This paper aims to describe different approaches for studying the overall diet with advantages and limitations. Studies of the overall diet have emerged because the relationship between dietary intake and health is very complex with all kinds of interactions. These cannot be captured well by studying single dietary components. Three main approaches to study the overall diet can be distinguished. The first method is researcher-defined scores or indices of diet quality. These are usually based on guidelines for a healthy diet or on diets known to be healthy. The second approach, using principal component or cluster analysis, is driven by the underlying dietary data. In principal component analysis, scales are derived based on the underlying relationships between food groups, whereas in cluster analysis, subgroups of the population are created with people that cluster together based on their dietary intake. A third approach includes methods that are driven by a combination of biological pathways and the underlying dietary data. Reduced rank regression defines linear combinations of food intakes that maximally explain nutrient intakes or intermediate markers of disease. Decision tree analysis identifies subgroups of a population whose members share dietary characteristics that influence (intermediate markers of) disease. It is concluded that all approaches have advantages and limitations and essentially answer different questions. The third approach is still more in an exploration phase, but seems to have great potential with complementary value. More insight into the utility of conducting studies on the overall diet can be gained if more attention is given to methodological issues.

Food synergy is the concept that the non-random mixture of food constituents operates in concert for the life of the organism eaten and presumably for the life of the eater. Isolated nutrients have been extensively studied in well-designed, long-term, large randomised clinical trials, typically with null and sometimes with harmful effects. Therefore, although nutrient deficiency is a known phenomenon, serious for the sufferer, and curable by taking the isolated nutrient, the effect of isolated nutrients or other chemicals derived from food on chronic disease, when that chemical is not deficient, may not have the same beneficial effect. It appears that the focus on nutrients rather than foods is in many ways counterproductive. This observation is the basis for the argument that nutrition research should focus more strongly on foods and on dietary patterns. Unlike many dietary phenomena in nutritional epidemiology, diet pattern appears to be highly correlated over time within person. A consistent and robust conclusion is that certain types of beneficial diet patterns, notably described with words such as ‘Mediterranean’ and ‘prudent’, or adverse patterns, often described by the word ‘Western’, predict chronic disease. Food is much more complex than drugs, but essentially uninvestigated as food or pattern. The concept of food synergy leads to new thinking in nutrition science and can help to forge rational nutrition policy-making and to determine future nutrition research strategies.

Technologic advances now make it possible to collect large amounts of genetic, epigenetic, metabolomic and gut microbiome data. These data have the potential to transform approaches towards nutrition counselling by allowing us to recognise and embrace the metabolic, physiologic and genetic differences among individuals. The ultimate goal is to be able to integrate these multi-dimensional data so as to characterise the health status and disease risk of an individual and to provide personalised recommendations to maximise health. To this end, accurate and predictive systems-based measures of health are needed that incorporate molecular signatures of genes, transcripts, proteins, metabolites and microbes. Although we are making progress within each of these omics arenas, we have yet to integrate effectively multiple sources of biologic data so as to provide comprehensive phenotypic profiles. Observational studies have provided some insights into associative interactions between genetic or phenotypic variation and diet and their impact on health; however, very few human experimental studies have addressed these relationships. Dietary interventions that test prescribed diets in well-characterised study populations and that monitor system-wide responses (ideally using several omics platforms) are needed to make correlation–causation connections and to characterise phenotypes under controlled conditions. Given the growth in our knowledge, there is the potential to develop personalised dietary recommendations. However, developing these recommendations assumes that an improved understanding of the phenotypic complexities of individuals and their responses to the complexities of their diets will lead to a sustainable, effective approach to promote health and prevent disease – therein lies our challenge.

Although personalised nutrition is frequently considered in the context of diet–gene interactions, increasingly, personalised nutrition is seen to exist at three levels. The first is personalised dietary advice using Internet-delivered services, which ultimately will become automated and which will also draw on mobile phone technology. The second level of personalised dietary advice will include phenotypic information on anthropometry, physical activity, clinical parameters and biochemical markers of nutritional status. It remains possible that in addition to personalised dietary advice based on phenotypic data, advice at that group or metabotype level may be offered where metabotypes are defined by a common metabolic profile. The third level of personalised nutrition will involve the use of genomic data. While the genomic aspect of personalised nutrition is often considered as its main driver, there are significant challenges to translation of data on SNP and diet into personalised advice. The majority of the published data on SNP and diet emanate from observational studies and as such do not offer any cause–effect associations. To achieve this, purpose-designed dietary intervention studies will be needed with subjects recruited according to their genotype. Extensive research indicates that consumers would welcome personalised dietary advice including dietary advice based on their genotype. Unlike personalised medicine where genotype data are linked to the risk of developing a disease, in personalised nutrition the genetic data relate to the optimal diet for a given genotype to reduce disease risk factors and thus there are few ethical and legal issues in personalised nutrition.

