Growing evidence has emerged about the role of dietary patterns and components in heart failure (HF) incidence and severity. The objective here is to provide a comprehensive summary of the current evidence regarding dietary patterns/components and HF. A comprehensive search of online databases was conducted using multiple relevant keywords to identify relevant human studies. The Dietary Approaches to Stop Hypertension (DASH) and Mediterranean diets have consistently been associated with decreased HF incidence and severity. Regarding specific dietary components, fruit, vegetables, legumes and whole grains appear beneficial. Current evidence suggests that red/processed meats, eggs and refined carbohydrates are harmful, while fish, dairy products and poultry remain controversial. However, there is a notable lack of human intervention trials. The existing but limited observational and interventional evidence from human studies suggests that a plant-based dietary pattern high in antioxidants, micronutrients, nitrate and fibre but low in saturated/trans-fat and Na may decrease HF incidence/severity. Potential mechanisms include decreased oxidative stress, homocysteine and inflammation but higher antioxidant defence and NO bioavailability and gut microbiome modulation. Randomised, controlled trials are urgently required.

The spectrum of gluten-related disorders includes coeliac disease (CD), wheat allergy (WA) and the suggested entity of non-coeliac gluten sensitivity (NCGS). An increasing number of the world’s population are avoiding gluten due to the assumption of health benefits and self-diagnosed gastrointestinal and/or extra-intestinal symptoms. Unlike CD and WA, NCGS is a relatively new entity with an unknown prevalence and mechanisms, complicated by recent literature suggesting that gluten is not the only food component that may trigger symptoms experienced by this group of patients. The term ‘non-coeliac wheat sensitivity’ has been proposed as a more accurate term, allowing inclusion of other non-gluten wheat components such as fructans and amylase–trypsin inhibitors. There is inconsistent evidence when evaluating the effects of a gluten challenge in patients with suspected NCGS and there is a need for a standardised procedure to confirm the diagnosis, ultimately enabling the optimisation of clinical care. The present review will give an overview of the different gluten-related disorders and discuss the most recent scientific evidence investigating NCGS.

The WHO encourages national diet survey (NDS) implementation to obtain relevant data to inform policies addressing all forms of malnutrition, which remains a pressing issue throughout Europe. This paper provides an up-to-date review on energy, macro- and selected micronutrient intakes in children across WHO Europe using the latest available NDS intakes. It assesses these against WHO recommended nutrient intakes (RNI) to highlight vulnerable groups and areas of concern. Dietary survey information was gathered by Internet searches, contacting survey authors and nutrition experts. Survey characteristics, energy and nutrient intakes were extracted and weighted means calculated and presented by region. Child energy and nutrient intakes were extracted from twenty-one NDS across a third (n 18) of the fifty-three WHO Europe countries. Of these, 38 % (n 6) reported intakes by socio-economic group, but by various indicators. Energy and macronutrients, where boys and older children had higher intakes, were more widely reported than micronutrients. Most countries met under half of the WHO RNI for nutrients reported in their NDS. Micronutrient attainment was higher than macronutrients, but worst in girls and older children. Only a third, mainly Western, WHO European member states provided published data on child nutrient intakes. Gaps in provision mean that dietary inadequacies may go unidentified, preventing evidence-based policy formation. WHO RNI attainment was poor, particularly in girls and older children. Inconsistent age groups, dietary methodologies, nutrient composition databases and under-reporting hinder inter-country comparisons. Future efforts should encourage countries to conduct NDS in a standardised format by age and sociodemographic variables.

It has been nearly 70 years since the discovery that strict adherence to a diet low in phenylalanine prevents severe neurological sequelae in patients with phenylalanine hydroxylase deficiency (phenylketonuria; PKU). Today, dietary treatment with restricted phenylalanine intake supplemented with non-phenylalanine amino acids to support growth and maintain a healthy body composition remains the mainstay of therapy. However, a better understanding is needed of the factors that influence N balance in the context of amino acid supplementation. The aim of the present paper is to summarise considerations for improving N balance in patients with PKU, with a focus on gaining greater understanding of amino acid absorption, disposition and utilisation. In addition, the impact of phenylalanine-free amino acids on 24 h blood phenylalanine/tyrosine circadian rhythm is evaluated. We compare the effects of administering intact protein v. free amino acid on protein metabolism and discuss the possibility of improving outcomes by administering amino acid mixtures so that their absorption profile mimics that of intact protein. Protein substitutes with the ability to delay absorption of phenylalanine and tyrosine, mimicking physiological absorption kinetics, are expected to improve the rate of assimilation into protein and minimise fluctuations in quantitative plasma amino acid levels. They may also help maintain normal glycaemia and satiety sensation. This is likely to play an important role in improving the management of patients with PKU.

