Informing Evidence-based Practice in Nutritional Genomics: An Educational Needs Assessment of Nutrition Care Providers in Canada.

Purpose: To investigate why Canadian nutrition care providers choose, or not, to integrate nutritional genomics into practice, and to evaluate the nutritional genomics training/education experiences and needs of nutrition providers in Canada, while comparing those of dietitians to non-dietitians.Methods: A cross-sectional online survey was distributed across Canada from June 2021 to April 2022.Results: In total, 457 healthcare providers (HCPs) [n = 371 dietitians (81.2%)] met the inclusion criteria. The majority (n = 372; 82.1%) reported having no experience offering nutritional genomics to clients (n = 4 did not respond). Of the 81 respondents with experience (17.9%), the most common reason to integrate nutrigenetic testing into practice was the perception that clients would be more motivated to change their eating habits (70.4%), while the most common reason for not integrating such tests was the perception that the nutrigenetic testing process is too complicated (n = 313; 84.1%). Dietitians were more likely than non-dietitians to view existing scientific evidence as an important educational topic (p = 0.002). The most selected useful educational resource by all HCPs was clinical practice guidelines (n = 364; 85.4%).Conclusions: Both dietitians and non-dietitians express a desire for greater nutritional genomics training/education; specific educational needs differ by type of HCP. Low implementation of nutrigenetic testing may be partly attributed to other identified barriers.

Homocysteine, blood pressure and gene-diet interactions in relation to vascular function measures of black South Africans.

BACKGROUND AND AIMS: We investigated circulating homocysteine (Hcy), a cardiovascular disease (CVD) risk factor, examining its dietary associations to provide personalized nutrition advice. This study addressed the inadequacy of current dietary interventions to ultimately address the disproportionately high incidence of CVD in Black populations. METHODS AND RESULTS: Cross-sectional analyses of 1,867 Black individuals of the PURE-SA study allowed the identification of dietary intake and cardiovascular measure interactions on three sub-categories: (1) normal blood pressure (BP), hypertension or Hcy-related hypertension (H-type), (2) low, normal or high Hcy concentrations, and (3) Hcy-related genetic combinations. Favorable body composition, but adverse dietary intake and cardiovascular determinants, were observed in higher Hcy categories. H-types, compared to regular hypertensives, had higher alcohol and lower macronutrient and micronutrient consumption. Inverse associations with carotid-radial pulse wave velocity were evident between monounsaturated fatty acid (FA) consumption and H-type hypertension as well as polyunsaturated FA and CBS883/ins68 TT carriers. Energy intake was positively associated with vascular cell adhesion molecule-1 (VCAM-1) in variant CBST883C/ins68 and CBS9276 GG carriers. VCAM-1 was also positively associated with plant protein intake in CBS9276 GG and MTR2756 AA carriers and negatively with total protein intake and CBS9276 GG carriers. Alcohol intake was positively associated with intercellular adhesion molecule-1 in MTR2756 minor allele carriers. CONCLUSION: Because Hcy gene-diet interactions are evident, personalized nutrition, by adjusting diets based on genetic profiles (e.g., CBS and MTR variations) and dietary interactions (e.g., FAs and proteins), can enhance cardiovascular outcomes by managing Hcy and related hypertension in genetically susceptible individuals.

Community pharmacy professionals' knowledge, attitude, and practice toward nutrition and lifestyle counseling in Gondar City, Ethiopia.

