Malnutrition is frequently undetected in care homes. It is recommended that residents are screened on admission and at suitable intervals thereafter. It is aimed to implement the ‘Malnutrition Universal Screening Tool’ (‘MUST’) in all care homes in Norfolk in order to fulfil this recommendation. Following a pilot of successful (but time-consuming) ‘MUST’ training a train-the-trainer package was developed as a practical way of achieving this goal. Courses were held in 2007, each comprising a study day and an assessment of each trainer delivering training. Trainers were provided with a dossier of training support materials. Data were collected at the study day and 3 months after the course to evaluate its effectiveness. Sixty-seven trainers were trained, all of whom rated the course as effective in preparing them to deliver training. At their assessments 96% were able to explain ‘MUST’ accurately. Of the new trainers 44% returned follow-up questionnaires and copies of sample care plans. The majority of care plans showed ‘MUST’ scores had been calculated accurately and appropriate nutrition care plans had been set up and evaluated. The train-the-trainer model is an effective method of training large numbers of care-home staff to use ‘MUST’. One of the unexpected benefits observed was the ownership taken by the trainers, which was demonstrated by the enthusiasm and confidence with which they subsequently trained their colleagues.

Changing individuals' health behaviour seems to be the key to solving many of the world's health problems. Although there is a multitude of potential influences, many interventions to improve health seek to change intrinsic psychological determinants of health behaviour. To date, most attention has been paid to cognitions, such as attitudes and beliefs, and a number of social cognition models (SCM) are in current use. SCM all describe cognitions as determinants of behaviour, thereby implying that changes in cognitions will lead to changes in behaviour. Although SCM are widely used to predict a range of health behaviours, they are associated with a number of important limitations, including poor levels of predictive power, particularly in relation to eating behaviour, and limited guidance about the operationalisation of theoretical constructs. These limitations may explain why very few interventions to change behaviour are explicitly theory-based, despite the widely-held view that having a clear theoretical underpinning will improve effectiveness. Ultimately, advances in understanding and changing health behaviour will come about only if psychological theory and practice are integrated. The recently-published taxonomy of behaviour-change techniques used in interventions is a good example of integrated research, but more work of this type is essential and will require respectful collaboration between researchers and practitioners working from a range of different disciplines such as health psychology, public health nutrition and health promotion.

Human epidemiological studies have indicated that the risk of developing non-communicable diseases in later life may be related to exposures during the developmental period. Developmental life is a vulnerable period of the lifespan during which adverse environmental factors have the potential to disturb the processes of cell proliferation and differentiation or to alter patterns of epigenetic remodelling. Animal models have been instrumental in demonstrating the biological plausibility of the associations observed in human populations, providing proof of principle to the theory of the developmental origins of health and disease (DOHaD). A variety of large- and small-animal models have made important contributions to the field, providing strong evidence of a causal relationship between early-life exposures and metabolic risk factors in later life. Studies of animal models are continuing to contribute to improving the understanding of the mechanisms of the developmental origins of disease. All models have their advantages and disadvantages, and the model that is most appropriate for any particular study is hypotheses dependent. The present review aims to briefly summarise the contributions that animal models have made to the DOHaD field, before reviewing the strengths and weaknesses of these animal models. It is proposed that the integration of evidence from a variety of different models is required for the advancement of understanding within the field.

Cystic fibrosis (CF) is a complex multisystem disorder affecting mainly the gastrointestinal tract and respiratory system. Intestinal malabsorption occurs in approximately 90% of patients. In the past, malnutrition was an inevitable consequence of disease progression, leading to poor growth, impaired respiratory muscle function, decreased exercise tolerance and immunological impairment. A positive association between body weight and height and survival has been widely reported. The energy requirements of patients with CF vary widely and generally increase with age and disease severity. For many young adults requirements will be 120–150% of the age-related estimated average requirement. To meet these energy needs patients are encouraged to eat a high-fat high-energy diet with appropriate pancreatic enzyme supplements. Many patients are unable to achieve an adequate intake as a result of a variety of factors including chronic poor appetite, infection-related anorexia, gastro-oesophageal reflux and abdominal pain. Oral energy supplements and enteral tube feeding are widely used. Nutritional support has been shown to improve nutritional status and stabilise or slow the rate of decline in lung function. With such emphasis on nutritional intake and nutritional status throughout life, poor adherence to therapies and issues relating to body image are emerging. The median survival of patients with CF is increasing. CF is now considered a life-limiting disease of adulthood rather than a terminal childhood illness. With increased longevity new challenges are emerging that include the transition of young adults with CF to adult services, CF-related diabetes, disordered eating, osteoporosis, liver disease and transplantation.

