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1.
Nutrients ; 11(11)2019 Nov 13.
Artigo em Inglês | MEDLINE | ID: mdl-31766143

RESUMO

Leptin is a hormone crucial in the regulation of food intake and body-weight maintenance. However, the genes and gene variants that influence its plasma levels are still not well known. Results of studies investigating polymorphisms in candidate genes have been inconsistent, and, in addition, very few genome-wide association studies (GWAS) have been undertaken. Our aim was to investigate the genes and gene variants most associated with plasma leptin concentrations in a high-cardiovascular-risk Mediterranean population. We measured plasma leptin in 1011 men and women, and analyzed the genetic factors associated using three approaches: (1) Analyzing the single nucleotide polymorphisms (SNPs) reported in a GWAS meta-analysis in other populations (including an SNP in/near each of these LEP, SLC32A1, GCKR, CCNL, COBLL1, and FTO genes); (2) Investigating additional SNPs in/near those genes, also including the RLEP gene; and (3) Undertaking a GWAS to discover new genes. We did not find any statistically significant associations between the previously published SNPs and plasma leptin (Ln) in the whole population adjusting for sex and age. However, on undertaking an extensive screening of other gene variants in those genes to capture a more complete set of SNPs, we found more associations. Outstanding among the findings was the heterogeneity per sex. We detected several statistically significant interaction terms with sex for these SNPs in the candidate genes. The gene most associated with plasma leptin levels was the FTO gene in men (specifically the rs1075440 SNP) and the LEPR in women (specifically the rs12145690 SNP). In the GWAS on the whole population, we found several new associations at the p < 1 × 10-5 level, among them with the rs245908-CHN2 SNP (p = 1.6 × 10-6). We also detected a SNP*sex interaction at the GWAS significance level (p < 5 × 10-8), involving the SLIT3 gene, a gene regulated by estrogens. In conclusion, our study shows that the SNPs selected as relevant for plasma leptin levels in other populations, are not good markers for this Mediterranean population, so supporting those studies claiming a bias when generalizing GWAS results to different populations. These population-specific differences may include not only genetic characteristics, but also age, health status, and the influence of other environmental variables. In addition, we have detected several sex-specific effects. These results suggest that genomic analyses, involving leptin, should be estimated by sex and consider population-specificity for more precise estimations.

2.
Database (Oxford) ; 20192019 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-31665759

RESUMO

Habitual consumption of certain foods has shown beneficial and protective effects against multiple chronic diseases. However, it is not clear by which molecular mechanisms they may exert their beneficial effects. Multiple -omic experiments available in public databases have generated gene expression data following the treatment of human cells with different food nutrients and bioactive compounds. Exploration of such data in an integrative manner offers excellent possibilities for gaining insights into the molecular effects of food compounds and bioactive molecules at the cellular level. Here we present NutriGenomeDB, a web-based application that hosts manually curated gene sets defined from gene expression signatures, after differential expression analysis of nutrigenomics experiments performed on human cells available in the Gene Expression Omnibus (GEO) repository. Through its web interface, users can explore gene expression data with interactive visualizations. In addition, external gene signatures can be connected with nutrigenomics gene sets using a gene pattern-matching algorithm. We further demonstrate how the application can capture the primary molecular mechanisms of a drug used to treat hypertension and thus connect its mode of action with hosted food compounds.

3.
Atherosclerosis ; 290: 118-124, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31605877

RESUMO

BACKGROUND AND AIMS: Recent evidence suggests that postprandial hypertriglyceridemia (PPT) is associated with the incidence of CVD. Several non-modifiable factors (genetics, age, gender) and lifestyle factors (physical activity, smoking, regular alcohol) have shown their ability to modulate PPT. We evaluate the influence of regular alcohol intake, physical activity and smoking habit modulating PPT in the CORDIOPREV study (NCT00924937). METHODS: 1002 patients were subject to an oral fat load test meal and serial blood samples were drawn at 0, 1, 2, 3 and 4 h during postprandial state. A PPT concentration above 2.5 mmol/L (220 mg/dL) at any time point has been established as a detrimental response. Alcohol consumption was defined as non-drinkers, moderate and severe intake; regular physical activity exceeding than or lower than 1000 MET/week; smoking habit was classified in current, never, recent ex-smokers and long-term ex-smokers. RESULTS: The prevalence of undesirable PPT response was 68% in current, 58% in recent ex-smokers, 49% in long-term ex-smokers and 48% in never smokers (p < 0.001). Current and recent ex-smokers displayed higher PPT response as well as a greater area under the curve (AUC) and higher incremental (iAUC) of triglycerides (TG) compared with long-term ex-smokers and never smokers (p < 0.05), without differences among these subgroups. No differences were observed in the magnitude of PPT according to regular physical activity or alcohol intake habits. CONCLUSIONS: Smoking is an independent risk factor modulating the magnitude of PPT. However, after tobacco cessation, ex-smokers show a progressive decrease on their PPT to reach levels similar to those of never smokers.

