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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-DII TM ) 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.

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.

This study evaluated the association between inflammatory diets as measured by the Dietary Inflammatory index (DII), inflammation biomarkers and the development of preeclampsia among the Chinese population. We followed the reporting guidelines of the Strengthening the Reporting of Observational Studies in Epidemiology statement for observational studies. A total of 466 preeclampsia cases aged over 18 years were recruited between March 2016 and June 2019, and 466 healthy controls were 1:1 ratio matched by age (±3 years), week of gestation (±1 week) and gestational diabetes mellitus. The energy-adjusted DII (E-DII) was computed based on dietary intake assessed using a seventy-nine item semiquantitative FFQ. Inflammatory biomarkers were analysed by ELISA kits. The mean E-DII scores were -0·65 ± 1·58 for cases and -1·19 ± 1·47 for controls ( P value < 0·001). E-DII scores positively correlated with interferon- γ ( r s = 0·194, P value = 0·001) and IL-4 ( r s = 0·135, P value = 0·021). After multivariable adjustment, E-DII scores were positively related to preeclampsia risk ( P trend < 0·001). The highest tertile of E-DII was 2·18 times the lowest tertiles (95 % CI = 1·52, 3·13). The odds of preeclampsia increased by 30 % (95 % CI = 18 %, 43 %, P value < 0·001) for each E-DII score increase. The preeclampsia risk was positively associated with IL-2 (OR = 1·07, 95 % CI = 1·03, 1·11), IL-4 (OR = 1·26, 95 % CI = 1·03, 1·54) and transforming growth factor beta (TGF- β ) (OR = 1·17, 95 % CI = 1·06, 1·29). Therefore, proinflammatory diets, corresponding to higher IL-2, IL-4 and TGF- β levels, were associated with increased preeclampsia risk.

The aim of the study was to assess the inflammatory potential of the Brazilian population's diet and its association with demographic, socio-economic and anthropometric characteristics. A cross-sectional study was performed with 34 003 individuals aged 10 years and older, evaluated by the National Diet and Nutrition Survey from the Consumer Expenditure Survey (POF 2008-2009). The Energy-adjusted Dietary Inflammatory Index (E-DII™) was determined using thirty-four dietary parameters calculated through non-consecutive 2-d dietary records. Positive scores indicate a pro-inflammatory diet, while negative scores indicate an anti-inflammatory diet. A bivariate and multivariate linear regression analysis based on a hierarchical theoretical model was performed to verify the factors associated with the E-DII. The mean of the E-DII was 1·04 (range of -4·77 to +5·98). The highest values of the pro-inflammatory E-DII were found among adolescents (1·42; P < 0·001) and individuals with higher income (1·10; P < 0·001) and level of education (1·18; P < 0·001). In the final model, the E-DII was associated with higher income quartiles and was higher in the Northeast and South regions, in white people, individuals with ≥9 years of education and adults and adolescents age group. The Brazilian population consumes a diet with high inflammatory potential, especially adolescents, white people and those with higher income and level of education. Thus, the index presented uneven distribution among the population, emphasising groups with higher dietary inflammatory potential. The socio-economic risk profile of a diet with higher inflammatory potential in medium-income countries is different from what is observed in high-income nations.

Diet has direct and indirect effects on health through inflammation and the gut microbiome. We investigated total dietary inflammatory potential via the literature-derived index (Dietary Inflammatory Index (DII®)) with gut microbiota diversity, composition and function. In cancer-free patient volunteers initially approached at colonoscopy and healthy volunteers recruited from the medical centre community, we assessed 16S ribosomal DNA in all subjects who provided dietary assessments and stool samples (n 101) and the gut metagenome in a subset of patients with residual fasting blood samples (n 34). Associations of energy-adjusted DII scores with microbial diversity and composition were examined using linear regression, permutational multivariate ANOVA and linear discriminant analysis. Spearman correlation was used to evaluate associations of species and pathways with DII and circulating inflammatory markers. Across DII levels, α- and β-diversity did not significantly differ; however, Ruminococcus torques, Eubacterium nodatum, Acidaminococcus intestini and Clostridium leptum were more abundant in the most pro-inflammatory diet group, while Akkermansia muciniphila was enriched in the most anti-inflammatory diet group. With adjustment for age and BMI, R. torques, E. nodatum and A. intestini remained significantly associated with a more pro-inflammatory diet. In the metagenomic and fasting blood subset, A. intestini was correlated with circulating plasminogen activator inhibitor-1, a pro-inflammatory marker (rho = 0·40), but no associations remained significant upon correction for multiple testing. An index reflecting overall inflammatory potential of the diet was associated with specific microbes, but not overall diversity of the gut microbiome in our study. Findings from this preliminary study warrant further research in larger samples and prospective cohorts.

