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Evidence suggests that diets with high pro-inflammatory potential may play a substantial role in the origin of gastric inflammation. This study aimed to examine the association between the energy-adjusted dietary inflammatory index (E-DIITM) and gastric diseases at baseline and after a mean follow-up of 7.4 years in a Korean population. A total of 144,196 participants from the Korean Genome and Epidemiology Study_Health Examination (KoGES_HEXA) cohort were included. E-DII scores were computed using a validated semi-quantitative food frequency questionnaire. Multivariate logistic regression and Cox proportional hazards regression were used to assess the association between the E-DII and gastric disease risk. In the prospective analysis, the risk of developing gastric disease was significantly increased among individuals in the highest quartile of E-DII compared to those in the lowest quartile (HRquartile4vs1 = 1.22; 95% CI = 1.08–1.38). Prospective analysis also showed an increased risk in the incidence of gastritis (HRquartile4vs1 = 1.19; 95% CI = 1.04–1.37), gastric ulcers (HRquartile4vs1 = 1.47; 95% CI = 1.16–1.85), and gastric and duodenal ulcers (HRquartile4vs1 = 1.46; 95% CI = 1.17–1.81) in the highest E-DII quartile compared to the lowest quartile. In the cross-sectional analysis, the E-DII score was not associated with the risk of gastric disease. Our results suggest that a pro-inflammatory diet, indicated by high E-DII scores, is prospectively associated with an increased risk of gastric diseases. These results highlight the significance of an anti-inflammatory diet in lowering the risk of gastric disease risk in the general population.

Obesity has consistently been associated with an increased risk of metabolic abnormalities such as diabetes, hyperlipidemia, and cardiovascular diseases, as well as the development of several types of cancer. In recent decades, unfortunately, the rate of overweight/obesity has increased significantly among adults and children. A growing body of evidence shows that there is a relationship between metabolic disorders such as obesity and the composition of the gut microbiota. Additionally, inflammation is considered to be a driving force in the obesity–gut microbiota connection. Therefore, it seems that anti-inflammatory nutrients, foods, and/or diets can play an essential role in the management of obesity by affecting the intestinal flora and controlling inflammatory responses. In this review, we describe the links between the gut microbiota, obesity, and inflammation, and summarize the benefits of anti-inflammatory diets in preventing obesity.

Background Hashimoto's thyroiditis (HT) is an inflammatory autoimmune disease and patients with HT may benefit from interventions that incorporate anti‐inflammatory components. This study aimed to assess the combined effects of an anti‐inflammatory diet and curcumin supplementation on thyroid hormones and lipid profile in patients with HT. Methods This randomised controlled clinical trial was conducted on 57 patients with HT. Patients were randomly assigned to receive either an anti‐inflammatory diet plus 1320 mg/day curcumin or an anti‐inflammatory diet plus placebo for 12 weeks. Anthropometric indices, anti‐thyroid peroxidase (anti‐TPO), thyroid‐stimulating hormone (TSH), thyroxine (T4), triiodothyronine (T3), and lipid profile parameters were assessed at baseline and after the 12‐week intervention. The trial was registered in the Clinical Trials Database (registration number NCT05975866). Results After 12 weeks of intervention, both groups showed reductions in waist circumference and waist‐to‐hip ratio, with greater changes observed in the curcumin group. However, between‐group differences were not statistically significant. A significant reduction in anti‐TPO levels was observed in the curcumin group compared to placebo (p = 0.006). Although TSH and T3 levels significantly decreased within the curcumin group (p = 0.014 and p = 0.001, respectively), between‐group differences were not statistically significant after adjustment. Additionally, HDL‐C levels showed a non‐significant trend toward improvement in the curcumin group (p = 0.053), whereas other lipid parameters remained unchanged. Conclusion Curcumin may have possible benefits for thyroid autoimmunity, but further studies are required before any clinical use. Trial Registration The trial was registered in the Clinical Trials Database (Registration number: NCT05975866, 08 August 2023). National Nutrition and Food Technology Research Institute NCT0597586 https://www.clinicaltrials.gov/study/NCT05975866?term=NCT05975866&rank=1 Anti‐TPO levels, along with waist circumference and waist‐to‐hip ratio, showed notable reductions in the curcumin group compared to placebo, while other thyroid‐related and metabolic markers remained largely unchanged.

