The obesity epidemic and its associated morbidity and mortality have led to major research efforts to identify mechanisms that regulate appetite. Gut hormones have recently been found to be an important element in appetite regulation as a result of the signals from the periphery to the brain. Candidate hormones include ghrelin, peptide YY, glucagon-like peptide-1 and gastric inhibitory polypeptide, all of which are currently being investigated as potential obesity treatments. Bariatric surgery is currently the most effective therapy for substantial and sustained weight loss. Understanding how levels of gut hormones are modulated by such procedures has greatly contributed to the comprehension of the underlying mechanisms of appetite and obesity. The present paper is a review of how appetite and levels of gastrointestinal hormones are altered after bariatric surgery. Basic principles of common bariatric procedures and potential mechanisms for appetite regulation by gut hormones are also addressed.

Coeliac disease (CD), traditionally perceived as a rare childhood condition presenting with malabsorption, is instead an autoimmune multisystem disorder usually presenting in adulthood, affecting ⩾1% of the population and linked to the genetic expression of human leucocyte antigens (HLA) DQ2 and DQ8. Presentation occurs most often in the 40–60 years age-group, but potentially at any age. Symptoms attributable to the gut or to malabsorption may be mild, non-specific or absent; under one-third of patients have diarrhoea and almost half are overweight. Histological diagnosis no longer requires small intestine villous atrophy. The Marsh classification recognizes increased intraepithelial lymphocytes and crypt hyperplasia with intact villi as part of the gluten enteropathy spectrum, while some individuals have more subtle abnormalities identified only on electron microscopy. Serological testing for CD autoantibodies (to endomysium and tissue transglutaminase) has revolutionized diagnosis, shifting the process towards primary care. However, a substantial number of patients with CD are seronegative, particularly those without villous atrophy. The autoantibody to endomysium may be produced before histological change. The immune response to transglutaminase is crucial to the disease process. An exciting new development is the link between antibodies to organ-specific transglutaminases and clinical presentation; transglutaminases 2 (gut), 3 (skin) and 6 (nervous system). Negative testing for CD does not preclude its development later and HLA testing may allow ‘once and for all’ exclusion. In conclusion, an increasing proportion of patients with CD do not meet the ‘classic’ picture of malabsorption, positive serological testing and villous atrophy. Insisting on all these criteria for diagnosis will result in under diagnosis.

The vast majority of patients with coeliac disease will derive benefit from a gluten-free diet. However, some patients will not improve on the gluten-free diet or they will have a relapse of their symptoms. The present review will focus on this group of patients. Definitions for non-responsive coeliac disease and refractory coeliac disease will be provided. The most common reason for recurrent symptoms is continued gluten exposure. Other causes of persisting symptoms are discussed, including alternative causes of villous atrophy or co-existent pathology. Current literature is reviewed, including an initial investigation strategy for patients with persisting symptoms. A pragmatic management plan is described that can be initiated by any clinician. Finally, the current optimal investigational pathway for patients with refractory (or suspected refractory) coeliac disease is discussed and the reported effects of a number of therapeutic options are summarised. The aim of the present article is to provide clinicians with an up-to-date review of the literature in this clinical field and allow them to determine the most appropriate management strategy.

It seems obvious to healthcare professionals that patients with coeliac disease should receive regular follow-up. Surprisingly, there is little evidence that patients benefit in terms of reduced morbidity or mortality. However, several authoritative bodies have published guidelines on the management of coeliac disease that recommend regular follow-up. There is good evidence that compliance with a gluten-free diet reduces the risk of complications such as osteoporosis or small bowel lymphoma. Compliance is enhanced particularly by education about the disease and the gluten-free diet and by support from peers or professionals. Such input can be provided by regular follow-up, which thereby should improve compliance and hence long-term health. The consensus of the recommendations for follow-up suggests an annual review by a physician and dietitian. At annual follow-up the disease status can be checked and nutritional advice can be given, including checking the adequacy of, and the compliance with, the gluten-free diet. Complications and associated medical conditions can be sought, genetic risks explained and support and reassurance given. Specialist dietitians have particular expertise in relation to diet and nutritional management; specialist clinicians have a broader range of expertise in many aspects of management of the disease. A team approach for providing follow-up is the ideal, with a clinician and dietitian, both with expertise in coeliac disease, being involved. No one particular group of healthcare professionals is necessarily better than the other at providing follow-up.

