The omics technologies of metabolomics, transcriptomics, proteomics, and metagenomics are playing an increasingly important role in nutrition science. With the emergence of the concept of precision nutrition and the need to understand individual responses to dietary interventions, it is an opportune time to examine the impact of these tools to date in human nutrition studies. Advances in our mechanistic understanding of dietary interventions were realized through incorporation of metabolomics, proteomics, and, more recently, metagenomics. A common observation across the studies was the low intra-individual variability of the omics measurements and the high inter-individual variation. Harnessing this data for use in the development of precision nutrition will be important. Metabolomics in particular has played a key role in the development of biomarkers of food intake in an effort to enhance the accuracy of dietary assessments. Further work is needed to realize the full potential of such biomarkers and to demonstrate integration with current strategies, with the goal of overcoming the well-established limitations of self-reported approaches. Although many of the nutrigenomic studies performed to date were labelled as proof-of-concept or pilot studies, there is ample evidence to support the use of these technologies in nutrition science. Incorporating omic technologies from the start of study designs will ensure that studies are sufficiently powered for such data. Furthermore, multi-disciplinary collaborations are likely to become even more important to aid analyses and interpretation of the data.

The efficacy by which dietary interventions influence risk markers of multi-factorial diseases is mainly determined by taking population-based approaches. However, there exists considerable inter-individual variation in response to dietary interventions, and some interventions may benefit certain individuals or population subgroups more than others. This review evaluates the application of nutrigenomic technologies to further the concept of personalised nutrition, as well as the process to take personalised nutrition to the marketplace. The modulation of an individual's response is influenced by both genetic and environmental factors. Many nutrigenetics studies have attempted to explain variability in responses based on a single or a few genotypes so that a genotype may be used to define personalised dietary advice. It has, however, proven very challenging to define an individual's responsiveness to complex diets based on common genetic variations. In addition, there is a limited understanding of what constitutes an optimal response because we lack key health biomarkers and signatures. In conclusion, advances in nutrigenomics will undoubtedly further the understanding of the complex interplay between genotype, phenotype and environment, which are required to enhance the development of personalised nutrition in the future. At the same time, however, issues relating to consumer acceptance, privacy protection as well as marketing and distribution of personalised products need to be addressed before personalised nutrition can become commercially viable.

Food phytochemicals are increasingly considered to play a key role in the cardiometabolic health effects of plant foods. However, the heterogeneity in responsiveness to their intake frequently observed in clinical trials can hinder the beneficial effects of these compounds in specific subpopulations. A range of factors, including genetic background, gut microbiota, age, sex and health status, could be involved in these interindividual variations; however, the current knowledge is limited and fragmented. The European network, European Cooperation in Science and Technology (COST)-POSITIVe, has analysed, in a systematic way, existing knowledge with the aim to better understand the factors responsible for the interindividual variation in response to the consumption of the major families of plant food bioactives, regarding their bioavailability and bioefficacy. If differences in bioavailability, likely reflecting differences in human subjects’ genetics or in gut microbiota composition and functionality, are believed to underpin much of the interindividual variability, the key molecular determinants or microbial species remain to be identified. The systematic analysis of published studies conducted to assess the interindividual variation in biomarkers of cardiometabolic risk suggested some factors (such as adiposity and health status) as involved in between-subject variation. However, the contribution of these factors is not demonstrated consistently across the different compounds and biological outcomes and would deserve further investigations. The findings of the network clearly highlight that the human subjects’ intervention studies published so far are not adequate to investigate the relevant determinants of the absorption/metabolism and biological responsiveness. They also emphasise the need for a new generation of intervention studies designed to capture this interindividual variation.

Cardiovascular disease (CVD) is the major cause of morbidity and mortality worldwide. The consumption of a healthy diet rich in polyphenols has been inversely associated with the development of CVD. This study evaluated the effects of green coffee bean extract (GCBE) and yerba mate phenolic extract (YMPE), the main phenolic and methylxanthine constituents (5-caffeoylquinic acid, 3,5-dicaffeoylquinic acid, caffeine, and theobromine), and their main metabolites (caffeic acid, ferulic acid, dihydrocaffeic acid (DHCA) and dihydroferulic acid (DHFA)) on platelet activation in vitro. Upon incubation with different doses (0.01–100 μg mL⁻¹ or μM) of each compound, adenosine 5′-diphosphate-induced P-selectin expression and fibrinogen binding were determined using whole blood flow cytometry. Platelet P-selectin expression was significantly decreased by YMPE and all phenolic and methylxanthine constituents at physiological concentrations, compared with control, whereas fibrinogen binding on platelets was significantly increased. The colonic metabolites (DHCA and DHFA) had stronger inhibitory effects on P-selectin expression than their phenolic precursors, suggesting an increase in the efficacy to modulate platelet activation with the metabolism of the phenolic compounds.

Diet is a key modifiable risk factor for non-communicable diseases. However, we currently are not benefitting from the full potential of its protective effects. This is due to a number of reasons, including high individual variability in response to certain diets. It is now well acknowledged that in order to gain the full benefit of dietary regimes it is essential to take into account individual responses. With this in mind, the present review examines the concept of precision nutrition and the performance of n-of-1 studies, and discusses the development of certain approaches that will be critical for development of the concepts.