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BACKGROUND: Previous studies of dietary patterns and pancreatic cancer risk have been inconclusive; we aimed to investigate the association of Mediterranean Diet Score (MDS), Alternative Healthy Eating Index-2010 (AHEI-2010), and Dietary Inflammatory Index (DII®) with risk of pancreatic cancer. METHODS: We used data from the Melbourne Collaborative Cohort Study including 33,690 men and women aged 40-69 years at recruitment in 1990-1994. A total of 258 incident cases of pancreatic cancer was identified over an average of 23.7 years of follow-up. Hazard ratios (HR) were estimated using Cox regression, with age as the underlying time metric, adjusting for potential confounders including sex, height, country of birth, education, socio-economic position, physical activity, energy intake, smoking status, pack-years smoking, years since quitting smoking, and alcohol intake. RESULTS: A healthier diet as assessed by the AHEI-2010 was associated with a lower risk of pancreatic cancer [HRQuartile4 vs Quartile1 = 0.58; 95%CI 0.40 - 0.85; p for trend 0.003]. Weaker but consistent evidence was observed for the other indexes [DII® HRQuartile4 vs Quartile1 = 1.30; 95%CI 0.82 - 2.06; p for trend 0.1], [MDS HRCategory3 vs Category1 = 0.79; 95%CI 0.49 - 1.26; p for trend 0.06]. CONCLUSION: Adherence to a healthier diet, as assessed by the AHEI-2010, may reduce the risk of pancreatic cancer.

Abstract Background Higher levels of time spent sitting (sedentary behavior) contribute to adverse health outcomes, including earlier death. This effect may be modified by other lifestyle factors. We examined the association of television viewing (TV), a common leisure-time sedentary behavior, with all-cause mortality, and whether this is modified by body mass index (BMI), physical activity, smoking, alcohol intake, soft drink consumption, or diet-associated inflammation. Methods Using data from participants in the Melbourne Collaborative Cohort Study, flexible parametric survival models assessed the time-dependent association of self-reported TV time (three categories: < 2 h/day, 2–3 h/day, > 3 h/day) with all-cause mortality. Interaction terms were fitted to test whether there was effect modification of TV time by the other risk factors. Results From 19,570 participants, 4,417 deaths were reported over a median follow up of 14.5 years. More TV time was associated with earlier mortality; however, this relationship diminished with increasing age. The hazard ratio (HR) and 95% confidence interval (95% CI) for > 3 h/day compared with < 2 h/day of TV time was 1.34 (1.16, 1.55) at 70 years, 1.14 (1.04, 1.23) at 80 years, and 0.95 (0.84, 1.06) at 90 years. The TV time/mortality relationship was more evident in participants who were physically inactive (compared with active; p for interaction < 0.01) or had a higher dietary inflammatory index score (compared with a lower score; p for interaction = 0.03). No interactions were detected between TV time and BMI, smoking, alcohol intake, nor soft-drink consumption (all p for interaction&

BACKGROUND: Higher levels of time spent sitting (sedentary behavior) contribute to adverse health outcomes, including earlier death. This effect may be modified by other lifestyle factors. We examined the association of television viewing (TV), a common leisure-time sedentary behavior, with all-cause mortality, and whether this is modified by body mass index (BMI), physical activity, smoking, alcohol intake, soft drink consumption, or diet-associated inflammation. METHODS: Using data from participants in the Melbourne Collaborative Cohort Study, flexible parametric survival models assessed the time-dependent association of self-reported TV time (three categories: < 2 h/day, 2-3 h/day, > 3 h/day) with all-cause mortality. Interaction terms were fitted to test whether there was effect modification of TV time by the other risk factors. RESULTS: From 19,570 participants, 4,417 deaths were reported over a median follow up of 14.5 years. More TV time was associated with earlier mortality; however, this relationship diminished with increasing age. The hazard ratio (HR) and 95% confidence interval (95% CI) for > 3 h/day compared with < 2 h/day of TV time was 1.34 (1.16, 1.55) at 70 years, 1.14 (1.04, 1.23) at 80 years, and 0.95 (0.84, 1.06) at 90 years. The TV time/mortality relationship was more evident in participants who were physically inactive (compared with active; p for interaction < 0.01) or had a higher dietary inflammatory index score (compared with a lower score; p for interaction = 0.03). No interactions were detected between TV time and BMI, smoking, alcohol intake, nor soft-drink consumption (all p for interaction > 0.16). CONCLUSIONS: The relationship between TV time and all-cause mortality may change with age. It may also be more pronounced in those who are otherwise inactive or who have a pro-inflammatory diet.

(1) Background: Developing countries have experienced a rapid recent rise in Inflammatory Bowel Disease (IBD) incidence and emerging evidence suggests processed foods and food additives may predispose one to the development and perpetuation of Crohn's disease (CD). The aim of this study was to evaluate processed food and food additive intake in CD patients and controls, in Australia (high CD incidence), Hong Kong (intermediate incidence) and mainland China (emerging incidence). (2) Methods: In 274 CD patients (CD), 82 first-degree relatives (FDR), 83 household members (HM) and 92 healthy unrelated controls (HC) from Australia (n = 180), Hong Kong (HK) (n = 160) and mainland China (n = 191) we estimated early life (0-18 years), recent (12 months), and current processed and food additive intake, using validated questionnaires and a 3-day-food diary. (3) Results: Early life processed food intake: Combining all regions, CD were more likely to have consumed soft drinks and fast foods than HM, more likely to have consumed processed fruit and snacks than their FDR, and more likely to have consumed a range of processed foods than HC. HK and China CD patients were more likely to have consumed a range of processed foods than HC. Recent food-additive intake (12-months): Combining all regions, CD patients had significantly higher intakes of aspartame and sucralose, and polysorbate-80, than HC, and more total emulsifiers, artificial sweeteners, and titanium dioxide than FDR and HC. HK and China CD patients had a higher intake of almost all food additives than all controls. Current additive intake (3-days): Australian and HK CD patients had higher total food-additive intake than FDR, and HK CD patients had a higher intake of total food-additives and emulsifiers than HM. (4) Conclusions: CD patients have been exposed to more processed food and food additives than control groups, which may predispose them to CD development and ongoing inflammation.

