Allura Red AC is a xenobiotic. Is it also a carcinogen?

Merriam-Webster and Oxford define a xenobiotic as any substance foreign to living systems. Allura Red AC (a.k.a., E129; FD&C Red No. 40), a synthetic food dye extensively used in manufacturing ultra-processed foods and therefore highly prevalent in our food supply, falls under this category. The surge in synthetic food dye consumption during the 70s and 80s was followed by an epidemic of metabolic diseases and the emergence of early-onset colorectal cancer in the 1990s. This temporal association raises significant concerns, particularly given the widespread inclusion of synthetic food dyes in ultra-processed products, notably those marketed toward children. Given its interactions with key contributors to colorectal carcinogenesis such as inflammatory mediators, the microbiome, and DNA damage, there is growing interest in understanding Allura Red AC's potential impact on colon health as a putative carcinogen. This review discusses the history of Allura Red AC, current research on its effects on the colon and rectum, potential mechanisms underlying its impact on colon health, and provides future considerations. Indeed, although no governing agencies classify Allura Red AC as a carcinogen, its interaction with key guardians of carcinogenesis makes it suspect and worthy of further molecular investigation. The goal of this review is to inspire research into the impact of synthetic food dyes on colon health.

The association between dietary inflammatory index with risk rheumatoid arthritis: A case-control study.

Diet represents an important set of potential risk factors for rheumatoid arthritis (RA), a known inflammatory condition. This case-control study examined the association between the inflammatory potential of diet, as determined by the dietary inflammatory index (DII®), and RA risk in an Iranian population. The present Case-control study was conducted on 100 RA patients and 200 age- and sex-matched controls in Isfahan, Iran. The presence of RA was determined by expert Rheumatologist assessment based on the American College of Rheumatology definitions. A 168-item food frequency questionnaire was used to collect dietary intake from which DII scores were computed. Odds ratios (OR) and 95 % confidence intervals (CI) for the association between the DII, expressed in tertiles, and RA risk were estimated by two multivariable logistic regression models, one crude model and one in which we controlled for important potential confounders. In the crude model, individuals in the top DII tertile (most pro-inflammatory diet) had more than triple the risk of RA compared to those in the lowest tertile (ORtertile3vs1= 3.57; 95 % CI, 1.95-6.53; p< 0.001). The association was essentially unchanged after controlling for potential confounders (OR tertile3vs1 = 3.83; 95 % CI, 1.66-8.81; p<0.001). We found that a pro-inflammatory diet is associated with increased risk of RA. Higher volume studies are needed to confirm the results.

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.

Association of a dietary inflammatory index with cardiometabolic, endocrine, liver, renal and bones biomarkers: cross-sectional analysis of the UK Biobank study.

BACKGROUND AND AIMS: Research into the relationship between an Energy-adjusted Diet-Inflammatory Index (E-DII) and a wider health-related biomarkers profile is limited. Much of the existing evidence centers on traditional metabolic biomarkers in populations with chronic diseases, with scarce data on healthy individuals. Thus, this study aims to investigate the association between an E-DII score and 30 biomarkers spanning metabolic health, endocrine, bone health, liver function, cardiovascular, and renal functions, in healthy individuals. METHODS AND RESULTS: 66,978 healthy UK Biobank participants, the overall mean age was 55.3 (7.9) years were included in this cross-sectional study. E-DII scores, based on 18 food parameters, were categorised as anti-inflammatory (E-DII < -1), neutral (-1 to 1), and pro-inflammatory (>1). Regression analyses, adjusted for confounding factors, were conducted to investigate the association of 30 biomarkers with E-DII. Compared to those with an anti-inflammatory diet, individuals with a pro-inflammatory diet had increased levels of 16 biomarkers, including six cardiometabolic, five liver, and four renal markers. The concentration difference ranged from 0.27 SD for creatinine to 0.03 SD for total cholesterol. Conversely, those on a pro-inflammatory diet had decreased concentrations in six biomarkers, including two for endocrine and cardiometabolic. The association range varied from -0.04 for IGF-1 to -0.23 for SHBG. CONCLUSION: This study highlighted that a pro-inflammatory diet was associated with an adverse profile of biomarkers linked to cardiometabolic health, endocrine, liver function, and renal health.

