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This review discusses the personalised dietary approach with respect to inflammatory bowel disease (IBD). It identifies gene-nutrient interactions associated with the nutritional deficiencies that people with IBD commonly experience, and the role of the Western diet in influencing these. It also discusses food intolerances and how particular genotypes can affect these. It is well established that with respect to food there is no "one size fits all" diet for those with IBD. Gene-nutrient interactions may help explain this variability in response to food that is associated with IBD. Nutrigenomic research, which examines the effects of food and its constituents on gene expression, shows that-like a number of pharmaceutical products-food can have beneficial effects or have adverse (side) effects depending on a person's genotype. Pharmacogenetic research is identifying gene variants with adverse reactions to drugs, and this is modifying clinical practice and allowing individualised treatment. Nutrigenomic research could enable individualised treatment in persons with IBD and enable more accurate tailoring of food intake, to avoid exacerbating malnutrition and to counter some of the adverse effects of the Western diet. It may also help to establish the dietary pattern that is most protective against IBD.

Competing Interests: Competing interests: We have read and understood BMJ policy on declaration of interests and declare the following interests: JMO is part of Habit advisory board.

Chronic diseases, including obesity, are major causes of morbidity and mortality in most countries. The adverse impacts of obesity and associated comorbidities on health remain a major concern due to the lack of effective interventions for prevention and management. Precision nutrition is an emerging therapeutic approach that takes into account an individual's genetic and epigenetic information, as well as age, gender, or particular physiopathological status. Advances in genomic sciences are contributing to a better understanding of the role of genetic variants and epigenetic signatures as well as gene expression patterns in the development of diverse chronic conditions, and how they may modify therapeutic responses. This knowledge has led to the search for genetic and epigenetic biomarkers to predict the risk of developing chronic diseases and personalizing their prevention and treatment. Additionally, original nutritional interventions based on nutrients and bioactive dietary compounds that can modify epigenetic marks and gene expression have been implemented. Although caution must be exercised, these scientific insights are paving the way for the design of innovative strategies for the control of chronic diseases accompanying obesity. This document provides a number of examples of the huge potential of understanding nutrigenetic, nutrigenomic, and nutriepigenetic roles in precision nutrition., (© 2017 S. Karger AG, Basel.)

Nutrigenetics considers the influence of individual genetic variation on differences in response to dietary components, nutrient requirements and predisposition to disease. Nutrigenomics involves the study of interactions between the genome and diet, including how nutrients affect the transcription and translation process plus subsequent proteomic and metabolomic changes, and also differences in response to dietary factors based on the individual genetic makeup. Personalized characteristics such as age, gender, physical activity, physiological state and social status, and special conditions such as pregnancy and risk of disease can inform dietary advice that more closely meets individual needs. Precision nutrition has a promising future in treating the individual according to their phenotype and genetic characteristics, aimed at both the treatment and prevention of disease. However, many aspects are still in progress and remain as challenges for the future of nutrition. The integration of the human genotype and microbiome needs to be better understood. Further advances in data interpretation tools are also necessary, so that information obtained through newer tests and technologies can be properly transferred to consumers. Indeed, precision nutrition will integrate genetic data with phenotypical, social, cultural and personal preferences and lifestyles matters to provide a more individual nutrition, but considering public health perspectives, where ethical, legal and policy aspects need to be defined and implemented., (© 2016 S. Karger AG, Basel.)

