scholarly journals Dietary inflammatory index, risk of incident hypertension, and effect modification from BMI

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Conor-James MacDonald ◽  
Nasser Laouali ◽  
Anne-Laure Madika ◽  
Francesca Romana Mancini ◽  
Marie-Christine Boutron-Ruault
2020 ◽  
Author(s):  
Conor-James MacDonald ◽  
Nasser Laouali ◽  
Anne-Laure Madika ◽  
Francesca Romana Mancini ◽  
Marie-Christine Boutron-Ruault

Abstract Introduction: Previous studies have identified a positive association between the inflammatory potential of the diet and hypertension. It is not known if BMI is an effect modifier for this association, nor if the association is dose-respondent. This study aimed to assess the association between the dietary inflammatory index (DII) and the risk of hypertension, and assess any effect modification from BMI.Methods: Data from the E3N cohort study, a French prospective population-based study initiated in 1990 was used. From the women in the study, we included those who completed a detailed diet history questionnaire, and who did not have prevalent hypertension or cardiovascular disease at baseline, resulting in 46,652 women. The adapted DII was assessed with data from the dietary questionnaire. Hypertension cases were self-reported and verified through a drug-reimbursement database. Cox proportional hazard models were used to calculate hazard ratios. Spline regression was used to determine any dose-respondent relationship.Results: During 884,267 person-years, 13,183 cases of incident hypertension were identified. The median DII in the population was slightly pro-inflammatory (DII = + 0.44). A highly pro-inflammatory diet (DII > 3.0) was associated with a slight increase in hypertension risk (HRQ1-Q5 = 1.07 [1.02: 1.13]). Evidence was observed for effect modification from BMI, with associations strongest amongst women in the 18.5 - 21.0 BMI range (HRQ1-Q5 = 1.17 [1.06: 1.29]). A weak dose-respondent relationship was observed.Conclusion: Evidence for a weak association between DII and hypertension was observed. Associations were stronger amongst healthy-lean women.


2020 ◽  
Author(s):  
Conor-James MacDonald ◽  
Nasser Laouali ◽  
Anne-Laure Madika ◽  
Francesca Romana Mancini ◽  
Marie-Christine Boutron-Ruault

Abstract Introduction Previous studies have identified a positive association between the inflammatory potential of the diet and hypertension. It is not known if BMI is an effect modifier for this association, nor if the association is dose-respondent. This study aimed to assess the association between the dietary inflammatory index (DII) and the risk of hypertension, and assess any effect modification from BMI. Methods Data from the E3N cohort study, a French prospective population-based study initiated in 1990 was used. From the women in the study, we included those who completed a detailed diet history questionnaire, and who did not have prevalent hypertension or cardiovascular disease at baseline, resulting in 46,652 women. The adapted DII was assessed with data from the dietary questionnaire. Hypertension cases were self-reported and verified through a drug-reimbursement database. Cox proportional hazard models were used to calculate hazard ratios. Spline regression was used to determine any dose-respondent relationship. Results During 884,267 person-years, 13,183 cases of incident hypertension were identified. The median DII in the population was slightly pro-inflammatory (DII = + 0.44). A highly pro-inflammatory diet (DII > 3.0) was associated with a slight increase in hypertension risk (HR Q1-Q5 = 1.07 [1.02: 1.13]). Evidence was observed for effect modification from BMI, with associations strongest amongst women in the 18.5 - 21.0 BMI range (HR Q1-Q5 = 1.17 [1.06: 1.29]). A weak dose-respondent relationship was observed. Conclusion Evidence for a weak association between DII and hypertension was observed. Associations were stronger amongst leaner women.


2021 ◽  
pp. 1-27
Author(s):  
Chichen Zhang ◽  
Shi Qiu ◽  
Haiyang Bian ◽  
Bowen Tian ◽  
Haoyuan Wang ◽  
...  

Abstract Objective: We evaluate the association between the Dietary Inflammatory Index (DII) and kidney stones. Design: We performed a cross-sectional analysis using data from National Health and Nutrition Examination Survey. Dietary intake information was assessed using first 24-HR dietary recall interviews, and the Kidney Conditions was presented by questionnaire. The primary outcome was to investigate the association between DII and incidence of kidney stones, and the secondary outcome was to assess the association between DII and nephrolithiasis recurrence. Setting: The National Health and Nutrition Examination Survey (NHANES), 2007-2016. Participants: The study included 25984 NHANES participants, whose data on DII and kidney stones were available, of whom 2439 reported a history of kidney stones. Results: For the primary outcome, after fully multivariate adjustment, DII score is positively associated with the risk of kidney stones (OR = 1.07; 95% CI: [1.04–1.10]). Then, compared Q4 with Q1, a significant 38% increased likelihood of nephrolithiasis was observed. (OR=1.38; 95% CI: [1.19–1.60]). For the secondary outcome, the multivariate regression analysis showed that DII score is positively correlated with nephrolithiasis recurrence (OR=1.07; 95% CI: [1.00–1.15]). The results noted that higher DII scores (Q3 and Q4) are positively associated with a significant 48% and 61% increased risk of nephrolithiasis recurrence compared with the reference after fully multivariate adjustment. (OR=1.48; 95% CI: [1.07–2.05]; OR=1.61; 95% CI: [1.12–2.31]). Conclusions: Our findings revealed that increased intake of pro-inflammatory diet, as a higher DII score, is correlated with increased odds of kidney stones incidence and recurrence.


