The human diet has undergone profound changes over recent generations and this trend is likely to accelerate in the 21st century. Innovations in food technology, new ways of producing and processing foods and the increasing use of artificial vitamins and novel ingredients are changing the human diet in ways that our dietary monitoring systems struggle to keep pace with. There is a growing awareness of the importance of diet, but little understanding of how these changes may affect the health of current and future generations. Epigenetic programming, and specifically the persistence of functional epigenetic states following nutritional exposure, is particularly relevant to the issue of dietary change. Epigenetics is emerging as perhaps the most important mechanism through which diet and nutrition can directly influence the genome and there is now considerable evidence for nutritional epigenetic programming of health and the response to diet itself. A number of nutrients and food components that are changing in the human diet have been shown to produce epigenetic states that are stable across different timescales. We need to better understand the nutritional programming of epigenetic states, the persistence of these marks in time and their effect on biological function and the response to diet.

The aim of this review is to summarise the evidence linking vitamin D to bone health outcomes in older adults. A plethora of scientific evidence globally suggests that large proportions of people have vitamin D deficiency and are not meeting recommended intakes. Older adults are at particular risk of the consequences of vitamin D deficiency owing to a combination of physiological and behavioural factors. Epidemiological studies show that low vitamin D status is associated with a variety of negative skeletal consequences in older adults including osteomalacia, reduced bone mineral density, impaired Ca absorption and secondary hyperparathyroidism. There seems to be inconsistent evidence for a protective role of vitamin D supplementation alone on bone mass. However, it is generally accepted that vitamin D (17·5 μg/d) in combination with Ca (1200 mg/d) reduces bone loss among older white subjects. Evidence for a benefit of vitamin D supplementation alone on reducing fracture risk is varied. According to a recent Agency for Healthcare Research and Quality review in the USA the evidence base shows mixed results for a beneficial effect of vitamin D on decreasing overall fracture risk. Limitations such as poor compliance with treatment, incomplete assessment of vitamin D status and large drop-out rates however, have been highlighted within some studies. In conclusion, it is generally accepted that vitamin D in combination with Ca reduces the risk of non-vertebral fractures particularly those in institutional care. The lack of data on vitamin D and bone health outcomes in certain population groups such as diverse racial groups warrants attention.

The scaling up nutrition (SUN) policy framework requires extensive public–private partnership (PPP). Malnutrition is multi-dimensional and should engage multi-sectoral platforms. The SUN policy however did not fully embrace the dynamics of harnessing PPP. The objectives of the present paper are to highlight the reasons for the apprehension around PPP and illustrate how effective coordination of PPP in West Africa has contributed to implementing large-scale food fortification with micronutrients as a complementary nutrition intervention. The experience of Helen Keller International (HKI) in scaling up food fortification was emphasised with understanding of the factors contributing to indifference by the international community to private sector contribution to SUN. The roles of different stakeholders in a PPP are elucidated and the process linked to who, why and how to engage. The private sector provides direct nutrition services while the public sector creates the enabling environment for the private sector to thrive on social values. Through this approach fortified vegetable oil and wheat flour are now reaching over 70% of the population in West Africa. As a neutral broker HKI coordinated and facilitated dialogue among the different stakeholders. The core competencies of each stakeholder were harnessed and each partner was held accountable. It concludes that multi-sectoral relationship must be transparent, equitable and based on shared mutual interests. The rules and values of PPP offer opportunities for SUN.

Diet-related chronic diseases are major public health concerns in England and the associated costs to the National Health Service and society are considerable. Poor diet and other lifestyle factors are estimated to account for about one-third of all deaths from CVD in England. UK dietary recommendations were set by the Committee on Medical Aspects of Food Policy and are now set by the Scientific Advisory Committee on Nutrition. For cardiovascular health, dietary recommendations are set for nutrients (saturated fat, trans-fat and carbohydrates), foods (fruits, vegetables and oily fish) and salt. The National Diet and Nutrition Survey demonstrates that the majority of the UK population have poor diets. Average intakes of saturated fat and salt are above recommendations while fruit, vegetables, fibre and oily fish are below recommendations. The Department of Health in England is committed to working to improve diet and lifestyle. Current work includes the Public Health Responsibility Deal, under which organisations pledge to increase fruits and vegetables and reduce levels of salt, trans-fat and energy in manufactured foods and menus, the provision of information to help improve food choice through better food labels and provision of information, including a NHS Choices website and the social marketing campaign Change4Life.

