Obesity is a public health concern worldwide, arising from multifaceted and complex causes that relate to individual choice and lifestyle, and the influences of wider society. In addition to a long-standing focus on both childhood and adult obesity, there has been more recent concern relating to maternal obesity. This review explores the published evidence relating to maternal obesity incidence and associated inequalities, the impact of obesity on maternity services, and associated guidelines. Epidemiological data comprising three national maternal obesity datasets within the UK have identified a significant increase in maternal obesity in recent years, and reflect broad socio-demographic inequalities particularly deprivation, ethnicity and unemployment. Obese pregnancies present increased risk of complications that require more resource intensive antenatal and perinatal care, such as caesarean deliveries, gestational diabetes, haemorrhage, infections and congenital anomalies. Healthcare professionals also face difficulties when managing the care of women in pregnancy as obesity is an emotive and stigmatising topic. There is a lack of good-quality evidence for effective interventions to tackle maternal obesity. Recently published national guidelines for the clinical management and weight management of maternal obesity offer advice for professionals, but acknowledge the limitations of the evidence base. The consequence of these difficulties is an absence of support services available for women. Further evaluative research is thus required to assess the effectiveness of interventions with women before, during and after pregnancy. Qualitative work with women will also be needed to help inform the development of more sensitive risk communication and women-centred services.

Excess weight gain during pregnancy and post-partum weight retention are risk factors for obesity. While many studies report average weight retained from pregnancy is only 0·5–3·0 kg; between 14 and 20% of women are 5 kg heavier at 6–18 months post-partum than they were before pregnancy. Among normal-weight women, lactation usually promotes weight loss to a moderate extent, but not among those with BMI≥35 kg/m2. While exercise and energy restriction may promote weight loss during lactation, their effect on milk volume and composition and, consequently, infant growth must be considered. The effect of exercise on lactation performance has been investigated. Moderate aerobic exercise of 45 min/d, 5 d/week improved cardiovascular fitness, plasma lipids and insulin response; however, it did not promote post-partum weight loss. Breast milk volume and composition were not affected. The effect of exercise with energy restriction in overweight women on the growth of their infants has also been studied. At 1 month post-partum, women restricted their energy intake by 2092 kJ/d and exercised 45 min/d, 4 d/week for 10 weeks. Women in the diet and exercise group lost more weight than the control group (4·8 (sd 1·7) kg v. 0·8 (sd 2·3) kg); however, there were no differences in infant growth. Based on the current evidence, it is recommended that once lactation is established, overweight women may restrict their energy intake by 2092 kJ/d and exercise aerobically 4 d/week to promote a weight loss of 0·5 kg/week.

These days, we are bombarded with nutrition information from diverse sources and of varying quality. There has been a dramatic increase in communication channels, including more television channels with airtime to fill, and the emergence of the Internet and ‘new media’ such as social networking sites. Part of this culture is to deliver ever changing and novel angles. The background ‘noise’ that this creates can make delivery of evidence-based advice about healthy eating that generally carries less novelty value, a huge challenge. This paper illustrates ways in which complex scientific information can be translated into meaningful health promoting strategies that can be applied across the life course. The examples used are nutrition in the context of healthy ageing, communicating the concept of energy density in the context of satiety, healthy hydration, health effects of probiotics and resources for use by teachers in the classroom. This selection of examples demonstrates the processes adopted at the British Nutrition Foundation to identify the evidence base for a particular topic and then to communicate this information to various target audiences. The British Nutrition Foundation's approach typically starts with preparation of a detailed review of the evidence, often with the involvement of external expertise, followed by peer review. For much of this work conventional science communication routes are used, but use is also made of the Internet and various forms of new media.

An optimal nutritional state is an important consideration in providing successful operative outcomes. Unfortunately, many aspects of surgery are not constructive to providing this. In addition, the metabolic and immune response to injury induces a catabolic state and insulin resistance, a known risk factor of post-operative complications. Aggressive insulin therapy post-operatively has been shown to reduce morbidity and mortality but similar results can be achieved when insulin resistance is lessened by the use of pre-operative carbohydrate loading. Consuming carbohydrate-containing drinks up to 2 h before surgery has been found to be an effective way to attenuate insulin resistance, minimise protein losses, reduce hospital stays and improve patient comfort without adversely affecting gastric emptying. Enhanced recovery programmes have employed carbohydrate loading as one of several strategies aimed at reducing post-operative stress and improving the recovery process. Studies examining the benefits of these programmes have demonstrated significantly shorter post-operative hospital stays, faster return to normal functions and lower occurrences of surgical complications. As a consequence of the favourable evidence they are now being implemented in many surgical units. Further benefit to post-operative recovery may be found with the use of immune-enhancing diets, i.e. supplementation with n-3 fatty acids, arginine, glutamine and/or nucleotides. These have the potential to boost the immune system, improve wound healing and reduce inflammatory markers. Research exploring the benefits of immunonutrition and solidifying the use of carbohydrate loading is ongoing; however, there is strong evidence to link good pre-operative nutrition and improved surgical outcomes.

