IgE-mediated dietary hypersensitivity affects approximately 1% of the canine population. There are no breed associations and ≤50% of the patients are aged <1 year at presentation. The most common causative allergens are beef, chicken, milk, eggs, maize, wheat and soyabean. Affected dogs generally display cutaneous disease and 10–15% of the patients may have concurrent alimentary involvement. Diagnosis is currently based on dietary restriction followed by provocation. Procedures for the detection of serum allergen-specific IgE and IgG antibodies are widely available, but these tests correlate poorly with clinical presentation and dietary testing. Recent studies have demonstrated the allergen specificity of IgE antibodies by immunoblotting and have described blood lymphocyte proliferative responses to food allergens. In addition to investigations of spontaneously-arising dietary hypersensitivity, it has also proved possible to study this disorder experimentally. Small colonies of dogs sensitive to particular dietary proteins have been used to study clinical and serological responses to allergen challenge. Hypersensitivity has been experimentally induced in dogs of an atopic phenotype by repeated subcutaneous injection of alum-adjuvanted dietary allergen during neonatal life. These models have been used to trial a range of modified protein or hydrolysate diets. The dog provides a unique large-animal model for investigation of the immunopathogenesis of human dietary hypersensitivity. The dog is closely related genetically to man and shares environmental disease triggers with man. Spontaneously arising canine dietary hypersensitivity is a good clinical mimic of the human disease, and ability to therapeutically manipulate this adverse response in the dog might lead to benefits for human patients.

Crohn's disease is associated with osteoporosis, malnutrition and altered function of peripheral blood mononuclear cells (PBMC). The responses of circulating immune cells and extra-intestinal manifestations to increased inflammatory activity and to modulation by dietary supplementation are uncertain. The relationships between disease status, bone turnover and body mass and composition, PBMC function and fatty acid availability have been investigated in patients with Crohn's disease. The availability of n-3 and n-6 PUFA is altered in adult patients and interferon (IFN)-γ production by PBMC is lower. Increased inflammatory activity is associated with increased bone resorption in adult patients and decreased body mass in paediatric patients. In healthy male subjects there is a proportionate relationship between supplementary intake of EPA and DHA (0.3–2.0 g as fish oil/d) in combination with antioxidants (vitamins A, C and E and Se) and incorporation into plasma phospholipids and PBMC, and a non-linear relationship with PBMC synthesis of TNF-α, IL-6 and prostaglandin E2 (decrease) and IFN-γ (increase). In adults with Crohn's disease high-dose fish oil (2.7 g EPA+DHA/d) in combination with antioxidants (vitamins A, C and E and Se) increases the EPA and DHA content of PBMC and decreases the production of IFN-γ by PBMC, but is not associated with effects on bone turnover or nutritional status.

The regulation of energy balance is complex and, in man, imprecise. Nevertheless, in many individuals intake and expenditure are balanced with <1% error with little or no conscious effect. Essential components of such a regulatory system are signals, leptin and insulin, that reflect the size of lipid stores. Leptin receptors signal via phosphatidylinositol 3-kinase (as do insulin receptors) and via the transcription factor signal transducer and activator of transcription-3 to activate various types of neurone. Obese rodents, and possibly man, are resistant to leptin; in some cases because of genetic or perinatal programming (primary resistance), but commonly in response to high leptin levels (secondary resistance). Secondary leptin resistance may be a result of reduced transport of leptin to the brain or down-regulation of leptin signalling. Signals that reflect lipid stores form the tonic homeostatic regulatory system. They interact with episodic homeostatic signals carried by neurones, hormones and metabolites to regulate meal size and frequency. They also interact with signals related to the palatability of food, biorhythms and learning. Many neurotransmitters and hormones mediate responses to more than one input (e.g. gastric and adipocyte leptin), but are nevertheless most involved with particular inputs (e.g. leptin with adipocyte fat stores). Feeding can be divided into appetitive (preparation for feeding) and consummatory phases, which can both be further subdivided. Different sets of neurotransmitters and hormones are involved at each stage. In the long term it may be possible to customise obesity therapies according to those inputs and outputs that are most disturbed and most amenable to intervention in individual subjects.

