The purpose of this systematic review and meta-analysis was to investigate the effects of hesperidin supplementation on inflammatory and oxidative stress biomarkers in human adults. A systematic literature search was conducted in PubMed, EMBASE and Cochrane Central Register of Controlled Trials from inception to 4 January 2025 to identify eligible randomised controlled trials. Ten randomised controlled trials with a total of 532 participants were included. The results indicated that hesperidin supplementation significantly reduced the serum levels of C-reactive protein or high-sensitivity C-reactive protein (SMD: –0·43; 95 % CI –0·71, –0·15; P = 0·002) and TNF-α (SMD: –0·51; 95 % CI –0·95, –0·07; P = 0·02) in adults, while no significant beneficial effect of hesperidin on IL-6 was observed (SMD: –0·25; 95 % CI –0·52, 0·01; P = 0·06). In addition, hesperidin intake showed a beneficial impact on the IL-6 level in patients with diseases (type 2 diabetes and myocardial infarction) (SMD: –0·38; 95 % CI –0·72, –0·04; P = 0·03) yet not in healthy adults without diagnosed diseases. Our findings demonstrated that hesperidin supplementation could lower the serum levels of C-reactive protein or high-sensitivity C-reactive protein and TNF-α in adults.

Vitamin D has been associated with depression, potentially via anti-inflammatory mechanisms, yet data are scarce, particularly in adolescence. We investigated (1) whether lower vitamin D status is associated with greater depression severity and (2) whether this association is statistically moderated by inflammation in patients of a child and adolescent psychiatry department. At admission, fasting morning venous blood was drawn. Serum vitamin D (25-hydroxy-cholecalciferol (25(OH)D)) and C-reactive protein (CRP) were analysed in all participants (n 465 (64·7 %♀; 11·3–18·9 years)). In a subsample (n 177), we additionally measured tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin (IL)-1β, IL-6, IL-8 and IL-10. Depression severity was assessed by the Beck Depression Inventory II (BDI-II) (n 450), the Diagnostic System for Mental Disorders in Childhood and Adolescence via self-assessment (DISYPS Self) (n 441) and parent-assessment (DISYPS Proxy) (n 422). Overall, 43·2 % (n 201) were at risk for vitamin D deficiency (< 30 nmol/l), and 73·5–83·2 % – depending on assessment tool – showed at least mild depression. Linear regression revealed an inverse association between 25(OH)D and BDI-II in both crude and CRP-adjusted full-sample models. Logistic regressions showed a robust inverse association between 25(OH)D and DISYPS Proxy, but not for DISYPS Self. Although 25(OH)D was inversely correlated with some pro-inflammatory markers, neither their inclusion in regression models nor formal mediation analyses supported inflammation as a mediator of the vitamin D–depression association. Overall, our results suggest that vitamin D relates modestly to both depression and inflammation in adolescence. However, based on the measured parameters, we cannot confirm that anti-inflammatory effects are the link between vitamin D and depression.

This study aimed to explore whether health effects of dietary nitrate depend on its source, by investigating associations between plant and animal-sourced dietary nitrate groups with markers of inflammation and CVD risk factors. Among 100 non-smoking adults (mean age 49 (sd 13) years, 31 % male), dietary nitrate intake was assessed using FFQ (n 100) and 3-d food diary (n 89), combined with nitrate food composition databases. Nitrate intake was classified into plant, naturally occurring animal and additive-permitted meat-sourced groups. Associations between source-dependent nitrate intakes and lipoprotein-associated phospholipase A2 (Lp-PLA2), C-reactive protein (CRP), fasting plasma lipids, anthropometry and blood pressure were examined using multivariable linear regression, adjusted for socio-demographic, lifestyle and dietary confounders. Each 1 sd (∼57 mg/d) increment in plant-sourced nitrate intake was associated with a 0·191 sd lower LDL-cholesterol (β = −0·191, 95 % CI (–0·369, −0·004), P = 0·045; equivalent to −0·21 mmol/l) in primary models, though this association was attenuated in sensitivity analyses. Naturally occurring animal-sourced nitrate intake was not associated with any outcomes. A 1 sd (0·08 mg/d) increment in additive-permitted meat-sourced nitrate intake was associated with a 0·208 sd lower HDL-cholesterol (β = −0·208, (–0·362, −0·054), P = 0·009; equivalent to −0·10 mmol/l) and a 0·192 sd higher waist circumference (β = 0·192, (0·005, 0·380), P = 0·042; equivalent to +1·29 cm) but not with LDL-cholesterol, TAG, blood pressure, Lp-PLA2 or CRP. These preliminary findings suggest potential differential associations between nitrate source and cardiometabolic markers that warrant confirmation in larger studies.

