Dietary reference values for essential trace elements are designed to meet requirements with minimal risk of deficiency and toxicity. Risk–benefit analysis requires data on habitual dietary intakes, an estimate of variation and effects of deficiency and excess on health. For some nutrients, the range between the upper and lower limits may be extremely narrow and even overlap, which creates difficulties when setting safety margins. A new approach for estimating optimal intakes, taking into account several health biomarkers, has been developed and applied to selenium, but at present there are insufficient data to extend this technique to other micronutrients. The existing methods for deriving reference values for Cu and Fe are described. For Cu, there are no sensitive biomarkers of status or health relating to marginal deficiency or toxicity, despite the well-characterised genetic disorders of Menkes and Wilson's disease which, if untreated, lead to lethal deficiency and overload, respectively. For Fe, the wide variation in bioavailability confounds the relationship between intake and status and complicates risk–benefit analysis. As with Cu, health effects associated with deficiency or toxicity are not easy to quantify, therefore status is the most accessible variable for risk–benefit analysis. Serum ferritin reflects Fe stores but is affected by infection/inflammation, and therefore additional biomarkers are generally employed to measure and assess Fe status. Characterising the relationship between health and dietary intake is problematic for both these trace elements due to the confounding effects of bioavailability, inadequate biomarkers of status and a lack of sensitive and specific biomarkers for health outcomes.

The health benefits associated with soya food consumption have been widely studied, with soya isoflavones and soya protein implicated in the protection of CVD, osteoporosis and cancers such as those of the breast and prostate. Equol (7-hydroxy-3-(4’-hydroxyphenyl)-chroman), a metabolite of the soya isoflavone daidzein, is produced via the formation of the intermediate dihydrodaidzein, by human intestinal bacteria, with only approximately 30–40% of the adult population having the ability to perform this transformation following a soya challenge. Inter-individual variation in conversion of daidzein to equol has been attributed, in part, to differences in the diet and in gut microflora composition, although the specific bacteria responsible for the colonic biotransformation of daidzein to equol are yet to be identified. Equol is a unique compound in that it can exert oestrogenic effects, but is also a potent antagonist of dihydrotestosterone in vivo. Furthermore, in vitro studies suggest that equol is more biologically active than its parent compound, daidzein, with a higher affinity for the oestrogen receptor and a more potent antioxidant activity. Although some observational and intervention studies suggest that the ability to produce equol is associated with reduced risk of breast and prostate cancer, CVD, improved bone health and reduced incidence of hot flushes, others have reported null or adverse effects. Studies to date have been limited and well-designed studies that are sufficiently powered to investigate the relationship between equol production and disease risk are warranted before the clinical relevance of the equol phenotype can be fully elucidated.

Health claims on food products, which aim at informing the public about the health benefits of the product, represent one type of nutrition communication; the use of these is regulated by the European Union. This paper provides an overview of the research on health claims, including consumers’ perceptions of such claims and their intention to buy products that carry health-related claims. This is followed by a discussion on the results from some recent studies investigating public perceptions and willingness to use products with health claims. In these studies, claims are presented in the form of messages of different lengths, types, framing, with and without qualifying words and symbols. They also investigate how perceptions and intentions are affected by individual needs and product characteristics. Results show that adding health claims to products does increase their perceived healthiness. Claim structure was found to make a difference to perceptions, but its influence depended on the level of relevance, familiarity and individuals’ need for information. Further, the type of health benefit proposed and the base product used also affected perceptions of healthiness. The paper concludes that while healthiness perceptions relating to products with health claims may vary between men and women, old and young and between countries, the main factor influencing perceived healthiness and intention to buy a product with health claim is personal relevance.

