Concerns exist about adequacy of vitamin D in pregnant women relative to both maternal and fetal adverse health outcomes. Further contributing to these concerns is the prevalence of inadequate and deficient vitamin D status in pregnant women, which ranges from 5 to 84% globally. Although maternal vitamin D metabolism changes during pregnancy, the mechanisms underlying these changes and the role of vitamin D during development are not well understood. Observational evidence links low maternal vitamin D status with an increased risk of non-bone health outcome in the mother (pre-eclampsia, gestational diabetes, obstructed labour and infectious disease), the fetus (gestational duration) and the older offspring (developmental programming of type 1 diabetes, inflammatory and atopic disorders and schizophrenia); but the totality of the evidence is contradictory (except for maternal infectious disease and offspring inflammatory and atopic disorders), lacking causality and, thus, inconclusive. In addition, recent evidence links not only low but also high maternal vitamin D status with increased risk of small-for-gestational age and schizophrenia in the offspring. Rigorous and well-designed randomised clinical trials need to determine whether vitamin D has a causal role in non-bone health outcomes in pregnancy.

CVD is the most common cause of death in people over 65 years. This review considers the latest evidence for a potential protective effect of C1 donors (folate and the metabolically related B-vitamins) in CVD. Such an effect may or may not be mediated via the role of these nutrients in maintaining plasma homocysteine concentrations within a desirable range. Despite predictions from epidemiological studies that lowering plasma homocysteine would reduce cardiovascular risk, several secondary prevention trials in at-risk patients published since 2004 have failed to demonstrate a benefit of homocysteine-lowering therapy with B-vitamins on CVD events generally. All these trials were performed in CVD patients with advanced disease; thus current evidence suggests that intervention with high-dose folic acid is of no benefit in preventing another event, at least in the case of heart disease. The evidence at this time, however, is stronger for stroke, with meta-analyses of randomised trials showing that folic acid reduces the risk of stroke, particularly in people with no history of stroke. Genetic studies provide convincing evidence to support a causal relationship between sub-optimal B-vitamin status and CVD. People homozygous for the common C677T variant in the gene encoding the folate-metabolising enzyme, methylenetetrahydrofolate reductase (MTHFR), typically have a 14–21% higher risk of CVD. Apart from folate, riboflavin is required as a co-factor for MTHFR. New evidence shows that riboflavin intervention results in marked lowering of blood pressure, specifically in patients with the MTHFR 677TT genotype. This novel gene–nutrient interaction may provide insights as to the mechanism that links C1 metabolism with CVD outcomes.

Recent global fluctuations in food prices and continuing environmental degradation highlight the future challenge of feeding a growing world population. However, current dialogues rarely address the relationship between agricultural changes and health. This relationship is traditionally associated with the role of food in nutrition and with food safety, and while these are key interactions, we show in this paper that the relationship is far more complex and interesting. Besides the direct effects of agriculture on population nutrition, agriculture also influences health through its impact on household incomes, economies and the environment. These effects are felt particularly in low- and middle-income countries, where dramatic changes are affecting the agriculture–health relationship, in particular the growth of nutrition-related chronic disease and the associated double burden of under- and over-nutrition. Greater understanding of the negative effects of agriculture on health is also needed. While lengthening food value chains make the chain of influence between agricultural policy, food consumption, nutrition and health more complex, there remain opportunities to improve health by changing agricultural systems. The first challenge in doing this, we suggest, is to improve our capacity to measure the impact of agricultural interventions on health outcomes, and vice versa.

Health claims on food products are often used as a means to highlight scientifically proven health benefits associated with consuming those foods. But do consumers understand and trust health claims? This paper provides an overview of recent research on consumers and health claims including attitudes, understanding and purchasing behaviour. A majority of studies investigated selective product–claim combinations, with ambiguous findings apart from consumers’ self-reported generic interest in health claims. There are clear indications that consumer responses differ substantially according to the nature of carrier product, the type of health claim, functional ingredient used or a combination of these components. Health claims tend to be perceived more positively when linked to a product with an overall positive health image, whereas some studies demonstrate higher perceived credibility of products with general health claims (e.g. omega-3 and brain development) compared to disease risk reduction claims (e.g. bioactive peptides to reduce risk of heart disease), others report the opposite. Inconsistent evidence also exists on the correlation between having a positive attitude towards products with health claims and purchase intentions. Familiarity with the functional ingredient and/or its claimed health effect seems to result in a more favourable evaluation. Better nutritional knowledge, however, does not automatically lead to a positive attitude towards products carrying health messages. Legislation in the European Union requires that the claim is understood by the average consumer. As most studies on consumers’ understanding of health claims are based on subjective understanding, this remains an area for more investigation.