This study aimed to assess the relationship between the Dietary Inflammatory Index (DII®), a validated tool for evaluating diet-associated inflammation, and anthropometric indices in children and adolescents. This multicentre survey was conducted on 5427 school students selected via multistage cluster sampling from thirty provinces of Iran. This survey was conducted under the framework of the weight disorders survey, which is part of a national surveillance programme entitled Childhood and Adolescence Surveillance and Prevention of Adult Non-communicable Diseases-IV. For calculating the DII scores, twenty-five dietary factors were obtained from a validated 168-item FFQ. Height, weight, wrist circumference, neck circumference (NC), waist circumference (WC) and hip circumference (HC) were measured. BMI z-score, waist circumference:hip circumference ratio (WHR), waist circumference:height ratio (WHtR) and parental BMI were computed. Linear regression models were used to evaluate the association of DII and anthropometric indices. Significant trends were observed across quartiles of DII score for all anthropometric indices in all participants (P &lt;0·05), except for WHR and WHtR. After adjustment for potential confounders, the multiple linear regression analysis for each anthropometric index revealed that participants in the highest DII quartile had higher BMI z-score, WC, HC and parental BMI compared with those in the first (or lowest) quartile. In summary, we found that a pro-inflammatory diet was associated with higher BMI z-score, wrist circumference, NC, WC, HC and parental BMI. The large sample size of the present study may influence the statistical significance of observed associations. Hence, the findings should be clinically interpreted with caution.

Chronic kidney disease (CKD) is described as a progressive alteration of kidney function, resulting from multiple factors, including behaviours. We investigated the association of the Dietary Inflammatory Index (DII®) with prevalent CKD in adult Americans. National Health and Nutrition Examination Survey participants with measured data on kidney function markers from 2005 to 2012 were included in this study. Prevalent CKD was based on an estimated glomerular filtration rate (eGFR) <60 ml/min per 1·73 m2 or urinary albumin/creatinine≥30 mg/g. Energy-adjusted DII (E-DIITM) scores were calculated from 24-h dietary recalls. Statistical analyses accounted for the survey design and sample weights. We included 21 649 participants, with 1634 (6·8 %) having prevalent CKD. Participants with high E-DII scores had greater BMI, fasting blood glucose and systolic blood pressure, and were more likely to be diabetic or hypertensive (all P<0·001) compared with those with lower E-DII scores. In regression models adjusted for age, sex, race, fasting blood glucose, blood pressure, BMI, hypertension and diabetes status, mean eGFR significantly decreased across increasing quartiles of E-DII, whereas serum uric acid level and log urinary albumin:creatinine ratio significantly increased (all P<0·001). Prevalent CKD increased from 5·3 % in the lowest to 9·3 % in the highest E-DII quartile (P=0·02). In multivariable-adjusted logistic regression models, the odds of prevalent CKD were 29 % higher in the highest compared with the lowest E-DII quartile. Pro-inflammatory diet is associated with declining kidney function and high prevalence of CKD. Dietary changes that reduce inflammation have a potential to prevent CKD.

Diet has been shown to have an effect on both inflammation and oesophageal cancer. This study investigated the association between the dietary inflammatory index (DII®) and the risk of oesophageal cancer in Xinjiang Uyghur Autonomous Region, China. A case-control study was conducted during 2008-2009 in Urumqi and Shihezi. DII scores were calculated based on dietary intake assessed by a validated FFQ administered to 359 incident oesophageal cancer patients and 380 hospital-based controls. Higher DII scores indicate more pro-inflammatory diets. Logistic regression analyses were performed to assess the association between DII scores and oesophageal cancer risk. Oesophageal cancer patients had a significantly higher median DII score (-0·35; interquartile range (IQR)=-2·25, 1·86) than that of controls (-1·41; IQR -3·07, 0·40). Multivariable logistic analysis revealed a positive association between higher DII scores and oesophageal cancer risk (ORQuartile 4 v. 1 2·55; 95 % CI 1·61, 4·06; P trend<0·001). A pro-inflammatory diet appears to be associated with an increased risk of oesophageal cancer in Xinjiang Uyghur Autonomous Region. Specific carcinogenic mechanisms are discussed. Accumulating evidence, to which the study contributes, indicates that encouraging the intake of more anti-inflammatory foods may be a strategy to protect against oesophageal cancer in this high-risk area of China.