As long as health communications have existed in the USA, Americans have faced the task of sorting the agenda of the source from the advice it provides. That task has become more complicated as advances in the science of nutrition and the technology used to present it have heightened the complexity of nutrition communications. Getting consumers to adopt a healthier diet has been a protracted undertaking with limited successes along the way. The obesity epidemic has added urgency to this discourse: not only do we need to eat better, but most of us also need to eat less. This paper reviews the dynamics that have made the communication of accurate and actionable health behaviour information an ongoing challenge, and outlines strategies for moving ahead. It considers the interplay of four sets of factors: the evolutionary nature of the science on which recommendations are based; the many sources of communication about that science; the agendas or motivations of each source; and finally the multifaceted nature of consumers, the recipients of these communications. Communication alone has not been, and will not be, sufficient for consumers to adopt the behavioural changes endorsed by experts. Broad environmental interventions coupled with individual skills development will need to be part of the process. Ultimately, it is the consumer who decides what is for dinner. Media literacy will play a critical role in building consumer efficacy in sorting fact from fiction in order to select food for a healthful diet.

These days, we are bombarded with nutrition information from diverse sources and of varying quality. There has been a dramatic increase in communication channels, including more television channels with airtime to fill, and the emergence of the Internet and ‘new media’ such as social networking sites. Part of this culture is to deliver ever changing and novel angles. The background ‘noise’ that this creates can make delivery of evidence-based advice about healthy eating that generally carries less novelty value, a huge challenge. This paper illustrates ways in which complex scientific information can be translated into meaningful health promoting strategies that can be applied across the life course. The examples used are nutrition in the context of healthy ageing, communicating the concept of energy density in the context of satiety, healthy hydration, health effects of probiotics and resources for use by teachers in the classroom. This selection of examples demonstrates the processes adopted at the British Nutrition Foundation to identify the evidence base for a particular topic and then to communicate this information to various target audiences. The British Nutrition Foundation's approach typically starts with preparation of a detailed review of the evidence, often with the involvement of external expertise, followed by peer review. For much of this work conventional science communication routes are used, but use is also made of the Internet and various forms of new media.

Epigenetic changes are inherited alterations in DNA that affect gene expression and function without altering the DNA sequence. DNA methylation is one epigenetic process implicated in human disease that is influenced by diet. DNA methylation involves addition of a 1-C moiety to cytosine groups in DNA. Methylated genes are not transcribed or are transcribed at a reduced rate. Global under-methylation (hypomethylation) and site-specific over-methylation (hypermethylation) are common features of human tumours. DNA hypomethylation, leading to increased expression of specific proto-oncogenes (e.g. genes involved in proliferation or metastasis) can increase the risk of cancer as can hypermethylation and reduced expression of tumour suppressor (TS) genes (e.g. DNA repair genes). DNA methyltransferases (DNMT), together with the methyl donor S-adenosylmethionine (SAM), facilitate DNA methylation. Abnormal DNA methylation is implicated not only in the development of human cancer but also in CVD. Polyphenols, a group of phytochemicals consumed in significant amounts in the human diet, effect risk of cancer. Flavonoids from tea, soft fruits and soya are potent inhibitors of DNMT in vitro, capable of reversing hypermethylation and reactivating TS genes. Folates, a group of water-soluble B vitamins found in high concentration in green leafy vegetables, regulate DNA methylation through their ability to generate SAM. People who habitually consume the lowest level of folate or with the lowest blood folate concentrations have a significantly increased risk of developing several cancers and CVD. This review describes how flavonoids and folates in the human diet alter DNA methylation and may modify the risk of human colon cancer and CVD.