There is evidence from epidemiological studies suggesting that increased consumption of cruciferous vegetables may protect against specific cancers more effectively than total fruit and vegetable intake. These beneficial effects are attributed to the glucosinolate breakdown products, isothiocyanates (ITC). Similarly, selenium (Se) consumption has also been inversely associated with cancer risk and as an integral part of many selenoproteins may influence multiple pathways in the development of cancer. This paper will briefly review the current state of knowledge concerning the effect of Se and ITC in cancer development with a particular emphasis on its antioxidant properties, and will also address whether alterations in DNA methylation may be a potential mechanism whereby these dietary constituents protect against the carcinogenic process. Furthermore, we will discuss the advantages of combining ITC and Se to benefit from their complementary mechanisms of action to potentially protect against the alterations leading to neoplasia. Based on this review it may be concluded that an understanding of the impact of ITC and Se on aberrant DNA methylation in relation to factors modulating gene-specific and global methylation patterns, in addition to the effect of these food constituents as modulators of key selenoenzymes, such as gastrointestinal glutathione peroxidase-2 (GPx2) and thioredoxin reductase-1 (TrxR1), may provide insights into the potential synergy among various components of a plant-based diet that may counteract the genetic and epigenetic alterations that initiate and sustain neoplasia.

There is considerable interest in the potential of a group of dietary-derived phytochemicals known as flavonoids in modulating neuronal function and thereby influencing memory, learning and cognitive function. The present review begins by detailing the molecular events that underlie the acquisition and consolidation of new memories in the brain in order to provide a critical background to understanding the impact of flavonoid-rich diets or pure flavonoids on memory. Data suggests that despite limited brain bioavailability, dietary supplementation with flavonoid-rich foods, such as blueberry, green tea and Ginkgo biloba lead to significant reversals of age-related deficits on spatial memory and learning. Furthermore, animal and cellular studies suggest that the mechanisms underpinning their ability to induce improvements in memory are linked to the potential of absorbed flavonoids and their metabolites to interact with and modulate critical signalling pathways, transcription factors and gene and/or protein expression which control memory and learning processes in the hippocampus; the brain structure where spatial learning occurs. Overall, current evidence suggests that human translation of these animal investigations are warranted, as are further studies, to better understand the precise cause-and-effect relationship between flavonoid intake and cognitive outputs.

Energy restriction (ER) to control weight is a potential strategy for breast cancer prevention. The protective effects of habitual continuous energy restriction (CER) and weight loss on breast tumour formation have been conclusively demonstrated in animal studies over the past 100 years, and more recently in women using data from observational studies and bariatric surgery. Intermittent energy restriction (IER) and intermittent fasting (IF) are possible alternative preventative approaches which may be easier for individuals to undertake and possibly more effective than standard CER. Here, we summarise the available data on CER, IER and IF with special emphasis on their potential for breast cancer prevention. In animals, IER is superior or equivalent to CER with the exception of carcinogen-induced tumour models when initiated soon after carcinogen exposure. There are no human data on IER and breast cancer risk, but three studies demonstrated IER and CER to be equivalent for weight loss. IF regimens also reduce mammary tumour formation in animal models and also led to weight loss in human subjects, but have not been directly compared with CER. Animal and some human data suggest that both IER and IF may differ mechanistically compared with CER and may bring about greater reduction in hepatic and visceral fat stores, insulin-like growth factor 1 (IGF-1) levels and cell proliferation, and increased insulin sensitivity and adiponectin levels. Although IER and IF were first studied 65 years ago, we conclude that further studies are required to assess their values compared with CER.

The huge health burden accompanying obesity is not only attributable to inadequate dietary and sedentary lifestyle habits, since a predisposing genetic make-up and other putative determinants concerning easier weight gain and fat deposition have been reported. Thus, several investigations aiming to understand energy metabolism and body composition maintenance have been performed considering the participation of perinatal nutritional programming and epigenetic processes as well as inflammation phenomena. The Developmental Origins of Health and Disease hypothesis and inheritance-oriented investigations concerning gene–nutrient interactions on energy homoeostasis and metabolic functions have suggested that inflammation could be not only a comorbidity of obesity but also a cause. There are several examples about the role of nutritional interventions in pregnancy and lactation, such as energetic deprivation, protein restriction and excess fat, which determine a cluster of disorders affecting energy efficiency in the offspring as well as different metabolic pathways, which are mediated by epigenetics encompassing the chromatin information encrypted by DNA methylation patterns, histone covalent modifications and non-coding RNA or microRNA. Epigenetic mechanisms may be boosted or impaired by dietary and environmental factors in the mother, intergenerationally or transiently transmitted, and could be involved in the obesity and inflammation susceptibility in the offspring. The aims currently pursued are the early identification of epigenetic biomarkers concerned in individual's disease susceptibility and the description of protocols for tailored dietary treatments/advice to counterbalance adverse epigenomic events. These approaches will allow diagnosis and prognosis implementation and facilitate therapeutic strategies in a personalised ‘epigenomically modelled’ manner to combat obesity and inflammation.

