Obesity has been described as the health crisis of the 21st century. It is a chronic lifelong medical condition, whose pattern often starts in childhood, and is demographically worsening in every developed country. The cost of treating the many medical conditions associated with obesity threatens to overwhelm healthcare resources. Medical treatments produce at most no more than 10% weight loss in the severely obese, with high failure rates. In this article, we review the available evidence regarding long-term reduction in weight, reduced mortality and improvement in most, if not all, obesity-related comorbidities. There is a need for daily multivitamins and extra minerals, especially with gastric bypass, and nutritional deficiencies of vitamins D and B12, Ca, Fe and folate need monitoring and prevention. Currently there is no medical therapy on the near horizon that will match the effect of surgery, which, if done safely, remains the only effective therapy. Bariatric surgery is cost effective, and health providers should embrace the development and rapid expansion of services.

The interaction between nutrition and infection was the subject of important work by several groups in the 1960s. The explosion of knowledge in immunology, including innate immunity, has led to increased understanding of the impact of nutrition on host defence, but much more work needs to be done in this area. In the last decade an increasing volume of work has opened up the previously obscure world of human endogenous flora. This work suggests that the microbiome, the total genetic pool of the microbiota, contributes to the already complex interaction between nutrition and infectious disease. The established concept that nutritional status, host defence and infection all impact on each other now has to be expanded into a multiple interaction, with the microbiota interacting with all three other elements. There is good evidence that the microbiome programmes host defence and drives a metabolome that impacts on energy balance, and indeed on some micronutrients. In turn, host defence shapes the microbiome, and nutritional status, particularly micronutrient status, helps determine several elements of host defence. While interventions in this area are in their infancy, the understanding of interactions that already have an enormous impact on global health is now at a threshold. The present review explores the evidence for these interactions with a view to putting potential interventions into the context of a conceptual framework.

Obesity leads to several chronic morbidities including type 2 diabetes, dyslipidaemia, atherosclerosis and hypertension, which are major components of the metabolic syndrome. White adipose tissue (WAT) metabolism and WAT-derived factors (fatty acids and adipokines) play an important role in the development of these metabolic disturbances. In fact, dysregulated adipokine secretion from the expanded WAT of obese individuals contributes to the development of systemic low-grade inflammation, insulin resistance and metabolic syndrome. The n-3 PUFA EPA and DHA have been widely reported to have protective effects in a range of chronic inflammatory conditions including obesity. In fact, n-3 PUFA have been shown to ameliorate low-grade inflammation in adipose tissue associated with obesity and up-regulate mitochondrial biogenesis and induce beta-oxidation in WAT in mice. Moreover, the ability of n-3 PUFA to regulate adipokine gene expression and secretion has been observed both in vitro and in vivo in rodents and human subjects. The present article reviews: (1) the physiological role of adiponectin, leptin and pre-B cell colony-enhancer factor/visfatin, three adipokines with immune-modulatory properties involved in the regulation of metabolism and insulin sensitivity and (2) the actions of n-3 PUFA on these adipokines focusing on the underlying mechanisms and the potential relationship with the beneficial effects of these fatty acids on obesity-associated metabolic disorders. It can be concluded that the ability of n-3 PUFA to improve obesity and insulin resistance conditions partially results from the modulation of WAT metabolism and the secretion of bioactive adipokines including leptin, adiponectin and visfatin.

Epidemiological studies have provided convincing evidence that obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colon, pancreas, breast (post-menopausal), endometrium and kidney. The magnitude of the increase in risk varies between cancer sites. For an increase in BMI of 10 kg/m2 relative risks are approximately 2·3 for adenocarcinoma of the oesophagus, 1·5 for colon cancer in men, 1·2 for colon cancer in women, 1·4 for post-menopausal breast cancer, 2·9 for endometrial cancer and >1·5 for kidney cancer, while the size of the effect on cancer of the pancreas is uncertain. There is also evidence that obesity increases the risks for cancers of the gallbladder, malignant melanoma, ovary, thyroid, non-Hodgkin lymphoma, multiple myeloma and leukaemia. Estimates of the percentage of cancers that can be attributed to excess body weight suggest that in the UK and similar countries approximately 5% of all cancers are attributable to overweight and obesity.

Several epidemiological and clinical studies have evaluated the effects of a Mediterranean diet (Med-Diet) on total cardiovascular mortality, and all concluded that adherence to the traditional Med-Diet is associated with reduced cardiovascular risk. However, the molecular mechanisms involved are not fully understood. Since atherosclerosis is nowadays considered a low-grade inflammatory disease, recent studies have explored the anti-inflammatory effects of a Med-Diet intervention on serum and cellular biomarkers related to atherosclerosis. In a pilot study of the PREvencion con DIeta MEDiterranea (PREDIMED) trial, we analysed the short-term effects of two Med-Diet interventions, one supplemented with virgin olive oil and another with nuts, on vascular risk factors in 772 subjects at high risk for CVD, and in a second study we evaluated the effects of these interventions on cellular and serum inflammatory biomarkers in 106 high-risk subjects. Compared to a low-fat diet, the Med-Diet produced favourable changes in all risk factors. Thus, participants in both Med-Diet groups reduced blood pressure, improved lipid profile and diminished insulin resistance compared to those allocated a low-fat diet. In addition, the Med-Diet supplemented with virgin olive oil or nuts showed an anti-inflammatory effect reducing serum C-reactive protein, IL-6 and endothelial and monocytary adhesion molecules and chemokines, whereas these parameters increased after the low-fat diet intervention. In conclusion, Med-Diets down-regulate cellular and circulating inflammatory biomarkers related to atherogenesis in subjects at high cardiovascular risk. These results support the recommendation of the Med-Diet as a useful tool against CVD.

This review details the practicalities of providing nutrition support to obese patients who experience complications following bariatric surgery and highlights some of the nutritional challenges encountered by this group of patients. Bariatric surgery to treat morbid obesity has significantly increased internationally over the past decade with hospital admissions rising annually. The gastric bypass is currently the most commonly performed procedure. The complication rate can be up to 16%, with a considerable proportion having nutritional implications. The treatment can involve avoidance of oral diet and nutrition support, i.e. enteral or parenteral nutrition. Opposition to nutrition support can be encountered. It is useful to clarify the aims of nutrition support, these being: the avoidance of overfeeding and its consequences, preservation of lean body mass and promotion of healing. Evidence suggests that hypoenergic nutrition is not harmful and may actually be beneficial. There is a lack of consensus regarding the optimum method to predict the nutritional requirements in the obese acutely unwell patient. The literature suggests that the predicted equations are fairly accurate compared to measured energy expenditure in free living obese patients before and after bariatric surgery. However, these findings cannot be directly applied to those obese patients experiencing complications of bariatric surgery, who will be acutely unwell exhibiting inflammatory response. It is therefore necessary to refer to the literature on energy expenditure in hospitalized obese patients, to help guide practice. More research examining the energy and protein requirements of obese patients needing nutrition support following bariatric surgery is urgently required.