Gut bacterial markers involved in association of dietary inflammatory index with visceral adiposity.

OBJECTIVE: To deepen the understanding of the influence of diet on weight gain and metabolic disturbances, we examined associations between diet-related inflammation and body composition and fecal bacteria abundances in participants of the Nutritionists' Health Study. METHODS: Early-life, dietary and clinical data were obtained from 114 women aged ≤45 years. A validated food frequency questionnaire was used to calculate the energy-adjusted dietary inflammatory index (E-DII). Participants' data were compared by E-DII quartiles using ANOVA or Kruskal-Wallis. Associations of DXA-determined body composition with the E-DII were tested by multiple linear regression using DAG-oriented adjustments. Fecal microbiota was analyzed targeting the V4 region of the 16S rRNA gene. Spearman correlation coefficients were used to test linear associations; differential abundance of genera across the E-DII quartiles was assessed by pair-wise comparisons. RESULTS: E-DII score was associated with total fat (b=1.80, p<0.001), FMI (b=0.08, p<0.001) and visceral fat (b=1.19, p=0.02), independently of maternal BMI, birth type and breastfeeding. E-DII score was directly correlated to HOMA-IR (r=0.30; p=0.004), C-reactive protein (r=0.29; p=0.003) and to the abundance of Actinomyces, and inversely correlated to the abundance of Eubacterium.xylanophilum.group. Actinomyces were significantly more abundant in the highest (most proinflammatory) E-DII quartile. CONCLUSIONS: Association of E-DII with markers of insulin resistance, inflammation, body adiposity and certain gut bacteria are consistent with beneficial effects of anti-inflammatory diet on body composition and metabolic profile. Bacterial markers, such as Actinomyces, could be involved in the association between the dietary inflammation with visceral adiposity. Studies designed to explore how a pro-inflammatory diet affects both central fat deposition and gut microbiota are needed.

The association between dietary inflammatory index (DII) scores and c-reactive protein (CRP) and nonalcoholic fatty liver disease (NAFLD) in a general population cohort.

BACKGROUND AND AIMS: Although there is extensive literature showing the ability of the dietary inflammation index (DII®) to predict concentrations of plasma inflammatory markers, few studies are testing the association between DII scores and nonalcoholic fatty liver disease (NAFLD). Considering the high prevalence of NAFLD and its complications, we conducted a validation study of DII scores and examined its association with NAFLD in the general adult population of Iran. METHODS: This cross-sectional study was conducted on 3110 adult participants in the Amol Cohort Study (AmolCS) who underwent abdominal ultrasonography to diagnose NAFLD. DII and energy-adjusted DII (E-DII™) scores were computed using data from a valid semi-quantitative 168-item food frequency questionnaire (FFQ). Multivariable logistic regression adjusting for socio-demographic, lifestyle, and health-related factors was used to assess association. RESULTS: The EDII was associated with CRP inflammatory biomarker. Participants in the highest, i.e., most pro-inflammatory tertile had the highest odds of NAFLD by ultrasound in all models [fully adjusted model: OR (95 % CI) tertile3vs.1:1.54 (1.05-2.05); Ptrend = 0.04, and 1.63 (1.19-2.21); Ptrend = 0.03 in women and men, respectively]. The highest tertile had the highest OR for NAFLD by fatty liver index (FLI) only in men [fully adjusted model OR (95 % CI) tertile3vs.1: 1.77 (1.15-2.71); Ptrend = 0.01]. Similar results were also obtained for NAFLD by hepatic steatosis index (HSI) in women [fully adjusted model: OR (95 % CI) tertile3vs.1: 1.70 (1.12-2.58); Ptrend = 0.03]. The results of the fully adjusted multivariable model of liver markers and NAFLD status, stratified by gender and abdominal obesity, revealed that the highest tertiles had the highest OR for NAFLD by ultrasound and NAFLD by FLI only in men without abdominal obesity [fully adjusted model: OR (95 % CI) tertile3vs.1: 1.83 (1.17-2.84); Ptrend = 0.03, and, respectively]. NAFLD by FLI tended to increase strongly with tertile E-DII scores in men without abdominal obesity in crude and three adjusted models [full-adjusted model: OR (95 % CI) tertile3vs.1: 3.64 (1.56-8.46); Ptrend = 0.005]. By contrast, women with abdominal obesity in the highest tertile had the highest OR for NAFLD by ultrasound in all models [full-adjusted model: OR (95 % CI) tertile3vs.1: 1.67 (1.07-2.62); Ptrend = 0.02]. CONCLUSIONS: Our results suggest that diet plays a role in regulating inflammation. Additionally, we observed an inflammatory diet predicts the risk of NAFLD in Iranian adults. However, longitudinal studies are required in order to further substantiate the utility of the DII in the development of more effective dietary interventions among populations at risk of chronic disease.

