In 1798, Thomas Robert Malthus published ‘An essay on the principle of population’ in which he concluded that: ‘The power of population is so superior to the power of the earth to produce subsistence for man, that premature death must in some shape or other visit the human race.’ Over the following century he was criticised for underestimating the potential for scientific and technological innovation to provide positive change. Since then, he has been proved wrong, with a number of papers published during the past few decades pointing out why he has been proved wrong so many times. In the present paper, I briefly review the main changes in food production in the past that have allowed us to continue to meet ever growing demand for food, and I examine the possibility of these same innovations delivering food security in the future. On the basis of recent studies, I conclude that technological innovation can no longer be relied upon to prove Malthus wrong as we strive to feed 9–10 billion people by 2050. Unless we are prepared to accept a wide range of significant, undesirable environmental consequences, technology alone cannot provide food security in 2050. Food demand, particularly the demand for livestock products, will need to be managed if we are to continue to prove Malthus wrong into the future.

This review uses production and climate data to examine global and local production trends that can be related to events such as drought. UK grain quality data is also available and provides an overview of trends in protein content. Literature surveys show a consistent reduction in grain size due to the effects of temperature and/or drought. A review of gene expression studies showed that most genes involved in starch synthesis are down regulated under heat stress. Net protein production is also reduced under heat and/or drought stress but apparently to a lesser degree as the reduction in grain mass is larger, resulting in an increase in protein concentration. Modelling has suggested that adaptation could be achieved by moving production to more extreme latitudes but other research suggests that simply transferring germplasm from one region to another is unlikely to be successful. Another review has identified drought tolerance phenotypes that could be used to breed more drought tolerant crops. At the time of the review, the authors concluded that phenotypic selection was generally preferable to forms of marker-assisted breeding and have used the approach to produce drought tolerant wheat cultivars. Transgenic approaches have also been shown to improve drought tolerance under controlled environment conditions but there are no results to show how well these results translate into improved crop performance under field conditions. The recent advances in genomic data and detecting marker–trait associations suggest that marker-assisted breeding will play a much more important role in breeding drought tolerant cereals in the future.

There are many quality targets in cereals that could generate step-change improvements in nutritional or food-processing characteristics. For instance, levels of acrylamide, soluble and insoluble fibre, antioxidants, allergens and intolerance factors in food are, to a large extent, determined by the genetics of the raw materials used. However, improvements to these traits pose significant challenges to plant breeders. For some traits, this is because the underlying genetic and biochemical basis of the traits is not fully understood but for others, there is simply a lack of natural genetic variation in commercially useful germplasm. One strategy to overcome the latter hindrance is to use wide crosses with more exotic germplasm; however, this can bring other difficulties such as yield loss and linkage drag of deleterious alleles. As DNA sequencing becomes cheaper and faster, it drives the research fields of reverse genetics and functional genomics which in turn will enable the incorporation of desirable traits into crop varieties via molecular breeding and biotechnology. I will discuss the evolution of these techniques from conventional genetic modification to more recent developments in targeted gene editing and the potential of biotechnology to complement conventional breeding methods. I will also discuss the role of risk assessment and regulation in the commercialisation of GM crops.

Autism spectrum disorders represent a diverse and heterogeneous array of conditions unified by the variable presence of specific behaviours impacting social and communicative functions (social affect) alongside other presentation. Common overt characteristics may come about as a consequence of several different genetic and biological processes differentially manifesting across different people or groups. The concept of plural ‘autisms’ is evolving, strengthened by an increasingly important evidence base detailing different developmental trajectories across the autism spectrum and the appearance of comorbidity variably interacting with core symptoms and onwards influencing quality of life. Reports that dietary intervention, specifically the removal of foods containing gluten and/or casein from the diet, may impact on the presentation of autism for some, complement this plural view of autism. Evidence suggestive of differing responses to the use of a gluten- and casein-free diet, defined as best- and non-response, has combined with some progress on determining the underlying genetic and biological correlates potentially related to such dietary elements. The preliminary suggestion of a possible diet-related autism phenotype is the result. This review will highlight several pertinent aspects onwards to an effect of food in some cases of autism including research on the pharmacological activity of food metabolites, immune response, issues with gut barrier function and some contribution from the gut microbiota. These represent promising areas in need of far greater research inspection in order to potentially define such a diet-related subgroup on the autism spectrum.

