Biological Rhythms, Chrono-Nutrition, and Gut Microbiota: Epigenomics Insights for Precision Nutrition and Metabolic Health.

Circadian rhythms integrate a finely tuned network of biological processes recurring every 24 h, intricately coordinating the machinery of all cells. This self-regulating system plays a pivotal role in synchronizing physiological and behavioral responses, ensuring an adaptive metabolism within the environmental milieu, including dietary and physical activity habits. The systemic integration of circadian homeostasis involves a balance of biological rhythms, each synchronically linked to the central circadian clock. Central to this orchestration is the temporal dimension of nutrient and food intake, an aspect closely interwoven with the neuroendocrine circuit, gut physiology, and resident microbiota. Indeed, the timing of meals exerts a profound influence on cell cycle regulation through genomic and epigenetic processes, particularly those involving gene expression, DNA methylation and repair, and non-coding RNA activity. These (epi)genomic interactions involve a dynamic interface between circadian rhythms, nutrition, and the gut microbiota, shaping the metabolic and immune landscape of the host. This research endeavors to illustrate the intricate (epi)genetic interplay that modulates the synchronization of circadian rhythms, nutritional signaling, and the gut microbiota, unravelling the repercussions on metabolic health while suggesting the potential benefits of feed circadian realignment as a non-invasive therapeutic strategy for systemic metabolic modulation via gut microbiota. This exploration delves into the interconnections that underscore the significance of temporal eating patterns, offering insights regarding circadian rhythms, gut microbiota, and chrono-nutrition interactions with (epi)genomic phenomena, thereby influencing diverse aspects of metabolic, well-being, and quality of life outcomes.

A Pilot Study of Dietetic, Phenotypic, and Genotypic Features Influencing Hypertensive Disorders of Pregnancy in Women with Pregestational Diabetes Mellitus.

Hypertensive disorders of pregnancy (HDP) are a leading cause of maternal and perinatal morbimortality. Dietetic, phenotypic, and genotypic factors influencing HDP were analyzed during a nutrigenetic trial in Rio de Janeiro, Brazil (2016-2020). Pregnant women with pregestational diabetes mellitus (n = 70) were randomly assigned to a traditional or DASH diet group. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured during prenatal visits and HDP were diagnosed using international criteria. Phenotypic data were obtained from medical records and personal interviews. Genotyping for FTO and ADRB2 polymorphisms used RT-PCR. Linear mixed-effect models and time-to-event analyses were performed. The variables with significant effect on the risk for progression to HDP were: black skin color (adjusted hazard ratio [aHR] 8.63, p = 0.01), preeclampsia in previous pregnancy (aHR 11.66, p < 0.01), SBP ≥ 114 mmHg in the third trimester (aHR 5.56, p 0.04), DBP ≥ 70 mmHg in the first trimester (aHR 70.15, p = 0.03), mean blood pressure > 100 mmHg (aHR 18.42, p = 0.03), and HbA1c ≥ 6.41% in the third trimester (aHR 4.76, p = 0.03). Dietetic and genotypic features had no significant effect on the outcome, although there was limited statistical power to test both.

Crosstalk between Gut Microbiota and Epigenetic Markers in Obesity Development: Relationship between Ruminococcus, BMI, and MACROD2/SEL1L2 Methylation.

Changes in gut microbiota composition and in epigenetic mechanisms have been proposed to play important roles in energy homeostasis, and the onset and development of obesity. However, the crosstalk between epigenetic markers and the gut microbiome in obesity remains unclear. The main objective of this study was to establish a link between the gut microbiota and DNA methylation patterns in subjects with obesity by identifying differentially methylated DNA regions (DMRs) that could be potentially regulated by the gut microbiota. DNA methylation and bacterial DNA sequencing analysis were performed on 342 subjects with a BMI between 18 and 40 kg/m2. DNA methylation analyses identified a total of 2648 DMRs associated with BMI, while ten bacterial genera were associated with BMI. Interestingly, only the abundance of Ruminococcus was associated with one BMI-related DMR, which is located between the MACROD2/SEL1L2 genes. The Ruminococcus abundance negatively correlated with BMI, while the hypermethylated DMR was associated with reduced MACROD2 protein levels in serum. Additionally, the mediation test showed that 19% of the effect of Ruminococcus abundance on BMI is mediated by the methylation of the MACROD2/SEL1L2 DMR. These findings support the hypothesis that a crosstalk between gut microbiota and epigenetic markers may be contributing to obesity development.

