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OBJECTIVE: To investigate whether the genetic burden of type 2 diabetes modifies the association between the quality of dietary fat and the incidence of type 2 diabetes.DESIGN: Individual participant data meta-analysis.DATA SOURCES: Eligible prospective cohort studies were systematically sourced from studies published between January 1970 and February 2017 through electronic searches in major medical databases (Medline, Embase, and Scopus) and discussion with investigators.REVIEW METHODS: Data from cohort studies or multicohort consortia with available genome-wide genetic data and information about the quality of dietary fat and the incidence of type 2 diabetes in participants of European descent was sought. Prospective cohorts that had accrued five or more years of follow-up were included. The type 2 diabetes genetic risk profile was characterized by a 68-variant polygenic risk score weighted by published effect sizes. Diet was recorded by using validated cohort-specific dietary assessment tools. Outcome measures were summary adjusted hazard ratios of incident type 2 diabetes for polygenic risk score, isocaloric replacement of carbohydrate (refined starch and sugars) with types of fat, and the interaction of types of fat with polygenic risk score.RESULTS: Of 102 305 participants from 15 prospective cohort studies, 20 015 type 2 diabetes cases were documented after a median follow-up of 12 years (interquartile range 9.4-14.2). The hazard ratio of type 2 diabetes per increment of 10 risk alleles in the polygenic risk score was 1.64 (95% confidence interval 1.54 to 1.75, I2=7.1%, τ2=0.003). The increase of polyunsaturated fat and total omega 6 polyunsaturated fat intake in place of carbohydrate was associated with a lower risk of type 2 diabetes, with hazard ratios of 0.90 (0.82 to 0.98, I2=18.0%, τ2=0.006; per 5% of energy) and 0.99 (0.97 to 1.00, I2=58.8%, τ2=0.001; per increment of 1 g/d), respectively. Increasing monounsaturated fat

OBJECTIVE To investigate whether the genetic burden of type 2 diabetes modifies the association between the quality of dietary fat and the incidence of type 2 diabetes. DESIGN Individual participant data meta-analysis. DATA SOURCES Eligible prospective cohort studies were systematically sourced from studies published between January 1970 and February 2017 through electronic searches in major medical databases (Medline, Embase, and Scopus) and discussion with investigators. REVIEW METHODS Data from cohort studies or multicohort consortia with available genome-wide genetic data and information about the quality of dietary fat and the incidence of type 2 diabetes in participants of European descent was sought. Prospective cohorts that had accrued five or more years of follow-up were included. The type 2 diabetes genetic risk profile was characterized by a 68-variant polygenic risk score weighted by published effect sizes. Diet was recorded by using validated cohort-specific dietary assessment tools. Outcome measures were summary adjusted hazard ratios of incident type 2 diabetes for polygenic risk score, isocaloric replacement of carbohydrate (refined starch and sugars) with types of fat, and the interaction of types of fat with polygenic risk score. RESULTS Of 102 305 participants from 15 prospective cohort studies, 20 015 type 2 diabetes cases were documented after a median follow-up of 12 years (interquartile range 9.4-14.2). The hazard ratio of type 2 diabetes per increment of 10 risk alleles in the polygenic risk score was 1.64 (95% confidence interval 1.54 to 1.75, I-2 = 7.1%, tau(2) = 0.003). The increase of polyunsaturated fat and total omega 6 polyunsaturated fat intake in place of carbohydrate was associated with a lower risk of type 2 diabetes, with hazard ratios of 0.90 (0.82 to 0.98, I-2 = 18.0%, tau(2) = 0.006; per 5% of energy) and 0.99 (0.97 to 1.00, I-2 = 58.8%, tau(2) = 0.001; per increment of 1 g/d), respectively. Increasing monounsaturated fat in pl

Type 2 diabetes (T2D) is widespread, affecting the health of hundreds of millions worldwide. The disease results from the complex interplay of lifestyle factors acting on a backdrop of inherited DNA risk variants. Detecting and understanding biomarkers, whether genotypes or other downstream biological features that dictate a person's phenotypic response to different lifestyle exposures, may have tremendous utility in the prevention of T2D. Here, we explore (i) evidence of how human genetic adaptation to diverse local environments might interact with lifestyle factors in T2D, (ii) the key challenges facing the research area of gene x lifestyle interactions in T2D, and (iii) the solutions that might be pursued in future studies. Overall, many preliminary examples of such interactions exist, but none is sufficient to have a major impact on clinical decision making. Future studies, integrating genetics and other biological markers into regulatory networks, are likely to be necessary to facilitate the integration of genomics into lifestyle medicine in T2D.

