As needed, the Society will establish committees to handle scientific and educational aspects and develop statements to be approved by the Board. Subsequent statements will be on the ISNN position on genetic testing, ethical, social and legal aspects. Some of the statements may be developed in collaboration with other institutes and national societies. Individuals respond differently to lifestyle interventions, especially those modulating diet, because of genetic variants that influence how dietary components are absorbed, metabolized and utilized [ 2 , 3 ].
Therefore, dietary advice that is specific to individuals with a particular genotype should be more effective at preventing chronic diseases than general recommendations about diet [ 4 ]. Some consumer genetic testing companies are beginning to provide information as to how diet should be modified, based on the genotype, to prevent disease or improve health, i.
The sequencing of the human genome and consequent increased knowledge regarding human genetic variation is contributing to the emergence of personalized nutrition [ 2 ]. Recognition of diverse individual nutritional needs and responses to diet are changing standards of nutritional care, creating new possibilities for this field.
Dietary reference intake values such as recommended dietary allowance and safe upper limits established by the Food and Nutrition Board of the National Academy of Medicine are based on recommendations for populations rather than for specific individuals or groups of individuals [ 5 ]. Promotion of dietary patterns believed to be beneficial, such as the Mediterranean diet, is another way to express healthy nutrition [ 8 ].
Most dietary recommendations are stratified according to gender and age, but these are not the only factors that should be considered when giving advice on nutrient intake. Diversity in the genetic profile between individuals and specific ethnic groups affects nutrient requirements, metabolism and response to nutritional and dietary interventions [ 9 , 10 ].
Environmental, cultural and economic factors also play a crucial role in individual food choices and accessibility [ 10 ]. Malnutrition in the form of undernutrition or obesity can also modify gene expression and genome stability, resulting in changes in phenotype, and hence it is difficult to choose one population as a reference [ 11 ]. New statistical approaches are urgently needed for estimating reference values in different population groups [ 12 ].
Features such as age, gender, physical activity, physiological state, social status and special conditions such as pregnancy and risk of disease [ 13 ] can inform dietary advice that more closely meets individual needs [ 14 ]. Improved health care can be achieved if nutritional recommendations are personalized according to individual genetic profile, phenotype, health status, food preferences and environmental characteristics [ 10 ]. Personalized nutrition is an important part of personalized medicine and may assist in establishing guidelines for specific subgroups based on phenotype and genotype.
All these techniques can be applied separately or in an integrated manner for a better understanding of health metabolism and disease progression [ 10 ]. With this perspective, the omics tools most immediately relevant to personalized nutrition include nutrigenetics, nutrigenomics and nutriepigenetics. Nutrigenetics investigates the influence of the genotype variants of the DNA sequence on the response to nutritional change and on the risk of nutrition-related disease. Nutrigenomic studies investigate the effect of nutrition on gene expression and, consequently, on the proteome and the metabolome [ 17 ].
Nutriepigenetic studies explore the chromatin structure and DNA modifications that do not alter the underlying DNA sequence, but affect gene expression [ 18 ]. These advances in genetic science are raising numerous questions regarding how personalized nutrition can contribute solutions to emerging problems in public health, by reducing the risk and prevalence of nutrition-related disease.
The availability of genetic information also raises questions from health-care professionals as to how to apply such knowledge, and from individuals regarding how to use such information. Furthermore, commercialization of genetic information raises ethical and moral issues. Hence, the interpretation and inclusion of genetic components into nutrition recommendations and products may generate ethical and financial difficulties while simultaneously promoting a revolution in nutrition. Genome-wide association studies GWAS have identified a large number of genetic variants associated with complex diseases and traits [ 19 ], but have failed to explain a large part of their heritability [ 20 ].
GWAS usually measure the impact of genes on disease using correlations rather than studying interactions between genes and environmental factors such as diet or exercise. These interactions cause genotypic effects to be more pronounced under particular environmental conditions. Therefore, failing to control for such variations means that GWAS data provide only a partial picture of genetic variation contributing to disease development, particularly with regard to heritability [ 21 ].
GWAS should be considered as only a first step in the understanding of the molecular basis of complex diseases. The advances in nutrigenetics, nutrigenomics and nutriepigenetics will help to identify the variability in interactions not controlled for in GWAS. This situation means that new bioinformatics and biostatistics tools will be necessary to make this new information useful for health-care professionals [ 22 ].