Correlation research demonstrates that an inflammatory diet is a risk factor for calcium oxalate renal stone formation.

BACKGROUND AND AIMS: Previous studies have demonstrated associations between the Dietary Inflammatory Index (DII®), an analytical tool which evaluates the inflammatory potential of the diet according to the pro- and anti-inflammatory properties of its components, and renal stone formation. However, these have not comprehensively addressed important parameters such as stone type, gender, DII scores in stone formers (SFs) and healthy controls (Cs) and associations of DII with urine and blood chemistries. These were adopted as the survey parameters for the present study, the purpose of which was to test whether the contributory role of an inflammatory diet on stone formation could be further confirmed. METHODS: 97 calcium oxalate (CaOx) SFs and 63 Cs, matched for age and gender each completed a semi-quantitative food frequency questionnaire from which nutrient composition was computed. These data were used to calculate the DII® score. To control the effect of energy intake, energy-adjusted DII scores were calculated per 1000 kcal consumed (E-DII™). A single blood sample and two consecutive overnight (8h) urine samples were collected from a subset (n = 59 SFs and n = 54 Cs) of the overall number of particpants (n = 160). These were analysed for renal stone risk factors. Data were analysed using regression models fit in R software. RESULTS: E-DII scores were found to fit the data better than DII, so they were used throughout. E-DII scores were significantly more positive (more pro-inflammatory) in SFs than in controls in the combined gender group (-0.34 vs. -1.73, p < 0.0001) and separately in males (-0.43 vs. -1.78, p = 0.01) and females (-0.26 vs. - 1.61, p = 0.05). In blood, a significant negative correlation was seen between E-DII and HDL cholesterol. In urine significant positive correlations were seen between E-DII and each of calcium (ρ = 0.25, p = 0.02), phosphate (ρ = 0.48, p < 0.001), magnesium (ρ = 0.33, p < 0.0001) and uric acid (ρ = 0.27, p = 0.004) concentrations. A significant negative correlation was seen between E-DII and urinary volume ρ = -0.27, p = 0.003). There was no correlation between E-DII scores and the relative supersaturations of urinary CaOx, calcium phosphate (brushite) and uric acid. CONCLUSIONS: Our findings provide hitherto unreported quantitative evidence in support of the notion that the diet of calcium oxalate renal stone patients is significantly more pro-inflammatory than that of healthy controls.

The association of dietary antioxidants and the inflammatory potential of the diet with poor physical function and disability in older Australian men: the Concord Health and Ageing in Men Project.

Our objective was to evaluate the association of antioxidant intake and the inflammatory potential of the diet with functional decline in older men. A diet history questionnaire was used to collect dietary intake data from men aged ≥ 75 years (n 794) participating in the Concord Health and Aging in Men Project cohort study. Intake of vitamins A, C, E and Zn were compared with the Australian Nutrient Reference Values to determine adequacy. The Energy-adjusted Dietary Inflammatory Index (E-DIITM) was used to assess the inflammatory potential of the diet. Physical performance data were collected via handgrip strength and walking speed tests, and activities of daily living (ADL) and instrumental activities of daily living (IADL) questionnaires, at baseline and 3-year follow-up (n 616). Logistic regression analysis was used to identify associations between diet and incident poor physical function and disability. Both poor antioxidant intake and high E-DII scores at baseline were significantly associated with poor grip strength and ADL disability at 3-year follow-up. No significant associations with walking speed or IADL disability were observed. Individual micronutrient analysis revealed a significant association between the lowest two quartiles of vitamin C intake and poor grip strength. The lowest quartiles of intake for vitamins A, C, E and Zn were significantly associated with incident ADL disability. The study observed that poor antioxidant and anti-inflammatory food intake were associated with odds of developing disability and declining muscle strength in older men. Further interventional research is necessary to clarify the causality of these associations.

The Brazilian Cardioprotective Nutritional (BALANCE) Program improves diet quality in patients with established cardiovascular disease: Results from a multicenter randomized controlled trial.

Dietary modifications are essential strategies for cardiovascular disease prevention. However, studies are needed to investigate the diet quality of individuals undergoing secondary prevention in cardiology and who received dietary intervention based on cardiovascular disease management. We prospectively evaluated the diet quality in the Brazilian Cardioprotective Nutritional Program Trial (BALANCE Program Trial). We hypothesized that the BALANCE Program could improve patients' dietary pattern according to different indices of diet quality such as the Dietary Inflammatory Index (DII); the dietary total antioxidant capacity; overall, healthful, and unhealthful Plant-Based Diet Index (PDI, hPDI, and uPDI, respectively); and modified Alternative Healthy Eating Index (mAHEI). This multicenter randomized, controlled trial included patients aged ≥45 years randomly assigned to either the experimental or control group. Data from 2185 participants at baseline and after 12, 24, 36, and 48 months showed that the intervention group (n = 1077) had lower mean values of DII and higher dietary total antioxidant capacity, PDI, hPDI, and mAHEI than the control group. The results also showed differences between the follow-up times for DII, hPDI, and uPDI (48 months vs baseline) and for PDI and mAHEI (24 months vs baseline), regardless of group. The interaction analysis demonstrated that the intervention group showed better results than the control group at 12, 24, 36, and 48 months for the DII and at months 12, 36, and 48 for the mAHEI. Our results provide prospective evidence that the BALANCE Program improved the diet quality in those in secondary cardiovascular prevention according to different indices, with the intervention group showing better results than the control group.