4.
Mayo Clin Proc ; 94(11): 2178-2188, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31623843

RESUMO

OBJECTIVE: To assess the prospective association between ultra-processed food consumption and all-cause mortality and to examine the effect of theoretical iso-caloric non-processed foods substitution. PATIENTS AND METHODS: A population-based cohort of 11,898 individuals (mean age 46.9 years, and 50.5% women) were selected from the ENRICA study, a representative sample of the noninstitutionalized Spanish population. Dietary information was collected by a validated computer-based dietary history and categorized according to their degree of processing using NOVA classification. Total mortality was obtained from the National Death Index. Follow-up lasted from baseline (2008-2010) to mortality date or December 31th, 2016, whichever was first. The association between quartiles of consumption of ultra-processed food and mortality was analyzed by Cox models adjusted for the main confounders. Restricted cubic-splines were used to assess dose-response relationships when using iso-caloric substitutions. RESULTS: Average consumption of ultra-processed food was 385 g/d (24.4% of the total energy intake). After a mean follow-up of 7.7 years (93,599 person-years), 440 deaths occurred. The hazard ratio (and 95% CI) for mortality in the highest versus the lowest quartile of ultra-processed food consumption was 1.44 (95% CI, 1.01-2.07; P trend=.03) in percent of energy and 1.46 (95% CI, 1.04-2.05; P trend=.03) in grams per day per kilogram. Isocaloric substitution of ultra-processed food with unprocessed or minimally processed foods was associated with a significant nonlinear decrease in mortality. CONCLUSION: A higher consumption of ultra-processed food was associated with higher mortality in the general population. Furthermore, the theoretical iso-caloric substitution ultra-processed food by unprocessed or minimally processed foods would suppose a reduction of the mortality risk. If confirmed, these findings support the necessity of the development of new nutritional policies and guides at the national and international level. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01133093.

5.
Clin Epigenetics ; 11(1): 142, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31615550

RESUMO

BACKGROUND: Epigenome-wide association studies using DNA methylation have the potential to uncover novel biomarkers and mechanisms of cardiovascular disease (CVD) risk. However, the direction of causation for these associations is not always clear, and investigations to-date have often failed to replicate at the level of individual loci. METHODS: Here, we undertook module- and region-based DNA methylation analyses of incident CVD in the Women's Health Initiative (WHI) and Framingham Heart Study Offspring Cohort (FHS) in order to find more robust epigenetic biomarkers for cardiovascular risk. We applied weighted gene correlation network analysis (WGCNA) and the Comb-p algorithm to find methylation modules and regions associated with incident CVD in the WHI dataset. RESULTS: We discovered two modules whose activation correlated with CVD risk and replicated across cohorts. One of these modules was enriched for development-related processes and overlaps strongly with epigenetic aging sites. For the other, we showed preliminary evidence for monocyte-specific effects and statistical links to cumulative exposure to traditional cardiovascular risk factors. Additionally, we found three regions (associated with the genes SLC9A1, SLC1A5, and TNRC6C) whose methylation associates with CVD risk. CONCLUSIONS: In sum, we present several epigenetic associations with incident CVD which reveal disease mechanisms related to development and monocyte biology. Furthermore, we show that epigenetic modules may act as a molecular readout of cumulative cardiovascular risk factor exposure, with implications for the improvement of clinical risk prediction.

