The Nutrition Society Spring Conference 2018, held in Glasgow, brought together experts focusing on the interaction between different nutrients and how this impacts absorption, metabolism and health from biochemical and physiological perspectives. This cross-cutting theme was examined from a range of perspectives, bringing together experts on topics ranging from food processing to the impact of inflammation on nutrient status. Two plenary lectures provided a food landscape and lifecourse background to the proceedings, with on the first day a focus on processed/ultra-processed foods and their nutrient composition and, on the second day, a plenary lecture exploring the role that nutrient–nutrient interactions within the maternal diet have for the lifelong health of the offspring. The meeting was framed around three symposia, examining the competition and bioavailability of dietary components, nutrient–nutrient interactions and their role in protection from chronic diseases and the mechanisms of nutrient–nutrient interactions. The meeting ended with a round table, and an overall conclusion highlighting the opportunities to derive further understanding of the short- and long-term implications of diets through the study of nutrient–nutrient interactions.

The NOVA food categorisation recommends ‘avoiding processed foods (PF), especially ultra-processed foods (UPF)’ and selecting minimally PF to address obesity and chronic disease. However, NOVA categories are drawn using non-traditional views of food processing with additional criteria including a number of ingredients, added sugars, and additives. Comparison of NOVA's definition and categorisation of PF with codified and published ones shows limited congruence with respect to either definition or food placement into categories. While NOVA studies associate PF with decreased nutrient density, other classifications find nutrient-dense foods at all levels of processing. Analyses of food intake data using NOVA show UPF provide much added sugars. Since added sugars are one criterion for designation as UPF, such a proof demonstrates a tautology. Avoidance of foods deemed as UPF, such as wholegrain/enriched bread and cereals or flavoured milk, may not address obesity but could decrease intakes of folate, calcium and dietary fibre. Consumer understanding and implementation of NOVA have not been tested. Neither have outcomes been compared with vetted patterns, such as Dietary Approaches to Stop Hypertension, which base food selection on food groups and nutrient contribution. NOVA fails to demonstrate the criteria required for dietary guidance: understandability, affordability, workability and practicality. Consumers’ confusion about definitions and food categorisations, inadequate cooking and meal planning skills and scarcity of resources (time, money), may impede adoption and success of NOVA. Research documenting that NOVA can be implemented by consumers and has nutrition and health outcomes equal to vetted patterns is needed.

Iron deficiency remains the largest nutritional deficiency worldwide and the main cause of anaemia. Severe iron deficiency leads to anaemia known as iron deficiency anaemia (IDA), which affects a total of 1·24 billion people, the majority of whom are children and women from resource-poor countries. In sub-Saharan Africa, iron deficiency is frequently exacerbated by concomitant parasitic and bacterial infections and contributes to over 120 000 maternal deaths a year, while it irreparably limits the cognitive development of children and leads to poor outcomes in pregnancy.

Currently available iron compounds are cheap and readily available, but constitute a non-physiological approach to providing iron that leads to significant side effects. Consequently, iron deficiency and IDA remain without an effective treatment, particularly in populations with high burden of infectious diseases. So far, despite considerable investment in the past 25 years in nutrition interventions with iron supplementation and fortification, we have been unable to significantly decrease the burden of this disease in resource-poor countries.

If we are to eliminate this condition in the future, it is imperative to look beyond the strategies used until now and we should make an effort to combine community engagement and social science approaches to optimise supplementation and fortification programmes.

This review aims to describe approaches used to estimate bioavailability when deriving dietary reference values (DRV) for iron and zinc using the factorial approach. Various values have been applied by different expert bodies to convert absorbed iron or zinc into dietary intakes, and these are summarised in this review. The European Food Safety Authority (EFSA) derived zinc requirements from a trivariate saturation response model describing the relationship between zinc absorption and dietary zinc and phytate. The average requirement for men and women was determined as the intercept of the total absorbed zinc needed to meet physiological requirements, calculated according to body weight, with phytate intake levels of 300, 600, 900 and 1200 mg/d, which are representative of mean/median intakes observed in European populations. For iron, the method employed by EFSA was to use whole body iron losses, determined from radioisotope dilution studies, to calculate the quantity of absorbed iron required to maintain null balance. Absorption from the diet was estimated from a probability model based on measures of iron intake and status and physiological requirements for absorbed iron. Average dietary requirements were derived for men and pre- and post-menopausal women. Taking into consideration the complexity of deriving DRV for iron and zinc, mainly due to the limited knowledge on dietary bioavailability, it appears that EFSA has made maximum use of the most relevant up-to-date data to develop novel and transparent DRV for these nutrients.

