It is beneficial for both the public health community and the food industry to meet nutritional needs of elderly consumers through product formats that they want. The heterogeneity of the elderly market poses a challenge, however, and calls for market segmentation. Although many researchers have proposed ways to segment the elderly consumer population, the elderly food market has received surprisingly little attention in this respect. Therefore, the present paper reviewed eight potential segmentation bases on their appropriateness in the context of functional foods aimed at the elderly: cognitive age, life course, time perspective, demographics, general food beliefs, food choice motives, product attributes and benefits sought, and past purchase. Each of the segmentation bases had strengths as well as weaknesses regarding seven evaluation criteria. Given that both product design and communication are useful tools to increase the appeal of functional foods, we argue that elderly consumers in this market may best be segmented using a preference-based segmentation base that is predictive of behaviour (for example, attributes and benefits sought), combined with a characteristics-based segmentation base that describes consumer characteristics (for example, demographics). In the end, the effectiveness of (combinations of) segmentation bases for elderly consumers in the functional food market remains an empirical matter. We hope that the present review stimulates further empirical research that substantiates the ideas presented in this paper.

The intestine is the only gate for the entry of Ca to the body in humans and mammals. The entrance of Ca occurs via paracellular and intracellular pathways. All steps of the latter pathway are regulated by calcitriol and by other hormones. Dietary and pharmacological compounds also modulate the intestinal Ca absorption process. Among them, dietary Ca and P are known to alter the lipid and protein composition of the brush-border and basolateral membranes and, consequently, Ca transport. Ca intakes are below the requirements recommended by health professionals in most countries, triggering important health problems. Chronic low Ca intake has been related to illness conditions such as osteoporosis, hypertension, renal lithiasis and incidences of human cancer. Carbohydrates, mainly lactose, and prebiotics have been described as positive modulators of intestinal Ca absorption. Apparently, high meat proteins increase intestinal Ca absorption while the effect of dietary lipids remains unclear. Pharmacological compounds such as menadione, dl-butionine-S,R-sulfoximine and ursodeoxycholic acid also modify intestinal Ca absorption as a consequence of altering the redox state of the epithelial cells. The paracellular pathway of intestinal Ca absorption is poorly known and is under present study in some laboratories. Another field that needs to be explored more intensively is the influence of the gene × diet interaction on intestinal Ca absorption. Health professionals should be aware of this knowledge in order to develop nutritional or medical strategies to stimulate the efficiency of intestinal Ca absorption and to prevent diseases.

Obesity is a chronic disorder caused by an imbalance of the energy metabolism with high associated burdens. Therefore, huge efforts are being currently devoted in studying new types of hypoenergetic diets and their composition, in order to characterise more specific, long-lasting and safe slimming protocols. A number of investigations are trying to determine the specific influence of the macronutrient distribution in energy-restricted diets on the management of excessive body weight. In this context, very-low-energy diets supplying between 1670 and 3350 kJ (400 and 800 kcal)/d have been beneficial in short-term treatments causing a weight loss of 300–500 g/d. Such strategies place more emphasis on energy restriction than on the macronutrient composition of the diet prescription. Weight loss produced by either low-carbohydrate or low-fat moderately energy-restricted diets ranges from 0·5 to 1·0 kg/week, while diets with high or moderately high protein content have also been applied in weight-reducing programmes by inducing losses of 0·2–0·4 kg/week. Other factors that determine weight loss by dieting are sex, age, initial body weight, race, genetics, regional fat deposition, etc, which must be taken into account to explain the variability in the outcomes of different low-energy diets. Therefore, more research is needed about the impact of diets with different fuel substrates and foods on the characteristics of the weight-loss process.

Obesity represents one of major health problems strongly linked to other co-morbidities, such as type 2 diabetes, CVD, gastrointestinal disorders and cognitive impairment. In this context, nutritional stress, such as an excess of fat intake, promotes a systemic oxidative stress, characterised by hyperproduction of reactive oxygen species, leading to cellular alterations that include impaired energy metabolism, altered cell signalling and cell cycle control, impaired cell transport mechanisms and overall dysfunctional biological activity. Flavonoids, dietary components of plant foods, are endowed with a wide spectrum of biological activities, including antioxidant activity, and have been proposed to reduce the risk of major chronic diseases. The present review intends to highlight and critically discuss the current scientific evidence on the possible effects of flavonoids in counteracting obesity and related co-morbidities (i.e. type 2 diabetes mellitus, CVD, gastrointestinal disorders and cognitive impairment) through a decrease in oxidative stress and related inflammatory conditions.

