The primary role of the extensive and complex modern food legislation is to protect the consumer. Providing a framework for industry and enabling free trade are secondary aims. In the EU the 2006 Regulation on nutrition and health claims made on foods was adopted in December 2006. This Regulation defines detailed lists of permitted claims with precise conditions, requires foods making claims to meet specific nutrient profiles and requires the submission of a dossier for approval of new health claims. Nutrient profiles and an initial list of existing health claims will not be agreed until January 2009 and January 2010 respectively. The uncertainty about profiles and the initial list of claims as well as the prescriptive nature of the Regulation will have a major impact, some negative but some positive, on food innovation. Worldwide legislation on nutrition and health claims continues to develop. The current paper also provides an outline of some other key pieces of European legislation that affect food innovation. However, currently, all this legislation remains in development and up-to-date information can be sought from the reference material provided.

Internationally, socio-economic trends reinforce the complex physiological mechanisms that favour positive energy balance, leading to an accumulation of excess body weight and associated metabolic disorders. This so-called ‘obesogenic environment’ is characterised by increasing accessibility and affordability of energy-dense foods and declining levels of physical activity. In the face of such rapidly-rising obesity rates there is general consensus that strategies to address trends in weight gain must go forwards in the absence of complete evidence of cause or effective prevention strategy. Thus, strategy implementation and evaluation must contribute to, as well as be informed by, the evidence base. Social marketing research and practice has a track record that strongly indicates that it can contribute to both the evolving knowledge base on obesity and overweight control policy and the development of effective intervention strategies. Social marketing draws pragmatically on many disciplines to bring about voluntary behaviour change as well as requisite supporting policy and environmental change. Key objectives include: generating insights into the drivers of current behaviour patterns; important barriers to change; client-oriented approaches to new desirable diet and lifestyle choices. Social marketing recognises that target clients have the power to ensure success or failure of obesity control policies. Social marketing seeks to identify genuine exchange of benefits for target adopters of behaviour change and the advocates of change, and how they may be developed and offered within an appropriate relevant context. Social marketing adopts a cyclical approach of learning, strategic development and evaluation, and therefore is well placed to integrate with the multi-disciplinary demands of obesity prevention strategies.

Sweat evaporation can be a key thermoregulatory mechanism and it causes a loss of water from all compartments of the body. Hypohydration can also develop with restricted fluid intake or with intake of diuretics. Hypohydration can affect physical and/or mental performance and/or have implications for dietary recommendations. A variety of different types and modes of exercise performance can be influenced by hydration state. Reviews of the published literature are currently most conclusive for endurance exercise. Dehydration equivalent to 2% body mass loss during exercise in a hot environment (31–32°C) impairs endurance performance, but when the exercise is performed in a temperate environment (20–21°C) a 2% body mass loss appears to have a lesser and inconsequential effect. In cold environments a body mass loss >2% may be tolerable for endurance exercise. There is a less conclusive picture as to the effects of hypohydration on other types of physical performance, including strength and power activities, team sports and the skills component of many sports, and for mental performance. A number of physiological mechanisms are responsible for the effects observed. Fluid consumption can be used to attenuate the development of a water deficit or to correct it. The composition and temperature of a drink and the volume and rate of its consumption can all influence the physiological responses to ingestion and can impact on exercise performance.

The importance of nutrition in sport has been recognised since the ancient Olympians, and its role in improving both health and sports performance has widespread acceptance. However, in sporting circles nutritional knowledge, beliefs and practices are extremely varied. Within any sporting organisation the sports dietitian or nutritionist must be able to work with athletes, their family, coaches and other support staff to develop and monitor realistic and practical strategies that work best for each performer, contributing to a positive and sustained outcome on performance. The present review examines the practical application of current key issues in performance nutrition, highlighting the advantages of early intervention in youth development and comprehensive and integrated nutrition services.

Regular and goal-appropriate exercise is critical to improving and maintaining both health and performance. However, the frequency, intensity, duration and type of activities needed to optimise health or achieve successful sports performance will differ considerably depending on an individual's goals and capabilities. Although sport is one of many forms of exercise that can be counted towards daily physical activity, participation in sport is not necessary to meet current physical activity recommendations. The current consensus is that the minimum amount of physical activity needed to improve and maintain good health is 30 min moderate-intensity activity/d on ≥5 d/week. The evidence supporting this consensus is based on predominantly observational evidence that performing regular aerobic (endurance)-type physical activity is associated with reduced morbidity and premature mortality from CVD, CHD, stroke and colo-rectal cancer. The exact dose needed to improve health and the slope of the dose–response gradient between physical activity and mortality for various diseases are not known, and one major limitation of the existing evidence is the lack of objective measurement of physical activity. Limited evidence indicates that a much higher dose of activity (45–90 min each day on ≥5 d/week) may be needed to prevent overweight and obesity and to avoid weight regain in previously overweight and obese individuals. The role of resistance training and heavy domestic work in reducing morbidity and premature mortality for various diseases is unclear. As most adults do not meet current recommendations there is a critical need for innovative approaches to increase physical activity across large-scale populations.