Optimising nutrition during lactation is critical for the mother and infant. The relationship between fermented food consumption and the mother’s gut microbiota and nutritional and inflammation status is unknown. Mageu is a fermented grain commonly consumed in Southern Africa. We randomised South African mothers to consume a live-culture mageu, pasteurised store-bought mageu or no mageu from 4 to 10 weeks postpartum. Clinical and dietary data, stool microbiota and nutritional and inflammatory biomarkers were assessed until week 15. Plant protein intake was higher among mageu users than non-users. Live-culture mageu increased gut α-diversity from weeks 4 to 10. Circulating ferritin was lower among live-culture mageu users at week 10 compared with non-users. In systems analyses, mageu intake was associated with distinct bacterial, inflammatory and nutritional signatures, primarily driven by interleukin (IL)-6, ferritin, soluble transferrin receptor and Eubacterium hallii. These results suggest that mageu has benefits for lactating mothers’ gut health and, therefore, possibly their infants.

Phenolic compounds may reduce oxidative stress and inflammation, but evidence on inflammatory markers is limited. This study investigated associations between phenolic compounds intake and ten inflammatory markers in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). The cross-sectional analysis included participants from the full cohort (n 14 151) and a São Paulo subsample (n 681). Food intake was assessed using a semiquantitative FFQ, and phenolic content was estimated from Phenol-Explorer and Brazilian Food Composition Database. Logistic regression models compared the highest v. lowest tertiles of phenolic intake for high-sensitivity C-reactive protein (hs-CRP), glycoprotein acetylation (GlycA), monocyte chemoattractant protein-1 (MCP-1), E-selectin, transforming growth factor β1, TNF α, IL-6, IL-10, fibrinogen and leptin levels. Inflammatory markers were dichotomised as low (tertiles 1–2) or high (tertile 3), except hs-CRP (> 3 mg/l). Multiple testing was corrected using P < 0·0036. Mean age was 52·1 years for hs-CRP/GlycA and 45·6 years for other markers. Compared with T1, participants in T3 of total phenolics, phenolic acids and flavonoids had 14 %, 18 % and 18 % lower odds of elevated hs-CRP, respectively. For GlycA, higher intakes of phenolic acids, stilbenes and other phenolics were associated with 18–48 % lower odds of high levels (all P ≤ 0·003). Higher intake of hydroxybenzoic acids and stilbenes was associated with lower E-selectin levels, while phenolic acid intake showed an inverse association with MCP-1. No associations were observed for other markers. Higher intakes of phenolic compounds were associated with lower systemic inflammation, suggesting a role in preventing inflammation-related chronic diseases.

Iron deficiency (ID) represents the most prevalent nutritional disorder and a major public health concern. As part of the HYDRIA 2013–2014 National Health and Nutrition study, a cross-sectional survey of a nationally representative sample of adults in Greece, serum ferritin levels (SFL) were measured in participants aged ≥ 55 years, and dietary intake was assessed using two non-consecutive 24-h dietary recalls per participant. The study aimed to evaluate SFL, determine the prevalence of ID among older adults and explore associations with dietary iron intake and adherence to the Mediterranean diet (MD). Among individuals over 55 years, ID prevalence was 6·5 % for SFL < 15 ng/ml and 12·7 % for SFL < 30 ng/ml. SFL were significantly associated with sex and age (P < 0·001), with men showing higher SFL than women. Advancing age, particularly among individuals over 74 years, increased the risk of ID. Dietary iron intake declined with age, and women had significantly lower intake than men (P < 0·001). Overall, 57·2 % of participants had inadequate daily iron intake. SFL were not associated with total or haem iron intake. High adherence to MD was associated with higher energy-adjusted total iron intake but lower haem iron intake. Weighted logistic regression for SFL < 15 ng/ml showed that MD adherence was significantly associated with reduced odds of ID (P = 0·007), likely due to the protective effect of intermediate adherence (OR = 0·10, P = 0·002). Conclusively, while ID prevalence among older adults in Greece is low, over half of the population presents inadequate daily iron intake, especially women. High adherence to MD may have a protective effect against ID.

