Micronutrient malnutrition, the deficiency of vitamins or minerals, impacts on physical and mental health, in clinical and general populations, across the life course. In older western populations the high prevalence and impact of micronutrient malnutrition is less well recognised. Low- and middle-income countries are experiencing the ‘double burden of disease’ where malnutrition coexists alongside the non-communicable diseases of aging, obesity, type 2 diabetes and cardiovascular disease. Held in December 2020, the Winter Conference of the Nutrition Society was designed to cover new areas of research and concern in micronutrient malnutrition across the life course. Common themes arising from the conference were: 1) The continuing high prevalence of micronutrient malnutrition across the life-course, in diverse populations, in high, middle and low-income countries. 2) That multiple deficiencies of micronutrients frequently exist. 3) The primary cause of deficiency is poor quality diets, of low diversity, low in micronutrient dense foods. 4) Clinical conditions, medications for common non-communicable diseases, and environmental conditions, interact with and exacerbate the effects of poor diet quality. 5) Understanding of the mechanistic effects of micronutrients is still emerging. 6) Micronutrients are necessary for maintaining immune function, which has importance for the COVID-19 epidemic. 7) Better biomarkers are needed detect and understand the effects of deficiency. 7) Dietary recommendations need to be updated regularly. Further research is needed in all these areas. Comprehensive public health and government approaches to ensure access and affordability of good quality foods to populations of all ages, particularly during the ongoing COVID-19 epidemic, are crucial.

The Spring Conference 2021 focused on the theme of the gut microbiome and health that was divided across three separate but inter-related areas from the impact of nutrition on the gut microbiome, the cause and effect of nutrition and health on the gut microbiome to the interaction between pathogens and gut microbiota. The programme was supported by two plenary lectures, the first discussed the computational methods commonly employed to examine gut microbiota and the concluding lecture presented the interaction between the gut microbiome, nutrition and health in older populations. This short report provides a summary and highlights of the conference.

Nutrition support involves the use of oral supplements, enteral tube feeding or parenteral nutrition. These interventions are considered when oral intake alone fails to meet nutritional requirements. Special diets and oral supplements are usually the first approach to managing malnutrition; however, their role becomes limited when oral intake is restricted or if swallowing is unsafe. Enteral tube feeding or parenteral nutrition are alternative means of providing nutrition support for this select group of patients. Percutaneous endoscopic gastrostomy (PEG) feeding was introduced into clinical practice in 1980. It describes a feeding tube placed directly into the stomach under endoscopic guidance. It is an established means of providing enteral nutrition to those who have functionally normal gastrointestinal tracts, but who cannot meet their nutritional requirements due to inadequate oral intake. The intervention is usually reserved when nutritional intake is likely to be inadequate for more than 4–6 weeks. Although the benefits of PEG have been shown for a select group of patients, there currently exists concerns about the increasing frequency of this intervention, and also uncertainty about the long-term benefits for certain patients. The 2004 UK National Confidential Enquiry into Patient Outcome and Death report emphasised this concern, with almost a fifth of PEG being undertaken for futile indications that negatively influenced morbidity and mortality. The present review paper discusses the indications for, controversies surrounding and complications of gastrostomy feeding and provides practical advice on optimising patient selection for this intervention.

Dietary protein is a pre-requisite for the maintenance of skeletal muscle mass; stimulating increases in muscle protein synthesis (MPS), via essential amino acids (EAA), and attenuating muscle protein breakdown, via insulin. Muscles are receptive to the anabolic effects of dietary protein, and in particular the EAA leucine, for only a short period (i.e. about 2–3 h) in the rested state. Thereafter, MPS exhibits tachyphylaxis despite continued EAA availability and sustained mechanistic target of rapamycin complex 1 signalling. Other notable characteristics of this ‘muscle full’ phenomenon include: (i) it cannot be overcome by proximal intake of additional nutrient signals/substrates regulating MPS; meaning a refractory period exists before a next stimulation is possible, (ii) it is refractory to pharmacological/nutraceutical enhancement of muscle blood flow and thus is not induced by muscle hypo-perfusion, (iii) it manifests independently of whether protein intake occurs in a bolus or intermittent feeding pattern, and (iv) it does not appear to be dependent on protein dose per se. Instead, the main factor associated with altering muscle full is physical activity. For instance, when coupled to protein intake, resistance exercise delays the muscle full set-point to permit additional use of available EAA for MPS to promote muscle remodelling/growth. In contrast, ageing is associated with blunted MPS responses to protein/exercise (anabolic resistance), while physical inactivity (e.g. immobilisation) induces a premature muscle full, promoting muscle atrophy. It is crucial that in catabolic scenarios, anabolic strategies are sought to mitigate muscle decline. This review highlights regulatory protein turnover interactions by dietary protein, exercise, ageing and physical inactivity.