Atopic allergic conditions and prostate cancer risk and survival in the Multiethnic Cohort study.

BACKGROUND: Previous studies investigating relationship between atopic allergic conditions (AACs)-a highly reactive immune state-and prostate cancer (PCa) risk were inconclusive, and few have studied diverse racial/ethnic populations. METHODS: We analysed 74,714 men aged ≥45 years at enrollment in Multiethnic Cohort study. Using multivariable Cox regression, we estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for self-reported AAC status on PCa outcomes. RESULTS: Through 2017, 8697 incident PCa and 1170 related deaths occurred. Twenty-one percent of men reported a history of AACs. AACs were not associated with incident PCa (HR = 0.98, 95% CI: 0.93-1.03) but were significantly inversely associated with PCa mortality (HR = 0.79, 95% CI: 0.67-0.92). This inverse association was consistently observed across all racial/ethnic groups (HR range: 0.60-0.90). Among men diagnosed with PCa, AACs were inversely associated with PCa-specific death (HR = 0.75, 95% CI: 0.63-0.89). Adjusting for potential confounding effect of PSA screening did not meaningfully change the results. No significant heterogeneity was observed in the effect of AACs on PCa incidence or mortality by Dietary Inflammatory Index. CONCLUSIONS: Hyper-allergic conditions were not associated with PCa incidence but were inversely associated with PCa mortality, suggesting a potential role in reducing tumour progression. Further aetiological research is warranted to understand underlying mechanisms.

Association between dietary inflammatory potential and mortality after cancer diagnosis in the Women's Health Initiative.

BACKGROUND: Chronic inflammation is implicated in cancer prognosis and can be modulated by diet. We examined associations between post-diagnosis dietary inflammatory potential and mortality outcomes among post-menopausal women diagnosed with cancer in the Women's Health Initiative (WHI). METHODS: Energy-adjusted dietary inflammatory index scores (E-DII) were calculated from dietary and supplemental intake data collected on the first food frequency questionnaire following the diagnosis of primary invasive cancer for 3434 women in the WHI. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CIs) for risk of death from any cause, cancer, cardiovascular disease (CVD) and other causes by post-diagnosis quartiles of E-DII. Subgroup analyses by cancer stage and grade were performed. RESULTS: There were 1156 deaths after a median 13 years of follow-up from the date of a cancer diagnosis. In the multivariable-adjusted analyses, a more anti-inflammatory diet plus supplements after cancer diagnosis was associated with lower all-cause mortality, cancer mortality, CVD mortality and mortality from other causes with HRsQ1vs.Q4 ranging from 0.47 to 0.68 (all P-trends < 0.05). Associations were stronger for cancers diagnosed at more distant stages or moderately differentiated grades. CONCLUSION: A more anti-inflammatory diet plus supplements after a cancer diagnosis may improve survival for post-menopausal cancer survivors.

Association of inflammation-related exposures and ovarian cancer survival in a multi-site cohort study of Black women.

BACKGROUND: An association was observed between an inflammation-related risk score (IRRS) and worse overall survival (OS) among a cohort of mostly White women with invasive epithelial ovarian cancer (EOC). Herein, we evaluated the association between the IRRS and OS among Black women with EOC, a population with higher frequencies of pro-inflammatory exposures and worse survival. METHODS: The analysis included 592 Black women diagnosed with EOC from the African American Cancer Epidemiology Study (AACES). Cox proportional hazards models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs) for the association of the IRRS and OS, adjusting for relevant covariates. Additional inflammation-related exposures, including the energy-adjusted Dietary Inflammatory Index (E-DIITM), were evaluated. RESULTS: A dose-response trend was observed showing higher IRRS was associated with worse OS (per quartile HR: 1.11, 95% CI: 1.01-1.22). Adding the E-DII to the model attenuated the association of IRRS with OS, and increasing E-DII, indicating a more pro-inflammatory diet, was associated with shorter OS (per quartile HR: 1.12, 95% CI: 1.02-1.24). Scoring high on both indices was associated with shorter OS (HR: 1.54, 95% CI: 1.16-2.06). CONCLUSION: Higher levels of inflammation-related exposures were associated with decreased EOC OS among Black women.