Body fat distribution plays an important role in determining metabolic health. Whereas central obesity is closely associated with the development of CVD and type 2 diabetes, lower body fat appears to be protective and is paradoxically associated with improved metabolic and cardiovascular profiles. Physiological studies have demonstrated that fatty acid handling differs between white adipose tissue depots, with lower body white adipose tissue acting as a more efficient site for long-term lipid storage. The regulatory mechanisms governing these regional differences in function remain to be elucidated. Although the local microenvironment is likely to be a contributing factor, recent findings point towards the tissues being intrinsically distinct at the level of the adipocyte precursor cells (pre-adipocytes). The multi-potent pre-adipocytes are capable of generating cells of the mesenchymal lineage, including adipocytes. Regional differences in the adipogenic and replicative potential of these cells, as well as metabolic and biochemical activity, have been reported. Intriguingly, the genetic and metabolic characteristics of these cells can be retained through multiple generations when the cells are cultured in vitro. The rapidly emerging field of epigenetics may hold the key for explaining regional differences in white adipose tissue gene expression and function. Epigenetics describes the regulation of gene expression that occurs independently of changes in DNA sequence, for instance, DNA methylation or histone protein modification. In this review, we will discuss the contribution of DNA methylation to the determination of cells of adipogenic fate as well as the role DNA methylation may play during adipocyte terminal differentiation.

The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also strongly influences the risk of developing such diseases in later life. Human studies have shown that low birth weight is associated with an increased risk of CVD, type II diabetes, obesity and hypertension, although recent studies have shown that over-nutrition in early life can also increase susceptibility to future metabolic disease. These findings have been replicated in a variety of animal models, which have shown that both maternal under- and over-nutrition can induce persistent changes in gene expression and metabolism within the offspring. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of chronic diseases raises the possibility that nutritional or pharmaceutical interventions may be used to modify long-term cardio-metabolic disease risk and combat this rapid rise in chronic non-communicable diseases.

Under- and over-nutrition during pregnancy has been linked to the later development of diseases such as diabetes and obesity. Epigenetic modifications may be one mechanism by which exposure to an altered intrauterine milieu or metabolic perturbation may influence the phenotype of the organism much later in life. Epigenetic modifications of the genome provide a mechanism that allows the stable propagation of gene expression from one generation of cells to the next. This review highlights our current knowledge of epigenetic gene regulation and the evidence that chromatin remodelling and histone modifications play key roles in adipogenesis and the development of obesity. Epigenetic modifications affecting processes important to glucose regulation and insulin secretion have been described in the pancreatic β-cells and muscle of the intrauterine growth-retarded offspring, characteristics essential to the pathophysiology of type-2 diabetes. Epigenetic regulation of gene expression contributes to both adipocyte determination and differentiation in in vitro models. The contributions of histone acetylation, histone methylation and DNA methylation to the process of adipogenesis in vivo remain to be evaluated.

The world has experienced a marked shift in the global BMI distribution towards reduced undernutrition and increased obesity. The collision between human biology, shaped over the millennia and modern technology, globalization, government policies and food industry practices have worked to create far-reaching energy imbalance across the globe. A prime example is the clash between our drinking habits and our biology. The shift from water and breast milk as the only beverages available, to a vast array of caloric beverages was very rapid, shaped both by our tastes and aggressive marketing of the beverage industry. Our biology, shaped over millennia by daily consumption of water and seasonal availability of food, was not ready to compensate for the liquid energies. Other dietary changes were similarly significant, particularly the shift towards increased frequency of eating and larger portions. The roles of the food and beverage production, distribution and marketing sectors in not only shaping our diet but also accelerating these changes must be understood. Apart from the role of beverages, there is much less consensus about the role of various components of our diet in energy imbalance. Understanding the determinants of change in the key components of our diet through an array of research provides insights into some of the options we face in attempting to attain a great balance between energy intake and expenditures while creating an overall healthier dietary pattern. A few countries are systematically addressing the causes of poor dietary and physical activity patterns and high energy imbalance.