The objective of this study was to examine the association between dietary inflammatory potential and memory and cognitive functioning among a representative sample of the US older adult population. Cross-sectional data from the 2011-2012 and 2013-2014 National Health and Nutrition Examination Survey were utilised to identify an aggregate sample of adults 60-85 years of age (n 1723). Dietary inflammatory index (DII®) scores were calculated using 24-h dietary recall interviews. Three memory-related assessments were employed, including the Consortium to Establish a Registry for Alzheimer's disease (CERAD) Word Learning subset, the Animal Fluency test and the Digit Symbol Substitution Test (DSST). Inverse associations were observed between DII scores and the different memory parameters. Episodic memory (CERAD) (b adjusted=-0·39; 95 % CI -0·79, 0·00), semantic-based memory (Animal Fluency Test) (b adjusted=-1·18; 95 % CI -2·17, -0·20) and executive function and working-memory (DSST) (b adjusted=-2·80; 95 % CI -5·58, -0·02) performances were lowest among those with the highest mean DII score. Though inverse relationships were observed between DII scores and memory and cognitive functioning, future work is needed to further explore the neurobiological mechanisms underlying the complex relationship between inflammation-related dietary behaviour and memory and cognition.

We aimed to examine the association between the Alternative Healthy Eating Index updated in 2010 (AHEI-2010), the Dietary Inflammatory Index (DIITM) and risk of mortality in the Whitehall II study. We also conducted a meta-analysis on the DII-based results from previous studies to summarise the overall evidence. Data on dietary behaviour assessed by self-administered repeated FFQ and on mortality status were available for 7627 participants from the Whitehall II cohort. Cox proportional hazards regression models were performed to assess the association between cumulative average of AHEI-2010 and DII scores and mortality risk. During 22 years of follow-up, 1001 participants died (450 from cancer, 264 from CVD). Both AHEI-2010 (mean=48·7 (sd 10·0)) and DII (mean=0·37 (sd 1·41)) were associated with all-cause mortality. The fully adjusted hazard ratio (HR) per sd, were 0·82; 95 % CI 0·76, 0·88 for AHEI-2010 and 1·18; 95 % CI 1·08, 1·29 for DII. Significant associations were also observed with cardiovascular and cancer mortality risk. For DII, a meta-analysis (using fixed effects) from this and four previous studies showed a positive association of DII score with all-cause (HR=1·04; 95 % CI 1·03, 1·05, 28 891deaths), cardiovascular (HR=1·05; 95 % CI 1·03, 1·07, 10 424 deaths) and cancer mortality (HR=1·05; 95 % CI 1·03, 1·07, n 8269).The present study confirms the validity to assess overall diet through AHEI-2010 and DII in the Whitehall II cohort and highlights the importance of considering diet indices related to inflammation when evaluating all-cause, cardiovascular and cancer mortality risk.

Arterial wall thickening, stimulated by low-grade systemic inflammation, underlies many cardiovascular events. As diet is a significant moderator of systemic inflammation, the dietary inflammatory index (DIITM) has recently been devised to assess the overall inflammatory potential of an individual's diet. The primary objective of this study was to assess the association of the DII with common carotid artery-intima-media thickness (CCA-IMT) and carotid plaques. To substantiate the clinical importance of these findings we assessed the relationship of DII score with atherosclerotic vascular disease (ASVD)-related mortality, ischaemic cerebrovascular disease (CVA)-related mortality and ischaemic heart disease (IHD)-related mortality more. The study was conducted in Western Australian women aged over 70 years (n 1304). Dietary data derived from a validated FFQ (completed at baseline) were used to calculate a DII score for each individual. In multivariable-adjusted models, DII scores were associated with sub-clinical atherosclerosis: a 1 sd (2·13 units) higher DII score was associated with a 0·013-mm higher mean CCA-IMT (P=0·016) and a 0·016-mm higher maximum CCA-IMT (P=0·008), measured at 36 months. No relationship was seen between DII score and carotid plaque severity. There were 269 deaths during follow-up. High DII scores were positively associated with ASVD-related death (per sd, hazard ratio (HR): 1·36; 95 % CI 1·15, 1·60), CVA-related death (per sd, HR: 1·30; 95 % CI 1·00, 1·69) and IHD-related death (per sd, HR: 1·40; 95 % CI 1·13, 1·75). These results support the hypothesis that a pro-inflammatory diet increases systemic inflammation leading to development and progression of atherosclerosis and eventual ASVD-related death.

