Epigenetic changes may be causal in the ageing process and may be influenced by diet, providing opportunities to improve health in later life. The aim of this review is to provide an overview of several areas of research relevant to this topic and to explore a hypothesis relating to a possible role of epigenetic effects, mediated by sirtuin 1, in the beneficial effects of dietary restriction, including increased lifespan. Epigenetic features of ageing include changes in DNA methylation, both globally and at specific loci, which differ between individuals. A major focus of research on dietary influences on epigenetic status has been on nutrition in utero, because the epigenome is probably particularly malleable during this life-course window and because epigenetic marking by early exposures is a compelling mechanism underlying effects on lifelong health. We explore the potential of diet during adulthood, including the practice of dietary restriction, to affect the epigenetic architecture. We report progress with respect to deriving data to support our hypothesis that sirtuin 1 may mediate some of the effects of dietary restriction through effects on DNA methylation and note observations that resveratrol affects DNA methylation and other epigenetic features. Disentangling cause and effect in the context of epigenetic change and ageing is a challenge and requires better understanding of the underlying mechanisms and also the development of more refined experimental tools to manipulate the epigenetic architecture, to facilitate hypothesis-driven research to elucidate these links and thus to exploit them to improve health across the full life-course through dietary measures.

The recent rise in the prevalence of obesity in the UK population includes women of reproductive age and children. For both groups there are specific health concerns consequent on excess bodyweight, including obstetric complications, fetal growth abnormalities and a range of obesity co-morbidities seen in children that were rarely found in young people a generation earlier. This paper identifies some of the issues which challenge policy-makers: guidelines for gestational weight gain and for weight loss after pregnancy; inequalities and interventions in pregnancy; interventions to prevent child obesity; and the role of individuals, government and the commercial sector in implementing policies for promoting healthy weight.

Ageing is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk for developing chronic metabolic diseases such as diabetes. The age-related loss of skeletal muscle mass results from a chronic disruption in the balance between muscle protein synthesis and degradation. As basal muscle protein synthesis rates are likely not different between healthy young and elderly human subjects, it was proposed that muscles from older adults lack the ability to regulate the protein synthetic response to anabolic stimuli, such as food intake and physical activity. Indeed, the dose–response relationship between myofibrillar protein synthesis and the availability of essential amino acids and/or resistance exercise intensity is shifted down and to the right in elderly human subjects. This so-called ‘anabolic resistance’ represents a key factor responsible for the age-related decline in skeletal muscle mass. Interestingly, long-term resistance exercise training is effective as a therapeutic intervention to augment skeletal muscle mass, and improves functional performance in the elderly. The consumption of different types of proteins, i.e. protein hydrolysates, can have different stimulatory effects on muscle protein synthesis in the elderly, which may be due to their higher rate of digestion and absorption. Current research aims to elucidate the interactions between nutrition, exercise and the skeletal muscle adaptive response that will define more effective strategies to maximise the therapeutic benefits of lifestyle interventions in the elderly.

Epidemiological and animal studies have demonstrated that early-life nutrition alters the metabolic responses and generates structural changes in complex tissues, such as the kidneys, which may lead to a reduction in the offspring lifespan. Independently, obesity induces a spontaneous low-grade chronic inflammatory response by modulating several of the major metabolic pathways that ultimately compromise long-term renal health. However, the combined effects of maternal nutrition and early-life obesity in the development of renal diseases are far from conclusive. Previous results, using the ovine model, demonstrated that the combination of a reduction in fetal nutrition and juvenile obesity induced a series of adaptations associated with severe metabolic syndrome in the heart and adipose tissue. Surprisingly, exposure to an obesogenic environment in the kidney of those offspring produced an apparent reduction in glomerulosclerosis in relation to age- and weight-matched controls. However, this reduction in cellular apoptosis was accompanied by a rise in glomerular filtration rate and blood pressure of equal intensity when compared with obese controls. The intention of this review is to explain the adaptive responses observed in this model, based on insights into the mechanism of renal fetal programming, and their potential interactions with some of the metabolic changes produced by obesity.

Kiwifruit is a good source of several vitamins and minerals and dietary fibre, and contains a number of phytochemicals; so kiwifruit potentially provides health benefits beyond basic nutrition. Consumption of green kiwifruit can have positive effects on cardiovascular health through antioxidant activity, inhibition of platelet aggregation and lowered TAG levels, and gut health through improving laxation, aiding digestion and promoting a healthy gut microflora. The importance of nutrition on immune function is well recognised, with deficiencies in vitamins A, C, E, B6 and B12, folic acid, Zn, Cu, Fe and Se being associated with impaired immune function and increased susceptibility to diseases. Evidence is growing that kiwifruit enhances immunity, with several small murine studies showing enhancement of innate and adaptive immune function. Few studies have examined the effect of kiwifruit on immune function in human subjects, but a recent study has revealed that kiwifruit up-regulates several ‘immune’ and ‘DNA and repair’-related gene sets, and down-regulates one gene set related to Ig secretion. Taken together, the evidence from the literature provides supporting data for designing a human intervention trial to validate the ability of kiwifruit to support immune function in healthy and immunocompromised populations.

The prevalence of obesity is high in older persons and recent trends show a rapid increase in this prevalence. Results from observational and intervention studies (i.e. weight loss studies) show the strong negative impact of obesity on functional status in old age. There are different potential pathways through which obesity may lead to functional decline in older persons. Furthermore, the presence of overweight and obesity during the life course and trends in medical care are likely to influence the impact of obesity on disability. The concepts sarcopenia (age-related loss of muscle mass) and dynapenia (age-related loss of muscle strength) receive a lot of research attention as potential determinants of functional decline in old age. There is no consensus on the definitions of these concepts. Recent studies conducted in large cohort studies of mainly community-dwelling older persons show that poor muscle strength is strongly associated with functional decline compared to low muscle mass. In several studies, no association between muscle mass and functional status was observed. Current research on the combination of obesity with poor muscle strength (dynapenic-obesity) suggests a potential additive effect of both components on poor functional status in old age which seems independent of the level of physical activity.

Despite extensive research it has proved difficult to establish the role of diet in the aetiology of common types of cancer. Obesity and alcohol definitely increase the risk for several types of cancer, but the importance of particular foods and nutrients is not clear. Part of the difficulty is our poor understanding of the physiological changes that might mediate the effect of diet on cancer risk. Recent research in prospective studies with biobanks of stored blood samples has shown that the serum concentration of insulin-like growth factor-1 (IGF-1) is positively associated with the risk for both breast cancer in women and prostate cancer in men. It is also known that circulating IGF-1 concentrations can change in response to nutritional changes including energy and protein restriction, and some studies suggest that, even within well-nourished western populations, men and women with relatively high intakes of protein from dairy products have higher blood levels of IGF-1. These observations have led to the hypothesis that high intakes of protein from dairy products might increase the risk for some cancers by increasing the endogenous production of IGF-1. Further evaluation of this hypothesis requires clinical nutritional studies of the effects of diet on IGF-1 metabolism, and large epidemiological studies of cancer risk incorporating reliable measures of diet and serum IGF-1 concentrations.