An unhealthy diet is a recognized risk factor in the pathophysiology of numerous chronic noncommunicable diseases (NCD), including obesity, type 2 diabetes (T2DM), and cardiovascular diseases (CVD). This is, at least in part, due to unhealthy diets causing chronic low-grade inflammation in the gut and systemically. To characterize the inflammatory potential of diet, we developed the Dietary Inflammatory Index (DII®). Following this development, around 500 papers have been published, which examined the association between the DII, energy-adjusted DII (E-DII™), and the children's DII (C-DII™) and many chronic NCDs including obesity and cardiometabolic diseases. Although a previous narrative review published in 2019 briefly summarized the evidence in this area, there was a significant increase in papers on this topic since 2020. Therefore, the purpose of this narrative review is to provide an in-depth updated review by including all papers until July 2021 on DII and its relationship with obesity, T2DM, and CVD. Furthermore, we aim to identify potential gaps in the literature and provide future directions for research. Most studies found that DII was associated with an increased risk of obesity, T2DM, and CVD with some relationships being sex-specific. However, we identified the paucity of papers describing associations between dietary inflammation and T2DM and its risk factors. Few studies used gold-standard measures of cardiometabolic risk factors. We also identified the lack of interventional studies designed to change the inflammatory potential of diets and study its effect on cardiometabolic risk factors and diseases. We recommend that such interventional studies are needed to assess if changes in DII, representing the inflammatory potential of diet, independently of changes in body composition can modulate cardiometabolic risk factors and diseases.

Lifestyle and environmental factors are known to contribute to allergic disease development, especially very early in life. However, the link between diet composition and allergic outcomes remains unclear. In the present population-based cohort study we evaluated the dietary intake of 10-year-old children and analyses were performed with particular focus on atopic dermatitis or food allergy, allergic diseases known to be affected by dietary allergens. Dietary intake was assessed via semi-quantitative food frequency questionnaires. Based on these data, individual nutrient intake as well as children’s Dietary Inflammatory Index (C-DII TM) scores were calculated. Information about atopic manifestations during the first 10 years of life and confounding factors were obtained from standardized questionnaires during pregnancy and annually thereafter. Analyses from confounder-adjusted logistic regression models (n=211) revealed that having atopic outcomes was associated with having a pro-inflammatory pattern at the age of 10 years: OR=2.22 (95% CI: 1.14–4.31) for children with atopic dermatitis and OR=3.82 (95% CI: 1.47-9.93) for children with food allergy in the first 10 years of life. A pro-inflammatory dietary pattern might worsen the atopic outcome and reduce the buffering capacity of the individual against harmful environmental exposures or triggers. For paediatricians it is recommended to test for the individual tolerance of allergenic foods and to increase the nutrient density of tolerable food items to avoid undesirable effects of eating a pro-inflammatory diet.

BACKGROUND: Adverse birth outcomes are major causes of morbidity and mortality during childhood and associate with a higher risk of noncommunicable diseases in adult life. Maternal periconception and antenatal nutrition, mostly focusing on single nutrients or foods, has been shown to influence infant birth ou

An unhealthy diet is a recognized risk factor in the pathophysiology of numerous chronic noncommunicable diseases (NCD), including obesity, type 2 diabetes (T2DM), and cardiovascular diseases (CVD). This is, at least in part, due to unhealthy diets causing chronic low-grade inflammation in the gut and systemically. To characterize the inflammatory potential of diet, we developed the Dietary Inflammatory Index (DII). Following this development, around 500 papers have been published, which examined the association between the DII, energy-adjusted DII (E-DIITM), and the children's DII (C-DIITM) and many chronic NCDs including obesity and cardiometabolic diseases. Although a previous narrative review published in 2019 briefly summarized the evidence in this area, there was a significant increase in papers on this topic since 2020. Therefore, the purpose of this narrative review is to provide an in-depth updated review by including all papers until July 2021 on DII and its relationship with obesity, T2DM, and CVD. Furthermore, we aim to identify potential gaps in the literature and provide future directions for research. Most studies found that DII was associated with an increased risk of obesity, T2DM, and CVD with some relationships being sex-specific. However, we identified the paucity of papers describing associations between dietary inflammation and T2DM and its risk factors. Few studies used gold-standard measures of cardiometabolic risk factors. We also identified the lack of interventional studies designed to change the inflammatory potential of diets and study its effect on cardiometabolic risk factors and diseases. We recommend that such interventional studies are needed to assess if changes in DII, representing the inflammatory potential of diet, independently of changes in body composition can modulate cardiometabolic risk factors and diseases.Copyright © 2021 World Obesity Federation

OBJECTIVE: To ascertain which of the Alternative Healthy Eating Index 2010 (AHEI), Dietary Inflammatory Index (DII) and Mediterranean Diet Score (MDS) best predicted body mass index (BMI) and waist-to-hip circumference ratio (WHR). DESIGN: Body size was measured at baseline (1990-94) and in 2003-7. Diet was assessed at baseline using a food frequency questionnaire, along with age, sex, socioeconomic status, smoking, alcohol drinking, physical activity, and country of birth. Regression coefficients and 95% confidence intervals 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. SETTING: Population-based cohort in Melbourne, Australia. PARTICIPANTS: Included were data from 11,030 men and 16,774 women aged 40 to 69 years at baseline. RESULT(S): Median (IQR) follow up was 11.6 (10.7 - 12.8) years. BMI and WHR at follow-up were associated with baseline DII (Q5 vs Q1 (BMI 0.41 95%CI (0.21, 0.61) and WHR 0.009 95%CI (0.006, 0.013)), and AHEI (Q5 vs 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 vs 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. CONCLUSION(S): 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.

BACKGROUND: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. OBJECTIVE(S): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. METHOD(S): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). RESULT(S): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. CONCLUSION(S): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Background: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. Objective(s): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. Method(s): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). Result(s): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. Conclusion(s): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

An unhealthy diet is a recognized risk factor in the pathophysiology of numerous chronic noncommunicable diseases (NCD), including obesity, type 2 diabetes (T2DM), and cardiovascular diseases (CVD). This is, at least in part, due to unhealthy diets causing chronic low-grade inflammation in the gut and systemically. To characterize the inflammatory potential of diet, we developed the Dietary Inflammatory Index (DII). Following this development, around 500 papers have been published, which examined the association between the DII, energy-adjusted DII (E-DIITM), and the children's DII (C-DIITM) and many chronic NCDs including obesity and cardiometabolic diseases. Although a previous narrative review published in 2019 briefly summarized the evidence in this area, there was a significant increase in papers on this topic since 2020. Therefore, the purpose of this narrative review is to provide an in-depth updated review by including all papers until July 2021 on DII and its relationship with obesity, T2DM, and CVD. Furthermore, we aim to identify potential gaps in the literature and provide future directions for research. Most studies found that DII was associated with an increased risk of obesity, T2DM, and CVD with some relationships being sex-specific. However, we identified the paucity of papers describing associations between dietary inflammation and T2DM and its risk factors. Few studies used gold-standard measures of cardiometabolic risk factors. We also identified the lack of interventional studies designed to change the inflammatory potential of diets and study its effect on cardiometabolic risk factors and diseases. We recommend that such interventional studies are needed to assess if changes in DII, representing the inflammatory potential of diet, independently of changes in body composition can modulate cardiometabolic risk factors and diseases.Copyright © 2021 World Obesity Federation