The dietary inflammatory indexTM (DII) has been shown to correlate with concentrations of several inflammatory markers and a variety of chronic disease endpoints, including cancers of various anatomic sites. We investigated whether the DII was associated with the risk for death among women with breast cancer (BrCa). This retrospective cohort study included 1453 women with BrCa, diagnosed between 1990 and 1994, and previously enrolled in a case-control study in northern Italy. With a median follow-up of 12·6 years, we observed 503 deaths, among which 398 were due to BrCa. The usual diet was assessed at BrCa diagnosis using a validated FFQ. DII scores were calculated using thirty-one foods/nutrients. Hazard ratios (HR) of death from all causes or from BrCa, with corresponding 95 % CI, were calculated using the Cox models, adjusted for age at diagnosis, tumour stage, oestrogen/progesterone receptor status and other potential confounders. The median DII score of the study women was -1·23, with a relatively narrow range (interquartile range -2·24 to -0·11), indicating a mainly anti-inflammatory diet. There was no difference in survival according to DII tertiles, neither considering all-cause mortality (HRtertile III v. I 1·00; 95 % CI 0·78, 1·28) nor BrCa-specific mortality (HRtertile III v. I 0·97; 95 % CI 0·73, 1·27). Study findings did not suggest an association between the inflammatory potential of diet, measured by the DII, and the survival of BrCa women. However, further studies are needed in populations reporting higher DII scores and a broader range of variability in the scores.

Previous studies have investigated the association between dietary inflammatory potential and the development of cancer. For breast cancer the results have been equivocal. The present study aimed to investigate whether higher Dietary Inflammatory IndexTM (DII) scores were associated with increased risk of breast cancer among Chinese women. A total of 867 cases and 824 controls were recruited into the present case-control study from September 2011 to February 2016. DII scores were computed based on baseline dietary intake assessed by a validated 81-item FFQ. The OR and 95 % CI were assessed by multivariable logistic regression after adjusting for various potential confounders. DII scores in this study ranged from -5·87 (most anti-inflammatory score) to +5·71 (most proinflammatory score). A higher DII score was associated with a higher breast cancer risk (adjusted ORquartile 4 v. 1 2·28; 95 % CI 1·71, 3·03; adjusted ORcontinuous 1·40; 95 %CI 1·25, 1·39). In stratified analyses, positive associations also were observed except for underweight women or women with either oestrogen receptor+ or progesterone receptor+ status (but not both). Results from this study indicated that higher DII scores, corresponding to more proinflammatory diets, were positively associated with breast cancer risk among Chinese women.

The dietary inflammatory index (DIITM) is a novel composite score based on a range of nutrients and foods known to be associated with inflammation. DII scores have been linked to the risk of a number of cancers, including oesophageal squamous cell cancer and oesophageal adenocarcinoma (OAC). Given that OAC stems from acid reflux and that the oesophageal epithelium undergoes a metaplasia-dysplasia transition from the resulting inflammation, it is plausible that a high DII score (indicating a pro-inflammatory diet) may exacerbate risk of OAC and its precursor conditions. The aim of this analytical study was to explore the association between energy-adjusted dietary inflammatory index (E-DIITM) in relation to risk of reflux oesophagitis, Barrett's oesophagus and OAC. Between 2002 and 2005, reflux oesophagitis (n 219), Barrett's oesophagus (n 220) and OAC (n 224) patients, and population-based controls (n 256), were recruited to the Factors influencing the Barrett's Adenocarcinoma Relationship study in Northern Ireland and the Republic of Ireland. E-DII scores were derived from a 101-item FFQ. Unconditional logistic regression analysis was applied to determine odds of oesophageal lesions according to E-DII intakes, adjusting for potential confounders. High E-DII scores were associated with borderline increase in odds of reflux oesophagitis (OR 1·87; 95 % CI 0·93, 3·73), and significantly increased odds of Barrett's oesophagus (OR 2·05; 95 % CI 1·22, 3·47), and OAC (OR 2·29; 95 % CI 1·32, 3·96), when comparing the highest with the lowest tertiles of E-DII scores. In conclusion, a pro-inflammatory diet may exacerbate the risk of the inflammation-metaplasia-adenocarcinoma pathway in oesophageal carcinogenesis.