Diversity in the genetic profile between individuals and specific ethnic groups affects nutrient requirements, metabolism and response to nutritional and dietary interventions. Indeed, individuals respond differently to lifestyle interventions (diet, physical activity, smoking, etc.). The sequencing of the human genome and subsequent increased knowledge regarding human genetic variation is contributing to the emergence of personalized nutrition. These advances in genetic science are raising numerous questions regarding the mode that precision nutrition can contribute solutions to emerging problems in public health, by reducing the risk and prevalence of nutrition-related diseases. Current views on personalized nutrition encompass omics technologies (nutrigenomics, transcriptomics, epigenomics, foodomics, metabolomics, metagenomics, etc.), functional food development and challenges related to legal and ethical aspects, application in clinical practice, and population scope, in terms of guidelines and epidemiological factors. In this context, precision nutrition can be considered as occurring at three levels: (1) conventional nutrition based on general guidelines for population groups by age, gender and social determinants; (2) individualized nutrition that adds phenotypic information about the person's current nutritional status (e.g. anthropometry, biochemical and metabolic analysis, physical activity, among others), and (3) genotype-directed nutrition based on rare or common gene variation. Research and appropriate translation into medical practice and dietary recommendations must be based on a solid foundation of knowledge derived from studies on nutrigenetics and nutrigenomics. A scientific society, such as the International Society of Nutrigenetics/Nutrigenomics (ISNN), internationally devoted to the study of nutrigenetics/nutrigenomics, can indeed serve the commendable roles of (1) promoting science and favoring scientific communication and (2) permanently working as a 'clearing house' to prevent disqualifying logical jumps, correct or stop unwarranted claims, and prevent the creation of unwarranted expectations in patients and in the general public. In this statement, we are focusing on the scientific aspects of disciplines covering nutrigenetics and nutrigenomics issues. Genetic screening and the ethical, legal, social and economic aspects will be dealt with in subsequent statements of the Society., (© 2016 S. Karger AG, Basel.)

Crohn's disease is a chronic relapsing condition that has no certain cure. Both genetic susceptibility and nutrition have key roles, but their level of involvement varies between patients. Interacting gene pathways influence the probability of disease development, but these are affected by stress and various environmental factors, including diet. In addition, the role of the gut microbiome must not be underestimated, as it is substantially altered in patients with Crohn's disease. Although an elemental diet might lead to disease remission, reintroducing real foods and sustainable diets in patients with Crohn's disease is currently difficult, and would benefit from the sensitivity and rapid feedback provided by the field of nutrigenomics. Nutrigenomics utilizes high-throughput genomics technologies to reveal changes in gene and protein expression that are modulated by the patient's nutrition. The most widely used technique thus far is transcriptomics, which permits measurement of changes in the expression of thousands of genes simultaneously in one sample. Given the volume of numbers generated in such studies, data-basing and bioinformatics are essential to ensure the correct application of nutrigenomics at the population level. These methods have been successfully applied to animal models of Crohn's disease, and the time is right to move them to human studies.

Nutritional genomics reflects gene/nutrient interactions, utilising high-throughput genomic tools in nutrition research. The field also considers the contribution of individual genotypes to wellness and the risk of chronic disease (nutrigenetics), and how such genetic predisposition may be modified by appropriate diets. For example, high consumption of brassicaceous vegetables, including broccoli, has regularly associated with low cancer risk. Bioactive chemicals in broccoli include glucosinolates, plant pigments including kaempferol, quercetin, lutein and carotenoids, various vitamins, minerals and amino acids. Cancer prevention is hypothesised to act through various mechanisms including modulation of xenobiotic metabolising enzymes, NF-E2 p45-related factor-2 (Nrf2)-mediated stress-response mechanisms, and protection against genomic instability. Broccoli and broccoli extracts also regulate the progression of cancer through anti-inflammatory effects, effects on signal transduction, epigenetic effects and modulation of the colonic microflora. Human intervention studies with broccoli and related foods, using standard biomarker methodologies, reveal part of a complex picture. Nutrigenomic approaches, especially transcriptomics, enable simultaneous study of various signalling pathways and networks. Phenotypic, genetic and/or metabolic stratification may identify individuals most likely to respond positively to foods or diets. Jointly, these technologies can provide proof of human efficacy, and may be essential to ensure effective market transfer and uptake of broccoli and related foods., (Copyright © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Background/aims: Prostate cancer runs in families and shows a clear dietary involvement. Until recently, the key risk gene(s) have proved elusive. We summarise current understandings of nutrient-gene interactions in prostate cancer risk and progression., Methods: A MEDLINE-based literature search was conducted., Results: Hypothesis-directed candidate gene approaches provide plausible, albeit statistically weak, nutrient-gene interactions. These are based on early understandings of factors likely to impact on carcinogenesis, including both nutrient and genetic effects on androgen biosynthesis and action, xenobiotic metabolism, DNA damage and DNA repair. Non-hypothesis-directed genome-wide association studies provide much stronger evidence for other genes, not hitherto suspected for involvement. Although only a few of these have been formally tested for dietary associations in well-designed epidemiologic studies, the nature of many of the genes suggests that their activity may be regulated by nutrients. These effects may not only be relevant to prostate cancer susceptibility, but also to disease progression., Conclusions: It will be important to move beyond studying single nucleotide polymorphisms, into more complex chromosomal rearrangements and to epigenetic changes. For future progress, large international cohorts will not only need to provide proof of individual nutrient-gene interactions, but also to relate these to more complex nutrient-gene-gene interactions, as parts of pathways. Bioinformatics and biostatistics will be increasingly important tools in nutrigenetic studies beyond 2011., (Copyright © 2011 S. Karger AG, Basel.)

