It is estimated that over half the population of the European Union (EU) is overweight or obese due to an imbalance between energy expenditure and energy intake; this is related to an obesogenic environment of sociocultural, economic and marketing challenges to the control of body weight. Excess body fat is associated with nine cancer sites - oesophagus, colorectum, gall bladder, pancreas, postmenopausal breast, endometrium, ovary, kidney and prostate (advanced) - and 4-38% of these cancers (depending on site and gender) can be attributed to overweight/obesity status. Metabolic alterations which accompany excess body weight are accompanied by increased levels of inflammation, insulin, oestrogens and other hormonal factors. There are some indications that intentional weight loss is associated with reduced cancer incidence (notably in postmenopausal breast and endometrial cancers). Excess body weight is also a risk factor for several other diseases, including diabetes and heart disease, and is related to higher risk of premature death. In reviewing the current evidence related to excess body fat and cancer, the European Code against Cancer Nutrition Working Group has developed the following recommendation: 'Take action to be a healthy body weight'.
The UK Food Standards Agency convened a group of expert scientists to review current research investigating emerging diet-related surrogate end points for colorectal cancer (CRC). The workshop aimed to overview current research and establish priorities for future research. The workshop considered that the validation of current putative diet-related surrogate end points for CRC and the development of novel ones, particularly in the emerging fields of proteomics, genomics and epigenomics, should be a high priority for future research.
BACKGROUND: Impaired iron handling in riboflavin deficiency is thought to be partially a result of significant morphological and cytokinetic changes within the small intestine. AIMS: The aim of the study was to find out if the responses of the rat small intestine to riboflavin deficiency induced at weaning could be reversed upon repletion. SUBJECTS: 48 female weanling Wistar rats were used for the purpose of the study. METHODS: Rats were fed a riboflavin deficient diet or a complete control diet for a period of five weeks followed by a repletion period of up to three weeks. Rats were killed on day 0, 2, 7, or 21 of repletion. The duodenum was removed and fixed for subsequent analysis. RESULTS: Five weeks of riboflavin deficiency significantly changed the morphology and cytokinetics of the duodenum; the changes were not reversed within the 21 day repletion period despite biochemical evidence for a correction of the deficiency. CONCLUSIONS: The results show that the small intestine cannot readily recover from a period of riboflavin deficiency induced at weaning, supporting the notion that the weaning period is a critical time for gastrointestinal development and highlighting the importance of adequate nutrition during infancy.
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Chapter 1 The Importance of Nutrition Chapter 2 Body Composition and Energy balance Chapter 3 Food consumption Chapter 4 Main dietary components Chapter 5 Minor dietary components Chapter 6 Diet and the lifecycle Chapter 7 Diet for sport and exercise Chapter 8 Diet and disease Chapter 9 Nutrition and the hard tissues Chapter 10 Diet and the gastrointestinal tract Chapter 11 Diet and genotype interactions: nutritional genomics Chapter 12 Nutritional epidemiology and nutritional assessment Chapter 13 Public Health Nutrition Appendices: Glossary Dietary reference values Index
This chapter provides an overview of biochemical assessment. Biochemical assessment forms part of a coordinated set of nutritional investigations that may also include dietary assessment, anthropometry, physiological tests, and clinical investigations. The design of the biochemical aspect of a nutritional assessment depends on there being an available and suitable sample of body fluid or tissue for analysis. The chapter looks into the necessary precautions to be taken during sample selection, storage, and analysis, before providing an outline of essential fieldwork and laboratory methodologies. It covers the correlation between status and nutritional adequacy by considering inter-relationships between the biochemical and other indices of nutritional status.
Gestational trophoblastic neoplasia is a rare malignancy, which can occur after any type of pregnancy. The incidence varies according to the geographical location and ethnic origin. Although most patients with gestational trophoblastic neoplasia are cured by conventional chemotherapy and surgery, some suffer resistant disease and may die. New therapeutic agents are needed to reduce the toxicity associated with conventional chemotherapy and treat those with resistant or refractory disease. Molecular targeted treatment provides an exciting avenue; however, the biology of gestational trophoblastic neoplasia is not well understood. This review briefly summarises recent advances in the understanding of the pathogenesis and molecular biology of this group of diseases and sheds light on molecules that could provide potential therapeutic targets.
Hyperhomocysteinaemia is considered to be an independent risk factor for vascular disease. Elevated plasma homocysteine may pose an oxidative stress, leading to the development of vascular damage. A component of this effect may be a disturbance of the extracellular aminothiol redox state. The relative contributions of plasma total homocysteine (tHcy) and plasma total cysteine (tCys) to the total antioxidant capacity (TAOC) of plasma was established in subjects with normal and elevated plasma tHcy. A total of 10 subjects with severe hyperhomocysteinaemia (due to inherited metabolic defects), 13 of their heterozygous parents and 72 normal healthy subjects were recruited to the study. The mean plasma tHcy in the patients was 91.8 µmol/l, compared with 13.2 µmol/l in the parents and 14.7 µmol/l in healthy control subjects. Plasma tCys and plasma TAOC were significantly lower in the subjects with severe hyperhomocysteinaemia compared with the parents and healthy control subjects (P < 0.05). In blood samples from subjects with a normal tHcy, a positive correlation was observed between tCys and tHcy (P = 0.0001). In contrast, in blood samples with tHcy ⩾ 20 µmol/l, plasma tCys was negatively correlated with tHcy (P = 0.0001). In samples with tHcy ⩾ 20 µmol/l, tHcy was inversely correlated with TAOC (P = 0.0001), whereas tCys was positively associated with TAOC (P = 0.0001). Multiple regression analysis revealed that tCys was the most important independent determinant of TAOC in the patient and control groups when the effects of tHcy and several factors known to influence TAOC, such as urate, were taken into account. Thus hyperhomocysteinaemia may pose an oxidative stress not only through the direct cytotoxicity of homocysteine, but also from an associated fall in plasma cysteine.
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