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.

Taste perception has been studied frequently in young and older adult groups. This paper systematically reviews these studies to determine the effect of ageing on taste perception and establish the reported extent of sensory decline. Five databases were searched from 1900 to April 2012. Articles relating to healthy ageing in human subjects were included, reviewed and rated (Downs and Black scoring system). Sixty-nine studies investigated the effect of ageing on taste perception; forty examined detection thresholds of which twenty-three provided sufficient data for meta-analysis, eighteen reported identification thresholds and twenty-five considered supra-threshold intensity perception. Researchers investigating detection thresholds considered between one and thirteen taste compounds per paper. Overall, the consensus was that taste detection thresholds increased with age (Hedges’ g = 0·91, P < 0·001), across all taste modalities. Identification thresholds were reported to be higher for older adults in seventeen out of eighteen studies. Sixteen out of twenty-five studies reported perception of taste intensity at supra-threshold levels to be significantly lower for older adults. However, six out of nine studies concerning sucrose found perceived intensity of sweet taste not to diminish with age. The findings of this systematic review suggest taste perception declines during the healthy ageing process, although the extent of decline varies between studies. Overall, the studies reviewed had low Downs and Black scores (mean 16 (SD 2)) highlighting the need for more robust large scale and longitudinal studies monitoring the impact of ageing on the sensory system, and how this influences the perception of foods and beverages.

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.

The inequality of nutrition and obesity re-focuses concern on who in society is consuming the worst diet. Identification of individuals with the worst of dietary habits permits for targeting interventions to assuage obesity among the population segment where it is most prevalent. We argue that the use of fiscal interventions does not appropriately take into account the economic, social and health circumstances of the intended beneficiaries of the policy. This paper reviews the influence of socio-demographic factors on nutrition and health status and considers the impacts of nutrition policy across the population drawing on methodologies from both public health and welfare economics. The effects of a fat tax on diet are found to be small and while other studies show that fat taxes saves lives, we show that average levels of disease risk do not change much: those consuming particularly bad diets continue to do so. Our results also suggest that the regressivity of the policy increases as the tax becomes focused on products with high saturated fat contents. A fiscally neutral policy that combines the fat tax with a subsidy on fruit and vegetables is actually more regressive because consumption of these foods tends to be concentrated in socially undeserving households. We argue that when inequality is of concern, population-based measures must reflect this and approaches that target vulnerable populations which have a shared propensity to adopt unhealthy behaviours are appropriate.

Diet can significantly influence athletic performance, but recent research developments have substantially changed our understanding of sport and exercise nutrition. Athletes adopt various nutritional strategies in training and competition in the pursuit of success. The aim of training is to promote changes in the structure and function of muscle and other tissues by selective modulation of protein synthesis and breakdown in response to the training stimulus. This process is affected by the availability of essential amino acids in the post-exercise period. Athletes have been encouraged to eat diets high in carbohydrate, but low-carbohydrate diets up-regulate the capacity of muscle for fat oxidation, potentially sparing the limited carbohydrate stores. Such diets, however, do not enhance endurance performance. It is not yet known whether the increased capacity for fat oxidation that results from training in a carbohydrate-deficient state can promote loss of body fat. Preventing excessive fluid deficits will maintain exercise capacity, and ensuring adequate hydration status can also reduce subjective perception of effort. This latter effect may be important in encouraging exercise participation and promoting adherence to exercise programmes. Dietary supplement use is popular in sport, and a few supplements may improve performance in specific exercise tasks. Athletes must be cautious, however, not to contravene the doping regulations. There is an increasing recognition of the role of the brain in determining exercise performance: various nutritional strategies have been proposed, but with limited success. Nutrition strategies developed for use by athletes can also be used to achieve functional benefits in other populations.

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.

Nutritional interventions that might influence sarcopenia, as indicated by literature reporting on sarcopenia per se as well as dynapenia and frailty, are reviewed in relation to potential physiological aetiological factors, i.e. inactivity, anabolic resistance, inflammation, acidosis and vitamin D deficiency. As sarcopenia occurs in physically active and presumably well-nourished populations, it is argued that a simple nutritional aetiology is unlikely and unequivocal evidence for any nutritional influence is extremely limited. Dietary protein is probably the most widely researched nutrient but only for frailty is there one study showing evidence of an aetiological influence and most intervention studies with protein or amino acids have proved ineffective with only a very few exceptions. Fish oil has been shown to attenuate anabolic resistance of muscle protein synthesis in one study. There is limited evidence for a protective influence of antioxidants and inducers of phase 2 proteins on sarcopenia, dynapenia and anabolic resistance in human and animal studies. Also fruit and vegetables may protect against acidosis-induced sarcopenia through their provision of dietary potassium. While severe vitamin D deficiency is associated with dynapenia and sarcopenia, the evidence for a beneficial influence of increasing vitamin D status above the severe deficiency level is limited and controversial, especially in men. On this basis there is insufficient evidence for any more specific nutritional advice than that contained in the general healthy lifestyle–healthy diet message: i.e. avoiding inactivity and low intakes of food energy and nutrients and maintain an active lifestyle with a diet providing a rich supply of fruit and vegetables and frequent oily fish.

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.

The rise in gluten consumption over time has led to the increasing recognition of coeliac disease (CD) with associated complications. However, only recently has there been an appreciation that the spectrum of gluten-related disorders is greater than just CD, which may explain the growing global popularity in gluten-free products. Current literature suggests that a newly recognised clinical entity in the form of non-coeliac gluten sensitivity (NCGS) may be the most common gluten-related disorder encountered by healthcare professionals, although its exact prevalence is as yet unknown. This article will review the historical relationship between mankind and gluten as well as the progressive recognition that it is possible for gluten to have a deleterious effect on our health. To this effect we discuss the prevalence, diagnosis and complications of CD including the benefits derived from a gluten-free diet (GFD). Finally, we discuss our current understanding of NCGS, in addition to highlighting the need for further research to determine the extent, clinicopathological features and serological biomarkers to help recognise this emerging condition in clinical practice.

EU legislation on nutrition and health claims made on foods (Regulation (EC) No. 1924/2006) specifies that health claims should be only authorised for use in the Community after a scientific assessment of the highest possible standard is carried out by the European Food Safety Authority (EFSA). This paper focuses on the scientific substantiation of health claims within the context of the EU Regulation. The evaluation of the substantiation of health claims is carried out by the EFSA Scientific Panel on Dietetic Products, Nutrition and Allergies (NDA). The EFSA has published extensive guidance to assist applicants in the preparation of applications for authorisations of health claims. This guidance summarises the general principles applied by the NDA Panel in the evaluation of health claims, including the scientific criteria for substantiation, as well as the scientific requirements for the substantiation of specific health claims. To date, the EFSA NDA Panel has concluded that a wide range of health claims has been substantiated. These include claims for many well-established functions of nutrients, as well as beneficial effects of foods and food constituents on a range of body functions. In addition, claims have been substantiated on the role of nutrients in growth and development of children and on the effects of nutrients and food constituents on reduction of risk factors for disease. EFSA evaluations and guidance have made an important contribution to the understanding of the scientific substantiation of health claims which will help to set new directions for research and will guide future innovation.