Associations Between Eating Speed, Diet Quality, Adiposity, and Cardiometabolic Risk Factors.

OBJECTIVE: To assess the associations between eating speed, adiposity, cardiometabolic risk factors, and diet quality in a cohort of Spanish preschool-children. STUDY DESIGN: A cross-sectional study in 1371 preschool age children (49% girls; mean age, 4.8 ± 1.0 years) from the Childhood Obesity Risk Assessment Longitudinal Study (CORALS) cohort was conducted. After exclusions, 956 participants were included in the analyses. The eating speed was estimated by summing the total minutes used in each of the 3 main meals and then categorized into slow, moderate, or fast. Multiple linear and logistic regression models were fitted to assess the ß-coefficient, or OR and 95% CI, between eating speed and body mass index, waist circumference, fat mass index (FMI), blood pressure, fasting plasma glucose, and lipid profile. RESULTS: Compared with participants in the slow-eating category, those in the fast-eating category had a higher prevalence risk of overweight/obesity (OR, 2.9; 95% CI, 1.8-4.4; P < .01); larger waist circumference (ß, 2.6 cm; 95% CI, 1.5-3.8 cm); and greater FMI (ß, 0.3 kg/m2; 95% CI, 0.1-0.5 kg/m2), systolic blood pressure (ß, 2.8 mmHg; 95% CI, 0.6-4.9 mmHg), and fasting plasma glucose levels (ß, 2.7 mg/dL, 95% CI, 1.2-4.2 mg/dL) but lower adherence to the Mediterranean diet (ß, -0.5 points; 95% CI, -0.9 to -0.1 points). CONCLUSIONS: Eating fast is associated with higher adiposity, certain cardiometabolic risk factors, and lower adherence to a Mediterranean diet. Further long-term and interventional studies are warranted to confirm these associations.

The Role of Nutrition on Meta-inflammation: Insights and Potential Targets in Communicable and Chronic Disease Management.

PURPOSE OF REVIEW: Chronic low-grade inflammation may contribute to the onset and progression of communicable and chronic diseases. This review examined the effects and eventual mediation roles of different nutritional factors on inflammation. RECENT FINDINGS: Potential nutritional compounds influencing inflammation processes include macro and micronutrients, bioactive molecules (polyphenols), specific food components, and culinary ingredients as well as standardized dietary patterns, eating habits, and chrononutrition features. Therefore, research in this field is still required, taking into account critical aspects of heterogeneity including type of population, minimum and maximum intakes and adverse effects, cooking methods, physiopathological status, and times of intervention. Moreover, the integrative analysis of traditional variables (age, sex, metabolic profile, clinical history, body phenotype, habitual dietary intake, physical activity levels, and lifestyle) together with individualized issues (genetic background, epigenetic signatures, microbiota composition, gene expression profiles, and metabolomic fingerprints) may contribute to the knowledge and prescription of more personalized treatments aimed to improving the precision medical management of inflammation as well as the design of anti-inflammatory diets in chronic and communicable diseases.

Holistic Integration of Omics Tools for Precision Nutrition in Health and Disease.

The combination of multiple omics approaches has emerged as an innovative holistic scope to provide a more comprehensive view of the molecular and physiological events underlying human diseases (including obesity, dyslipidemias, fatty liver, insulin resistance, and inflammation), as well as for elucidating unique and specific metabolic phenotypes. These omics technologies include genomics (polymorphisms and other structural genetic variants), epigenomics (DNA methylation, histone modifications, long non-coding RNA, telomere length), metagenomics (gut microbiota composition, enterotypes), transcriptomics (RNA expression patterns), proteomics (protein quantities), and metabolomics (metabolite profiles), as well as interactions with dietary/nutritional factors. Although more evidence is still necessary, it is expected that the incorporation of integrative omics could be useful not only for risk prediction and early diagnosis but also for guiding tailored dietary treatments and prognosis schemes. Some challenges include ethical and regulatory issues, the lack of robust and reproducible results due to methodological aspects, the high cost of omics methodologies, and high-dimensional data analyses and interpretation. In this review, we provide examples of system biology studies using multi-omics methodologies to unravel novel insights into the mechanisms and pathways connecting the genotype to clinically relevant traits and therapy outcomes for precision nutrition applications in health and disease.