Chronic low-grade inflammation has been recognised as a key underlying mechanism for several chronic diseases, including cancer and CVD. Nutrition represents a host of key modifiable factors that influence chronic inflammation. Dietary inflammatory scores were developed to assess the inflammatory potential of the diet and have been associated with inflammatory biomarkers in cross-sectional and short-term longitudinal studies. The objective of this study was to investigate the relationship between the dietary inflammatory index (DII), the alternate dietary inflammatory index (ADII) and long-term C-reactive protein (CRP). We also tested age as an effect modifier of this relationship. Participants were selected in the Supplémentation en Vitamines et Minéraux Antioxydants study, which included subjects aged 45-60 years old for men and 35-60 years old for women in 1994. Participants with ≥3 24-h dietary records at baseline and a CRP measurement at the 12-year follow-up evaluation were included in the present study (n 1980). The relationships between the DII and ADII and elevated CRP (>3 mg/l) were investigated using logistic multivariable regression. All analyses were stratified by age (cut-off at median age=50 years old). The overall associations between DII and ADII and long-term CRP were not statistically significant (P trend across tertiles=0·16 for DII and 0·10 for ADII). A quantitative interaction was found between ADII score and age (P=0·16 for ADII, 0·36 for DII). In stratified analyses the ADII was significantly prospectively associated with CRP only in younger participants: OR tertile 3 v. tertile 1: 1·79 (95 % CI 1·04, 3·07). Pro-inflammatory diets may have long-term effect on CRP only in younger subjects.

Recent evidence suggests that a pro-inflammatory diet could be associated with prostate cancer (PC) risk. To evaluate the association between dietary inflammatory index (DII) and PC risk as well as aggressiveness, we conducted a case-control study in Mexico City. Cases were 394 individuals with incident, histologically confirmed PC, who were matched by age (±5 years) with 794 population controls. Dietary information was obtained through a semi-quantitative FFQ with a 3-year frame of reference before diagnosis, for cases, or interview, for controls. On the basis of twenty-eight food parameters, we estimated the energy-adjusted DII (E-DII). According to the Gleason score at diagnosis, PC cases were categorised as high (≥8), moderate (=7) and low (≤6) PC risk. Independent, unconditional logistic regression models adjusted for potential confounders were used to estimate PC risk and PC aggressiveness. There were no significant associations between overall PC risk and E-DII (OR3rd v. 1st tertile 1·18; 95 % CI 0·85, 1·63; P=0·33) or among men with high-risk PC (Gleason≥8) (OR 1·46; 95 % CI 0·88, 2·42; P=0·14). These results do not support the hypothesis that a pro-inflammatory diet is related to PC risk and PC aggressiveness. However, further studies with larger sample sizes, with sufficient statistical power and of varying designs should be conducted to address this hypothesis.

Dietary factors and inflammation markers have been shown to play a role in the development of depression. However, there are very few studies that have explored the association between inflammatory potential of diet and risk of depression. In this study, we examined the association between the dietary inflammatory index (DII), which was developed specifically to measure the inflammatory potential of diet, and risk of depression in the middle-aged cohort of the Australian Longitudinal Study on Women's Health. A total of 6438 women with a mean age of 52·0 (sd 1·4) years at baseline were followed-up at five surveys over 12 years (2001-2013). Depression was defined as a score of ≥10 on the Center for Epidemiologic Studies Depression-10 scale. The DII score, a literature-derived, population-based dietary index that has been validated against several inflammatory markers, was computed on the basis of dietary intake assessed using a validated FFQ. Generalised estimating equations were used to estimate relative risk (RR) of depression according to DII score. Models were adjusted for energy intake, highest education completed, marital status, menopause status and symptoms, personal illness or injury, smoking status, physical activity, BMI and depression diagnosis or treatment. In total, 1156 women (18 %) had scores≥10 on the CESD scale over the course of 9 years. Women with the most anti-inflammatory diet had an approximately 20 % lower risk of developing depression compared with women with the most pro-inflammatory diet (RRDII quartile 1 v. 4: 0·81; 95 % CI 0·69, 0·96; P trend=0·03). These results suggest that an anti-inflammatory diet is associated with lower risk of depression in middle-aged Australian women.