OBJECTIVE: To ascertain which of the Alternative Healthy Eating Index 2010 (AHEI), Dietary Inflammatory Index (DII) and Mediterranean Diet Score (MDS) best predicted body mass index (BMI) and waist-to-hip circumference ratio (WHR). DESIGN: Body size was measured at baseline (1990-94) and in 2003-7. Diet was assessed at baseline using a food frequency questionnaire, along with age, sex, socioeconomic status, smoking, alcohol drinking, physical activity, and country of birth. Regression coefficients and 95% confidence intervals 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. SETTING: Population-based cohort in Melbourne, Australia. PARTICIPANTS: Included were data from 11,030 men and 16,774 women aged 40 to 69 years at baseline. RESULT(S): Median (IQR) follow up was 11.6 (10.7 - 12.8) years. BMI and WHR at follow-up were associated with baseline DII (Q5 vs Q1 (BMI 0.41 95%CI (0.21, 0.61) and WHR 0.009 95%CI (0.006, 0.013)), and AHEI (Q5 vs 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 vs 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. CONCLUSION(S): 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.

BACKGROUND: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. OBJECTIVE(S): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. METHOD(S): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). RESULT(S): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. CONCLUSION(S): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

Background: Nutritional epidemiology research using self-reported dietary intake is prone to measurement error. Objective methods are being explored to overcome this limitation. Objective(s): We aimed to examine 1) the association between plasma markers related to inflammation and derive marker scores for dietary patterns [Mediterranean dietary score (MDS), energy-adjusted Dietary Inflammatory Index (E-DIITM), Alternative Healthy Eating Index 2010 (AHEI)] and 2) the associations of these marker scores with mortality. Method(s): Weighted marker scores were derived from the cross-sectional association between 30 plasma markers and each dietary score (assessed using food-frequency questionnaires) using linear regression for 770 participants in the Melbourne Collaborative Cohort Study (aged 50-82 y). Prospective associations between marker scores and mortality (n = 249 deaths) were assessed using Cox regression (median follow-up: 14.4 y). Result(s): The MDS, E-DII, and AHEI were associated (P < 0.05) with 9, 14, and 11 plasma markers, respectively. Healthier diets (higher MDS and AHEI, and lower anti-inflammatory, E-DII) were associated with lower concentrations of kynurenines, neopterin, IFN-gamma, cytokines, and C-reactive protein. Five of 6 markers common to the 3 dietary scores were components of the kynurenine pathway. The 3 dietary-based marker scores were highly correlated (Spearman rho: -0.74, -0.82, and 0.93). Inverse associations (for 1-SD increment) were observed with all-cause mortality for the MDS marker score (HR: 0.84; 95% CI: 0.72-0.98) and the AHEI marker score (HR: 0.76; 95% CI: 0.66-0.89), whereas a positive association was observed with the E-DII marker score (HR: 1.18; 95% CI: 1.01-1.39). The same magnitude of effect was not observed for the respective dietary patterns. Conclusion(s): Markers involved in inflammation-related processes are associated with dietary quality, including a substantial overlap between markers associated with the MDS, the E

BACKGROUND: Adverse birth outcomes are major causes of morbidity and mortality during childhood and associate with a higher risk of noncommunicable diseases in adult life. Maternal periconception and antenatal nutrition, mostly focusing on single nutrients or foods, has been shown to influence infant birth outcomes. However, evidence on whole diet that considers complex nutrient and food interaction is rare and conflicting. We aim to elucidate the influence of whole-diet maternal dietary inflammatory potential and quality during periconceptional and antenatal periods on birth outcomes. METHODS AND FINDINGS: We harmonized and pooled individual participant data (IPD) from up to 24,861 mother-child pairs in 7 European mother-offspring cohorts [cohort name, country (recruitment dates): ALSPAC, UK (1 April 1991 to 31 December 1992); EDEN, France (27 January 2003 to 6 March 2006); Generation R, the Netherlands (1 April 2002 to 31 January 2006); Lifeways, Ireland (2 October 2001 to 4 April 2003); REPRO_PL, Poland (18 September 2007 to 16 December 2011); ROLO, Ireland (1 January 2007 to 1 January 2011); SWS, United Kingdom (6 April 1998 to 17 December 2002)]. Maternal diets were assessed preconceptionally (n = 2 cohorts) and antenatally (n = 7 cohorts). Maternal dietary inflammatory potential and quality were ranked using the energy-adjusted Dietary Inflammatory Index (E-DII) and Dietary Approaches to Stop Hypertension (DASH) index, respectively. Primary outcomes were birth weight and gestational age at birth. Adverse birth outcomes, i.e., low birth weight (LBW), macrosomia, small-for-gestational-age (SGA), large-for-gestational-age (LGA), preterm and postterm births were defined according to standard clinical cutoffs. Associations of maternal E-DII and DASH scores with infant birth outcomes were assessed using cohort-specific multivariable regression analyses (adjusted for confounders including maternal education, ethnicity, prepregnancy body mass index (BMI), maternal hei

BACKGROUND: Mounting evidence suggests that maternal diet influences pregnancy and birth outcomes, but its contribution to the global epidemic of childhood obesity has not as yet been definitively characterized. We investigated whether maternal whole diet quality and inflammatory potential influence childhood adiposity. METHODS: We harmonized and pooled individual participant data from 16,295 mother-child pairs in seven European birth cohorts. Maternal pre-, early-, late-, and whole-pregnancy (any time during pregnancy) dietary quality and inflammatory potential assessed with the Dietary Approaches to Stop Hypertension (DASH) score and the energy-adjusted Dietary Inflammatory Index (E-DII™) score, respectively. Primary outcome was childhood overweight and obesity (OWOB) (age-and-sex-specific BMI z-score > 85th percentile). Secondary outcomes were sum of skinfold thickness (SST), fat mass index (FMI) and fat-free mass index (FFMI). We used multivariable regression analyses (adjusting for maternal lifestyle and sociodemographic factors) to assess the associations of maternal DASH and E-DII scores with offspring adiposity outcomes in cohort-specific analyses, with subsequent random-effect meta-analyses. RESULTS: The study mothers had a mean (SD) age of 30.2 (4.6) years and a mean BMI of 23.4 (4.2) kg/m2. Higher early-pregnancy E-DII scores (more pro-inflammatory diet) tended to be associated with a higher odds of late-childhood [10.6 (1.2) years] OWOB [OR (95% CI) 1.09 (1.00, 1.19) per 1-SD E-DII score increase], whereas an inverse association was observed for late-pregnancy E-DII score and early-childhood [2.8 (0.3) years] OWOB [0.91 (0.83, 1.00)]. Higher maternal whole pregnancy DASH score (higher dietary quality) was associated with a lower odds of late-childhood OWOB [OR (95% CI) 0.92 (0.87, 0.98) per 1-SD DASH score increase]; associations were of similar magnitude for early and late-pregnancy [0.86 (0.72, 1.04) and 0.91 (0.85, 0.98), respectively]. These associat