Hashimoto's thyroiditis (HT) is a chronic autoimmune condition characterized by persistent thyroid inflammation. Patients with HT may benefit from anti‐inflammatory strategies. This study was designed to examine the combined impact of an anti‐inflammatory diet and curcumin supplementation on inflammatory markers in individuals with HT. In this randomized controlled clinical trial, 57 individuals diagnosed with Hashimoto's thyroiditis (HT) in Tehran, Iran, were recruited and randomly allocated to two intervention arms. One group received an anti‐inflammatory diet in conjunction with 1500 mg of curcumin daily, while the other group followed the same diet but was administered a placebo. Inflammatory biomarkers including high‐sensitivity C‐reactive protein (hs‐CRP), interleukin‐6 (IL‐6), and nuclear factor kappa B (NF‐κB) were measured at the start of the study and again following a 12‐week supplementation period to assess the additive effect of curcumin. Curcumin supplementation resulted in a reduction in IL‐6 (−5.28 ± 9.75, p = 0.009). Additionally, it decreased hs‐CRP levels in patients with HT, with a mean reduction of −1.17 ± 5.70 mg/L, whereas the placebo group exhibited an increase of +1.53 ± 3.33 mg/L (p = 0.305). Also, curcumin supplementation significantly reduced NF‐κB levels in patients with HT (−0.09 ± 0.22 vs. 0.03 ± 0.15, p = 0.019), while the placebo group showed a slight increase (0.65 ± 0.16 to 0.68 ± 0.13). Curcumin, by reducing inflammation, can be effective as an adjunctive treatment alongside an anti‐inflammatory diet in individuals with HT. Additional studies are warranted. Name of the Registry: National Nutrition and Food Technology Research Institute. Trial Registration Number: NCT0597586. Date of Registration: 2023‐08‐04. URL of Trial Registry Record: https://www.clinicaltrials.gov/study/NCT05975866?term = NCT05975866&rank = 1. Curcumin supplementation resulted in a reduction in IL‐6. Additionally, it decreased hs‐CRP levels in patients with HT, with a mean reduction of whereas the placebo group exhibited an increase of +1.53 ± 3.33 mg/L (p = 0.305). Also, curcumin supplementation significantly reduced NF‐κB levels in patients with HT, while the placebo group showed a slight increase. Curcumin, by reducing inflammation, can be effective as an adjunctive treatment alongside an anti‐inflammatory diet in individuals with HT.

Colorectal cancer is one of the most common cancers and a primary cause of death. The increased incidence in low‐ and middle‐income nations highlights the need for better prevention. Chronic inflammation, obesity, and gut microbial dysbiosis are major risk factors for CRC, making nutritional interventions attractive. This study aims to examine the association between adherence to an anti‐inflammatory diet and anthropometric, biochemical, inflammatory, molecular, and gut microbiota parameters related to colorectal cancer risk. In this retrospective analysis, anti‐inflammatory diet adherents (n = 515) and non‐adherents (n = 435) were compared. Hematological, hepatic, inflammatory, tumor, genetic/molecular, and gut microbiota tests were performed, and chi‐square tests were used for categorical outcomes. Multiple regression was used to examine the association between adherence to an anti‐inflammatory diet and the development of colorectal cancer. Multiple logistic regression analysis indicated that anti‐inflammatory diets were associated with improved clinical, biochemical, and microbiome outcomes in patients with CRC. Diet adherence was associated with a lower risk of obesity, central obesity, dyslipidemia, anemia, and leukocytosis after adjusting for age, sex, BMI, smoking, and caloric intake (β = −1.90, SE = 0.26, OR = 0.15, 95% CI: 0.09–0.25). Several inflammatory markers, including CRP, IL‐6, CEA, and MMP‐9, decreased markedly (p < 0.001). Molecular alterations associated with CRC, including p53 mutation, Ki‐67 overexpression, microsatellite instability, APC mutation, and β‐catenin nuclear expression, were significantly decreased (p < 0.001). Bifidobacterium, Lactobacillus, Faecalibacterium prausnitzii, and Akkermansia muciniphila were increased, and pathogenic species decreased in the gut (ORs 2.10–2.30; Fusobacterium nucleatum, Clostridium difficile, pathogenic Escherichia coli; ORs 0.16–0.18). Anti‐inflammatory diets significantly improve metabolic, inflammatory, tumor‐related, and microbiome profiles in patients with CRC. Adherence to an anti‐inflammatory dietary pattern is significantly associated with improved metabolic, inflammatory, molecular, and gut microbiota profiles, all of which are linked to colorectal cancer risk. These findings support anti‐inflammatory dietary strategies as cost‐effective and non‐invasive approaches for colorectal cancer prevention and adjunctive management. This retrospective study evaluates whether greater adherence to an anti‐inflammatory diet is associated with biomarkers and gut microbiota profiles linked to reduced colorectal cancer risk. The study seeks to clarify how dietary patterns influence inflammation and gut microbiota, providing insights to guide effective prevention strategies for individuals at risk of colorectal cancer.