The AMP-activated protein kinase (AMPK) is a sensor of cellular energy status, and a regulator of energy balance at both the cellular and whole body levels. Although ubiquitously expressed, its function is best understood in skeletal muscle. AMPK contains sites that reversibly bind AMP or ATP, with an increase in cellular AMP:ATP ratio (signalling a fall in cellular energy status) switching on the kinase. In muscle, AMPK activation is therefore triggered by sustained contraction, and appears to be particularly important in the metabolic changes that occur in the transition from resistance to endurance exercise. Once activated, AMPK switches on catabolic processes that generate ATP, while switching off energy-requiring processes not essential in the short term. Thus, it acutely activates glucose uptake (by promoting translocation of the transporter GLUT4 to the membrane) and fatty acid oxidation, while switching off glycogen synthesis and protein synthesis (the later via inactivation of the mammalian target-of-rapamycin pathway). Prolonged AMPK activation also causes some of the chronic adaptations to endurance exercise, such as increased GLUT4 expression and mitochondrial biogenesis. AMPK contains a glycogen-binding domain that causes a sub-fraction to bind to the surface of the glycogen particle, and it can inhibit glycogen synthesis by phosphorylating glycogen synthase. We have shown that AMPK is inhibited by exposed non-reducing ends in glycogen. We are working on the hypothesis that this ensures that glycogen synthesis is rapidly activated when glycogen becomes depleted after exercise, but is switched off again as soon as glycogen stores are replenished.

Growing evidence supports the conclusion that consumption of protein in close temporal proximity to the performance of resistance exercise promotes greater muscular hypertrophy. We can also state with good certainty that merely consuming energy, as carbohydrate for example, is also not sufficient to maximise muscle protein synthesis leading to anabolism and net new muscle protein accretion. Recent work also indicates that certain types of proteins, particular those that are rapidly digested and high in leucine content (i.e. whey protein), appear to be more efficient at stimulating muscle protein synthesis. Continued practice of consumption of these types or proteins after exercise should lead to greater hypertrophy. Reviews of numerous training studies indicate that studies in which milk proteins and principally whey protein show an advantage of these proteins over and above isoenergetic carbohydrate and soya protein in promoting hypertrophy. Thus, the combined evidence suggests a strategic advantage of practising early post-exercise consumption of whey protein or dairy-based protein to promote muscle protein synthesis, net muscle protein accretion and ultimately hypertrophy.

Ageing is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk for developing chronic metabolic diseases such as diabetes. The age-related loss of skeletal muscle mass results from a chronic disruption in the balance between muscle protein synthesis and degradation. As basal muscle protein synthesis rates are likely not different between healthy young and elderly human subjects, it was proposed that muscles from older adults lack the ability to regulate the protein synthetic response to anabolic stimuli, such as food intake and physical activity. Indeed, the dose–response relationship between myofibrillar protein synthesis and the availability of essential amino acids and/or resistance exercise intensity is shifted down and to the right in elderly human subjects. This so-called ‘anabolic resistance’ represents a key factor responsible for the age-related decline in skeletal muscle mass. Interestingly, long-term resistance exercise training is effective as a therapeutic intervention to augment skeletal muscle mass, and improves functional performance in the elderly. The consumption of different types of proteins, i.e. protein hydrolysates, can have different stimulatory effects on muscle protein synthesis in the elderly, which may be due to their higher rate of digestion and absorption. Current research aims to elucidate the interactions between nutrition, exercise and the skeletal muscle adaptive response that will define more effective strategies to maximise the therapeutic benefits of lifestyle interventions in the elderly.

The prevalence of obesity is high in older persons and recent trends show a rapid increase in this prevalence. Results from observational and intervention studies (i.e. weight loss studies) show the strong negative impact of obesity on functional status in old age. There are different potential pathways through which obesity may lead to functional decline in older persons. Furthermore, the presence of overweight and obesity during the life course and trends in medical care are likely to influence the impact of obesity on disability. The concepts sarcopenia (age-related loss of muscle mass) and dynapenia (age-related loss of muscle strength) receive a lot of research attention as potential determinants of functional decline in old age. There is no consensus on the definitions of these concepts. Recent studies conducted in large cohort studies of mainly community-dwelling older persons show that poor muscle strength is strongly associated with functional decline compared to low muscle mass. In several studies, no association between muscle mass and functional status was observed. Current research on the combination of obesity with poor muscle strength (dynapenic-obesity) suggests a potential additive effect of both components on poor functional status in old age which seems independent of the level of physical activity.

