The effects of maternal broccoli powder (BP) intake on inflammation and AMPK activation in weaning offspring programmed by maternal undernutrition remain poorly understood. This study aimed to investigate whether maternal BP intake during lactation ameliorates inflammation and affects AMPK phosphorylation in the hypothalamus and liver of weaning offspring subjected to maternal undernutrition. Pregnant rats received either a normal protein (NP, 20% casein) or a low protein (LP, 8% casein) diet. During lactation, dams were provided with either a normal protein diet without or with 0.74% BP (NP/NP or NP/NPBP) or a low protein diet without or with 0.74% BP (LP/LP or LP/LPBP). Blood, liver (left lateral lobular region), and hypothalamic samples (region estimated to include the arcuate nucleus and ventromedial hypothalamus) were collected on postnatal day 21. In the liver, macrophage count, NFκB p65 protein expression, and TNF-α mRNA expression were lower in LP/LPBP than in LP/LP. In the hypothalamus, Iba1 mRNA expression, NFκB p65 protein expression, and TNF-α mRNA expression were reduced in LP/LPBP compared to LP/LP. AMPK phosphorylation was upregulated in both the liver and hypothalamus of LP/LPBP offspring relative to LP/LP. In the liver, mTOR and Akt phosphorylation were downregulated in LP/LPBP compared to LP/LP. Additionally, Dnmt1 levels were lower in LP/LPBP than in LP/LP in the liver, whereas in the hypothalamus, Dnmt1 and Dnmt3a mRNA expression levels were higher in NP/NPBP than in NP/NP. In conclusion, maternal BP intake during lactation decreased inflammation and increased AMPK phosphorylation in the liver and hypothalamus of weaning rats programmed by maternal undernutrition.

Using NHANES data (2011–2020), we assessed the association between the Nutritional Risk Index (NRI) and stroke risk among 22,839 adults (mean age, 49.61 ± 17.07 years), including 910 individuals (3.98%) with stroke. Weighted multivariable logistic regression and restricted cubic spline (RCS) analysis were used to characterize the association, with subgroup analyses to examine consistency across populations and mediation analyses to investigate the roles of lipid and inflammatory biomarkers. Higher continuous NRI was inversely associated with stroke, with each 1-unit increase associated with 4% lower odds (OR = 0.96, 95% CI: 0.95–0.97), and participants in the highest NRI quartile (Q4) had a significantly lower stroke risk than those in the lowest NRI quartile (Q1) (OR 0.60, 95% CI 0.42–0.85). RCS analysis indicated a linear relationship (P for nonlinearity >0.05), and the protective effect of higher NRI remained robust across nearly all subgroups examined. Mediation analyses revealed that total cholesterol, systemic immune-inflammation index, platelet-neutrophil product, neutrophil-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio each partially mediated the NRI–stroke association, with mediation effects ranging from 1.71% to 13.65%. These findings suggest that favorable nutritional status, reflected by higher NRI, is linked to lower stroke risk, with lipid metabolism and inflammation playing mediating roles in this association. Further longitudinal and mechanistic studies are warranted.

Tail biting in pigs is a serious problem both from an animal welfare and an economic perspective. Once the behaviour starts, it is important to identify it and intervene immediately to restrict the spread and risk of secondary problems, such as infections. In this study, we tested whether thermal camera imaging could be used as an aid for early detection of tail biting. We also assessed links between skin temperature, tail health and saliva biomarkers for stress and inflammation. Bitten tails were slightly warmer based on thermal imaging than non-lesioned tails. However, the difference was not sufficiently large or specific to enable its use as a practical tool in the early detection of tail lesions. The methodology, however, warrants further investigation. Shortened, but healed tails had a lower skin temperature than tails of other health categories. In combination with a lower saliva cortisol level in pigs with shortened tails, potentially indicative of chronic stress, this supports previous studies indicating chronic pain in shortened pig tails, and/or chronic stress as a result of being a victim of tail biting. These findings provide a further insight into the link between stress, infections and tail biting, while also illustrating potential for skin temperature changes to be used as an early indicator of health and welfare challenges in pigs.

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.

High-energy, sugar-rich diets are associated with obesity and pancreatic disorders. We investigated the effects of consumption of a high-fat and high-fructose diet (HFFrD) on gene expression related to insulin synthesis, inflammation and apoptosis in pancreatic β-cells. Weaned Wistar rats were fed either a control diet (CD; 11 % kcal from fat and 0 % from fructose) or an HFFrD (48 % kcal from fat and 33 % from fructose) for 22 weeks; after a 6-h fast, animals were euthanised. Body weight and total fat were recorded. Serum analyses included: glucose, insulin, triacylglycerides (TAG), malondialdehyde (MDA), TNFα, IL-6, IL-10 and advanced glycation end-products (AGE). Pancreatic islets were analysed for gene expression linked to insulin synthesis, inflammation and apoptosis. Pancreatic assessments included TUNEL assay and immunohistochemistry. HFFrD increased body weight, total fat, MDA, insulin, homeostatic model assessment for insulin resistance, AGE, TAG and IL-6 concentrations in both sexes. Gene expression revealed sex-dependent differences: Glut2, Gck, Khk, Ins2 and the transcription factor Mafa were downregulated in males but upregulated in females. Pdx1 expression increased in females, whereas NeuroD1 increased in males. Pro-inflammatory markers (Il-1β, Il-6) increased in both sexes, whereas Il-10 decreased in males and increased in females. Bax/Bcl2 ratio decreased in males but increased in females; antioxidant and apoptotic markers Nrf2 and Casp3 increased in females. Endocannabinoid receptors (Cnr1, Cnr2) increased in both sexes. HFFrD altered the expression of genes involved in insulin synthesis, inflammation and apoptosis in a sex-specific manner. Compared with males, females showed lower vulnerability, possibly because of adaptive responses in insulin synthesis signalling influenced by sex hormones.