Nutrigenetics and nutrigenomics hold much promise for providing better nutritional advice to the public generally, genetic subgroups and individuals. Because nutrigenetics and nutrigenomics require a deep understanding of nutrition, genetics and biochemistry and ever new 'omic' technologies, it is often difficult, even for educated professionals, to appreciate their relevance to the practice of preventive approaches for optimising health, delaying onset of disease and diminishing its severity. This review discusses (i) the basic concepts, technical terms and technology involved in nutrigenetics and nutrigenomics; (ii) how this emerging knowledge can be applied to optimise health, prevent and treat diseases; (iii) how to read, understand and interpret nutrigenetic and nutrigenomic research results, and (iv) how this knowledge may potentially transform nutrition and dietetic practice, and the implications of such a transformation. This is in effect an up-to-date overview of the various aspects of nutrigenetics and nutrigenomics relevant to health practitioners who are seeking a better understanding of this new frontier in nutrition research and its potential application to dietetic practice., (Copyright © 2011 S. Karger AG, Basel.)

The field of nutrigenomics recognizes gene-diet interactions, with regard to both the impact of genetic variation on nutrient requirements, and conversely nutrient regulation of the expression of genes. Crohn's disease and ulcerative colitis are inflammatory bowel diseases for which twin studies reveal genetic susceptibility that is impacted by diet and environment. Apparently contradictory data on the role of diet in inflammatory bowel disease would be entirely explainable if genetic variability determined dietary requirements and intolerances. Considering Crohn's disease, we recognize three major classes of genes. The first of these involves bacterial recognition through pattern recognition receptors and autophagy genes, while the second act through secondary immune response, and the third concern epithelial barrier integrity. Despite genetic overlap with CD, the first two groups of genes appear to be less important in ulcerative colitis, while other genes, particularly those involved in barrier function, gain prominence. Case-control studies suggest that these different genetic groups reflect distinct dietary requirements. Such studies suggest nutrigenomic approaches to maintaining disease remission at present, and preventing disease development in the future.

By definition, functional foods benefit human health beyond the effect of nutrients alone. However, few are accompanied by convincing health claims, partly because human responses are variable. Nutritional biochemistry explains why polymorphisms in genes for the absorption, circulation, or metabolism of essential nutrients, such as n-3 polyunsaturated fatty acids, would affect the efficacy of that nutrient. However, functional foods often incorporate bioactive compounds, such as epigallocatechin-3-gallate, without considering the interaction with genetic polymorphisms. For either example there will be individuals whose genotype precludes their deriving significant benefit from an increased intake of such foods, and a small segment of the population that may be disadvantaged. Large-scale, whole-genome association studies are providing unprecedented understanding of the genetic basis of health and chronic disease. This rapidly evolving genomic science often fails to consider the interaction with environmental exposure like diet. It is important that the dietetics profession ensures rigorous nutrition science alongside genetic evaluation as part of future study design to derive informed information on gene-diet interactions that may enable clients to rationally select foods leading to optimal health or reduced risk of chronic disease.