Hashimoto's thyroiditis (HT) and Graves’ disease (GD) are examples of autoimmune thyroid disease (AITD), the commonest autoimmune condition. Antibodies to thyroid peroxidase (TPO), the enzyme that catalyses thyroid-hormone production and antibodies to the receptor for the thyroid-stimulating hormone, are characteristic of HT and GD, respectively. It is presently accepted that genetic susceptibility, environmental factors, including nutritional factors and immune disorders contribute to the development of AITD. Aiming to investigate the effect of iodine, iron and selenium in the risk, pathogenesis and treatment of thyroid disease, PubMed and the Cochrane Library were searched for relevant publications to provide a narrative review. Iodine: chronic exposure to excess iodine intake induces autoimmune thyroiditis, partly because highly-iodinated thyroglobulin (Tg) is more immunogenic. The recent introduction of universal salt iodisation can have a similar, although transient, effect. Iron: iron deficiency impairs thyroid metabolism. TPO is a haem enzyme that becomes active only after binding haem. AITD patients are frequently iron-deficient since autoimmune gastritis, which reduces iron absorption and coeliac disease which causes iron loss, are frequent co-morbidities. In two-thirds of women with persistent symptoms of hypothyroidism despite appropriate levothyroxine therapy, restoration of serum ferritin above 100 µg/l ameliorated symptoms. Selenium: selenoproteins are essential to thyroid action. In particular, the glutathione peroxidases remove excessive hydrogen peroxide produced there for the iodination of Tg to form thyroid hormones. There is evidence from observational studies and randomised controlled trials that selenium, probably as selenoproteins, can reduce TPO-antibody concentration, hypothyroidism and postpartum thyroiditis. Appropriate status of iodine, iron and selenium is crucial to thyroid health.

Bone health is determined by the rate of accrual in early life, followed by the rate of age-associated bone loss. Dietary protein intake might have a role in bone health across both of these phases via pleiotropic mechanistic pathways. Herein we summarise the pathways through which protein may exert either a positive or negative influence on bone. In the introduction, we describe the acid-ash hypothesis, which states that a high-protein intake may lead to an acidic residue that must be neutralised through the leaching of calcium and other minerals from the bone, subsequently leading to demineralisation and bone weakening. Conversely, and as described in the ‘Against: mechanisms through which protein may negatively impact bone’ section, protein intake may act to strengthen the bone by stimulating the activity of various anabolic hormones and growth factors, or by optimising muscle mass and functionality, which itself has an osteogenic influence. The net effect of these contrasting pathways is described in the ‘For: mechanisms through which protein may positively impact bone’ section, where a number of meta-analyses have demonstrated that higher protein intakes have a small positive impact on bone mass and fracture risk. Sometimes higher than recommended protein intakes are advised, e.g. during the earlier and later phases of the lifespan or during reduced energy availability. We conclude that protein is an essential nutrient for bone health, although further research is required to clarify the mechanistic pathways through which it exerts its influence, along with the clarification of the quantities, food sources and timing to allow for the optimisation of this protective influence and ultimately a reduction in fracture risk.

Micronutrients such as trace elements and vitamins are important as enzyme cofactors in the metabolism of all cells in the body and therefore key to determining nutritional status. The present systematic review examined the evidence of the impact of the systemic inflammatory response on plasma micronutrient status in acute (surgical) and chronic tissue injury. A literature review using targeted subject headings was carried out. Plasma C-reactive protein was used to classify minor (<10 mg/l), moderate (11–80 mg/l) and major (>80 mg/l) inflammation. The literature search produced 2344 publications and plasma vitamin D, zinc and carotenoids were most commonly studied and plasma vitamins K, B2 and B6 were least studied. In acute injury thirteen studies (all prospective) and in chronic injury twenty-four studies (largely retrospective) were included in the review. There was consistent evidence that most common measured micronutrients in the plasma (zinc, selenium, vitamins A, D, E, K, B2, B6, B12, C, lutein, lycopene, α- and β-carotene) were significantly lowered from minor to moderate to major inflammation. The results of the present systematic review indicate that most plasma micronutrients fall as part of the systemic inflammatory response irrespective of acute or chronic injury. Therefore, in the presence of a systemic inflammation, plasma micronutrient concentrations should be interpreted with caution. There are a number of methods applied to adjust plasma micronutrient concentrations to avoid misdiagnosis of deficiency. Alternatively, intracellular measurements appear to obviate the need for such plasma adjustment to assess micronutrient status.

