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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 (rs = 0·194, P value = 0·001) and IL-4 (rs = 0·135, P value = 0·021). After multivariable adjustment, E-DII scores were positively related to preeclampsia risk (Ptrend < 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.
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.
Dietary factors play a role in modulating chronic inflammation and in the development of CVD. We aimed to investigate the association between the dietary inflammatory index (DII) and cardiometabolic risk factors among adolescents. A total of 31 684 Brazilian adolescents (aged 12–17 years) from the Study of Cardiovascular Risks in Adolescents (ERICA) were included. Dietary intake was assessed using a 24-h dietary recall. The energy-adjusted dietary inflammatory index (E-DII) score was calculated based on data for twenty-five available nutrients. The anthropometric profile, blood pressure, lipid profile, glucose, Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and glycated Hb were measured. Poisson regression models were used to examine the associations between sex-specific quartiles of the E-DII and cardiometabolic risk factors. In the energy-adjusted models, when comparing a high pro-inflammatory diet (quartile 4) with an anti-inflammatory diet (quartile 1), there was a positive association with high HOMA-IR among boys (prevalence ratios (PR)Q4 = 1·37, 95 % CI: 1·04, 1·79); and with high fasting glucose (PRQ4 = 1·96, 95 % CI: 1·02, 3·78), high TAG (PRQ4 = 1·92, 95 % CI: 1·06, 3·46), low HDL-cholesterol (PRQ4 = 1·16, 95 % CI: 1·02, 1·32) and high LDL-cholesterol (PRQ4 = 1·93, 95 % CI: 1·12, 3·33) among girls. Additionally, a moderately pro-inflammatory diet was positively associated with high HOMA-IR (PRQ2 = 1·14, 95 % CI: 1·02, 1·29) among girls and high total cholesterol (PRQ3 = 1·56, 95 % CI: 1·20, 2·01) among boys. In conclusion, this study provides new evidence on the association between inflammatory diets with cardiometabolic risk factors among adolescents.
This study aimed to investigate the relationships between diet quality, the relative abundance of butyrate-producing bacteria of the gut microbiome and muscle mass, strength and function. In this cross-sectional study, n = 490 men (64.4 ± 13.5 years) from the Geelong Osteoporosis Study provided food frequency questionnaire data, from which the Australian Recommended Food Score (ARFS) and Dietary Inflammatory Index (DII) score were calculated. Muscle mass (skeletal muscle index from DXA-derived lean mass), muscle strength (handgrip strength) and muscle function (Timed Up-and-Go test) were measured. Participants provided stool samples for 16S rRNA gene sequencing. There was no evidence of associations between alpha or beta diversity and muscle health measures. A healthier ARFS score was positively associated with the relative abundance of butyrate-producing bacteria (β 0.09, 95%CI 0.03, 0.15) and a higher (pro-inflammatory) DII score was associated with lower relative abundance of butyrate-producing bacteria (β −0.60, 95%CI −1.06, −0.15). The relative abundance of butyrate-producing bacteria was positively associated with healthier muscle mass, strength and function; however, these relationships were attenuated in multivariable models. These findings support the role of diet quality in achieving a healthier gut microbiome, however, further evidence is required for a gut-muscle axis in humans.
To investigate the association between the Children’s Dietary Inflammatory Index (C-DIITM) scores and atherogenic risk in Brazilian schoolchildren.
A cross-sectional representative study. Three 24-h dietary recalls were performed to evaluate food consumption and to calculate C-DII scores. Blood samples were collected for the lipid profile analysis (serum total cholesterol (TC), HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol and triglycerides (TAG)) and to determine atherogenic indexes (Castelli risk indexes I and II, lipoprotein combined index (LCI), and atherogenic index of plasma and atherogenic coefficient (AC)). A semi-structured questionnaire was used to obtain sociodemographic characteristics and screen time. Body fat was assessed by dual-energy X-ray absorptiometry. We compared the distributions of outcomes by C-DII categories using multivariable linear regression.
Viçosa, Minas Gerais, Brazil.
Three hundred seventy-eight children between the ages of 8 and 9 years.
The mean C-DII score was 0·60 ± 0·94, and the prevalence of dyslipidaemia was 70 %. Children with hypercholesterolaemia and hypertriglyceridaemia had higher C-DII scores. The C-DII was directly associated with atherogenic risk. Every 1 sd of C-DII was associated with a 0·07 (0·01, 0·13), 1·94 (0·20, 3·67), 0·06 (0·002, 0·12) and 0·12 (0·02, 0·22) units higher TC:HDL cholesterol ratio, LCI, AC and accumulation of altered dyslipidaemia markers (high TC + high LDL-cholesterol + high TAG + low HDL-cholesterol), respectively.
Dietary inflammatory potential, as estimated by the C-DII, is directly associated with atherogenic risk in Brazilian schoolchildren. This results reinforce the importance of effective nutritional policies to promote healthy eating habits and improve children’s lipid profiles.