Current views on personalized nutrition encompass omics technologies, functional foods, existing products, future challenges - particularly those relating to legal and ethical aspects, application in clinical practice, and population scope, in terms of guidelines and epidemiological factors fig. A major contribution of the Human Genome Project was to lay the foundation that led to the discovery of millions of differences in the nucleotide sequence of genes. Some SNPs may affect the synthesis and function of proteins, and may therefore alter nutritional requirements and nutrient metabolism [ 24 , 25 ], as well as playing important roles in an individual's risk of developing disease [ 26 ].
Some of them appear to play an important role in human health [ 28 , 29 ] through association with the risk of disease development and progression [ 30 ]. One example of this is phenylketonuria PKU , an inborn error of metabolism caused by mutations in the gene that encodes the hepatic enzyme phenylalanine hydroxylase [ 31 ].
Individuals with PKU need to avoid foods rich in the amino acid phenylalanine. Another example is lactase persistence, which evolved a few thousand years ago in response to the development of dairy farming. Lactose milk sugar is a disaccharide, made from glucose and galactose. Recent studies investigating genetic variants associated with obesity risk or with resistance to weight loss in human populations [ 32 , 33 ] have helped clarify molecular mechanisms involved in obesity [ 34 ].
One such example is the fat mass and obesity-associated FTO gene. Variants in numerous other obesity candidate genes, such as peroxisome proliferator-activated receptor, uncoupling proteins UCP1 and UCP3 , leptin receptor and melanocortin 4 receptor, can also affect weight gain or loss in genetically predisposed subjects [ 32 , 36 ]. Variants in genes necessary for lipid metabolism, such as those encoding cholesteryl ester transfer protein, lipoprotein lipase, low-density lipoprotein receptor and apolipoprotein E, may increase the risk of coronary artery disease [ 37 , 38 , 39 , 40 ].
Further variants are associated with the development of diabetes, cancer and other diseases. Dietary advice specifically tailored to some of these variants may reduce the elevated disease risk better than genetic counselling without knowledge of the genetic information [ 41 ]. Many other metabolic pathways and biological functions have similarly identifiable genetic vulnerabilities that are amenable to tailoring of dietary intakes. For example, the combination of low folate intake, a low-activity variant of the 5,methylene tetrahydrofolate reductase gene MTHFR , increases susceptibility to disease, while either of them on their own will not [ 42 , 43 ].
Technologies such as next-generation sequencing NGS platforms arrays, bead chips and sequencing approaches provide a rapid scan of known genetic variants to define genetic differences between individuals [ 44 , 45 ]. Assessing the role of single gene variants in complex traits influenced by many genes [e. Therefore, simultaneous examination of multiple variants is necessary, given the fact that several of them may affect the function of a particular gene and that multiple genes may contribute to disease development and progression. This approach assists with defining biological response to food components and food patterns, thereby advancing strategies to identify, treat and prevent disease [ 45 ].
In particular, the analysis of groups of gene variants haplotypes that are related or physically close to each other on the same DNA strand can promote our understanding of biological events and conditions [ 46 ]. Telomere length TL has also been linked to the risk of several diseases, such as cancer and CVD [ 47 ]. TL is a biomarker of cumulative oxidative stress, biological age, and an independent predictor of survival and therapeutic treatment requirements. Thus, leukocyte TL has been proposed as a biomarker of biological age [ 47 ]. Studies have shown that dietary patterns can protect or damage telomeres.
For example, high consumption of fruits and vegetables and a higher intake of omega-3 fatty acids or fiber were associated with longer telomeres [ 49 , 50 ], whereas higher intake of saturated fatty acids and higher consumption of processed meats were both associated with telomere shortening [ 51 ]. Furthermore, recent studies have shown that total dietary antioxidant capacity was associated with longer telomeres, while higher white bread consumption was associated with telomere shortening in a population of Spanish children and adolescents [ 52 ].
Nutrients and food components can affect and regulate gene activity both directly and indirectly, including acting as ligands of transcription factors and playing a regulatory role in intermediate metabolites of signaling pathways, with positive or negative effects [ 53 ]. Hence, nutrigenomics seeks to show how dietary factors influence gene expression and subsequently impact protein and metabolite levels [ 54 , 55 ].