Associations between an inflammatory diet index and severe non-alcoholic fatty liver disease: a prospective study of 171,544 UK Biobank participants.

BACKGROUND: Although non-alcoholic fatty liver disease (NAFLD) is linked to inflammation, whether an inflammatory diet increases the risk of NAFLD is unclear. This study aimed to examine the association between the Energy-adjusted Diet Inflammatory Index (E-DII) score and severe NAFLD using UK Biobank. METHODS: This prospective cohort study included 171,544 UK Biobank participants. The E-DII score was computed using 18 food parameters. Associations between the E-DII and incident severe NAFLD (defined as hospital admission or death) were first investigated by E-DII categories (very/moderately anti-inflammatory [E-DII < - 1], neutral [E-DII - 1 to 1] and very/moderately pro-inflammatory [E-DII > 1]) using Cox proportional hazard models. Nonlinear associations were investigated using penalised cubic splines fitted into the Cox proportional hazard models. Analyses were adjusted for sociodemographic, lifestyle and health-related factors. RESULTS: Over a median follow-up of 10.2 years, 1489 participants developed severe NAFLD. After adjusting for confounders, individuals in the very/moderately pro-inflammatory category had a higher risk (HR: 1.19 [95% CI: 1.03 to 1.38]) of incident severe NAFLD compared with those in the very/moderately anti-inflammatory category. There was some evidence of nonlinearity between the E-DII score and severe NAFLD. CONCLUSIONS: Pro-inflammatory diets were associated with a higher risk of severe NAFLD independent of confounders such as the components of the metabolic syndrome. Considering there is no recommended treatment for the disease, our findings suggest a potential means to lower the risk of NAFLD.

The special sauce of the Cancer Prevention and Control Research Network: 20 years of lessons learned in developing the evidence base, building community capacity, and translating research into practice.

PURPOSE: The Cancer Prevention and Control Research Network (CPCRN) is a national network focused on accelerating the translation of cancer prevention and control research evidence into practice through collaborative, multicenter projects in partnership with diverse communities. From 2003 to 2022, the CPCRN included 613 members. METHODS: We: (1) characterize the extent and nature of collaborations through a bibliometric analysis of 20 years of Network publications; and (2) describe key features and functions of the CPCRN as related to organizational structure, productivity, impact, and focus on health equity, partnership development, and capacity building through analysis of 22 in-depth interviews and review of Network documentation. RESULTS: Searching Scopus for multicenter publications among the CPCRN members from their time of Network engagement yielded 1,074 collaborative publications involving two or more members. Both the overall number and content breadth of multicenter publications increased over time as the Network matured. Since 2004, members submitted 123 multicenter grant applications, of which 72 were funded (59%), totaling more than $77 million secured. Thematic analysis of interviews revealed that the CPCRN's success-in terms of publication and grant productivity, as well as the breadth and depth of partnerships, subject matter expertise, and content area foci-is attributable to: (1) its people-the inclusion of members representing diverse content-area interests, multidisciplinary perspectives, and geographic contexts; (2) dedicated centralized structures and processes to enable and evaluate collaboration; and (3) focused attention to strategically adapting to change. CONCLUSION: CPCRN's history highlights organizational, strategic, and practical lessons learned over two decades to optimize Network collaboration for enhanced collective impact in cancer prevention and control. These insights may be useful to others seeking to leverage collaborative networks to address public health problems.

Interaction between Meal-timing and Dietary Inflammatory Potential: Association with Cardiometabolic Endpoints in a 3-month Prospective Analysis.

