Satiety, which is the inhibition of eating following the end of a meal, is influenced by a number of food characteristics, including compositional and structural factors. An increased understanding of these factors and the mechanisms whereby they exert their effects on satiety may offer a food-based approach to weight management. Water and gas, which are often neglected in nutrition, are major components of many foods and contribute to volume, and to sensory and other characteristics. A review of previous short-term studies that evaluated the effects of water or gas in foods on satiety showed that while satiety was generally increased, effects on subsequent intakes were not always apparent. These studies were diverse in terms of design, timings and food matrices, which precludes definitive conclusions. However, the results indicate that solids may be more effective at increasing satiety than liquids, but gas may be as effective as water. Although increased gastric distension may be the main mechanism underlying these effects, pre-ingestive and ingestive impacts on cognitive, anticipatory and sensory responses also appear to be involved. Furthermore, there is limited evidence that water on its own may be effective at increasing satiety and decreasing intakes when drunk before, but not with, a meal. Longer-term extrapolation suggests that increasing food volumes with water or gas may offer weight-management strategies. However, from a practical viewpoint, the effects of water and gas on satiety may be best exploited by using these non-nutrients to manipulate perceived portion sizes, without increasing energy contents.

Unlike energy expenditure, energy intake occurs during discrete events: snacks and meals. The prevailing view is that meal size is governed by physiological and psychological events that promote satiation towards the end of a meal. This review explores an alternative and perhaps controversial proposition. Specifically that satiation plays a secondary role, and that meal size (kJ) is controlled by decisions about portion size, before a meal begins. Recently, techniques have been developed that enable us to quantify ‘expected satiation’ and ‘expected satiety’ (respectively, the fullness and the respite from hunger that foods are expected to confer). When compared on a kJ-for-kJ basis, these expectations differ markedly across foods. Moreover, in self-selected meals, these measures are remarkably good predictors of the energy content of food that ends up on our plate, even more important than palatability. Expected satiation and expected satiety are influenced by the physical characteristics of a food (e.g. perceived volume). However, they are also learned. Indeed, there is now mounting evidence for ‘expected-satiation drift’, a general tendency for a food to have higher expected satiation as it increases in familiarity. Together, these findings show that important elements of control (discrimination and learning/adaptation) are clearly evident in plans around portion size. Since most meals are eaten in their entirety, understanding the nature of these controls should be given high priority.

Liquids have been shown to have a low satiating efficiency. The may be related to the high rate of consumption for liquids which may be higher than 200 g/min. In a number of studies, we showed that the positive relationship between eating rate and energy intake is mediated by oro-sensory exposure time. Longer sensory exposure times are consistently associated with lower food intakes. This observation maybe linked to the role of cephalic phase responses to foods. Cephalic phase responses are a set of physiological responses, which are conceived to prepare the digestive system for the incoming flow of nutrients after ingestion, with the aim of maintaining homeostasis. Results from various studies suggest that cephalic phase responses are much smaller (absent) for liquids compared to solids. It is hypothesised that the absence of cephalic phase responses to liquid foods may be one of the causes why liquid energies enter the body undetected and lead to weak energy intake compensation. This idea fits with the concept of the taste system as a nutrient-sensing system that informs the brain and the gastro-intestinal system about what is coming into our body. With liquids, this system is bypassed. Slower eating may help the human body to associate the sensory signals from food with their metabolic consequences. Foods that are eaten quickly may impair this association, and may therefore lead to overconsumption of energy, and ultimately to weight gain.

Investigations of the impact of physical activity on appetite control have the potential to throw light on the understanding of energy balance and therefore, upon body weight regulation and the development of obesity. Given the complexity of the landscape influencing weight regulation, research strategies should reflect this complexity. We have developed a research approach based on the concept of the psychobiological system (multi-level measurement and analysis) and an experimental platform that respects the operations of an adaptive regulating biological system. It is important that both sides of the energy balance equation (activity and diet) receive similar detailed levels of analysis. The experimental platform uses realistic and fully supervised levels of physical activity, medium-term (not acute) interventions, measurement of body composition, energy metabolism (indirect calorimetry), satiety physiology (gut peptides), homeostatic and hedonic processes of appetite control, non-exercise activity, obese adult participants and both genders. This research approach has shown that the impact of physical activity on appetite control is characterised by large individual differences. Changes in body composition, waist circumference and health benefits are more meaningful than changes in weight. Further, we are realising that the acute effects do not predict what will happen in the longer term. The psychobiological systems approach offers a strategy for simultaneously investigating biological and behavioural processes relevant to understanding obese people and how obesity can be managed. This experimental platform provides opportunities for industry to examine the impact of foods under scientifically controlled conditions relevant to the real world.