In contrast to the decline in mortality from many non-infectious, chronic diseases in the UK, death from liver disease has increased exponentially in men and women over the past 40 years. This is primarily because of the over consumption of alcohol, but also the increased prevalence of obesity, which is linked to early pathology through the accumulation of liver fat. Supra-physiological intakes of fructose-containing sugar can produce acute, adverse effects on lipid metabolism, and deliver excess energy that increases bodyweight and the deposition of fat in sites other than adipose tissue, including the liver. This review addresses the variable metabolic origins of liver fat, and the key importance of postprandial lipid metabolism in this respect. The effects of supra-physiological intakes of sugar are also considered in context of the real world and established threshold for the adverse effects of sugar on cardio-metabolic risk factors. The review concludes that while the average intake of sugar in the UK falls well below this critical threshold, intakes in subgroups of adults, and especially adolescents, may be cause for concern. There is also evidence to suggest that raised liver fat, acquired, in part, through an impaired removal of postprandial lipaemia, can increase sensitivity to the adverse effects of sugar at all ages.

Carbohydrates provide the major source of energy in the diet and hence the type and amount of carbohydrate consumed is an important consideration for weight control. Recent risk assessments have shown that there is no consistent association between the proportions of energy consumed as carbohydrate and body weight and reinforce the dominance of total energy intake as the primary determinant of body weight. However, they have highlighted evidence that different types of carbohydrate have specific effects on the risk of obesity. Short-term experimental studies suggest that some types of dietary fibre may be linked to increased satiation and cohort studies are supportive of an association between low intakes of fibre-rich, whole-grain foods and weight gain. But these observations are not supported by evidence of effects on body weight in randomised controlled trials, suggesting that high-fibre or whole-grain intake may simply be a marker of a broader dietary pattern. Recent attention has focused on the growing evidence of a positive association between the intake of free sugars and weight gain and particularly the risks linked to consumption of sugar-sweetened beverages (SSB). Given the high population-level intake of free sugars the challenge is to identify actions that will successfully reduce consumption to contribute to reductions in the prevalence of obesity. The present paper considers the range of policy options available, using the Nuffield ladder of intervention to provide a framework for risk management, with a focus on the consumption of SSB. Current policy interventions are largely based around consumer education and encouragement to industry to renovate products to reduce the sugar content of food and drinks and/or reduce portion size, but dietary change has been slow. Further measures, including the use of specific incentives/disincentives may be needed to change consumption patterns, some of which may infringe personal or commercial freedom. For these policies to be implemented will require sustained efforts to create a climate in which such interventions are acceptable or even welcomed by society as an appropriate protection against obesity and other diet-related ill-health.

Mankind has existed for 2·5 million years but only in the last 10 000 years have we been exposed to wheat. Wheat was first cultivated in the Fertile Crescent (South Western Asia) with a farming expansion that lasted from about 9000BC to 4000BC. Thus it could be considered that wheat (and gluten) is a novel introduction to man'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 5-fold. Perhaps as a result the epidemiology of coeliac disease (CD) or gluten sensitive enteropathy has changed. CD is a state of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals. CD now affects 1 % or more of all adults, for which the treatment is a strict lifelong gluten-free diet. However, there is a growing body of evidence to show that a far greater proportion of individuals without coeliac disease are taking a gluten-free diet of their own volition. This clinical entity has been termed non-coeliac gluten sensitivity (NCGS), although the condition is fraught with complexities due to overlap with other gluten-based constituents that can also trigger similar clinical symptoms. This review will explore the relationship between gluten, the rising prevalence of modern coeliac disease, and the new entity of NCGS along with its associated uncertainties.

