Diet and chronic inflammation have been suggested to be risk factors in the development of cardiovascular disease (CVD) and related mortality. The possible link between the inflammatory potential of ...diet measured through the Dietary Inflammatory Index (DII
) and CVD has been investigated in several populations across the world. The aim of this study was to conduct a meta-analysis on studies exploring this association. Data from 14 studies were eligible, of which two were case-control, eleven were cohort, and one was cross-sectional. Results from the random-effects meta-analysis showed a positive association between increasing DII, indicating a pro-inflammatory diet, and CVD. Individuals in the highest versus the lowest (reference) DII category showed a 36% increased risk of CVD incidence and mortality, with moderate evidence of heterogeneity (relative risk (RR) = 1.36, 95% confidence interval (CI): 1.19, 1.57; heterogeneity index
² = 69%,
< 0.001). When analyzed as a continuous variable, results showed an increased risk of CVD risk and mortality of 8% for each one-point increase in the DII score. Results remained unchanged when analyses were restricted to the prospective studies. Results of our meta-analysis support the importance of adopting a healthier anti-inflammatory diet for preventing CVD incidence and related mortality. In conclusion, a pro-inflammatory diet is associated with increased risk of CVD and CVD mortality. These results further substantiate the utility of DII as tool to characterize the inflammatory potential of diet and to predict CVD incidence and mortality.
We examined the associations between muscular strength, markers of overall and central adiposity, and cancer mortality in men.
A prospective cohort study including 8,677 men ages 20 to 82 years ...followed from 1980 to 2003. Participants were enrolled in The Aerobics Centre Longitudinal Study, the Cooper Institute in Dallas, Texas. Muscular strength was quantified by combining 1-repetition maximal measures for leg and bench presses. Adiposity was assessed by body mass index (BMI), percent body fat, and waist circumference.
Cancer death rates per 10,000 person-years adjusted for age and examination year were 17.5, 11.0, and 10.3 across incremental thirds of muscular strength (P = 0.001); 10.9, 13.4, and 20.1 across BMI groups of 18.5-24.9, 25.0-29.9, and > or =30 kg/m(2), respectively (P = 0.008); 11.6 and 17.5 for normal (<25%) and high percent body fat (> or =25%), respectively (P = 0.006); and 12.2 and 16.7 for normal (< or =102 cm) and high waist circumference (>102 cm), respectively (P = 0.06). After adjusting for additional potential confounders, hazard ratios (95% confidence intervals) were 1.00 (reference), 0.65 (0.47-0.90), and 0.61 (0.44-0.85) across incremental thirds of muscular strength, respectively (P = 0.003 for linear trend). Further adjustment for BMI, percent body fat, waist circumference, or cardiorespiratory fitness had little effect on the association. The associations of BMI, percent body fat, or waist circumference with cancer mortality did not persist after further adjusting for muscular strength (all P > or = 0.1).
Higher levels of muscular strength are associated with lower cancer mortality risk in men, independent of clinically established measures of overall and central adiposity, and other potential confounders.
Inflammation-related mechanisms may contribute to the link between diet and cancer. We sought to investigate the inflammatory impact of diet on cancer risk using the Dietary inflammatory index (DII) ...and an adapted Mediterranean diet score (MDS).
This population-based, prospective cohort study used self-reported dietary data from the Västerbotten Intervention Programme, including 100,881 participants, of whom 35,393 had repeated measures. Associations between dietary patterns and cancer risk were evaluated using Cox proportional hazards regression. We also used restricted cubic splines to test for potential non-linear associations.
A total of 9,250 incident cancer cases were diagnosed during a median follow-up of 15 years. The two dietary patterns were moderately correlated to each other and had similar associations with cancer risk, predominantly lung cancer in men (DII per tertile decrease: Hazard ratio (HR) 0.81 (0.66-0.99), MDS per tertile increase: HR 0.86 (0.72-1.03)), and gastric cancer in men (DII: 0.73 (0.53-0.99), MDS: 0.73 (0.56-0.96)). Associations were, in general, found to be linear. We found no longitudinal association between 10-year change in diet and cancer risk.
We confirm small, but consistent and statistically significant associations between a more anti-inflammatory or healthier diet and reduced risk of cancer, including a lower risk of lung and gastric cancer in men. The dietary indexes produced similar associations with respect to the risk of cancer.