Optimal health and well-being are now considered the true measures of human development. Integrated strategies for infant, child and adult nutrition are required that take a life-course perspective to achieve life-long health. The major nutrition challenges faced today include: (a) addressing the pending burden of undernutrition (low birth weight, severe wasting, stunting and Zn, retinol, Fe, iodine and folic acid deficits) affecting those individuals living in conditions of poverty and deprivation; (b) preventing nutrition-related chronic diseases (obesity, diabetes, CVD, some forms of cancer and osteoporosis) that, except in sub-Saharan Africa, are the main causes of death and disability globally. This challenge requires a life-course perspective as effective prevention starts before conception and continues at each stage of life. While death is unavoidable, premature death and disability can be postponed by providing the right amount and quality of food and by maintaining an active life; (c) delaying or avoiding, via appropriate nutrition and physical activity interventions, the functional declines associated with advancing age. To help tackle these challenges, it is proposed that the term ‘malnutrition in all its forms’, which encompasses the full spectrum of nutritional disorders, should be used to engender a broader understanding of global nutrition problems. This term may prove particularly helpful when interacting with policy makers and the public. Finally, a greater effort by the UN agencies and private and public development partners is called for to strengthen local, regional and international capacity to support the much needed change in policy and programme activities focusing on all forms of malnutrition with a unified agenda.

Use of the energy balance equation for understanding the causation of obesity is discussed. Its basis on the thermodynamic laws is expressed in mathematical models for body-weight changes. Only a very small net energy surplus per time unit constitutes the energy deposition during weight gain, making measurements of its components difficult. The physical laws provide exact quantitative relationships between energy intake, energy expenditure and deposition of energy, but cannot disentangle the initiating and driving forces of the energy imbalance, which may also be an active storage of fat in adipose tissue. These and various other limitations of the energy balance model warrant cautiousness in using the model in studies of obesity causation. Weight gain may be self-promoting and mathematical feedback models allowing estimation of such effects show that they are realistic. Predisposition and susceptibility should be distinguished, and susceptibility as a modifiable predisposition, the genetic and environmental contribution to predisposition and its usefulness as targets for prevention and treatment are discussed. Current progress in unravelling genetic predisposition, the complex genetically-determined mechanisms, the slower progress in unravelling the environmental influences, the different nature of genetic and environmental influences, the possible pathways of environmental influences and the environmental influences as mediators of genetic effects are addressed. The evidence behind the prevailing concept of the ‘obesogenic’ environment is critically analysed. Finally, particular opportunities for the identification of the causes of the obesity epidemic by detailed analysis of an observed irregular development of the epidemic over long time periods are presented, and evidence for predisposition as a result of postnatal environmental influences is inferred from these studies.

Diabetes mellitus is escalating globally and it is predicted that 200 million individuals worldwide will have diabetes by 2010 and 300 million by 2025. However, there is compelling evidence from many studies that for subjects with impaired fasting glucose or impaired glucose tolerance the presentation of type 2 diabetes can be delayed by lifestyle modification. The aim of the present review is to present a summary of lifestyle modification interventions that have included a dietary component in their overall diabetes prevention programme. Medline, allied health literature and diabetes journals were searched for peer-reviewed literature using the terms ‘diet*’ and ‘diabetes’ and ‘intervention’. Inclusion criteria were: peer-reviewed studies from 1975 to 2008; a sample of at least fifty subjects; a healthy eating and/or physical activity component; prevention of diabetes as a primary goal. Generally, the participants were in a high-risk category for the development of diabetes. Outcomes were evaluated at two points in time (pre- and post-intervention) in terms of knowledge, behaviour change and clinical improvement, which included weight, blood pressure, BMI, body fat, waist circumference, waist:hip ratio and physiological and/or biochemical measures. Findings indicate that the most successful interventions combine individual dietary counselling with an activity component. Further factors predicting success are weight loss achieved, duration and intensity of the intervention and dietary compliance.

Whilst previously type 2 diabetes occurred in older adults, its incidence, together with obesity, has increased rapidly in children. An improved understanding of this disease pathway from a developmental view point is critical. It is likely that subtle changes in dietary patterns over an extended period of time contribute to diabetes, although this type of rationale is largely ignored in animal studies aimed at determining the mechanisms involved. Small-animal studies in which large, and often extreme, changes in the diet are imposed at different stages of the life cycle can have substantial effects on fat mass and/or pancreatic functions. These responses are not representative of the much more gradual changes seen in the human population. An increasing number of studies indicate that it is growth rate per se, rather than the type of dietary intervention that determines pancreatic function during development. Epigenetic mechanisms that regulate insulin secretion by the pancreas can be re-set by more extreme changes in dietary supply in early life. The extent to which these changes may contribute to more subtle modulations in glucose homeostasis that can accompany excess fat growth in childhood remains to be established. For human subjects there is much less information as to whether specific dietary components determine disease onset. Indeed, it is highly likely that genotype has a major influence, although recent data relating early diet to physical activity and the FTO gene indicate the difficulty of establishing the relative contribution of diet and changes in body mass to diabetes.