The promise of nutrigenomics is of personalized nutrition that will lead to optimization or maintenance of good health and/or prevention of the development of chronic diseases. Type 2 diabetes mellitus (T2DM) is a leading health problem throughout the world. Adherence to a Mediterranean-style diet, regulation of carbohydrate intake, and regular exercise may be desirable. Four key genes were originally identified: KCNJ11, potassium inwardly rectifying channel, subfamily J, member 11 gene; PPAR-gamma, peroxisome proliferator activated receptor-gamma; TCF2, transcription factor 2, hepatic; WFS1, Wolfram syndrome 1. However, genome-wide association studies are accelerating our knowledge of the genetics of complex diseases, and have identified seven other key genes in T2DM: CDKAL1, CDK5 regulatory subunit associated protein-like 1; CDKN2, cyclin-dependent kinase inhibitor 2A; FTO, fat mass and obesity associated; HHEX, haematopoietically expressed homeobox; IDE, insulin-degrading enzyme; IGF2BP2, insulin-like growth factor 2 mRNA-binding protein 2; SLC30A8, solute carrier family 30 (zinc transporter), member 8; TCF7L2, transcription factor 7-like 2 (T-cell specific, HMG-box). Gene-nutrient or gene-environment interactions may be important. For example, the PPAR-gamma variant genotype is responsive to different types and levels of lipids, while the effect of the FTO variant can be partly overcome by exercise. Several of these genes act through their effect on the gastrointestinal tract. There are analytical challenges in analyzing the high-dimensional datasets relating genes, nutrients, and other variables to their influence on health and disease processes. An even greater challenge may be in implementing population level changes in diet and behavior to fully exploit the potential of this field.

Inflammatory bowel disease is the umbrella term for a group of diseases whose incidence has been increasing over the past century. Although initial literature analyses had suggested a small number of genes, perhaps between 10 and 20, responsible for disease susceptibility, subsequent national and international collaborations have significantly modified those estimations to greater than 240, with more expected as the technologies continue to advance. As well as direct effects on the genome providing possible targets for therapy or functional foods, it is clear that the immune system, the epi-genome and the gut microbiome also play an important role in disease development and progression. While certain foods accelerate disease development in individuals carrying specific genotypes, the same foods appear beneficial to other genetic groups. Gene-nutrient-microbiota interactions also become important, and tissue culture or animal models are available to initially test hypotheses. However, genomic technologies are necessary to reveal all major effects, whether beneficial or otherwise, in animal or human studies. These technologies include transcriptomics, proteomics and metabolomics, which reveal details of what has happened in a gene-diet or gene-drug interaction. At an international level, the field originally called nutrigenomics, has now been divided into two complementary fields: nutrigenetics and nutrigenomics. [ABSTRACT FROM AUTHOR]

Aim: Nutrigenomics reflects gene-diet interactions. In recent years, the science of nutrigenomics has become more sophisticated. We seek to answer the question as to what this might mean for the dietetics profession. Methods: We have critically reviewed recent developments in the area, and considered the importance of new business opportunities being opened up, which exploit the full potential of nutrigenomics for dietitians. Results: Whereas early business models sold genetic test results through direct-to-consumer testing, new business initiatives move dietitians to a central role. This now provides a robust framework that can inform dietitians in their practice. Conclusion: This field represents an important advance for dietitians. [ABSTRACT FROM AUTHOR]

Traditional views of nutritional carcinogenesis depend on the identification of exogenous carcinogens as major risk factors. As our understanding evolves, it is clear that the pattern of events involves not only exogenous carcinogens, but also metabolic processes and endogenous and exogenous anticarcinogens. The process is modulated by the immune system, and genetics plays a significant role. New monitoring methods provide much-needed tools for providing proof of involvement of various factors at the level of human populations. [Copyright &y& Elsevier]

Abstract: Nutrigenomics seeks to understand the interplay between an individual''s genes and their diet. This approach can potentially be harnessed to reduce the incidence or symptoms of chronic diseases, such as inflammatory bowel disease (IBD). It becomes desirable to interrogate the vast number of discrete compounds present in foods for their ability to influence the phenotype of a cell carrying a variant single nucleotide polymorphism (SNP). Here we describe two cell-based assays that can now be used to test the ability of food components or extracts, to overcome the functional effects of certain variant SNPs that may be important in human IBD. The first monitors the signal transduction pathways of key pattern recognition receptors, in which SNPs associated with IBD have been identified, and tests for food components or extracts that can modulate these pathways for potential therapeutic benefit. The second models the NOD2 3020insC SNP, which is the most common and highest risk variant in Crohn''s disease, and examines the ability of food components or extracts to restore the normal phenotype in the mutant cell line. Such screens provide a scientific basis for the rational choice of foods to be more rigorously investigated in animal models of IBD. [Copyright &y& Elsevier]