Inflammation plays a key role in many common conditions and diseases. Fatty acids can influence inflammation through a variety of mechanisms acting from the membrane to the nucleus. They act through cell surface and intracellular receptors that control inflammatory cell signalling and gene expression patterns. Modifications of inflammatory cell membrane fatty acid composition can modify membrane fluidity, lipid raft formation and cell signalling leading to altered gene expression and can alter the pattern of lipid and peptide mediator production. Cells involved in the inflammatory response usually contain a relatively high proportion of the n-6 fatty acid arachidonic acid in their membrane phospholipids. Eicosanoids produced from arachidonic acid have well-recognised roles in inflammation. Oral administration of the marine n-3 fatty acids EPA and DHA increases the contents of EPA and DHA in the membranes of cells involved in inflammation. This is accompanied by a decrease in the amount of arachidonic acid present. EPA is a substrate for eicosanoid synthesis and these are often less potent than those produced from arachidonic acid. EPA gives rise to E-series resolvins and DHA gives rise to D-series resolvins and protectins. Resolvins and protectins are anti-inflammatory and inflammation resolving. Thus, the exposure of inflammatory cells to different types of fatty acids can influence their function and so has the potential to modify inflammatory processes.

Obesity has been associated with low-grade systemic inflammation and with micronutrient deficiencies. Obese individuals have been found to have lower vitamin A levels and lower vitamin A intake compared with normal-weight individuals. Vitamin A plays a major role in the immune function, including innate immunity, cell-mediated immunity and humoral antibody immunity. It has also been recognised recently that vitamin A has important regulatory functions. Vitamin A status has an important effect on the chronic inflammatory response. Vitamin A deficiency increases a T-helper type 1 (Th1) response, elevates levels of pro-inflammatory cytokines, increases the expression of leptin, resistin and uncoupling proteins (UCP) and promotes adipogenesis. The effect of vitamin A deficiency on obesity might be increasing the risk of fat deposition and also the risk of chronic inflammation associated with obesity. Supplementation with vitamin A in vitro and in animal models has been found to reduce concentrations of adipocytokines, such as leptin and resistin. In conclusion, vitamin A deficiency increases a Th1 response in the presence of obesity and thus, increases the inflammatory process involved in chronic inflammation and fat deposition. The metabolism of leptin and other adipocytokines may play a critical role in the effect of vitamin A deficiency in the inflammatory response observed in obesity.

There is strong evidence indicating that excess adiposity negatively impacts immune function and host defence in obese individuals. This is a review of research findings concerning the impact of obesity on the immune response to infection, including a discussion of possible mechanisms. Obesity is characterised by a state of low-grade, chronic inflammation in addition to disturbed levels of circulating nutrients and metabolic hormones. The impact of these metabolic abnormalities on obesity-related comorbidities has undergone intense scrutiny over the past decade. However, relatively little is known of how the immune system and host defence are influenced by the pro-inflammatory and excess energy milieu of the obese. Epidemiological data suggest obese human subjects are at greater risk for nosocomial infections, especially following surgery. Additionally, the significance of altered immunity in obese human subjects is emphasised by recent studies reporting obesity to be an independent risk factor for increased morbidity and mortality following infection with the 2009 pandemic influenza A (H1N1) virus. Rodent models offer important insight into how metabolic abnormalities associated with excess body weight can impair immunity. However, more research is necessary to understand the specific aspects of immunity that are impaired and what factors are contributing to reduced immunocompetence in the obese. Additionally, special consideration of how infection in this at-risk population is managed is required, given that this population may not respond optimally to antimicrobial drugs and vaccination. Obesity impacts millions globally, and greater understanding of its associated physiological disturbances is a key public health concern.

The benefits of moderate amounts of alcohol for a better health and longer life expectancy compared with abstinence have been suggested by the findings of numerous studies. However, controversies have emerged regarding the influence of confounding factors and the systematic errors that might have been inadvertently disregarded in the early studies. This review includes a description of the findings of those research studies published in the last 5 years on the effects of moderate alcohol consumption on all-cause mortality, CVD and inflammation, the immune system, insulin sensitivity, non-alcoholic fatty liver disease (NAFLD) and cancer. Promising evidences exist from both animal studies and human clinical trials regarding intermediate end-points of CHD and insulin sensitivity, such as HDL, adiponectin or fibrinogen. However, controversies and inconsistent findings exist regarding many of these diseases and related functions and biomarkers. Further research and human randomised-controlled trials with adequate standardisation of the study conditions are necessary in order to draw a comparison between studies, establish the causal effect of moderate alcohol intake on disease protection and reach consensus on the circumstances that allow the recommendation of moderate alcohol habitual intakes as a strategy for health maintenance.