Excess weight gain during pregnancy and post-partum weight retention are risk factors for obesity. While many studies report average weight retained from pregnancy is only 0·5–3·0 kg; between 14 and 20% of women are 5 kg heavier at 6–18 months post-partum than they were before pregnancy. Among normal-weight women, lactation usually promotes weight loss to a moderate extent, but not among those with BMI≥35 kg/m2. While exercise and energy restriction may promote weight loss during lactation, their effect on milk volume and composition and, consequently, infant growth must be considered. The effect of exercise on lactation performance has been investigated. Moderate aerobic exercise of 45 min/d, 5 d/week improved cardiovascular fitness, plasma lipids and insulin response; however, it did not promote post-partum weight loss. Breast milk volume and composition were not affected. The effect of exercise with energy restriction in overweight women on the growth of their infants has also been studied. At 1 month post-partum, women restricted their energy intake by 2092 kJ/d and exercised 45 min/d, 4 d/week for 10 weeks. Women in the diet and exercise group lost more weight than the control group (4·8 (sd 1·7) kg v. 0·8 (sd 2·3) kg); however, there were no differences in infant growth. Based on the current evidence, it is recommended that once lactation is established, overweight women may restrict their energy intake by 2092 kJ/d and exercise aerobically 4 d/week to promote a weight loss of 0·5 kg/week.

Epithelial cells lining the inner surface of the intestinal epithelium are in direct contact with a lumenal environment that varies dramatically with diet. It has long been suggested that the intestinal epithelium can sense the nutrient composition of lumenal contents. It is only recently that the nature of intestinal nutrient-sensing molecules and underlying mechanisms have been elucidated. There are a number of nutrient sensors expressed on the luminal membrane of endocrine cells that are activated by various dietary nutrients. We showed that the intestinal glucose sensor, T1R2+T1R3 and the G-protein, gustducin are expressed in endocrine cells. Eliminating sweet transduction in mice in vivo by deletion of either gustducin or T1R3 prevented dietary monosaccharide- and artificial sweetener-induced up-regulation of the Na+/glucose cotransporter, SGLT1 observed in wild-type mice. Transgenic mice, lacking gustducin or T1R3 had deficiencies in secretion of glucagon-like peptide 1 (GLP-1) and, glucose-dependent insulinotrophic peptide (GIP). Furthermore, they had an abnormal insulin profile and prolonged elevation of postprandial blood glucose in response to orally ingested carbohydrates. GIP and GLP-1 increase insulin secretion, while glucagon-like peptide 2 (GLP-2) modulates intestinal growth, blood flow and expression of SGLT1. The receptor for GLP-2 resides in enteric neurons and not in any surface epithelial cells, suggesting the involvement of the enteric nervous system in SGLT1 up-regulation. The accessibility of the glucose sensor and the important role that it plays in regulation of intestinal glucose absorption and glucose homeostasis makes it an attractive nutritional and therapeutic target for manipulation.

Colorectal cancer (CRC) is a major cause of premature death in the UK and many developed countries. However, the risk of developing CRC is well recognised to be associated not only with diet but also with obesity and lack of exercise. While epidemiological evidence shows an association with factors such as high red meat intake and low intake of vegetables, fibre and fish, the mechanisms underlying these effects are only now being elucidated. CRC develops over many years and is typically characterised by an accumulation of mutations, which may arise as a consequence of inherited polymorphisms in key genes, but more commonly as a result of spontaneously arising mutations affecting genes controlling cell proliferation, differentiation, apoptosis and DNA repair. Epigenetic changes are observed throughout the progress from normal morphology through formation of adenoma, and the subsequent development of carcinoma. The reasons why this accumulation of loss of homoeostatic controls arises are unclear but chronic inflammation has been proposed to play a central role. Obesity is associated with increased plasma levels of chemokines and adipokines characteristic of chronic systemic inflammation, and dietary factors such as fish oils and phytochemicals have been shown to have anti-inflammatory properties as well as modulating established risk factors such as apoptosis and cell proliferation. There is also some evidence that diet can modify epigenetic changes. This paper briefly reviews the current state of knowledge in relation to CRC development and considers evidence for potential mechanisms by which diet may modify risk.

