Diet and detox teas are commonly marketed as over-the-counter products that claim to support weight loss through detoxification and metabolic enhancement. Despite their widespread use, the evidence base supporting these claims remains unclear. This mini review summarizes and critically examines the existing literature on the safety and efficacy of diet and detox teas marketed for weight loss. A focused review of the literature identified 10 studies spanning experimental research, case reports, product analyses, and marketing assessments. Overall, the available evidence provides limited support for weight loss benefits. A small number of experimental studies suggested modest effects on body weight or metabolic outcomes, while the majority of evidence consisted of case reports and product analyses. Notably, multiple reports described serious adverse health outcomes associated with diet and detox tea consumption, including electrolyte disturbances, cardiovascular events, and liver injury in otherwise healthy individuals. In addition, analytical studies identified undeclared pharmaceutical ingredients, high levels of stimulants, and inconsistencies between labeled and actual product contents in teas marketed as natural. Altogether, current evidence suggests that diet and detox teas marketed for weight loss offer minimal demonstrated benefit and may pose meaningful health risks. The findings highlight important gaps in the evidence base and underscore the need for improved regulatory oversight, clearer labeling, and higher-quality research to better inform consumers and health professionals regarding the use of these products for weight management.

Background Dihydromyricetin (DHM) is a food-derived flavonoid widely investigated as a nutraceutical candidate for metabolic dysfunction–associated steatotic liver disease (MASLD) in preclinical models; however, its overall efficacy in diet-induced MASLD/NAFLD models has not been systematically quantified. Methods This PRISMA 2020 systematic review and meta-analysis was registered in PROSPERO (CRD420251119087). PubMed, Embase, Web of Science Core Collection, the Cochrane Library, and four major Chinese databases were searched from inception to December 15, 2025. Controlled murine studies comparing DHM monotherapy with high-fat diet controls were included. Random-effects meta-analyses pooled standardized mean differences (SMDs) with 95% confidence intervals; risk of bias was assessed using SYRCLE’s tool. Results Fourteen controlled studies were included. Compared with controls, DHM reduced hepatic triglycerides and total cholesterol, improved liver enzymes (ALT, AST, ALP), and decreased body weight and liver index. DHM improved serum lipid profiles (lower total cholesterol and LDL; higher HDL) and glucose homeostasis (lower fasting glucose and insulin). Antioxidant defenses increased (SOD, CAT, GSH, GSH-Px) with reduced malondialdehyde, while inflammatory markers (TNF- α and IL-6) decreased. At the signaling level, DHM increased the pAMPK/AMPK ratio. Heterogeneity was moderate to high for several outcomes, partly explained by dose and treatment duration. Conclusion In murine diet-induced MASLD/NAFLD models, DHM shows promising multidomain benefits across various physiological outcomes, though some variability remains due to differences in study design. More standardized preclinical designs and well-controlled nutraceutical/clinical studies are needed to define clinically relevant, bioavailable dosing and efficacy. Systematic review registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420251119087 , PROSPERO, Identifier CRD420251119087.

Background There is an established correlation between obesity and dyslipidemia in individuals who have undergone kidney transplantation (KT). Body composition is a more accurate indicator of obesity than body mass index (BMI). However, the relationship between pre-operative body composition and post-transplant dyslipidemia remains unexplored. Methods We analyzed 333 participants who underwent KT between 2021 and 2024. Using pre-transplantation computed tomography (CT), we assessed the cross-sectional areas of skeletal muscle (SM) and adipose tissue at the level of the third lumbar vertebra. Participants were categorized into high and low body composition groups based on the highest quartile, and into dyslipidemia and non-dyslipidemia groups according to post-transplant blood lipid levels. Skeletal muscle (SM) and adipose tissue metrics were subsequently used to model dyslipidemia after KT. Generalized estimating equations (GEE) were then employed to assess the impact of body composition on blood lipid levels at 45 days, and at 3, 6 months, and 1 year post-transplant. Results Univariate analysis revealed that BMI ( P = 0.006), visceral adipose tissue (VAT) area ( P < 0.001), intermuscular adipose tissue (IMAT; P = 0.005), subcutaneous adipose tissue (SAT; P = 0.003), and skeletal muscle ( P = 0.019) were identified as risk factors for dyslipidemia 1 year post-transplant. A predictive model was further developed, indicating that VAT was a more reliable predictor than BMI and other body composition metrics. Statistically significant associations were observed for both VAT (OR = 1.005, 95% CI: 1.001–1.009; P = 0.014) and VATI (OR = 1.013, 95% CI: 1.002–1.025; P = 0.027). Sensitivity analysis indicated that the observed effect sizes were near the detection limit for a study of this sample size, reinforcing the modest magnitude of these associations. REE analysis demonstrated that VAT influenced triglyceride (TG) levels ( P = 0.006), high-density lipoprotein cholesterol (HDL-C) levels ( P = 0.001), and low-density lipoprotein cholesterol (LDL-C) levels ( P = 0.033). Conclusions High pre-transplant VAT was associated with low HDL-C, elevated TG, and LDL-C levels after KT. These findings may have significant implications for reducing the incidence of dyslipidemia post-KT.

