This paper presents emerging evidence linking visceral adiposity and the metabolic syndrome (MetSyn) with carcinogenesis. The link between obesity and cancer has been clearly identified in a multitude of robust epidemiological studies. Research is now focusing on the role of visceral adipose tissue in carcinogenesis; as it is recognised as an important metabolic tissue that secretes factors that systemically alter the immunological, metabolic and endocrine milieu. Excess visceral adipose tissue gives rise to a state of chronic systemic inflammation with associated insulin resistance and dysmetabolism, collectively known as the MetSyn. Prospective cohort studies have shown associations between visceral adiposity, the MetSyn and increased risk of breast cancer, colorectal cancer and oesophageal adenocarcinoma. Furthermore, visceral adiposity and the MetSyn have been associated with increased tumour progression and reduced survival. The mechanisms by which visceral adiposity and the MetSyn are thought to promote tumorigenesis are manifold. These include alterations in adipokine secretion and cell signalling pathways. In addition, hyperinsulinaemia, subsequent insulin resistance and stimulation of the insulin-like growth factor-1 axis have all been linked with visceral adiposity and promote tumour progression. Furthermore, the abundance of inflammatory cells in visceral adipose tissue, including macrophages and T-cells, create systemic inflammation and a pro-tumorigenic environment. It is clear from current research that excess visceral adiposity and associated dysmetabolism play a central role in the pathogenesis of certain cancer types. Further research is required to elucidate the exact mechanisms at play and identify potential targets for intervention. Visceral adiposity: Metabolic syndrome: Insulin resistance: Inflammation: TumorigenesisThe prevalence of obesity has increased rapidly in recent years (1) . Being overweight or obese is now the most prevalent body composition in some countries, accounting for 71% of males and 62 % of females in the United States (2) . Similar trends exist in Western Europe with greater than 66% of men and 49-57 % of women being overweight or obese in the UK and Ireland (3,4) . This pattern shows no signs of abating as obesity rates are increasing among children (5) and overweight children tend to become overweight adults (6) . In countries where sedentary lifestyles and high-energy foods are abundant it is easy to see how energy intake exceeds that expended. It has been estimated that ingestion of 5 % more energy than expended may result in an accumulation of 5 kg adipose tissue in a single year (7) . Epidemiological studies have demonstrated a robust link between obesity and cancer development at numerous sites, in particular the oesophagus, pancreas, colorectum, breast (postmenopausal), endometrium and kidney (8,9) . This association carries relative risk (RR) estimates of 1 . 1-1 . 6 per 5 kg/m 2 incremental increase in BMI (8) . Obesity also increases cancer-related mo...

BackgroundThere is a well established link between obesity and cancer. Emerging research is characterising this relationship further and delineating the specific role of excess visceral adiposity, as opposed to simple obesity, in promoting tumorigenesis. This review summarises the evidence from an epidemiological and pathophysiological perspective.MethodsRelevant medical literature was identified from searches of PubMed and references cited in appropriate articles identified. Selection of articles was based on peer review, journal and relevance.ResultsNumerous epidemiological studies consistently identify increased risk of developing carcinoma in the obese. Adipose tissue, particularly viscerally located fat, is metabolically active and exerts systemic endocrine effects. Putative pathophysiological mechanisms linking obesity and carcinogenesis include the paracrine effects of adipose tissue and systemic alterations associated with obesity. Systemic changes in the obese state include chronic inflammation and alterations in adipokines and sex steroids. Insulin and the insulin-like growth factor axis influence tumorigenesis and also have a complex relationship with adiposity. There is evidence to suggest that insulin and the IGF axis play an important role in mediating obesity associated malignancy.ConclusionsThere is much evidence to support a role for obesity in cancer progression, however further research is warranted to determine the specific effect of excess visceral adipose tissue on tumorigenesis. Investigation of the potential mechanisms underpinning the association, including the role of insulin and the IGF axis, will improve understanding of the obesity and cancer link and may uncover targets for intervention.

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Malabsorption and malnutrition are prevalent in survivorship of esophageal and stomach cancer. This may be underappreciated, and both gut and pancreatic insufficiency represent modifiable targets in the interdisciplinary approach to recovery of HR-QL.

This novel study examined the differential role of the IGF system in esophageal adenocarcinoma and SCC, and its association with visceral obesity. These results indicate that the IGF-1 axis has a key role in malignant progression of esophageal cancer, and represents a plausible mechanism through which visceral obesity impacts on esophageal adenocarcinoma risk and tumor biology.

As the prevalence of obesity continues to rise in society, an increasing number of patients undergoing non-bariatric surgery will be obese. Obesity is known to increase morbidity and mortality in the general population and thus is perceived as a risk factor for adverse post-surgical outcomes. This association is not clear-cut, however, and there is a lack of consensus in the literature on the risk between obesity and specific complications, in particular relating to infection, wound healing, respiratory and venous thromboembolism. The paucity of studies, as well as a lack of consistency of definition of obesity, with an over-reliance on body mass index rather than body composition analysis, may underlie this confusion. Emerging concepts position central/visceral adipose tissue as potentially key to the pathogenesis of the comorbidities associated with obesity, thus this article reviews emerging research investigating the association between visceral obesity, the metabolic syndrome and resulting post-operative complications. It is hypothesized that the state of chronic inflammation and dysmetabolism observed in visceral obese patients negatively influences post-operative outcomes and represents a potential target for pharmaconutrition. The need for further research investigating the influence of visceral adiposity on immune function post surgery and its impact on post-operative morbidity and mortality is highlighted.

NCT03314311.

The thesis that EPA impacts on anabolism, immune function, and clinical outcomes post-esophagectomy was not supported. Compliance with home EN was excellent, but weight, muscle, and fat loss was significant in 30% of patients, highlighting the complexity of postoperative weight loss.