Animal studies have demonstrated that altering the maternal diet during pregnancy affects offspring disease risk. Data from human subjects on the early-life determinants of disease have been derived primarily from birth-weight associations; studies of the impact of the maternal diet are scarce and inconsistent. Investigating CVD risk factors in the offspring of women who have participated in maternal supplementation trials provides a useful resource in this research field, by virtue of employing an experimental design (as compared with observational studies). To date, follow-up studies have been published only for a small number of trials; these trials include the impact of maternal protein–energy, multiple-micronutrient and Ca supplementation on offspring disease risk. In Nepal maternal micronutrient supplementation has been shown to be associated with lower offspring systolic blood pressure at 2 years of age. Data from Guatemala on a pre- and postnatal protein–energy community intervention have suggested long-term improvements in fasting glucose and body composition but not in blood pressure. In The Gambia no association has been found between prenatal protein–energy supplementation and markers of CVD risk including body composition, blood pressure and fasting glucose and insulin in childhood and adolescence. Little evidence of an effect of maternal Ca supplementation on offspring blood pressure has been demonstrated in four trials, although the risk of high systolic blood pressure was found to be reduced in one trial. The present paper reviews the current evidence relating maternal nutritional supplementation during pregnancy to offspring CVD risk and explores the potential explanations for the lack of association.

Dietary fat is an important factor in the aetiology of obesity and the metabolic syndrome. It has been widely debated whether gastric emptying (GE) is altered in obesity. GE times have been reported as both longer and shorter in obese individuals compared with matched lean individuals. However, the general consensus is that GE is accelerated and satiety is lower in obesity. Research has implicated a high-fat (HF) diet in these findings. A single HF meal has a longer GE time than a low-fat meal and can even delay GE of the subsequent meal. However, an HF diet has shown different effects. Feeding a HF diet adapts gastrointestinal function to reduce GE times in comparison with a low-fat diet. Increased GE may lead to decreased satiety and faster onset of subsequent eating episodes. Further results have suggested that consuming an HF diet for 14 d increases the GE rate of HF food but not low-fat food. Consuming HF diets for 2 weeks has also been shown to increase food intake. Decreased satiation following an HF diet may cause increased food intake and a positive energy balance, potentially resulting in a gradual increase in adiposity. Recent results have suggested that gastrointestinal transit is accelerated following only 3 d on a HF diet. The variable GE times reported in obesity may be associated with interactions between the HF diet and obesity and not simply the obese state.

Companion animals represent an under-utilised resource. The present paper is designed to encourage collaborative studies. Dogs and cats are out-bred animals that are willing to consume a consistent diet for long periods, so are ideal candidates for prospective studies of naturally-occurring disease. In some studies the effect of diet on survival has been substantial. Food restriction, for example, slows the development of osteoarthritis and increases the lifespan of Labrador retrievers by 2 years, protein and P restriction more than doubles the median survival time of dogs and cats with chronic kidney disease and adding n-3 fats and arginine to the diet of dogs with stage 3 lymphoma improves median survival time by one-quarter. Obesity is also very common in both dogs and cats and is also associated with disease as in human subjects. When interpreting these results, however, it is essential to take into account pathophysiological differences among species. Dogs and cats do not display all the characteristics of metabolic disease in human subjects, they metabolise fat well and atherosclerosis and cardiac infarction are uncommon. Such differences should not, however, preclude further study because differences among species often clarify knowledge. Monitoring of disease in companion animals may also provide a surveillance system for the safety of the food supply, as illustrated by recent outbreaks of acute renal failure and liver failure in cats and dogs in the USA caused respectively by melamine and mycotoxin contamination of pet foods.

Over several decades a number of epidemiological studies have identified the inverse associations between cruciferous vegetables and the risk of several cancers, including gastric, breast, colo-rectal, lung, prostate, bladder and endometrial cancers, via plausible physiological mechanisms. Although retrospective case–control studies have consistently reported inverse associations between the risk of these cancers and the intake of cruciferous vegetables and isothiocyanate-containing plants, current prospective cohort studies have found these associations to be weaker and less consistent. Genetic variations affecting the metabolism of glucosinolate hydrolysis products may modulate the effects of cruciferous vegetable consumption on cancer risk, which may be one of the reasons for the discrepancies between retrospective and prospective studies. In addition, methodological issues such as measurement errors of dietary exposure, misclassification, recall bias, publication bias, confounding and study design should be carefully considered in interpreting the results of case–control and cohort studies and in drawing conclusions in relation to the potential effects of cruciferous vegetables on cancers. Although recent comprehensive reviews of numerous studies have purported to show the specific protective role of cruciferous vegetables, and particularly Brassicas, against cancer risk, the current epidemiological evidence suggests that cruciferous vegetable consumption may reduce the risk only of gastric and lung cancers. However, there is at present no conclusive evidence that the consumption of cruciferous vegetables attenuates the risk of all other cancers.