This review will describe the evidence for changing the hospital environment to improve nutrition of older people, with particular emphasis on the role of additional mealtime assistance. Poor nutrition among older people in hospital is well recognised in many countries and is associated with poor outcomes of hospital care including increased mortality and longer lengths of stay. Factors recognised to contribute to poor dietary intake include acute illness, co-morbidities, cognitive impairment, low mood and medication. The hospital environment has also been scrutinised with reports from many countries of food being placed out of reach or going cold because time-pressured ward and catering staff often struggle to help an increasingly dependent group of patients at mealtimes. Routine screening in hospital for people at risk of under nutrition is recommended. Coloured trays and protected mealtimes are widespread although there is relatively little evidence for their impact on dietary intake. Volunteers can be trained to sfely give additional mealtime assistance including feeding to older patients on acute medical wards. They can improve the quality of mealtime care for patients and nursing staff although the evidence for improved dietary intake is mixed. In conclusion, improving the nutrition of older patients in hospital is challenging. Initiatives such as routine screening, the use of coloured trays, protected mealtimes and additional mealtime assistance can work together synergistically. Volunteers are likely to be increasingly important in an era when healthcare systems are generally limited in both financial resources and the ability to recruit sufficient nursing staff.

The use of taxes to promote healthy nutritional behaviour has gained ground in the past decade. The present paper reviews existing applications of fiscal instruments in nutrition policy and derives some perspectives and recommendations from the experiences gained with these instruments. Many countries in different parts of the world have experiences with the taxation of sugar-sweetened beverages, in some cases in combination with taxes on unhealthy food commodities such as confectionery or high-fat foods. These tax schemes have many similarities, but also differ in their definitions of tax objects and in the applied tax rates. Denmark has been the only country in the world to operate a tax on saturated fat content in foods, from 2011 to 2012. Most of the existing food tax schemes have been introduced from fiscal motivations, with health promotion as a secondary objective, but a few have been introduced with health promotion as the primary objective. The diversity in experiences from existing tax schemes can provide valuable insights for future use of fiscal instruments to promote healthy nutrition, in terms of designing effective and efficient tax or subsidy instruments, and in terms of smooth and politically viable implementation of the instruments.

Poor diets are a significant contributor to non-communicable diseases and obesity. Despite years of health promotion, change in dietary habits is slow and there is growing recognition of the need to provide greater support to individuals and to complement individual efforts with changes in the food environment to shift the default towards healthier diets. The present paper summarises opportunities for intervention at the individual and population level. It discusses the role of voluntary or mandatory approaches to drive change in the food industry and the need for improved methods to monitor and evaluate progress. It concludes with a call to action from all stakeholders to accelerate change towards a healthier diet.

CVD are characterised by a multi-factorial pathogenesis. Key pathogenetic steps in the development of CVD are the occurrence of endothelial dysfunction and formation of atherosclerotic lesions. Reduced nitric oxide (NO) bioavailability is a primary event in the initiation of the atherosclerotic cascade. NO is a free radical with multiple physiological functions including the regulation of vascular resistance, coagulation, immunity and oxidative metabolism. The synthesis of NO proceeds via two distinct pathways identified as enzymatic and non-enzymatic. The former involves the conversion of arginine into NO by the NO synthases, whilst the latter comprises a two-step reducing process converting inorganic nitrate $({\rm NO}_3^ - )$ into nitrite and subsequently NO.

Inorganic ${\rm NO}_3^ - $ is present in water and food, particularly beetroot and green leafy vegetables. Several investigations have therefore used the non-enzymatic NO pathway as a target for nutritional supplementation (${\rm NO}_3^ - $ salts) or dietary interventions (high-${\rm NO}_3^ - $ foods) to increase NO bioavailability and impact on cardiovascular outcomes. Some studies have reported positive effects of dietary ${\rm NO}_3^ - $ on systolic blood pressure and endothelial function in patients with hypertension and chronic heart failure. Nevertheless, results have been inconsistent and the size of the effect appears to be declining in older individuals. Additionally, there is a paucity of studies for disorders such as diabetes, CHD and chronic kidney failure. Thus, whilst dietary ${\rm NO}_3^ - $ supplementation could represent an effective and viable strategy for the primary and secondary prevention of age-related cardiovascular and metabolic diseases, more large-scale, robust studies are awaited to confirm or refute this notion.

Globally, an estimated 46 million people are currently living with dementia and this figure is projected to increase 3-fold by 2050, highlighting this major public health concern and its substantial associated healthcare costs. With pharmacological treatment yet to reach fruition, the emphasis on evidence-based preventative lifestyle strategies is becoming increasingly important and several modifiable lifestyle factors have been identified that may preserve cognitive health. These include good cardiovascular health, physical activity, low alcohol intake, smoking and a healthy diet, with growing interest in vitamin D. The aim of the present paper is to review the evidence supporting the potential roles of vitamin D in ageing and cognitive health in community-dwelling older adults. Furthermore, to describe the utility and challenges of cognitive assessments and outcomes when investigating vitamin D in this context. Evidence indicates that serum 25-hydroxyvitamin D (25(OH)D) may impact brain health. There is a biological plausibility from animal models that vitamin D may influence neurodegenerative disorders, through several mechanisms. Epidemiological evidence supports associations between low serum 25(OH)D concentrations and poorer cognitive performance in community-dwelling older populations, although an optimal 25(OH)D level for cognitive health could not be determined. The effect of raising 25(OH)D concentrations on cognitive function remains unclear, as there is a paucity of interventional evidence. At a minimum, it seems prudent to aim to prevent vitamin D deficiency in older adults, with other known common protective lifestyle factors, as a viable component of brain health strategies.