Background Remnant cholesterol (RC) has been established as an independent risk factor for atherosclerotic cardiovascular disease. While the association between RC and diabetic kidney disease (DKD) remains unclear. Methods This cross-sectional study included 1,893 patients with T2D hospitalized across multiple centers from 2019 to 2024. The correlation of RC and DKD was analyzed by multiple logistic regression and restricted cubic spline (RCS) models. The subgroup analysis was to assess the stability of the correlation between RC and DKD. Results The participants comprise 1,340 without DKD and 553 with DKD. RC was significantly higher in DKD patients compared non-DKD patients ( P = 0.012). In multiple logistic regression analysis, the results revealed a 43% increased DKD risk per 0.1 mmol/L RC increment (adjusted OR = 1.43, 95% CI = 1.10–1.86). Additionally, when analyzed as quartiles, participants in the highest RC quartile (Q4: >0.700 mmol/L) demonstrated 1.77-fold higher DKD risk compared to the lowest quartile (95% CI = 1.28–2.45, P = 0.001), with significant linear trend across quartiles ( P < 0.001). Furthermore, RCS model demonstrated a biphasic relationship: risk increased linearly with RC levels below 0.96 mmol/L (β = 2.25 per 0.1 mmol/L, P = 0.001), transitioning to a plateau (β = 0.86, P = 0.588) with RC levels exceeded 0.96, suggesting lipid-mediated renal injury pathways may reach saturation. Subgroup analyses confirmed stability across demographic or clinical strata (all P > 0.05). Conclusions Our study establishes RC as an independent DKD biomarker in Chinese T2D patient, suggesting its dual utility as a pathophysiological indicator and preventive therapeutic target.

Inflammation and oxidative stress are the key pathogenic mechanisms for the occurrence and development of liver fibrosis. After liver cell damage, excessive reactive oxygen species (ROS) are released, which is a key trigger for the activation of hepatic stellate cells (HSCs). Once activated, HSCs transform into myofibroblasts, leading to excessive extracellular matrix (ECM) deposition and promoting the formation of liver fibrosis. The above processes interact with each other, mutually amplifying and forming a vicious cycle, jointly accelerating the development process of liver fibrosis. The commonly used antioxidants in clinical practice, such as SOD, CAT, and anthocyanins, play a significant role in clinical antioxidant therapy. Vitamins, as common and natural antioxidants, have the characteristic of being both food and medicine, and are relatively safe. Compared with the commonly used antioxidants in clinical settings, vitamins have higher bioavailability, lower adverse reactions and side effects, are widely available, and are easy to obtain. Patients with liver fibrosis often suffer from multiple vitamin deficiencies due to reduced intake, absorption disorders, and increased consumption. This may further accelerate the disease progression. However, the anti-inflammatory and antioxidant effects of vitamins in liver fibrosis and their underlying mechanisms have not been fully elucidated. Moreover, systematic studies on various vitamins are still relatively scarce. Based on the above background, this article systematically elaborates on the research progress of various vitamins in the prevention and treatment of liver fibrosis through their antioxidant and anti-inflammatory mechanisms, with a focus on correcting the deficiency state. The aim is to provide a theoretical basis for precise nutritional intervention for patients with liver fibrosis due to vitamin deficiency.