The microbial community populating the human digestive tract has been linked to the development of obesity, diabetes and liver diseases. Proposed mechanisms on how the gut microbiota could contribute to obesity and metabolic diseases include: (1) improved energy extraction from diet by the conversion of dietary fibre to SCFA; (2) increased intestinal permeability for bacterial lipopolysaccharides (LPS) in response to the consumption of high-fat diets resulting in an elevated systemic LPS level and low-grade inflammation. Animal studies indicate differences in the physiologic effects of fermentable and non-fermentable dietary fibres as well as differences in long- and short-term effects of fermentable dietary fibre. The human intestinal microbiome is enriched in genes involved in the degradation of indigestible polysaccharides. The extent to which dietary fibres are fermented and in which molar ratio SCFA are formed depends on their physicochemical properties and on the individual microbiome. Acetate and propionate play an important role in lipid and glucose metabolism. Acetate serves as a substrate for de novo lipogenesis in liver, whereas propionate can be utilised for gluconeogenesis. The conversion of fermentable dietary fibre to SCFA provides additional energy to the host which could promote obesity. However, epidemiologic studies indicate that diets rich in fibre rather prevent than promote obesity development. This may be due to the fact that SCFA are also ligands of free fatty acid receptors (FFAR). Activation of FFAR leads to an increased expression and secretion of enteroendocrine hormones such as glucagon-like-peptide 1 or peptide YY which cause satiety. In conclusion, the role of SCFA in host energy balance needs to be re-evaluated.

The recent availability of high-throughput nucleic acid sequencing technologies has rapidly advanced approaches to analysing the role of the gut microbiome in governance of human health, including gut health, and also metabolic, cardiovascular and mental health, inter alia. Recent scientific studies suggest that energy intake (EI) perturbations at the population level cannot account for the current obesity epidemic, and significant work is investigating the potential role of the microbiome, and in particular its metabolic products, notably SCFA, predominantly acetate, propionate and butyrate, the last of which is an energy source for the epithelium of the large intestine. The energy yield from dietary residues may be a significant factor influencing energy balance. This review posits that the contribution towards EI is governed by EI diet composition (not just fibre), the composition of the microbiome and by the levels of physical activity. Furthermore, we hypothesise that these factors do not exist in a steady state, but rather are dynamic, with both short- and medium-term effects on appetite regulation. We suggest that the existing modelling strategies for bacterial dynamics, specifically for growth in chemostat culture, are of utility in understanding the dynamic interplay of diet, activity and microbiomic organisation. Such approaches may be informative in optimising the application of dietary and microbial therapy to promote health.

This review summarises evidence for an association between vitamin D status and CVD and the mechanisms involved. Vitamin D3 is predominantly provided by the action of UVB from sunlight on skin. Average UK diets supply 2–3 μg/d vitamin D but diets containing at least one portion of oily fish per week supply about 7 μg/d. Pharmacological doses of vitamin D2 (bolus injection of 7500 μg or intakes >50 μg/d) result in a smaller increase in plasma 25(OH)D than those of D3 but physiological doses 5–25 μg/d seem equivalent. Plasma 25(OH)D concentrations are also influenced by clothing, obesity and skin pigmentation. Up to 40 % of the population have plasma 25(OH)D concentrations <25 nmol/l in the winter compared with <10 % in the summer. The relative risk of CVD death is 1·41 (95 % CI 1·18, 1·68) greater in the lowest quintile of plasma 25(OH)D according to meta-analysis of prospective cohort studies. Acute deficiency may inhibit insulin secretion and promote inflammation thus increasing the risk of plaque rupture and arterial thrombosis. Chronic insufficiency may increase arterial stiffness. There is no evidence to support claims of reduced CVD from existing trials with bone-related health outcomes where vitamin D was usually co-administered with calcium. Although several trials with cardiovascular endpoints are in progress, these are using pharmacological doses. In view of the potential toxicity of pharmacological doses, there remains a need for long-term trials of physiological doses of D2 and D3 with CVD incidence as the primary outcome.