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.

Diet-related sources of ill health, including Fe-deficiency anaemia, are prevalent in the local South Asian population. This population also has a high prevalence of low-birth-weight babies. A need for preventative measures that take a holistic view to dietary change was identified in a South Asian community in Southampton, UK. A peer-led approach was used, training and developing a local workforce to become community food assistants. This workforce, drawn from local black and minority ethnic communities, ran practical ‘hands-on’ culturally-appropriate food-related activities within their communities that were successful in achieving long-term change in the diets of local women and their families. This model has the potential for achieving sustained behaviour change and is able to engage key target groups that can often be difficult to reach through more traditional routes.

It is now apparent that one key factor determining the current obesity epidemic within the developed world is the extent to which adipose tissue growth and function can be reset in early life. Adipose tissue can be either brown or white, with brown fat being characterised as possessing a unique uncoupling protein (uncoupling protein 1) that enables the rapid generation of heat by non-shivering thermogenesis. In large mammals this function is recruited at approximately the time of birth, after which brown fat is lost, not normally reappearing again throughout the life cycle. The origin and developmental regulation of brown fat in large mammals is therefore very different from that of small mammals in which brown fat is retained throughout the life cycle and may have the same origin as muscle cells. In contrast, white adipose tissue increases in mass after birth, paralleled by a rise in glucocorticoid action and macrophage accumulation. This process can be reset by changes in the maternal nutritional environment, with the magnitude of response being further determined by the timing at which such a challenge is imposed. Importantly, the long-term response within white adipocytes can occur in the absence of any change in total fat mass. The present review therefore emphasises the need to further understand the developmental regulation of the function of fat through the life cycle in order to optimise appropriate and sustainable intervention strategies necessary not only to prevent obesity in the first place but also to reverse excess fat mass in obese individuals.

Pharmacological, surgical and technological advances have resulted in children now surviving through adolescence into adulthood with conditions that were previously unseen by adult services. Arranging transition for young people on home parenteral nutrition (HPN) to the adult sector is one of greatest challenges for health services that care for young people. Transition is not only a key quality issue for health services, but is a multidimensional process covering psychosocial, educational and vocational aspects. Poorly-planned transition may result in difficulties when young people access adult specialist services. As a consequence, there may be increased risk of non-adherence or lack of follow-up, which carries dangers of morbidity and mortality as well as poor social and educational outcomes. Transition does not end at the exit from the paediatric clinic, but continues into the adult sector, which needs to provide developmentally-appropriate clinical care. Recent Department of Health initiatives are aimed at ensuring that young people do not miss out on healthcare during the transfer between paediatric and adult services. Transfer can be a major, often daunting, event for young people. Parents may also fear transfer and need to learn to ‘let go’ of some control, which may be particularly difficult with a young person on HPN.

There are a range of government food policies at national and international level. Overall, their aims are diverse but all will have an impact on women and thus impact on the developmental origins of adult disease through their role as mothers of future generations. The present paper describes the approach of the Food Standards Agency to help consumers choose, cook and eat healthy safe food by influencing individuals, products and the food environment. Examples of activity at the national, local and international level are used to demonstrate this approach.

Non-communicable chronic diseases are now a worldwide epidemic. Diet and physical activity throughout life are among its main determinants. In countries undergoing the early stages of the nutrition transition weight gain from birth to 2 years of life is related to lean mass gain, while ponderal gain after age 2 years is related to adiposity and later diabetes and CVD risk. Evidence from developing countries undergoing the more advanced stages of the nutrition transition is limited. The early growth patterns of a cohort of Chilean children born in 2002 with normal birth weight who at 4 years had a high prevalence of obesity and CVD risk factors have been assessed. Results indicate that BMI gain in early life, particularly from 6 months to 24 months, is positively associated with adiposity and CVD risk status at 4 years. These results together with existing evidence suggest that actions to prevent obesity and nutrition-related chronic diseases in developing countries should start early in life, possibly after 6 months of age. This approach should consider assessing the effect of mode of feeding and the amount and type of energy fed, as well as the resulting growth patterns. The challenge for researchers addressing the nutrition transition is to define the optimal nutrition in early life, considering not only the short- and long-term health consequences but also taking into account the stage of the nutritional transition for the given population of interest. The latter will probably require redefining optimal postnatal growth based on the context of maternal size and fetal growth.