The health benefits of fruit, vegetables and dietary fibre have been promoted for many years. Much of the supporting evidence is circumstantial or even contradictory and mechanisms underlying health benefits of specific foods are poorly understood. Colorectal cancer shows marked geographical differences in incidence, probably linked with diet, and explanations for this require knowledge of the complex interactions between diet, microbiota and the gut epithelium. Dietary fibres can act as prebiotics, encouraging growth of saccharolytic bacteria, but other mechanisms are also important. Some but not all soluble fibres have a ‘contrabiotic’ effect inhibiting bacterial adherence to the epithelium. This is particularly a property of pectins (galacturonans) whereas dietary fructans, previously regarded as beneficial prebiotics, can have a proinflammatory effect mediated via toxic effects of high butyrate concentrations. This also suggests that ulcerative colitis could in part result from potentially toxic faecal butyrate concentrations in the presence of a damaged mucus layer. Epithelial adherence of lectins, either dietary lectins as found in legumes, or bacterial lectins such as the galactose-binding lectin expressed by colon cancer-associated Fusobacterium nucleatum, may also be important and could be inhibitable by specific dietary glycans. Conversely, emulsifiers in processed foods may increase bacterial translocation and alter the microbiota thus promoting inflammation or cancer. Focusing on one condition is of limited value although in developing public health messages and growing evidence for impacts of dietary components on all-cause mortality is gaining more attention. We are only just starting to understand the complex interactions between food, the microbiota and health.

The aim of this review is to provide an overview of the complex interactions between dietary fibre and the resident microbial community in the human gut. The microbiota influences both health maintenance and disease development. In the large intestine, the microbiota plays a crucial role in the degradation of dietary carbohydrates that remain undigested in the upper gut (non-digestible carbohydrates or fibre). Dietary fibre contains a variety of different types of carbohydrates, and its breakdown is facilitated by many different microbial enzymes. Some microbes, termed generalists, are able to degrade a range of different carbohydrates, whereas others are more specialised. Furthermore, the physicochemical characteristics of dietary fibre, such as whether it enters the gut in soluble or insoluble form, also likely influence which microbes can degrade it. A complex nutritional network therefore exists comprising primary degraders able to attack complex fibre and cross feeders that benefit from fibre breakdown intermediates or fermentation products. This leads predominately to the generation of the short-chain fatty acids (SCFA) acetate, propionate and butyrate, which exert various effects on host physiology, including the supply of energy, influencing glucose and lipid metabolism and anti-carcinogenic and anti-inflammatory actions. In order to effectively modulate the gut microbiota through diet, there is a need to better understand the complex competitive and cooperative interactions between gut microbes in dietary fibre breakdown, as well as how gut environmental factors and the physicochemical state of fibre originating from different types of diets influence microbial metabolism and ecology in the gut.

The aim of this review paper is to explore the strategies employed to tackle micronutrient deficiencies with illustrations from field-based experience. Hidden hunger is the presence of multiple micronutrient deficiencies (particularly iron, zinc, iodine and vitamin A), which can occur without a deficit in energy intake as a result of consuming an energy-dense, but nutrient-poor diet. It is estimated that it affects more than two billion people worldwide, particularly in low- and middle-income countries where there is a reliance on low-cost food staples and where the diversity of the diet is limited. Finding a way to improve the nutritional quality of diets for the poorest people is central to meeting the UN sustainable development goals particularly sustainable development goal 2: end hunger, achieve food security and improved nutrition and promote sustainable agriculture. As we pass the midpoint of the UN's Decade for Action on Nutrition, it is timely to reflect on progress towards achieving sustainable development goal 2 and the strategies to reduce hidden hunger. Many low- and middle-income countries are falling behind national nutrition targets, and this has been exacerbated by the COVID-19 pandemic as well as other recent shocks to the global food system which have disproportionately impacted the world's most vulnerable communities. Addressing inequalities within the food system must be central to developing a sustainable, cost-effective strategy for improving food quality that delivers benefit to the seldom heard and marginalised communities.

High-protein meals and foods are promoted for their beneficial effects on satiety, weight loss and glucose homeostasis. However, the mechanisms involved and the long-term benefits of such diets are still debated. We here review how the characterisation of intestinal gluconeogenesis (IGN) sheds new light on the mechanisms by which protein diets exert their beneficial effects on health. The small intestine is the third organ (in addition to the liver and kidney) contributing to endogenous glucose production via gluconeogenesis. The particularity of glucose produced by the intestine is that it is detected in the portal vein and initiates a nervous signal to the hypothalamic nuclei regulating energy homeostasis. In this context, we demonstrated that protein diets initiate their satiety effects indirectly via IGN and portal glucose sensing. This induction results in the activation of brain areas involved in the regulation of food intake. The μ-opioid-antagonistic properties of protein digests, exerted in the portal vein, are a key link between IGN induction and protein-enriched diet in the control of satiety. From our results, IGN can be proposed as a mandatory link between nutrient sensing and the regulation of whole-body homeostasis. The use of specific mouse models targeting IGN should allow us to identify several metabolic functions that could be controlled by protein diets. This will lead to the characterisation of the mechanisms by which protein diets improve whole-body homeostasis. These data could be the basis of novel nutritional strategies targeting the serious metabolic consequences of both obesity and diabetes.