Previous studies on the association between fruit juice consumption and type 2 diabetes remain controversial, which might be due to heterogeneity in the polygenic risk score (PRS) for type 2 diabetes. We examined the association between fruit juice and type 2 diabetes by PRS for type 2 diabetes. We investigated whether fruit juice influences type 2 diabetes risk differently among individuals with varying genetic risks. Data from the Japan Multi-Institutional Collaborative Cohort (J-MICC) study, a cross-sectional study of 13 769 Japanese individuals was used for our analysis. The primary exposure was the frequency of fruit juice, categorised as do not drink, less than 1 cup per day or more than 1 cup per day. We selected PGS002379, a PRS for type 2 diabetes developed using East Asian populations. The primary outcome was physician-diagnosed type 2 diabetes, reported by participants. The consumption of fruit juice was significantly inversely associated with type 2 diabetes in the group with a high PRS for type 2 diabetes (OR: 0·78, 95 % CI: 0·65, 0·93 for < 1 cup/d and OR: 0·54, 95 % CI: 0·30, 0·96 for > 1/d), but this association was not observed in the low PRS group. Fruit juice consumption was inversely associated with type 2 diabetes, especially in genetically high-risk populations for type 2 diabetes.

The effects of high plant-based proteins (PP) used as alternative protein sources in aquafeeds on muscle cellularity and myogenic factors of rainbow trout, Oncorhynchus mykiss, remain unclear. This study explored muscle fibre growth phases and the impact of two additive mixtures (A) in high-PP diets on muscle physiology. Over a seven-month trial, 2000 fish (2·22 g) were divided into four groups (five replicates each) and fed isonitrogenous (fry, 46 %; fingerling, 44 %; and grow-out, 42 % crude protein) and isolipidic (20 % lipid) diets: control (30 % fishmeal), PP, PP + A1 (krill meal, taurine, selenium) and PP + A2 (proline, hydroxyproline, vitamin C). Sampling for muscle histology and myogenic gene expression was conducted at ten sampling points from Day 0 to Day 214. Muscle histology (fibre distribution: small, 0–20 μm; small-medium, 20–60 μm; large-medium, 60–100 μm and large, ≥ 100 μm diameter) revealed four growth phases: hyperplasia (2·2–15 g), hypertrophy (15–50 g), hyperplasia (50–150 g) and hypertrophy (150–350 g). MyoD2 and myogenic regulatory factor 4 (MRF4) were upregulated during hyperplasia, while myostatin 1 (MSTN1)/myostatin 2 (2) and reduced Paired box 7 indicating growth inhibition and fewer satellite cells. The PP diet without additives altered fibre recruitment, while PP + A2 enhanced hypertrophy, increasing large (> 100 μm) fibres. Additive mixtures modulated myogenic gene expression, with PP + A2 promoting MyoD2, myogenin and MRF4 and reducing MEF2A/C, contrary to known hypertrophy markers. PP + A1 and PP + A2 diets reduced MSTN1 expression, potentially mitigating growth inhibition. Additive supplementation in PP diets alleviates negative impacts on muscle cellularity and myogenic regulation. The identified growth phases provide insights for precision nutrition, supporting improved feeding strategies for sustainable aquaculture.

