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.

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.

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.

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.

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.

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.

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.

Blood 25-hydroxyvitamin D (25(OH)D) concentrations vary considerably by season and sex. The present study aimed to determine associations between vitamin D deficiency and mortality in Japanese adults and identify risk thresholds according to 25(OH)D concentrations. This was a cohort study with an 11-year follow-up. Participants were 8285 community-dwelling Japanese adults aged 40–74 years. Plasma 25(OH)D concentrations were measured by chemiluminescent immunoassay at baseline and divided into quintiles for each of the subgroups stratified by season and sex (denoted as season- and sex-stratified quintiles). The main outcome was all-cause mortality. Hazard ratios (HR) were calculated using a Cox proportional hazards model. Mean age and 25(OH)D concentration were 59·9 years (sd = 9·1) and 50·1 nmol/l (sd = 18·1), respectively. Lower season- and sex-stratified quintiles were associated with higher hazards of all-cause mortality (Pfor trend = 0·0015), with the first quintile (median = 28·2 nmol/l) having a higher HR (HR = 1·46, 95 % CI, 1·13, 1·88) than the highest quintile (reference). When crude quintiles were used, the overall association was similar (Pfor trend = 0·0027), with the first (median = 28·0 nmol/l) and second (median = 39·7 nmol/l) quintiles having higher HR (HR = 1·40, 95 % CI, 1·06, 1·85 and 1·38, 95 % CI, 1·07, 1·77, respectively) than the reference. The risk threshold difference was estimated to be approximately 10 nmol/l. In conclusion, low blood 25(OH)D concentrations are associated with high mortality risk. Crude blood 25(OH)D concentration may modulate the estimated risk threshold for vitamin D deficiency associated with mortality.

This study examined the associations between cold and hot food and beverage consumption and various health outcomes among Asians and Whites in the USA. Data were drawn from 212 Asian and 203 White adults (aged 18–65 years) in the Healthy Ageing Survey. Participants reported their frequency of cold and hot drink and meal intake, along with symptoms of depression, anxiety, insomnia and gastrointestinal issues (e.g. gas, abdominal fullness). Multivariable analyses adjusted for confounders were used to assess these associations. Among Asians, higher cold consumption in summer was associated with increased anxiety (β = 0·24, 95 % CI: 0·05, 0·44) and abdominal fullness (β = 0·05, 95 % CI: 0·01, 0·86). In contrast, among Whites, higher winter hot drink intake was linked to lower insomnia (β = –0·23, 95 % CI: –0·42, –0·04) and gas symptoms (β = –0·05, 95 % CI: –0·09, –0·01). Tertile analyses showed that, compared with tertile 1, Asians in the highest tertile of summer cold drink intake had higher insomnia scores (β = 1·26, 95 % CI: 0·19, 2·33), while Whites in the highest tertile of winter hot drink intake had lower depression scores (β = –1·73, 95 % CI: –3·28, –0·18). These associations were stronger among individuals with cold hands but not observed in those without. Findings suggest that the temperature of foods and beverages may influence mental and gut health, underscoring the need to consider temperature-related dietary habits in public health and nutrition strategies, particularly across diverse populations.

This study explored whether lifestyle therapy that promoted adherence to a Mediterranean-style diet as a treatment for depression led to environmental co-benefits. Participants (n 75 complete case) were Australian adults in the Curbing Anxiety and Depression using Lifestyle Medicine non-inferiority, randomised controlled trial, which showed that lifestyle therapy was non-inferior to psychotherapy in reducing depressive symptoms, when delivered in group format via video conferencing over an 8-week treatment period. In this secondary analysis, we hypothesised that the lifestyle arm would be superior to the psychotherapy arm in reducing the environmental impact of self-reported diet over time. Dietary intake derived from FFQ at baseline and 8 weeks was transformed into environmental impact scores by calculating global warming potential (GWP)*. GWP* was calculated for total dietary intake and distinct food groups (Australian Dietary Guidelines and NOVA classifications). Within-arm changes in GWP* over time were calculated using the median difference. Neither arm showed significant changes. Between-arm differences in percentage change in GWP* scores over time were analysed using generalised estimating equations models. No between-arm difference for total GWP* score was found (β = 11·06 (–7·04, 29·15)). When examining distinct food groups, results were mixed. These novel findings contribute to the sparse evidence base that has measured the environmental impact of diets in a clinical trial context. Whilst lifestyle therapy that reduced depressive symptoms did not have clear environmental benefits relative to psychotherapy, nutritional counselling that focuses on the environmental impact of food choices may drive more pronounced planetary co-benefits.