Inflammation is associated with a number of chronic conditions, such as cancer and cardiovascular disease. Reducing inflammation may help prevent or treat these conditions. Diet has consistently been ...shown to modulate inflammation. To facilitate research into the inflammatory effect of diet on health in humans, we sought to develop and validate an Inflammatory Index designed to assess the inflammatory potential of individuals' diets. An Inflammatory Index was developed based on the results of an extensive literature search. Using data from a longitudinal observational study that carefully measured diet and the inflammatory marker, serum high-sensitivity (hs) C-reactive protein (CRP), in ~600 adults for 1 y, we conducted analyses to test the effect of Inflammatory Index score on hs-CRP as a continuous and dichotomous (less-than or equal to3 mg/L, >3 mg/L) indicator of inflammatory response, while controlling for important potential confounders. Results based on continuous measures of hs-CRP suggested that an increasing Inflammatory Index score (representing movement toward an antiinflammatory diet) was associated with a decrease in hs-CRP. Analyses using hs-CRP as a dichotomous variable showed that an antiinflammatory diet was associated with a decrease in the odds of an elevated hs-CRP (P = 0.049). The results are consistent with the ability of the Inflammatory Index to predict hs-CRP and provide additional evidence that diet plays a role in the regulation of inflammation, even after careful control of a wide variety of potential confounders.
Summary
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.
Previous research has shown that nutrients and certain food items influence inflammation. However, little is known about the associations between diet, as a whole, and inflammatory markers. In the ...present study, we examined the ability of a FFQ-derived dietary inflammatory index (DII) to predict inflammation. Data from a Belgian cross-sectional study of 2524 generally healthy subjects (age 35-55 years) were used. The DII is a population-based, literature-derived dietary index that was developed to predict inflammation and inflammation-related chronic diseases. The DII was calculated from FFQ-derived dietary information and tested against inflammatory markers, namely C-reactive protein (CRP), IL-6, homocysteine and fibrinogen. Analyses were performed using multivariable logistic regression, adjusting for energy, age, sex, BMI, smoking status, education level, use of non-steroidal anti-inflammatory drugs, blood pressure, use of oral contraceptives, anti-hypertensive therapy, lipid-lowering drugs and physical activity. Multivariable analyses showed significant positive associations between the DII and the inflammatory markers IL-6 (>1·6 pg/ml) (OR 1·19, 95 % CI 1·04, 1·36) and homocysteine (>15 μmol/l) (OR 1·56, 95 % CI 1·25, 1·94). No significant associations were observed between the DII and the inflammatory markers CRP and fibrinogen. These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation.
Accumulating evidence identifies diet and inflammation as potential mechanisms contributing to cardiometabolic risk. However, inconsistent reports regarding dietary inflammatory potential, biomarkers ...of cardiometabolic health and metabolic syndrome (MetS) risk exist. Our objective was to examine the relationships between a food frequency questionnaire (FFQ)-derived dietary inflammatory index (DII
), biomarkers of lipoprotein metabolism, inflammation and glucose homeostasis and MetS risk in a cross-sectional sample of 1992 adults. Energy-adjusted DII (E-DII) scores derived from an FFQ were calculated. Lipoprotein particle size and subclass concentrations were measured using nuclear magnetic resonance (NMR) spectroscopy. Serum acute-phase reactants, adipocytokines, pro-inflammatory cytokines and white blood cell (WBC) counts were determined. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Our data indicate that a more pro-inflammatory diet, reflected by higher E-DII scores, was associated with potentially pro-atherogenic lipoprotein profiles characterised by increased numbers of large very low density lipoprotein (VLDL), small dense low density lipoprotein (LDL) and high density lipoprotein (HDL) particles and less large LDL and HDL particles (all
< 0.001). Inflammatory profiling identified a range of adverse phenotypes among those with higher E-DII scores, including higher complement component C3 (C3), C-reactive protein (CRP), (both
< 0.05), interleukin 6 (IL-6) and tumour necrosis factor (TNF)-α concentrations, higher WBC counts and neutrophil to lymphocyte ratio (NLR) and lower adiponectin levels (all
< 0.001). MetS risk was increased among those with higher E-DII scores (OR 1.37, 95% CI (1.01, 1.88),
< 0.05), after adjusting for potential confounders. In conclusion, habitual intake of a more pro-inflammatory diet is associated with unfavourable lipoprotein and inflammatory profiles and increased MetS risk.
Beyond intakes of total energy and individual nutrient, eating patterns may influence health, and thereby the risk of adverse outcomes. How different diet measures relate to frailty-a general measure ...of increased vulnerability to unfavorable health outcomes-and mortality risk, and how this might vary across the life course, is not known. We investigated the associations of five dietary indices (Nutrition Index (NI), the energy-density Dietary Inflammatory Index (E-DII™), Healthy Eating Index-2015 (HEI-2015), Mediterranean Diet Score (MDS), and Dietary Approaches to Stop Hypertension (DASH)) with frailty and mortality.
We included 15,249 participants aged ≥ 20 years from the 2007-2012 cohorts of the National Health and Nutrition Examination Survey (NHANES). The NI combined 31 nutrition-related deficits. The E-DII is a literature-derived dietary index associated with inflammation. The HEI-2015 assesses adherence to the Dietary Guidelines of Americans. The MDS represents adherence to the traditional Mediterranean diet. DASH combines macronutrients and micronutrients to prevent hypertension. Frailty was evaluated using a 36-item frailty index. Mortality status was ascertained up to December 31, 2015.
