Physical activity is one of the major non-pharmacological methods for increasing and maintaining bone mineral density (BMD) and geometry. As such, it has an important role in maintaining peak bone mass and strength, thus reducing the risk of future osteoporotic fracture. However, not all exercise is effective, so a prescription in terms of optimal type, intensity, frequency and duration is required. Studies using animal models suggest that loading that is high in magnitude, rapidly applied and novel is most effective, whilst duration is less important beyond a threshold number of cycles. In human subjects cross-sectional studies comparing different athletic populations suggest that those who participate in high- or odd-impact sports have higher BMD; whilst impact exercise, strength training and brief high-impact-jump training interventions increase BMD in premenopausal women. In order to further elucidate exercise recommendations to optimise bone health in this population, the usefulness of brief high-impact unilateral exercises has been evaluated. Brief hopping exercises were shown to be feasible for sedentary premenopausal women, producing ground-reaction forces as high as those from jumping. Regularly performing these hopping exercises over 6 months was found to increase femoral-neck BMD of the trained leg relative to the control leg. Unilateral high-impact exercise may therefore improve bone strength of the trained limb and provide a useful model for comparing exercise prescriptions to help define the most efficient and effective exercise recommendations for the bone health of premenopausal women.

It is becoming increasingly evident that (a) risk for developmental and degenerative disease increases with more DNA damage, which in turn is dependent on nutritional status, and (b) the optimal concentration of micronutrients for prevention of genome damage is also dependent on genetic polymorphisms that alter the function of genes involved directly or indirectly in the uptake and metabolism of micronutrients required for DNA repair and DNA replication. The development of dietary patterns, functional foods and supplements that are designed to improve genome-health maintenance in individuals with specific genetic backgrounds may provide an important contribution to an optimum health strategy based on the diagnosis and individualised nutritional prevention of genome damage, i.e. genome health clinics. The present review summarises some of the recent knowledge relating to micronutrients that are associated with chromosomal stability and provides some initial insights into the likely nutritional factors that may be expected to have an impact on the maintenance of telomeres. It is evident that developing effective strategies for defining nutrient doses and combinations or ‘nutriomes’ for genome-health maintenance at the individual level is essential for further progress in this research field.

Dietary n-3 PUFA have many beneficial effects on cell and tissue function and on human health. In mammals the n-3 essential fatty acid α-linolenic acid (ALNA) can be converted into longer-chain (LC) n-3 PUFA such as EPA and DHA via a series of desaturase and elongase enzymes that are mainly active in the liver. Human studies have identified that males and females appear to differ in their ability to synthesise EPA and DHA from ALNA, with associated differences in circulating concentrations. Based on studies of women using the contraceptive pill or hormone-replacement therapy and of trans-sexual subjects it is suggested that sex hormones play a role in these differences. The rat has been used to investigate gender differences in n-3 PUFA status since this model allows greater dietary control than is possible in human subjects. Like human subjects, female rats have higher plasma DHA concentrations than males. Rats also respond to increased dietary ALNA in a way that is comparable with available human data. The concentrations of LC n-3 PUFA in rat plasma and tissues are positively associated with circulating concentrations of oestradiol and progesterone and negatively associated with circulating concentrations of testosterone. These findings suggest that sex hormones act to modify plasma and tissue n-3 PUFA content, possibly by altering the expression of desaturase and elongase enzymes in the liver, which is currently under investigation.

Advances in the understanding of appetite are leading to a refined concept of disease cachexia and point to novel therapeutic strategies based on the manipulation of appetite. The complex social and psychological short-term influences on appetite obscure the fact that over the longer term appetite is tightly regulated by physiological considerations; the homeostatic control of energy balance. Like obesity, which is now viewed as a disorder of homeostasis, cachexia can be seen as an adaptive response to the disease state that becomes harmful when prolonged. Several lines of evidence implicate a disorder of appetite regulation in the pathogenesis of cachexia. As the only known circulating mediator of increased appetite the peptide hormone ghrelin has attracted attention as a potential therapy. Trials in patients with various chronic illnesses, including cancer and kidney failure, have demonstrated short-term increases in energy intake. Trials in patients with emphysema and heart failure have also shown benefits in clinical outcomes such as lean body mass and exercise capacity, and longer-term trials using oral analogues are being undertaken. As well as improving nutrition, ghrelin has a number of other actions that may be useful, including an anti-inflammatory effect; of interest since many cachexias are associated with inappropriate immune activation. The manipulation of appetite, in particular by ghrelin agonism, is emerging as an exciting potential therapy for disease cachexia. Future research should focus on the ascertainment of clinically-relevant outcomes, and further characterisation of the non-nutritional effects of this pathway.

Childhood obesity has multiple causes, most of them capable of explaining only one part of the problem. The population-wide impact of sedentary lifestyles and availability of energy-dense food is undeniable, but substantial individual differences in body weight persist, suggesting that individuals respond differently to the ‘obesogenic’ environment. One plausible mechanism for this variation is the early expression of appetitive traits, including low responsiveness to internal satiety signals, high responsiveness to external food cues, high subjective reward experienced when eating liked foods and preferences for energy-dense foods. Case–control studies support the existence of abnormalities in these traits among obese children compared with normal-weight children, and correlations between psychometric measures of child appetite and child weight suggest that appetitive trait profiles may not only promote obesity but also protect against it. The origins of appetitive traits are as yet uncharted, but will include both genetic and environmental influences. Parental feeding style may affect the development of appetite but the exact nature of the relevant behaviours is unclear and many studies are cross-sectional or begin late in childhood, obscuring causal relationships. Future research should explore determinants and biological mechanisms by using prospective designs beginning early in life, measuring relevant biomarkers such as gut hormones and incorporating neuroimaging and genotyping technologies. Potential clinical applications include the identification of ‘at risk’ children early in life and interventions to modify appetitive traits or ameliorate their impact on intake and weight.

Nasogastric enteral feeding is not tolerated in patients with gastric atony and in many critically-ill patients in whom gastric emptying may be delayed and in whom gastro-oesophageal regurgitation may lead to pulmonary aspiration of enteral feed and the development of pneumonia. Initial attempts to overcome these problems led to the development of post pyloric enteral feeding techniques with the infusion port of the tubes positioned in the duodenum. In many centres this technique is still the most practised post-pyloric enteral feeding technique. Nasoduodenal feeding tubes often retroperistalse into the stomach. The technique of choice, therefore, in these difficult patients is to position the infusion port of the feeding tube well distal to the ligament of trietz (post ligament of trietz nasojejunal enteral tube feeding). While nasogastric and nasoduodenal enteral feeding techniques have been shown to elicit a stimulatory exocrine pancreatic response, distal jejunal enteral feeding does not. During this mode of feeding the ileal brake is activated and pancreatic exocrine pancreatic secretion inhibited by the action of the released peptide YY and glucagon-like peptide-1 hormones, in turn the inhibition of pancreatic secretion being the result of inhibition of trypsin secretion. In the light of the findings showing the absence of a stimulatory pancreatic exocrine response to nasojejunal enteral feeding these patients should receive a predigested rather than a polymeric enteral diet.