Background: Joint data analysis from multiple nutrition studies may improve the ability to answer complex questions regarding the role of nutritional status and diet in health and disease.Objective: The objective was to identify nutritional observational studies from partners participating in the European Nutritional Phenotype Assessment and Data Sharing Initiative (ENPADASI) Consortium, as well as minimal requirements for joint data analysis.Methods: A predefined template containing information on study design, exposure measurements (dietary intake, alcohol and tobacco consumption, physical activity, sedentary behavior, anthropometric measures, and sociodemographic and health status), main health-related outcomes, and laboratory measurements (traditional and omics biomarkers) was developed and circulated to those European research groups participating in the ENPADASI under the strategic research area of "diet-related chronic diseases." Information about raw data disposition and metadata sharing was requested. A set of minimal requirements was abstracted from the gathered information.Results: Studies (12 cohort, 12 cross-sectional, and 2 case-control) were identified. Two studies recruited children only and the rest recruited adults. All studies included dietary intake data. Twenty studies collected blood samples. Data on traditional biomarkers were available for 20 studies, of which 17 measured lipoproteins, glucose, and insulin and 13 measured inflammatory biomarkers. Metabolomics, proteomics, and genomics or transcriptomics data were available in 5, 3, and 12 studies, respectively. Although the study authors were willing to share metadata, most refused, were hesitant, or had legal or ethical issues related to sharing raw data. Forty-one descriptors of minimal requirements for the study data were identified to facilitate data integration.Conclusions

Excess sodium intake is associated with high blood pressure, a major risk factor for cardiovascular disease (CVD). It is unknown whether decreasing sodium intake to <2300 mg/d has an effect on CVD or all-cause mortality.The objective was to assess whether reductions in sodium intake to <2300 mg/d were associated with either an increased or a decreased risk of fatal and nonfatal CVD and all-cause mortality.This observational prospective study of the PREvención con DIeta MEDiterránea (PREDIMED) trial included 3982 participants at high CVD risk. Sodium intake was evaluated with a validated food-frequency questionnaire and categorized as low (<1500 mg/d), intermediate (?1500 to ?2300 mg/d), high (>2300 to ?3400 mg/d), or very high (>3400 mg/d). Subsequently, 1-y and 3-y changes in sodium intake were calculated. Multivariate relative risks were assessed by using Cox proportional hazards ratios. Marginal structural models with inverse probability weighting were used to test the effect of changes in sodium intake and the Mediterranean diet (MedDiet).We documented 125 CVD events and 131 deaths after a 4.8-y median follow-up. Sodium intake <2300 mg/d was associated with a lower risk of all-cause mortality: 48% (HR: 0.52; 95% CI: 0.30, 0.91; P = 0.02) and 49% (HR: 0.51; 95% CI: 0.26, 0.98; P = 0.04) after 1 and 3 y, respectively. Increasing sodium intake after 1 y was associated with a 72% (HR: 1.72; 95% CI: 1.01, 2.91; P = 0.04) higher risk of CVD events. The incidence rate of CVD was reduced for those who reduced their sodium intake and were randomly assigned to MedDiet interventions [4.1/10,000 (95% CI: 3.1, 8.0) compared with 4.4/10,000 (95% CI: 2.7, 12.4) person-years; P = 0.002].Decreasing sodium intake to <2300 mg/d was associated with a reduced risk of all-cause mortality

Some individuals with cardiovascular risk are unable to achieve even the lower internationally recommended level of physical activity (PA). We aimed to study the impact of a lower-than-advised level of PA on small artery vascular function and oxidative stress in overweight and obese postmenopausal women.Forty-seven overweight and obese postmenopausal women completed a 4-month program of 1-hour low-intensity PA for 2 days per week. Before and after the intervention, PA level (metabolic equivalent tasks/h/wk), endogenous antioxidant status (superoxide dismutase and erythrocyte lysate and glutathione peroxidase erythrocyte lysate concentrations, superoxide dismutase plasma and glutathione peroxidase plasma [GPXa] activities, and oxidized low-density lipoprotein), asymmetrical dimethylarginine concentrations, endothelial function by small artery reactive hyperemia index (saRHI), and resting heart rate (RHR) were assessed.After the intervention, a significant increase in GPXa and decreases in asymmetrical dimethylarginine concentrations and RHR (P < 0.001 for all) were observed. Increases in PA were positively associated with increases in saRHI (r = 0.330, P = 0.027) and GPXa (r = 0.299, P = 0.05) and a decrease in RHR (r = -0.297, P = 0.047). Multivariate analyses showed that the independent predictors of saRHI improvement were an increase in PA (? = 2.63; 95% CI, 1.24-4.19; P = 0.019), a decrease in RHR (? = 1.96; 95% CI, 1.01-5.03; P = 0.048), and an increase in GPXa (? = 2.64; 95% CI, 1.18-5.08; P = 0.021).Even low-intensity PA improves antioxidant capacity, RHR, and saRHI in postmenopausal women. Advising postmenopausal women to increase their PA at any level seems warranted based on our preliminary and hypothesis-generating data.