Low muscle mass is associated with reduced independence and increased risk for falls and fractures. Identification of modifiable risk factors for low muscle mass is thus imperative. This study aimed to examine the longitudinal relationship between both diet quality and patterns and lean mass in Australian women. Data from n = 494 participants of the Geelong Osteoporosis Study's 10- and 15-year women's follow-ups were used (conducted in 2004-08 and 2011-14, respectively), and participants were aged 21-89 years. Self-reported lifestyle and demographics were collected, and food frequency questionnaire data informed the dietary exposure variables: the Australian Recommended Food Score (ARFS); the Dietary Inflammatory Index (DII); and a posteriori dietary patterns. The outcome, Skeletal Muscle Index (SMI), was calculated from DXA-derived appendicular lean mass (ALM) relative to height (ALM kg/m2). Analyses employed Generalised Estimating Equations. A higher ARFS score positively predicted SMI over 5-years, and adjustments for age and physical activity did not attenuate this relationship (B:0.044, (95%CI 0.004, 0.084) kg/m2). Following adjustment, both an anti-inflammatory diet (B:-0.034, (95%CI -0.070, -0.002) kg/m2) and a 'traditional' dietary pattern predicted higher SMI (B:0.081, (95%CI 0.004, 0.158) kg/m2). No other associations were observed. Our study reinforces the importance of diet quality for healthy, aging muscle mass. Furthermore, a less inflammatory diet and a diet comprising a wide variety of plant and animal foods may be conducive to maintenance of muscle mass in women. Further studies investigating diet quality's impact on various muscle health measures over longer time periods are warranted.

Type 2 diabetes mellitus is a common condition whose incidence is increasing worldwide, and for which obesity and diet are important risk factors. The aim of this study was to assess the association of three diet quality scores with diabetes risk and how much of the association was mediated through body size. The Melbourne Collaborative Cohort Study recruited 41,513 men and women aged 40-69 years during 1990-1994. At baseline, data were collected on lifestyle and diet, anthropometric measures were performed. Incident diabetes was assessed by self-report at follow-up surveys in 1994-1998 and 2003-2007. The associations between the dietary inflammatory index (DII®), Mediterranean Diet Score (MDS) and the Alternative Healthy Eating Index-2010 and incident diabetes were assessed using Poisson regression, adjusting for age, sex, physical activity, smoking, alcohol consumption, socio-economic status (area based) and family history of diabetes. Data from 39,185 participants were included in the analysis and 1989 cases of diabetes were identified. Both DII and AHEI-2010 were associated with diabetes incidence, but MDS was not. In the top quintile of DII (most pro-inflammatory) vs. the least inflammatory quintile IRR was 1.49 95% CI (1.30, 1.72), p trend across quintiles <0.001. For AHEI-2010 the IRR was 0.67 (0.58, 0.78), p trend <0.001 for the healthiest vs. the least healthy quintile. Mediation analysis indicated that body size (body mass index/waist to hip ratio) mediated 35-48% of the association with incident diabetes for the AHEI and DII. Healthier diets may reduce risk of diabetes both by reducing weight gain and other mechanisms such as reducing inflammation.

Background: Mounting evidence suggests that maternal diet influences pregnancy and birth outcomes, but its contribution to the global epidemic of childhood obesity has not as yet been definitively characterized. We investigated whether maternal whole diet quality and inflammatory potential influence childhood adiposity. Methods: We harmonized and pooled individual participant data from 16,295 mother-child pairs in seven European birth cohorts. Maternal pre-, early-, late-, and whole-pregnancy (any time during pregnancy) dietary quality and inflammatory potential assessed with the Dietary Approaches to Stop Hypertension (DASH) score and the energy-adjusted Dietary Inflammatory Index (E-DII™) score, respectively. Primary outcome was childhood overweight and obesity (OWOB) (age-and-sex-specific BMI z-score > 85th percentile). Secondary outcomes were sum of skinfold thickness (SST), fat mass index (FMI) and fat-free mass index (FFMI). We used multivariable regression analyses (adjusting for maternal lifestyle and sociodemographic factors) to assess the associations of maternal DASH and E-DII scores with offspring adiposity outcomes in cohort-specific analyses, with subsequent random-effect meta-analyses. Results: The study mothers had a mean (SD) age of 30.2 (4.6) years and a mean BMI of 23.4 (4.2) kg/m2. Higher early-pregnancy E-DII scores (more pro-inflammatory diet) tended to be associated with a higher odds of late-childhood [10.6 (1.2) years] OWOB [OR (95% CI) 1.09 (1.00, 1.19) per 1-SD E-DII score increase], whereas an inverse association was observed for late-pregnancy E-DII score and early-childhood [2.8 (0.3) years] OWOB [0.91 (0.83, 1.00)]. Higher maternal whole pregnancy DASH score (higher dietary quality) was associated with a lower odds of late-childhood OWOB [OR (95% CI) 0.92 (0.87, 0.98) per 1-SD DASH score increase]; associations were of similar magnitude for early and late-pregnancy [0.86 (0.72, 1.04) and 0.91 (0.85, 0.98), respectively