Participants' mean age was 47.2 ± 16.7 years and 51.7% were women. After adjusting for age, sex, race, educational level, marital and employment status, smoking, BMI, and study cohort, higher NI and E-DII scores and lower HEI-2015, MDS, and DASH scores were individually significantly associated with frailty. All dietary scores were significantly associated with 8-year mortality risk after adjusting for basic covariates and frailty: NI (hazard ratio per 0.1 point, 1.15, 95%CI 1.10-1.21), E-DII (per 1 point, 1.05, 1.01-1.08), HEI-2015 (per 10 points, 0.93, 0.89-0.97), MDS (per 1 point, 0.94, 0.90-0.97), and DASH (per 1 point, 0.96, 0.93-0.99). The associations of E-DII, HEI-2015, and MDS scores with 8-year mortality risk persisted after additionally adjusting for NI.
NI, E-DII, HEI-2015, MDS, and DASH scores are associated with frailty and 8-year mortality risk in adults across all ages. Nevertheless, their mechanisms and sensitivity to predict health outcomes may differ. Nutrition scores have the potential to include measures of both consumption and laboratory and physical measures of exposure.
Diet and inflammation are both associated with type 2 diabetes mellitus (T2DM). In the present study, we aimed to assess the relation between the dietary inflammatory index (DII) and the presence of ...T2DM in Mexican adults participating in the Diabetes Mellitus Survey administered in Mexico City (DMS-MC). The study involved 1174 subjects (48.5% men) between 20-69 years of age. A validated semi-quantitative food frequency questionnaire was employed to evaluate dietary intake and to compute DII. The DII is based on scientific evidence about the association between dietary compounds and six established inflammatory biomarkers. Multivariate logistic regression models were used to estimate the odds ratios (ORs) and 95% confidence intervals (95% CIs) of DII in relation to T2DM. Our results suggest that subjects in the highest quintile of the DII had higher odds of T2DM (OR = 3.02; 95% CI: 1.39, 6.58;
= 0.005) compared to subjects in the lowest quintile of DII scores. Assessing possible effect modification, an association with T2DM was evident when comparing DII quintile 5 to quintile 1 for participants aged ≥ 55 years (OR = 9.77; 95% CI: 3.78, 25.50;
= 0.001). These results suggest that a pro-inflammatory diet is associated with significantly higher odds of T2DM among adult Mexicans.
Sleep disturbances, chronotype and social jetlag (SJL) have been associated with increased risks for major chronic diseases that take decades to develop, such as obesity, metabolic syndrome and ...cardiovascular disease. Potential relationships between poor sleep, chronotype and SJL as they relate to metabolic risk factors for chronic disease have not been extensively investigated. This prospective study examined chronotype, SJL and poor sleep in relation to both obesity and elevated blood pressure among healthy young adults. SJL and objective sleep measures (total sleep time, sleep onset latency, wake after sleep onset and sleep efficiency) were derived from personal rest/activity monitoring (armband actigraphy) among 390 healthy adults 21-35 years old. Participants wore the device for 6-10 days at 6-month intervals over a 2-year period (n = 1431 repeated observations). Chronotypes were categorized into morning, intermediate and evening groups using repeated measures latent class analysis. Means of SJL and sleep measures among latent chronotype groups were compared using partial F-tests in generalized linear mixed models. Generalized linear mixed models also were used to generate odds ratios (ORs) with 95% confidence intervals (CIs) examining the relationship between repeated measures of chronotype, SJL, sleep and concurrent anthropometric outcome measures (body mass index, percentage of body fat, waist-to-hip ratio, waist-to-height ratio), systolic blood pressure and diastolic blood pressure. Sleep latency ≥12 min was associated with increased odds of a high waist-to-height ratio (OR = 1.37; CI: 1.03-1.84). Neither chronotype nor SJL was independently associated with anthropometric outcomes or with blood pressure. Relationships between poor sleep and anthropometric outcomes or blood pressure varied by chronotype. Morning types with total sleep time <6 h, sleep efficiency <85% or wake after sleep onset ≥60 min were more likely to have an increased percentage of body fat, waist-to-hip ratio and waist-to-height ratio relative to those with an intermediate chronotype. Similarly, sleep latency ≥12 min was associated with increased odds of elevated systolic blood pressure (OR = 1.90; CI: 1.15-3.16, p
= 0.02) among morning versus intermediate chronotypes. No relationships between poor sleep and obesity or elevated blood pressure were observed among evening chronotypes. The results from this study among healthy young adults suggest that poor sleep among morning types may be more strongly associated with obesity and elevated blood pressure relative to those with an intermediate (neutral) chronotype. Sleep-related metabolic alterations among different chronotypes warrant further investigation.
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