Background: Community pharmacy professionals play a vital role in health care, have a greater impact on public health programs, and play a critical role in patient counseling for both non-pharmacological and pharmacological management. This study aimed to evaluate the knowledge, attitude, and practice of community pharmacy professionals toward nutrition and lifestyle counseling in Gondar City, Ethiopia. Methods: A cross-sectional survey was undertaken in Northwestern Ethiopia from May to June 2021. Face-to-face structured interviews were performed to collect data using a specially created questionnaire. Descriptive, independent t-test, and one-way ANOVA analyses were used. A significant difference was defined as a p-value of less than 0.05. Results: This survey drew 100 community pharmacy professional from a pool of 105 participants, with a 95.2% response rate. More than a third of the participants (n = 43, 43%) defined medical nutrition therapy as the use of food to prevent disease, and almost half of the participants (n = 51, 51%) viewed therapeutic nutrition to be part of their job responsibilities. More than half (64%) believe that patients should be provided a combination of nutritional and pharmacological treatments in the majority of cases. The majority of participants (75%) gave patients counseling on drug-food interactions. Conclusion: The majority of community pharmacy professionals said they knew a lot about medical nutrition therapy and were enthusiastic about nutrition evaluation and medical nutrition therapy, they see these tasks as part of their job, and they practiced dietary counseling that was limited to pregnancy and chronic diseases.

Host genetics and nutrition.

Optimal nutrition is essential for health and physiological performance. Nutrition-related diseases such as obesity and diabetes are major causes of death and reduced quality of life in modern Western societies. Thanks to combining nutrigenetics and nutrigenomics, genomic nutrition allows the study of the interaction between nutrition, genetics and physiology. Currently, interrelated multi-genetic and multifactorial phenotypes are studied from a multiethnic and multi-omics approach, step by step identifying the important role of pathways, in addition to those directly related to metabolism. It allows the progressive identification of genetic profiles associated with specific susceptibilities to diet-related phenotypes, which may facilitate individualised dietary recommendations to improve health and quality of life.

Effect of ADORA2A Gene Polymorphism and Acute Caffeine Supplementation on Hormonal Response to Resistance Exercise: A Double-Blind, Crossover, Placebo-Controlled Study.

Previous studies have reported that TT genotype carriers of the adenosine A2a receptor (ADORA2A) gene rs5751876 polymorphism have better ergogenic and anti-inflammatory responses to caffeine intake compared to C allele carriers. The aim of the present study was twofold: (1) to investigate the association of the ADORA2A rs5751876 polymorphism with acute caffeine supplementation on hormonal (growth hormone and testosterone) response to resistance exercise (RE); (2) to examine the relationship between the rs5751876 polymorphism and the resting levels of growth hormone and testosterone in athletes who are light caffeine consumers. A double-blind, crossover, placebo-controlled study involving 30 resistance-trained men (age 21.7 ± 4.1) was conducted to assess the impact of caffeine supplementation on serum growth hormone (GH) and testosterone (TS) levels before, immediately after, and 15 min post-RE. One hour before engaging in resistance exercise, subjects were randomly administered 6 mg of caffeine per kg of body mass or a placebo (maltodextrin). After a 7-day washout period, the same protocol was repeated. Resting testosterone and growth hormone levels were examined in the sera of 94 elite athletes (31 females, age 21.4 ± 2.8; 63 males, age 22.9 ± 3.8). Caffeine consumption led to significantly greater increases in GH and TS in men with the TT genotype compared to C allele carriers. Furthermore, in the group of athletes, carriers of the TT genotype had significantly higher testosterone (p = 0.0125) and growth hormone (p = 0.0365) levels compared to C allele carriers. In conclusion, the ADORA2A gene rs5751876 polymorphism may modify the effect of caffeine intake on the hormonal response to exercise.

Integrated Analysis of Genomic and Genome-Wide Association Studies Identified Candidate Genes for Nutrigenetic Studies in Flavonoids and Vascular Health: Path to Precision Nutrition for (Poly)phenols.

Flavonoids exert vasculoprotective effects in humans, but interindividual variability in their action has also been reported. This study aims to identify genes that are associated with vascular health effects of flavonoids and whose polymorphisms could explain interindividual variability in response to their intake. Applying the predetermined literature search criteria, we identified five human intervention studies reporting positive effects of flavonoids on vascular function together with global genomic changes analyzed using microarray methods. Genes involved in vascular dysfunction were identified from genome-wide association studies (GWAS). By extracting data from the eligible human intervention studies, we obtained 5807 differentially expressed genes (DEGs). The number of identified upstream regulators (URs) varied across the studies, from 227 to 1407. The search of the GWAS Catalog revealed 493 genes associated with vascular dysfunction. An integrative analysis of transcriptomic data with GWAS genes identified 106 candidate DEGs and 42 candidate URs, while subsequent functional analyses and a search of the literature identified 20 top priority candidate genes: ALDH2, APOE, CAPZA1, CYP11B2, GNA13, IL6, IRF5, LDLR, LPL, LSP1, MKNK1, MMP3, MTHFR, MYO6, NCR3, PPARG, SARM1, TCF20, TCF7L2, and TNF. In conclusion, this integrated analysis identifies important genes to design future nutrigenetic studies for development of precision nutrition for polyphenols.