Dietary Inflammatory Potential and the Risk of Serrated and Adenomatous Colorectal Polyps.

Studies of dietary inflammation potential and risks of colorectal cancer precursors are limited, particularly for sessile serrated lesions (SSLs). This study examines the association using the energy-adjusted dietary inflammatory index (E-DIITM), a measure of anti- and/or pro-inflammatory diet, in a large US colonoscopy-based case-control study of 3246 controls, 1530 adenoma cases, 472 hyperplastic polyp cases, and 180 SSL cases. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived from logistic regression models. Analyses were stratified by participant characteristics, and urinary prostaglandin E2 metabolite (PGE-M) and high-sensitivity plasma C-reactive protein (hs-CRP) levels, inflammation biomarkers. Highest E-DII™ intake was associated with significantly increased risks of colorectal adenomas (OR 1.36, 95% CI 1.11, 1.67), and hyperplastic polyps (OR 1.43, 95% CI 1.06, 1.98), compared with participants consuming the lowest E-DII™ quartile. A similar, but non-significant, increased risk was also observed for SSLs (OR 1.41, 95% CI 0.82, 2.41). The positive association was stronger in females (pinteraction <0.001), normal weight individuals (ptrend 0.01), and in individuals with lower inflammatory biomarkers (ptrend 0.02 and 0.01 for PGE-M and hs-CRP, respectively). A high E-DII™ is associated with colorectal polyp risk, therefore promoting an anti-inflammatory diet may aid in preventing colorectal polyps.

Dietary inflammatory index and renal cancer risk: a prospective study.

Background: High dietary inflammatory index (DII®) scores, representing pro-inflammatory diets, have been associated with increased risks for numerous cancers. However, the evidence for renal cancer is limited. In the present study, we aimed to assess the association between DII and renal cancer risk in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cohort. Methods: Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using a Cox proportional hazards model with adjustment for various potential confounders. Results: After a median 12.2 years of follow-up, this study recorded 443 renal cancer cases among 101 190 individuals. The DII score was positively associated with renal cancer risk in multivariable analyses. The HR in the highest DII tertile compared to the lowest tertile was 1.38 (95% CI 1.03-1.84). This was also true when DII was analyzed as a continuous variable. The HR of one-unit increment in DII for renal cancer risk was 1.07 (95% CI 1.01-1.12). Conclusion: In this large American cohort, pro-inflammatory diet, as estimated by higher DII scores, was significantly associated with a greater risk of renal cancer. Future large prospective studies are warranted to verify these preliminary findings.

Beneficial Short-Term Effects of Bariatric Surgery on Nutritional Inflammatory Profile and Metabolic Biomarkers.

PURPOSE: Bariatric surgery (BS) has several potential metabolic benefits. However, little is known about its impact on changes in the inflammatory potential of diet and its effect on inflammatory and metabolic markers. This study aimed to assess the short-term beneficial effects of BS on dietary inflammatory potential and inflammatory and metabolic markers. MATERIALS AND METHODS: Participants (n = 20) were evaluated 3 months before and after BS. Body mass, body mass index, anthropometric measurements, fat mass, fat-free mass, visceral fat, skeletal muscle mass, basal metabolic rate, serum lipids, HOMA-IR, QUICKI and inflammatory markers, including leptin, adiponectin, adiponectin/leptin ratio and plasminogen activator inhibitor-1 (PAI-1), were evaluated. Diet data were collected using a 3-day diet record and the dietary inflammatory index (DII®) and energy-adjusted dietary inflammatory index (E-DIITM) scores were computed. RESULTS: There was a reduction in DII® (2.56 vs 2.13) and E-DIITM (2.18 vs 0.45) indicating an improvement in inflammatory nutritional profile. Moreover, there were increases in the adiponectin/leptin ratio (0.08 vs 0.21) and QUICKI scores (0.31 vs 0.37), and reductions in leptin (36.66 vs 11.41 ng/ml) and HOMA-IR scores (3.93 vs 1.50). There were also improvements in body composition and anthropometric parameters. CONCLUSIONS: BS promotes changes in metabolic profile, inflammatory state and food intake and these modifications appeared to be associated with improvements in diet-related inflammation, an increase in the adiponectin/leptin ratio and a reduction in leptin. These results contribute to knowledge on the contribution bariatric surgery can make to the treatment of obesity and the reduction of related comorbidities.

