According to the adipostat hypothesis for body-weight control, alterations in body weight should always be compensated by adequate alterations in food intake and thermogenesis. Thus, increased thermogenesis should not be able to counteract obesity because food intake would be increased. However evidence is presented here that thermogenesis in different forms (through artificial uncouplers, exercise, cold exposure) may counteract obesity and is not always fully compensated by increased food intake. Correspondingly, a decreased capacity for metaboloregulatory thermogenesis (i.e. non-functional brown adipose tissue) may in itself lead to obesity. This is evident in mice and may be valid for human subjects, as a substantial proportion of adults possess brown adipose tissue, and those with less or without brown adipose tissue would seem to be more prone to obesity. Thus, increased thermogenesis may counteract obesity, without dietary intervention.

Nutrition can affect the brain throughout the life cycle, with profound implications for mental health and degenerative disease. Many aspects of nutrition, from entire diets to specific nutrients, affect brain structure and function. The present short review focuses on recent insights into the role of nutrition in cognition and mental health and is divided into four main sections. First, the importance of nutritional balance and nutrient interactions to brain health are considered by reference to the Mediterranean diet, energy balance, fatty acids and trace elements. Many factors modulate the effects of nutrition on brain health and inconsistencies between studies can be explained in part by differences in early environment and genetic variability. Thus, these two factors are considered in the second and third parts of the present review. Finally, recent findings on mechanisms underlying the actions of nutrition on the brain are considered. These mechanisms involve changes in neurotrophic factors, neural pathways and brain plasticity. Advances in understanding the critical role of nutrition in brain health will help to fulfil the potential of nutrition to optimise brain function, prevent dysfunction and treat disease.

The diets of young women are important not just for their own health but also for the long-term health of their offspring. Unbalanced unvaried diets are more common amongst poor and disadvantaged women. If the diets of these women are to be improved, it is first necessary to understand why they make the food choices they do. Influences on women's food choices range from the global to the individual: environmental factors, such as difficulty in acquiring and affording good-quality healthy foods; social support and social relationships, such as those with parents, spouses and children; life transitions, such as leaving home, living with a partner or having children; individual factors, such as having low perceived control or self-efficacy in making food choices and placing a low value on health in general and on their own health in particular. These interrelated factors all influence food choice, suggesting that if the diets of disadvantaged women are to be improved, it will be necessary to do more than simply educate about the link between diet and health.

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.

Chris Pennington was an archetypal team player, strategist and networker. Clinical nutritional support has progressed remarkably since the 1970s and it has been a privilege to work in this field over this period during which teamwork, strategy development and networking have been crucial. British experience has been characterised by groups of individuals of differing professions and specialties coming together to enable progress to be made. This approach was initially in the form of nutrition support teams orientated to patient-centred ward-based care, then as hospital strategic committees and the concept of the ‘patient journey’. Indeed, the formation of the British Association for Parenteral and Enteral Nutrition (now known as BAPEN) in 1992 required the statesmanlike burying of jealousies as societies came together into a multiprofessional association. With the understanding that disease-related malnutrition was highly prevalent it became apparent that it must be managed on a broad and organised clinical front. In the Organisation of Food and Nutritional Support in Hospitals a group of professionals developed for BAPEN concepts of hospital-wide organisation to tackle malnutrition that were based on previous reports, both national and international, and were made easily accessible from the BAPEN website, especially the ‘Malnutrition Universal Screening Tool’ and the National Institute for Health and Clinical Excellence nutrition guidelines. The coming together of six national clinical societies to develop evidence-based consensus guidelines for intravenous saline therapy (also on the BAPEN website) has shown that BAPEN can catalyse opinion well beyond its own nutritional constituency. In England Chris Pennington's Scottish lead is being followed by developing a patient-centred strategic framework for a managed home parenteral nutrition and intestinal failure national network. In research, education or clinical practice the engines of progress have been teams, strategies and networks.

