Seventy-two women aged 19–39 completed the study. The median UIC was 76 μg/l. Compared with the 24HR, the I-screener placed 83 % of the participants in the same/adjacent tertial, with a slight agreement between the methods (Cohen's kappa = 0⋅187). The present study shows an acceptable correlation between the I-screener and the 24HR (r = 0⋅318), but not between the I-screener and UIC (r = 0⋅122). Despite its varying iodine estimate abilities, the I-screener may be used as an initial screening tool to rank fertile women on an individual level into deficient inadequate, and sufficient iodine intake. However, due to the relatively high risk of misclassification, further assessment of iodine status should follow.

Mitochondrial dysfunction is a common feature of brain disorders. Mitochondria play a central role in oxidative phosphorylation; thus changes in energy metabolism in the brain have been reported in conditions such as Alzheimer’s disease, Parkinson’s disease, and stroke. In addition, mitochondria regulate cellular responses associated with neuronal damage such as the production of reactive oxygen species (ROS), opening of the mitochondrial permeability transition pore (mPTP), and apoptosis. Therefore, interventions that aim to protect mitochondria may be effective against brain disorders. Fucoxanthin is a marine carotenoid that has recently gained recognition for its neuroprotective properties. However, the cellular mechanisms of fucoxanthin in brain disorders, particularly its role in mitochondrial function, have not been thoroughly discussed. This review summarises the current literature on the effects of fucoxanthin on oxidative stress, neuroinflammation, and apoptosis using in vitro and in vivo models of brain disorders. We further present the potential mechanisms by which fucoxanthin protects mitochondria, with the objective of developing dietary interventions for a spectrum of brain disorders. Although the studies reviewed are predominantly preclinical studies, they provide important insights into understanding the cellular and molecular functions of fucoxanthin in the brain. Future studies investigating the mechanisms of action and the molecular targets of fucoxanthin are warranted to develop translational approaches to brain disorders.