Obesity is characterised by chronic low-grade inflammation, which is a key factor in the development of obesity-related co-morbidities. Intake of n-3 long-chain PUFAs is associated with anti-inflammatory effects. Recent studies suggest that also n-11 long-chain MUFAs may reduce the concentrations of inflammatory markers, possibly by increasing the biosynthesis of EPA. The primary aim was to investigate if diets added herring oil containing cetoleic acid (CA, C22:1n-11) or a CA concentrate (CECO) affected the fatty acid composition in tissues from obese rats with chronic inflammation. Secondary aims included investigating the effects on inflammatory markers. Thirty male obese Zucker fa/fa rats were fed diets containing herring oil (HERO) or a CECO, containing 0·70 or 1·40 wt% CA, respectively, with a comparable content of EPA (0·17 and 0·20 wt%, respectively), or a control diet with soyabean oil for 5 weeks. Data were analysed using one-way ANOVA. CA from HERO and CECO diets were recovered in liver, adipose tissue, muscle and blood cells. The EPA concentration was similar between HERO and CECO groups in tissues, whereas the hepatic concentrations of fatty acid desaturases were lower or similar to Controls. The concentrations of TNFα, matrix metalloproteinase-3, IL6, monocyte chemotactic protein 1 and integrin α M in adipose tissue, and the hepatic concentration of CD68 were lower after CECO intake but were not affected by the HERO diet. To conclude, rats fed the CECO diet had lower concentrations of inflammatory and macrophage infiltration markers, but this effect was probably not mediated through increased EPA biosynthesis.

This study examined whether supplementation with collagen peptides (CP) affects appetite and post-exercise energy intake in healthy active females. In this randomised, double-blind cross-over study, fifteen healthy females (23 (sd 3) years) consumed 15 g/d of CP or a taste matched non-energy control (CON) for 7 d. On day 7, participants cycled for 45 min at ∼55 % Wmax, before consuming the final supplement. Sixty-min post supplementation an ad libitum meal was provided, and energy intake recorded. Subjective appetite sensations were measured daily for 6 d (pre- and 30 min post-supplement) and pre (0 min) to 280 min post-exercise on day 7. Blood glucose and hormone concentrations (total ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), cholecystokinin (CCK), dipeptidyl peptidase-4 (sDPP-4), leptin, and insulin) were measured fasted at baseline (day 0), then pre-breakfast (0 min), post-exercise (100 min), post-supplement (115, 130, 145, 160 min) and post-meal (220, 280 min) on day 7. Ad libitum energy intake was ∼10 % (∼41 kcal) lower in the CP trial (P = 0·037). There was no difference in gastrointestinal symptoms or subjective appetite sensations throughout the trial (P ≥ 0·412). Total plasma GLP-1 (AUC, CON: 6369 (sd 2330); CP: 9064 (sd 3021) pmol/l; P < 0·001) and insulin (+80 % at peak) were higher after CP (P < 0·001). Plasma ghrelin and leptin were lower in CP (condition effect; P ≤ 0·032). PYY, CCK and glucose were not different between CP and placebo (P ≥ 0·100). CP supplementation following exercise increased GLP-1 and insulin concentrations and reduced ad libitum energy intake at a subsequent meal in physically active females.

Although numerous clinical studies suggest that ginseng supplementation may benefit CVD risk factors, results remain inconclusive. This systematic review and meta-analysis evaluated the effects of ginseng supplementation on CVD-related risk factors. Relevant studies were identified through electronic searches in Embase, Web of Science, Scopus, PubMed and CENTRAL up to August 2024. Statistical analyses, including a random effects model, meta-regression and non-linear modelling, were used to assess heterogeneity, dose–response relationships and the overall effects of ginseng supplementation. A total of 70 studies, published between 1998 and 2024 and involving 4506 participants, were included. Ginseng supplementation significantly affected several biochemical markers, including high-sensitivity C-reactive protein (standardised mean difference (SMD): −0·23; 95 % CI: −0·38, −0·08; P = 0·002), gamma-glutamyl transferase (SMD: −0·20; 95 % CI: −0·36, −0·04; P = 0·015), glutathione reductase (SMD: 0·90; 95 % CI: 0·38, 1·42; P = 0·001), reactive oxygen species (SMD: −0·94; 95 % CI: −1·27, −0·60; P < 0·001) and superoxide dismutase (SMD: 0·48; 95 % CI: 0·10, 0·87; P = 0·014). Meta-regression analysis showed significant linear associations between ginseng dosage and Homeostatic Model Assessment for Insulin Resistance (P = 0·044) and between supplementation duration and malondialdehyde (P = 0·007). Dose–response analysis revealed significant associations between ginseng dose and fasting blood glucose (P < 0·001), high-sensitivity C-reactive protein (P = 0·043), IL-6 (P = 0·041), diastolic blood pressure (P = 0·022), IL-10 (P = 0·048), fasting insulin (P = 0·012) and total protein (P = 0·010). Supplementation duration was positively associated with malondialdehyde levels (P = 0·008). Ginseng supplementation was associated with improvements in inflammatory markers, liver function and oxidative stress parameters. No significant effects were observed on anthropometric indices, blood pressure, glycaemic profile, lipid profile, adipokines or heart rate.