In recent years there has been a proliferation of nutrition screening tools but undernutrition remains prevalent amongst older subjects. Screening tools commonly include BMI as the widely-accepted ‘gold standard’ indicator of malnutrition. Whilst BMI may be an appropriate tool for population studies when it can be measured accurately in research conditions, the use of BMI in clinical practice may mask important weight changes and result in a failure to alert healthcare staff to a nutritional problem. The inclusion of BMI has been identified as a barrier to completing the screening process at ward level. Also, feedback from dietitians working with older subjects indicates that 72.5% of those using BMI express concerns that it is of limited use for practical reasons or that the reference range (20–25 kg/m2) is not appropriate to older subjects. Further evidence questions whether or not BMI is applicable for inclusion in methods used to identify an older subject at risk of undernutrition in a variety of care settings. In view of these findings it is advocated that weight change over a period of time together with clinical judgement is a far superior prognostic indicator of undernutrition. Despite screening, there is evidence that inpatients continue to lose weight before discharge. Further experiential evidence from both community and ward settings suggests that inadequacies in care planning, food provision and a lack of assistance with feeding are common. In order to improve the management of undernutrition in older subjects it is therefore recommended that the focus of attention should be on addressing these practical issues and on the effective monitoring of these processes.

There is no branch of medicine in which nutritional considerations do not play some part. Overnutrition, undernutrition or unbalanced nutrition are the major causes of ill health in the world. Conversely, illness causes important nutritional and metabolic problems. The spectrum from lack to excess of nutrients is seamless as a clinical and scientific discipline, the two extremes being linked by the Barker effect by which intrauterine malnutrition and low birth weight predispose to obesity, diabetes and CVD in later life. However, the teaching of nutrition in medical and nursing schools remains sparse. Nutritional care cannot be practised satisfactorily in isolation from other aspects of management, since factors such as drugs, surgery and fluid and electrolyte balance affect nutritional status. Nutritional treatment may also have adverse or beneficial effects according to the composition, amount and mode of delivery of the diet and the clinical context in which it is given. Any benefits of nutritional support may also be negated by shortcomings in other aspects of treatment and must therefore be fully integrated into overall care. One example of this approach is the enhanced recovery after a surgery protocol incorporating immediate pre-operative carbohydrate and early post-operative oral intake with strict attention to zero fluid balance, epidural analgesia and early mobilisation. Other examples include the deleterious effect on surgical outcome of salt and water overload or hyperglycaemia, either of which may negate the benefits of nutritional support. There is a need, therefore, to integrate clinical nutrition more closely, not just into medical and surgical practice, but also into the organisation of health services in the hospital and the community, and into the training of doctors and nurses. Societies originally devoted to parenteral and enteral nutrition need to widen their scope to embrace wider aspects of clinical nutrition.

Allergy is caused by an immune reaction that is out of all proportion to the antigenic stimuli. Classical allergy is a type I hypersensitivity reaction mediated by the interaction of mast cells (and eosinophils) coated with allergen-specific IgE and a cross-linking allergen. The physiological outcome is inflammation commonly displayed by urticaria, rhinitis, vomiting and diarrhoea, depending on the route of allergen entry. In extreme reactions anaphylactic shock can result that may lead to death. Chronic allergic responses most commonly present themselves as asthma and eczema. All these symptoms are the consequence of an imbalanced immune system making an unsuitable response to an environmental or food antigen. On bacterial colonisation of the colon after birth the appropriate microbiological stimuli is essential to redress the balance of the skewed T-helper 2 immune response present in the newborn. This normal interaction between baby and microbes is thought to be compromised in the Western world, with a reduction in bifidobacteria and an increase in clostridial species, particularly in bottle-fed infants. The use of probiotic therapy to prevent allergic disease has been demonstrated in two studies using a probiotic Lactobacillus rhamnosus GG in neonates. A long-term reduction in allergy has been shown in the test group, with lactobacillus reducing the incidence of atopic eczema. Management of allergy through probiotics has also been demonstrated in infants, using lactobacilli to control atopic eczema and cow's milk allergy. Unfortunately, these positive results have not been repeated in studies with older children and young adults.