FTO and ADRB2 Genetic Polymorphisms Are Risk Factors for Earlier Excessive Gestational Weight Gain in Pregnant Women with Pregestational Diabetes Mellitus: Results of a Randomized Nutrigenetic Trial.

Excessive gestational weight gain (GWG) is associated with increased risk of maternal and neonatal complications. We investigated obesity-related polymorphisms in the FTO gene (rs9939609, rs17817449) and ADRB2 (rs1042713, rs1042714) as candidate risk factors concerning excessive GWG in pregnant women with pregestational diabetes. This nutrigenetic trial, conducted in Brazil, randomly assigned 70 pregnant women to one of the groups: traditional diet (n = 41) or DASH diet (n = 29). Excessive GWG was the total weight gain above the upper limit of the recommendation, according to the Institute of Medicine guidelines. Genotyping was performed using real-time PCR. Time-to-event analysis was performed to investigate risk factors for progression to excessive GWG. Regardless the type of diet, AT carriers of rs9939609 (FTO) and AA carriers of rs1042713 (ADRB2) had higher risk of earlier exceeding GWG compared to TT (aHR 2.44; CI 95% 1.03-5.78; p = 0.04) and GG (aHR 3.91; CI 95% 1.12-13.70; p = 0.03) genotypes, respectively, as the AG carriers for FTO haplotype rs9939609:rs17817449 compared to TT carriers (aHR 1.79; CI 95% 1.04-3.06; p = 0.02).

Cardiorespiratory Fitness and Muscular Strength Moderates the Relationship between FNDC5 Polymorphism and Adiposity in Children and Adolescents.

The human locus FNDC5 rs16835198 contributes positively to anthropometric phenotypes in children and adolescents. However, the role of specific components of physical fitness in this relationship is not known. The present study aimed to verify the moderator role of cardiorespiratory fitness (CRF) and muscular strength in the relationship between rs16835198 polymorphism FNDC5 and adiposity in children and adolescents. This cross-sectional study was carried out by genotyping the rs16835198 FNDC5 polymorphism in 1701 children and adolescents (mean age 11.73 ± 2.75 years). Obesity was assessed using waist circumference and body mass index (BMI) z-scores. To evaluate CRF and muscular strength, the 6 min run/walk test and lower limb strength (LLS) were used. Linear regression models were applied, and all analyses were adjusted for age, sex, skin color, living area, and school type. A significant interaction term for CRF (p = 0.038) and LLS (p = 0.040) × rs16835198 FNDC5 with WC was identified. Regarding BMI, a significant interaction term for CRF (p = 0.007) and LLS (p = 0.044) × rs16835198 FNDC5 was observed. Moreover, medium and high CRF and LLS levels protected against higher WC and BMI. In conclusion, adiposity levels of children and adolescents with a genetic predisposition to obesity might be modified by improving CRF and muscular strength.

Proinflammatory and Hepatic Features Related to Morbidity and Fatal Outcomes in COVID-19 Patients.