TNF-α polymorphisms may influence dyslipidaemia, but their role remains unclear. This case–control study investigated associations between TNF-α gene polymorphisms (–1031T/C, −863C/A, −857C/T, −308G/A and −238G/A) and dyslipidaemia in 595 participants (162 cases, 433 controls) from the Chaoshan region of China. Anthropometric, biochemical and genetic data were analysed using χ2 tests and logistic regression, with the false discovery rate (FDR) method applied to correct for multiple comparisons. Results revealed that only the −1031T/C and −863C/A polymorphisms were significantly associated with dyslipidaemia. Carriers of the TC + CC genotype for −1031T/C (OR = 0·48; 95 % CI: 0·30, 0·78; PFDR = 0·006) and the CA + AA genotype for −863C/A (OR = 0·41; 95 % CI: 0·24, 0·70; PFDR = 0·004) had lower odds of dyslipidaemia. Protective effects were observed for the C allele at −1031T/C (OR = 0·58, PFDR = 0·012) and the A allele at −863C/A (OR = 0·47, PFDR = 0·004). Stratified analyses showed that these associations were significant in males but not females. Functional annotation linked these TNF-α gene polymorphisms to transcription factors (e.g. HNF-1A, STAT1β) in the adipogenesis pathway. This study reveals genetic associations between TNF-α polymorphisms and dyslipidaemia, particularly in males, and provides mechanistic insights into their role in transcriptional regulation.

Thyroglobulin (Tg) has been considered a measure of iodine status, but there is no global guidance. This analysis examines the relationship between serum Tg and spot urinary iodine concentration (UIC) data to identify Tg concentrations that correspond to current WHO thresholds for population iodine status. We analysed data from 730 non-pregnant Guatemalan women aged 15–49 years who had both UIC and Tg measurements. Correlations were examined. Bootstrap stratified finite sampling with replacement was used to generate cluster k-medians of UIC (mUIC) and Tg (mTg) that served as the population unit of analyses. Non-linear restricted cubic spline regression dose–response curve functions and ordinary differential equations were then used to derive the Tg threshold corresponding to WHO definitions for UIC. Mean age was 30·2 (sd 9·3) years. mTg was 10·4 ng/ml (9·9, 10·8), and mUIC was 148·7 μg/l (139·1, 161·0). Correlations between spot UIC and Tg were NS at the individual level, but correlations based on population k-medians were significant (Spearman r = −0·21 to −0·06, each P < 0·0001) and demonstrated a U-shaped relationship according to WHO categories. Derived mTg cutoffs were 14·2 ng/ml predictive of UIC insufficiency, 10·2 ng/ml for UIC adequacy, 8·5 ng/ml for UIC above adequate and 10·8 ng/ml for UIC excess. The significant and graded mUIC–mTg correlations suggest that Tg concentrations predictive of UIC categories are obtainable for non-pregnant Guatemalan women aged 15–49 years. The newly derived mTg cutoff may be more discriminant at a lower spectrum of UIC in terms of identifying iodine-deficient women, more so than in the UIC excess category.