BACKGROUND: Diet quality is a moderator of cardiometabolic markers. The timing of dietary intake may be an important determinant; however, previous results have been mixed. Complex mechanisms may result in an interaction between diet timing and quality. OBJECTIVES: This study aimed to examine the association between fasting duration and first and last mealtime and inflammatory and lipid biomarkers. We also explored the interactions between Energy-density Dietary Inflammatory Index (E-DII) scores and meal-timing on inflammatory and lipid biomarkers. METHODS: This study was a secondary data analysis of a dietary intervention. Assessments occurred at baseline and 3-months. Three unannounced 24-hour dietary recalls estimated diet for calculation of E-DII scores, nighttime fasting duration, and first and last mealtime. Cardiometabolic markers were obtained from a fasting blood sample. Multiple linear regression of baseline data was used for Aim 1. For Aim 2, the interaction between E-DII change over 3 months and the meal-timing metrics were used to estimate changes in cardiometabolic markers. RESULTS: Most participants (n=95) were female (81%) and White (62%) and they had an average age of 46.9 ± 13.4 years and BMI of 31.4 ± 7.1 kg/m2. Every one-hour longer fasting duration was associated with increased total cholesterol (ß=5.79, p=0.01), LDL-cholesterol (ß=4.47, p=0.03), and LDL:HDL ratio (ß=0.08, p=0.04). For every 30-minute later first mealtime, increases in total cholesterol, LDL-cholesterol and LDL:HDL ratios also were observed. Anti-inflammatory E-DII changes were associated with reduced total cholesterol and LDL-C (among participants with shorter fasting durations, later last mealtime, or earlier first mealtime) and C-reactive protein (CRP, among earlier first mealtime and shorter fasting duration). CONCLUSIONS: This study provides evidence for interaction between dietary timing and quality on cardiometabolic biomarkers. Worsening lipid profiles seen with longer fasting durations may be an artifact of skipped or delayed breakfast, underlining the potential importance of food consumption early in the morning. GOV IDENTIFIER: NCT02382458 (https://clinicaltrials.gov/ct2/show/NCT02382458).

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.

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.

A pro-inflammatory diet in people with multiple sclerosis is associated with an increased rate of relapse and increased FLAIR lesion volume on MRI in early multiple sclerosis: A prospective cohort study.

BACKGROUND: A pro-inflammatory diet has been posited to induce chronic inflammation within the central nervous system (CNS), and multiple sclerosis (MS) is an inflammatory disease of the CNS. OBJECTIVE: We examined whether Dietary Inflammatory Index (DII®)) scores are associated with measures of MS progression and inflammatory activity. METHODS: A cohort with a first clinical diagnosis of CNS demyelination was followed annually (10 years, n = 223). At baseline, 5- and 10-year reviews, DII and energy-adjusted DII (E-DIITM) scores were calculated (food frequency questionnaire) and assessed as predictors of relapses, annualised change in disability (Expanded Disability Status Scale) and two magnetic resonance imaging measures; fluid-attenuated inversion recovery (FLAIR) lesion volume and black hole lesion volume. RESULTS: A more pro-inflammatory diet was associated with a higher relapse risk (highest vs. lowest E-DII quartile: hazard ratio = 2.24, 95% confidence interval (CI) = -1.16, 4.33, p = 0.02). When we limited analyses to those assessed on the same manufacturer of scanner and those with a first demyelinating event at study entry (to reduce error and disease heterogeneity), an association between E-DII score and FLAIR lesion volume was evident (ß = 0.38, 95% CI = 0.04, 0.72, p = 0.03). CONCLUSION: There is a longitudinal association between a higher DII and a worsening in relapse rate and periventricular FLAIR lesion volume in people with MS.

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.

Maternal obesity, gestational diabetes mellitus, and diet in association with neurodevelopment of 2-year-old children.

