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.

Seventy years have elapsed since the Nutrition Society was founded and John Boyd Orr became its first Chairman. Over the intervening period, nutrition research has embraced and responded to a wide variety of challenges as the requirements of research have evolved and changed. This paper reflects on some of the major challenges that have influenced nutrition research over the past 70 years and considers where nutrition stands today along with the challenges for the future. In the past, these challenges have included food security and improvements in animal nutrition to enhance production through problems of overnutrition, such as CVD and obesity, as well as the recognition of the importance of early-life nutrition. The challenges for the future include how to translate the increasingly comprehensive and complex understanding of the relationship between nutrition and health, being gained as a result of the genomic revolution, into simple and accessible policy advice. It also includes how we learn more about the ways in which diet can help in the prevention of obesity as well as the ways in which we prevent the rise in complex diseases in emerging nations as they undergo nutritional transition. From this, it is clear that nutrition research has moved a long way from its initial focus on nutritional deficiencies to a subject, which is at the heart of public health consideration. This evolution of nutrition research means that today diet and health are high on the political agenda and that nutrition remains a priority area for research. It has been 70 years since 1941 when the Nutrition Society was established, under its first Chairman, John Boyd Orr. At that time there were many who believed that nutrition research had reached its peak and there was little left to discover. This view stemmed from the fact that most vitamins and minerals had been discovered and that the syndromes associated with nutritional deficiencies in these were largely known. Despite this gloomy prognosis, the intervening 70 years have witnessed a remarkable evolution in nutrition research, which has underpinned key Government policies, ranging from food security right through to public health. This review considers some major developments that have helped to shape nutrition research over the past 70 years and in so doing have changed its frontiers.

The consequences of sub-optimal nutrition through alterations in the macronutrient content of the maternal diet will not simply be reflected in altered neonatal body composition and increased mortality, but are likely to continue into adulthood and confer greater risk of metabolic disease. One mechanism linking manipulations of the maternal environment to an increased risk of later disease is enhanced fetal exposure to glucocorticoids (GC). Tissue sensitivity to cortisol is regulated, in part, by the GC receptor and 11β-hydroxysteroid dehydrogenase (11β-HSD) types 1 and 2. Several studies have shown the effects of maternal undernutrition, particularly low-protein diets, on the programming of GC action in the offspring; however, dietary excess is far more characteristic of the diets consumed by contemporary pregnant women. This study investigated the programming effects of moderate protein supplementation in pigs throughout pregnancy. We have demonstrated an up-regulation of genes involved in GC sensitivity, such as GC receptor and 11β-HSD, in the liver, but have yet to detect any other significant changes in these piglets, with no differences observed in body weight or composition. This increase in GC sensitivity was similar to the programming effects observed following maternal protein restriction or global undernutrition during pregnancy.