Nutrigenetic and Epigenetic Mechanisms of Maternal Nutrition-Induced Glucolipid Metabolism Changes in the Offspring.

Maternal nutrition during pregnancy regulates the offspring's metabolic homeostasis, including insulin sensitivity and the metabolism of glucose and lipids. The fetus undergoes a crucial period of plasticity in the uterus; metabolic changes in the fetus during pregnancy caused by maternal nutrition not only influence fetal growth and development but also have a long-term or even life-long impact for the offspring. Epigenetic modifications, such as DNA methylation, histone modification, and non-coding RNAs, play important roles in intergenerational and transgenerational effects. In this context, this narrative review comprehensively summarizes and analyzes the molecular mechanisms underlying how maternal nutrition, including a high-fat diet, polyunsaturated fatty acid diet, methyl donor nutrient supplementation, feed restriction, and protein restriction during pregnancy, impacts the genes involved in glucolipid metabolism in the liver, adipose tissue, hypothalamus, muscle, and oocytes of the offspring in terms of the epigenetic modifications. This will provide a foundation for the further exploration of nutrigenetic and epigenetic mechanisms for integrative mother-child nutrition and promotion of the offspring's health through the regulation of maternal nutrition during pregnancy. Note: This paper is part of the Nutrition Reviews Special Collection on Precision Nutrition.

Exploring genetic variants in congenital monosaccharide-disaccharide metabolism: Carrier ratios and phenotypic insights.

OBJECTIVES: Adverse food reactions, often underestimated, encompass congenital monosaccharide-disaccharide metabolism disorders, yielding diverse outcomes such as abdominal pain, diarrhea, bleeding disorders, and even death. This study retrospectively scrutinized genetic variants linked to these disorders in a cohort subjected to whole-exome sequence analysis (WES), determining carrier frequencies and genotype-phenotype correlations. METHODS: Data from 484 patients, were retrospectively analyzed using a gene panel (ALDOB, FBP1, GALE, GALK1, GALM, GALT, LCT, SLC2A2, SLC5A1, SI) for congenital monosaccharide-disaccharide metabolism disorders. WES was performed on patients using the xGen Exome Research Panel v2 kit, utilizing Next Generation Sequence Analysis (NGS). The study encompassed pathogenic, likely pathogenic, and variant of uncertain significance (VUS) variants. RESULTS: Among 484 patients (244 female, 240 male), 17.35% carried 99 variants (67 distinct) in the analyzed genes. Pathogenic/likely pathogenic allele frequency stood at 0.013, while VUS allele frequency was 0.088. Notably, 44% (37/84) of patients harboring mutations manifested at least one relevant phenotype. Carriage frequencies ranged from 1:25 (SI gene) to 1:968 (GALE gene), with the estimated disease frequency spanning from 1:2500 to 1:3748000. CONCLUSIONS: Our study underscores clinical manifestations in heterozygous carriers of recessive genetic disorders, addressing gaps in carrier frequencies and phenotypic effects for congenital monosaccharide-disaccharide metabolism disorders. This knowledge can improve these conditions' diagnosis and management, potentially preventing adverse food reactions and their associated complications.

FTO rs9939609: T>A Variant and Physical Inactivity as Important Risk Factors for Class III Obesity: A Cross-Sectional Study.