OBJECTIVE: to screen putative associations between liver markers and proinflammatory-related features concerning infectious morbidity and fatal outcomes in COVID-19 patients. METHODS: a total of 2094 COVID-19 positive patients from the COVID-DATA-SAFE-LIFES cohort (HM hospitals consortium) were classified according to median values of hepatic, inflammatory, and clinical indicators. Logistic regression models were fitted and ROC cures were generated to explain disease severity and mortality. RESULTS: intensive care unit (ICU) assistance plus death outcomes were associated with liver dysfunction, hyperinflammation, respiratory insufficiency, and higher associated comorbidities. Four models including age, sex, neutrophils, D-dimer, oxygen saturation lower than 92%, C-reactive protein (CRP), Charlson Comorbidity Index (CCI), FIB-4 and interactions with CRP, neutrophils, and CCI explained ICU plus death variance in more than 28%. The predictive values of ROC curves were: FIB-4 (0.7339), AST/ALT ratio (0.7107), CRP (0.7003), CCI index (0.6778), neutrophils (0.6772), and platelets (0.5618) concerning ICU plus death outcomes. CONCLUSIONS: the results of this research revealed that liver and proinflammatory features are important determinants of COVID-19 morbidity and fatal outcomes, which could improve the current understanding of the COVID-19 physiopathology as well as to facilitate the clinical management and therapy decision-making of this disease under a personalized medicine scope.

Precision nutrition based on phenotypical traits and the (epi)genotype: nutrigenetic and nutrigenomic approaches for obesity care.

PURPOSE OF REVIEW: The purpose of this article is to rationally review and critically appraise the current knowledge in the most relevant nongenetic and genetic factors influencing obesity predisposition. This information may be translated into the implementation of personalized nutrition approaches involving precision nutrigenetic and nutrigenomic strategies for obesity monitoring and weight management. RECENT FINDINGS: The importance and influence of several nongenetic contributors to obesity onset and individual responses to weight-loss interventions have been highlighted including the role of age, sex or perinatal feeding and others related to an individual's lifestyle and modifiable. Nutrigenetic studies have analysed potential interactions between polymorphisms influencing energy homeostasis/body composition and dietary factors in relation to adiposity phenotypes and therapy responsiveness. A second approach comprises the Nutrigenomic analysis of gene expression modifications in response to the consumption of specific nutrients or dietary bioactive compounds, which may involve epigenetic mechanisms including deoxyribonucleic acid methylation and micro-ribonucleic acid expression profiles. SUMMARY: Taken together, these findings encompass the importance of taking into account up-to-date advances in Nutrigenetic and Nutrigenomic hallmarks, globally analysing the risk of weight gain and related outcomes after following nutrition counselling, this contributing to improve obesity care considering phenotypical traits and the genetic make-up for precision obesity care.

Diet-induced obesity in animal models: points to consider and influence on metabolic markers.

Overweight and obesity are a worldwide public health problem. Obesity prevalence has increased considerably, which indicates the need for more studies to better understand these diseases and related complications. Diet induced-obesity (DIO) animal models can reproduce human overweight and obesity, and there are many protocols used to lead to excess fat deposition. So, the purpose of this review was to identify the key points for the induction of obesity through diet, as well as identifying which are the necessary endpoints to be achieved when inducing fat gain. For this, we reviewed the literature in the last 6 years, looking for original articles that aimed to induce obesity through the diet. All articles evaluated should have a control group, in order to verify the results found, and had worked with Sprague-Dawley and Wistar rats, or with C57BL-/-6 mice strain. Articles that induced obesity by other methods, such as genetic manipulation, surgery, or drugs were excluded, since our main objective was to identify key points for the induction of obesity through diet. Articles in humans, in cell culture, in non-rodent animals, as well as review articles, articles that did not have obesity induction and book chapters were also excluded. Body weight and fat gain, as well as determinants related to inflammation, hormonal concentration, blood glycemia, lipid profile, and liver health, must be evaluated together to better determination of the development of obesity. In addition, to select the best model in each circumstance, it should be considered that each breed and sex respond differently to diet-induced obesity. The composition of the diet and calorie overconsumption are also relevant to the development of obesity. Finally, it is important that a non-obese control group is included in the experimental design.

Kefir and Intestinal Microbiota Modulation: Implications in Human Health.