The recently discovered SCFA-activated G-coupled protein receptors FFA receptor 2 and FFA receptor 3 are co-localised in l-cells with the anorexigenic ‘ileal brake’ gut hormone peptide YY, and also in adipocytes, with activation stimulating leptin release. Thus, SCFA such as acetate and propionate show promise as a candidate to increase satiety-enhancing properties of food. We therefore postulate SCFA may have a role in appetite regulation and energy homeostasis. SCFA can be delivered either directly within food, or indirectly via the colon by the provision of fermentable non-digestible carbohydrates. A review of studies investigating the effects of oral SCFA ingestion on appetite suggests that while oral SCFA ingestion is associated with enhanced satiety, this may be explained by product palatability rather than a physiological effect of SCFA. Colon-derived SCFA generated during microfloral fermentation have also been suggested to explain satiety-enhancing properties of non-digestible carbohydrates. However, findings are mixed from investigations into the effects of the prebiotic inulin-type fructans on appetite. Overall, data presented in this review do not support a role for SCFA in appetite regulation.

The British Bangladeshi community is one of the youngest and fastest growing ethnic minority groups in the UK. Many report poor socio-economic and health profiles with the existence of substantial health inequalities, particularly in relation to type 2 diabetes. Although there is compelling evidence for the effectiveness of lifestyle interventions in the prevention of type 2 diabetes, there is little understanding of how best to tailor treatments to the needs of minority ethnic groups. Little is known about nutrition related lifestyle choices in the Bangladeshi community or the factors influencing such decisions. Only by exploring these factors will it be possible to design and tailor interventions appropriately. The Bangladeshi Initiative for the Prevention of Diabetes study explored lay beliefs and attitudes, religious teachings and professional perspectives in relation to diabetes prevention in the Bangladeshi community in Tower Hamlets, London. Contrary to the views of health professionals and previous research, poor knowledge was not the main barrier to healthy lifestyle choices. Rather the desire to comply with cultural norms, particularly those relating to hospitality, conflicted with efforts to implement healthy behaviours. Considerable support from Islamic teachings for diabetes prevention messages was provided by religious leaders, and faith may have an important role in supporting health promotion in this community. Some health professionals expressed outdated views on community attitudes and were concerned about their own limited cultural understanding. The potential for collaborative working between health educators and religious leaders should be explored further, and the cultural competence of health professionals addressed.

Taste is often cited as the factor of greatest significance in food choice, and has been described as the body's ‘nutritional gatekeeper’. Variation in taste receptor genes can give rise to differential perception of sweet, umami and bitter tastes, whereas less is known about the genetics of sour and salty taste. Over twenty-five bitter taste receptor genes exist, of which TAS2R38 is one of the most studied. This gene is broadly tuned to the perception of the bitter-tasting thiourea compounds, which are found in brassica vegetables and other foods with purported health benefits, such as green tea and soya. Variations in this gene contribute to three thiourea taster groups of people: supertasters, medium tasters and nontasters. Differences in taster status have been linked to body weight, alcoholism, preferences for sugar and fat levels in food and fruit and vegetable preferences. However, genetic predispositions to food preferences may be outweighed by environmental influences, and few studies have examined both. The Tastebuddies study aimed at taking a holistic approach, examining both genetic and environmental factors in children and adults. Taster status, age and gender were the most significant influences in food preferences, whereas genotype was less important. Taster perception was associated with BMI in women; nontasters had a higher mean BMI than medium tasters or supertasters. Nutrient intakes were influenced by both phenotype and genotype for the whole group, and in women, the AVI variation of the TAS2R38 gene was associated with a nutrient intake pattern indicative of healthy eating.