High BMI is an important risk factor for female colon and rectal, ovarian and uterine cancers. Current comprehensive studies on its effects on these cancers are limited. This paper aims to explore regional and age differences in the impact of high BMI on these cancers and the commonalities among the three by using the Global Burden of Disease 2021. Deaths, disability-adjusted life years and their age-standardised rates for these cancers were retrieved from 1990 to 2021, and burden trends were assessed using the estimated annual percentage change and percentage changes. The study also analysed the correlation between age-standardised rate and socio-demographic index across twenty-one regions and projected future disease burden trends using the Bayesian Age-Period-Cohort model. Results showed that the global burden of female colon and rectal cancer declined since 1990 but remained at the highest level among the three cancers in 2021. At the same time, these three cancers had high burdens in high-income areas. Since 1990, ovarian and uterine cancer burdens attributable to high BMI increased, and all three burdens grew fastest in low-middle-income regions and among younger people. The burden of all three is projected to continue increasing through 2050. This study confirms that high BMI’s impact on these cancers is regional and age-specific, with long-term effects. Therefore, subsequent public health interventions should adopt more targeted obesity prevention and control strategies based on national and regional situations to effectively mitigate the adverse effects of high BMI on these cancers.

Age is the main risk factor for many neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and frontotemporal dementia. Despite our limited understanding of cellular mechanisms of ageing-associated neuronal loss, an increasing number of studies demonstrate that oxidative stress and inflammation are key drivers. Epidemiological studies indicate that diet during middle adulthood can influence the risk of developing neurodegenerative diseases later in life, so it is important to investigate dietary interventions to combat oxidative stress and inflammation. In this study, we hypothesised that treatment with fucoxanthin, a marine carotenoid with strong antioxidant properties, prevents ageing-associated oxidative stress that is known to be related to natural brain ageing. Treatment with fucoxanthin protected rat primary hippocampal neurons against oxidative stress and ageing in vitro. In our in vivo study, middle-aged male Sprague-Dawley rats were gavaged with fucoxanthin (1 mg/kg, 5 d/week, n 6) or vehicle (n 6) for 4 weeks. After supplementation was completed, brain samples were harvested and subjected to quantitative and bioinformatic analyses. Fucoxanthin was detected and shown to decrease lipid peroxidation in the brains of the animals supplemented with fucoxanthin. Microarray analysis showed that treatment with fucoxanthin changed 5602 genes. Together, our results suggest that treatment with fucoxanthin prevents ageing-associated oxidative stress and is capable of regulating genes that potentially ameliorate age-related changes to the brain.

The effect of dietary FODMAP (fermentable oligo-, di- and mono-saccharides and polyols) in healthy adults is poorly documented. This study compared the specific effects of low and moderate FODMAP intake (relative to typical intake) on the faecal microbiome, participant-reported outcomes and gastrointestinal physiology. In a single-blind cross-over study, twenty-five healthy participants were randomised to one of two provided diets, ‘low’ (LFD) <4 g/d or ‘moderate’ (MFD) 14–18 g/d, for 3 weeks each, with ≥ 2-week washout between. Endpoints were assessed in the last week of each diet. The faecal bacterial/archaeal and fungal communities were characterised by eighteen participants from whom high-quality DNA was extracted by 16S rRNA and internal transcribed spacer 2 (ITS2) profiling and metagenomic sequencing. There were no differences in gastrointestinal or behavioural symptoms (fatigue, depression, anxiety) or faecal characteristics and biochemistry (including SCFA). Mean colonic transit time (telemetry) was 23 (95 % CI: 15, 30) h with the MFD compared with 34 (24, 44) h with LFD (n 12; P = 0·009). Fungal diversity (richness) increased in response to MFD, but the bacterial richness was reduced, coincident with the expansion of the relative abundances of Bifidobacterium, Anaerostipes and Eubacterium. Metagenomic analysis showed expansion of polyol-utilising Bifidobacteria and Anaerostipes with MFD. In conclusion, short-term alterations of FODMAP intake are not associated with symptomatic, stool or behavioural manifestations in healthy adults, but remarkable shifts within the bacterial and mycobiome populations were observed. These findings emphasise the need to quantitatively assess all microbial domains and their interrelationships to improve understanding of the consequences of diet on gut function.