Inflammation and diet have been suggested to be important risk factors for hepatocellular cancer (HCC). This Italian multicentre hospital-based case-control study conducted between 1999 and 2002 and including 185 cases with incident, histologically confirmed HCC, and 404 controls hospitalised for acute non-neoplastic diseases provided an opportunity to investigate the association between HCC and the dietary inflammatory index (DII). The DII was computed on the basis of dietary intake assessed 2 years before the date of interview by a validated sixty-three-item FFQ. Logistic regression models were used to estimate OR adjusted for age, sex, study centre, education, BMI, smoking, physical activity, serum markers of hepatitis B and C infection and energy intake. Energy adjustment for DII was performed using the residual method. Participants in the highest tertile of DII scores (i.e. with a more pro-inflammatory diet) had a higher risk for HCC (ORtertile 3 v, 1 2·43; 95 % CI 1·27, 4·68; P trend=0·03). When stratified by the presence or absence of hepatitis B/C infection and sex, DII was strongly associated with HCC in hepatitis B- and C-negative participants (ORtertile 3 v. 1 4·18; 95 % CI 1·53, 11·39; P trend=0·02) and among males (ORtertile 3 v. 1 3·60; 95 % CI 1·65, 7·87; P trend=0·001). These results indicate that a pro-inflammatory diet is associated with increased risk for HCC, in those without a history of hepatitis B/C infection and among males.

The relation between inflammation deriving from diet and endometrial cancer risk has not yet been investigated. In this study, we explored the association between the dietary inflammatory index (DII) and endometrial cancer risk in an Italian case-control study. Cases comprised 454 patients with incident, histologically confirmed carcinoma of the endometrium, and controls comprised 908 subjects admitted to the same network of hospitals as cases for a wide spectrum of acute, non-neoplastic conditions. DII scores were computed on the basis of dietary intake assessed using a reproducible and valid seventy-eight-item FFQ. OR were calculated through logistic regression models conditioned on age and study centre and adjusted for recognised confounding factors, including total energy intake. Women with the most pro-inflammatory diet had a higher risk for endometrial cancer compared with women with the most anti-inflammatory diet (OR(Quartile) 4 v. 1 1·46; 95% CI 1·02, 2·11; P(trend)=0·04). A pro-inflammatory diet may increase the risk for endometrial cancer.

Convincing evidence has identified inflammation as an initiator of atherosclerosis, underpinning CVD. We investigated (i) whether dietary inflammation, as measured by the 'dietary inflammatory index (DII)', was predictive of 5-year CVD in men and (ii) its predictive ability compared with that of SFA intake alone. The sample consisted of 1363 men enrolled in the Geelong Osteoporosis Study who completed an FFQ at baseline (2001-2006) (excluding participants who were identified as having previous CVD). DII scores were computed from participants' reported intakes of carbohydrate, micronutrients and glycaemic load. DII scores were dichotomised into a pro-inflammatory diet (positive values) or an anti-inflammatory diet (negative values). The primary outcome was a formal diagnosis of CVD resulting in hospitalisation over the 5-year study period. In total, seventy-six events were observed during the 5-year follow-up period. Men with a pro-inflammatory diet at baseline were twice as likely to experience a CVD event over the study period (OR 2·07; 95 % CI 1·20, 3·55). This association held following adjustment for traditional CVD risk factors and total energy intake (adjusted OR 2·00; 95 % CI 1·03, 3·96). This effect appeared to be stronger with the inclusion of an age-by-DII score interaction. In contrast, SFA intake alone did not predict 5-year CVD events after adjustment for covariates (adjusted OR 1·40; 95 % CI 0·73, 2·70). We conclude that an association exists between a pro-inflammatory diet and CVD in Australian men. CVD clinical guidelines and public health recommendations may have to expand to include dietary patterns in the context of vascular inflammation.

Only one prospective study has analysed the relationship between the inflammatory properties of diet and risk of depression thus far. The aim of this study was to assess the association between the dietary inflammatory index (DII) and the incidence of depression. In a cohort study of 15 093 university graduates, participants completed a validated FFQ at baseline and after 10 years of follow-up. The DII was calculated based on the FFQ. Each of the twenty-eight nutrients or foods received a score based on findings from the peer-reviewed literature reporting on the relationships between diet and inflammatory biomarkers (IL-1β, IL-4, IL-6, IL-10, TNF-α and C-reactive protein). Participants were classified as having depression if they reported a new clinical diagnosis of depression by a physician, antidepressant drugs, or both. Multivariable Cox regression models were used to estimate hazard ratios (HR) of depression according to quintiles of the DII. After a median 8·5 years of follow-up, we observed 1051 incident cases of depression. The HR for participants in the highest quintile of DII (strongly pro-inflammatory) was 1·47 (95% CI 1·17, 1·85) compared with those in the bottom quintile, with a significant dose-response relationship (P trend=0·01). In the subgroup analyses, the association between DII and depression was stronger among participants >55 years and among those with cardiometabolic comorbidities (HR 2·70; 95% CI 1·22, 5·97 and HR 1·80; 95% CI 1·27, 2·57, respectively). A pro-inflammatory diet was associated with a significantly higher risk of depression in a Mediterranean population. This association was stronger among older subjects and subjects with cardiometabolic diseases.