β-Carotene intake and tissue/blood concentrations have been associated with reduced incidence of several chronic diseases. Further bioactive carotenoid-metabolites can modulate the expression of specific genes mainly via the nuclear hormone receptors: retinoic acid receptor- and retinoid X receptor-mediated signalling. To better understand the metabolic conversion of β-carotene, inter-individual differences regarding β-carotene bioavailability and bioactivity are key steps that determine its further metabolism and bioactivation and mediated signalling. Major carotenoid metabolites, the retinoids, can be stored as esters or further oxidised and excreted via phase 2 metabolism pathways. In this review, we aim to highlight the major critical control points that determine the fate of β-carotene in the human body, with a special emphasis on β-carotene oxygenase 1. The hypothesis that higher dietary β-carotene intake and serum level results in higher β-carotene-mediated signalling is partly questioned. Alternative autoregulatory mechanisms in β-carotene / retinoid-mediated signalling are highlighted to better predict and optimise nutritional strategies involving β-carotene-related health beneficial mediated effects.

Nutritional science has traditionally used the reductionist approach to understand the roles of individual nutrients in growth and development. The macronutrient dense but micronutrient poor diets consumed by many in the Western world may not result in an overt deficiency; however, there may be situations where multiple mild deficiencies combine with excess energy to alter cellular metabolism. These interactions are especially important in pregnancy as changes in early development modify the risk of developing non-communicable diseases later in life. Nutrient interactions affect all stages of fetal development, influencing endocrine programming, organ development and the epigenetic programming of gene expression. The rapidly developing field of stem cell metabolism reveals new links between cellular metabolism and differentiation. This review will consider the interactions between nutrients in the maternal diet and their influence on fetal development, with particular reference to energy metabolism, amino acids and the vitamins in the B group.

In the past, vitamins and minerals were used to cure deficiency diseases. Supplements nowadays are used with the aim of reducing the risk of chronic diseases of which the origins are complex. Dietary supplement use has increased in the UK over recent decades, contributing to the nutrient intake in the population, but not necessarily the proportion of the population that is sub-optimally nourished; therefore, not reducing the proportion below the estimated average requirement and potentially increasing the number at risk of an intake above the safety limits. The supplement nutrient intake may be objectively monitored using circulation biomarkers. The influence of the researcher in how the supplements are grouped and how the nutrient intakes are quantified may however result in different conclusions regarding their nutrient contribution, the associations with biomarkers, in general, and dose–response associations specifically. The diet might be sufficient in micronutrients, but lacking in a balanced food intake. Since public-health nutrition guidelines are expressed in terms of foods, there is potentially a discrepancy between the nutrient-orientated supplement and the quality of the dietary pattern. To promote health, current public-health messages only advocate supplements in specific circumstances, but not in optimally nourished populations.

The objective of this review paper is to evaluate the impact of undertaking aerobic exercise in the overnight-fasted v. fed-state, in the context of optimising the health benefits of regular physical activity. Conducting a single bout of aerobic exercise in the overnight-fasted v. fed-state can differentially modulate the aspects of metabolism and energy balance behaviours. This includes, but is not limited to, increased utilisation of fat as a fuel source, improved plasma lipid profiles, enhanced activation of molecular signalling pathways related to fuel metabolism in skeletal muscle and adipose tissue, and reductions in energy intake over the course of a day. The impact of a single bout of overnight-fasted v. fed-state exercise on short-term glycaemic control is variable, being affected by the experimental conditions, the time frame of measurement and possibly the subject population studied. The health response to undertaking overnight-fasted v. fed-state exercise for a sustained period of time in the form of exercise training is less clear, due to a limited number of studies. From the extant literature, there is evidence that overnight-fasted exercise in young, healthy men can enhance training-induced adaptations in skeletal muscle metabolic profile, and mitigate against the negative consequences of short-term excess energy intake on glucose tolerance compared with exercising in the fed-state. Nonetheless, further long-term studies are required, particularly in populations at-risk or living with cardio-metabolic disease to elucidate if feeding status prior to exercise modulates metabolism or energy balance behaviours to an extent that could impact upon the health or therapeutic benefits of exercise.