A common approach is the examination of individual mRNA levels relative to intake of certain food components. Nutrigenomic strategies thus include analysis of gene expression and biochemical profiles. The study of the transcriptome the complete set of RNA transcripts [ 23 ], provides a tool for observing such changes in gene expression in response to different factors including dietary changes [ 59 ]. Diet, physical activity, alcohol and smoking habits all modify gene expression and consequently affect the risk of pathological outcome [ 36 , 60 ].
Dietary components, such as macronutrients and micronutrients influence gene expression, thereby altering metabolism and the development of disease [ 23 ]. Transcriptome analysis can evaluate the expression of thousands of genes before and after dietary intervention, showing the difference between healthy and unhealthy individuals and helping to establish new biomarkers for disease diagnosis [ 23 ].
Transcriptomics requires the study of cells in which genes are expressed, because gene expression is often tissue specific. It is difficult to access the most relevant human tissues, meaning that samples are usually available only from the more accessible tissues such as subcutaneous adipose tissue, blood mononuclear cells and skeletal muscle [ 61 ]. Polymerase chain reaction has been used to measure gene expression in the interaction of the genome and diet [ 31 ].
Newer microarray technologies can identify most changes in gene expression and in metabolic pathways after nutritional intervention. Epigenetic processes bring about reversible modifications in chromatin structure and DNA modification without altering the underlying sequence.
Epigenetic changes include DNA methylation and histone modification [ 33 , 62 , 63 ]. Different classes of small noncoding RNAs such as microRNAs or long noncoding RNAs have been proposed as key regulators of gene expression, chromatin remodeling and epigenetic changes through multiple mechanism, showing a potential as biomarkers of human diseases [ 64 , 65 ]. Additionally, external effects including diet on the epigenome alter the expression of genes, providing a link between environment, nutrition and disease [ 66 ].
DNA methylation is the most widely studied form of epigenetic modification. The added methyl group often silences the gene by blocking the binding of transcription factors [ 61 , 67 ]. In recent years, development of new technologies such as NGS has allowed the detection of site-specific methylation patterns with great accuracy and led to the discovery of new types of epigenetic modifications [ 68 , 69 , 70 ]. Histone modifications, consisting of acetylation, methylation, phosphorylation and ubiquitination, affect transcription through compacting DNA.
This process can activate or repress gene expression by controlling accessibility of genes to transcriptional regulators [ 71 , 72 ]. Epigenetics depends on the presence of enzymes and dietary nutrients, and can occur in a gene-specific or in a global manner [ 73 ]. The availability of SAM can be diminished under some circumstances by insufficient availability of folic acid, vitamin B 12 , vitamin B 6 , vitamin B 2 , choline, betaine and methionine, both due to low intake and individual genetic vulnerabilities [ 74 , 75 ].
Some studies have shown a relationship between nutritional intake during pregnancy and changes in methylation patterns in rats [ 76 , 77 ]. Nutritional interventions in pregnancy and lactation such as energy restriction and excessive dietary fat can alter epigenetic modifications [ 78 ].
Epigenetics - Wikipedia
Other studies have shown that epigenetic modifications change the risk of inflammation, obesity and chronic diseases [ 79 ]. A study of obese men on a hypocaloric diet to lose weight found distinct differences in DNA methylation patterns between individuals with high weight loss compared to those with little weight loss [ 80 ]. New NGS and microarray technologies have enabled the study of DNA methylation at high resolution across the genome, helping to characterize epigenetic outcomes though epigenome-wide association studies [ 82 ].
Transcriptomics does not show the number of expressed proteins.
Thus, one transcript can be translated into numerous proteins, just as many factors can stop or modify the translation process or cause posttranslational modifications [ 6 ]. Proteomics analyzes protein expressed over a given time, and is the most precise method for identifying the effect of nutrients and food components on the genome [ 6 , 23 ].
Each cell will have a corresponding proteome, depending on the cell's type and function [ 83 ]. Proteins are commonly analyzed in blood samples [ 84 ], but there is not a single platform capable of evaluating the full spectrum of proteins in blood or tissue samples [ 85 ]. Lipids play an important role in nutrition and metabolism [ 86 ]. Lipidomics produces a global profile of lipids found in cells, tissues and fluids [ 87 ], studying the interactions between genes, diet, nutrients and human metabolism [ 86 , 88 ].
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