6.
Mol Nutr Food Res ; : e1900399, 2019 Sep 18.
Artigo em Inglês | MEDLINE | ID: mdl-31533195

RESUMO

SCOPE: A better understanding of factors contributing to interindividual variability in biomarkers of vitamin K can enhance the understanding of the equivocal role of vitamin K in cardiovascular disease. Based on the known biology of phylloquinone, the major form of vitamin K, it is hypothesized that plasma lipids contribute to the variable response of biomarkers of vitamin K metabolism to phylloquinone supplementation. METHODS AND RESULTS: The association of plasma lipids and 27 lipid-related genetic variants with the response of biomarkers of vitamin K metabolism is examined in a secondary analysis of data from a 3-year phylloquinone supplementation trial in men (n = 66) and women (n = 85). Year 3 plasma triglycerides (TG), but not total cholesterol, LDL-cholesterol, or HDL-cholesterol, are associated with the plasma phylloquinone response (men: ß = 1.01, p < 0.001, R2  = 0.34; women: ß = 0.61, p = 0.008, R2  = 0.11; sex interaction p = 0.077). Four variants and the TG-weighted genetic risk score are associated with the plasma phylloquinone response in men only. Plasma lipids are not associated with changes in biomarkers of vitamin K function (undercarboxylated osteocalcin and matrix gla protein) in either sex. CONCLUSION: Plasma TG are an important determinant of the interindividual response of plasma phylloquinone to phylloquinone supplementation, but changes in biomarkers of vitamin K carboxylation are not influenced by lipids.

7.
J Nutr ; 2019 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-31504696

RESUMO

BACKGROUND: Transcription factor 7-like 2 (TCF7L2) genetic variants that predispose individuals to type 2 diabetes (T2D) show inconsistent associations with anthropometric traits. Interaction between TCF7L2 genotypes and dietary factors may help explain these observations. OBJECTIVE: We aimed to examine the potential modulation of TCF7L2-rs7903146 and rs12255372 on anthropometric markers by a Mediterranean diet (MedDiet). METHODS: Cross-sectional analysis was conducted in 1120 participants (aged 45-75 y) of the Boston Puerto Rican Health Study. Anthropometric variables were measured, and polymorphisms were genotyped using standardized protocols. Diet was assessed using a validated FFQ. The MedDiet was defined based on adherence to 9 food and nutrient components using sex-specific population-based median cut-offs; high adherence was defined as meeting ≥4 components. Haplotypes were tested for association with obesity traits, independently and via interaction with the MedDiet. RESULTS: TCF7L2-rs7903146 showed significant interaction with the MedDiet influencing BMI, weight, and waist circumference. The T risk-allele carriers (CT + TT) with a high MedDiet score had lower weight (77.3 ± 1.0 compared with CC 80.9 ± 1.0 kg; P = 0.013) and waist circumference (99.2 ± 0.9 compared with CC 102.2 ± 0.9 cm; P = 0.021), when compared with CC participants. A low MedDiet score resulted in no significant differences between genotypes. For TCF7L2-rs12255372, we found significant interactions with the MedDiet for weight (P-interaction = 0.034) and BMI (P-interaction = 0.036). The T allele carriers with a higher MedDiet score showed a trend of lower but no significant differences when compared with CC participants for BMI (P = 0.19), weight (P = 0.09), and waist circumference (P = 0.11). We found significant interactions between the 2 risk-carrying haplotypes and the MedDiet compared with the common haplotype (GC), with lower BMI (ß ± SE, TT: -1.53 ± 0.68; P-interaction = 0.024), weight (TT: -4.16 ± 1.77; P-interaction = 0.019), and waist circumference (GT: -5.07 ± 2.50; P-interaction = 0.042) at a high MedDiet score. CONCLUSION: Puerto Ricans with the TCF7L2-rs7903146 and rs12255372 T2D risk genotypes, although still high, had better anthropometric profiles when adhering to a MedDiet, suggesting that this diet may offset unfavorable genetic predisposition.

8.
Mol Nutr Food Res ; 63(22): e1900226, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31432628

RESUMO

SCOPE: Insulin resistance (IR) and inflammation are hallmarks of type 2 diabetes (T2D). The nod-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a metabolic sensor activated by saturated fatty acids (SFA) initiating IL-1ß inflammation and IR. Interactions between SFA intake and NLRP3-related genetic variants may alter T2D risk factors. METHODS: Meta-analyses of six Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium (n = 19 005) tested interactions between SFA and NLRP3-related single-nucleotide polymorphisms (SNPs) and modulation of fasting insulin, fasting glucose, and homeostasis model assessment of insulin resistance. RESULTS: SFA interacted with rs12143966, wherein each 1% increase in SFA intake increased insulin by 0.0063 IU mL-1 (SE ± 0.002, p = 0.001) per each major (G) allele copy. rs4925663, interacted with SFA (ß ± SE = -0.0058 ± 0.002, p = 0.004) to increase insulin by 0.0058 IU mL-1 , per additional copy of the major (C) allele. Both associations are close to the significance threshold (p < 0.0001). rs4925663 causes a missense mutation affecting NLRP3 expression. CONCLUSION: Two NLRP3-related SNPs showed potential interaction with SFA to modulate fasting insulin. Greater dietary SFA intake accentuates T2D risk, which, subject to functional validation, may be further elaborated depending on NLRP3-related genetic variants.