Humankind has existed for 2·5 million years but only in the past 10 000 years have we been exposed to wheat. Therefore, it could be considered that wheat (gluten) is a novel introduction to humankind's diet! Prior to 1939, the rationing system had already been devised. This led to an imperative to try to increase agricultural production. Thus, it was agreed in 1941 that there was a need to establish a Nutrition Society. The very roots of the Society were geared towards necessarily increasing the production of wheat. This goal was achieved and by the end of the 20th century, global wheat output had expanded by 5-fold. Perhaps, as a result, the epidemiology of coeliac disease (CD) or gluten sensitive enteropathy has changed. CD now affects 1 % or more of all adults. Despite this, delays in diagnosis are common, for every adult patient diagnosed approximately three–four cases are undetected. This review explores humankind's relationship with gluten, wheat chemistry, the rising prevalence of modern CD and the new entity of non-coeliac gluten or wheat sensitivity. The nutritional interventions of a low fermentable oligo-, di- and mono-saccharides and polyols diet and gluten-free diet (GFD) for irritable bowel syndrome and the evidence to support this approach (including our own published work) are also reviewed. There appears to be a rising interest in the GFD as a ‘lifestyler’, ‘free from’ or ‘clean eater’ choice, causing concern. Restrictive diets may lead to potential nutritional implications, with long-term effects requiring further exploration.

When we consume dietary fat, a series of complex metabolic processes ensures that fatty acids are absorbed, transported around the body and used/stored appropriately. The liver is a central metabolic organ within the human body and has a major role in regulating fat and carbohydrate metabolism. Studying hepatic metabolism in human subjects is challenging; the use of stable isotope tracers and measurement of particles or molecules secreted by the liver such as VLDL-TAG and 3-hydroxybutyrate offers the best insight into postprandial hepatic fatty acid metabolism in human subjects. Diet derived fatty acids are taken up by the liver and mix with fatty acids coming from the lipolysis of adipose tissue, and those already present in the liver (cytosolic TAG) and fatty acids synthesised de novo within the liver from non-lipid precursors (known as de novo lipogenesis). Fatty acids are removed from the liver by secretion as VLDL-TAG and oxidation. Perturbations in these processes have the potential to impact on metabolic health. Whether fatty acids are partitioned towards oxidation or esterification pathways appears to be dependent on a number of metabolic factors; not least ambient insulin concentrations. Moreover, along with the phenotype and lifestyle factors (e.g. habitual diet) of an individual, it is becoming apparent that the composition of the diet (macronutrient and fatty acid composition) may play pivotal roles in determining if intra-hepatic fat accumulates, although what remains to be elucidated is the influence these nutrients have on intra-hepatic fatty acid synthesis and partitioning.

This review evaluates evidence on dietary interventions for cancer survivors giving an overview of people's views and preferences for service attributes and provides a narrative review. After cancer, people often want to change their diet and there is a plethora of evidence why dietary optimisation would be beneficial. However, cancer survivors have different preferences about attributes of services including: place, person and communication mode. Randomised control trials have been reviewed to provide a narrative summary of evidence of dietary interventions. Most studies were on survivors of breast cancer, with a few on colorectal, prostate and gynaecological survivors. Telephone interventions were the most frequently reported means of providing advice and dietitians were most likely to communicate advice. Dietary assessment methods used were FFQ, food diaries and 24-h recalls. Dietary interventions were shown to increase intake of fruit and vegetables, dietary fibre, and improve diet quality in some studies but with contradictory findings in others. Telephone advice increased fruit and vegetable intake primarily in women with breast cancer and at some time points in people after colorectal cancer, but findings were inconsistent. Findings from mail interventions were contradictory, although diet quality improved in some studies. Web-based and group sessions had limited benefits. There is some evidence that dietary interventions improve diet quality and some aspects of nutritional intake in cancer survivors. However, due to contradictory findings between studies and cancer sites, short term follow-up and surrogate endpoints it is difficult to decipher the evidence base.