This review describes historical iodine deficiency in the UK, gives current information on dietary sources of iodine and summarises recent evidence of iodine deficiency and its association with child neurodevelopment. Iodine is required for the production of thyroid hormones that are needed for brain development, particularly during pregnancy. Iodine deficiency is a leading cause of preventable brain damage worldwide and is associated with impaired cognitive function. Despite a global focus on the elimination of iodine deficiency, iodine is a largely overlooked nutrient in the UK, a situation we have endeavoured to address through a series of studies. Although the UK has been considered iodine-sufficient for many years, there is now concern that iodine deficiency may be prevalent, particularly in pregnant women and women of childbearing age; indeed we found mild-to-moderate iodine deficiency in pregnant women in Surrey. As the major dietary source of iodine in the UK is milk and dairy produce, it is relevant to note that we have found the iodine concentration of organic milk to be over 40% lower than that of conventional milk. In contrast to many countries, iodised table salt is unlikely to contribute to UK iodine intake as we have shown that its availability is low in grocery stores. This situation is of concern as the level of UK iodine deficiency is such that it is associated with adverse effects on offspring neurological development; we demonstrated a higher risk of low IQ and poorer reading-accuracy scores in UK children born to mothers who were iodine-deficient during pregnancy. Given our findings and those of others, iodine status in the UK population should be monitored, particularly in vulnerable subgroups such as pregnant women and children.

A high intake of fruit and vegetables (FV) is associated with reduced risk of chronic disease, although the evidence base is mostly observational. Blood biomarkers offer an objective indicator of FV intake, potentially improving estimates of intakes based on traditional methods. A valid biomarker of overall FV intake would be able to confirm population intakes, more precisely evaluate the association between intakes and health outcomes and confirm compliance in FV interventions. Several substances have been proposed as biomarkers of FV intake: vitamin C, the carotenoids and polyphenols. Certain biomarkers are strong predictors of single FV; however, the proposed single biomarkers of FV consumption are only modestly predictive of overall FV consumption. This is likely to be due to the complexity of the FV food group. While accurately measuring FV intake is important in nutrition research, another critical question is: how best can an increase in FV intake be achieved? Increased FV intake has been achieved in efficacy studies using intensive dietary advice. Alternative, less intensive methods for encouraging FV consumption need to be developed and tested for population level intervention. Systematic reviews suggest peer support to be an effective strategy to promote dietary change. This review will describe the evidence for a link between increased FV intake and good health, outline possible novel biomarkers of FV consumption, present the most recently available data on population intake of FV and examine the usefulness of different approaches to encourage increased consumption of FV.

Over the past two centuries human life expectancy has increased by nearly 50 years. Genetic factors account for about one-third of the variation in life expectancy so that most of the inter-individual variation in lifespan is explained by stochastic and environmental factors, including diet. In some model organisms, dietary (energy) restriction is a potent, and highly reproducible, means of increasing lifespan and of reducing the risk of age-related dysfunction although whether this strategy is effective in human subjects is unknown. This is ample evidence that the ageing process is plastic and research demonstrates that ageing is driven by the accumulation of molecular damage, which causes the changes in cell and tissue function that characterise the ageing phenotype. This cellular, tissue and organ damage results in the development of age-related frailty, disabilities and diseases. There are compelling observational data showing links between eating patterns, e.g. the Mediterranean dietary pattern, and ageing. In contrast, there is little empirical evidence that dietary changes can prolong healthy lifespan and there is even less information about the intervention modalities that can produce such sustainable dietary behaviour changes. In conclusion, current research needs include (1) a better understanding of the causal biological pathways linking diet with the ageing trajectory, (2) the development of lifestyle-based interventions, including dietary changes, which are effective in preventing age-related disease and disability and (3) the development of robust markers of healthy ageing, which can be used as surrogate outcome measures in the development and testing of dietary interventions designed to enhance health and well-being long into old age.

The aim of this review paper is to consider how the principles of clinical audit could be applied to the development of an audit of nutritional care in hospitals and care homes, based on criteria derived from the Essence of Care: Food and Drink. A literature review identified fifteen key papers that included guidance or standards for nutritional care in hospitals or care homes. These were used to supplement the ten factors suggested by the Essence of Care to develop a set of potential audit criteria covering all aspects of the nutritional care pathway including the identification of risk of malnutrition, implementation of nutritional care plans, referral to healthcare professionals for further nutritional assessment and nutritional support strategies. A series of audit tools have been developed, including an organisational level audit tool, a staff questionnaire, a patients' and residents' records audit tool and a patients' and residents' experiences questionnaire. Further issues to consider in designing a national nutritional audit include the potential role of direct observation of care, the use of trained auditors and the scope for including the results of pre-existing local audits. In conclusion, a national audit would need to encompass a very large number of health and care organisations of widely varying sizes and types and a diverse range of people.