BACKGROUND: The prevalence of obesity has been increasing worldwide. It has been reported that physiological and environmental factors such as diet, culture, physical activity, and genetics are the principal factors related to obesity. The fat mass and obesity-associated (FTO) gen variant (rs9939609: T>A) has been associated with class III obesity. The A variant has been correlated with anthropometric and metabolic alterations. Therefore, the purpose of this study was to analyze the association of the FTO rs9939609: T>A variant and environmental factors with clinical, anthropometric, and biochemical variables in subjects with class III obesity. RESULTS: The A variant frequency was higher in the class III obesity group compared with the normal weight group (44% vs. 25%, p < 0.001). Subjects with the AA genotype had a higher body mass index (BMI) than those with the AT genotype (35.46 kg/m2 (31-39.8) vs. 26.91 kg/m2 (23.7-30), p = 0.005). Women with the AA genotype showed higher waist circumferences than the AT group (101.07 cm (90.9-111.1) vs. 85.45 cm (77-93.8) p = 0.047). The FTO A variant increases the risk by 3.54 times and physical inactivity increases the risk by 6.37 times for class III obesity. CONCLUSIONS: Our results suggest that among the studied variables, those most related to class III obesity were the FTO risk genotype (A allele) and physical inactivity.

The role of interaction between vitamin D and VDR FokI gene polymorphism (rs2228570) in sleep quality of adults.

To evaluate association of vitamin D with sleep quality in adults and the influence of VDR-gene polymorphism FokI (rs2228570;A > G). Cross-sectional population-based study in adults, conducted in Brazil. The outcome was sleep-quality, evaluated by the Pittsburgh Sleep Quality Index. Vitamin D was determined by indirect electrochemiluminescence and classified as deficiency (VDD), 25(OH)D < 20 ng/mL in a healthy population or 25(OH)D < 30 ng/mL for groups at risk for VDD. FokI polymorphism in the VDR-gene was genotyped by qPCR and classified as homozygous wild (FF or AA), heterozygous (Ff or AG), or homozygous mutant (ff or GG). Multivariate logistic analysis was used to estimate the association between vitamin D and FokI polymorphism with sleep-quality. In a total of 1674 individuals evaluated, 53.6% had poor-sleep-quality, 31.5% had VDD, and the genotype frequency of the FokI polymorphism was 9.9% FF, 44.6% Ff, and 45.5% ff. In multivariate analysis, individuals with VDD had 1.51 times the chance of poor-sleep-quality, and individuals with the ff genotype had 1.49 times the chance of poor-sleep-quality (OR:1.49;95%CI:1.05-2.12) when compared to individuals with the FF or Ff genotype. In the combined analysis, individuals with VDD and ff genotype had more chance of poor-sleep-quality than individuals with sufficient vitamin D and genotype Ff or FF (OR:2.19;95%CI:1.27-3.76). Our data suggest that VDD and VDR FokI gene polymorphism are associated with poor-sleep-quality, and combining the two factors increases the chance of poor-sleep-quality compared to separate groups.

Understanding and applying gene-environment interactions: a guide for nutrition professionals with an emphasis on integration in African research settings.

Noncommunicable diseases (NCDs) are influenced by the interplay between genetics and environmental exposures, particularly diet. However, many healthcare professionals, including nutritionists and dietitians, have limited genetic background and, therefore, they may lack understanding of gene-environment interactions (GxEs) studies. Even researchers deeply involved in nutrition studies, but with a focus elsewhere, can struggle to interpret, evaluate, and conduct GxE studies. There is an urgent need to study African populations that bear a heavy burden of NCDs, demonstrate unique genetic variability, and have cultural practices resulting in distinctive environmental exposures compared with Europeans or Americans, who are studied more. Although diverse and rapidly changing environments, as well as the high genetic variability of Africans and difference in linkage disequilibrium (ie, certain gene variants are inherited together more often than expected by chance), provide unparalleled potential to investigate the omics fields, only a small percentage of studies come from Africa. Furthermore, research evidence lags behind the practices of companies offering genetic testing for personalized medicine and nutrition. We need to generate more evidence on GxEs that also considers continental African populations to be able to prevent unethical practices and enable tailored treatments. This review aims to introduce nutrition professionals to genetics terms and valid methods to investigate GxEs and their challenges, and proposes ways to improve quality and reproducibility. The review also provides insight into the potential contributions of nutrigenetics and nutrigenomics to the healthcare sphere, addresses direct-to-consumer genetic testing, and concludes by offering insights into the field's future, including advanced technologies like artificial intelligence and machine learning.