This randomised controlled trial examined the effect of a 4-week, high-dose (Lf-High, 600 mg/d) or low-dose (Lf-Low, 200 mg/d) oral lactoferrin (Lf) intervention v. placebo on immune cell responses to respiratory virus, immune cell subsets and systemic inflammation. In healthy older adults (n 103, ≥50 years old), ex vivo cytokine release of interferon (IFN)-α2, IFN-γ, IL-6 and TNF-α from rhinovirus A-16 (RV-16) or influenza A virus (H1N1) stimulated peripheral blood mononuclear cells, circulating immune cell subsets, and plasma IL-6, C-reactive protein (CRP) and TNF-α were assessed. Ninety-seven participants completed the 4-week intervention (Lf-High n 32, Lf-Low n 31, placebo n 34, withdrawals n 6). There was no difference in RV-16 or H1N1-induced IFN-γ release between groups. RV-16-induced IL-6 was lower in Lf-High v. placebo (P = 0·001), and RV-16-induced IFN-α2 was higher in Lf-High v. Lf-Low (P = 0·04). Lf-High increased total T cells (P = 0·03) and CD4+ T cells (P = 0·03) v. placebo. Lf-Low reduced neutrophil (P = 0·04), natural killer cell (P = 0·045), activated CD8+ T cell (P = 0·03) and γδ T cell (P = 0·03) frequency v. placebo. Plasma IL-6 (P = 0·004) and CRP (P = 0·03) were lower following Lf-High v. Lf-Low, but not placebo. Both high- and low-dose Lf altered ex vivo immune cell responses after 4 weeks. High-dose increased T-cell subsets, promoting adaptive immunity, and reduced systemic inflammation, while low-dose reduced proinflammatory and cytotoxic immune cells. High- and low-dose Lf supplements may have immunoceutical benefits in older adults.

Patients with chronic liver disease (CLD) often experience hypozincemia. The clinical factors associated with hypozincemia have not been established. We investigated clinical factors that may be useful to predict hypozincemia in patients with CLD. The serum zinc levels CLD patients were measured; Study 1 investigated the predictive factors of hypozincemia, and Study 2 was performed to validate the factors identified in Study 1. Study 1 included 197 participants, of whom 28 and 106 had serum zinc levels <60 µg/dL and <80 µg/dL, respectively. A multivariate analysis revealed that serum zinc levels <60 µg/dL or <80 µg/dL were associated with the albumin–bilirubin (ALBI) score and serum albumin level. A receiver operating characteristic curve analysis revealed that the ALBI score ≥ −1.83 and the serum albumin level ≤3.3 g/dL were the cut-off values for a serum zinc level <60 µg/dL, whereas the ALBI score ≥ −2.44 and the serum albumin level ≤3.6 g/dL were the cut-off values for a serum zinc level <80 µg/dL. In Study 2 (n = 177), the diagnostic accuracy rates for serum zinc <60 µg/dL were 81.9% for the ALBI score and 75.1% for the serum albumin level, and those for serum zinc <80 µg/dL were 70.1% for both parameters. Together these findings indicate that the ALBI score may serve as a predictive factor of hypozincemia in CLD patients.

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.

Vitamin A deficiency (VAD) poses significant health risks and is prevalent in children and adolescents in India. This study aimed to determine the effect of seasonal variation and availability of vitamin A-rich (VA-rich) foods on serum retinol in adolescents. Data on serum retinol levels from adolescents (n 2297, mean age 14 years) from the Comprehensive National Nutrition Survey (2016–2018) in India were analysed, with VAD defined as serum retinol < 0·7 µmol/L. Five states were selected based on a comparable under-five mortality rate and the seasonal spread of the data collection period. Dietary data from adolescents and children ≤ 4 years old were used to assess VA-rich food consumption. A linear mixed model framework was employed to analyse the relationship between serum retinol, month of the year and VA-rich food consumption, with a priori ranking to control for multiple hypothesis testing. Consumption of VA-rich foods, particularly fruits and vegetables/roots and tubers, showed seasonal patterns, with higher consumption during summer and monsoon months. Significant associations were found between serum retinol concentrations and age, month of sampling, consumption of VA-rich foods and fish. VAD prevalence was lowest in August, coinciding with higher consumption of VA-rich fruits and foods. Findings highlight the importance of considering seasonality in assessing VAD prevalence and careful interpretation of survey findings. Intentional design, analysis and reporting of surveys to capture seasonal variation is crucial for accurate assessment and interpretation of VAD prevalence, including during monitoring and evaluation of programmes, and to ensure that public health strategies are appropriately informed.

