Food consumption patterns are influenced by a number of factors, including social and cultural factors. It is difficult to effect dietary change, and one possible barrier to dietary change is optimistic bias. Research indicates that individuals tend to believe that they are less likely to experience negative events, and more likely to experience positive events than their peers; this phenomenon is known as optimistic bias. It has been argued that optimistic bias may have a negative impact both on self-protective behaviour and on efforts to promote risk-reducing behaviours. The present article reviews the literature investigating optimistic bias specifically in the food domain. The review indicated that many food and nutrition issues are associated with optimistic bias. This has important implications for health-promotion activities in the food domain. The paper also describes key aspects of the methodology used to investigate optimistic bias and details the conditions under which optimistic bias has been demonstrated. The importance of identifying the causes of optimistic bias is discussed, and empirical attempts designed to reduce optimistic bias by countering the causes are reviewed. Finally, directions for future research are suggested.

Despite continued efforts to prevent and control food-borne illness it remains a major cause of morbidity and mortality throughout the world. The problem is made worse by the continuous threat from emerging pathogens that can evolve to adapt to the different environments resulting from ongoing changes in farming or food production. The present review discusses the impact of genomics and post-genomic technologies on research in the area of food-borne bacterial pathogens. Genomics research is moving at a fast pace and these are exciting times for microbial research. The genome sequences of approximately ninety bacterial genomes have recently been completed and genome sequences are already available for several food-borne pathogens and closely related species. Comparative genomics is providing new insights into mechanisms of bacterial evolution and has helped in determining virulence factors of pathogens. Genomics has also provided tools such as DNA microarrays that can be used to examine the genetic composition and whole genome expression profiles of bacterial strains by hybridisation of fluorescently labelled DNA. This is helping to identify genes associated with particular phenotypes such as virulence and host preference, and to identify genes in uncharacterised genomes of closely related organisms. Microarrays are also being developed for the detection of food-borne pathogens and investigation of the evolutionary relationship between different species of bacteria. The review concludes with a discussion of the use of functional genomics tools to investigate bacterial responses to environmental stresses and also host–pathogen interactions. These research areas will be valuable in designing future strategies for controlling food-borne pathogens.

The diversity of the human genome leads to many functional differences between individuals. The present review focuses on genetic variations, both rare and common, that are of relevance to digestion of the sugars and starches that form a major part of human diets, and considers these in relation to the evolution of our species. For example, intolerances of dietary saccharides are not usually life-threatening because symptoms can be avoided by removal of the offending sugar from the diet, and deficiencies of the relevant enzymes are in some cases found at relatively high frequencies in certain populations. This is of evolutionary interest in relation to changes in the human diet, and the lactase-persistence polymorphism, in particular, provides an interesting model. More of the world's adult population are lactase-deficient than have high lactase. The other deficiencies are however much more rare, but the significance of variant alleles at these loci, and also heterozygosity for deficiency alleles, to human nutrition and health is an area that is relatively unexplored.

The metalloid Se is ubiquitous in soils, but exists mainly in insoluble forms in high-Fe, low-pH and certain leached soils, and hence is often of limited availability to plants. Consequently, it is often supplied by plants to animals and human consumers at levels too low for optimum health. Se deficiency and suboptimality are manifested in populations as increased rates of thyroid dysfunction, cancer, severe viral diseases, cardiovascular disease and various inflammatory conditions. Se deficiency probably affects at least a billion individuals. Optimal cancer protection appears to require a supra-nutritional Se intake, and involves several mechanisms, which include promotion of apoptosis and inhibition of neo-angiogenesis. Evidence suggests that in some regions Se is declining in the food chain, and new strategies to increase its intake are required. These could include education to increase consumption of higher-Se foods, individual supplementation, food fortification, supplementation of livestock, Se fertilisation of crops and plant breeding for enhanced Se accumulation. Se levels in Australian residents and wheat appear to be above the global estimated mean. Wheat is estimated to supply nearly half the Se utilised by most Australians. Increasing the Se content of wheat represents a food systems approach that would increase population intake, with consequent probable improvement in public health and large health cost savings. The strategies that show most promise to achieve this are biofortification by Se fertilisation and breeding wheat varieties that are more efficient at increasing grain Se density. Research is needed in Australia to determine the most cost-effective fertilisation methods, and to determine the extent of genetic variability for grain Se accumulation. Before recommending large-scale fortification of the food supply with Se, it will be necessary to await the results of current intervention studies with Se on cancer, HIV and AIDS, and asthma.