Athletes and exercisers have utilised high-protein diets for centuries. The objective of this review is to examine the evidence for the efficacy and potential dangers of high-protein diets. One important factor to consider is the definition of a ‘high-protein diet’. There are several ways to consider protein content of a diet. The composition of the diet can be determined as the absolute amount of the protein (or other nutrient of interest), the % of total energy (calories) as protein and the amount of protein ingested per kg of body weight. Many athletes consume very high amounts of protein. High-protein diets most often are associated with muscle hypertrophy and strength, but now also are advocated for weight loss and recovery from intense exercise or injuries. Prolonged intake of a large amount of protein has been associated with potential dangers, such as bone mineral loss and kidney damage. In otherwise healthy individuals, there is little evidence that high protein intake is dangerous. However, kidney damage may be an issue for individuals with already existing kidney dysfunction. Increased protein intake necessarily means that overall energy intake must increase or consumption of either carbohydrate or fat must decrease. In conclusion, high protein intake may be appropriate for some athletes, but there are potential negative consequences that must be carefully considered before adopting such a diet. In particular, care must be taken to ensure that there is sufficient intake of other nutrients to support the training load.

Compelling evidence exists for the cardioprotective benefits resulting from consumption of fatty acids from fish oils, EPA (20:5n-3) and DHA (22:6n-3). EPA and DHA alter membrane fluidity, interact with transcription factors such as PPAR and sterol regulatory element binding protein, and are substrates for enzymes including cyclooxygenase, lipoxygenase and cytochrome P450. As a result, fish oils may improve cardiovascular health by altering lipid metabolism, inducing haemodynamic changes, decreasing arrhythmias, modulating platelet function, improving endothelial function and inhibiting inflammatory pathways. The independent effects of EPA and DHA are poorly understood. While both EPA and DHA decrease TAG levels, only DHA appears to increase HDL and LDL particle size. Evidence to date suggests that DHA is more efficient in decreasing blood pressure, heart rate and platelet aggregation compared to EPA. Fish oil consumption appears to improve arterial compliance and endothelial function; it is not yet clear as to whether differences exist between EPA and DHA in their vascular effects. In contrast, the beneficial effect of fish oils on inflammation and insulin sensitivity observed in vitro and in animal studies has not been confirmed in human subjects. Further investigation to clarify the relative effects of consuming EPA and DHA at a range of doses would enable elaboration of current understanding regarding cardioprotective effects of consuming oily fish and algal sources of long chain n-3 PUFA, and provide clearer evidence for the clinical therapeutic potential of consuming either EPA or DHA-rich oils.

In nutritional epidemiology, development of valid dietary assessment instruments specific to populations in diverse settings is of paramount importance. Such instruments are essential when trying to characterise dietary patterns and intake, investigate diet–disease associations, inform and evaluate nutrition interventions, assess nutrient–gene interactions, conduct cross-country comparison studies and monitor nutrition transitions. The FFQ is a relatively inexpensive tool for measuring long-term dietary intake for large populations and for allowing researchers to track dietary changes over time. However, FFQ must be population specific to capture the local diet and available foods. Collecting 24-h dietary recalls and utilising community feedback to build the FFQ ensures that a culturally appropriate instrument is developed. This article presents several examples describing FFQ development and utilisation in different settings globally. In the Canadian Arctic, FFQ were developed and utilised to inform and evaluate a community-based intervention programme, characterise the diet and track dietary changes occurring among Inuit and Inuvialuit, populations experiencing rising rates of chronic disease and likely to be extremely vulnerable to the potential effects of climate change. Another example is an FFQ developed to assess sodium intake and evaluate a sodium reduction trial in a high-risk population in Barbados. An example is provided from Brazil, where an FFQ was developed to assess associations between diet, heterocyclic aromatic amines and colorectal adenoma among Japanese Brazilians and to conduct cross-country comparisons. These and other case studies highlight the diversity in dietary intake between populations and the need for FFQ to be developed to capture this diversity.

