One of the greatest challenges we face in the twenty-first century is to sustainably feed nine to ten billion people by 2050 while at the same time reducing environmental impact (e.g. greenhouse gas (GHG) emissions, biodiversity loss, land use change and loss of ecosystem services). To this end, food security must be delivered. According to the United Nations definition, ‘food security exists when all people, at all times, have physical and economic access to sufficient, safe and nutritious food to meet their dietary needs and food preferences for an active and healthy life’. At the same time as delivering food security, we must also reduce the environmental impact of food production. Future climate change will make an impact upon food production. On the other hand, agriculture contributes up to about 30% of the anthropogenic GHG emissions that drive climate change. The aim of this review is to outline some of the likely impacts of climate change on agriculture, the mitigation measures available within agriculture to reduce GHG emissions and outlines the very significant challenge of feeding nine to ten billion people sustainably under a future climate, with reduced emissions of GHG. Each challenge is in itself enormous, requiring solutions that co-deliver on all aspects. We conclude that the status quo is not an option, and tinkering with the current production systems is unlikely to deliver the food and ecosystems services we need in the future; radical changes in production and consumption are likely to be required over the coming decades.

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.

The gastrointestinal microbiota is a complex ecosystem with each human individual hosting at least 160 different bacterial strains. Our understanding of its role is rapidly expanding as a result of the molecular microbiological techniques that can accurately characterise its composition and ‘omics’ technologies that measure its metabolic activity. Since 1995, extensive research has investigated the prebiotic concept, which describes how supplementation of some non-digestible oligosaccharides can stimulate the growth and/or activity of specific genera including bifidobacteria. However, the vast majority of studies are in healthy human subjects, with few undertaken in patients with disorders relevant to clinical nutrition. Marked alterations of the luminal microbiota have been demonstrated in patients with digestive disorders, highlighting mechanisms through which they might be involved in their pathogenesis, including higher clostridia in patients who develop diarrhoea during enteral nutrition and the influence of bifidobacteria on intestinal dendritic cell phenotype in Crohn's disease. The impact of prebiotics on the intestinal microbiota of healthy people has not been consistently replicated in patients with digestive disorders. For example, a number of studies show that inulin/oligofructose do not increase bifidobacteria in enteral nutrition and Crohn's disease. Indeed, in Crohn's disease and irritable bowel syndrome there is evidence that some prebiotics in high doses worsen functional symptoms. Unlike healthy human subjects, patients experience a number of issues that may alter their gastrointestinal microbiota (disease, antibiotics and inflammation) and the use of microbiota modifying therapies, such as prebiotics, do not always elicit the same effects in patients as they do in healthy people.

The global food system makes a significant contribution to climate changing greenhouse gas emissions with all stages in the supply chain, from agricultural production through processing, distribution, retailing, home food preparation and waste, playing a part. It also gives rise to other major environmental impacts, including biodiversity loss and water extraction and pollution. Policy makers are increasingly aware of the need to address these concerns, but at the same time they are faced with a growing burden of food security and nutrition-related problems, and tasked with ensuring that there is enough food to meet the needs of a growing global population. In short, more people need to be fed better, with less environmental impact. How might this be achieved? Broadly, three main ‘takes’ or perspectives, on the issues and their interactions, appear to be emerging. Depending on one's view point, the problem can be conceptualised as a production challenge, in which case there is a need to change how food is produced by improving the unit efficiency of food production; a consumption challenge, which requires changes to the dietary drivers that determine food production; or a socio-economic challenge, which requires changes in how the food system is governed. This paper considers these perspectives in turn, their implications for nutrition and climate change, and their strengths and weaknesses. Finally, an argument is made for a reorientation of policy thinking which uses the insights provided by all three perspectives, rather than, as is the situation today, privileging one over the other.

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.

A well-functioning immune system is key to providing good defence against pathogenic organisms and to providing tolerance to non-threatening organisms, to food components and to self. The immune system works by providing an exclusion barrier, by identifying and eliminating pathogens and by identifying and tolerating non-threatening sources of antigens, and by maintaining a memory of immunological encounters. The immune system is complex involving many different cell types distributed throughout the body and many different chemical mediators some of which are involved directly in defence while others have a regulatory role. Babies are born with an immature immune system that fully develops in the first few years of life. Immune competence can decline with ageing. The sub-optimal immune competence that occurs early and late in life increases susceptibility to infection. Undernutrition decreases immune defences, making an individual more susceptible to infection. However, the immune response to an infection can itself impair nutritional status and alter body composition. Practically all forms of immunity are affected by protein–energy malnutrition, but non-specific defences and cell-mediated immunity are most severely affected. Micronutrient deficiencies impair immune function. Here, vitamins A, D and E, and Zn, Fe and Se are discussed. The gut-associated lymphoid tissue is especially important in health and well-being because of its close proximity to a large and diverse population of organisms in the gastrointestinal tract and its exposure to food constituents. Certain probiotic bacteria which modify the gut microbiota enhance immune function in laboratory animals and may do so in human subjects.

Although personalised nutrition is frequently considered in the context of diet–gene interactions, increasingly, personalised nutrition is seen to exist at three levels. The first is personalised dietary advice using Internet-delivered services, which ultimately will become automated and which will also draw on mobile phone technology. The second level of personalised dietary advice will include phenotypic information on anthropometry, physical activity, clinical parameters and biochemical markers of nutritional status. It remains possible that in addition to personalised dietary advice based on phenotypic data, advice at that group or metabotype level may be offered where metabotypes are defined by a common metabolic profile. The third level of personalised nutrition will involve the use of genomic data. While the genomic aspect of personalised nutrition is often considered as its main driver, there are significant challenges to translation of data on SNP and diet into personalised advice. The majority of the published data on SNP and diet emanate from observational studies and as such do not offer any cause–effect associations. To achieve this, purpose-designed dietary intervention studies will be needed with subjects recruited according to their genotype. Extensive research indicates that consumers would welcome personalised dietary advice including dietary advice based on their genotype. Unlike personalised medicine where genotype data are linked to the risk of developing a disease, in personalised nutrition the genetic data relate to the optimal diet for a given genotype to reduce disease risk factors and thus there are few ethical and legal issues in personalised nutrition.

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.

Ten years ago, it was assumed that disease risk prediction and personalised nutrition based on genetic information would now be in widespread use. However, this has not (yet) transpired. The interaction of genetic make-up, diet and health is far more complex and subtle than originally thought. With a few notable exceptions, the impact of identified common genetic variants on phenotype is relatively small and variable in their penetrance. Furthermore, the known variants account for only a fraction of what we believe to be the total genetic contribution to disease risk and heterogeneity in response to environmental change. Here, the question ‘how far have we progressed and are we likely to get there’ (Rimbach and Minihane, 2009) is revisited with regard to the translation of genetic knowledge into public health benefit. It is concluded that progress to date has been modest. It is hoped that recent technological developments allowing the detection of rarer variants and future use of more hypothesis-driven targeted data analysis will reveal most of the currently ‘hidden’ significant genetic variability.