In the last decades changes in the pattern of health and disease in Latin America and in the world has been observed, with an increase in cases of chronic non-communicable diseases. Changes in intestinal microbiota composition can contribute to the development of these diseases and be useful in their management. In this context, the consumption of fermented foods with probiotic properties, such as kefir, stands out due to its gut microbiota-modulating capacity. There is an increasing interest in the commercial use of kefir since it can be marketed as a natural beverage containing health-promoting bacteria and has been gaining international popularity in Latin America. Also the consumption of these drinks in Latin America seems to be even more relevant, given the socioeconomic situation of this population, which highlights the need for disease prevention at the expense of its treatment. In this narrative review, we discuss how kefir may work against obesity, diabetes mellitus, liver disease, cardiovascular disorders, immunity, and neurological disorders. Peptides, bioactive compounds and strains occurring in kefir, can modulate gut microbiota composition, low-grade inflammation and intestinal permeability, which consequently may generate health benefits. Kefir can also impact on the regulation of organism homeostasis, with a direct effect on the gut-brain axis, being a possible strategy for the prevention of metabolic diseases. Further studies are needed to standardize these bioactive compounds and better elucidate the mechanisms linking kefir and intestinal microbiota modulation. However, due to the benefits reported, low cost and ease of preparation, kefir seems to be a promising approach to prevent and manage microbiota-related diseases in Latin America and the rest of the world.

Epigenetic signatures underlying inflammation: an interplay of nutrition, physical activity, metabolic diseases, and environmental factors for personalized nutrition.

AIM AND OBJECTIVE: Emerging translational evidence suggests that epigenetic alterations (DNA methylation, miRNA expression, and histone modifications) occur after external stimuli and may contribute to exacerbated inflammation and the risk of suffering several diseases including diabetes, cardiovascular diseases, cancer, and neurological disorders. This review summarizes the current knowledge about the harmful effects of high-fat/high-sugar diets, micronutrient deficiencies (folate, manganese, and carotenoids), obesity and associated complications, bacterial/viral infections, smoking, excessive alcohol consumption, sleep deprivation, chronic stress, air pollution, and chemical exposure on inflammation through epigenetic mechanisms. Additionally, the epigenetic phenomena underlying the anti-inflammatory potential of caloric restriction, n-3 PUFA, Mediterranean diet, vitamin D, zinc, polyphenols (i.e., resveratrol, gallic acid, epicatechin, luteolin, curcumin), and the role of systematic exercise are discussed. METHODS: Original and review articles encompassing epigenetics and inflammation were screened from major databases (including PubMed, Medline, Science Direct, Scopus, etc.) and analyzed for the writing of the review paper. CONCLUSION: Although caution should be exercised, research on epigenetic mechanisms is contributing to understand pathological processes involving inflammatory responses, the prediction of disease risk based on the epigenotype, as well as the putative design of therapeutic interventions targeting the epigenome.

Impact of APOE Alleles-by-Diet Interactions on Glycemic and Lipid Features- A Cross-Sectional Study of a Cohort of Type 2 Diabetes Patients from Western Mexico: Implications for Personalized Medicine.

PURPOSE: To analyze clinically relevant interactions between the apolipoprotein E (APOE) ε2, ε3 and ε4 alleles and nutritional factors on glycemic control and lipid levels in a cohort of type 2 diabetes (T2D) patients from western Mexico. PATIENTS AND METHODS: In this cross-sectional study of the cohort of T2D patients, a total of 224 individuals were selected for interaction studies. Clinical and anthropometric data were obtained from pre-designed medical records. Dietary intake was assessed by validated three-day food consumption records. Biochemical measurements were determined by automated methods. APOE genotyping was performed by a real-time allelic discrimination assay. Gene-diet interactions were tested by corrected multiple linear regression analyses, which were adjusted by potential confounding factors such as age, sex, energy intake, BMI and anti-hyperglycemic therapy (Metformin, Glibenclamide or Insulin), and years with T2D. RESULTS: Seventy-six percent of patients with T2D were on Metformin therapy. The frequencies of the APOE alleles were ε2 (5.8%), ε3 (74.1%) and ε4 (20.1%). After statistical settings, significant APOE alleles-by-diet interactions in relation to the metabolic profile were found. Interestingly, higher blood levels of total cholesterol (p int. = 0.016), non-HDL-c (p int. = 0.024), and LDL-c (p int. = 0.030) were found only in carriers of the APOE ε2 allele with a low consumption of MUFA. In contrast, carriers of the APOE ε4 allele with a high ω-6:ω-3 PUFA ratio in the diet had higher %HbA1c blood concentrations (p int. = 0.035). CONCLUSION: This study suggests a differential metabolic impact of APOE alleles on lipid/glycemic phenotypes depending on the dietary intake, with important potential implications in the personalized medicine and nutritional management of patients with type 2 diabetes mellitus.