2,3-Diphosphoglycerate (2,3-DPG), found primarily in red blood cells, plays a key role in regulating hemoglobin’s (Hb) affinity for oxygen. Increased 2,3-DPG levels shift the oxygen dissociation curve to the right, reducing Hb’s oxygen affinity and enhancing oxygen delivery to tissues—particularly important in conditions like anemia and high-altitude adaptation. Despite its physiological significance, research on 2,3-DPG is outdated and limited. This review aims to summarize current knowledge and identify research gaps. Measuring 2,3-DPG is challenging due to its instability and the need for careful sample handling. Chromatography and enzymatic methods are commonly used. Several factors influence 2,3-DPG levels, including diet, physiological state, and disease. Dietary phosphorus, for example, can acutely affect 2,3-DPG levels, though the impact of different meal compositions remains unexplored. Age, pregnancy, and physical activity also modulate 2,3-DPG, yet little is known about its role in infants and children. While changes in 2,3-DPG levels under various pathological conditions have been described, the molecular mechanisms behind these alterations remain poorly understood and warrant further investigation.

The objective of this study was to evaluate the impact of incorporating group-based nutritional education into usual care on adherence to nutritional counselling among outpatients with type 2 diabetes (T2DM). This parallel-group, randomised controlled superiority trial was conducted with outpatients diagnosed with T2DM and poor glycaemic control. The control group received individual usual care, while the intervention group received usual care plus group-based nutritional education, which included three sessions: ‘Let’s Go Shopping,’ ‘Healthy Plate’ and ‘Hunger and Satiety.’ Baseline and four-month follow-up assessments were conducted, and outcome measures included adherence to nutritional counselling, glycaemic control, weight and physical activity. A total of 213 participants were included: 61·9 % were women, aged 60 years (interquartile range (IQR) = 53–65), 67·6 % with low socio-economic status, 67·3 % had obesity and the glycated Hb (HbA1c) was 9·3 % (IQR = 8·3–10·2 %). The intervention did not result in superior glycaemic control; however, short-term reductions in HbA1c were observed across all participants (–0·3 % (IQR = –0·7–0·3 %)). The intervention group demonstrated an increase in physical activity levels between visits (262 metabolic equivalent tasks (IQR = 99–257); P = 0·038), but no significant difference between the groups. Participants in the intervention group adhered to 67 % of combinations, compared with 50 % in the control group (P = 0·012), and adherence to the diabetes plate method was significantly higher in this group (75·9 % v. 62·2 %; P = 0·05). In conclusion, no significant between-group differences in glycaemic control were found, although both groups improved HbA1c short-term. Group-based nutritional education increased dietary adherence, particularly to the diabetes plate method and physical activity. Long-term effects on metabolic outcomes warrant further study.

Type 2 diabetes (T2D) incidence has been steadily increasing over the past few decades. Several studies have evaluated the effect of plant-based, vegetarian or vegan diets on the risk of T2D, although their potential benefits need to be confirmed and characterised. We performed a literature search up to 10 July 2025, using the terms/keywords related to plant-based index (PDI), vegetarian/vegan diets and T2D. We included observational non-experimental studies evaluating adherence to such diets in adult subjects assessing T2D risk. We specifically considered overall PDI and related healthy PDI (hPDI) and unhealthy PDI (uPDI), assessing intake of different food groups. We included 36 studies published between 1999 and 2025. We found an inverse association between adherence to vegetarian/plant-based dietary patterns and T2D risk. This association was stronger, though statistically imprecise, for the vegan diet (RR = 0·65, 95 % CI 0·42, 1·00) and for lacto-ovo-vegetarian diet (RR = 0·68, 0·57, 0·82). For studies using plant-based indices, the RR were 0·82 (0·69, 0·82), 0·76 (0·69, 0·82) and 1·13 (0·98, 1·30) for overall PDI, hPDI and uPDI, respectively. In the dose–response meta-analysis, overall PDI and hPDI showed an inverse and almost linear association with T2D risk. Conversely, adherence to uPDI directly correlated with T2D risk. Overall, adherence to vegan/vegetarian diets may reduce T2D risk, while an unhealthy plant-based diet appears to linearly increase disease risk, indicating caution in the consumption of such unhealthy foods even if of plant origin. The beneficial association between vegetarian and healthy plant-based diets may have major public health implications.

