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Dietary inflammatory index and all-cause mortality in large cohorts: The SUN and PREDIMED studies.
Garcia-Arellano, A, Martínez-González, MA, Ramallal, R, Salas-Salvadó, J, Hébert, JR, Corella, D, Shivappa, N, Forga, L, Schröder, H, Muñoz-Bravo, C, et al
Clinical nutrition (Edinburgh, Scotland). 2019;(3):1221-1231
Abstract
BACKGROUND Inflammation is known to be related to the leading causes of death including cardiovascular disease, several types of cancer, obesity, type 2 diabetes, depression-suicide and other chronic diseases. In the context of whole dietary patterns, the Dietary Inflammatory Index (DII®) was developed to appraise the inflammatory potential of the diet. OBJECTIVE We prospectively assessed the association between DII scores and all-cause mortality in two large Spanish cohorts and valuated the consistency of findings across these two cohorts and results published based on other cohorts. DESIGN We assessed 18,566 participants in the "Seguimiento Universidad de Navarra" (SUN) cohort followed-up during 188,891 person-years and 6790 participants in the "PREvencion con DIeta MEDiterránea" (PREDIMED) randomized trial representing 30,233 person-years of follow-up. DII scores were calculated in both cohorts from validated FFQs. Higher DII scores corresponded to more proinflammatory diets. A total of 230 and 302 deaths occurred in SUN and PREDIMED, respectively. In a random-effect meta-analysis we included 12 prospective studies (SUN, PREDIMED and 10 additional studies) that assessed the association between DII scores and all-cause mortality. RESULTS After adjusting for a wide array of potential confounders, the comparison between extreme quartiles of the DII showed a positive and significant association with all-cause mortality in both the SUN (hazard ratio [HR] = 1.85; 95% CI: 1.15, 2.98; P-trend = 0.004) and the PREDIMED cohort (HR = 1.42; 95% CI: 1.00, 2.02; P-trend = 0.009). In the meta-analysis of 12 cohorts, the DII was significantly associated with an increase of 23% in all-cause mortality (95% CI: 16%-32%, for the highest vs lowest category of DII). CONCLUSION Our results provide strong and consistent support for the hypothesis that a pro-inflammatory diet is associated with increased all-cause mortality. The SUN cohort and PREDIMED trial were registered at clinicaltrials.gov as NCT02669602 and at isrctn.com as ISRCTN35739639, respectively.
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Effect of the glycemic index of the diet on weight loss, modulation of satiety, inflammation, and other metabolic risk factors: a randomized controlled trial.
Juanola-Falgarona, M, Salas-Salvadó, J, Ibarrola-Jurado, N, Rabassa-Soler, A, Díaz-López, A, Guasch-Ferré, M, Hernández-Alonso, P, Balanza, R, Bulló, M
The American journal of clinical nutrition. 2014;(1):27-35
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Abstract
BACKGROUND Low-glycemic index (GI) diets have been proven to have beneficial effects in such chronic conditions as type 2 diabetes, ischemic heart disease, and some types of cancer, but the effect of low-GI diets on weight loss, satiety, and inflammation is still controversial. OBJECTIVE We assessed the efficacy of 2 moderate-carbohydrate diets and a low-fat diet with different GIs on weight loss and the modulation of satiety, inflammation, and other metabolic risk markers. DESIGN The GLYNDIET study is a 6-mo randomized, parallel, controlled clinical trial conducted in 122 overweight and obese adults. Participants were randomly assigned to one of the following 3 isocaloric energy-restricted diets for 6 mo: 1) a moderate-carbohydrate and high-GI diet (HGI), 2) a moderate-carbohydrate and low-GI diet (LGI), and 3) a low-fat and high-GI diet (LF). RESULTS At weeks 16 and 20 and the end of the intervention, changes in body mass index (BMI; in kg/m(2)) differed significantly between intervention groups. Reductions in BMI were greater in the LGI group than in the LF group, whereas in the HGI group, reductions in BMI did not differ significantly from those in the other 2 groups (LGI: -2.45 ± 0.27; HGI: -2.30 ± 0.27; LF: -1.43 ± 0.27; F = 4.616, P = 0.012; pairwise comparisons: LGI compared with HGI, P = 1.000; LGI compared with LF, P = 0.016; HGI compared with LF, P = 0.061). The decrease in fasting insulin, homeostatic model assessment of insulin resistance, and homeostatic model assessment of β cell function was also significantly greater in the LGI group than in the LF group (P < 0.05). Despite this tendency for a greater improvement with a low-GI diet, the 3 intervention groups were not observed to have different effects on hunger, satiety, lipid profiles, or other inflammatory and metabolic risk markers. CONCLUSION A low-GI and energy-restricted diet containing moderate amounts of carbohydrates may be more effective than a high-GI and low-fat diet at reducing body weight and controlling glucose and insulin metabolism. This trial was registered at Current Controlled Trials (www.controlled-trials.com) as ISRCTN54971867.