Alterations in the composition and metabolic activity of the gut microbiota appear to contribute to the development of obesity and associated metabolic diseases. However, the extent of this relationship remains unknown. Modulating the gut microbiota with non-digestible carbohydrates (NDC) may exert anti-obesogenic effects through various metabolic pathways including changes to appetite regulation, glucose and lipid metabolism and inflammation. The NDC vary in physicochemical structure and this may govern their physical properties and fermentation by specific gut bacterial populations. Much research in this area has focused on established prebiotics, especially fructans (i.e. inulin and fructo-oligosaccharides); however, there is increasing interest in the metabolic effects of other NDC, such as resistant dextrin. Data presented in this review provide evidence from mechanistic and intervention studies that certain fermentable NDC, including resistant dextrin, are able to modulate the gut microbiota and may alter metabolic process associated with obesity, including appetite regulation, energy and lipid metabolism and inflammation. To confirm these effects and elucidate the responsible mechanisms, further well-controlled human intervention studies are required to investigate the impact of NDC on the composition and function of the gut microbiota and at the same time determine concomitant effects on host metabolism and physiology.

Olive oil (OO) is the primary source of fat in the Mediterranean diet and has been associated with longevity and a lower incidence of chronic diseases, particularly CHD. Cardioprotective effects of OO consumption have been widely related with improved lipoprotein profile, endothelial function and inflammation, linked to health claims of oleic acid and phenolic content of OO. With CVD being a leading cause of death worldwide, a review of the potential mechanisms underpinning the impact of OO in the prevention of disease is warranted. The current body of evidence relies on mechanistic studies involving animal and cell-based models, epidemiological studies of OO intake and risk factor, small- and large-scale human interventions, and the emerging use of novel biomarker techniques associated with disease risk. Although model systems are important for mechanistic research nutrition, methodologies and experimental designs with strong translational value are still lacking. The present review critically appraises the available evidence to date, with particular focus on emerging novel biomarkers for disease risk assessment. New perspectives on OO research are outlined, especially those with scope to clarify key mechanisms by which OO consumption exerts health benefits. The use of urinary proteomic biomarkers, as highly specific disease biomarkers, is highlighted towards a higher translational approach involving OO in nutritional recommendations.

Epidemiological and experimental evidence suggests that non-digestible carbohydrates (NDC) including resistant starch are protective against colorectal cancer. These anti-neoplastic effects are presumed to result from the production of the SCFA, butyrate, by colonic fermentation, which binds to the G-protein-coupled receptor GPR43 to regulate inflammation and other cancer-related processes. The WNT pathway is central to the maintenance of homeostasis within the large bowel through regulation of processes such as cell proliferation and migration and is frequently aberrantly hyperactivated in colorectal cancers. Abnormal WNT signalling can lead to irregular crypt cell proliferation that favours a hyperproliferative state. Butyrate has been shown to modulate the WNT pathway positively, affecting functional outcomes such as apoptosis and proliferation. Butyrate's ability to regulate gene expression results from epigenetic mechanisms, including its role as a histone deacetylase inhibitor and through modulating DNA methylation and the expression of microRNA. We conclude that genetic and epigenetic modulation of the WNT signalling pathway may be an important mechanism through which butyrate from fermentation of resistant starch and other NDC exert their chemoprotective effects.

The role of dietary fibre in promoting sustained health has been studied for several decades and in adults there is good evidence that diets rich in high-fibre foods reduce the risk of chronic diseases, including CVD and cancer. Research in this area, however, has been hampered by uncertainties about the definition of dietary fibre which has resulted in many studies measuring fibre in different ways. There is also a wide range of properties and actions of different fibres in the human body, depending on their solubility, viscosity and fermentability by the colonic microbiota. This review considers the epidemiological evidence for dietary fibre and health in children and the current dietary recommendations and measured intakes in several countries using national surveys. In children and adolescents, there is a particular lack of relevant research on which to formulate appropriate dietary fibre recommendations and these are often based on extrapolation from adult data. However, children are not little adults and have differing physiology and nutritional needs as they grow. The dietary recommendations in different countries are based on varying premises and daily amounts. Intakes vary from country to country and on the whole do not meet recommendations. Much more research is needed in children to fully understand the impact of dietary fibre on growth and health in the young to allow more appropriate recommendations to be made.