Osteoporosis is an important contributor to the global burden of disease, and in the UK alone results in one in three women and one in twelve men aged >50 years experiencing a fragility fracture. Optimising peak bone mass in early adulthood is thought to reduce osteoporosis risk by offsetting bone losses in later life. Ensuring sufficient vitamin D status (measured as 25-hydroxyvitamin D (25OHD) in plasma), among other factors, is believed to facilitate the achievement of optimum peak bone mass. Lower 25OHD is associated with a higher plasma concentration of parathyroid hormone (PTH). As PTH is associated with increased bone turnover and bone loss, maintenance of sufficient 25OHD is thought to have a protective effect on bone health. However, there is a lack of consensus internationally on what constitutes an optimum 25OHD concentration, and values between 30 and 80 nmol/l have been suggested. These values have been based on findings from various studies in adults in which PTH has been observed to plateau at a 25OHD concentration of >30 nmol/l; however, not all studies have found such a plateau. Although studies in younger adolescents (14–16 years) have shown an inverse relationship between PTH and 25OHD, the concentration of 25OHD required for achievement of optimum peak bone mass is unknown. The present review examines the evidence defining vitamin D insufficiency thresholds, and the relevance of such thresholds to adolescent bone health.

While investigating the reversible seasonal obesity of Siberian hamsters, direct sympathetic nervous system (SNS) postganglionic innervation of white adipose tissue (WAT) has been demonstrated using anterograde and retrograde tract tracers. The primary function of this innervation is lipid mobilization. The brain SNS outflow to WAT has been defined using the pseudorabies virus (PRV), a retrograde transneuronal tract tracer. These PRV-labelled SNS outflow neurons are extensively co-localized with melanocortin-4 receptor mRNA, which, combined with functional data, suggests their involvement in lipolysis. The SNS innervation of WAT also regulates fat cell number, as noradrenaline inhibits and WAT denervation stimulates fat cell proliferation in vitro and in vivo respectively. The sensory innervation of WAT has been demonstrated by retrograde tract tracing, electrophysiological recording and labelling of the sensory-associated neuropeptide calcitonin gene-related peptide in WAT. Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey information about body fat levels to the brain. Finally, parasympathetic nervous system innervation of WAT has been suggested, but the recent finding of no WAT immunoreactivity for the possible parasympathetic marker vesicular acetylcholine transporter (VAChT) argues against this claim. Collectively, these data suggest several roles for efferent and afferent neural innervation of WAT in body fat regulation.

Exaggerated postprandial lipaemia may increase the risk of CHD by contributing to both thrombotic and atherogenic processes. Previous research has focused on the quantity and composition of dietary fat, whereas the effect of triacylglycerol (TAG) structure on postprandial lipaemia and clotting factor VII activity has received little attention. TAG with similar fatty acid composition may have different biochemical and physical properties that are dependent on their TAG structure, and these differences may affect lipid metabolism. Recent findings suggest that differences in the physical properties of stearic acid-rich fats are associated with differences in postprandial lipaemia, and may play an important role in determining their rates of digestion and absorption.

Strategies are needed for community-based treatment of disease-related malnutrition (DRM), which is a common debilitating condition that in the UK is estimated to cost >£7×109 annually. Whilst dietary fortification and counselling are often used as a first-line treatment for malnutrition, the numbers of dietitians available to undertake and oversee such practices are currently insufficient to address the extent of DRM in primary care. Although dietary fortification and counselling can improve nutritional (primarily energy) intake, the evidence base for this practice is weak and it needs addressing with well-designed trials that assess clinically-relevant outcome measures and costs. Liquid oral nutritional supplements (ONS) are increasingly used in the community, often in combination with dietary counselling. The larger evidence base of trials that have assessed ONS suggests that nutritional intake and some functional outcomes can be improved in some patient groups in the community. Although meta-analysis indicates significant reductions in mortality (odds ratio 0.59 (95% CI 0.48, 0.72), n 3258) and complication rates (odds ratio 0.41 (95% CI 0.31, 0.53), n 1710) with ONS v. routine care, few of these studies are community based. Thus, the impact of ONS on clinical outcome, healthcare use and costs requires further assessment. Similarly, the clinical and cost efficacy of other strategies (e.g. sensory enhancement, music, behavioural therapy), alone or in combination with other treatments, requires greater investigation in order to meet the challenge of treating DRM more effectively and cheaply in the future.