Genotype-based precision nutrition strategies for the prediction and clinical management of type 2 diabetes mellitus.

Globally, type 2 diabetes mellitus (T2DM) is one of the most common metabolic disorders. T2DM physiopathology is influenced by complex interrelationships between genetic, metabolic and lifestyle factors (including diet), which differ between populations and geographic regions. In fact, excessive consumptions of high fat/high sugar foods generally increase the risk of developing T2DM, whereas habitual intakes of plant-based healthy diets usually exert a protective effect. Moreover, genomic studies have allowed the characterization of sequence DNA variants across the human genome, some of which may affect gene expression and protein functions relevant for glucose homeostasis. This comprehensive literature review covers the impact of gene-diet interactions on T2DM susceptibility and disease progression, some of which have demonstrated a value as biomarkers of personal responses to certain nutritional interventions. Also, novel genotype-based dietary strategies have been developed for improving T2DM control in comparison to general lifestyle recommendations. Furthermore, progresses in other omics areas (epigenomics, metagenomics, proteomics, and metabolomics) are improving current understanding of genetic insights in T2DM clinical outcomes. Although more investigation is still needed, the analysis of the genetic make-up may help to decipher new paradigms in the pathophysiology of T2DM as well as offer further opportunities to personalize the screening, prevention, diagnosis, management, and prognosis of T2DM through precision nutrition.

PNPLA3 Genotype and Dietary Fat Modify Concentrations of Plasma and Fecal Short Chain Fatty Acids and Plasma Branched-Chain Amino Acids.

The GG genotype of the Patatin-like phosphatase domain-containing 3 (PNPLA3), dietary fat, short-chain fatty acids (SCFA) and branched-chain amino acids (BCAA) are linked with non-alcoholic fatty liver disease. We studied the impact of the quality of dietary fat on plasma (p) and fecal (f) SCFA and p-BCAA in men homozygous for the PNPLA3 rs738409 variant (I148M). Eighty-eight randomly assigned men (age 67.8 ± 4.3 years, body mass index 27.1 ± 2.5 kg/m2) participated in a 12-week diet intervention. The recommended diet (RD) group followed the National and Nordic nutrition recommendations for fat intake. The average diet (AD) group followed the average fat intake in Finland. The intervention resulted in a decrease in total p-SCFAs and iso-butyric acid in the RD group (p = 0.041 and p = 0.002). Valeric acid (p-VA) increased in participants with the GG genotype regardless of the diet (RD, 3.6 ± 0.6 to 7.0 ± 0.6 µmol/g, p = 0.005 and AD, 3.8 ± 0.3 to 9.7 ± 8.5 µmol/g, p = 0.015). Also, genotype relation to p-VA was seen statistically significantly in the RD group (CC: 3.7 ± 0.4 to 4.2 ± 1.7 µmol/g and GG: 3.6 ± 0.6 to 7.0 ± 0.6 µmol/g, p = 0.0026 for time and p = 0.004 for time and genotype). P-VA, unlike any other SCFA, correlated positively with plasma gamma-glutamyl transferase (r = 0.240, p = 0.025). Total p-BCAAs concentration changed in the AD group comparing PNPLA3 CC and GG genotypes (CC: 612 ± 184 to 532 ± 149 µmol/g and GG: 587 ± 182 to 590 ± 130 µmol/g, p = 0.015 for time). Valine decreased in the RD group (p = 0.009), and leucine decreased in the AD group (p = 0.043). RD decreased total fecal SCFA, acetic acid (f-AA), and butyric acid (f-BA) in those with CC genotype (p = 0.006, 0.013 and 0.005, respectively). Our results suggest that the PNPLA3 genotype modifies the effect of dietary fat modification for p-VA, total f-SCFA, f-AA and f-BA, and total p-BCAA.