Optimising nutrition is known to improve outcome in a variety of specialities from elderly care to orthopaedics. The National Institute for Health and Clinical Excellence guidelines of 2006 have provided standards to positively influence the profile of nutrition within the National Health Service. However, what role do doctors have in this process? Clearly, not all doctors are competent in nutrition. In a recent US survey only 14% of resident physicians reported feeling adequately trained to provide nutrition counselling. A lack of knowledge has also been demonstrated by general practitioners (GP). The Intercollegiate Group on Nutrition is working to improve nutritional knowledge in British medical graduates. In addition, nutritional care is now a core competency assessed in the UK Foundation Programme curriculum, which can only be a positive step. The assessment process may even influence some of the supervising consultants. What about those doctors currently practising in the UK? Recently, a questionnaire study was undertaken to look at healthcare professionals' knowledge of the benefits and risks of percutaneous endoscopic gastrostomy (PEG) feeding. Important gaps in knowledge were found that were positively correlated with whether respondents had received relevant education. Referral for a PEG was considered to be appropriate for patients with advanced dementia by 31% of the GP compared with 10% of the consultants. Only 4% of these GP had received any training in this ethically-sensitive area at a time when they may be asked to countersign consent forms for patients who lack competence. So, what is the way forward? Positive steps are being taken in the undergraduate curriculum and Foundation Programme. Perhaps it is the responsibility of those doctors with the skills and opportunities to promote good nutritional knowledge in those doctors already practising in the UK.

Observational evidence suggests that improving the diets of women of child-bearing age from disadvantaged backgrounds might be an important component of public health strategies aimed at reducing the burden of chronic disease in their offspring. The development of an intervention to improve the nutrition of young women needs to be informed by a systematic collation of evidence. Such a systematic collation of evidence from systematic reviews of interventions directed at changing health behaviours including diet, breast-feeding, physical activity and smoking has been conducted. Of 1847 potentially-relevant abstracts, fourteen systematic reviews met inclusion criteria. Four aspects of intervention design were identified that were effective at changing one or more of the health behaviours considered in the present review: the use of an educational component; provision of continued support after the initial intervention; family involvement; social support from peers or lay health workers. The findings of the present review suggest that interventions to change the health behaviour of women of child-bearing age from disadvantaged backgrounds will require an educational approach and should provide continued support after the initial intervention. Family involvement and social support from peers may also be important features of interventions that aim to improve diet.

Changes in maternal diet at different stages of reproduction can have pronounced influences on the health and well-being of the resulting offspring, especially following exposure to an obesogenic environment. The mechanisms mediating adaptations in development of the embryo, placenta, fetus and newborn include changes in the maternal metabolic environment. These changes include reductions in a range of maternal counter-regulatory hormones such as cortisol, leptin and insulin. In the sheep, for example, targeted maternal nutrient restriction coincident with the period of maximal placental growth has pronounced effects on the development of the kidney and adipose tissue. As a consequence, the response of these tissues varies greatly following adolescent-onset obesity and ultimately results in these offspring exhibiting all the symptoms of the metabolic syndrome earlier in young adult life. Leptin administration to the offspring after birth can have some long-term differential effects, although much higher amounts are required to cause a response in small compared with large animal models. At the same time, the responsiveness of the offspring is gender dependent, which may relate to the differences in leptin sensitivity around the time of birth. Increasing maternal food intake during pregnancy, either globally or of individual nutrients, has little positive impact on birth weight but does impact on liver development. The challenge now is to establish which components of the maternal diet can be sustainably modified in order to optimise the maternal endocrine environment through pregnancy, thus ensuring feto–placental growth is appropriate in relation to an individual's gender and body composition.

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.

Nutrition in early life, a critical period for human development, can have long-term effects on health in adulthood. Supporting evidence comes from epidemiological studies, animal models and experimental interventions in human subjects. The mechanism is proposed to operate through nutritional influences on growth. Substantial evidence now supports the hypothesis that ‘accelerated’ or too fast infant growth increases the propensity to the major components of the metabolic syndrome (glucose intolerance, obesity, raised blood pressure and dyslipidaemia), the clustering of risk factors that predispose to cardiovascular morbidity and mortality. The association between infant growth and these risk factors is strong, consistent, shows a dose–response effect and is biologically plausible. Moreover, experimental data from prospective randomised controlled trials strongly support a causal link between infant growth and later risk factors for atherosclerosis. Evidence that infant growth affects the development of atherosclerosis therefore suggests that the primary prevention of CVD should begin from as early as the first few months of life. The present review considers this evidence, the underlying mechanisms involved and its implications for public health.

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.