Persistent malnutrition is associated with poor clinical outcomes in cancer. However, assessing its reversibility can be challenging. The present study aimed to utilise machine learning (ML) to predict reversible malnutrition (RM) in patients with cancer. A multicentre cohort study including hospitalised oncology patients. Malnutrition was diagnosed using an international consensus. RM was defined as a positive diagnosis of malnutrition upon patient admission which turned negative one month later. Time-series data on body weight and skeletal muscle were modelled using a long short-term memory architecture to predict RM. The model was named as WAL-net, and its performance, explainability, clinical relevance and generalisability were evaluated. We investigated 4254 patients with cancer-associated malnutrition (discovery set = 2977, test set = 1277). There were 2783 men and 1471 women (median age = 61 years). RM was identified in 754 (17·7 %) patients. RM/non-RM groups showed distinct patterns of weight and muscle dynamics, and RM was negatively correlated to the progressive stages of cancer cachexia (r = –0·340, P < 0·001). WAL-net was the state-of-the-art model among all ML algorithms evaluated, demonstrating favourable performance to predict RM in the test set (AUC = 0·924, 95 % CI = 0·904, 0·944) and an external validation set (n 798, AUC = 0·909, 95 % CI = 0·876, 0·943). Model-predicted RM using baseline information was associated with lower future risks of underweight, sarcopenia, performance status decline and progression of malnutrition (all P < 0·05). This study presents an explainable deep learning model, the WAL-net, for early identification of RM in patients with cancer. These findings might help the management of cancer-associated malnutrition to optimise patient outcomes in multidisciplinary cancer care.

The purpose of this study was to confirm reduced training metrics previously associated with a ketogenic low-carbohydrate (CHO) high-fat diet (LCHF) and investigate their attenuation with caffeine supplementation. At baseline, n 21 elite race-walkers followed a high CHO availability (HCHO) diet and performed a tempo hill session (14 km with a 450 m elevation gain). Athletes were then assigned to either the HCHO or LCHF in a parallel groups design for 3 weeks, where the 14 km tempo hill session was repeated each week. On weeks 2 and 3, in a randomised crossover allocation, all participants received 3 mg/kg caffeine or placebo (gum), 20 min before the session. Race-walking speed, heart rate, ratings of perceived exertion, blood metabolites and Stroop word-colour test metrics were collected. Although LCHF athletes walked faster at baseline compared with HCHO (P = 0·049), the HCHO group improved by week 2 (P = 0·009) and week 3 (P = 0·007), whereas the LCHF group was significantly slower in Week 1 (P < 0·001) and Week 2 (P = 0·026) compared with baseline. During the 14 km hill session, within-group analysis shows that athletes walked significantly faster (P = 0·010) and at a higher percentage of vVO2max (P = 0·007) when using caffeine compared with a placebo. Between-group differences remained present, with HCHO athletes walking at a higher percentage of vVO2max than those adhering to the LCHF diet (P = 0·035). No interaction between supplement treatment and dietary group occurred (P = 0·640). Caffeine supplementation partially reversed the performance impairment associated with an LCHF diet, but training quality remained lower than the combination of caffeine and high CHO availability.