Energy-Adjusted Dietary Inflammatory Index and Diabetes Risk in Postmenopausal Hispanic Women.

BACKGROUND: Type 2 diabetes is a major public health concern in the United States and worldwide. The dietary inflammatory index (DII) and the energy-adjusted DII (E-DII) are tools that assess dietary inflammation. Previous evidence suggests that obesity can modify the association between inflammation and disease. OBJECTIVE: The aim of this study was to evaluate the association between the DII/E-DII and incident diabetes in self-identified Hispanic women from the Women's Health Initiative (WHI). The secondary aim was to evaluate whether obesity modifies the association between the DII/E-DII scores and incident diabetes. DESIGN: Participants were from the WHI Observational Study and the Clinical Trial Components (except women from the treatment arm in the Dietary Modification Trial) conducted among postmenopausal women in the United States. DII/E-DII scores were calculated from a self-administered food frequency questionnaire at baseline that included 122 food items, of which 12 are representative of Hispanic eating patterns. PARTICIPANTS/SETTINGS: Participants included 3,849 postmenopausal women who self-identified as Hispanic that were recruited for the WHI from 1993 to 1998 at 40 US clinical centers. MAIN OUTCOME MEASURES: The outcome was incident diabetes. STATISTICAL ANALYSIS PERFORMED: Cox regression models were used to assess the association between DII/E-DII and incident diabetes. Models were adjusted for age at baseline, lifestyle-related risk factors, known type 2 diabetes mellitus (T2DM) risk factors, and neighborhood socioeconomic status. Interaction was tested between the DII/E-DII scores and obesity. RESULTS: The incidence of diabetes was 13.1% after a median follow-up of 13 years. Higher E-DII scores were associated with a higher risk of incident diabetes (hazard ratio [HR], 1.09; 95% confidence interval [CI], 1.04-1.14). There was no interaction between E-DII scores and obesity (P = 0.73). CONCLUSIONS: Pro-inflammatory diets, as measured by higher E-DII scores, were associated with a higher risk of incident diabetes. Future research is needed for understanding how the inflammatory potential of diets can be decreased.

Associations between dietary inflammatory scores and biomarkers of inflammation in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

BACKGROUND: Since the first version of the dietary inflammatory index (DII®) developed in the past decade, several other versions have been developed. However, to date no study has attempted to compare these versions with respect to their associations with biomarkers of inflammation. OBJECTIVE: We aimed to investigate the relationship between four dietary inflammatory scores [DII, two energy-adjusted derivatives (E-DII and E-DIIr), and the Inflammatory Score of the Diet (ISD)], and circulating levels of several inflammatory markers and adipokines. METHODS: This study included 17 637 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort with at least one marker of inflammation measured in blood. Associations between the four scores and C-reactive protein (CRP), interleukin (IL)6, IL10, IL1RA, tumor necrosis factor-α (TNFα), soluble tumor necrosis factor receptor-1 (sTNFR1), sTNFR2, leptin, soluble leptin receptor (sLeptin R), adiponectin, and High Molecular Weight (HMW) adiponectin were evaluated using multivariable linear regressions adjusted for potential confounders. RESULTS: Positive associations were observed between the four dietary inflammatory scores and levels of CRP, IL6, sTNFR1, sTNFR2 and leptin. However, only the DII and the ISD were positively associated with IL1RA levels and only the DII and the E-DIIr were positively associated with TNFα levels. The proportion of variance of each biomarker explained by the scores was lower than 2%, which was equivalent to the variance explained by smoking status but much lower than that explained by body mass index. CONCLUSIONS: Our results suggest that the four dietary inflammatory scores were associated with some biomarkers of inflammation and could be used to assess the inflammatory potential of diet in European adults but are not sufficient to capture the inflammatory status of an individual. These findings can help to better understand the inflammatory potential of diet, but they need to be replicated in studies with repeated dietary measurements.

The effect of low dietary inflammatory index score formula on inflammatory, metabolic, and clinical outcomes in critically ill traumatic brain injury patients: A single-blind randomized controlled pilot study.

