Micronutrient deficiency persists throughout the world, and although the burden is higher in low-resource settings, it is also prevalent in wealthy countries, a phenomenon termed ‘hidden hunger’. Due to their high requirements for vitamins and minerals relative to their energy intake, young women and children are particularly vulnerable to hidden hunger. As they share several risk factors and impact on overlapping outcomes, we consider how deficiency of iron, iodine and vitamin D can have profound impacts on perinatal health and infant development. We review the epidemiology of these micronutrient deficiencies during pregnancy, including social, environmental and dietary risk factors. We identify the main challenges in defining nutritional status of these nutrients using validated diagnostic criteria linked with meaningful clinical outcomes. Public health strategies are urgently required to improve the overall health and nutritional status of women of reproductive age. Obesity prevention and early detection of malnutrition with standardised screening methods would detect pregnant women at increased risk of iron deficiency. Development of sensitive, individual biomarkers of iodine status is required to protect maternal health and fetal/infant brain development. Risk assessments of vitamin D requirements during pregnancy need to be revisited from the perspective of fetal and neonatal requirements. International consensus on standardised approaches to micronutrient assessment, analysis and reporting as well as sensitive, clinically validated infant and child neuro-behavioural outcomes will enable progression of useful observational and intervention studies.

Dietary restriction of fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) is clinically effective and a commonly utilised approach in the management of functional symptoms in irritable bowel syndrome. Despite this, the low FODMAP diet has a number of challenges: it can alter the gut microbiota; impact nutrient intake and diet quality; is complex to understand; requires the patient to be adequately supported to follow the diet accurately and safely; and lastly, not all patients respond to the diet. The current review highlights the evidence for the clinical effectiveness of the low FODMAP diet, but focusses on the challenges associated with the diet to the patient, health professionals and the wider healthcare service. Finally, the review discusses research findings and practical guidance for how these challenges can be minimised and mitigated. The low FODMAP diet is a useful management strategy for irritable bowel syndrome, with data from clinical trials suggesting a 50–80% response rate, and when administered appropriately, the challenges to implementing the diet can be overcome so that these outcomes can be realised effectively and safely in clinical practice.

Research characterising the gut microbiota in different populations and diseases has mushroomed since the advent of next-generation sequencing techniques. However, there has been less emphasis on the impact of dietary fibres and other dietary components that influence gut microbial metabolic activities. Dietary fibres are the main energy source for gut bacteria. However, fibres differ in their physicochemical properties, their effects on the gut and their fermentation characteristics. The diversity of carbohydrates and associated molecules in fibre-rich foods can have a major influence on microbiota composition and production of bioactive molecules, for example SCFAs and phenolic acids. Several of these microbial metabolites may influence the functions of body systems including the gut, liver, adipose tissues and brain. Dietary fibre intake recommendations have recently been increased (to 30 g daily) in response to growing obesity and other health concerns. Increasing intakes of specific fibre and plant food sources may differentially influence the bacteria and their metabolism. However, in vitro studies show great individual variability in the response of the gut microbiota to different fibres and fibre combinations, making it difficult to predict which foods or food components will have the greatest impact on levels of bioactive molecules produced in the colon of individuals. Greater understanding of individual responses to manipulation of the diet, in relation to microbiome composition and production of metabolites with proven beneficial impact on body systems, would allow the personalised approach needed to best promote good health.

The aetiology of inflammatory bowel disease (IBD) is multifactorial, with diet and gut microbiota playing an important role. Nonetheless, there are very few studies, particularly clinical research, which have explored the interaction between diet and gut microbiota. In the current review, we summarise the evidence from clinical trials exploring the interactions between the gut microbiota and diet in the management of IBD. Data from the effect of exclusive enteral nutrition (EEN) on the gut microbiota of children with active Crohn's disease (CD), receiving induction treatment, offer opportunities to understand the role of gut microbiota in underlying disease pathogenesis and develop novel dietary and pharmacological microbial therapeutics. In contrast, the evidence which links the effectiveness of food-based dietary therapies for IBD with mechanisms involving the gut microbiota is far less convincing. The microbial signals arising from these dietary therapies are inconsistent and vary compared to the effects of effective treatment with EEN in CD.

Sometimes referred to as hidden hunger, micronutrient deficiencies persist on a global scale. For some micronutrients this appears to be due to inadequate intake, for others intake may not match increased requirements. However, for most micronutrient deficiencies there is uncertainty as to the dominant driver, and the question about the contribution of malabsorption is open. Environmental enteropathy (EE), formerly referred to as tropical enteropathy and also referred to as environmental enteric dysfunction, is an asymptomatic disorder of small intestinal structure and function which is very highly prevalent in many disadvantaged populations. Recent studies of the pathology and microbiology of this disorder suggest that it is driven by very high pathogen burdens in children and adults living in insanitary environments and is characterised by major derangements of the epithelial cells of the intestinal mucosa. Transcriptomic data suggest that it may lead to impaired digestion and absorption of macronutrients. Given the very high prevalence of EE, marginal malabsorption could have large impacts at population scales. However, the relative contributions of inadequate soil and crop micronutrient contents, inadequate intake, malabsorption and increased requirements are unknown. Malabsorption may compromise attempts to improve micronutrient status, but with the exception of zinc there is currently little evidence to confirm that malabsorption contributes to micronutrient deficiency. Much further research is required to understand the role of malabsorption in hidden hunger, especially in very disadvantaged populations where these deficiencies are most prevalent.