The proportion of adults aged 60 years and over is expected to increase over the coming decades. This ageing of the population represents an important health issue, given that marked reductions to cerebral macro- and microstructural integrity are apparent with increasing age. Reduced cerebral structural integrity in older adults appears to predict poorer cognitive performance, even in the absence of clinical disorders such as dementia. As such, it is becoming increasingly important to identify those factors predicting cerebral structural integrity, especially factors that are modifiable. One such factor is nutritional intake. While the literature is limited, data from available cross-sectional studies indicate that increased intake of nutrients such as B vitamins (for example, B6, B12 and folate), choline, n-3 fatty acids and vitamin D, or increased adherence to prudent whole diets (for example, the Mediterranean diet) predicts greater cerebral structural integrity in older adults. There is even greater scarcity of randomised clinical trials investigating the effects of nutritional supplementation on cerebral structure, though it appears that supplementation with B vitamins (B6, B12 and folic acid) or n-3 fatty acids (DHA or EPA) may be beneficial. The current review presents an overview of available research examining the relationship between key nutrients or adherence to select diets and cerebral structural integrity in dementia-free older adults.

Increased oxidative stress has been implicated as a potential causal factor in the development of several diseases. In the last decade, an extensive literature has been produced on vitamin D, not limited to its well-known function like a steroid hormone on skeletal tissue, but for its potential pleiotropic role in human health. Several researchers have suggested relationships between vitamin D intake and health outcomes such as cancer prevention and increased immunity, or possible role in preventing diabetes, and in inflammation. Little is known about its antioxidant effect. The aim of the present review was to explore major evidence regarding the potential scavenger capacity of vitamin D in high-evidence human studies. Studies considered by the present review suggest that the potential role of vitamin D as an antioxidant could not be confirmed. Current literature showed controversial effects about the ability of cholecalciferol to prevent or ameliorate oxidative stress biomarkers, and there is need of further and high-quality studies testing the antioxidant effect of vitamin D supplementation.

Existing reviews suggest that milk and other dairy products do not play a role in the development of obesity in childhood, but they do make an important contribution to children’s nutrient intake. It is thus curious that public health advice on the consumption of dairy products for children is often perceived as unclear. The present review aimed to provide an overview of the totality of the evidence on the association between milk and other dairy products, and obesity and indicators of adiposity, in children. Our search identified forty-three cross-sectional studies, thirty-one longitudinal cohort studies and twenty randomised controlled trials. We found that milk and other dairy products are consistently found to be not associated, or inversely associated, with obesity and indicators of adiposity in children. Adjustment for energy intake tended to change inverse associations to neutral. Also, we found little evidence to suggest that the relationship varied by type of milk or dairy product, or age of the children, although there was a dearth of evidence for young children. Only nine of the ninety-four studies found a positive association between milk and other dairy products and body fatness. There may be some plausible mechanisms underlying the effect of milk and other dairy products on adiposity that influence energy and fat balance, possibly through fat absorption, appetite or metabolic activity of gut microbiota. In conclusion, there is little evidence to support a concern to limit the consumption of milk and other dairy products for children on the grounds that they may promote obesity.

Early-life nutrition plays a critical role in fetal growth and development. Food intake absence and excess are the two main types of energy malnutrition that predispose to the appearance of diseases in adulthood, according to the hypothesis of ‘developmental origins of health and disease’. Epidemiological data have shown an association between early-life malnutrition and the metabolic syndrome in later life. Evidence has also demonstrated that nutrition during this period of life can affect the development of the immune system through epigenetic mechanisms. Thus, epigenetics has an essential role in the complex interplay between environmental factors and genetics. Altogether, this leads to the inflammatory response that is commonly seen in non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of the metabolic syndrome. In conjunction, DNA methylation, covalent modification of histones and the expression of non-coding RNA are the epigenetic phenomena that affect inflammatory processes in the context of NAFLD. Here, we highlight current understanding of the mechanisms underlying developmental programming of NAFLD linked to epigenetic modulation of the immune system and environmental factors, such as malnutrition.

We provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent intake of lean seafood, as compared with intake of terrestrial meats, reduces energy intake by 4–9 %, sufficient to prevent a positive energy balance and obesity. At equal energy intake, lean seafood reduces fasting and postprandial risk markers of insulin resistance, and improves insulin sensitivity in insulin-resistant adults. Energy restriction combined with intake of lean and fatty seafood seems to increase weight loss. Marine n-3 PUFA are probably of importance through n-3 PUFA-derived lipid mediators such as endocannabinoids and oxylipins, but other constituents of seafood such as the fish protein per se, trace elements or vitamins also seem to play a largely neglected role. A high intake of fatty seafood increases circulating levels of the insulin-sensitising hormone adiponectin. As compared with a high meat intake, high intake of seafood has been reported to reduce plasma levels of the hepatic acute-phase protein C-reactive protein level in some, but not all studies. More studies are needed to confirm the dietary effects on energy intake, obesity and insulin resistance. Future studies should be designed to elucidate the potential contribution of trace elements, vitamins and undesirables present in seafood, and we argue that stratification into responders and non-responders in randomised controlled trials may improve the understanding of health effects from intake of seafood.