In traumatic brain injury (TBI) patients, a complex cascade of inflammatory responses are frequently observed following trauma. Numerous dietary agents have long been found to have potential in modulating inflammatory responses. This pilot study, designed an enteral formula with low inflammatory properties based on the dietary inflammatory index (DII®) and evaluated its effect on inflammatory and metabolic factors in critically ill TBI patients. This single-blind randomized controlled pilot study was conducted at the Neurosurgical ICU of Shahid Kamyab Hospital (Mashhad, Iran). A total of 20 TBI patients were randomly assigned to receive either low-DII score or standard formula at the intensive care unit (ICU). The primary outcomes of the study included clinical status, inflammatory biomarkers, APACHE II, SAPS II, SOFA, and NUTRIC scores. The trial groups did not differ significantly in baseline values. Following 14 days of intervention, there was a statistically significant decrease in the APACHE II, SAPS II, and NUTRIC scores and a significant increase in the GCS score in the low-DII score formula group compared to the standard formula group. Over 2 weeks, high sensitivity C-reactive protein (hs-CRP) values of -2.73 (95% CI: -3.67, -1.79) mg/dL in the low-DII score formula group versus 0.65 (95% CI: -0.29, 1.58) mg/dL in controls were obtained. Moreover, the length of hospital stay was longer for the standard formula group than for the low-DII score formula group. The low-DII score formula improves inflammatory factors (serum hs-CRP) and metabolic biomarkers (LDL-c and FBS). Furthermore, clinical outcomes, including the length of hospital stay and disease severity, appear to be enhanced.

Energy-Adjusted Dietary Inflammatory Index in pregnancy and maternal cardiometabolic health: findings from the ROLO study.

Background: Excessive inflammation during pregnancy has been linked to adverse long-term health outcomes for both mothers and their children. One such outcome is maternal cardiometabolic dysfunction. The Energy-Adjusted Dietary Inflammatory Index is a method of scoring the overall inflammatory potential of the diet. Research on how the inflammatory potential of the maternal diet during pregnancy affects maternal cardiometabolic factors is limited. Objective: We investigated if the maternal Energy-Adjusted Dietary Inflammatory Index was associated with maternal cardiometabolic factors during pregnancy. Study design: This is a secondary analysis of 518 individuals who participated in the ROLO (Randomized cOntrol trial of a LOw glycemic index diet in pregnancy) study. Maternal Energy-Adjusted Dietary Inflammatory Index scores were calculated in early (12-14 weeks' gestation) and late pregnancy (34 weeks' gestation) using data collected from 3-day food diaries. Body mass index, blood pressure, fasting lipid profiles, glucose levels, and HOMA1-IR were obtained in early and late pregnancy. Multiple linear regression examined associations between early-pregnancy Energy-Adjusted Dietary Inflammatory Index and early and late maternal cardiometabolic markers. In addition, the relationship between late-pregnancy Energy-Adjusted Dietary Inflammatory Index and late cardiometabolic factors was explored. Regression models were adjusted for maternal ethnicity, maternal age at delivery, education level, smoking status, and original randomized control trial group allocation. In regression models examining late-pregnancy Energy-Adjusted Dietary Inflammatory Index with late lipids, change in lipid level from early to late pregnancy was also adjusted for. Results: Women's mean (standard deviation) age at delivery was 32.8 (±4.01) years, with median (interquartile range) body mass index of 24.45 (23.34-28.20) kg/m2. Mean (standard deviation) Energy-Adjusted Dietary Inflammatory Index was 0.59 (±1.60) in early pregnancy and 0.67 (±1.59) in late pregnancy. In adjusted linear regression analysis, first-trimester maternal Energy-Adjusted Dietary Inflammatory Index was positively associated with maternal body mass index (B=0.007; 95% confidence interval, 0.003-0.011; P=.001), early-pregnancy cardiometabolic markers including total cholesterol (B=0.155; 95% confidence interval, 0.061-0.249; P=.001), triglycerides (B=0.043; 95% confidence interval, 0.005-0.080; P=.03), low-density lipoproteins (B=0.129; 95% confidence interval, 0.049-0.209; P=.002), and diastolic blood pressure (B=0.538; 95% confidence interval, 0.070-1.006; P=.02), and late-pregnancy cardiometabolic markers including total cholesterol (B=0.127; 95% confidence interval, 0.012-0.243; P=.01) and low-density lipoproteins (B=0.110; 95% confidence interval, 0.010-0.209; P=.03). In the third trimester, Energy-Adjusted Dietary Inflammatory Index was associated with late-pregnancy diastolic blood pressure (B=0.624; 95% confidence interval, 0.103-1.145; P=.02), HOMA1-IR (B=0.030; 95% confidence interval, 0.005-0.054; P=.02), and glucose (B=0.003; 95% confidence interval, 0.003-0.034; P=.03). No associations were observed between third-trimester Energy-Adjusted Dietary Inflammatory Index and late-pregnancy lipid profiles. Conclusion: Maternal diets with a higher Energy-Adjusted Dietary Inflammatory Index, which were low in anti-inflammatory foods and rich in proinflammatory foods, were associated with increased levels of cardiometabolic health risk factors in pregnancy. Promoting dietary intakes that have a lower inflammatory potential may support more favorable maternal cardiometabolic profiles during pregnancy.

Diet-related inflammation increases the odds of multiple sclerosis: Results from a large population-based prevalent case-control study in Jordan.