Sensing of nutrients by chemosensory cells in the gastrointestinal tract plays a key role in transmitting food-related signals, linking information about the composition of ingested foods to digestive processes. In recent years, a number of G protein-coupled receptors (GPCR) responsive to a range of nutrients have been identified. Many are localised to intestinal enteroendocrine (chemosensory) cells, promoting hormonal and neuronal signalling locally, centrally and to the periphery. The field of gut sensory systems is relatively new and still evolving. Despite huge interest in these nutrient-sensing GPCR, both as sensors for nutritional status and targets for preventing the development of metabolic diseases, major challenges remain to be resolved. However, the gut expressed sweet taste receptor, resident in L-enteroendocrine cells and responsive to dietary sweetener additives, has already been successfully explored and utilised as a therapeutic target, treating weaning-related disorders in young animals. In addition to sensing nutrients, many GPCR are targets for drugs used in clinical practice. As such these receptors, in particular those expressed in L-cells, are currently being assessed as potential new pathways for treating diabetes and obesity. Furthermore, growing recognition of gut chemosensing of microbial-produced SCFA acids has led further attention to the association between nutrition and development of chronic disorders focusing on the relationship between nutrients, gut microbiota and health. The central importance of gut nutrient sensing in the control of gastrointestinal physiology, health promotion and gut–brain communication offers promise that further therapeutic successes and nutritional recommendations will arise from research in this area.

Sarcopenia, a skeletal muscle disorder that is characterised by loss of muscle strength and mass, is common in older populations and associated with poorer health outcomes. Although the individual and economic costs of sarcopenia are widely recognised, current understanding of its pathophysiology is incomplete, limiting efforts to translate research evidence into effective preventive and treatment strategies. While nutrition is a key field of sarcopenia research, the role of differences in habitual diets, and the effectiveness of dietary change as a prevention or treatment strategy, is uncertain. There is a growing evidence base that links low micronutrient intakes to sarcopenia risk and/or its components (low muscle strength and mass, impaired physical performance), although there remain many gaps in understanding. There is some consistency in findings across studies highlighting potential roles for antioxidant nutrients, B vitamins and magnesium; however, the evidence is largely observational and from cross-sectional studies, often describing associations with different muscle outcomes. As low intakes of some micronutrients are common in older populations, there is a need for new research, particularly from well-characterised prospective cohorts, to improve the understanding of their role and importance in the aetiology of sarcopenia and to generate the evidence needed to inform dietary guidelines to promote muscle health.

In recent years, the importance of the gut microbiota in human health has been revealed and many publications have highlighted its role as a key component of human physiology. Owing to the use of modern sequencing approaches, the characterisation of the microbiome in healthy individuals and in disease has demonstrated a disturbance of the microbiota, or dysbiosis, associated with pathological conditions. The microbiota establishes a symbiotic crosstalk with their host: commensal microbes benefit from the nutrient-rich environment provided by the gut and the microbiota produces hundreds of proteins and metabolites that modulate key functions of the host, including nutrient processing, maintenance of energy homoeostasis and immune system development. Many bacteria-derived metabolites originate from dietary sources. Among them, an important role has been attributed to the metabolites derived from the bacterial fermentation of dietary fibres, namely SCFA linking host nutrition to intestinal homoeostasis maintenance. SCFA are important fuels for intestinal epithelial cells (IEC) and regulate IEC functions through different mechanisms to modulate their proliferation, differentiation as well as functions of subpopulations such as enteroendocrine cells, to impact gut motility and to strengthen the gut barrier functions as well as host metabolism. Recent findings show that SCFA, and in particular butyrate, also have important intestinal and immuno-modulatory functions. In this review, we discuss the mechanisms and the impact of SCFA on gut functions and host immunity and consequently on human health.

All tissues are in a constant state of turnover, with a tightly controlled regulation of protein synthesis and breakdown rates. Due to the relative ease of sampling skeletal muscle tissue, basal muscle protein synthesis rates and the protein synthetic responses to various anabolic stimuli have been well defined in human subjects. In contrast, only limited data are available on tissue protein synthesis rates in other organs. Several organs such as the brain, liver and pancreas, show substantially higher (basal) protein synthesis rates when compared to skeletal muscle tissue. Such data suggest that these tissues may also possess a high level of plasticity. It remains to be determined whether protein synthesis rates in these tissues can be modulated by external stimuli. Whole-body protein synthesis rates are highly responsive to protein intake. As the contribution of muscle protein synthesis rates to whole-body protein synthesis rates is relatively small considering the large amount of muscle mass, this suggests that other organ tissues may also be responsive to (protein) feeding. Whole-body protein synthesis rates in the fasted or fed state can be quantified by measuring plasma amino acid kinetics, although this requires the production of intrinsically labelled protein. Protein intake requirements to maximise whole-body protein synthesis may also be determined by the indicator amino acid oxidation technique, but the technique does not allow the assessment of actual protein synthesis and breakdown rates. Both approaches have several other methodological and inferential limitations that will be discussed in detail in this paper.