There are no studies in the literature examining the inflammatory content and effects of the diets of patients with primary Sjögren’s syndrome (PSS). This study aimed to investigate the relationship between the Energy-Adjusted Dietary Inflammatory Index (E-DII) and anthropometric measurements, disease activity, inflammatory markers, and blood lipid concentrations in female patients with PSS. A cross-sectional study was conducted between November 2020 and November 2021, including 102 female patients with a confirmed diagnosis of PSS. Dietary intake was assessed using the multiple-pass, 3-day food record method to calculate E-DII scores. Physical activity was evaluated using the International Physical Activity Questionnaire (Short Form), anthropometric measurements were taken, and the European League Against Rheumatism Sjögren’s Syndrome Disease Activity Index (ESSDAI) was used to determine disease activity. Lipid profile and inflammatory markers were analyzed in blood samples. Patients had a median E-DII value of –2·36. An anti-inflammatory diet was associated with lower anthropometric measurements and reduced total cholesterol, triglycerides, and low-density lipoprotein cholesterol concentrations. Logistic regression analysis revealed a significant association between E-DII and complement C3 (OR: 1·03, 95 % CI: 1·00, 1·05, P = 0·021) and C4 (OR: 1·08, 95 % CI: 1·01, 1·13, P = 0·019) after adjusting for age, disease score, drug use for SS, smoking, and physical activity. However, no significant correlation was found between E-DII and ESSDAI scores, C-reactive protein, or erythrocyte sedimentation rate. In conclusion, a pro-inflammatory diet was associated with higher anthropometric measurements and adverse lipid profiles in PSS patients, but its relationship with disease activity and inflammation remains unclear.

Modern Western diets, characterised by a substantial proportion of kilocalories derived from ultra-processed foods (UPF), have been associated with systemic inflammation. This study examines the association between UPF consumption and inflammation, assessed through alterations in C-reactive protein (CRP) concentrations, among Brazilian adolescents. This is a cross-sectional study involving a sub-sample of 6316 adolescents aged 12–17 years, participants in the Study of Cardiovascular Risk in Adolescents (ERICA), from seven capitals in Brazil. Dietary intake was assessed using a 24-hour recall, and foods were categorised based on their degree of processing according to the NOVA classification. UPF consumption was then divided into quartiles. For CRP evaluation, blood samples were collected after a 12-hour fasting period and categorised as > 3 mg/l, indicating low-grade inflammation. Poisson regression models with robust variance were employed to assess the association between UPF consumption and high CRP concentrations. High UPF consumption (highest quartile, ≥ 44·9 % kcal/d) was slightly associated with a higher prevalence of CRP after adjusting for potential confounders (prevalence ratio = 1·039; 95 % CI: 1·006, 1·073), compared with those in the lowest quartile of UPF consumption. However, when evaluating different groups of UPF separately (such as sugary beverages, processed meats and sweets), the previous association was no longer observed. These findings suggest a modest association between overall UPF consumption and early indicators of unhealthy low-grade inflammation in adolescents. Further experimental and cohort studies are necessary to clarify the role of UPF in inflammatory processes.

Although adverse childhood experiences (ACEs) are commonly associated with depressive symptoms in adulthood, studies frequently collapse ACEs into a single unitary index, making it difficult to identify specific targets for intervention and prevention. Furthermore, studies rarely explore sex differences in this area despite males and females often differing in the experiences of ACEs, depressive symptoms, and inflammatory activity. To address these issues, we used data from the National Longitudinal Study of Adolescent to Adult Health to model the effects of 10 different ACEs on C-reactive protein (CRP) and depressive symptoms in adulthood. Path modeling was used to measure the effects of ACEs on CRP and depressive symptoms conjointly while also assigning covariances among ACEs to assess their interrelations. Sex-by-ACE interaction terms and sex-disaggregated models were used to test for potential differences. Emotional abuse and parental incarceration were consistently related to both CRP and depressive symptoms for males and females. Childhood maltreatment was associated with depressive symptoms for females, whereas sexual abuse was associated with inflammation for males. Several covariances among ACEs were identified, indicating potential networks through which ACEs are indirectly associated with CRP and depressive symptoms. These data demonstrate that ACEs have differing direct effects on CRP and depressive symptoms – and that they differ with respect to how they cluster – for males versus females. These differences should be considered in theory and clinical workflows aiming to understand, treat, and prevent the long-term impacts of ACEs on depressive symptoms and inflammation-related health conditions in adulthood.