Background: Multiple sclerosis, a chronic inflammatory disease in young and middle-aged adults, is one of the leading causes of non-traumatic disability in adults. Diet is known to have an important role in the modulating inflammatory processes and influencing molecular pathways. Purpose: This study aims to examine the association of the inflammatory capacity of diet measured by DII with MS in Jordan. Methods: This prevalent case-control study included participants of both sexes, aged between 20 and 60 years. The cases (n = 541) had a confirmed diagnosis of prevalent Multiple Sclerosis (MS) in the previous 3 years, and controls (n = 607) were apparently healthy individuals matched on sex and age (42 ± 4 years). A validated Arabic food frequency questionnaire (FFQ) was utilized to obtain estimated dietary intake. Dietary data from the FFQ were analyzed using ESHA's Food Processor® nutrition analysis software, and the results were used to calculate the DII scores. Logistic regression analyses, controlling for covariates such as age, sex, body mass index, and smoking status, were used to measure the association between DII score and MS outcomes. Results: Cases represent a mixed sample of MS phenotypes and controls were comparable on age and sex. However, controls tended to be taller, lighter, had a lower BMI, and had a lower smoking rate. After controlling for age, BMI, sex, and smoking status, there was a consistent increase in MS risk according to DII score, with a 10-fold increase in odds in quartile 4 vs. quartile 1 [ORquartile 4vs1 = 10.17 (95% CI: 6.88; 15.04)]. For each point increase in DII score, there was nearly a doubling of odds [OR1 = 1.75 (95% CI: 1.59; 1.92)]. Individual nutrients and food values aligned according to their contribution to the DII score calculations. Conclusion: The findings of this study, obtained in MS patients with varied illness duration over the previous 3 years, are consistent with an association between the overall inflammatory potential of diet and MS odds. Our findings among MS participants showed a significantly more pro-inflammatory DII scores than age- and sex-matched controls. Our results also suggest that MS group had a diet rich in pro-inflammatory foods and nutrients.

The association between inflammatory and immune system biomarkers and the dietary inflammatory index in patients with COVID-19.

Background: Inflammation and cytokine storm have been reported to be the main cause of acute symptoms of coronavirus disease (COVID-19). Diet-induced inflammation may affect the condition of patients with COVID-19. Therefore, this study aimed to investigate the relationship between disease severity, inflammatory and immune system biomarkers, and the dietary inflammatory index (DII) in patients with COVID-19. Methods: This cross-sectional study was conducted on 500 adult patients with COVID-19. Patients were divided into mild, moderate, and severe conditions based on clinical and laboratory evidence. A validated food frequency questionnaire (FFQ) was used to determine DII and energy-adjusted DII (E-DII) scores. The serum C-reactive protein (CRP) level and blood cell count were measured for all patients. Multiple linear regression was used to explore the association between DII and E-DII and CRP, blood cell counts, and hospitalization in patients with COVID-19. Results: Coronavirus disease (COVID-19) patients with higher DII had higher consumption of fat and carbohydrate and lower intakes of protein, anti-inflammatory nutrients, garlic, caffeine, tea, onion, and fiber (P < 0.05). There was a positive association between DII and CRP (ß = 1.024, P < 0.001), hospitalization (ß = 1.062, P < 0.001), WBC count (ß = 0.486, P < 0.009), neutrophil count (ß = 0.565, P < 0.001), and neutrophil-to-lymphocyte ratio (ß = 0.538, P < 0.001) and a negative association between DII and the lymphocyte count (ß = -0.569, P < 0.001). There was a positive association between E-DII and hospitalization (ß = 1.645, P < 0.001), WBC count (ß = 0.417, P < 0.02), and neutrophil-to-lymphocyte ratio (ß = 0.35, P < 0.03). Conclusion: There is a positive correlation between DII and inflammation, immune hyperactivation, and length of hospital stay in patients with COVID-19. Further longitudinal studies are necessary.

The Association of the Inflammatory Index of the Maternal Diet with the Type of Delivery, Maternal Nutritional Status, and the Lipid Profile of Human Milk.

Objective: To evaluate the association of the dietary inflammatory index adjusted for energy (E-DII®) with the evolution of maternal body mass index and human milk lipid (HM) profile in the first 6 months postpartum. Methods: This is a cohort study with 260 Brazilian women (19-43 years old) in the postpartum period. Sociodemographic, gestational, and anthropometric data of the mother were obtained in the immediate postpartum period and in the six monthly meetings. A food frequency questionnaire was applied at baseline and used to calculate the E-DII score. Mature HM was collected, analyzed by gas chromatography coupled with mass spectrometry and the Rose Gottlib method. Generalized estimation equation models were built. Results: Women with >E-DII showed lower adherence to physical activity during pregnancy (p = 0.027), higher frequency of cesarean delivery (p = 0.024), and higher body mass index over time (p < 0.001). At the end of the 6th month, 35 women remained in the study. As for HM, 151 analyses were performed, detecting in the 3rd collection greater fat (%) among those with >E-DII (4.27 ± 1.98 vs. 3.75 ± 2.48; p = 0.003). Conclusion: Diets with >E-DII can impact the type of delivery, change the evolution of maternal nutritional status, and the stability of the lipid profile of HM.