Background In addition to the elimination diet, dietary composition may influence disease severity in patients with eosinophilic esophagitis (EoE) through modulation of the immune response. Aim To explore the immunomodulatory role of nutrition before and during elimination diet in adult EoE patients. Methods Nutritional intake was assessed in 39 Dutch adult EoE patients participating in the Supplemental Elemental Trial (Dutch trial registry NL6014, NTR6778) using 3‐day food diaries. In this randomized controlled trial, diagnosed patients received either a four‐food elimination diet alone (FFED) or FFED with addition of an amino acid‐based formula for 6 weeks. Multiple linear regression analyses were performed to assess associations between the intake of nutrients and food groups per 1000 kCal and peak eosinophil count/high power field (PEC), both at baseline and after 6 weeks. Results At baseline, we found a statistically significant negative (thus favorable) relationship between the intake of protein, total fat, phosphorus, zinc, vitamin B12, folate, and milk products and PEC (p < .05), while calcium (p = .058) and full‐fat cheese/curd (p = .056) were borderline (favorably) significant. In contrast, total carbohydrates, prepacked fruit juice, and white bread were significantly positively (unfavorable) related to PEC (p < .05), while ultra‐processed meals (p = .059) were borderline (unfavorably) significant. After dietary intervention, coffee/tea were significantly negatively (favorably) related to PEC, hummus/legumes were significantly positively (unfavorably) related with PEC, while peanuts were borderline significantly positively related (p = .058). Conclusion Dietary composition may be related to inflammation in adult EoE patients. High‐quality and anti‐inflammatory diets may be a promising adjuvant therapy in the dietary management of EoE.

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of liver disease in children. Following earlier reports on an increase in the prevalence of childhood obesity, NAFLD is now becoming increasingly common in children. Although no definitive cure exists, early management, early diagnosis, and treatment can reduce its complications. This study aims to determine the effectiveness of the combination of ginger and an anti‐inflammatory diet (AID) in children with obesity on fatty liver management. This randomized clinical trial was conducted on 160 children with obesity aged 8–11 years, with a mean (SD) weight of 65.01 (9.67) kg, mean (SD) height of 139.87 (7.37) cm, and mean (SD) body mass index of 33.40 (5.59) kg/m2. The study duration was 12 weeks. Children were divided into four groups: ginger (G), AID, ginger plus an AID (GPA), and control. Ginger capsules comprised 1000 mg of ginger, whereas the AID comprised fruits and vegetables, fish, turkey, and chicken (without skin) with lean meat, omega‐3 sources, nuts, legumes, probiotic products, and elimination of inflammatory food. Following the intervention, serum fasting blood sugar and high‐sensitivity C‐reactive protein levels were significantly decreased in the AID (p = .006 and .002, respectively), G (p = .04 and <.001, respectively), and GPA (p <.001 in both cases, respectively) groups. Further, in the G and GPA groups, there was a significant decrease in body mass index (p = .04 in both cases, respectively), waist circumference (p = .009 and .003, respectively), waist‐to‐height ratio (p = .02 and .005, respectively), alanine aminotransferase (p = .004 and <.001, respectively), total cholesterol (p = .0002 and .0001, respectively) and low‐density lipoprotein‐cholesterol (p < .001 and <.001, respectively). Eventually, serum aspartate aminotransferase was decreased (p < .001) and high‐density lipoprotein‐cholesterol (p = .03) was increased significantly in the GPA group. As a main finding of this study, hepatic steatosis significantly decreased in the G and GPA groups. Ginger supplementation can effectively improve NAFLD in children, and its effectiveness was further increased when combined with an AID. Ginger as a nonmedicinal supplement can improve fatty liver in children with obesity, while adherence to an anti‐inflammatory diet will increase its overall effectiveness. This work is part of Negin Kamari's MSc thesis on children aged 8–11 with fatty liver. We investigated the effectiveness of ginger and an anti‐inflammatory diet after a 12‐week intervention period.