To ascertain which of the Alternative Healthy Eating Index (AHEI) 2010, Dietary Inflammatory Index (DII®) and Mediterranean Diet Score (MDS) best predicted BMI and waist-to-hip circumference ratio (WHR).
Body size was measured at baseline (1990–1994) and in 2003–2007. Diet was assessed at baseline using a FFQ, along with age, sex, socio-economic status, smoking, alcohol drinking, physical activity and country of birth. Regression coefficients and 95 % CI for the association of baseline dietary scores with follow-up BMI and WHR were generated using multivariable linear regression, adjusting for baseline body size, confounders and energy intake.
Population-based cohort in Melbourne, Australia.
Included were data from 11 030 men and 16 774 women aged 40–69 years at baseline.
Median (IQR) follow-up was 11·6 (10·7–12·8) years. BMI and WHR at follow-up were associated with baseline DII® (Q5 v. Q1 (BMI 0·41, 95 % CI 0·21, 0·61) and WHR 0·009, 95 % CI 0·006, 0·013)) and AHEI (Q5 v. Q1 (BMI −0·51, 95 % CI −0·68, −0·35) and WHR −0·011, 95 % CI −0·013, −0·008)). WHR, but not BMI, at follow-up was associated with baseline MDS (Group 3 most Mediterranean v. G1 (BMI −0·05, 95 % CI −0·23, 0·13) and WHR −0·004, 95 % CI −0·007, −0·001)). Based on Akaike’s Information Criterion and Bayesian Information Criterion statistics, AHEI was a stronger predictor of body size than the other diet scores.
Poor quality or pro-inflammatory diets predicted overall and central obesity. The AHEI may provide the best way to assess the obesogenic potential of diet.
Many arthritic patients have the belief that dietary habits can worsen or ameliorate their symptoms. Whether diet quality can modify the risk of rheumatoid arthritis (RA) is an issue of continued scientific debate and interest. Therefore, we aimed to examine the association between both overall diet quality and the overall diet inflammatory potential on the risk of RA.
Overall diet quality and the overall inflammatory potential of the diet were evaluated with the use of Dietary Inflammatory Index (DII) and the Healthy Eating Index (HEI)-2015, respectively. Both DII and HEI-2015 scores were calculated based on a validated semi-quantitative FFQ. Multivariable-adjusted odds of RA were calculated across tertiles of HEI, and energy-adjusted DII (E-DII) scores using binary logistic regression.
Fifty newly diagnosed RA cases and 100 well-matched healthy people controls.
Individuals in the highest tertile of DII scores, indicating the most pro-inflammatory diet, were about three times more likely to have RA than those in the lowest tertile (OR: 2·99; 95 % CI 1·08, 8·24; P-trend: 0·037), whereas individuals in the highest tertile of HEI scores, indicating more top dietary quality, had a significantly lower odds of RA than those in the lowest tertile (OR: 0·33; 95 % CI 0·12, 0·87; P-trend: 0·024).
Our findings show that E-DII and HEI-2015 are positively and negatively associated, respectively, with the odds of RA in a convenience sample of Iranians. These results highlight the importance of overall diet quality in modulating the risk of RA.
To evaluate the association of dietary inflammatory index (DII®) with the occurrence of cardiovascular events, cardiometabolic risk factors and with the consumption of processed, ultra-processed, unprocessed or minimally processed foods and culinary ingredients.
This was a cross-sectional study that analysed the baseline data from 2359 cardiac patients. Data on socio-demographic, anthropometric, clinical and food consumption were collected. Energy-adjusted food intake data were used to calculate DII, and the foods were classified according to the NOVA classification. Furthermore, the patients were grouped according to the number (1, 2 or ≥ 3) of manifested cardiovascular events. The data were analysed using linear and multinomial logistic regression.
Multicentre study from Brazil.
Patients with established cardiovascular events from the Brazilian Cardioprotective Nutritional Program Trial evaluated at baseline.
Most of the patients were male (58·8 %), older adults (64·2 %) and were overweight (68·8 %). Patients in the third tertile of DII (DII > 0·91) had were more likely to have 2 (OR 1·27, 95 % CI: 1·01–1·61) and ≥ 3 (OR 1·39, 95 % CI: 1·07–1·79) cardiovascular events, with poor cardiometabolic profile. They also were more likely to consume a higher percentage of processed, ultra-processed and culinary ingredients foods consumption compared with the patients in the first DII tertile (DII ≤ 0·91).
A more pro-inflammatory diet is associated with a greater chance of having 2 and ≥ 3 cardiovascular events and cardiometabolic risk factors and were more likely to consume processed, ultra-processed and culinary ingredients compared to those with a more anti-inflammatory diet.
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.