Low-carbohydrate diets have become increasingly popular for weight loss. Although they may improve some metabolic markers, particularly in type 2 diabetes mellitus (T2D) or the metabolic syndrome (MS), their net effect on arterial wall function remains unclear. The objective was to evaluate the relation between dietary macronutrient composition and the small artery reactive hyperaemia index (saRHI), a marker of small artery endothelial function, in a cohort of patients at increased cardiovascular (CV) risk. The present cross-sectional study included 247 patients. Diet was evaluated by a 3-d food-intake register and reduced to a novel low-carbohydrate diet score (LCDS). Physical examination, demographic, biochemical and anthropometry parameters were recorded, and the saRHI was measured in each patient. Individuals in the lowest LCDS quartile (Q1, 45 % carbohydrate; 20 % protein; 32 % fat) had higher saRHI values than those in the top quartile (Q4, 29 % carbohydrate, 24 % protein, 40 % fat; 1.66 (sd 0.41) v. 1.52 (sd 0.22), P= 0.037). These results were particularly strong in patients with the MS (Q1 = 1.82 (sd 0.32) v. Q4 = 1.61 (sd 027); P= 0.021) and T2D (Q1 = 1.78 (sd 0.31) v. Q4 = 1.62 (sd 0.35); P= 0.011). Multivariate analysis demonstrated that individuals in the highest LCDS quartile had a significantly negative coefficient of saRHI, which was independent of confounders (OR -0.85; 95 % CI 0.19, 0.92; P= 0.031). These findings suggest that a dietary pattern characterised by a low amount of carbohydrate, but high amounts of protein and fat, is associated with a poorer small artery vascular reactivity in patients with increased CV risk.

To describe clinical and epidemiological characteristics of patients with very high hypertriglyceridemia (HTG) who were attended in lipid units of the Spanish Society of Atherosclerosis (SEA).Patients of the HTG Registry of SEA with at least one triglyceride concentration greater than 1,000mg/dL (n=298, HTG severe group) and those whose baseline triglycerides were between 200 and 246mg/dL (HTG control group, n=272) were included.Patients with very high triglyceride levels were younger (46.9±11.5 years vs 52.7±13 years; p<0.0001), with a larger waist circumference (100.5±10.6cm vs 98.5±11.1cm; p=0.0426), higher alcohol intake (170.7±179.1g/wk vs 118.8±106.4g/wk; p=0,0473), active smoking status (45.6% vs 26.8%; p<0.0001) and a higher frequency of pancreatitis (10.2% vs 3%; p=0.0006) than HTG control group. There was a higher percentage of patients with atherogenic dietary pattern in severe HTG group compared with the control group (138 [46.3%] vs. 94 [34.5%]; p=0,001). The multivariate analysis showed that factors associated with a triglyceride concentration greater than 1,000mg/dl were age, male sex, weight, waist circumference, alcohol, physical inactivity in non-business hours and the presence of diabetes mellitus.Patients with very high HTG were usually men in the fourth decade of life, with abdominal obesity, smoking and alcohol consumption. In 60% of cases the HTG was primary, and pancreatitis the most frequently complication.Copyright © 2012 Elsevier España, S.L. and SEA. All rights reserved.

Es conegut que en les activitats de la construcció intervé el medi ambient, utilitzant els recursos extrets de l’escorça terrestre, per al que es requereixen grans quantitats d’energia, tant per a l’explotació dels recursos com en la transformació dels productes de construcció, depositant residus durant i al final del cicle de vida dels productes. (6) Els arquitectes i projectistes, considerats en ocasions gestors de recursos en el procés constructiu s’han de comprometre amb el medi ambient des del disseny i la selecció de productes de la construcció que generin menys impacte ambiental i que requereixin un menor consum energètic relacionat amb els processos al llarg de la seva vida. El sector de la construcció representa una de les activitats menys sostenibles del planeta: consumeix el 40% dels materials de l’economia global i genera entre el 40-50% de les emissions de gasos d’efecte hivernacle. El major impacte ambiental a dia d’avui, es genera durant la fase d’ús de l’edifici, degut al cost energètic per al seu condicionament tèrmic o estat de confort. (1) En aquest treball s’han calculat i donat diferents “eines”, que podrien ser útils per a una ponderació de la sostenibilitat en el cas que s’haguessin de comparar la construcció de diferents propostes arquitectòniques. Hem intentat dotar-nos d’eines de ponderació que, un cop verificades podríen introduir-se com a base de puntuació d’un concurs on es presenten diferents exemplars arquitectònics.