Kawakawa (Piper excelsum) is an endemic medicinal plant widely consumed by Māori in New Zealand. Presence of diverse biologically active phytochemicals in kawakawa may underpin its putative therapeutic anti‐inflammatory properties. However, no human studies on its anti‐inflammatory effects are yet undertaken. Blood samples from a randomized controlled dietary intervention exploring the impact of kawakawa compared to control on postprandial microRNAs (miRNA) abundances and their respective gene and protein targets in a cohort of healthy human volunteers (n = 26; Age; 33.6 ± 1.9 year and BMI; 22.5 ± 0.4 kg/m2) were analyzed. Postprandial levels of nine miRNAs showed differential abundances; hsa‐miR‐17‐5p, ‐21‐5p, ‐320a‐5p, let‐7g‐5p, ‐16‐5p, ‐122‐5p, and ‐144‐3p was upregulated while as hsa‐miR‐221‐3p and ‐223‐3p was downregulated in response to kawakawa compared to control. In silico analysis indicated enrichment of miRNAs in multiple inflammation‐related pathways, including apoptosis, cytokine signaling, MAPK signaling, and MTOR pathways. Furthermore, gene expression of IL‐8 (p = .03), IL‐6 (p = .01), and PPAR‐γ were significantly reduced following kawakawa intake compared to control. While as plasma IL‐6 showed a significant increase over 120 min in the kawakawa arm. These results highlight kawakawa to exert anti‐inflammatory effects by modulating the expression of miRNAs and their target genes and proteins in the inflammatory signaling pathways. Acute intake of kawakawa tea, derived from the indigenous New Zealand plant Piper excelsum, demonstrates promising anti‐inflammatory effects. This effect is mediated through the regulation of miRNA expression, which in turn influences their target genes and proteins associated with key inflammatory signaling pathways. The modulation of these pathways suggests that kawakawa tea could play a significant role in reducing inflammation by offering a natural and sustainable dietary intervention for managing inflammation‐related health conditions.

Anthocyanins are flavonoid compounds that are abundantly present in fruits and vegetables. These compounds contribute to the color of these foods and offer various health benefits to consumers due to their biological properties. There are more than 1000 types of anthocyanins in nature, all derived from 27 anthocyanidin aglycones that have different glycosylations and acylations. Malvidin is one of the most well-known anthocyanidins. Several studies, including those conducted on cell lines, animals, and humans, have suggested that malvidin and its glycosides possess anti-carcinogenic, diabetes-control, cardiovascular-disease-prevention, and brain-function-improvement properties. These health benefits are primarily attributed to their antioxidant and anti-inflammatory effects, which are influenced by the molecular mechanisms related to the expression and modulation of critical genes. In this article, we review the available information on the biological activity of malvidin and its glycosides concerning their health-promoting effects.

A complicated autoimmune illness known as systemic lupus erythematosus (SLE) is typified by multi‐organ dysfunction and ongoing inflammatory processes. Although medication is still the mainstay of managing SLE, tailored nutrition provides a mechanistically sound way to reduce inflammation and promote immunological balance. The present article links certain nutritional factors to pathways controlling cytokine equilibrium, oxidative damage, endothelium integrity, and regulatory T cell activity. These elements include unsaturated fats, vitamins, polyphenols, probiotics, and fiber‐derived short‐chain fatty acids (SCFAs). Additionally, it assesses microbiome‐based therapies and looks at nutritional habits that may have anti‐inflammatory properties, such as the Mediterranean style of eating. Based on these findings, we suggest an evidence‐based “anti‐lupus plate” approach that takes into consideration renal function, concurrent medical conditions, and drug–nutrient relationships while matching dietary habits to pathophysiological goals. Research limitations are highlighted as major obstacles, especially the lack of broad, biomarker‐driven research. These shortfalls must be filled in order to integrate food into a research‐based SLE treatment. Regulated procedures, extended follow‐up, and multimodal dietary treatments are necessary to achieve this. The present article links certain nutritional factors to pathways controlling cytokine equilibrium, oxidative damage, endothelium integrity, and regulatory T cell activity. These elements include unsaturated fats, vitamins, polyphenols, probiotics, and fiber‐derived short‐chain fatty acids (SCFAs).