Background Adverse birth outcomes are major causes of morbidity and mortality during childhood and associate with a higher risk of noncommunicable diseases in adult life. Maternal periconception and antenatal nutrition, mostly focusing on single nutrients or foods, has been shown to influence infant birth outcomes. However, evidence on whole diet that considers complex nutrient and food interaction is rare and conflicting. We aim to elucidate the influence of whole-diet maternal dietary inflammatory potential and quality during periconceptional and antenatal periods on birth outcomes. Methods and findings We harmonized and pooled individual participant data (IPD) from up to 24,861 mother-child pairs in 7 European mother-offspring cohorts [cohort name, country (recruitment dates): ALSPAC, UK (1 April 1991 to 31 December 1992); EDEN, France (27 January 2003 to 6 March 2006); Generation R, the Netherlands (1 April 2002 to 31 January 2006); Lifeways, Ireland (2 October 2001 to 4 April 2003); REPRO_PL, Poland (18 September 2007 to 16 December 2011); ROLO, Ireland (1 January 2007 to 1 January 2011); SWS, United Kingdom (6 April 1998 to 17 December 2002)]. Maternal diets were assessed preconceptionally (n = 2 cohorts) and antenatally (n = 7 cohorts). Maternal dietary inflammatory potential and quality were ranked using the energy-adjusted Dietary Inflammatory Index (E-DII) and Dietary Approaches to Stop Hypertension (DASH) index, respectively. Primary outcomes were birth weight and gestational age at birth. Adverse birth outcomes, i.e., low birth weight (LBW), macrosomia, small-for-gestational-age (SGA), large-for-gestational-age (LGA), preterm and postterm births were defined according to standard clinical cutoffs. Associations of maternal E-DII and DASH scores with infant birth outcomes were assessed using cohort-specific multivariable regression analyses (adjusted for confounders including maternal education, ethnicity, prepregnancy body mass index (BMI), maternal he

Background: The impact of maternal diet during pregnancy on child neurodevelopment is of public health and clinical relevance. We evaluated the associations of dietary quality based on the Dietary Approaches to Stop Hypertension (DASH) score and dietary inflammatory potential based on the energy-adjusted Dietary Inflammatory Index (E-DII) score during pregnancy with emotional and behavioral symptoms of offspring at 7 to 10 years of age. Methods: Individual participant data for 11,870 mother–child pairs from four European cohorts participating in the ALPHABET project were analyzed. Maternal antenatal DASH and E-DII scores were generated from self-completed food frequency questionnaires. Symptoms of depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder in children were assessed using mother-reported tests and classified within the normal or borderline/clinical ranges using validated cutoffs. Adjusted odds ratios were determined by multivariable logistic regression models and aggregated by the two-level individual participant data meta-analysis method. Results: Higher maternal DASH scores (indicating better dietary quality) were associated with lower risk of depressive and anxiety symptoms, aggressive behavior symptoms, and attention-deficit/hyperactivity disorder symptoms within the borderline/clinical ranges: odds ratio [OR] 0.97, 95% confidence interval [CI], 0.95–0.99; OR 0.97, 95% CI, 0.94–0.99; OR 0.97, 95% CI, 0.95–0.98, per one-unit DASH score increase, respectively. For depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder symptoms, a one-unit increase in E-DII scores (a more proinflammatory diet) was associated with a 7% increased risk of all three analyzed emotional and behavioral symptoms: OR 1.07, 95% CI, 1.03–1.11; OR 1.07, 95% CI, 1.02–1.13; OR 1.07, 95% CI, 1.01–1.13, respectively. Conclusions: Our findings suggest that a maternal low-quality and proinflammatory diet may increase

Background: The impact of maternal diet during pregnancy on child neurodevelopment is of public health and clinical relevance. We evaluated the associations of dietary quality based on the Dietary Approaches to Stop Hypertension (DASH) score and dietary inflammatory potential based on the energy-adjusted Dietary Inflammatory Index (E-DII) score during pregnancy with emotional and behavioral symptoms of offspring at 7 to 10 years of age. Methods: Individual participant data for 11,870 mother–child pairs from four European cohorts participating in the ALPHABET project were analyzed. Maternal antenatal DASH and E-DII scores were generated from self-completed food frequency questionnaires. Symptoms of depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder in children were assessed using mother-reported tests and classified within the normal or borderline/clinical ranges using validated cutoffs. Adjusted odds ratios were determined by multivariable logistic regression models and aggregated by the two-level individual participant data meta-analysis method. Results: Higher maternal DASH scores (indicating better dietary quality) were associated with lower risk of depressive and anxiety symptoms, aggressive behavior symptoms, and attention-deficit/hyperactivity disorder symptoms within the borderline/clinical ranges: odds ratio [OR] 0.97, 95% confidence interval [CI], 0.95–0.99; OR 0.97, 95% CI, 0.94–0.99; OR 0.97, 95% CI, 0.95–0.98, per one-unit DASH score increase, respectively. For depression and anxiety, aggressive behavior, and attention-deficit/hyperactivity disorder symptoms, a one-unit increase in E-DII scores (a more proinflammatory diet) was associated with a 7% increased risk of all three analyzed emotional and behavioral symptoms: OR 1.07, 95% CI, 1.03–1.11; OR 1.07, 95% CI, 1.02–1.13; OR 1.07, 95% CI, 1.01–1.13, respectively. Conclusions: Our findings suggest that a maternal low-quality and proinflammatory diet may increase th

Background & aims: Aging is characterized by progressive decline in physiologic reserves and functions as well as prolonged inflammation, increasing susceptibility to disease. Diet plays an important role in maintaining health, and reducing morbidity and mortality, especially in older populations. This study was designed to determine prospective associations between dietary inflammatory index (DII) scores and bone health, sarcopenia-related outcomes, falls risk and incident fractures in community-dwelling Australian older adults. Method(s): A total of 1098 [51% male; age (mean +/- SD) 63.0 +/- 7.5 years] non-institutionalized older adults who participated in the Tasmanian Older Adult Cohort Study (TASOAC) at baseline, 768 at 5 years, and 566 at 10 years follow-up were included in this analysis. Baseline energy-adjusted DII (E-DII) scores were calculated using a validated Food Frequency Questionnaire. Changes in bone mineral density (BMD) and appendicular lean mass (ALM) were measured over ten years using dual-energy x-ray absorptiometry. Ten-year changes in hand grip, knee extensor and whole lower-limb muscle strength and quality were assessed by dynamometers and change in falls risk score using the Physical Profile Assessment (PPA). Incident fractures at any site and non-vertebral fractures over 10 years were self-reported. Result(s): The E-DII range was -3.48 to +3.23 in men and -3.80 to +2.74 in women. Higher E-DII score (indicating a more pro-inflammatory diet) was associated with lower total hip (B: -0.009; 95% CI: -0.017, 0.000) and lumbar spine BMD (B: -0.013; 95% CI: -0.024, -0.002), and higher falls risk score (B: 0.040; 95% CI: 0.002, 0.078) over 10 years in men. Women with higher E-DII scores had higher whole lower-limb muscle quality over 10 years (B: 0.109; 95% CI: 0.002, 0.215). For every unit increase in E-DII score, incident fracture rates increased by 9.0% in men (IRR: 1.090; 95% CI: 1.011, 1.175) and decreased by 12.2% in women (IRR: 0.878; 95% CI