Prevalence of type 2 diabetes mellitus (T2DM) is rapidly increasingly and is a key risk for CVD development, now recognised as the leading cause of death globally. Dietary strategies to reduce CVD development include reduction of saturated fat intake. Milk and dairy products are the largest contributors to dietary saturated fats in the UK and reduced consumption is often recommended as a strategy for risk reduction. However, overall evidence from prospective cohort studies does not confirm a detrimental association between dairy product consumption and CVD risk. The present review critically evaluates the current evidence on the association between milk and dairy products and risk of CVD, T2DM and the metabolic syndrome (collectively, cardiometabolic disease). The effects of total and individual dairy foods on cardiometabolic risk factors and new information on the effects of the food matrix on reducing fat digestion are also reviewed. It is concluded that a policy to lower SFA intake by reducing dairy food consumption to reduce cardiometabolic disease risk is likely to have limited or possibly negative effects. There remain many uncertainties, including differential effects of different dairy products and those of differing fat content. Focused and suitably designed and powered studies are needed to provide clearer evidence not only of the mechanisms involved, but how they may be beneficially influenced during milk production and processing.

Beef and its products are an important source of nutrition in many human societies. Methods of production vary and include the use of hormonal compounds (‘hormones’) to increase growth and lean tissue with reduced fat deposition in cattle. The hormonal compounds are naturally occurring in animals or are synthetically produced xenobiotics and have oestrogenic (oestradiol-17β and its esters; zeranol), androgenic (testosterone and esters; trenbolone acetate) or progestogenic (progesterone; melengestrol acetate) activity. The use of hormones as production aids is permitted in North American countries but is no longer allowed in the European Union (EU), which also prohibits the importation of beef and its products derived from hormone-treated cattle. These actions have resulted in a trade dispute between the two trading blocs. The major concern for EU authorities is the possibility of adverse effects on human consumers of residues of hormones and metabolites. Methods used to assess possible adverse effects are typical of those used by international agencies to assess acceptability of chemicals in human food. These include analysis of quantities present in the context of known biological activity and digestive, absorptive, post-absorptive and excretory processes. Particular considerations include the low quantities of hormonal compounds consumed in meat products and their relationships to endogenous production particularly in prepubertal children, enterohepatic inactivation, cellular receptor- and non-receptor-mediated effects and potential for interference with growth, development and physiological function in consumers. There is particular concern about the role of oestradiol-17β as a carcinogen in certain tissues. Now subject to a ‘permanent’ EU ban, current evidence suggests that certain catechol metabolites may induce free-radical damage of DNA in cell and laboratory animal test systems. Classical oestrogen-receptor mediation is considered to stimulate proliferation in cells maintaining receptivity. Mathematical models describing quantitative relationships between consumption of small amounts of oestrogens in meat in addition to greater concentrations from endogenous production, chemical stoichiometry at cellular level and human pathology have not been developed. Such an approach will be necessary to establish ‘molecular materiality’ of the additional hormone intake as a component of relative risk assessment. The other hormones, although generally less well researched, are similarly subject to a range of tests to determine potentially adverse effects. The resulting limited international consensus relates to the application of the ‘precautionary principle’ and non-acceptance by the European Commission of the recommendations of the Codex Alimentarius Commission, which determined that meat from cattle, hormone-treated according to good practice, was safe for human consumers. The present review considers the hormone issue in the context of current international social methodology and regulation, recent advances in knowledge of biological activity of hormones and current status of science-based evaluation of food safety and risk for human consumers.

The WHO encourages national diet survey (NDS) implementation to obtain relevant data to inform policies addressing all forms of malnutrition, which remains a pressing issue throughout Europe. This paper provides an up-to-date review on energy, macro- and selected micronutrient intakes in children across WHO Europe using the latest available NDS intakes. It assesses these against WHO recommended nutrient intakes (RNI) to highlight vulnerable groups and areas of concern. Dietary survey information was gathered by Internet searches, contacting survey authors and nutrition experts. Survey characteristics, energy and nutrient intakes were extracted and weighted means calculated and presented by region. Child energy and nutrient intakes were extracted from twenty-one NDS across a third (n 18) of the fifty-three WHO Europe countries. Of these, 38 % (n 6) reported intakes by socio-economic group, but by various indicators. Energy and macronutrients, where boys and older children had higher intakes, were more widely reported than micronutrients. Most countries met under half of the WHO RNI for nutrients reported in their NDS. Micronutrient attainment was higher than macronutrients, but worst in girls and older children. Only a third, mainly Western, WHO European member states provided published data on child nutrient intakes. Gaps in provision mean that dietary inadequacies may go unidentified, preventing evidence-based policy formation. WHO RNI attainment was poor, particularly in girls and older children. Inconsistent age groups, dietary methodologies, nutrient composition databases and under-reporting hinder inter-country comparisons. Future efforts should encourage countries to conduct NDS in a standardised format by age and sociodemographic variables.