This review reappraises dietary advice to reduce and replace SFA for the prevention of CVD. In the 1970s, SFA accounted for about 18% UK food energy, by 2001 it had fallen to 13% and continues to be above the <11% target. Compared with carbohydrates, C12–C16 SFA raise serum total cholesterol (TC), LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) without affecting the TC:HDL-C ratio; other SFA have neutral effects on the fasting lipid profile. Replacing 3% dietary SFA with MUFA or PUFA lowers LDL-C by 2% and TC:HDL-C ratio by 0·03. No other specific adverse effects of SFA compared with MUFA on risk CVD factors have been proven. Meta-analyses of prospective cohort studies report the relative risks (95% CI) of high v. low intakes of SFA to be 1·07 (0·96, 1·19) for CHD, 0·81 (0·62, 1·05) for stroke and 1·00 (0·89, 1·11) for CVD mortality and were not statistically significant. Exchanging 5% energy SFA for PUFA or carbohydrates found hazard ratios (95% CI) for CHD death to be 26% (−23, −3) and 4% (−18, 12; NS) lower, respectively. Meta-analysis of randomised controlled trials with clinical endpoints reports mean reductions (95% CI) of 14% (4, 23) in CHD incidence and 6% (−25, 4; NS) in mortality in trials, where SFA was lowered by decreasing and/or modifying dietary fat. In conclusion, SFA intakes are now close to guideline amounts and further reductions may only have a minor impact on CVD.

A high intake of fruit and vegetables (FV) has been shown to be associated with reduced risk of a number of chronic diseases, including CVD. This review aims to provide an overview of the evidence that increased FV intake reduces risk of CVD, focusing on studies examining total FV intake. This evidence so far available is largely based on prospective cohort studies, with meta-analyses demonstrating an association between increased FV intake and reduced risk of both CHD and stroke. Controlled intervention trials examining either clinical or cardiovascular risk factor endpoints are scarce. However, such trials have shown that an increase in FV consumption can lower blood pressure and also improve microvascular function, both of which are commensurate with a reduced risk of CVD. The effects of increased FV consumption on plasma lipid levels, risk of diabetes and body weight have yet to be firmly established. In conclusion, evidence that FV consumption reduces the risk of CVD is so far largely confined to observational epidemiology, with further intervention studies required.

Despite strong prospective epidemiology and mechanistic evidence for the benefits of certain micronutrients in preventing CVD, neutral and negative outcomes from secondary intervention trials have undermined the efficacy of supplemental nutrition in preventing CVD. In contrast, evidence for the positive impact of specific diets in CVD prevention, such as the Dietary Approaches to Stop Hypertension (DASH) diet, has focused attention on the potential benefits of whole diets and specific dietary patterns. These patterns have been scored on the basis of current guidelines for the prevention of CVD, to provide a quantitative evaluation of the relationship between diet and disease. Using this approach, large prospective studies have reported reductions in CVD risk ranging from 10 to 60% in groups whose diets can be variously classified as ‘Healthy’, ‘Prudent’, Mediterranean’ or ‘DASH compliant’. Evaluation of the relationship between dietary score and risk biomarkers has also been informative with respect to underlying mechanisms. However, although this analysis may appear to validate whole-diet approaches to disease prevention, it must be remembered that the classification of dietary scores is based on current understanding of diet–disease relationships, which may be incomplete or erroneous. Of particular concern is the limited number of high-quality intervention studies of whole diets, which include disease endpoints as the primary outcome. The aims of this review are to highlight the limitations of dietary guidelines based on nutrient-specific data, and the persuasive evidence for the benefits of whole dietary patterns on CVD risk. It also makes a plea for more randomised controlled trials, which are designed to support food and whole dietary-based approaches for preventing CVD.