A genomics perspective of personalized prevention and management of obesity.

This review discusses the landscape of personalized prevention and management of obesity from a nutrigenetics perspective. Focusing on macronutrient tailoring, we discuss the impact of genetic variation on responses to carbohydrate, lipid, protein, and fiber consumption. Our bioinformatic analysis of genomic variants guiding macronutrient intake revealed enrichment of pathways associated with circadian rhythm, melatonin metabolism, cholesterol and lipoprotein remodeling and PPAR signaling as potential targets of macronutrients for the management of obesity in relevant genetic backgrounds. Notably, our data-based in silico predictions suggest the potential of repurposing the SYK inhibitor fostamatinib for obesity treatment in relevant genetic profiles. In addition to dietary considerations, we address genetic variations guiding lifestyle changes in weight management, including exercise and chrononutrition. Finally, we emphasize the need for a refined understanding and expanded research into the complex genetic landscape underlying obesity and its management.

Investigation of the Relationship Between Serum Low-Density Lipoprotein Cholesterol Levels with Genetic Polymorphisms, Gut Microbiota, and Nutrition.

Background: To prevent cardiovascular disease (CVD), it is important to determine the factors that are associated with its development. High serum low-density lipoprotein (LDL) cholesterol (LDL-C) levels are a modifiable prevention and treatment target known to contribute to the development of CVD, but the factors affecting blood cholesterol levels, including LDL-C, remain controversial. Objective: In this study, the factors (genetic, nutritional, and gut microbiota) thought to be effective on serum LDL-C levels were discussed from a holistic perspective, and the effects of the relationship between these factors on LDL-C levels were examined. Methods: The study was carried out with 609 adults (48% male) who applied to a private health institution between 2016 and 2022. Results: It was observed that serum LDL-C levels were positively correlated with body mass index (BMI) (P = 0.000) and different ApoE alleles had significant effects on LDL-C levels. It was observed that the highest LDL-C levels were in the ɛ4+ group, followed by ɛ3+ and ɛ2+ groups, respectively (P = 0.000). Results showed that dietary cholesterol and fiber consumption did not significantly affect serum LDL-C levels (P = 0.705 and P = 0.722, respectively). It was also observed that enterotypes and the butyrate synthesis potential of intestinal microbiota did not cause significant changes in serum LDL-C levels (P = 0.369 and P = 975, respectively). Conclusion: Serum LDL-C levels are affected by modifiable factors such as BMI and nonmodifiable factors such as APOE genotype. By identifying these factors and conducting further studies on them, new ways to improve serum LDL-C levels, which is an important factor in the development of CVD, can be identified. In addition, no significant effect of gene-nutrient or microbiota-nutrient interactions on serum LDL-C levels was detected. Further research is needed, especially on the relationship between intestinal microbiota and serum LDL levels.

Diet as an epigenetic factor in inflammatory bowel disease.

Inflammatory bowel disease (IBD) has as a main characteristic the exacerbation of the immune system against enterocytes, compromising the individual's intestinal microbiota. This inflammatory cascade causes several nutritional deficiencies, which further compromise immunological functioning and, as a result, worsen the prognosis. This vicious cycle can be interrupted as the patient's dietary pattern meets their needs according to their clinical condition, acting directly on the inflammatory process of IBD through the interaction of food, intestinal microbiota, and epigenome. Specific nutritional intervention for IBD has a crucial role in preventing and managing disease activity. This review addresses epigenetic modifications through dietary compounds as a mechanism for modulating the intestinal microbiota of patients with IBD.

A multi-omics approach to understand the influence of polyphenols in ovarian cancer for precision nutrition: a mini-review.