Diet and inflammation have been suggested to be important risk factors for colorectal cancer (CRC). In the present study, we examined the association between the dietary inflammatory index (DII) and the risk of CRC in a multi-centre case-control study conducted between 1992 and 1996 in Italy. The study included 1225 incident colon cancer cases, 728 incident rectal cancer cases and 4154 controls hospitalised for acute non-neoplastic diseases. The DII was computed based on dietary intake assessed using a validated seventy-eight-item FFQ that included assessment of alcohol intake. Logistic regression models were used to estimate the OR adjusted for age, sex, study centre, education, BMI, alcohol drinking, physical activity and family history of CRC. Energy intake was adjusted using the residual method. Subjects with higher DII scores (i.e. with a more pro-inflammatory diet) had a higher risk of CRC, with the DII being used both as a continuous variable (OR(continuous) 1.13, 95 % CI 1.09, 1.18) and as a categorical variable (OR(quintile 5 v. 1) 1.55, 95 % CI 1.29, 1.85; P for trend < 0.0001). Similar results were observed when the analyses were carried out separately for colon and rectal cancer cases. These results indicate that a pro-inflammatory diet is associated with an increased risk of CRC.

Diet is a strong moderator of systemic inflammation, an established risk factor for colorectal cancer (CRC). The dietary inflammatory index (DII) measures the inflammatory potential of individuals' diets. The association between the DII and incident CRC was examined, using the National Institutes of Health-American Associations of Retired Persons Diet and Health Study individuals (n 489,422) aged 50-74 years at recruitment, starting between 1995-6, and followed for a mean of 9·1 (sd 2·9) years. Baseline data from a FFQ were used to calculate the DII; higher scores are more pro-inflammatory, and lower scores are more anti-inflammatory. First, primary CRC diagnoses were identified through linkage to state cancer registries. Anatomic location and disease severity also were examined. Cox proportional hazards models estimated CRC hazard ratios (HR) and 95% CI using quartile 1 as the referent. DII quartile 4 compared to quartile 1 was associated with CRC risk among all subjects (HR 1·40, 95% CI 1·28, 1·53; P for trend < 0·01). Statistically significant associations also were observed for each anatomic site examined, for moderate and poorly differentiated tumours, and at each cancer stage among all subjects. Effects were similar when stratified by sex; however, results were statistically significant only in males. The only result reaching statistical significance in females was risk of moderately differentiated CRC tumours (DII quartile 4 v. quartile 1 HR 1·26, 95% CI 1·03, 1·56). Overall, the DII was associated with CRC risk among all subjects. The DII may serve as a novel way to evaluate dietary risk for chronic disorders associated with inflammation, such as CRC.

Previous research has shown that nutrients and certain food items influence inflammation. However, little is known about the associations between diet, as a whole, and inflammatory markers. In the present study, we examined the ability of a FFQ-derived dietary inflammatory index (DII) to predict inflammation. Data from a Belgian cross-sectional study of 2524 generally healthy subjects (age 35-55 years) were used. The DII is a population-based, literature-derived dietary index that was developed to predict inflammation and inflammation-related chronic diseases. The DII was calculated from FFQ-derived dietary information and tested against inflammatory markers, namely C-reactive protein (CRP), IL-6, homocysteine and fibrinogen. Analyses were performed using multivariable logistic regression, adjusting for energy, age, sex, BMI, smoking status, education level, use of non-steroidal anti-inflammatory drugs, blood pressure, use of oral contraceptives, anti-hypertensive therapy, lipid-lowering drugs and physical activity. Multivariable analyses showed significant positive associations between the DII and the inflammatory markers IL-6 (>1·6 pg/ml) (OR 1·19, 95 % CI 1·04, 1·36) and homocysteine (>15 μmol/l) (OR 1·56, 95 % CI 1·25, 1·94). No significant associations were observed between the DII and the inflammatory markers CRP and fibrinogen. These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation.