Non-alcoholic fatty liver disease (NAFLD) is now recognised as the hepatic component of metabolic syndrome (MetS). NAFLD is an example of ectopic fat accumulation in a visceral organ that causes organ-specific disease, and affects risk of other related diseases such as type 2 diabetes and CVD. NAFLD is a spectrum of fat-associated liver conditions that can culminate in end stage liver disease, hepatocellular carcinoma and the need for liver transplantation. Simple steatosis, or fatty liver, occurs early in NAFLD and may progress to non-alcoholic steatohepatitis, fibrosis and cirrhosis with increased risk of hepatocellular carcinoma. Prevalence estimates for NAFLD range from 2 to 44% in the general population and it has been estimated that NAFLD exists in up to 70% of people with type 2 diabetes. Although many obese people have NAFLD, there are many obese people who do not develop ectopic liver fat. The aim of this review which is based on a presentation at the Royal Society of Medicine, UK in December 2012 is to discuss development of NAFLD, ectopic fat accumulation and insulin resistance. The review will also describe the relationships between NAFLD, type 2 diabetes and CVD.

The objective of the present paper was to review the literature investigating the potential relationship between fruit and vegetables (FV) and psychological well-being. The rising prevalence of mental ill health is causing considerable societal burden. Inexpensive and effective strategies are therefore required to improve the psychological well-being of the population, and to reduce the negative impact of mental health problems. A growing body of literature suggests that dietary intake may have the potential to influence psychological well-being. For example, studies have suggested that particular dietary constituents, including vitamins and minerals, might be beneficial to psychological health. However, in order to better reflect normal dietary intake, health-based research has increasingly begun to focus on whole foods and dietary patterns, rather than individual nutrients. One food group that has received increasing attention with regard to psychological health is FV. This is probably a result of the strong evidence base, which exists in relation to their protective association with a number of chronic diseases, as well as the fact that they are a rich source of some of the nutrients which have been linked to psychological health. While some promising findings exist with regards to FV intake and psychological well-being, overall, results are inconsistent. Possible reasons for this, such as methodological issues related to study design and the measurement of psychological well-being and FV intake, are discussed within this review. Based on the predominantly observational nature of existing literature, the present paper concludes that future well-designed randomised controlled trials are required to investigate the relationship further.

This review aims to assess the efficacy and safety of voluntary fortification as an option to address the occurrence of inadequate micronutrient intakes in population subgroups in Europe. Although legislation is harmonised across the European Union, fortification practices and patterns of consumption of fortified foods vary considerably between countries. While the proportion of children consuming fortified foods is greater than adults, the proportion of dietary energy obtained from fortified foods is generally low (<10% in Ireland, where fortified foods are widely consumed). There are a few systematic studies on the overall nutritional impact of voluntary fortification, but there are several studies on the impact of fortified ready-to-eat breakfast cereals. The available evidence indicates that voluntary fortification can reduce the risk of sub-optimal intakes of a range of micronutrients at a population level and can also improve status for selected micronutrients (e.g. folate, vitamin D and riboflavin) in children and adults. Although concerns have been raised regarding the potential of food fortification to lead to unacceptably high micronutrient intakes, particularly for those consuming higher amounts of fortified foods, data from national surveys on total micronutrient intakes (including fortified foods) in Europe show that small proportions of the population, particularly children, may exceed the upper intake level (UL) for some micronutrients. The risk of adverse effects occurring in these individuals exceeding the UL by modest amounts is low. In conclusion, voluntary fortification practices have been shown to improve intake and status of key micronutrients in European Union population groups and do not contribute appreciably to risk of adverse effects.