Changes in Dietary Inflammatory Index Score over Time and Cancer Development in Rural Post-Menopausal Women.

Inflammation plays a key role in cancer development. As an important modulator of inflammation, the role of diet should be explored. The purpose of this study was to determine the association between diets with a higher inflammatory potential, as measured by the Dietary Inflammatory Index (DII®), and cancer development in a cohort of rural post-menopausal women. Dietary intake from a randomized controlled trial cohort of rural, post-menopausal women in Nebraska was used to compute energy-adjusted DII (E-DIITM) scores at baseline and four years later (visit 9). A linear mixed model analysis and multivariate logistic regression evaluated the association between E-DII scores (baseline, visit 9, change score) and cancer status. Of 1977 eligible participants, those who developed cancer (n = 91, 4.6%) had a significantly larger, pro-inflammatory change in E-DII scores (Non-cancer: Δ 0.19 ± 1.43 vs. Cancer: Δ 0.55 ± 1.43, p = 0.02). After adjustment, odds of cancer development were over 20% higher in those with a larger change (more pro-inflammatory) in E-DII scores than those with smaller E-DII changes (OR = 1.21, 95% CI [1.02, 1.42], p = 0.02). Shifting to a more pro-inflammatory diet pattern over four years was associated with increased odds of cancer development, but not with E-DII at baseline or visit 9 alone.

Association between inflammatory potential of diet and periodontitis disease risks: Results from a Korean population-based cohort study.

AIM: To examine the association between a pro-inflammatory diet, estimated using the energy-adjusted dietary inflammatory index (E-DII), and the risk of periodontitis. MATERIALS AND METHODS: Study subjects from the Korean Genome and Epidemiology Study Health Examinee (KoGES_HEXA) cohort were included for cross-sectional analysis (n = 168,378) using multivariate logistic regression and prospective analysis (n = 160,397) using Cox proportional hazard models respectively. DII and E-DII scores were calculated based on the intake reported on a validated semi-quantitative food frequency questionnaire (SQ-FFQ). RESULTS: Cox proportional hazard models revealed a significantly increased risk of incident periodontitis in individuals consuming high E-DII (more pro-inflammatory) diets in the total population (HRquartile4vs1 = 1.29; 95% CI: 1.13-1.48; ptrend <.001) and in both men (HRquartile4vs1 = 1.36; 95% CI: 1.07-1.73; ptrend = 0.02) and women (HRquartile4vs1 = 1.27; 95% CI: 1.08-1.50; ptrend = .002). The association remained significant even after excluding cases diagnosed early in the follow-up. In the cross-sectional analysis, a significant association was observed between the E-DII score and the prevalence of periodontitis among all study subjects (ORquartile4vs1 = 1.17; 95% CI: 1.03-1.34; ptrend = 0.01) and men (ORquartile4vs1 = 1.28; 95%CI: 1.01-1.63; ptrend <.001); however, the association did not reach statistical significance in women (ORquartile4vs1 = 1.13; 95% CI: 0.96-1.33; ptrend <.001). CONCLUSIONS: Findings from the current study support the hypothesis that diets with high pro-inflammatory potential increase the risk of periodontitis.

Maternal and Paternal Dietary Quality and Dietary Inflammation Associations with Offspring DNA Methylation and Epigenetic Biomarkers of Aging in the Lifeways Cross-Generation Study.

BACKGROUND: Early-life nutritional exposures may contribute to offspring epigenetic modifications. However, few studies have evaluated parental dietary quality effects on offspring DNA methylation (DNAm). OBJECTIVES: We aim to fill this gap by elucidating the influence of maternal and paternal whole-diet quality and inflammatory potential on offspring DNAm in the Lifeways Cross-generation cohort. METHODS: Families (n = 1124) were recruited around 16 weeks of gestation in the Republic of Ireland between 2001 and 2003. Maternal dietary intake during the first trimester and paternal diet during the 12 previous months were assessed with an FFQ. Parental dietary inflammatory potential and quality were determined using the energy-adjusted Dietary Inflammatory Index (E-DII), the Healthy Eating Index-2015 (HEI-2015), and the maternal DASH score. DNAm in the saliva of 246 children at age nine was measured using the Illumina Infinium HumanMethylationEPIC array. DNAm-derived biomarkers of aging, the Pediatric-Buccal-Epigenetic clock and DNAm estimator of telomere length, were calculated. Parental diet associations with the DNAm concentrations of 850K Cytosine-phosphate-guanine sites (CpG sites) and with DNAm-derived biomarkers of aging were examined using an epigenome-wide association study and linear regressions, respectively. RESULTS: Maternal HEI-2015 scores were inversely associated with DNAm at CpG site (cg21840035) located near the PLEKHM1 gene, whose functions involve regulation of bone development (ß = -0.0036, per 1 point increase in the score; P = 5.6 × 10-8). Higher paternal HEI-2015 score was related to lower methylation at CpG site (cg22431767), located near cell signaling gene LUZP1 (ß = -0.0022, per 1 point increase in the score, P = 4.1 × 10-8). There were no associations with parental E-DII and DASH scores, and no evidence of major effects on biomarkers of aging. CONCLUSIONS: Parental dietary quality in the prenatal period, evaluated by the HEI-2015, may influence offspring DNAm during childhood. Further research to improve our understanding of parental nutritional programming is warranted.