Author(s):  
Evertine Wesselink ◽  
Laura E. Staritsky ◽  
Moniek van Zutphen ◽  
Anne J.M.R. Geijsen ◽  
Dieuwertje E. Kok ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1194
Author(s):  
Vanessa Machado ◽  
João Botelho ◽  
João Viana ◽  
Paula Pereira ◽  
Luísa Bandeira Lopes ◽  
...  

Inflammation-modulating elements are recognized periodontitis (PD) risk factors, nevertheless, the association between dietary inflammatory index (DII) and PD has never been appraised. We aimed to assess the association between DII and PD and the mediation effect of DII in the association of PD with systemic inflammation. Using the National Health and Nutrition Examination Survey 2009–2010, 2011–2012 and 2013–2014, participants who received periodontal exam and provided dietary recall data were included. The inflammatory potential of diet was calculated via DII. PD was defined according to the 2012 case definition. White blood cells (WBC), segmented neutrophils and C-reactive protein (CRP) were used as proxies for systemic inflammation. The periodontal measures were regressed across DII values using adjusted multivariate linear regression and adjusted mediation analysis. Overall, 10,178 participants were included. DII was significantly correlated with mean periodontal probing depth (PPD), mean clinical attachment loss (CAL), thresholds of PPD and CAL, WBC, segmented neutrophils and DII (p < 0.01). A linear regression logistic adjusted for multiple confounding variables confirmed the association between DII and mean PPD (B = 0.02, Standard Error [SE]: 0.02, p < 0.001) and CAL (B = −0.02, SE: 0.01, p < 0.001). The association of mean PPD and mean CAL with both WBC and segmented neutrophils were mediated by DII (from 2.1 to 3.5%, p < 0.001). In the 2009–2010 subset, the association of mean CAL with serum CRP was mediated by DII (52.0%, p < 0.01). Inflammatory diet and PD may be associated. Also, the inflammatory diet significantly mediated the association of leukocyte counts and systemic inflammation with PD.


2021 ◽  
pp. 1-10
Author(s):  
Jiani Yang ◽  
Jun Ma ◽  
Yue Jin ◽  
Shanshan Cheng ◽  
Shan Huang ◽  
...  

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Yoshinari Matsumoto ◽  
Nitin Shivappa ◽  
Yuko Sugioka ◽  
Masahiro Tada ◽  
Tadashi Okano ◽  
...  

Abstract Background The dietary inflammatory index (DII®), a quantitative measure of the inflammatory potential of daily food and nutrient intake, and associations between a variety of health outcomes have been reported. However, the association between DII score and disease activity of rheumatoid arthritis (RA) is unclear. Therefore, this study was designed to test whether higher DII score contributes to disease activity and as a corollary, whether reducing DII score helps to achieve or maintain low disease activity or remission in patients with RA. Methods We performed a cross-sectional and longitudinal analysis using 6 years of data (from 2011 to 2017) in TOMORROW, a cohort study consisting of 208 RA patients and 205 gender- and age-matched controls started in 2010. Disease activity of RA patients was assessed annually using DAS28-ESR (disease activity score 28 joints and the erythrocyte sedimentation rate) as a composite measure based on arthritic symptoms in 28 joints plus global health assessment and ESR. Dietary data were collected in 2011 and 2017 using the brief-type self-administered diet history questionnaire (BDHQ). Energy-adjusted DII (E-DII™) score was calculated using 26 nutrients derived from the BDHQ. Data were analyzed with two-group comparisons, correlation analysis, and multivariable logistic regression analysis. Results One hundred and seventy-seven RA patients and 183 controls, for whom clinical and dietary survey data were available, were analyzed. RA patients had significantly higher E-DII (pro-inflammatory) score compared to controls both in 2011 and 2017 (p < 0.05). In RA patients, E-DII score was not a factor associated with significant change in disease activity. However, anti-inflammatory change in E-DII score was associated maintaining low disease activity (DAS28-ESR ≤ 3.2) or less for 6 years (OR 3.46, 95% CI 0.33–8.98, p = 0.011). Conclusions The diets of RA patients had a higher inflammatory potential than controls. Although E-DII score was not a factor associated with significant disease activity change, anti-inflammatory change in E-DII score appeared to be associated with maintaining low disease activity in patients with RA. Trial registration UMIN Clinical Trials Registry, UMIN000003876. Registered 7 Aug 2010—retrospectively registered.


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