9.
Adv Nutr ; 2019 08 06.
Artigo em Inglês | MEDLINE | ID: mdl-31386148

RESUMO

While conventional nutrition research has yielded biomarkers such as doubly labeled water for energy metabolism and 24-h urinary nitrogen for protein intake, a critical need exists for additional, equally robust biomarkers that allow for objective assessment of specific food intake and dietary exposure. Recent advances in high-throughput MS combined with improved metabolomics techniques and bioinformatic tools provide new opportunities for dietary biomarker development. In September 2018, the NIH organized a 2-d workshop to engage nutrition and omics researchers and explore the potential of multiomics approaches in nutritional biomarker research. The current Perspective summarizes key gaps and challenges identified, as well as the recommendations from the workshop that could serve as a guide for scientists interested in dietary biomarkers research. Topics addressed included study designs for biomarker development, analytical and bioinformatic considerations, and integration of dietary biomarkers with other omics techniques. Several clear needs were identified, including larger controlled feeding studies, testing a variety of foods and dietary patterns across diverse populations, improved reporting standards to support study replication, more chemical standards covering a broader range of food constituents and human metabolites, standardized approaches for biomarker validation, comprehensive and accessible food composition databases, a common ontology for dietary biomarker literature, and methodologic work on statistical procedures for intake biomarker discovery. Multidisciplinary research teams with appropriate expertise are critical to moving forward the field of dietary biomarkers and producing robust, reproducible biomarkers that can be used in public health and clinical research.

10.
BMJ ; 366: l4292, 2019 07 25.
Artigo em Inglês | MEDLINE | ID: mdl-31345923

RESUMO

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 in place of carbohydrate was associated with a higher risk of type 2 diabetes (hazard ratio 1.10, 95% confidence interval 1.01 to 1.19, I2=25.9%, τ2=0.006; per 5% of energy). Evidence of small study effects was detected for the overall association of polyunsaturated fat with the risk of type 2 diabetes, but not for the omega 6 polyunsaturated fat and monounsaturated fat associations. Significant interactions between dietary fat and polygenic risk score on the risk of type 2 diabetes (P>0.05 for interaction) were not observed. CONCLUSIONS: These data indicate that genetic burden and the quality of dietary fat are each associated with the incidence of type 2 diabetes. The findings do not support tailoring recommendations on the quality of dietary fat to individual type 2 diabetes genetic risk profiles for the primary prevention of type 2 diabetes, and suggest that dietary fat is associated with the risk of type 2 diabetes across the spectrum of type 2 diabetes genetic risk.


Assuntos
Diabetes Mellitus Tipo 2/epidemiologia , Diabetes Mellitus Tipo 2/etiologia , Dieta/efeitos adversos , Gorduras na Dieta/efeitos adversos , Adulto , Alelos , Diabetes Mellitus Tipo 2/genética , Feminino , Estudo de Associação Genômica Ampla , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Estudos Prospectivos , Fatores de Risco
11.
Diabetes Care ; 42(9): 1784-1791, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31213470

RESUMO

OBJECTIVE: We aimed to identify hemoglobin A1c (HbA1c)-associated genetic variants and examine their implications for glycemic status evaluated by HbA1c in U.S. Hispanics/Latinos with diverse genetic ancestries. RESEARCH DESIGN AND METHODS: We conducted a genome-wide association study (GWAS) of HbA1c in 9,636 U.S. Hispanics/Latinos without diabetes from the Hispanic Community Health Study/Study of Latinos, followed by a replication among 4,729 U.S. Hispanics/Latinos from three independent studies. RESULTS: Our GWAS and replication analyses showed 10 previously known and novel loci associated with HbA1c at genome-wide significance levels (P < 5.0 × 10-8). In particular, two African ancestry-specific variants, HBB-rs334 and G6PD-rs1050828, which are causal mutations for sickle cell disease and G6PD deficiency, respectively, had ∼10 times larger effect sizes on HbA1c levels (ß = -0.31% [-3.4 mmol/mol]) and -0.35% [-3.8 mmol/mol] per minor allele, respectively) compared with other HbA1c-associated variants (0.03-0.04% [0.3-0.4 mmol/mol] per allele). A novel Amerindian ancestry-specific variant, HBM-rs145546625, was associated with HbA1c and hematologic traits but not with fasting glucose. The prevalence of hyperglycemia (prediabetes and diabetes) defined using fasting glucose or oral glucose tolerance test 2-h glucose was similar between carriers of HBB-rs334 or G6PD-rs1050828 HbA1c-lowering alleles and noncarriers, whereas the prevalence of hyperglycemia defined using HbA1c was significantly lower in carriers than in noncarriers (12.2% vs. 28.4%, P < 0.001). After recalibration of the HbA1c level taking HBB-rs334 and G6PD-rs1050828 into account, the prevalence of hyperglycemia in carriers was similar to noncarriers (31.3% vs. 28.4%, P = 0.28). CONCLUSIONS: This study in U.S. Hispanics/Latinos found several ancestry-specific alleles associated with HbA1c through erythrocyte-related rather than glycemic-related pathways. The potential influences of these nonglycemic-related variants need to be considered when the HbA1c test is performed.