The current study aims to assess associations between trimethylamine N-oxide (TMAO) levels and mortality and to investigate modification effects of genetics. A total of 500 participants from a family-based cohort study were enrolled from 2005 to 2017 and followed up until 2020 in Fangshan District, Beijing, China. Serum TMAO levels were measured using the ELISA kit. The primary outcomes were all-cause mortality and deaths from CVD and stroke. During a median follow-up time of 7·38 years, thirty-eight deaths were recorded, including twenty deaths due to CVD and nineteen deaths due to stroke. Compared with the lowest TMAO quartile group, the HR for all-cause mortality was 1·35 (95 % CI: 0·44, 4·15), 1·65 (95 % CI: 0·58, 4·64) and 2·45 (95 % CI: 0·91, 6·57), respectively, in higher groups. No association was observed between TMAO and CVD mortality. However, compared with the lowest TMAO concentration group, the HR for stroke mortality was 1·93 (95 % CI: 0·40, 9·39), 1·91 (95 % CI: 0·41, 8·96) and 4·16 (95 % CI: 0·94, 18·52), respectively, in higher groups (Pfor trend = 0·046). Furthermore, polygenic risk score (PRS) for longevity modified the association of TMAO with all-cause mortality (Pfor interaction = 0·008). The risk of mortality (HR = 2·20, 95 % CI: 1·06, 4·57) was higher among participants with lower PRS compared with higher PRS (HR = 1·00, 95 % CI: 0·71, 1·40). The study indicates that elevated serum TMAO levels are potentially associated with long-term mortality risk in rural areas of northern China, especially for stroke deaths. Additionally, it provides novel evidence that genetic variations might modify the association.

Previous observational studies suggested that vitamin D may control the absorption of iron (Fe) by inhibition of hepcidin, but the causal relevance of these associations is uncertain. Using placebo-controlled randomisation, we assessed the effects of supplementation with vitamin D on biochemical markers of Fe status and erythropoiesis in community-dwelling older people living in the UK. The BEST-D trial, designed to establish the optimum dose of vitamin D3 for future trials, had 305 participants, aged 65 years or older, randomly allocated to 4000 IU vitamin D3 (n 102), 2000 IU vitamin D3 (n 102) or matching placebo (n 101). We estimated the effect of vitamin D allocation on plasma levels of hepcidin, soluble transferrin receptor (sTfR), ferritin, Fe, transferrin, saturated transferrin (TSAT%) and the sTfR–ferritin index. Despite increases in 25-hydroxy-vitamin D, neither dose had significant effects on biochemical markers of Fe status or erythropoiesis. Geometric mean concentrations were similar in vitamin D3 arms v. placebo for hepcidin (20·7 [se 0·90] v. 20·5 [1·21] ng/ml), sTfR (0·69 [0·010] v. 0·70 [0·015] µg/ml), ferritin (97·1 [2·81] v. 97·8 [4·10] µg/l) and sTfR–ferritin ratio (0·36 [0·006] v. 0·36 [0·009]), respectively, while arithmetic mean levels were similar for Fe (16·7 [0·38] v. 17·3 [0·54] µmol/l), transferrin (2·56 [0·014] v. 2·60 [0·021] g/dl) and TSAT% (26·5 [0·60] v. 27·5 [0·85]). The proportions of participants with ferritin < 15 µg/l and TSAT < 16 % were unaltered by vitamin D3 suggesting that 12 months of daily supplementation with moderately high doses of vitamin D3 are unlikely to alter the Fe status of older adults.