Serious attempts to estimate the impact of allergic reactions to foods on public health did not begin until the 1980s. Until about 15 years ago food allergy was considered a minor aspect of food safety. Two developments probably prompted a radical re-appraisal of that situation. The first was the apparently inexorable rise in the prevalence of atopic diseases, of which food allergy forms a part, with its possible consequences highlighted by some well-publicised severe reactions. The second was the growth of genetic modification technology, manifested by the commercialisation of transgenic crops. Each of these developments impacted on the food industry in distinct ways. On the one hand, consumers with food allergies had to be enabled to avoid specific allergens in products formulated with existing ingredients. Food manufacturers therefore had to identify those specific allergens down to trace amounts in all the ingredients forming the product and label or remove them. On the other hand, the introduction of products using ingredients from novel sources required an assessment of the allergenicity of these ingredients as an integral part of safety assurance. The approaches used by the food industry to protect existing consumers who have food allergies and those at potential risk of sensitisation from novel proteins will be illustrated, emphasising how they need to be built into every stage of the life cycle of a product.

Food allergy represents an increasingly important health problem, with prevalence in Western Europe continuing to rise. While some reactions are mild, others can include life-threatening anaphylactic shock. It is estimated that food allergies affect 1–2% of the adult population and ≤8% of children. Relatively few foods are to blame for a large majority of allergic reactions to food in the UK, with most reactions being to milk, eggs, peanuts (Arachis hypogea), nuts, fish, shellfish, soyabean, sesame (Sesamum indicum L.) and wheat. There is currently no cure for food allergy and the few available treatments are focused on relieving the specific symptoms. Consumers with food allergies and food intolerances rely on food labelling to enable them to make informed choices about the foods they eat. Whilst there have recently been important advances in the labelling of food allergens, these advances relate only to requirements for the labelling of the deliberate use of specified food allergens in foods sold pre-packed. In other areas the development of guidance for food manufacturers and retailers on how to assess the risks of possible allergen cross-contamination during food production and manufacture, and then to determine appropriate advisory labelling, is well advanced. Work to address the issue of how to provide appropriate allergen information for foods sold loose, or in catering establishments, is also in progress.

The development of gastrostomy placement has been an important technological advance in the enteral-access field. However, its rapid growth in popularity could be viewed as problematic. The endoscopist or intervention radiologist can no longer act as a technician but requires to follow-up this group of patients in order to determine outcomes that will inform future practice. There has been emphasis on the importance of the multidisciplinary team in informing and assessing patients referred for gastrostomy insertion. Communication between all the professionals caring for a patient and between the carers and the patient allows information to be collated that will determine the benefits and burdens of long-term gastrostomy feeding. At present much of the published experience is limited to the acute care setting. The incidence of complications varies, depending on the investigator's definition of complication and the diagnosis of the patient group. Many reported studies are retrospective, which puts limitations on documentation. Increasing numbers of patients with diverse needs are now being discharged into the community with gastrostomy tubes in place. Whilst the hospital should ensure that written protocols are provided and that all carers involved should have adequate training, it is not unusual for patients to receive mixed messages from the different care teams responsible for their care. In South Glasgow NHS Hospital Division key members of all teams caring for these patients (acute care, community district nurses, learning disabilities team, physical disabilities team and commercial homecare companies) meet regularly to discuss equipment and protocols. The members of this group feel that this approach has improved communication, standardised practice and reduced complications by providing a service that delivers artificial nutrition support but is primarily suited to the patient's disease process.

Obesity is taking on pandemic proportions. The laws of thermodynamics, however, remain unchanged, as energy will be stored if less energy is expended than consumed; the storage is usually in the form of adipose tissue. Several neural, humeral and psychological factors control the complex process known as appetite. Recently, a close evolutionary relationship between the gut and brain has become apparent. The gut hormones regulate important gastrointestinal functions such as motility, secretion, absorption, provide feedback to the central nervous system on availability of nutrients and may play a part in regulating food intake. Peptide YY (PYY) is a thirty-six amino acid peptide related to neuropeptide Y (NPY) and is co-secreted with glucagon-like peptide 1. Produced by the intestinal L-cells, the highest tissue concentrations of PYY are found in distal segments of the gastrointestinal tract, although it is present throughout the gut. Following food intake PYY is released into the circulation. PYY concentrations are proportional to meal energy content and peak plasma levels appear postprandially after 1 h. PYY3-36 is a major form of PYY in both the gut mucosal endocrine cells and the circulation. Peripheral administration of PYY3-36 inhibits food intake for several hours in both rodents and man. The binding of PYY3-36 to the Y2 receptor leads to an inhibition of the NPY neurones and a possible reciprocal stimulation of the pro-opiomelanocortin neurones. Thus, PYY3-36 appears to control food intake by providing a powerful feedback on the hypothalamic circuits. The effect on food intake has been demonstrated at physiological concentrations and, therefore, PYY3-36 may be important in the everyday regulation of food intake.