12.
J Nutr ; 149(8): 1377-1384, 2019 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-31162580

RESUMO

BACKGROUND: Commonly consumed mushrooms, portobello (PBM) and shiitake (SHM), are abundant in nutrients, soluble dietary fibers, and bioactive compounds that have been implicated as beneficial in reducing inflammation, improving lipid profiles, and ameliorating heart disease and atherosclerosis, an inflammatory disease of the arteries. OBJECTIVE: The aim of this study was to determine effects of PBM and SHM in preventing atherosclerosis and associated inflammation in an animal model. METHODS: Four-week-old Ldlr-/- male mice were divided into 5 dietary groups for 16 wk: a low-fat control (LF-C, 11 kcal% fat), high-fat control (HF-C, 18.9 kcal% fat), HF + 10% (wt:wt) PBM (HF-PBM, 19.5 kcal% fat) or SHM (HF-SHM, 19.7 kcal% fat) powder, and HF + mushroom control mix (MIX-C, 19.6 kcal% fat), a diet best matched to the average macronutrient content of both mushrooms. Body composition was measured using MRI. Aortic tricuspid valves and aortas were collected and stained to quantify plaque formation. Adhesion molecule expression was quantified by immunohistochemistry. Plasma lipid and cytokine concentrations were measured. RESULTS: We found that mice fed a HF-SHM diet had ∼86% smaller aortic lesion area than mice in both HF-C (P < 0.01) and MIX-C (P < 0.01) groups and also expressed 31-48% lower vascular cell adhesion molecule-1 levels (P < 0.05) than all other groups. Similarly, HF-PBM-fed mice displayed a 70% reduction in aortic lesion area in the tricuspid valve only (P < 0.05). Both mushroom-fed groups had lower weight gain and fat mass (P < 0.05) than the control groups. CONCLUSION: These results suggest that consumption of PBMs and particularly SHMs is effective in preventing development of high-fat diet-induced atherosclerosis in Ldlr-/- mice. Future studies will determine active components in mushrooms responsible for this beneficial effect.

13.
Eur J Clin Invest ; 49(8): e13146, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31166609

RESUMO

BACKGROUND: We try to explore whether long-term consumption of two healthy dietary patterns (low-fat [LF] diet or Mediterranean diet [MedDiet]) interacts with the apolipoprotein E (APOE) single-nucleotide polymorphisms (SNPs: rs439401, rs440446 and rs7412) modulating postprandial hypertriglyceridemia (ppHTG) in coronary heart disease (CHD) patients. METHODS AND RESULTS: We selected patients from the CORDIOPREV study with genotyping and who underwent an oral fat load test (FLT) at baseline and after 3 years follow-up (n = 506). After 3 years of follow-up, we found a gene-diet interaction between the APOE rs439401 SNP and MedDiet. Specifically, T-allele carriers in the MedDiet group showed a more significant decrease in postprandial triglycerides (TG: P = 0.03) and large triacylglycerol-rich lipoproteins (TRLs) TG (large TRLs TG; P = 0.01) compared with CC subjects. Consistently, the area under the curve of TG (AUC-TG; P-interaction = 0.03) and AUC-large TRLs TG (P-interaction = 0.02) were significantly lower in T-allele carriers compared with CC subjects. CONCLUSIONS: The long-term consumption of a MedDiet modulates ppHTG through APOE genetic variants in CHD patients. This gene-diet interaction may contribute to a more precise dietary advice in CHD patients.