The scientific community has become increasingly interested in the overall quality of diets rather than in single food-based or single nutrient-based approaches to examine diet-disease relationships. Despite the plethora of indices used to measure diet quality, there still exist questions as to which of these can best predict health outcomes. The present study aimed to compare the ability of five diet quality indices, namely the Recommendation Compliance Index (RCI), Diet Quality Index-International (DQI-I), Dietary Approaches to Stop Hypertension (DASH), Mediterranean Diet Score (MDS), and Dietary Inflammatory Index (DII), to detect changes in chronic disease risk biomarkers. Nutritional data from 1352 participants, aged 18-69 years, of the Luxembourg nationwide cross-sectional ORISCAV-LUX (Observation of Cardiovascular Risk Factors in Luxembourg) study, 2007-8, were used to calculate adherence to the diet quality index. General linear modelling was performed to assess trends in biomarkers according to adherence to different dietary patterns, after adjustment for age, sex, education level, smoking status, physical activity and energy intake. Among the five selected diet quality indices, the MDS exhibited the best ability to detect changes in numerous risk markers and was significantly associated with lower levels of LDL-cholesterol, apo B, diastolic blood pressure, renal function indicators (creatinine and uric acid) and liver enzymes (serum γ-glutamyl-transpeptidase and glutamate-pyruvate transaminase). Compared with other dietary patterns, higher adherence to the Mediterranean diet is associated with a favourable cardiometabolic, hepatic and renal risk profile. Diets congruent with current universally accepted guidelines may be insufficient to prevent chronic diseases. Clinicians and public health decision makers should be aware of needs to improve the current dietary guidelines.

Previous studies have shown that various dietary components may be implicated in the aetiology of prostate cancer, although the results remain equivocal. The possible relationship of inflammation derived from dietary exposures with prostate cancer risk has not been investigated. We examined the ability of a newly developed dietary inflammatory index (DII) to predict prostate cancer risk in a case-control study conducted in Italy between 1991 and 2002. A total of 1294 patients aged < 75 years with incident, histologically confirmed carcinoma of the prostate served as cases. A total of 1451 subjects aged < 75 years who were admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions served as controls. The DII was computed based on dietary intake assessed using a previously validated seventy-eight-item FFQ. Logistic regression models were used to estimate multivariable OR adjusted for age, study centre, years of education, social class, BMI, smoking status, family history of prostate cancer and total energy intake. Men with higher DII scores had a higher risk of prostate cancer when analysed using the DII as both continuous (OR 1.06, 95% CI 1.00, 1.13) and categorical, i.e., compared with men in the lowest quartile of the DII, men in the third and fourth quartiles were at elevated risk (OR(Quartile 3 v. 1) 1.32, 95% CI 1.03, 1.69 and OR(Quartile 4 v. 1) 1.33, 95% CI 1.01, 1.76; P trend= 0.04). These data suggest that a pro-inflammatory diet, as indicated by the increasing DII score, is a risk factor of prostate cancer in Italian men.

Previous studies have shown that various dietary components may be implicated in the aetiology of pancreatic cancer. However, the possible relationship between diet-related inflammation and the risk of pancreatic cancer has not yet been investigated. We examined the ability of a newly developed literature-derived dietary inflammatory index (DII) to predict the risk of pancreatic cancer in a case-control study conducted in Italy between 1991 and 2008. This included 326 incident cases and 652 controls admitted to the major teaching and general hospitals for non-neoplastic diseases, frequency-matched to cases by study centre, sex and age. The DII was computed based on dietary intake assessed using a validated and reproducible seventy-eight-item FFQ. Logistic regression models were used to estimate multivariable OR adjusted for age, sex, study centre, education, BMI, smoking status, alcohol drinking and history of diabetes. Energy adjustment was performed using the residual method. Subjects with higher DII scores (i.e., representing a more pro-inflammatory diet) had a higher risk of pancreatic cancer, with the DII being used as both a continuous variable (ORcontinuous 1.24, 95% CI 1.11, 1.38) and a categorical variable (i.e., compared with the subjects in the lowest quintile of the DII, those in the second, third, fourth and fifth quintiles had, respectively, OR(quintile2 v. 1) 1.70, 95% CI 1.02, 2.80; OR(quintile3 v. 1) 1.91, 95% CI 1.16, 3.16; OR(quintile4 v. 1) 1.98, 95% CI 1.20, 3.27; OR(quintile5 v. 1) 2.48, 95% CI 1.50, 4.10; P trend= 0.0015). These data suggest that a pro-inflammatory diet increases the risk of pancreatic cancer.