The WHO's Ottawa Charter highlights five priority areas for taking action in public health. Only one of them is at the individual level as action at more upstream intervention levels, such as community or policy levels, is critical for enabling individuals to succeed. The objective of the present paper is to give insight into the many complex processes involved in public health nutrition by describing the Ottawa Charter's five priority areas for taking action using public health nutrition initiatives I have been involved in. Evidence-based guidelines for healthy eating and infant feeding provide an essential basis for individuals to ‘develop personal skills’ (Action Area 1). ‘Re-orienting health services’ (Action Area 2) can address the needs of vulnerable population subgroups, such as the culturally sensitive diabetes prevention programme established for an Indo-Asian community in Canada. Identifying geographic areas at high risk of childhood obesity enables better strategic planning and targeting of resources to ‘strengthen community action’ (Action Area 3). Calorie menu labelling can ‘create supportive environments’ (Action Area 4) through encouraging a demand for less energy-dense, healthier food options. ‘Building healthy public policy’ (Action Area 5) to implement mandatory folic acid food fortification for prevention of birth defects has many advantages over a voluntary approach. In conclusion, evaluation and evidence-based decision-making needs to take account of different strategies used to take action in each of these priority areas. For this, the randomised control trial needs adaptation to determine the best practice in public health nutrition where interventions play out in real life with all its confounding factors.

Cereal-based foods are key components of the diet and they dominate most food-based dietary recommendations in order to achieve targets for intake of carbohydrate, protein and dietary fibre. Processing (milling) of grains to produce refined grain products removes key nutrients and phytochemicals from the flour and although in some countries nutrients may be replaced with mandatory fortification, overall this refinement reduces their potential nutritional quality. There is increasing evidence from both observational and intervention studies that increased intake of less-refined, whole-grain (WG) foods has positive health benefits. The highest WG consumers are consistently shown to have lower risk of developing CVD, type 2 diabetes and some cancers. WG consumers may also have better digestive health and are likely to have lower BMI and gain less weight over time. The bulk of the evidence for the benefits of WG comes from observational studies, but evidence of benefit in intervention studies and potential mechanisms of action is increasing. Overall this evidence supports the promotion of WG foods over refined grain foods in the diet, but this would require adoption of standard definitions of ‘whole grain’ and ‘whole-grain foods’ which will enable innovation by food manufacturers, provide clarity for the consumer and encourage the implementation of food-based dietary recommendations and public health strategies.

Dietary fibre alone does not fully explain the frequent association between greater intake of whole grains and reduced risk of disease in observational studies, and other phytochemicals or food structure may also play an important role. For all the observational evidence for the benefits of a whole-grain-rich diet, we have only limited knowledge of the mechanisms behind this reduction in disease risk, aside from the action of specific cereal fibres on reduction of blood cholesterol and the post-prandial glucose peak. Nutritional metabolomics, the global measurement and interpretation of metabolic profiles, assesses the interaction of food with the endogenous gene–protein cascade and the gut microbiome. This approach allows the generation of new hypotheses which account for systemic effects, rather than just focusing on one or two mechanisms or metabolic pathways. To date, animal and human trials using metabolomics to investigate mechanistic changes to metabolism on eating whole grains and cereal fractions have led to new hypotheses around mechanistic effects of whole grains. These include the role of cereals as a major source of dietary glycine betaine, a possible effect on phospholipid synthesis or metabolism, the role of branched-chain amino acids and improvements in insulin sensitivity, and the possibility that whole grains may have an effect on protein metabolism. These hypotheses help explain some of the observed effects of whole grains, although mechanistic studies using stable isotopes and fully quantitative measures are required to confirm these potential mechanisms.

In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2- or FFAR3-deficient animal models suggest that SCFA-mediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.