The role of nutrition is especially important in certain ‘lifestyle’ diseases that impact disproportionately on ethnic minority populations. The aim of this paper is to review the evidence of risk, health outcomes and interventions for certain diseases that affect the UK's largest ethnic minority group (South Asians) in order to help professionals better address the needs of this diverse population. Research evidence is presented on factors influencing access to services by ethnic minority populations and the changing UK policy background for public health and preventive care. The available research base on obesity, diabetes and CVD is discussed. Conditions such as type 2 diabetes, which are more prevalent among the South Asian population, are associated with poorer health outcomes and appear to exhibit links to diet and nutrition that start in childhood or even before birth; all making preventive care important. Obesity is a major risk factor and it appears that BMI thresholds may need to be lower for South Asians. Targeted interventions to improve diet and outcomes in the South Asian population also appear promising. Recent moves to promote access to evidence of ethnicity and health and to improve the cultural competence of organisations are discussed. Health professionals will increasingly need to promote lifestyle changes in a manner that meets the needs of a diverse population in order to address future public health challenges. Nutritionists and other professionals will need to ensure that interventions are culturally appropriate and involve engagement with extended family members and communities.

As a population subgroup, older people are more vulnerable to malnutrition especially those who are institutionalised. Recognition of deteriorating or poor nutritional status is key in reversing the effects of undernutrition and reinforces the value of regular weight checks and/or the use of screening tools. Commercially produced supplements are often the first option used to address undernutrition in both acute and community settings. They can be expensive and, although regularly prescribed, have undergone only limited evaluation of their effectiveness in community settings. An alternative but less researched approach to improve the nutritional status of undernourished people is food fortification. This approach may be particularly useful for older people, given their often small appetites. The ability to eat independently has been significantly related to decreased risk of undernutrition. Assisting people who have difficulty feeding themselves independently should become a designated duty and may be crucial in optimising nutritional status. Lack of nutrition knowledge has been identified as the greatest barrier to the provision of good nutritional care. Education and training of care staff are pivotal for the success of any intervention to address undernutrition. The development of undernutrition is a multi-factorial process and a package of approaches may be required to prevent or treat undernutrition. Nutrition must be at the forefront of care if national care standards are to be met.

Epidemiological and animal studies have demonstrated that early-life nutrition alters the metabolic responses and generates structural changes in complex tissues, such as the kidneys, which may lead to a reduction in the offspring lifespan. Independently, obesity induces a spontaneous low-grade chronic inflammatory response by modulating several of the major metabolic pathways that ultimately compromise long-term renal health. However, the combined effects of maternal nutrition and early-life obesity in the development of renal diseases are far from conclusive. Previous results, using the ovine model, demonstrated that the combination of a reduction in fetal nutrition and juvenile obesity induced a series of adaptations associated with severe metabolic syndrome in the heart and adipose tissue. Surprisingly, exposure to an obesogenic environment in the kidney of those offspring produced an apparent reduction in glomerulosclerosis in relation to age- and weight-matched controls. However, this reduction in cellular apoptosis was accompanied by a rise in glomerular filtration rate and blood pressure of equal intensity when compared with obese controls. The intention of this review is to explain the adaptive responses observed in this model, based on insights into the mechanism of renal fetal programming, and their potential interactions with some of the metabolic changes produced by obesity.

Kiwifruit is a good source of several vitamins and minerals and dietary fibre, and contains a number of phytochemicals; so kiwifruit potentially provides health benefits beyond basic nutrition. Consumption of green kiwifruit can have positive effects on cardiovascular health through antioxidant activity, inhibition of platelet aggregation and lowered TAG levels, and gut health through improving laxation, aiding digestion and promoting a healthy gut microflora. The importance of nutrition on immune function is well recognised, with deficiencies in vitamins A, C, E, B6 and B12, folic acid, Zn, Cu, Fe and Se being associated with impaired immune function and increased susceptibility to diseases. Evidence is growing that kiwifruit enhances immunity, with several small murine studies showing enhancement of innate and adaptive immune function. Few studies have examined the effect of kiwifruit on immune function in human subjects, but a recent study has revealed that kiwifruit up-regulates several ‘immune’ and ‘DNA and repair’-related gene sets, and down-regulates one gene set related to Ig secretion. Taken together, the evidence from the literature provides supporting data for designing a human intervention trial to validate the ability of kiwifruit to support immune function in healthy and immunocompromised populations.