14.
Artigo em Inglês | MEDLINE | ID: mdl-31132092

RESUMO

BACKGROUND: Ultra-processed food intake has been associated with chronic conditions and mortality. The aim of this study was to assess the relationship between ultra-processed food intake and incident frailty in community-dwelling older adults. METHODS: Prospective cohort study with 1,822 individuals aged ≥60 who were recruited during 2008-2010 in Spain. At baseline, food consumption was obtained using a validated computerized face-to-face dietary history. Ultra-processed foods were identified according to the nature and extent of their industrial processing (NOVA classification). In 2012, incident frailty was ascertained based on Fried's criteria. Statistical analyses were performed with logistic regression and adjusted for the main potential confounders. RESULTS: After a mean follow-up of 3.5 years, 132 cases of frailty were identified. The fully adjusted risks of frailty across increasing quartiles of the percentage of total energy intake from ultra-processed foods were: 0.04 (0.02-0.05), 0.05 (0.03-0.07), 0.09 (0.07-0.12), and 0.11 (0.08-0.14). Results were similar when food consumption was expressed as gram per day/body weight. Regarding ultra-processed food groups, the highest versus the lowest tertiles of consumption of yogurts and fermented milks, cakes and pastries, as well as non-alcoholic beverages (instant coffee and cocoa, packaged juices, and other non-alcoholic drinks, excluding soft drinks) were also significantly related to incident frailty. CONCLUSIONS: Consumption of ultra-processed foods is strongly associated with frailty risk in older adults. Substituting unprocessed or minimally processed foods for ultra-processed foods would play an important role in the prevention of age-related frailty.

15.
J Nutr ; 149(7): 1116-1121, 2019 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-31070756

RESUMO

BACKGROUND: Dietary intervention (DI) is a primary strategy to attenuate some of the metabolic abnormalities associated with metabolic syndrome (MetS), including low HDL cholesterol. There is no biomarker that can identify individuals who respond to DI by increasing HDL cholesterol. OBJECTIVE: The aim of this study was to assess the predictive power of a genetic predisposition score (GPS) in Mexican adults with MetS to identify HDL cholesterol responders to DI. METHODS: This study followed a prospective cohort design. Sixty-seven Mexican adults aged 20-60 y (21% men) with BMI ≥25 and ≤39.9 kg/m², who had at least 3 of 5 positive criteria for MetS, were included. Participants consumed a low saturated fat diet for 2.5 mo (<7% energy as saturated fat, <200 mg of cholesterol/d) and reduced their usual diet by ∼440 kcal/d, a reduction in total energy intake of about 25%. Anthropometry and serum biochemical markers, including HDL cholesterol, were measured before and after DI. A multilocus GPS was constructed using previously reported genetic variants associated with response to diet in subjects with MetS. GPS values, designed to predict the response of HDL cholesterol to the DI, were computed for each individual as the sum of the number of effect alleles across 14 SNPs. RESULTS: Individuals were dichotomized as high and low GPS according to median GPS (-2.12) and we observed a difference in HDL cholesterol changes on DI of +3 mg/dL (6.3%) in subjects with low GPS, whereas those with high GPS had HDL cholesterol decreases of -3 mg/dL (-7.9%) (P = 0.04). CONCLUSIONS: Individuals with low GPS showed greater increases in their HDL cholesterol than those with high GPS. Therefore, the GPS can be useful for predicting the HDL cholesterol response to diet.

16.
Clin Nutr ; 2019 Feb 21.
Artigo em Inglês | MEDLINE | ID: mdl-30852029

RESUMO

AIM: Our objective was to investigate the role of two healthy diets in modulating the risk of type 2 diabetes (T2DM) development associated with each prediabetes diagnosis criteria in coronary heart disease patients. Additionally, we explored the pathophysiological characteristics and the risk of developing T2DM in patients with different prediabetes criteria. METHODS: We included 462 patients from the CORDIOPREV study without T2DM at baseline: 213 had prediabetes defined by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (PreDM-IFG/IGT); 180 had prediabetes by isolated hemoglobin glycated plasma levels (PreDM-isolated-HbA1c), and 69 were not prediabetics (non-PreDM), according to the American Diabetes Association criteria. Patients were randomized to consume either a Mediterranean or a low-fat diet. We performed a COX proportional hazards regression analysis to determine the T2DM risk according to diet and the prediabetes criteria after a median follow-up of 60 months. RESULTS: We found higher T2DM risk (HR: 2.98; 95% CI 1.27-6.98) in PreDM-IFG/IGT than in PreDM-isolated-HbA1c (HR: 2.31; 95% CI 0.97-5.49) compared with non-PreDM. Long-term consumption of a low-fat diet was associated with a lower risk of T2DM when compared to the Mediterranean diet in the PreDM-IFG/IGT group (HR: 3.20; 95% CI 0.75-13.69 versus HR: 4.70; 95% CI 1.12-19.67, respectively). Moreover, we found the highest risk of T2DM development associated with patients who had both IFG and IGT (HR: 2.15; 95% CI 1.11-4.16). Patients who had both IFG and IGT and consumed a low-fat diet had a lower T2DM risk than those who consumed a Mediterranean diet (HR: 1.53; 95% CI 0.53-4.39 versus HR: 3.33; 95% CI 1.34-8.30, respectively). CONCLUSION: Our results suggest that the type of diet consumed may modulate the risk of T2DM development according to the prediabetes diagnosis criteria. Specifically, our study showed that the consumption of a low-fat diet was more beneficial than a Mediterranean diet in patients with IFG and IGT. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.govNCT00924937.