Epigenetic changes are inherited alterations in DNA that affect gene expression and function without altering the DNA sequence. DNA methylation is one epigenetic process implicated in human disease that is influenced by diet. DNA methylation involves addition of a 1-C moiety to cytosine groups in DNA. Methylated genes are not transcribed or are transcribed at a reduced rate. Global under-methylation (hypomethylation) and site-specific over-methylation (hypermethylation) are common features of human tumours. DNA hypomethylation, leading to increased expression of specific proto-oncogenes (e.g. genes involved in proliferation or metastasis) can increase the risk of cancer as can hypermethylation and reduced expression of tumour suppressor (TS) genes (e.g. DNA repair genes). DNA methyltransferases (DNMT), together with the methyl donor S-adenosylmethionine (SAM), facilitate DNA methylation. Abnormal DNA methylation is implicated not only in the development of human cancer but also in CVD. Polyphenols, a group of phytochemicals consumed in significant amounts in the human diet, effect risk of cancer. Flavonoids from tea, soft fruits and soya are potent inhibitors of DNMT in vitro, capable of reversing hypermethylation and reactivating TS genes. Folates, a group of water-soluble B vitamins found in high concentration in green leafy vegetables, regulate DNA methylation through their ability to generate SAM. People who habitually consume the lowest level of folate or with the lowest blood folate concentrations have a significantly increased risk of developing several cancers and CVD. This review describes how flavonoids and folates in the human diet alter DNA methylation and may modify the risk of human colon cancer and CVD.

Epithelial cells lining the inner surface of the intestinal epithelium are in direct contact with a lumenal environment that varies dramatically with diet. It has long been suggested that the intestinal epithelium can sense the nutrient composition of lumenal contents. It is only recently that the nature of intestinal nutrient-sensing molecules and underlying mechanisms have been elucidated. There are a number of nutrient sensors expressed on the luminal membrane of endocrine cells that are activated by various dietary nutrients. We showed that the intestinal glucose sensor, T1R2+T1R3 and the G-protein, gustducin are expressed in endocrine cells. Eliminating sweet transduction in mice in vivo by deletion of either gustducin or T1R3 prevented dietary monosaccharide- and artificial sweetener-induced up-regulation of the Na+/glucose cotransporter, SGLT1 observed in wild-type mice. Transgenic mice, lacking gustducin or T1R3 had deficiencies in secretion of glucagon-like peptide 1 (GLP-1) and, glucose-dependent insulinotrophic peptide (GIP). Furthermore, they had an abnormal insulin profile and prolonged elevation of postprandial blood glucose in response to orally ingested carbohydrates. GIP and GLP-1 increase insulin secretion, while glucagon-like peptide 2 (GLP-2) modulates intestinal growth, blood flow and expression of SGLT1. The receptor for GLP-2 resides in enteric neurons and not in any surface epithelial cells, suggesting the involvement of the enteric nervous system in SGLT1 up-regulation. The accessibility of the glucose sensor and the important role that it plays in regulation of intestinal glucose absorption and glucose homeostasis makes it an attractive nutritional and therapeutic target for manipulation.

Patients undergoing oesophagectomy often have nutritional needs at the time of diagnosis and in the post-operative period. The aim of this article is to review the current literature and report on the author's experience of routine feeding jejunostomy insertion following oesophagectomy. The records of forty-eight consecutive patients undergoing oesphagectomy under the author's care were reviewed. Although the evidence of benefit of peri-operative feeding in patients undergoing oesophagectomy is limited, there is a clear need to establish a feeding route at the time of surgery. Oesophagectomy is associated with a mortality rate of 5–10% and a morbidity rate of 30–40% even in high-volume specialist centres. Over 50% of patients developing complications will require an alternative to oral feeding beyond 30 d. The enteral route is preferred in terms of safety and cost. A surgical feeding jejunostomy is associated with a low complication rate and a mortality rate of less than 1%. In forty-eight patients undergoing oesophagectomy the average weight loss at 6 months was 8·4 kg with only 8% regaining their pre-operative weight. Large reductions in weight at 6 months post-operatively were recorded irrespective of the development of post-operative complications or early recurrent disease. Routine jejunostomy insertion is recommended to ensure adequate nutrition in patients who develop post-operative complications and for those patients with long-term reduced appetite and poor oral intake.

The prevalence of obesity in pregnancy is rising exponentially; about 15–20% of pregnant women now enter pregnancy with a BMI which would define them as obese. This paper provides a review of the strong links between obesity and adverse pregnancy outcome which operate across a range of pregnancy complications. For example, obesity is associated with an increased risk of maternal mortality, gestational diabetes mellitus, thromboembolism, pre-eclampsia and postpartum haemorrhage. Obesity also complicates operative delivery; it makes operative delivery more difficult, increases complications and paradoxically increases the need for operative delivery. The risk of the majority of these complications is amplified by excess weight gain in pregnancy and increases in proportion to the degree of obesity, for example, women with extreme obesity have OR of 7·89 for gestational diabetes and 3·84 for postpartum haemorrhage compared to their lean counterparts. The consequences of maternal obesity do not stop once the baby is born. Maternal obesity programmes a variety of long-term adverse outcomes, including obesity in the offspring at adulthood. Such an effect is mediated at least in part via high birthweight; a recent study has suggested that the odds of adult obesity are two-fold greater in babies weighing more than 4 kg at birth. The mechanism by which obesity causes adverse pregnancy outcome is uncertain. This paper reviews the emerging evidence that hyperglycaemia and insulin resistance may both play a role: the links between hyperglycaemia in pregnancy and both increased birthweight and insulin resistance have been demonstrated in two large studies. Lastly, we discuss the nature and rationale for possible intervention strategies in obese pregnant women.