The increased incidence of allergic disease seems to rely on many factors. Among them, the association between genetic variations of the immune response and environmental pressure by allergens, infectious agents and pollutants should be taken into consideration. In alternative to conventional treatments with corticosteroids and antihistaminics, nutraceuticals have been shown to act on allergic disease either during allergic sensitisation or on consolidated disease. In this review, special emphasis is placed on the effects of dietary polyphenols on three major allergic diseases, namely atopic eczema, food allergy and asthma. Interference of polyphenols with T-helper 2 activation seems to be the main mechanism of their inhibitory effects on allergy development. Moreover, deficits of T-regulatory cells seem to play a pathogenic role in allergic disease and, therefore, these cells may represent a major target of polyphenol activity.

We have reviewed effects of long chain (LC) n-3 PUFA on markers of atherosclerosis in human subjects with a focus on individual effects of EPA and DHA. Initial results from epidemiological studies suggested that LC n-3 PUFA from fish oils (FO) reduced incidence of CVD; those results have been confirmed in interventional studies. Dietary intervention with n-3 PUFA decreased fasting and postprandial TAG, number of remnant-like chylomicron particles, large VLDL, and total and small dense LDL particles. It increased mean size of LDL particles by increasing number of large and decreasing those of small dense particles. With some exceptions, n-3 PUFA decreased blood pressure (BP) and heart rate (HR), flow-mediated dilation (FMD) and plasma concentrations of inflammatory markers. n-3 PUFA also decreased circulating adhesion molecules and intima-media thickness (IMT) in some but not other studies. For IMT, results varied with the sex and artery being examined. EPA effects on FMD are endothelial cell dependent, while those of DHA seem to be endothelial cell independent. Individually, both EPA and DHA decreased TAG and inflammatory markers, but only DHA decreased HR, BP and number of small dense LDL particles. Results varied because of dose and duration of n-3 PUFA, EPA:DHA, health status of subjects and other reasons. Future studies are needed to determine optimal doses of EPA and DHA individually, their synergistic, additive or antagonistic effects, and to understand underlying mechanisms. In conclusion, n-3 PUFA decreased several risk factors for atherosclerosis without any serious adverse effects.

Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. The chronic inflammatory response has its origin in the links existing between the adipose tissue and the immune system. Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.

Dietary strategies that can help reduce hunger and promote fullness are beneficial for weight control, since these are major limiting factors for success. High-protein (HP) diets, specifically those that maintain the absolute number of grams ingested, while reducing energy, are a popular strategy for weight loss (WL) due to the effects of protein-induced satiety to control hunger. Nonetheless, both the safety and efficacy of HP WL diets have been questioned, particularly in combination with low-carbohydrate advice. Nonetheless, for short-to-medium-term intervention studies (over several months), increasing the energetic contribution of protein does appear effective. The effects of HP diets on appetite, bone health, renal function, blood pressure, cardiovascular bio-markers, antioxidant status, gut health and psychological function are discussed. Further research is warranted to validate the physiological effects of HP diets over longer periods of time, including studies that modify the quality of macronutrients (i.e. the type of carbohydrate, fat and protein) and the interaction with other interventions (e.g. exercise and dietary supplements).

The current review considers satiety-based approaches to weight management in the context of health claims. Health benefits, defined as beneficial physiological effects, are what the European Food Safety Authority bases their recommendations on for claim approval. The literature demonstrates that foods that target within-meal satiation and post-meal satiety provide a plausible approach to weight management. However, few ingredient types tested produce the sustainable and enduring effects on appetite accompanied by the necessary reductions in energy intake required to claim satiety/reduction in hunger as a health benefit. Proteins, fibre types, novel oils and carbohydrates resistant to digestion all have the potential to produce beneficial short-term changes in appetite (proof-of-concept). The challenge remains to demonstrate their enduring effects on appetite and energy intake, as well as the health and consumer benefits such effects provide in terms of optimising successful weight management. Currently, the benefits of satiety-enhancing ingredients to both consumers and their health are under researched. It is possible that such ingredients help consumers gain control over their eating behaviour and may also help reduce the negative psychological impact of dieting and the physiological consequences of energy restriction that ultimately undermine weight management. In conclusion, industry needs to demonstrate that a satiety-based approach to weight management, based on single-manipulated food items, is sufficient to help consumers resist the situational and personal factors that drive overconsumption. Nonetheless, we possess the methodological tools, which when employed in appropriate designs, are sufficient to support health claims.