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.

Bipolar disorder (BD) is associated with increased cardiometabolic risk, contributing to elevated morbidity and premature mortality. Childhood trauma (CT) is a common environmental risk factor in BD and may exacerbate metabolic dysfunction, but no prior systematic synthesis has focused on their intersection. The objective of this review was to systematically review and synthesize evidence on the association between childhood trauma exposure and metabolic biomarkers in adults with bipolar disorder. This review adhered to PRISMA 2020 guidelines and was registered in PROSPERO (ID CRD420251045565). A comprehensive search of PubMed/MEDLINE, Web of Science, Scopus, and Embase (from inception to September 2025) was conducted. Eligible studies were peer-reviewed observational studies assessing associations between CT and metabolic markers (eg, BMI, lipids, HbA1c, hs-CRP) in adult BD populations. Data extraction and NIH quality assessments were performed independently by multiple reviewers. Sixteen studies were included (total n ≈ 6,200 across study samples). CT was significantly associated with higher body mass index and elevated hs-CRP. Two third of studies reported adverse associations with lipid profiles, and one study showed increased HbA1c among CT-exposed BD patients. Most findings emerged from cross-sectional designs, though one longitudinal study revealed large effect sizes across multiple metabolic markers. CT is consistently associated with adverse metabolic outcomes in individuals with BD, particularly elevated BMI, inflammation, and dyslipidemia. These findings support the need for trauma-informed metabolic screening and personalized interventions in this subgroup BD population. Further prospective studies are warranted to elucidate causal pathways and inform personalized care.

Tryptophan is an essential amino acid required for protein synthesis, immune regulation and the production of serotonin, melatonin and kynurenine. Its metabolism proceeds through three major pathways – the kynurenine, serotonin and gut microbiota–derived indole pathways – which are influenced by diet, microbiota and inflammation. The Mediterranean diet generally improves tryptophan bioavailability, enhances serotonin synthesis and limits excessive kynurenine activation through anti-inflammatory and microbiota-mediated mechanisms. In contrast, Western diets promote systemic inflammation, increase kynurenine production and reduce serotonin and beneficial indole metabolites. High-protein and ketogenic diets elevate substrate availability but may increase microbial production of indoles such as skatole and alter the balance of tryptophan utilisation, while calorie-restricted diets appear to downregulate pro-inflammatory tryptophan degradation and improve serotonin-related satiety regulation. Collectively, these findings demonstrate that diet is a key regulator of tryptophan metabolism, with implications for mood, sleep, inflammation, cancer progression and cardiometabolic health. Despite these advances, several knowledge gaps remain, including limited standardisation of dietary assessment methods, insufficient databases on the tryptophan content of foods and a lack of controlled comparative trials. Addressing these limitations may enable the development of nutritional strategies that optimise tryptophan metabolism and improve health outcomes.

Metabolic dysregulation increases the risk of cognitive and motor deficits, exacerbated by diets high in refined carbohydrates and fats. Polyphenol-rich berries, such as red raspberries (RRB; Rubus idaeus), may offer protective benefits. This randomised, single-blinded, controlled crossover study evaluated the acute metabolic and cognitive effects of RRB intake in older adults (55–70 years) with overweight/obesity. Thirty-six adults (61 (sd 5) years, BMI: 30·0 (sd 2·8) kg/m2; 19 females: 17 males) consumed a high-carbohydrate, moderate-fat meal (56 % carbohydrate, 33 % fat) containing 0 g (control) or 25 g of freeze-dried RRB powder. Plasma was collected at baseline and postprandially over 7·5 h to assess glucose, insulin, triacylglyceride (TAG) and IL-6. In vitro, fasting and postprandial serum samples were applied to lipopolysaccharide (LPS)-stimulated microglial cells to assess neuroinflammatory responses (nitric oxide (NO) production, inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) expression). Cognitive and vascular function were assessed at baseline and postprandially. The RRB meal significantly reduced peak glucose (by 8 %), insulin concentrations at 0·5 h and overall insulin response compared with control (P < 0·05). Serum from RRB consumers attenuated LPS-induced NO, iNOS and COX-2 expression in microglial cells (P < 0·001). Cognitive performance improved following the RRB meal, with fewer attempts in the CANTAB (Cambridge Neuropsychological Test Automated Battery) Paired Associates Learning task (P < 0·05) and fewer errors with better strategy use in the Spatial Working Memory task (P < 0·05). No significant differences were observed in vascular function. These findings suggest that acute RRB supplementation attenuated postprandial metabolic stress, reduced markers of neuroinflammation and improved cognitive performance, supporting RRB’s potential role in a dietary strategy for ageing populations.