BACKGROUND: Maternal metabolic disturbances and diet may influence long-term infantile neurodevelopment. We investigated whether maternal gestational diabetes mellitus (GDM), obesity, and diet could affect the neurodevelopment of 2-year-old children. METHODS: Neurodevelopment of children (n = 243) born to mothers with overweight or obesity was assessed with the Bayley Scales of Infant and Toddler Development-Third Edition, and the Hammersmith Infant Neurological Examination. Maternal adiposity was determined by air displacement plethysmography, and GDM with an oral glucose tolerance test. Dietary assessment included diet quality and fish consumption questionnaires, and three-day food diaries, from which dietary inflammatory index (DII®) scores were computed. RESULTS: GDM was associated with weaker expressive language skills (adj.ß = -1.12, 95% CI = -2.10;-0.15), and higher maternal adiposity with weaker cognitive, language, and motor skills in children (adj.p < 0.05). Maternal good dietary quality (adj.ß = 0.87, 95% CI = 0.004;1.73) and higher fish consumption (adj.p = 0.02) were related to better expressive language skills. DII scores were not associated with children's neurodevelopment. CONCLUSIONS: Findings suggest that GDM and higher maternal adiposity may lead to weaker neurodevelopmental skills, although still within the mean normative range in this population of children. Good dietary quality and higher fish consumption during pregnancy could benefit a child's language development. IMPACT: Gestational diabetes mellitus and maternal higher adiposity may have unfavorable effects on a 2-year-old child's neurodevelopment. An overall good quality of diet and higher fish consumption during pregnancy may result in more favorable cognitive and language skills when the child is 2-year-old. Our findings reveal that women with overweight or obesity, a risk group for pregnancy complications, could benefit from dietary counseling to support their children's neurodevelopment.

Change in the inflammatory potential of diet over 10 years and subsequent mortality: the Multiethnic Cohort Study.

Dietary inflammatory potential assessed by the Dietary Inflammatory Index (DII®) has been associated with health outcomes. However, longitudinal changes in the DII in relation to health outcomes rarely have been studied. This study aimed to examine change in the DII score over 10 years and its association with subsequent mortality in the Multiethnic Cohort. The analysis included 56 263 African American, Japanese American, Latino, Native Hawaiian and White participants who completed baseline (45-75 years) and 10-year follow-up surveys, including a FFQ. Mean energy-adjusted DII (E-DII) decreased over 10 years in men (from -0·85 to -1·61) and women (from -1·80 to -2·47), reflecting changes towards a more anti-inflammatory diet. During an average follow-up of 13·0 years, 16 363 deaths were identified. In multivariable Cox models, compared with anti-inflammatory stable individuals, risk of all-cause mortality was increased with pro-inflammatory change in men (hazard ratio (HR) = 1·13, 95 % CI 1·03, 1·23) and women (HR = 1·22, 95 % CI 1·13, 1·32). Per one-point increase in E-DII score over time, HR was 1·02 (95 % CI 1·00, 1·03) for men and 1·06 (95 % CI 1·04, 1·07) for women (P for heterogeneity < 0·001). While no heterogeneity by race and ethnicity was observed for men, the increased risk per one-point increase among women was stronger in non-Whites than in Whites (P for heterogeneity = 0·004). Our findings suggest that a change towards a more pro-inflammatory diet is associated with an increased risk of mortality both in men and women, and that the association is stronger in women, especially non-White women, than in men.

Association of diet quality indices with serum and metabolic biomarkers in participants of the ORISCAV-LUX-2 study.

PURPOSE: Diet quality is a critical modifiable factor related to health, including the risk of cardiometabolic complications. Rather than assessing the intake of individual food items, it is more meaningful to examine overall dietary patterns. This study investigated the adherence to common dietary indices and their association with serum/metabolic parameters of disease risk. METHODS: Dietary intakes of the general adult population (n = 1404, 25-79 years) were assessed by a validated food-frequency questionnaire (174 items). The French ANSES-Ciqual food composition database was used to compute nutrient intakes. Seven indicators were calculated to investigate participants' diet quality: the Alternative Healthy Eating Index (AHEI), Dietary Approaches to Stop Hypertension Score (DASH-S), Mediterranean Diet Score (MDS), Diet Quality Index-International (DQI-I), Dietary Inflammatory Index (DII), Dietary Antioxidant Index (DAI), and Naturally Nutrient-Rich Score (NNRS). Various serum/metabolic parameters were used in the validity and association analyses, including markers of inflammation, blood glucose, and blood lipid status. RESULTS: Following linear regression models adjusted for confounders, the DASH-S was significantly associated with most metabolic parameters (14, e.g., inversely with blood pressure, triglycerides, urinary sodium, uric acid, and positively with serum vitamin D), followed by the DQI-I (13, e.g., total cholesterol, apo-A/B, uric acid, and blood pressure) and the AHEI (11, e.g., apo-A, uric acid, serum vitamin D, diastolic blood pressure and vascular age). CONCLUSION: Food-group-based indices, including DASH-S, DQI-I, and AHEI, were good predictors for serum/metabolic parameters, while nutrient-based indices, such as the DAI or NNRS, were less related to biological markers and, thus, less suitable to reflect diet quality in a general population.