The link between nutritional status and chemotherapy toxicity in cancer patients requires further clarification. This study used serum metabolomics to examine how nutritional status affects oxaliplatin-induced peripheral neuropathy (OIPN) in patients with colorectal cancer (CRC). We analyzed samples from 219 CRC patients receiving oxaliplatin-based therapy, grouped by nutritional risk using the Nutritional Risk Screening 2002 (NRS-2002) into two cohorts: malnourished (NRS ≥ 3) and well-nourished (NRS < 3) cohorts. Liquid chromatography-mass spectrometry (LC–MS) and multivariate statistics were used to identify differentially expressed metabolites (DEMs). We found 179 DEMs between OIPN and non-neuropathic controls (CONT), with amino acids and derivatives being the most prevalent. Enrichment analysis pinpointed arginine biosynthesis as a key pathway, exhibiting nutrition-dependent regulation. While L-arginine and ornithine were downregulated and L-glutamine was upregulated in OIPN patients overall, this pattern was reversed in the malnutrition subgroup. Concurrently, arginine pathway enrichment was reduced in malnourished patients. These results indicate that OIPN is associated with significant serum metabolite alterations, primarily affecting amino acid metabolism, which are distinctly modulated by malnutrition. Our findings highlight the role of nutritional status in OIPN occurrence and may provide a basis for future research into targeted nutritional support to alleviate this neurotoxicity in CRC patients, although confirmatory studies are needed.

Exercise-induced fatigue is a regular physiological event that impairs sports performance and prolongs recovery time. While conventional recovery methods exist, there is a pressing need for natural, effective, and sustainable alternatives. This review aims to comprehensively review the emerging role of plant-derived bioactive peptides (PBPs) in sports nutrition, highlighting their innovative potential compared to traditional supplements. We demonstrate that PBPs alleviate fatigue through multi-targeted remarkable mechanisms: scavenging reactive oxygen species (ROS) to mitigate oxidative stress, downregulating pro-inflammatory cytokines to protect muscle tissue, and activating specific metabolic pathways (e.g., AMPK) to accelerate glycogen resynthesis and optimize energy utilization. Consequently, the application of PBPs offers a compelling solution to delay fatigue and accelerate physical recovery. However, the field faces significant new challenges, including the lack of standardized dosages, unmapped structure-activity relationships, and a scarcity of human clinical trials. By addressing these unexplored aspects, this study provides a critical theoretical foundation and future directions for developing PBPs as next-generation functional ingredients in personalized sports nutrition.

Introduction Anemia of prematurity (AOP) is a common condition, often necessitating transfusion therapy. Although vitamin AD deficiency has been linked to anemia pathogenesis, the effect of supplementation timing on transfusion needs remains unclear. This study investigates the association between the initiation timing of vitamin AD supplementation and the number of transfusions received in preterm infants. Methods In this retrospective cohort study, we included 226 preterm infants (gestational age <37 weeks) who received both blood transfusions and vitamin AD supplementation in a neonatal intensive care unit (2018–2022). The association was assessed using Spearman correlation. Segmented Poisson regression compared transfusion incidence rates before and after supplementation, controlling for hospitalization timeline. A conditional Cox model (Anderson-Gill) evaluated the impact on subsequent transfusion risk, adjusting for covariates. Patients were stratified by supplementation timing (≤14 vs. >14 days), with propensity score matching applied to balance groups. Independent factors were identified using generalized linear models. Results The timing of vitamin AD initiation was positively correlated with transfusion number [Spearman’s ρ = 0.200(0.068–0.326), p = 0.003], an association that remained significant in subgroups including infants 28–37 weeks and those without complications. Multivariable analysis identified supplementation timing as an independent risk factor for transfusion frequency [ β = 0.016(0.007–0.025), p < 0.001]. Segmented Poisson regression showed a significantly lower incidence rate ratio after supplementation [IRR = 0.139(0.098–0.199)]. The conditional Cox model revealed no immediate change in risk [ HR = 10.858(0.725–162.663), p = 0.084] but a significant time-dependent protective effect [ HR per log(day+1) = 0.381(0.160–0.911), p = 0.03], with the hazard ratio becoming protective by day 5 and reaching 0.32 (68% risk reduction) by day 28. After propensity score matching, no significant difference in transfusion frequency was found between the ≤14-day and >14-day groups [median (IQR): 2 (1.5–3) vs. 2 (2–4), p = 0.544]. Conclusion This study suggests an association between earlier vitamin AD supplementation and reduced transfusion needs in preterm infants, supported by a time-dependent protective effect. The specific optimal timing requires further prospective investigation.