Lipids traditionally used in parenteral nutrition are based on n-6 fatty acid-rich vegetable oils such as soyabean oil. This practice may not be optimal because it may present an excessive supply of linoleic acid. Alternatives to the use of soyabean oil include its partial replacement by so-called medium-chain TAG (MCT), olive oil or fish oil, either alone or in combination. Lipid emulsions containing MCT are well established, but those containing olive oil and fish oil, although commercially available, are still undergoing trials in different patient groups. Emulsions containing olive oil or fish oil are well tolerated and without adverse effects in a wide range of adult patients. An olive oil–soyabean oil emulsion has been used in quite small studies in critically-ill patients and in patients with trauma or burns with little real evidence of advantage over soyabean oil or MCT–soyabean oil. Fish oil-containing lipid emulsions have been used in adult patients post surgery (mainly gastrointestinal). This approach has been associated with alterations in patterns of inflammatory mediators and in immune function and, in some studies, a reduction in the length of stay in the intensive care unit and in hospital. One study indicates that peri-operative administration of fish oil may be superior to post-operative administration. Fish oil has been used in critically-ill adults. Here, the influence on inflammatory processes, immune function and clinical end points is not clear, since there are too few studies and those that are available report contradictory findings. One important factor is the dose of fish oil required to influence clinical outcomes. Further studies that are properly designed and adequately powered are required in order to strengthen the evidence base relating to the use of lipid emulsions that include olive oil and fish oil in critically-ill patients and in patients post surgery.

The amino acid glutamine has numerous important roles including particularly antioxidant defence, immune function, the inflammatory response, acid–base balance and N economy. The present systematic review of randomised controlled trials of nutrition support with glutamine up to August 2008 has found that parenteral glutamine in critical illness is associated with a non-significant reduction in mortality (risk ratio 0·71 (95% CI 0·49, 1·03)) and may reduce infections. However, poor study quality and the possibility of publication bias mean that these results should be interpreted with caution. There is no evidence to suggest that glutamine is harmful in terms of organ failure and parenteral glutamine may reduce the development of organ failure.

The relationship between glutamine and malignancy can be traced back to the 1950s and the requirement for glutamine for malignant-cell growth in culture. Later studies demonstrated an association between the rate of proliferation of the malignant cells and glutamine usage. The excessive use of glutamine by malignant cells was seen as an opportunity for the development of a treatment using glutamine analogues, but unfortunately excessive toxicity was observed during clinical studies. In animal models glutamine supplementation, initially thought to increase tumour growth, actually causes tumour regression as a result of improved immune clearance of the tumour and appears to reduce the severity of the side effects of chemo- and radiotherapy. This finding led to human studies in both traditional cancer therapy and bone-marrow transplantation, which are reviewed here. Unfortunately, the majority of the studies performed are small and have poor methodological reporting. There is clinical heterogeneity in terms of routes of administration, dosing schedules, chemotherapy regimens and diseases. Studies of glutamine in non-bone-marrow transplantation chemo- and/or radiotherapy treatment suggest a possible trend towards reductions in objective mucositis but no effect on subjective symptoms. There is no evidence for its effect on other clinical outcomes. For bone-marrow transplantation there appears to be some benefit from oral glutamine in reducing mucositis and graft v. host disease, while intravenous glutamine may reduce infections but at the expense of an increased relapse rate. Good-quality studies are required in this area.

The systematic failure to recognise and appropriately treat children with severe malnutrition has been attributed to the elevated case-fatality rates, often as high as 50%, that still prevail in many hospitals in Africa. Children admitted to Kilifi District Hospital, on the coast of Kenya, with severe malnutrition frequently have life-threatening features and complications, many of which are not adequately identified or treated by WHO guidelines. Four main areas have been identified for research: early identification and better supportive care of sepsis; evidence-based fluid management strategies; improved antimicrobial treatment; rational use of nutritional strategies. The present paper focuses on the identification of children with sepsis and on fluid management strategies.

Anorexia nervosa has the highest mortality rate of any psychiatric condition and its management is complex and multi-faceted, requiring a multidisciplinary team approach. Dietitians are an important part of the multidisciplinary team, offering objective nutritional advice with the aim of helping the patient to develop an improved relationship with food. Refeeding patients with a low body weight requires careful management; nonetheless, refeeding the low-weight patient with anorexia presents many additional complications, largely of a psychological nature. Treatment plans need to consider psychological, physical, behavioural and psycho-social factors relating to anorexia nervosa. Currently, there is no consistent approach and a paucity of evidence to support best practice for weight restoration in this group of patients. Tube feeding is utilised at varying BMI in anorexia nervosa, mainly in an inpatient setting. However, its use should be seen as a last resort and limited to a life-saving intervention. Weight restoration is best managed by an experienced dietitian within a specialist eating disorders team, using normal foods. This approach is ideal for nutrition rehabilitation, promoting skills for eating and normal behaviour and providing a longer-term solution by challenging unhelpful coping strategies from the onset. Dietitians have a unique mix of skills and knowledge in numerous areas including nutrition, physiology, psychology, sociology and behaviour change, which can be applied to support patients with thoughts and behaviours around food, weight and appetite. Further research is required into the effectiveness of dietetic interventions in eating disorders in order to establish an evidence base for best practice.

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.

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.

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.

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.

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.