17.
Nutrients ; 11(1)2019 Jan 04.
Artigo em Inglês | MEDLINE | ID: mdl-30621171

RESUMO

Although, for decades, increased serum bilirubin concentrations were considered a threatening sign of underlying liver disease and had been associated with neonatal jaundice, data from recent years show that bilirubin is a powerful antioxidant and suggest that slightly increased serum bilirubin concentrations are protective against oxidative stress-related diseases, such as cardiovascular diseases. Therefore, a better understanding of the gene-diet interactions in determining serum bilirubin concentrations is needed. None of the previous genome-wide association studies (GWAS) on bilirubin concentrations has been stratified by sex. Therefore, considering the increasing interest in incorporating the gender perspective into nutritional genomics, our main aim was to carry out a GWAS on total serum bilirubin concentrations in a Mediterranean population with metabolic syndrome, stratified by sex. Our secondary aim was to explore, as a pilot study, the presence of gene-diet interactions at the GWAS level. We included 430 participants (188 men and 242 women, aged 55⁻75 years, and with metabolic syndrome) in the PREDIMED Plus-Valencia study. Global and sex-specific GWAS were undertaken to analyze associations and gene-diet interaction on total serum bilirubin. Adherence (low and high) to the Mediterranean diet (MedDiet) was analyzed as the dietary modulator. In the GWAS, we detected more than 55 SNPs associated with serum bilirubin at p < 5 × 10-8 (GWAS level). The top-ranked were four SNPs (rs4148325 (p = 9.25 × 10-24), rs4148324 (p = 9.48 × 10-24), rs6742078 (p = 1.29 × 10-23), rs887829 (p = 1.39 × 10-23), and the rs4148324 (p = 9.48 × 10-24)) in the UGT1A1 (UDP glucuronosyltransferase family 1 member A1) gene, which replicated previous findings revealing the UGT1A1 as the major locus. In the sex-specific GWAS, the top-ranked SNPs at the GWAS level were similar in men and women (the lead SNP was the rs4148324-UGT1A1 in both men (p = 4.77 × 10-11) and women (p = 2.15 × 10-14), which shows homogeneous genetic results for the major locus. There was more sex-specific heterogeneity for other minor genes associated at the suggestive level of GWAS significance (p < 1 × 10-5). We did not detect any gene-MedDiet interaction at p < 1 × 10-5 for the major genetic locus, but we detected some gene-MedDiet interactions with other genes at p < 1 × 10-5, and even at the GWAS level for the IL17B gene (p = 3.14 × 10-8). These interaction results, however, should be interpreted with caution due to our small sample size. In conclusion, our study provides new data, with a gender perspective, on genes associated with total serum bilirubin concentrations in men and women, and suggests possible additional modulations by adherence to MedDiet.


Assuntos
Bilirrubina/sangue , Estudo de Associação Genômica Ampla , Síndrome Metabólica/sangue , Idoso , Estudos Transversais , Dieta , Dieta Mediterrânea , Feminino , Genótipo , Glucuronosiltransferase/genética , Humanos , Estilo de Vida , Desequilíbrio de Ligação/genética , Masculino , Região do Mediterrâneo , Pessoa de Meia-Idade , Nutrigenômica/métodos , Projetos Piloto , Polimorfismo de Nucleotídeo Único/genética , Fatores Sexuais
18.
J Am Coll Cardiol ; 73(2): 134-144, 2019 01 22.
Artigo em Inglês | MEDLINE | ID: mdl-30654884