Exploring Host Genetic Polymorphisms Involved in SARS-CoV Infection Outcomes: Implications for Personalized Medicine in COVID-19.

OBJECTIVE: To systematically explore genetic polymorphisms associated with the clinical outcomes in SARS-CoV infection in humans. METHODS: This comprehensive literature search comprised available English papers published in PubMed/Medline and SCOPUS databases following the PRISMA-P guidelines and PICO/AXIS criteria. RESULTS: Twenty-nine polymorphisms located in 21 genes were identified as associated with SARS-CoV susceptibility/resistance, disease severity, and clinical outcomes predominantly in Asian populations. Thus, genes implicated in key pathophysiological processes such as the mechanisms related to the entry of the virus into the cell and the antiviral immune/inflammatory responses were identified. CONCLUSIONS: Although caution must be taken, the results of this systematic review suggest that multiple genetic polymorphisms are associated with SARS-CoV infection features by affecting virus pathogenesis and host immune response, which could have important applications for the study and understanding of genetics in SARS-CoV-2/COVID-19 and for personalized translational clinical practice depending on the population studied and associated environments.

PPARGC1A Gene Promoter Methylation as a Biomarker of Insulin Secretion and Sensitivity in Response to Glucose Challenges.

Methylation in CpG sites of the PPARGC1A gene (encoding PGC1-α) has been associated with adiposity, insulin secretion/sensitivity indexes and type 2 diabetes. We assessed the association between the methylation profile of the PPARGC1A gene promoter gene in leukocytes with insulin secretion/sensitivity indexes in normoglycemic women. A standard oral glucose tolerance test (OGTT) and an abbreviated version of the intravenous glucose tolerance test (IVGTT) were carried out in n = 57 Chilean nondiabetic women with measurements of plasma glucose, insulin, and C-peptide. Bisulfite-treated DNA from leukocytes was evaluated for methylation levels in six CpG sites of the proximal promoter of the PPARGC1A gene by pyrosequencing (positions -816, -783, -652, -617, -521 and -515). A strong correlation between the DNA methylation percentage of different CpG sites of the PPARGC1A promoter in leukocytes was found, suggesting an integrated epigenetic control of this region. We found a positive association between the methylation levels of the CpG site -783 with the insulin sensitivity Matsuda composite index (rho = 0.31; p = 0.02) derived from the OGTT. The CpG hypomethylation in the promoter position -783 of the PPARGC1A gene in leukocytes may represent a biomarker of reduced insulin sensitivity after the ingestion of glucose.

Changes of Physical Activity and Ultra-Processed Food Consumption in Adolescents from Different Countries during Covid-19 Pandemic: An Observational Study.

AIM: to describe physical activity and ultra-processed foods consumption, their changes and sociodemographic predictors among adolescents from countries in Europe (Italy and Spain) and Latin America (Brazil, Chile, and Colombia) during the SARS-CoV-2-pandemic period. METHODS: Cross-sectional study via web survey. International Physical Activity Questionnaire (IPAQ) and weekly ultra-processed food consumption data were used. To compare the frequencies of physical activity status with sociodemographic variables, a multinomial logistic and a multiple logistic regression for habitual ultra-processed foods was performed. In final models, p < 0.05 was considered significant. RESULTS: Sample of 726 adolescents, mostly females (59.6%) aged 16-19 years old (54.3%). Adolescents from Latin America presented odds ratio (OR) 2.98 (CI 95% 1.80-4.94) of being inactive and those whose mothers had higher level of education were less active during lockdown [OR 0.40 (CI 95% 0.20-0.84)]. The habitual ultra-processed consumption was also high during this period in all countries, and more prevalent in Latin America. CONCLUSION: A higher prevalence of inactivity was observed in this population, but reductions of physical activity and habitual ultra-processed consumption during the pandemic were more pronounced in Latin America. Our findings reinforce the importance of promoting a healthy lifestyle, i.e., exercise and diet, during periods of social isolation.