Obesity treatment remains a ‘Cinderella’ of all clinical management programmes, but generally without a happy ending. The great expectation for new therapeutic agents has not been fulfilled in clinical practice, whilst the restriction of eating through surgical division of the upper bowel seems strange in an age of advanced and sophisticated technology. The better understanding of the neuro-regulation of appetite, and its application as part of evidence-based clinical interventions, could lead to a more coherent approach to obesity treatment. Nevertheless, investigation of potential neuroendocrine targets for appetite suppression suggests redundancy in the systems, which make development of effective agents against single receptors impractical. Importantly, the progressive rise in the prevalence of obesity will inevitably mean that only a small proportion of afflicted patients will actually be treated by long-term drugs and surgery. Drugs and surgery are not currently the answer for the majority of obese individuals. What is required is a better way of identifying patients who may particularly benefit from such approaches. However, the major emphasis must be the development of effective population-wide interventions that halt the increase in fatness and ensure that future generations maintain and enjoy a healthy body weight.

The rising tide of obesity has led to a resurgence of interest in dietary strategies to prevent excess weight gain. Data from controlled intervention studies is sparse, but nonetheless evidence from other diverse sources has identified a number of specific dietary factors and aspects of eating behaviour that either promote or protect against obesity. The present paper reviews the evidence in relation to energy density, the macronutrient composition of the diet, including the nature of carbohydrate foods and sugar-rich drinks, portion size and snacking habits. It concludes that there is now sufficient evidence to develop clear dietary guidelines to prevent weight gain that are largely consistent with those for the prevention of CVD and cancer. However, coordinated action across multiple stakeholders is also required if these guidelines are to be translated into sustained changes in eating habits.

The present paper gives an insight from a parent's perspective into the roles of health professionals and service providers in the daily management of a child with complex needs that include enteral feeding. It focuses on the case of a 9-year-old boy and discusses some aspects of his diagnosis and treatment, and the support received. It highlights the need for a multi-agency approach based around the child, in which parents are consulted, the opinions of professionals from the different disciplines are valued by other professionals and professionals do not issue conflicting advice but share knowledge before giving advice. There should be national accessibility to support services and a standardised training programme for carers. Better communication between parents, carers, health professionals and service providers and working together can reduce the stress for the patient and carer, and put less strain on much-needed resources.

The European Food Safety Authority, following a request from the European Commission, has published a guidance document for the risk assessment of GM plants and derived food and feed to assist in the implementation of provisions of Regulation (EC) 1829/2003 of the European Parliament and Council on GM food and feed. This regulation has applied since 18 April 2004. In principle, hazard identification and characterisation of GM crops is conducted in four steps: characterisation of the parent crop and any hazards associated with it; characterisation of the transformation process and of the inserted recombinant DNA, including an assessment of the possible production of new fusion proteins or allergens; assessment of the introduced proteins (toxicity, allergenicity) and metabolites; identification of any other targetted and unexpected alterations in the GM crop, including changes in the plant metabolism resulting in compositional changes and assessment of their toxicological, allergenic or nutritional impact. In relation to allergenicity specifically, it is clear that this property of a given protein is not intrinsic and fully predictable but is a biological activity requiring an interaction with individuals with a predisposed genetic background. Allergenicity, therefore, depends on the genetic diversity and variability in atopic human subjects. Given this lack of complete predictability it is necessary to obtain, from several steps in the risk-assessment process, a cumulative body of evidence that minimises any uncertainty about the protein(s) in question.

Childhood obesity poses one of the greatest challenges to paediatric health in the 21st century. Developing effective strategies for treatment and prevention is therefore a priority for clinical medicine and public health. This process is taking place at a time of unprecedented change in the understanding of the role of genetic factors in human health and disease, and genetic research into obesity has challenged assumptions about causal processes. In the spirit of the conference theme, the present paper will discuss the implications of the understanding of genetic and environmental influences on obesity for the development of effective behavioural treatments.