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Beneficial effect of pistachio consumption on glucose metabolism, insulin resistance, inflammation, and related metabolic risk markers: a randomized clinical trial.
Hernández-Alonso, P, Salas-Salvadó, J, Baldrich-Mora, M, Juanola-Falgarona, M, Bulló, M
Diabetes care. 2014;(11):3098-105
Abstract
OBJECTIVE To examine whether a pistachio-rich diet reduces the prediabetes stage and improves its metabolic risk profile. RESEARCH DESIGN AND METHODS Prediabetic subjects were recruited to participate in this Spanish randomized clinical trial between 20 September 2011 and 4 February 2013. In a crossover manner, 54 subjects consumed two diets, each for 4 months: a pistachio-supplemented diet (PD) and a control diet (CD). A 2-week washout period separated study periods. Diets were isocaloric and matched for protein, fiber, and saturated fatty acids. A total of 55% of the CD calories came from carbohydrates and 30% from fat, whereas for the PD, these percentages were 50 and 35%, respectively (including 57 g/day of pistachios). RESULTS Fasting glucose, insulin, and HOMA of insulin resistance decreased significantly after the PD compared with the CD. Other cardiometabolic risk markers such as fibrinogen, oxidized LDL, and platelet factor 4 significantly decreased under the PD compared with the CD (P < 0.05), whereas glucagon-like peptide-1 increased. Interleukin-6 mRNA and resistin gene expression decreased by 9 and 6%, respectively, in lymphocytes after the pistachio intervention (P < 0.05, for PD vs. CD). SLC2A4 expression increased by 69% in CD (P = 0.03, for PD vs. CD). Cellular glucose uptake by lymphocytes decreased by 78.78% during the PD (P = 0.01, PD vs. CD). CONCLUSIONS Chronic pistachio consumption is emerging as a useful nutritional strategy for the prediabetic state. Data suggest that pistachios have a glucose- and insulin-lowering effect, promote a healthier metabolic profile, and reverse certain metabolic deleterious consequences of prediabetes.
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Nuts, inflammation and insulin resistance.
Casas-Agustench, P, Bulló, M, Salas-Salvadó, J
Asia Pacific journal of clinical nutrition. 2010;(1):124-30
Abstract
The beneficial effects of nut consumption on cardiovascular disease (CVD) have been widely documented. These protective effects are mainly attributed to the role of nuts in the metabolism of lipids and lipoproteins. As chronic inflammation is a key early stage in the atherosclerotic process that predicts future CVD events and is closely related to the pathogenesis of insulin resistance, many recent studies have focused on the potential effect of nut consumption on inflammation and insulin resistance. Through different mechanisms, some components of nuts such as magnesium, fiber, alpha-linolenic acid, L-arginine, antioxidants and MUFA may protect against inflammation and insulin resistance. This review evaluates the epidemiologic and experimental evidence in humans demonstrating an association between nut consumption and these two emergent cardio-protective mechanisms.