Psoriatic Arthritis (PsA) is a chronic inflammatory disease that are associated with multiple comorbidities, particularly metabolic syndrome (MetS), obesity, hypertension and diabetes. These findings brought up a potential link between adiposity and psoriasis/ PsA. Though a healthy diet could improve some aspects related to MetS, as well as painful joints and skin lesions in patients with PsA, the aim of this study is to describe the main particularities related to food intake and nutrient consumption, including the dietary inflammatory index (DII) and the healthy eating index (HEI), in patients with PsA. A total of 97 patients with PsA were included in this cross-sectional study. Food intake was evaluated by using a 3-day food-record, HEI and the DII. Energy was adjusted using the residual method in order to control the effects of energy intake when evaluating micronutrient intake. Weight, waist of circumference, Body Mass Index (BMI) and disease activity (PASI, BSA, BASDAI, DAS28-ESR, DAS28-CRP and MDA) were also evaluated. The inferential analysis included t-student test, Pearson's correlation and Tukey's test. Kolmogorov-Smirnov test was used to define normality. Level of significance was set as p < 0.05. Patients with PsA had hypercaloric diet and inadequate consumption of sodium, vitamin A, vitamin E, magnesium, zinc and copper when compared to Dietary Reference Intake. The HEI had low score (63.2 ± 10.2), suggesting that more than 90% of the patients had inappropriate diet and need nutritional intervention. Moreover, the DII score was high (+ 2.48 ± 0.9), highlighting a pro-inflammatory pattern. It was also observed an increase of BMI (mean 30.5 ± 5.7 kg/m2), waist circumference (103.13 ± 13.26 cm) and a high prevalence of MetS (54.6%). Our data showed patients with PsA had high prevalence of MetS, low quality of food intake, diet inadequacy and a pro-inflammatory pattern, especially regarding antioxidants intake.
The foetal programming hypothesis posits that optimising early life factors e.g. maternal diets can help avert the burden of adverse childhood outcomes e.g. childhood obesity. To improve applicability to public health messaging, we investigated whether maternal whole diet quality and inflammatory potential influence childhood adiposity in a large consortium.
We harmonized and pooled individual participant data from up to 8,769 mother-child pairs in 7 European mother-offspring cohorts. Maternal early-, late-, and whole-pregnancy dietary quality and inflammatory potential were assessed with Dietary Approaches to Stop Hypertension (DASH) and energy-adjusted Dietary Inflammatory Index (E-DII), respectively. Primary outcome was childhood overweight and obesity (OWOB), defined as age- and sex-specific body-mass-index-z score (BMIz) > 85th percentile based on WHO growth standard. Secondary outcomes were sum-of-skinfold-thickness (SST), fat-mass-index (FMI) and fat-free-mass-index (FFMI) in available cohorts. Outcomes were assessed in early- [mean (SD) age: 2.8 (0.3) y], mid- [6.2 (0.6) y], and late-childhood [10.6 (1.2) y]. We used multivariable regression analyses to assess the associations of maternal E-DII and DASH with offspring adiposity outcomes in cohort-specific analyses, with subsequent random-effects meta-analyses. Analyses were adjusted for maternal age, pre-pregnancy BMI, parity, lifestyle factors, energy intake, educational attainment, offspring age and sex.
A more pro-inflammatory maternal diet, indicated by higher E-DII, was associated with a higher risk of offspring late-childhood OWOB [pooled-OR (95% CI) comparing highest vs. lowest E-DII quartiles: 1.22 (1.01,1.47) for whole-pregnancy and 1.38 (1.05,1.83) for early-pregnancy; both P < 0.05]. Moreover, higher late-pregnancy E-DII was associated with higher mid-childhood FMI [pooled-β (95% CI): 0.11 (0.003,0.22) kg/m2; P < 0.05]; trending association was observed for whole-pregnancy E-DII [0.12 (-0.01,0.25) kg/m2; P = 0.07]. A higher maternal dietary quality, indicated by higher DASH score, showed a trending inverse association with late-childhood OWOB (pooled-OR (95% CI) comparing highest vs. lowest DASH quartiles: 0.58 (0.32,1.02; P = 0.06). Higher early-pregnancy DASH was associated with lower late-childhood SST [pooled-β (95% CI): -1.9 (-3.6,-0.1) cm; P < 0.05] and tended to be associated with lower late-childhood FMI [-0.34 (-0.71,0.04) kg/m2; P = 0.08]. Higher whole-pregnancy DASH tended to associate with lower early-childhood SST [-0.33 (-0.72,0.06) cm; P = 0.10]. Results were similar when modelling DASH and E-DII continuously.
Analysis of pooled data suggests that pro-inflammatory, low-quality maternal antenatal diets may influence offspring body composition and obesity risk, especially during mid- or late-childhood. Due to variation of data availability at each timepoint, our results should be interpreted with caution. Because most associations were observed at mid-childhood or later, future studies will benefit from a longer follow-up.
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 <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; Ptrend<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) (badjusted=−0·39; 95 % CI −0·79, 0·00), semantic-based memory (Animal Fluency Test) (badjusted=−1·18; 95 % CI −2·17, −0·20) and executive function and working-memory (DSST) (badjusted=−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.