Influence of FTO (Fat mass and obesity) gene and parental obesity on Brazilian children and adolescents adiposity.

Objectives Evaluate the influence of the genetic variant rs9939609 of the FTO gene on anthropometric characteristics and whether parental obesity is related to children and adolescents being overweight. Methods A total of 2,364 children and adolescents between 6 and 17 years old were genotyped and the lipid profile, plasma glucose level, and anthropometric characteristics were measured to assess adiposity. Results The AA genotype (risk) was associated with higher body mass index (BMI Z-score; p = 0.006), waist circumference (WC; p = 0.001), and triglycerides (p = 0.033). The association of the participants' adiposity characteristics with the parents' BMI and FTO genotypes showed an association of the BMI Z-score when either the mother or father was overweight or obese (p = 0.028 and p = 0.029). In the overweight or obese father/eutrophic mother, we also observe an association of FTO rs9939609 with WC (p = 0.039). The effect of these variables on the risk of obesity was also tested: overweight or obese mother (OR = 1.82, p = 0.041), overweight and obese parents (OR = 3.09, p < 0.0001), and FTO rs9939609 AA genotype (OR = 2.08, p = 0.0004) were associated. With regard to altered WC and high body fat percentage (BF%), either overweight or obese parents (OR = 2.39, p < 0.0001; OR = 1.92, p < 0.002) showed an association. The FTO rs9939609 AA genotype (OR = 1.99, p = 0.0002) was associated with altered WC. Conclusions The results show that parental weight also contributes to obesity and may interact with the FTO genetic make-up.

Food consumption by degree of processing and cardiometabolic risk: a systematic review.

Processed and ultra-processed foods (UPF) consumption has been associated with development of noncommunicable chronic diseases (NCD). This systematic review aims to summarise and discuss evidence of the relationship between food consumption according to degree of food processing and cardiometabolic risk. Data search was conducted in databases as PubMed, Bireme and Science Direct until July 2018. Studies have shown a positive association of UPF consumption with excess body weight, hypertension, dyslipidemia and metabolic syndrome features. However, disparities found in the studies analysed regarding dietary assessment, confounding factors and differences in food classifications makes comparisons between studies difficult. In conclusion, current evidences indicate the need to monitor UPF intake in global population. However, more studies are necessary to interpret better these associations with similar methodologies used in the studies. As well as longitudinal analyses can help to improve comparisons between outcomes and establish cause-effect relationship between UPF intake and cardiometabolic risk.

Biochemical profile, eating habits, and telomere length among Brazilian children and adolescents.

OBJECTIVES: Lifestyle, obesity, and eating habits are emerging as determinants for the instability of telomeres. The increase in childhood and adolescent obesity and the association of biochemical profiles and dietary components with telomere length (TL) makes it an important issue in nutritional research. The aim of the present study was to investigate TL and its association with ethnic background, adiposity, clinical and biochemical parameters, and dietary patterns among Brazilian children and adolescents. METHODS: A cross-sectional study encompassing 981 children and adolescents between 7 and 17 y of age was performed. Dietary intake habits, anthropometry, and clinical data were collected. TL analysis was performed by quantitative polymerase chain reaction. RESULTS: Children presented significantly longer TL than adolescents (P = 0.046). Participants who self-declared as black, mulatto, or brown (P < 0.001) also showed longer TL than those who were white. Regarding biochemical parameters, individuals with altered glucose levels had shorter TL than normoglycemic participants in the total sample (P = 0.014). Such difference remained statistically significant in adolescents (P = 0.019). Participants who reported eating fruits and vegetables regularly had longer TL than those who did not (P < 0.001). CONCLUSION: The results suggested that both biochemical parameters and the intake of antioxidant-rich food, such as fruits and vegetables, are associated with the stability of telomere biology among young Brazilians.