Intestinal failure (IF) occurs when intestinal absorptive function is inadequate to maintain hydration and nutrition without enteral or parenteral supplements. It has been classified into three types depending on duration of nutrition support and reversibility. Type 1 IF is commonly seen in the peri-operative period as ileus and usually spontaneously resolves within 14 d. Type 2 IF is uncommon and is often associated with an intra-abdominal catastrophe, intestinal resection, sepsis, metabolic disturbances and undernutrition. Type 3 IF is a chronic condition in a metabolically stable patient, which usually requires long-term parenteral nutrition. This paper focuses on Types 1 and 2 IF (or acute IF) that are usually found in surgical wards. The objectives of this paper are to review the incidence, aetiology, prevention, management principles and outcome of acute IF. The paper discusses the resources necessary to manage acute IF, the indications for inter-hospital transfer and the practicalities of how to transfer and receive a patient with acute IF.

The global pandemic of maternal obesity presents a major challenge for healthcare providers, and has significant short- and long-term implications for both maternal and fetal health. Currently, the evidence-base underpinning many of the interventions either currently in use or recommended to improve pregnancy outcome in obese women is limited. The nature and timing of these interventions vary widely, ranging from simple advice to more intensive dietary and exercise programmes, cognitive behavioural therapy and drug trials. In addition, a growing number of very severely obese women now enter pregnancy having had surgical interventions. Although surgical interventions such as gastric bypass or banding may be associated with improved pregnancy outcomes, these women have particular nutritional requirements, which need to be addressed to optimise pregnancy outcome. Until the outcomes of ongoing current trials are reported and provide a firm evidence base on which to base future intervention strategies and guide evidence based care for obese pregnant women, pregnancy outcome is best optimised by high-risk antenatal care delivered by healthcare providers who are experienced in supporting these high-risk women.

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.

Body fat distribution plays an important role in determining metabolic health. Whereas central obesity is closely associated with the development of CVD and type 2 diabetes, lower body fat appears to be protective and is paradoxically associated with improved metabolic and cardiovascular profiles. Physiological studies have demonstrated that fatty acid handling differs between white adipose tissue depots, with lower body white adipose tissue acting as a more efficient site for long-term lipid storage. The regulatory mechanisms governing these regional differences in function remain to be elucidated. Although the local microenvironment is likely to be a contributing factor, recent findings point towards the tissues being intrinsically distinct at the level of the adipocyte precursor cells (pre-adipocytes). The multi-potent pre-adipocytes are capable of generating cells of the mesenchymal lineage, including adipocytes. Regional differences in the adipogenic and replicative potential of these cells, as well as metabolic and biochemical activity, have been reported. Intriguingly, the genetic and metabolic characteristics of these cells can be retained through multiple generations when the cells are cultured in vitro. The rapidly emerging field of epigenetics may hold the key for explaining regional differences in white adipose tissue gene expression and function. Epigenetics describes the regulation of gene expression that occurs independently of changes in DNA sequence, for instance, DNA methylation or histone protein modification. In this review, we will discuss the contribution of DNA methylation to the determination of cells of adipogenic fate as well as the role DNA methylation may play during adipocyte terminal differentiation.

Over the past several decades, the incidence of atopic diseases such as asthma, atopic dermatitis and food allergies has increased dramatically. Although atopic diseases have a clear genetic basis, environmental factors, including early infant nutrition, may have an important influence on their development. Therefore, attempts have been made to reduce the risk of the development of allergy using dietary modifications, mainly focused on longer breast-feeding and delayed introduction or elimination of foods identified as potentially most allergenic. Recently, there is also an increasing interest in the active prevention of atopy using specific dietary components. Many studies have shown that breast-feeding may have the protective effect against future atopic dermatitis and early childhood wheezing. Concerning complementary feeding, there is evidence that the introduction of complementary foods before 4 months of age may increase the risk for atopic dermatitis. However, there is no current convincing evidence that delaying introduction of solids after 6 months of age has a significant protective effect on the development of atopic disease regardless of whether infants are fed cow's milk protein formula or human subject's milk, and this includes delaying the introduction of foods that are considered to be highly allergic, such as fish, eggs and foods containing peanut protein. In conclusion, as early nutrition may have profound implications for long-term health and atopy later in life, it presents an opportunity to prevent or delay the onset of atopic diseases.

Nutritional assessment and dietary advice are fundamental to inflammatory bowel disease (IBD) patient management and all patients should have access to a dietitian. Newly diagnosed patients often think that their pre-illness diet has contributed to the development of their IBD. However, epidemiological evidence to support diet as a risk factor is lacking. How the diet contributes to the gastrointestinal microbiota is interesting, although the role is not yet clearly defined. Nutritional problems in IBD are common. Malnutrition occurs in up to 85% of patients and weight loss affects up to 80% of patients with Crohn's disease and 18–62% of patients with ulcerative colitis. Nutritional deficiencies are prevalent, particularly in relation to anaemia and osteoporosis. Intestinal strictures can be problematic in Crohn's disease and limiting fibrous foods that may cause a mechanical obstruction in the gastrointestinal tract is helpful. Patients often explore dietary exclusion to alleviate symptoms but such changes may be self-directed or inappropriately advised and can lead to further nutritional deficiencies. Some patients experience concurrent functional symptoms (e.g. abdominal bloating, abdominal pain, flatulence and diarrhoea) that can significantly affect quality of life. Recently, a group of poorly absorbed carbohydrates that occur naturally in the diet called fermentable oligo-, di-, mono-saccharides and polyols have been associated with functional symptoms by intestinal bacterial fermentation leading to rapid gas production, and an osmotic effect increasing fluid delivery to the colon. Emerging evidence indicates that a diet low in fermentable oligo-, di-, mono-saccharides and polyols can alleviate functional symptoms in IBD.

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.

The rapid increase in the incidence of chronic non-communicable diseases over the past two decades cannot be explained solely by genetic and adult lifestyle factors. There is now considerable evidence that the fetal and early postnatal environment also strongly influences the risk of developing such diseases in later life. Human studies have shown that low birth weight is associated with an increased risk of CVD, type II diabetes, obesity and hypertension, although recent studies have shown that over-nutrition in early life can also increase susceptibility to future metabolic disease. These findings have been replicated in a variety of animal models, which have shown that both maternal under- and over-nutrition can induce persistent changes in gene expression and metabolism within the offspring. The mechanism by which the maternal nutritional environment induces such changes is beginning to be understood and involves the altered epigenetic regulation of specific genes. The demonstration of a role for altered epigenetic regulation of genes in the developmental induction of chronic diseases raises the possibility that nutritional or pharmaceutical interventions may be used to modify long-term cardio-metabolic disease risk and combat this rapid rise in chronic non-communicable diseases.