Advancements in image-based technologies and body composition research over the past decade has led to increased understanding of the importance of muscle abnormalities, such as low muscle mass (sarcopenia), and more recently low muscle attenuation (MA), as important prognostic indicators of unfavourable outcomes in patients with cancer. Muscle abnormalities can be highly prevalent in patients with cancer (ranging between 10 and 90 %), depending on the cohort under investigation and diagnostic criteria used. Importantly, both low muscle mass and low MA have been associated with poorer tolerance to chemotherapy, increased risk of post-operative infectious and non-infectious complications, increased length of hospital stay and poorer survival in patients with cancer. Studies have shown that systemic antineoplastic treatment can exacerbate losses in muscle mass and MA, with reported loss of skeletal muscle between 3 and 5 % per 100 d, which are increased exponentially with progressive disease and proximity to death. At present, no effective medical intervention to improve muscle mass and MA exists. Most research to date has focused on treating muscle depletion as part of the cachexia syndrome using nutritional, exercise and pharmacological interventions; however, these single-agent therapies have not provided promising results. Rehabilitation care to modify body composition, either increasing muscle mass and/or MA should be conducted, and its respective impact on oncology outcomes explored. Although the optimal timing and treatment strategy for preventing or delaying the development of muscle abnormalities are yet to be determined, multimodal interventions initiated early in the disease trajectory appear to hold the most promise.

Globally populations are ageing. By 2050, it is estimated that there will be two billion people aged 60 years or over, of which 131 million are projected to be affected by dementia, while depression is predicted to be the second leading cause of disability worldwide by 2020. Preventing or delaying the onset of these disorders should therefore be a public health priority. There is some evidence linking certain dietary patterns, particularly the Mediterranean diet, with a reduced risk of dementia and depression. Specific dietary components have also been investigated in relation to brain health, with emerging evidence supporting protective roles for n-3 PUFA, polyphenols, vitamin D and B-vitamins. At this time, the totality of evidence is strongest in support of a role for folate and the metabolically related B-vitamins (vitamin B12, vitamin B6 and riboflavin) in slowing the progression of cognitive decline and possibly reducing the risk of depression in ageing. Future studies incorporating new technologies, such as MRI and magnetoencephalography, offer much promise in identifying effective nutrition interventions that could reduce the risk of cognitive and mental disorders. This review will explore the ageing brain and the emerging evidence linking diet and specific nutrients with cognitive function and depression in ageing, with the potential to develop strategies that could improve quality of life in our ageing population.

Despite the inverse association between skin colour and efficiency of cutaneous vitamin D synthesis, in addition to the widely accepted racial disparity in vitamin D status, populations of ethnic minority are understudied in terms of setting target serum 25-hydroxyvitamin D concentrations and corresponding dietary requirements for vitamin D. In minority groups, prevention of vitamin D deficiency on a population basis is challenging due to the lack of clarity surrounding the metabolism and transport of vitamin D. Authoritative agencies have been unable to define pregnancy-specific dietary recommendations for vitamin D, owing to an absence of sufficient evidence to confirm whether nutritional requirements for vitamin D are altered during pregnancy. While the question of setting race- and pregnancy-specific dietary reference values for vitamin D has not been addressed to date, endemic vitamin D deficiency has been reported among gravidae worldwide, specifically among ethnic minorities and white women resident at high latitude. In light of the increased risk of nutritional rickets among infants of ethnic minority, coupled with growing evidence for potential non-skeletal roles of vitamin D in perinatal health, determination of the dietary vitamin D requirement that will prevent deficiency during pregnancy is a research priority. However, systematic approaches to establishing dietary requirements are limited by the quality of the available evidence and the under-representation of minority groups in clinical research. This review considers the evidence for racial differences in vitamin D status and response to vitamin D supplementation, with particular application to pregnancy-specific requirements among ethnic minorities resident at high latitudes.

The neurotransmitter serotonin has a role in affective disorders such as depression and anxiety, as well as sleep, cognitive function and appetite. This review examines the evidence that serotonin-related genotypes may moderate the behavioural effects of supplementation with the serotonin precursor amino acid l-tryptophan (TRP), on which synthesis of serotonin (or 5-hydroxytryptamine; 5-HT) depends. However, 95 % of serotonin is synthesised and used in the periphery, and TRP is also metabolised via non-5-HT routes such as the kynurenine pathway. Moreover, understanding of genotypes involved in regulation of serotonin raises questions over the generalisability of TRP effects on behaviour across individuals with varied serotonergic genotypes. To date, only differences between variants of the 5-HT transporter-linked promoter region (5-HTTLPR) have been investigated in relation to behavioural effects of TRP supplementation. Effects of 5-HTTLPR genotypes are usually compared between the alleles that are either high (L/L′) or low (S/S′) expressing of mRNA for the 5-HT transporter receptor. Yet, another key genetic variable is sex: in women, the S/S′ genotype predicts sensitivity to improved mood and reduced cortisol by TRP supplementation, during stressful challenges, whereas the L/L′ genotype protects against stress-induced mood deterioration. In men, the L/L′ genotype may confer risk of stress-induced increases in negative affect; there are insufficient data to assess effects on male S/S′ genotypes. However, better-powered studies to detect sex by genotype by stress by TRP interactions, as well as consideration of more genotypes, are needed before strong conclusions and recommendations for behavioural effects of TRP treatment can be reached.