Background: The relations between diet, chronic inflammation, and musculoskeletal health are unclear, especially among older men. Objective(s): This study aimed to determine associations of the Dietary Inflammatory Index (DII) with inflammatory biomarkers, musculoskeletal health, and falls risk in community-dwelling older men. Method(s): The cross-sectional analysis included 794 community-dwelling men, mean age 81.1 +/- 4.5 y, who participated in the 5-y follow-up of the Concord Health and Aging in Men Project. Of these, 616 were seen again 3 y later for the longitudinal analysis. Energy-adjusted DII (E-DII) was calculated from a validated diet history questionnaire. Bone mineral density (BMD) was measured using DXA. Twenty-four inflammatory biomarkers were analyzed. Incident falls over 3 y were determined through telephone interviews every 4 mo. Multiple regression, linear mixed effects models, negative binomial regression, and mediation analysis were utilized in this study. Result(s): A higher E-DII score (indicating a more proinflammatory diet) was associated with higher concentrations of IL-6 (beta: 0.028 pg/mL; 95% CI: 0.003, 0.053), IL-7 (beta: 0.020 pg/mL; 95% CI: 0.002, 0.037), and TNF-alpha (beta: 0.027 pg/mL; 95% CI: 0.003, 0.051). A higher E-DII score was also associated with lower appendicular lean mass adjusted for BMI (ALMBMI) (beta: -0.006 kg/m2; 95% CI: -0.010, -0.001). For every unit increase in E-DII (range: -4.91 to +3.66 units), incident falls rates increased by 13% (incidence rate ratio: 1.13; 95% CI: 1.05, 1.21) over 3 y. Mediation analysis showed that the association between E-DII and 3-y incident falls was influenced by the concentrations of IL-7 by 24%. There was no association between E-DII and BMD. Conclusion(s): Consumption of a proinflammatory diet was associated with increased concentrations of IL-6, IL-7, and TNF-alpha; increased falls risk; and lower ALMBMI in community-dwelling older men. The association between incident falls and E

Background & aims: Aging is characterized by progressive decline in physiologic reserves and functions as well as prolonged inflammation, increasing susceptibility to disease. Diet plays an important role in maintaining health, and reducing morbidity and mortality, especially in older populations. This study was designed to determine prospective associations between dietary inflammatory index (DII) scores and bone health, sarcopenia-related outcomes, falls risk and incident fractures in community-dwelling Australian older adults. Method(s): A total of 1098 [51% male; age (mean +/- SD) 63.0 +/- 7.5 years] non-institutionalized older adults who participated in the Tasmanian Older Adult Cohort Study (TASOAC) at baseline, 768 at 5 years, and 566 at 10 years follow-up were included in this analysis. Baseline energy-adjusted DII (E-DII) scores were calculated using a validated Food Frequency Questionnaire. Changes in bone mineral density (BMD) and appendicular lean mass (ALM) were measured over ten years using dual-energy x-ray absorptiometry. Ten-year changes in hand grip, knee extensor and whole lower-limb muscle strength and quality were assessed by dynamometers and change in falls risk score using the Physical Profile Assessment (PPA). Incident fractures at any site and non-vertebral fractures over 10 years were self-reported. Result(s): The E-DII range was -3.48 to +3.23 in men and -3.80 to +2.74 in women. Higher E-DII score (indicating a more pro-inflammatory diet) was associated with lower total hip (B: -0.009; 95% CI: -0.017, 0.000) and lumbar spine BMD (B: -0.013; 95% CI: -0.024, -0.002), and higher falls risk score (B: 0.040; 95% CI: 0.002, 0.078) over 10 years in men. Women with higher E-DII scores had higher whole lower-limb muscle quality over 10 years (B: 0.109; 95% CI: 0.002, 0.215). For every unit increase in E-DII score, incident fracture rates increased by 9.0% in men (IRR: 1.090; 95% CI: 1.011, 1.175) and decreased by 12.2% in women (IRR: 0.878; 95% CI

Background: The relations between diet, chronic inflammation, and musculoskeletal health are unclear, especially among older men. Objective(s): This study aimed to determine associations of the Dietary Inflammatory Index (DII) with inflammatory biomarkers, musculoskeletal health, and falls risk in community-dwelling older men. Method(s): The cross-sectional analysis included 794 community-dwelling men, mean age 81.1 +/- 4.5 y, who participated in the 5-y follow-up of the Concord Health and Aging in Men Project. Of these, 616 were seen again 3 y later for the longitudinal analysis. Energy-adjusted DII (E-DII) was calculated from a validated diet history questionnaire. Bone mineral density (BMD) was measured using DXA. Twenty-four inflammatory biomarkers were analyzed. Incident falls over 3 y were determined through telephone interviews every 4 mo. Multiple regression, linear mixed effects models, negative binomial regression, and mediation analysis were utilized in this study. Result(s): A higher E-DII score (indicating a more proinflammatory diet) was associated with higher concentrations of IL-6 (beta: 0.028 pg/mL; 95% CI: 0.003, 0.053), IL-7 (beta: 0.020 pg/mL; 95% CI: 0.002, 0.037), and TNF-alpha (beta: 0.027 pg/mL; 95% CI: 0.003, 0.051). A higher E-DII score was also associated with lower appendicular lean mass adjusted for BMI (ALMBMI) (beta: -0.006 kg/m2; 95% CI: -0.010, -0.001). For every unit increase in E-DII (range: -4.91 to +3.66 units), incident falls rates increased by 13% (incidence rate ratio: 1.13; 95% CI: 1.05, 1.21) over 3 y. Mediation analysis showed that the association between E-DII and 3-y incident falls was influenced by the concentrations of IL-7 by 24%. There was no association between E-DII and BMD. Conclusion(s): Consumption of a proinflammatory diet was associated with increased concentrations of IL-6, IL-7, and TNF-alpha; increased falls risk; and lower ALMBMI in community-dwelling older men. The association between incident falls and E

Diet and inflammation have been suggested to be important risk factors for oral and pharyngeal cancer. We examined the association between dietary inflammatory index (DIITM) and oral and pharyngeal cancer in a large case-control study conducted between 1992 and 2009 in Italy. This study included 946 cases with incident, histologically confirmed oral and pharyngeal cancer, and 2,492 controls hospitalized for acute non-neoplastic diseases. The DII was computed based on dietary intake assessed by a valid 78-item food frequency questionnaire and was adjusted for nonalcohol energy intake using the residual approach (E-DIITM). Logistic regression models were used to estimate odds ratios (ORs), and 95% confidence intervals (CIs), adjusted for age, sex, non-alcohol energy intake, study center, year of interview, education, body mass index, tobacco smoking, and alcohol drinking. Subjects with higher DII scores (i.e., with a more pro-inflammatory diet) had a higher risk of oral and pharyngeal cancer, the OR being 1.80 (95% CI 1.36–2.38) for the highest versus the lowest DII quartile and 1.17 (95% CI 1.10–1.25) for a one-unit increase (8% of the DII range). When stratified by selected covariates, a stronger association was observed among women (ORquartile4 v.1 3.30, 95% CI 1.95–5.57). We also observed a stronger association for oral cancers and a strong combined effect of higher DII score and tobacco smoking or alcohol consumption on oral and pharyngeal cancer. These results indicate that the pro-inflammatory potential of the diet, as shown by higher DII scores, is associated with higher odds of oral and pharyngeal cancer.