Dietary Inflammatory Index and Fractures in Midlife Women: Study of Women's Health Across the Nation.

CONTEXT: While evidence suggests that chronic, low-grade inflammation is a risk factor for bone loss and fractures, the potential relation between an inflammatory dietary profile and greater fracture risk is uncertain. OBJECTIVE: We examined whether a more inflammatory diet, consumed during pre- and early perimenopause, is associated with more incident fractures starting in the menopause transition (MT) and continuing into postmenopause. METHODS: Dietary inflammatory potential was quantified using 2 energy-adjusted dietary inflammatory index scores: one for diet only (E-DII), and one for diet plus supplements (E-DII-S). We included 1559 women from the Study of Women's Health Across the Nation, with E-DII and E-DII-S scores from the baseline visit (during pre- or early perimenopausal), and up to 20 years of follow-up. We excluded women using bone-beneficial medications at baseline; subsequent initiators were censored at first use. The associations of E-DII or E-DII-S (each tested as separate exposures) with incident fracture were examined using Cox proportional hazards regression. RESULTS: Adjusted for age, BMI, cigarette use, diabetes, MT stage, race/ethnicity, prior fracture, bone-detrimental medication use, aspirin or nonsteroidal anti-inflammatory drug use, and study site, greater E-DII and E-DII-S (tested separately) were associated with more future fractures. Each SD increment in E-DII and E-DII-S predicted 28% (P = .005) and 21% (P = .02) greater fracture hazard, respectively. Associations were essentially unchanged after controlling for bone mineral density. CONCLUSION: A more pro-inflammatory diet in pre- and early perimenopause is a risk factor for incident fracture. Future studies should consider whether reducing dietary inflammation in midlife diminishes fracture risk.

Maternal Diet Quality During Pregnancy and Offspring Hepatic Fat in Early Childhood: The Healthy Start Study.

BACKGROUND: Overnutrition in utero may increase offspring risk of nonalcoholic fatty liver disease (NAFLD), but the specific contribution of maternal diet quality during pregnancy to this association remains understudied in humans. OBJECTIVES: This study aimed to examine the associations of maternal diet quality during pregnancy with offspring hepatic fat in early childhood (median: 5 y old, range: 4-8 y old). METHODS: Data were from 278 mother-child pairs in the longitudinal, Colorado-based Healthy Start Study. Multiple 24-h recalls were collected from mothers during pregnancy on a monthly basis (median: 3 recalls, range: 1-8 recalls starting after enrollment), and used to estimate maternal usual nutrient intakes and dietary pattern scores [Healthy Eating Index-2010 (HEI-2010), Dietary Inflammatory Index (DII), and Relative Mediterranean Diet Score (rMED)]. Offspring hepatic fat was measured in early childhood by MRI. Associations of maternal dietary predictors during pregnancy with offspring log-transformed hepatic fat were assessed using linear regression models adjusted for offspring demographics, maternal/perinatal confounders, and maternal total energy intake. RESULTS: Higher maternal fiber intake and rMED scores during pregnancy were associated with lower offspring hepatic fat in early childhood in fully adjusted models [Back-transformed ß (95% CI): 0.82 (0.72, 0.94) per 5 g/1000 kcal fiber; 0.93 (0.88, 0.99) per 1 SD for rMED]. In contrast, higher maternal total sugar and added sugar intakes, and DII scores were associated with higher offspring hepatic fat [Back-transformed ß (95% CI): 1.18 (1.05, 1.32) per 5% kcal/d added sugar; 1.08 (0.99, 1.18) per 1 SD for DII]. Analyses of dietary pattern subcomponents also revealed that lower maternal intakes of green vegetables and legumes and higher intake of "empty calories" were associated with higher offspring hepatic fat in early childhood. CONCLUSIONS: Poorer maternal diet quality during pregnancy was associated with greater offspring susceptibility to hepatic fat in early childhood. Our findings provide insights into potential perinatal targets for the primordial prevention of pediatric NAFLD.