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.

Dietary inflammatory index and cardiovascular disease risk in Hispanic women from the Women's Health Initiative.

BACKGROUND: To evaluate the association between the dietary inflammatory index (DII®) and incident cardiovascular disease (CVD) in Hispanic women from the Women's Health Initiative (WHI), and to determine if body mass index (BMI) interacted with the DII scores. METHODS: Secondary analysis of baseline dietary data and long-term CVD outcomes among 3,469 postmenopausal women who self-identified as Hispanic enrolled in WHI. DII scores were calculated from self-administered food frequency questionnaires. The CVD outcomes included coronary heart disease (CHD) and stroke. Stratified Cox regression models were used to assess the relationship between DII scores and CVD in women with and without obesity. Models were adjusted for age, lifestyle risk factors, known risk factors, and neighborhood socioeconomic status. RESULTS: The incidence of CHD was 3.4 and 2.8% for stroke after a median follow-up of 12.9 years. None of the DIIs were associated with CVD risk in this sample of Hispanic women. BMI interacted with the DII (p < 0.20) and stratified models showed that the associations between the DII and CVD were only significant in women with overweight (p < 0.05). In this group, higher DII scores were associated with a higher risk of CHD (HR 1.27; 95% CI: 1.08, 1.51) and a higher risk of stroke (HR 1.32; 95% CI: 1.07, 1.64). CONCLUSION: Among postmenopausal Hispanic women with overweight, greater adherence to pro-inflammatory diets was associated with higher risk of CVD. Additional research is needed to understand how to promote long-term heart-healthy dietary habits to reduce inflammation and prevent CVD in at-risk Hispanic women.

Inflammatory diets are associated with lower total iron binding capacity in sera of young adults.

Chronic, systemic inflammation, which is associated with obesity and numerous other diseases, impairs iron status by increasing hepcidin concentration. Inflammation also decreases the concentration of transferrin, the main iron transport protein and a negative acute phase protein, which is indirectly assessed by measuring total iron binding capacity (TIBC). However, the contribution of diet-induced inflammation has not been studied. Data from two studies, namely Diet and Inflammation and Selenium and Inflammation Studies (total n=98) were used to assess the associations among Dietary Inflammatory Index (DII®) scores derived from three-day dietary records, body mass index (BMI=weight[kg]/height[m]2), inflammatory and hematological markers among young adults with normal-weight, overweight or obesity. Subjects' diets were also categorized as less inflammatory diets (LID) and inflammatory diets (ID) using cluster analysis. Independent t-test and regression analyses were used to assess associations in the data. Intakes of iron, proteins, fat, fiber, and calories were higher in the LID group compared to the ID group (p<0.05). Demographic characteristics and concentrations of C-reactive protein (CRP) and iron status biomarkers did not differ significantly between the two groups (p>0.05). Higher DII score was associated with increasing CRP (ß+SE=0.23+0.07, p=0.002) and lower TIBC (ß+SE=-8.46+3.44, p=0.02), independent of BMI category. The LID diet was associated with higher TIBC (ß+SE=29.87+10.75, p=0.007) compared to the ID diet. In conclusion, inflammatory diets may impair iron status by reducing the iron binding capacity of transferrin.