Inflammation and infections such as malaria affect concentrations of many micronutrient biomarkers and hence estimates of nutritional status. We aimed to assess the relationship between malaria infection and micronutrient biomarker concentrations in pre-school children (PSC), school-age children (SAC) and women of reproductive age (WRA) in Malawi and examine the potential role of malarial immunity on the relationship between malaria and micronutrient biomarkers. Data from the 2015/2016 Malawi micronutrient survey were used. The associations between current or recent malaria infection, detected by rapid diagnostic test and concentration of serum ferritin, soluble transferrin receptor (sTfR), zinc, serum folate, red blood cell folate and vitamin B12 were estimated using multivariable linear regression. Factors related to malarial immunity including age, altitude and presence of hemoglobinopathies were examined as effect modifiers. Serum ferritin, sTfR and zinc were adjusted for inflammation using the BRINDA method. Malaria infection was associated with 68 % (95 % CI 51, 86), 28 % (18, 40) and 34 % (13, 45) greater inflammation-adjusted ferritin in PSC, SAC and WRA, respectively (P < 0·001 for each). In PSC, the positive association was stronger in younger children, high altitude and children who were not carriers of the sickle cell trait. In PSC and SAC, sTfR was elevated (+ 25 % (16, 29) and + 15 % (9, 22) respectively, P < 0·001). Serum folate and erythrocyte folate were elevated in WRA with malaria (+ 18 % (3, 35) and + 11 % (1, 23), P = 0·01 and P = 0·003 respectively). Malaria affects the interpretation of micronutrient biomarker concentrations, and examining factors related to malarial immunity may be informative.

Triceps skinfold thickness (TSF) is a surrogate marker of subcutaneous fat. Evidence is limited about the association of sex-specific TSF with the risk of all-cause mortality among maintenance haemodialysis (MHD) patients. We aimed to investigate the longitudinal relationship of TSF with all-cause mortality among MHD patients. A multicenter prospective cohort study was performed on 1034 patients undergoing MHD. The primary outcome was all-cause mortality. The median (interquartile range) of TSF was 9·7 (6·3–13·3 mm) in males and 12·7 (10·0–18·0 mm) in females. Over a median follow-up of 4·4 years (interquartile range, 2·4–7·9 years), there were 548 (53·0 %) deaths. When TSF was assessed as sex-specific quartiles, compared with those in quartile 1, the adjusted hazard ratio (HR) (95 % CI) of all-cause mortality in quartile 2, quartile 3 and quartile 4 was 0·93 (0·73, 1·19), 0·75 (0·58, 0·97) and 0·69 (0·52, 0·92), respectively (P for trend = 0·005). Moreover, when analysed by sex, increased TSF (≥9·7 mm for males and ≥18 mm for females) was significantly associated with a reduced risk of all-cause mortality (quartile 3–4 v. quartile 1–2; HR, 0·70; 95 % CI: 0·55, 0·90 in males; quartile 4 v. quartile 1–3; HR, 0·69; 95 % CI: 0·48, 1·00 in females). In conclusion, high TSF was significantly associated with a lower risk of all-cause mortality in MHD patients.

Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL and MEDLINE) with 12,286 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n 11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n 7), are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be prospective, utilise rigorous research methods, assess the full range of index parameters, and examine biomarkers the tool was developed for.

This study investigates the effects of fat emulsion-based early parenteral nutrition in patients following hemihepatectomy, addressing a critical gap in clinical knowledge regarding parenteral nutrition after hemihepatectomy. We retrospectively analysed clinical data from 274 patients who received non-fat emulsion-based parenteral nutrition (non-fatty nutrition group) and 297 patients who received fat emulsion-based parenteral nutrition (fatty nutrition group) after hemihepatectomy. Fat emulsion-based early parenteral nutrition significantly reduced levels of post-operative aspartate aminotransferase, total bilirubin and direct bilirubin, while minor decreases in red blood cell and platelet counts were observed in the fatty nutrition group. Importantly, fat emulsion-based early parenteral nutrition shortened lengths of post-operative hospital stay and fasting duration, but did not affect the incidence of short-term post-operative complications. Subgroup analyses revealed that the supplement of n-3 fish oil emulsions was significantly associated with a reduced inflammatory response and risk of post-operative infections. These findings indicate that fat emulsion-based early parenteral nutrition enhances short-term post-operative recovery in patients undergoing hemihepatectomy.