Accumulating evidence indicates that, analogous to n-6 PUFA, n-3 PUFA are enzymatically converted into diverse families of bioactive mediators that play numerous roles in physiology. These mediators, which include the resolvins, protectins and maresins, are particularly important in resolving acute inflammation and also appear to play a role in enhancing host defence. Given the protective actions of n-3 PUFA in human subjects and in animal models of disease, active generation of bioactive mediators may in part underlie these protective effects. Several studies have demonstrated that bioactive autacoids generated from n-3 PUFA have direct anti-inflammatory and pro-resolution actions, and the structures of many of these endogenous mediators have been elucidated. The diverse roles of these lipid mediators in health and disease, regulation of their biosynthesis, as well as identification of specific receptors and cellular targets, are emerging. This brief review will highlight the biosynthesis of resolvins, protectins and maresins, and discuss their receptor-mediated biological actions in promoting the resolution of inflammation. Their potential use as a new class of pro-resolution therapeutics, as well as gaps in knowledge and challenges for future research, will also be discussed. Overall, the identification of these novel families of lipid mediators has yielded insight into the protective actions of n-3 PUFA and may lead to the development of an entirely new class of therapeutics aimed at regulating inflammation and host defence.

Following on from the discovery of cannabinoid receptors, of their endogenous agonists (endocannabinoids) and of the biosynthetic and metabolic enzymes of the endocannabinoids, significant progress has been made towards the understanding of the role of the endocannabinoid system in both physiological and pathological conditions. Endocannabinoids are mainly n-6 long-chain PUFA (LCPUFA) derivatives that are synthesised by neuronal cells and inactivated via a two-step process that begins with their transport from the extracellular to the intracellular space and culminates in their intracellular degradation by hydrolysis or oxidation. Although the enzymes responsible for the biosynthesis and metabolism of endocannabinoids have been well characterised, the processes involved in their cellular uptake are still a subject of debate. Moreover, little is yet known about the roles of endocannabinoids derived from n-3 LCPUFA such as EPA and DHA. Here, I provide an overview of what is currently known about the mechanisms for the biosynthesis and inactivation of endocannabinoids, together with a brief analysis of the involvement of the endocannabinoids in both food intake and obesity. Owing to limited space, recent reviews will be often cited instead of original papers.

The presence of an active and functioning endocannabinoid (EC) system within cardiovascular tissues implies that this system has either a physiological or pathophysiological role (or both), and there is a substantial literature to support the notion that, in the main, they are protective in the setting of various CVD states. Moreover, there is an equally extensive literature to demonstrate the cardio- and vasculo-protective effects of n-3 long-chain (LC)-PUFA. It is now becoming evident that there appears to be a close relationship between dietary intervention with n-3 LC-PUFA and changes in tissue levels of EC, raising the question as to whether or not EC may, at least in part, play a role in mediating the cardio-and vasculo-protective effects of n-3 LC-PUFA. This brief review summarises the current understanding of how both EC and n-3 LC-PUFA exert their protective effects in three major cardiovascular disorders (hypertension, atherosclerosis and acute myocardial infarction) and attempts to identify the similarities and differences that may indicate common or integrated mechanisms. From the data available, it is unlikely that in hypertension EC mediate any beneficial effects of n-3 LC-PUFA, since they do not share common mechanisms of blood pressure reduction. However, inhibition of inflammation is an effect shared by EC and n-3 LC-PUFA in the setting of both atherosclerosis and myocardial reperfusion injury, while blockade of L-type Ca2+ channels is one of the possible common mechanisms for their antiarrhythmic effects. Although both EC and n-3 LC-PUFA demonstrate vasculo- and cardio-protection, the literature overwhelmingly shows that n-3 LC-PUFA decrease tissue levels of EC through formation of EC–n-3 LC-PUFA conjugates, which is counter-intuitive to an argument that EC may mediate the effects of n-3 LC-PUFA. However, the discovery that these conjugates have a greater affinity for cannabinoid receptors than the native EC provides a fascinating avenue for further research into novel approaches for the treatment and prevention of atherosclerosis and myocardial injury following ischaemia/reperfusion.