RESUMO

BACKGROUND: Sleep duration and quality have been associated with increased cardiovascular risk. However, large studies linking objectively measured sleep and subclinical atherosclerosis assessed in multiple vascular sites are lacking. OBJECTIVES: The purpose of this study was to evaluate the association of actigraphy-measured sleep parameters with subclinical atherosclerosis in an asymptomatic middle-aged population, and investigate interactions among sleep, conventional risk factors, psychosocial factors, dietary habits, and inflammation. METHODS: Seven-day actigraphic recording was performed in 3,974 participants (age 45.8 ± 4.3 years; 62.6% men) from the PESA (Progression of Early Subclinical Atherosclerosis) study. Four groups were defined: very short sleep duration <6 h, short sleep duration 6 to 7 h, reference sleep duration 7 to 8 h, and long sleep duration >8 h. Sleep fragmentation index was defined as the sum of the movement index and fragmentation index. Carotid and femoral 3-dimensional vascular ultrasound and cardiac computed tomography were performed to quantify noncoronary atherosclerosis and coronary calcification. RESULTS: When adjusted for conventional risk factors, very short sleep duration was independently associated with a higher atherosclerotic burden with 3-dimensional vascular ultrasound compared to the reference group (odds ratio: 1.27; 95% confidence interval: 1.06 to 1.52; p = 0.008). Participants within the highest quintile of sleep fragmentation presented a higher prevalence of multiple affected noncoronary territories (odds ratio: 1.34; 95% confidence interval: 1.09 to 1.64; p = 0.006). No differences were observed regarding coronary artery calcification score in the different sleep groups. CONCLUSIONS: Lower sleeping times and fragmented sleep are independently associated with an increased risk of subclinical multiterritory atherosclerosis. These results highlight the importance of healthy sleep habits for the prevention of cardiovascular disease.


Assuntos
Aterosclerose/etiologia , Sono , Actigrafia , Adulto , Dieta , Feminino , Humanos , Inflamação , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Fatores de Risco , Privação do Sono/complicações
19.
Nutrients ; 11(1)2018 Dec 20.
Artigo em Inglês | MEDLINE | ID: mdl-30577445

RESUMO

Precision nutrition aims to make dietary recommendations of a more personalized nature possible, to optimize the prevention or delay of a disease and to improve health. Therefore, the characteristics (including sex) of an individual have to be taken into account as well as a series of omics markers. The results of nutritional genomics studies are crucial to generate the evidence needed so that precision nutrition can be applied. Although sex is one of the fundamental variables for making recommendations, at present, the nutritional genomics studies undertaken have not analyzed, systematically and with a gender perspective, the heterogeneity/homogeneity in gene-diet interactions on the different phenotypes studied, thus there is little information available on this issue and needs to be improved. Here we argue for the need to incorporate the gender perspective in nutritional genomics studies, present the general context, analyze the differences between sex and gender, as well as the limitations to measuring them and to detecting specific sex-gene or sex-phenotype associations, both at the specific gene level or in genome-wide-association studies. We analyzed the main sex-specific gene-diet interactions published to date and their main limitations and present guidelines with recommendations to be followed when undertaking new nutritional genomics studies incorporating the gender perspective.


Assuntos
Dieta/métodos , Nutrigenômica/métodos , Fenômenos Fisiológicos da Nutrição/genética , Medicina de Precisão/métodos , Fatores Sexuais , Feminino , Identidade de Gênero , Humanos , Masculino , Estado Nutricional , Fenótipo , Caracteres Sexuais
20.
Artigo em Inglês | MEDLINE | ID: mdl-30377248

RESUMO

BACKGROUND: Some of the previously reported health benefits of low-to-moderate alcohol consumption may derive from health status influencing alcohol consumption rather than the opposite. We examined whether health status changes influence changes in alcohol consumption, cessation included. METHODS: Data came from 571 current drinkers aged ≥60 years participating in the Seniors-ENRICA cohort in Spain. Participants were recruited in 2008-2010 and followed-up for 8.2 years, with four waves of data collection. We assessed health status using a 52-item deficit accumulation (DA) index with four domains: functional, self-rated health and vitality, mental health, and morbidity and health services use. To minimise reverse causation, we examined how changes in health status over a 3-year period (wave 0-wave 1) influenced changes in alcohol consumption over the subsequent 5 years (waves 1-3) using linear/logistic regression, as appropriate. RESULTS: Compared with participants in the lowest tertile of DA change (mean absolute 4.3% health improvement), those in the highest tertile (7.8% worsening) showed a reduction in alcohol intake (ß: -4.32 g/day; 95% CI -7.00 to -1.62; p trend=0.002) and were more likely to quit alcohol (OR: 2.80; 95% CI 1.54 to 5.08; p trend=0.001). The main contributors to decreasing drinking were increased functional impairment and poorer self-rated health, whereas worsening self-rated health, onset of diabetes or stroke and increased prevalence of hospitalisation influenced cessation. CONCLUSIONS: Health deterioration is related to a subsequent reduction and cessation of alcohol consumption contributing to the growing evidence challenging the protective health effect previously attributed to low-to-moderate alcohol consumption.

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