During ageing, a progressive loss of muscle mass has been well described in both man and rodents. This loss of proteins results from an imbalance between protein synthesis and degradation rates. Although some authors have shown a decrease of myofibrillar protein synthesis rates in human volunteers, this imbalance is not clearly apparent when basal rates of protein turnover are measured. A decrease in muscle protein synthesis stimulation was detected nevertheless in ageing rats during the postprandial period, suggesting that the ‘meal signal’ was altered during ageing. Many results now suggest that aged muscle is less sensitive to the stimulatory effect of amino acids at physiological concentrations but is still able to respond if the increase in aminoacidaemia is sufficiently large. Indeed amino acids play an important role in regulating muscle protein turnover both in vitro and in vivo. At the molecular level, amino acids modulate gene expression. Amino acid response elements have been characterised in the promoter of transcriptional factor CCAAT-enhancer binding protein homologous protein and asparagine synthetase genes. Among amino acids, leucine seems to play the major role in regulating the metabolic function. It inhibits proteolysis and stimulates muscle protein synthesis independently of insulin. Leucine has been shown to act as a real mediator by modulating specifically the activities of intracellular kinases linked to the translation of proteins such as phosphatidylinosinol 3′ kinase and mammalian target of rapamycin–70 kDa ribosomal protein S6 (p70S6K) kinases. We recently demonstrated in vitro that protein synthesis of ageing rat muscles becomes resistant to the stimulatory effect of leucine in its physiological concentration range. However, when leucine concentration was increased greatly above its postprandial level, protein synthesis was stimulated normally. Moreover, we studied the effect of meal leucine supplementation on in vivo protein synthesis in adult and ageing rats. Leucine supplementation had no additional effect on muscle protein synthesis in adults but totally restored its stimulation in ageing rats. Whether chronic oral leucine supplementation would be beneficial for maintaining muscle protein mass in elderly men and women remains to be studied.

Since 1953, the definition of ‘dietary fibre’ (DF) has evolved significantly following an international debate based on analytical progress, new nutritional and physiological knowledge and also private interests of the food industry. The overall tendency is towards an extension of the definition by including resistant starches as well as non-digestible oligosaccharides. This broadened definition is indeed based on physiological considerations as these compounds are not digested in the small intestine and become substrates for the colonic microflora, resulting in fermentation products that have a variety of local and possibly also systemic effects. A main reluctance to use this definition, however, is linked to the difficulty to quantify, with a universal method, the various compounds that fulfil the characteristics defined by this broad definition. At this point, if such a definition were adopted, there are two options, not necessarily antagonistic, which would be (1) to sum the content of NSP, resistant starches and non-digestible oligosaccharides quantified by distinct methods or (2) to use the Association of Official Analytical Chemists (AOAC) method of DF analysis (AOAC 985.29, 991.43) with complementary analyses of the different non-digestible oligosaccharides likely to be present in the food. With none of these solutions being fully satisfying from a scientific but also from a practical point of view, an innovative method has to be proposed within the next decade. The present review describes the various types of DF, effects of DF consumption on physiology and metabolism, past and current definitions, analytical aspects to measure DF and some aspects of DF claims and food labelling.

Leptin is a 16 kDa protein synthesized and secreted primarily from adipocytes. Leptin acts centrally to regulate appetite and energy expenditure and has peripheral effects to coordinate whole-body energy metabolism. Leptin acts as an energy balance and nutrient sensor; its expression and function are regulated by endocrine and dietary factors. Leptin regulates lipid metabolism, specifically lipid storage in adipocytes as well as in skeletal muscle, liver and the pancreas. Effects of leptin on tissue lipid metabolism include regulation of lipogenesis and fatty acid oxidation. Leptin resistance is a hallmark of rodent and human obesity and appears to be due to defects in leptin-receptor signalling (proximal and perhaps distal) as well as impaired leptin transport into the brain. Dietary composition, especially dietary fatty acid intake and profile, impacts on the expression of genes encoding leptin and leptin receptors as well as downstream leptin effectors. Dietary fat consumption, especially consumption of saturated fatty acids, can induce leptin resistance. Leptin has been implicated in nutritional programming during fetal and neonatal growth with long-term effects on susceptibility to obesity, diabetes and CHD in adults.

Exercise causes a dramatic increase in energy requirements because of the metabolic needs of working muscles. Exercise-dependent factors regulate fuel use. Absolute exercise intensity determines the exercise-induced increase in energy demands, whereas exercise intensity relative to an individual's maximal aerobic capacity (VO2max) determines the proportional contribution of different fuel sources (i.e. plasma glucose, plasma fatty acids, muscle glycogen and intramuscular triacylglycerols). Endurance training increases aerobic capacity in muscle and the oxidation of fat during exercise. In addition, exercise-independent factors, such as diet composition, sex, age, and body composition also influence substrate use during exercise. The present review discusses the regulation of substrate use during exercise in human subjects, with a focus on the role of exercise-independent factors.

The link between genome instability and adverse health outcomes during the various stages of life, such as infertility, fetal development and cancer, is briefly reviewed against a background of evidence indicating that genome instability, in the absence of overt exposure to genotoxins, is itself a sensitive marker of nutritional deficiency. The latter is illustrated with cross-sectional and dietary intervention data obtained using the micronucleus assay, an efficient biomarker for diagnosing genome instability and nutritional deficiency. The concept of recommended dietary allowances for genome stability and how this could be achieved is discussed together with the emerging field of nutritional genomics for genome stability. The review concludes with a vision for a disease-prevention strategy based on the diagnosis and nutritional treatment of genome instability, i.e. ‘Genome Health Clinics’.