Contaminants are a vast subject area of food safety and quality and can be present in our food chain from raw materials to finished products. Acrylamide, an α,β-unsaturated (conjugated) reactive molecule, can be detected as a contaminant in several foodstuffs including baby foods and infant formulas. It is anticipated that children will generally have intakes that are two to three times those of adults when expressed on a body-weight basis. Though exposure to acrylamide is inevitable, it is necessary to protect infant and children from high exposure. The present review focuses on the several adverse health effects of acrylamide including mutagenicity, genotoxicity, carcinogenicity, neurotoxicity and reproductive toxicity, and the possible outcomes of childhood exposure from baby foods and infant formulas.

The present review investigates the role of sleep and its alteration in triggering metabolic disorders. The reduction of the amount of time sleeping has become an endemic condition in modern society and the current literature has found important associations between sleep loss and alterations in nutritional and metabolic aspects. Studies suggest that individuals who sleep less have a higher probability of becoming obese. It can be related to the increase of ghrelin and decrease of leptin levels, generating an increase of appetite and hunger. Sleep loss has been closely associated with problems in glucose metabolism and a higher risk for the development of insulin resistance and diabetes, and this disturbance may reflect decreased efficacy of the negative-feedback regulation of the hypothalamic–pituitary–adrenal axis. The period of sleep is also associated with an increase of blood lipid concentrations, which can be intensified under conditions of reduced sleep time, leading to disorders in fat metabolism. Based on a review of the literature, we conclude that sleep loss represents an important risk factor for weight gain, insulin resistance, type 2 diabetes and dyslipidaemia. Therefore, an adequate sleep pattern is fundamental for the nutritional balance of the body and should be encouraged by professionals in the area.

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3), the active form of vitamin D3, is a central player in Ca and bone metabolism. More recently, important immunomodulatory effects have been attributed to this hormone. By binding to its receptor, the vitamin D receptor, 1,25(OH)2D3 regulates the expression of various genes and consequently affects the behaviour of different cell types within the immune system. 1,25(OH)2D3 can potently inhibit pathogenic T cells and gives rise to elevated numbers of regulatory T cells via the induction of tolerogenic dendritic cells. These immunomodulatory activities of 1,25(OH)2D3 have also been proven useful in vivo: administration of 1,25(OH)2D3 in several animal models can prevent or cure different autoimmune diseases and graft rejection. To overcome the dose-limiting side effects of 1,25(OH)2D3 on Ca and bone, less calcaemic structural analogues (alone or in combination with synergistically acting drugs or bone-resorption inhibitors) have been successfully used in animal models. Furthermore, as 1,25(OH)2D3 also contributes to host defence against infectious agents by the induction of antimicrobial responses, this molecule might provide a new strategy to deal with drug-resistant infections. According to the pleiotropic effects of 1,25(OH)2D3 in the immune system, increasing epidemiological data underline the importance of adequate vitamin D intakes in reducing the risk of several autoimmune diseases and infections such as tuberculosis.

Evidence from epidemiological studies suggests that diets rich in n-3 PUFA may be associated with reduced cancer risk. These observations have formed the rationale for exploring the mechanisms by which n-3 PUFA may be chemoprotective and have resulted in significant advances in our mechanistic understanding of n-3 PUFA action on tumour growth. Various interrelated and integrated mechanisms may be at work by which n-3 PUFA influence cancer at all stages of initiation, promotion, progression, and neoplastic transformation. More recently, experimental studies have reported enhanced tumour cell death with chemotherapy when fish oil is provided while toxic side effects to the host are reduced. Furthermore, cancer-associated wasting has been shown to be attenuated by fish oil supplementation. Clinical evidence suggests that the n-3 PUFA status of newly diagnosed cancer patients and individuals undergoing chemotherapy is low. Therefore, both the disease itself and therapeutic treatments may be contributing factors in the decline of n-3 PUFA status. Dietary supplementation to maintain and replenish n-3 PUFA status at key points in the cancer disease trajectory may provide additional health benefits and an enhanced quality of life. The present review will focus on and critically examine current research efforts related to the putative anti-cancer effects of n-3 PUFA and their suggested ability to palliate cancer-associated and treatment-associated symptoms.

The various positional isomers of oleic acid (18 : 1Δ9c or 9c-18 : 1) may have distinct biological effects. Detrimental effects of consumption of industrial trans-fatty acids (TFA) (elaidic acid; 18 : 1Δ9t) from partially hydrogenated vegetable oils on CVD risk factors are well documented. In addition, epidemiological data suggest that chronic consumption of industrial sources of TFA could alter insulin sensitivity and predispose for type 2 diabetes. However, intervention studies on this issue have remained inconclusive. Moreover, very little information is available on the effect of natural sources of TFA (vaccenic acid; 18 : 1Δ11t) coming from dairy products and ruminant meat on the development of CVD and type 2 diabetes. The review focuses on the impact of the consumption of ruminant TFA in relation to cardiovascular risk factors, inflammation and type 2 diabetes.

We provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent intake of lean seafood, as compared with intake of terrestrial meats, reduces energy intake by 4–9 %, sufficient to prevent a positive energy balance and obesity. At equal energy intake, lean seafood reduces fasting and postprandial risk markers of insulin resistance, and improves insulin sensitivity in insulin-resistant adults. Energy restriction combined with intake of lean and fatty seafood seems to increase weight loss. Marine n-3 PUFA are probably of importance through n-3 PUFA-derived lipid mediators such as endocannabinoids and oxylipins, but other constituents of seafood such as the fish protein per se, trace elements or vitamins also seem to play a largely neglected role. A high intake of fatty seafood increases circulating levels of the insulin-sensitising hormone adiponectin. As compared with a high meat intake, high intake of seafood has been reported to reduce plasma levels of the hepatic acute-phase protein C-reactive protein level in some, but not all studies. More studies are needed to confirm the dietary effects on energy intake, obesity and insulin resistance. Future studies should be designed to elucidate the potential contribution of trace elements, vitamins and undesirables present in seafood, and we argue that stratification into responders and non-responders in randomised controlled trials may improve the understanding of health effects from intake of seafood.

Nuts are rich in many nutrients that can benefit multiple cardiometabolic functions, including arterial compliance, blood pressure, inflammation, glucoregulation and endothelial vasodilatation. Impaired vasodilatation may contribute to impaired cognitive performance due to poor cerebral perfusion. The present narrative review examines associations between nut consumption, vascular health and cognitive function. It includes a systematic search which identified seventy-one epidemiological or intervention studies in which effects of chronic nut consumption on blood pressure, glucoregulation, endothelial vasodilator function, arterial compliance, inflammatory biomarkers and cognitive performance were evaluated. Weighted mean changes were estimated where data were available; they indicate that nut consumption reduces blood pressure and improves glucoregulation, endothelial vasodilator function and inflammation, whilst a limited number of studies suggest that nut consumption may also improve cognitive performance. Further clinical trials are warranted to explore relationships between nut consumption, endothelial function and cognitive function.

The possible role played by artificial sweeteners in the long-term maintenance of body weight is considered. Although artificial sweeteners can play a role in a short-term energy-controlled diet, the evidence that they are helpful over a longer period is limited. In those in the recommended weight range there is evidence of compensation; that is, the consumption of low-energy foods is followed by an increased energy intake to make up the lost energy. Energy compensation is more likely in those not displaying dietary restraint. The desire to remove sugar from the diet reflects an assumption that its intake is associated with obesity. However, the consumption of energy-dense food, that almost entirely reflects a high fat and low water content, is the best predictor of obesity. Diets offering a high proportion of energy in the form of carbohydrate tend to contain low levels of fat. There are several reports that the use of artificial sweeteners leads to an increased consumption of fat. The weak ability of fat to satisfy hunger makes it easy to overeat fatty foods; in contrast, carbohydrates promote a feeling of ‘fullness’. Various short-term studies have found that carbohydrate consumed as a liquid, rather than a solid, is more likely to result in weight gain.

Nutrition plays a central role in linking the fields of developmental neurobiology and cognitive neuroscience. It has a profound impact on the development of brain structure and function and malnutrition can result in developmental dysfunction and disease in later life. A number of diseases, including schizophrenia, may be related to neurodevelopmental insults such as malnutrition, hypoxia, viruses or in utero drug exposure. Some of the most significant findings on nutrition and neurodevelopment during the last three decades, and especially during the last few years, are discussed in this review. Attention is focused on the underlying cellular and molecular mechanisms by which diet exerts its effects. Randomized intervention studies have revealed important effects of early nutrition on later cognitive development, and recent epidemiological findings show that both genetics and environment are risk factors for schizophrenia. Particularly important is the effect of early nutrition on development of the hippocampus, a brain structure important in establishing learning and memory, and hence for cognitive performance. A major aim of future research should be to elucidate the molecular mechanisms underlying nutritionally-induced impairment of neurodevelopment and specifically to determine the mechanisms by which early nutritional experience affects later cognitive performance. Key research objectives should include: (1) increased understanding of mechanisms underlying the normal processes of ageing and neurodegenerative disorders; (2) assessment of the role of susceptibility genes in modulating the effects of early nutrition on neurodevelopment; and (3) development of nutritional and pharmaceutical strategies for preventing and/or ameliorating the adverse effects of early malnutrition on long-term programming.