Introduction Zhaqu Compound (ZQC), a traditional Chinese herbal formula, has shown promise in improving glucose and lipid metabolism, but its mechanisms in T2DM-MASLD remain unclear. Methods In this study, db/db mice with T2DM-MASLD were treated for 12 weeks with ZQC, metformin, or saline. Metabolic outcomes included blood glucose, insulin resistance indices, lipid profiles, hepatic steatosis, hepatocyte ultrastructure, gut microbiota (16S rRNA), fecal metabolomics, and liver transcriptomics. In high-glucose + palmitate–induced HepG2 cells, ZQC-containing serum and the PPARγ agonist GW1929 were applied to assess gluconeogenic and lipogenic proteins. Results ZQC improved glycemia, insulin resistance, lipid profiles, and hepatic steatosis. Gut microbiota analysis showed modulation of key metabolic genera, including Bacteroides, Mucispirillum, Lactobacillus, Lachnospiraceae , and Muribaculaceae , with correlations to glucose, lipid, and hepatic biochemical indices. Metabolomics and transcriptomics revealed regulation of amino acid metabolism, AGE-RAGE/mTOR pathways, and enrichment of hepatic PPARγ–related pathways, alongside modulation of fatty acid and arachidonic acid metabolism. In HepG2 cells, ZQC reduced lipid accumulation, decreased triglycerides and cholesterol, enhanced glucose uptake, and restrained PPARγ and its downstream transporters CD36 and FABP4. N-phenethylhexadecanamide, palmitic acid, and isoxanthohumol likely mediate these effects. Discussion Overall, ZQC improves glucose and lipid metabolism in T2DM with MASLD by modulating gut microbiota, influencing hepatic PPARγ–related pathways, and enhancing hepatocyte metabolic function.

Stroke represents the leading cause of disability and mortality worldwide, often resulting in long-term neurological deficits, extensive neuronal damage and inflammatory cascades. Ischemic stroke, which accounts for about 80% of stroke cases, is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. The blood supply interruption induced oxidative stress, mitochondrial dysfunction, neuroinflammation, and gut dysbiosis are involved in complex interactions within brain tissues. Moreover, the reperfusion induced inflammation produces more severe damage compared to the blood supply interruption. Current therapeutic interventions face critical limitations including narrow treatment windows, restricted patient eligibility, and significant adverse effects, underscoring the urgent need for safe, effective adjunctive strategies applicable during extended recovery periods. Recent research highlights the potential of nature biologically active substances, here we referred to food-derived and natural bioactive compounds, as promising therapeutic agents for post-stroke recovery. Administration of these compound by dietary route has the potential to support cellular repair processes via reducing oxidative stress, modulating neuroinflammation, promoting neurogenesis, inhibiting ferroptosis, and enhancing synaptic plasticity. This review examines the current evidence and emerging concepts on the roles of these bioactive compounds in post-stroke recovery and synthesizing mechanistic evidence. We discussed specific dietary sources and pharmacokinetics of selected compounds, providing insights into their bioavailability and potential synergistic effects with conventional therapies. Additionally, we examined clinical studies and evaluated the efficacy and safety of these interventions, offering a translational perspective on their integration into post-stroke rehabilitation. These findings underscore the therapeutic potential of dietary bioactive compounds as adjunctive treatments in post-stroke recovery and highlight the need for dose–response optimization, biomarker-guided precision nutrition approaches for patient stratification, and large-scale trials to validate long-term efficacy and safety in diverse stroke populations.