There are over 1,000,000 publications on diet and health and over 480,000 references on inflammation in the National Library of Medicine database. In addition, there have now been over 30,000 peer-reviewed articles published on the relationship between diet, inflammation, and health outcomes. Based on this voluminous literature, it is now recognized that low-grade, chronic systemic inflammation is associated with most non-communicable diseases (NCDs), including diabetes, obesity, cardiovascular disease, cancers, respiratory and musculoskeletal disorders, as well as impaired neurodevelopment and adverse mental health outcomes. Dietary components modulate inflammatory status. In recent years, the Dietary Inflammatory Index (DII®), a literature-derived dietary index, was developed to characterize the inflammatory poten

Severe mental illnesses (SMI), including major depressive disorder, bipolar disorder, and schizophrenia, are associated with increased inflammation. Given diet's role in modulating inflammatory processes, excessive calorie-dense, nutrient-deficient processed food intake may contribute toward the heightened inflammation observed in SMI. This review assesses the evidence from observational and experimental studies to investigate how diet may affect physical and mental health outcomes in SMI through inflammation-related pathways. Cross-sectional studies indicate that individuals with SMI, particularly schizophrenia, consume more pro-inflammatory foods and fewer anti-inflammatory nutrients than the general population. Cohort studies indicate that high levels of dietary inflammation are associated with increased risk of developing depression, but there is currently a lack of evidence for schizophrenia or bipolar disorder. Randomized controlled trials show that dietary interventions improve symptoms of depression, but none have tested the extent to which these benefits are due to changes in inflammation. This review summarizes evidence on dietary inflammation in SMI, explores the directionality of these links, and discusses the potential use of targeted nutritional interventions for improving psychological well-being and physical health outcomes in SMI. Establishing the extent to which diet explains elevated levels of inflammatory markers observed in SMI is a priority for future research.

Herbal medicines widely improved for primary health care because of better cultural acceptability and better compatibility with human body and lesser side effects. The aim of present study was to formulate and evaluate of herbal gel containing Allium cepa extract. Topical gel formulation was designed by using Allium cepa extract and carbopol 934 as a gelling agent and different excipients. The herbaceous plant Allium cepa (onion). It has great health significance and is consumed for nutritional and health benefits for last centuries. It contains flavonoids compound. Plant extract used for prevention of hair loss. Raw onion eaten in salad form this is play very important role in health benefits. Gel was prepared by incorporating extract of Allium cepa in gel at a particular step in order to prepare non greasy formulation. Gel Formulation F3 Batch was optimized in the concentration 1.5% of Carbopol 934. Different gel formulations were evaluated for their physical appearance; pH, Spreadability, Homogeneity in-vitro diffusion ,Viscosity and Drug Excipients comparability study are carried out.

Herbal medicines widely improved for primary health care because of better cultural acceptability and better compatibility with human body and lesser side effects. The aim of present study was to formulate and evaluate of herbal gel containing Allium cepa extract. Topical gel formulation was designed by using Allium cepa extract and carbopol 934 as a gelling agent and different excipients. The herbaceous plant Allium cepa (onion). It has great health significance and is consumed for nutritional and health benefits for last centuries. It contains flavonoids compound. Plant extract used for prevention of hair loss. Raw onion eaten in salad form this is play very important role in health benefits. Gel was prepared by incorporating extract of Allium cepa in gel at a particular step in order to prepare non greasy formulation. Gel Formulation F3 Batch was optimized in the concentration 1.5% of Carbopol 934. Different gel formulations were evaluated for their physical appearance; pH, Spreadability, Homogeneity in-vitro diffusion ,Viscosity and Drug Excipients comparability study are carried out.

Copyright © The Authors 2018. 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.

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 (OR Quartile 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.

To assess the possible association between a validated Dietary Inflammatory Index (DII) and specific dietary components with suitable non-invasive markers of liver status in overweight and obese subjects within the PREDIMED study.A cross-sectional study encompassing 794 randomized overweight and obese participants (mean ± SD age: 67.0 ± 5.0 y, 55% females) from the PREDIMED (PREvención con DIeta MEDiterránea) trial was conducted. DII is a validated tool evaluating the effect of diet on six inflammatory biomarkers (IL-1b, IL-4, IL-6, IL-10, TNF-? and C-reactive protein). Furthermore, a validated 137-item food-frequency-questionnaire was used to obtain the information about the food intake. In addition, anthropometric measurements and several non-invasive markers of liver status were assessed and the Fatty Liver Index (FLI) score was calculated.A higher DII and lower adherence to Mediterranean diet (MeDiet) were associated with a higher degree of liver damage (FLI > 60) in obese as compared to overweight participants. Furthermore, the DII score was positively associated with relevant non-invasive liver markers (ALT, AST, GGT and FLI) and directly affected FLI values. Interestingly, a positive correlation was observed between liver damage (>50th percentile FLI) and nutrients and foods linked to a pro-inflammatory dietary pattern.This study reinforced the concept that obesity is associated with liver damage and revealed that the consumption of a pro-inflammatory dietary pattern might contribute to obesity and fatty liver disease features. These data suggest that a well-designed precision diet including putative anti-inflammatory components could specifically prevent and ameliorate non-alcoholic fatty liver manifestations in addition to obesity.Copyright © 2017 Elsevier Ltd

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 (DII TM ) 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.