The impact of polyphenols in ovarian cancer is widely studied observing gene expression, epigenetic alterations, and molecular mechanisms based on new 'omics' technologies. Therefore, the combination of omics technologies with the use of phenolic compounds may represent a promising approach to precision nutrition in cancer. This article provides an updated review involving the current applications of high-throughput technologies in ovarian cancer, the role of dietary polyphenols and their mechanistic effects in ovarian cancer, and the current status and challenges of precision nutrition and their relationship with big data. High-throughput technologies in different omics science can provide relevant information from different facets for identifying biomarkers for diagnosis, prognosis, and selection of specific therapies for personalized treatment. Furthermore, the field of omics sciences can provide a better understanding of the role of polyphenols and their function as signaling molecules in the prevention and treatment of ovarian cancer. Although we observed an increase in the number of investigations, there are several approaches to data acquisition, analysis, and integration that still need to be improved, and the standardization of these practices still needs to be implemented in clinical trials.

Nutrigenomics and microbiome shaping the future of personalized medicine: a review article.

The relationship between nutrition and genes has long been hinted at and sometimes plainly associated with certain diseases. Now, after many years of research and coincidental findings, it is believed that this relationship, termed "Nutrigenomics," is certainly a factor of major importance in various conditions. In this review article, we discuss nutrigenomics, starting with basics definitions and enzymatic functions and ending with its palpable association with cancer. Now, diet is basically what we eat on a daily basis. Everything that enters through our alimentary tract ends up broken down to minute molecules and amino acids. These molecules interact with our microbiome and genome in discreet ways. For instance, we demonstrate how proper intake of probiotics enhances beneficial bacteria and may alleviate IBS and prevent colorectal cancer on the long term. We also show how a diet rich in folic acid is essential for methylenetetrahydrofolate reductase (MTHFR) function, which lowers risk of colorectal cancer. Also, we discuss how certain diets were associated with development of certain cancers. For example, red and processed meat are highly associated with colorectal and prostate cancer, salty diets with stomach cancer, and obesity with breast cancer. The modification of these diets significantly lowered the risk and improved prognosis of these cancers among many others. We also examined how micronutrients had a role in cancer prevention, as vitamin A and C exert anti-carcinogenic effects through their function as antioxidants. In addition, we show how folic acid prevent DNA mutations by enhancing protein methylation processes. Finally, after a systematic review of myriad articles on the etiology and prevention of cancer, we think that diet should be a crucial feature in cancer prevention and treatment programs. In the future, healthy diets and micronutrients may even be able to successively alter the liability to genetic mutations that result in cancer. It also will play a role in boosting treatment and improving prognosis of diagnosed cancers.

Genetic Variants in CD36 Involved in Fat Taste Perception: Association with Anthropometric and Clinical Parameters in Overweight and Obese Subjects Affected by Type 2 Diabetes or Dysglycemia-A Pilot Study.

Obesity and overweight represent a growing health problem worldwide. Genes regulating the intake and metabolism of different nutrients can positively or negatively influence the efficacy of nutritional interventions against obesity and its complications. The aim of this study was to assess changes in anthropometric and clinical parameters and the adherence to a Mediterranean diet (MedDiet) over time in relation to nutrigenetic variants in overweight or obese subjects affected by Type 2 Diabetes (T2D) or dysglycemia, who were included in a nutritional program. A total of 23 subjects were included in this study. Clinical parameters, physical activity levels, and the adherence to a MedDiet were evaluated at baseline, at 6 (T6), and at 12 months (T12) during and after a diet/lifestyle intervention. In a single blood sample from each subject, rs1984112 (A>G) and rs1761667 (G>A) in CD36; rs7950226 (G>A) in BMAL1; and rs1801260 (A>G), rs4864548 (A>G), and rs3736544 (G>A) in CLOCK were genotyped with Real-Time PCR. Significant associations were observed between CD36 rs1761667 and weight (p = 0.025), hip circumference (p = 0.042), triglycerides (p = 0.047), and HbA1c (p = 0.012) at baseline. Moreover, the genotype AA in CD36 rs1761667 was significantly associated with a lower BMI when compared to G carriers at baseline, at T6, and also at T12. In addition, subjects with the AA genotype at CD36 rs1984112 had significantly lower levels of HbA1c (p = 0.027) than the GG and AG genotypes at baseline. These results show that variants in CD36 can have an impact on anthropometric and clinical parameters in overweight or obese subjects affected by T2D or dysglycemia, and that it might influence the success of the diet/lifestyle intervention.