Background: Diet is known to influence systemic inflammation, a recognized risk factor for colorectal cancer (CRC). Studies in ethnically diverse populations that examine the association between dietary inflammatory potential and CRC incidence are limited. Objectives: We used the Dietary Inflammatory Index to clarify the relation between the inflammatory potential of diet and CRC incidence across racial/ethnic groups. We hypothesized that proinflammatory diets would be associated with an increased risk of CRC, and that these associations may differ across racial/ethnic groups. Methods: The Multiethnic Cohort (MEC) follows a prospective study design. It includes 190,963 white, African-American, native Hawaiian, Japanese-American, and Latino men and women aged 45-75 y at recruitment and followed over 20 y. Participants completed a food frequency questionnaire from which energy-adjusted Dietary Inflammatory Index (E-DII) scores were computed and categorized into quartiles. CRC incidence was documented through linkage to cancer registry programs. Cox proportional hazards regression was used to estimate HRs and 95% CIs, adjusting for known or expected CRC risk factors. Results: Among all participants, more-proinflammatory diets (highest quartile compared with lowest quartile) were associated with an increased risk of CRC (HR: 1.21; 95% CI: 1.11, 1.32). However, the effect size was larger for men (HR: 1.28; 95% CI: 1.13, 1.45) than for women (HR: 1.16; 95% CI: 1.02, 1.33), although the interaction term for sex was not statistically significant (P-interaction = 0.17). When stratified by race/ethnicity, the association was significantly different between groups for men (P-interaction = 0.01), although not for women (P-interaction = 0.20). Significant associations with HRs ranging from 2.33 to 1.04 were observed in white, Japanese-American, and Latino men, and native Hawaiian women. Conclusions: Overall, more-proinflammatory diets, as identified by the E-DII, were associated

Studies investigating the association of food and nutrient consumption with the risk of urothelial cell carcinoma (UCC) have produced mixed results. We used three common dietary scores, the Mediterranean Diet Score (MDS), the Alternate Healthy Eating Index 2010 (AHEI-2010) and the Dietary Inflammatory Index (DII) to assess the evidence of an association between diet and the risk of UCC. Over a median follow-up time of 21.3 years, 379 incident UCC cases were diagnosed. Dietary scores were calculated using data from a 121-item food frequency questionnaire administered at baseline. We used Cox models to compute hazard ratios (HR) for the association between dietary scores (per one standard deviation) and UCC risk. In order to reflect overall adherence to a healthy diet, a metascore was constructed by summing the quintiles of each of the three scores. None of the dietary scores was associated with the risk of UCC overall. A healthier diet was found to be inversely associated with the risk of invasive (MDS: HR = 0.86, 95% CI: 0.74-1.00, metascore: HR = 0.84, 95% CI: 0.71-0.98), but not superficial disease (heterogeneity between subtypes p = 0.04 and p = 0.03, respectively). Results were consistent but weaker for the DII and the AHEI-2010. We found some evidence of effect modification by smoking, in particular for the metascore (Current: HR = 0.77, 95% CI: 0.58-1.01, Former: HR = 0.77, 95% CI: 0.64-0.92, Never: HR = 1.01, 95% CI: 0.81-1.26, p for heterogeneity = 0.05). A healthy diet may be protective against the risk of invasive, but not superficial, UCC. Promoting healthy dietary habits may help lower the risk of invasive UCC, especially for current and former smokers.

Purpose: Components of diet can modulate inflammation and therefore may have an important role in the development of nasopharyngeal carcinoma (NPC). Little is known about the inflammatory potential of diet in relation to nasopharyngeal carcinogenesis. Methods: Data from an Italian multicenter case–control study conducted between 1992 and 2008 and including 198 cases with incident, histologically confirmed NPC, and 594 controls hospitalized for acute nonneoplastic diseases were used to estimate the relation between a dietary inflammatory index (DII) and the risk of NPC. The DII was computed based on the intake of selected dietary factors assessed by a validated 78-item food frequency questionnaire. Logistic regression models were used to estimate odds ratios (ORs) adjusted for study center, place of living, sex, age, year of interview, education, tobacco smoking, alcohol drinking, and energy intake using the residual method. Results: Subjects with higher DII scores had an increased risk of NPC, with each DII point increasing risk by nearly 20% [OR: 1.19; 95% confidence interval (CI): 1.05–1.36]. Compared to subjects in the lowest DII tertile, those in the highest tertile had >60% higher risk of NPC (OR: 1.64; 95% CI: 1.06–2.55; Ptrend = 0.04). Conclusion: These results indicate that inflammatory potential of diet plays a role in NPC.

Purpose: Many dietary factors have either proinflammatory or anti-inflammatory properties. We previously developed a dietary inflammatory index (DII) to assess the inflammatory potential of diet. In this study, we conducted a construct validation of the DII based on data from a food frequency questionnaire and three inflammatory biomarkers in a subsample of 2567 postmenopausal women in the Women's Health Initiative Observational Study. Methods: We used multiple linear and logistic regression models, controlling for potential confounders, to test whether baseline DII predicted concentrations of interleukin-6, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha receptor 2, or an overall biomarker score combining all three inflammatory biomarkers. Results: The DII was associated with the four biomarkers with beta estimates (95% confidence interval) comparing the highest with lowest DII quintiles as follows: interleukin-6: 1.26 (1.15-1.38), Ptrend < .0001; tumor necrosis factor alpha receptor 2: 81.43 (19.15-143.71), Ptrend=.004; dichotomized hs-CRP (odds ratio for higher vs. lower hs-CRP): 1.30 (0.97-1.67), Ptrend=.34; and the combined inflammatory biomarker score: 0.26 (0.12-0.40), Ptrend=.0001. Conclusions: The DII was significantly associated with inflammatory biomarkers. Construct validity of the DII indicates its utility for assessing the inflammatory potential of diet and for expanding its use to include associations with common chronic diseases in future studies.

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.© Copyright The Authors 2015.

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.© Copyright The Authors 2015.

Purpose: Many dietary factors have either proinflammatory or anti-inflammatory properties. We previously developed a dietary inflammatory index (DII) to assess the inflammatory potential of diet. In this study, we conducted a construct validation of the DII based on data from a food frequency questionnaire and three inflammatory biomarkers in a subsample of 2567 postmenopausal women in the Women's Health Initiative Observational Study. Methods: We used multiple linear and logistic regression models, controlling for potential confounders, to test whether baseline DII predicted concentrations of interleukin-6, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha receptor 2, or an overall biomarker score combining all three inflammatory biomarkers. Results: The DII was associated with the four biomarkers with beta estimates (95% confidence interval) comparing the highest with lowest DII quintiles as follows: interleukin-6: 1.26 (1.15-1.38), Ptrend < .0001; tumor necrosis factor alpha receptor 2: 81.43 (19.15-143.71), Ptrend=.004; dichotomized hs-CRP (odds ratio for higher vs. lower hs-CRP): 1.30 (0.97-1.67), Ptrend=.34; and the combined inflammatory biomarker score: 0.26 (0.12-0.40), Ptrend=.0001. Conclusions: The DII was significantly associated with inflammatory biomarkers. Construct validity of the DII indicates its utility for assessing the inflammatory potential of diet and for expanding its use to include associations with common chronic diseases in future studies.