The aim of the present paper is to give a brief overview on the role of dietary fat in carcinogenesis and as possible anticancer agents. Dietary fat is an essential nutrient and important source for the essential fatty acids (FA), linoleic and α-linolenic acids, which contribute to proper growth and development. However, dietary fat has been associated with the development of colorectal, breast, prostate, endometrial and ovarian cancers, with the type and quality of fat playing an underlying role. Tumour growth is the disruption of the homoeostatic balance regulating cell differentiation, proliferation and apoptosis and is associated with altered lipid metabolism. Animal cancer models and human cancer biopsy tissue demonstrate that a characteristic lipid profile is associated with the growth and development of neoplastic lesions. This entails alterations in membrane cholesterol, phospholipid and PUFA metabolism. Particularly, alterations in cell membrane FA metabolism involving the n-6 and n-3 PUFA, are associated with changes in membrane structure, function, cellular oxidative status, activity of enzymes and signalling pathways. These events are a driving force in sustaining the altered growth of cancerous lesions and provide unique targets for intervention/cancer modulation. Challenges in utilising FA in cancer modulation exist regarding intake and effect on cell structure and biochemical interactions within the cell in the prevention of cancer development. Therefore, utilising dietary PUFA in a specific n-6:n-3 ratio may be an important chemopreventive tool in altering the growth characteristics of cancer cells.

Eating more seasonal food is one proposal for moving towards more sustainable consumption patterns, based on the assumption that it could reduce the environmental impact of the diet. The aim of the present paper is to consider the implications of eating seasonal food on the different elements of sustainability (i.e. health, economics, society), not just the environment. Seasonality can be defined as either globally seasonal (i.e. produced in the natural production season but consumed anywhere in the world) or locally seasonal (i.e. produced in the natural production season and consumed within the same climatic zone). The environmental, health, economic and societal impact varies by the definition used. Global seasonality has the nutritional benefit of providing a more varied and consistent supply of fresh produce year round, but this increases demand for foods that in turn can have a high environmental cost in the country of production (e.g. water stress, land use change with loss of biodiversity). Greenhouse gas emissions of globally seasonal food are not necessarily higher than food produced locally as it depends more on the production system used than transportation. Eating more seasonal food, however, is only one element of a sustainable diet and should not overshadow some of the potentially more difficult dietary behaviours to change that could have greater environmental and health benefits (e.g. reducing overconsumption or meat consumption). For future guidelines for sustainable diets to be realistic they will need to take into account modern lifestyles, cultural and social expectations in the current food environment.

Health benefits or advocated health benefits of long-chain (LC) n-3 PUFA are better known by medical doctors as well as by consumers, so that consumption increases. In addition, the development of aquaculture requires more fishmeal and fish oil. Humanisation of care of companion animals is also associated with addition of LC n-3 PUFA in pet foods. The risk of the increased demand for LC n-3 PUFA is the excess harvesting of natural sources, especially of marine origin (oily fishes, krill). In order to improve sustainability, alternative sources of LC n-3 PUFA have been developed. These alternative sources are: (a) terrestrial plants naturally or genetically enriched in stearidonic acid (SDA), which bypasses the first limiting step of (i.e. ∆6 desaturase) of the biosynthesis of LC n-3 PUFA; (b) single-cell oils rich in LC n-3 PUFA (microalgae, Escherichia coli) and krill. Currently, plants rich in SDA are expensive, metabolic engineering is unfavourably accepted by consumers in many countries, cultivation of microalgae is very expensive even though their ability (for some of them) to synthesise biofuels could induce a decrease in industrial costs, and Antarctic krill harvest must be restricted. Thus, it is difficult to predict their real development in the future.

The aim of the present paper is to review nutrition transition (NT) ongoing in low and middle income countries and the associated dietary changes. NT is accompanied by demographic and epidemiological transition associated with economic development and urbanisation. In these countries, while the problems of hunger and undernourishment persist, there is an escalation of diet-related non-communicable diseases; making them face both problems of malnutrition, under and overnutrition. Indeed, in addition to protein energy malnutrition underweight and micronutrient deficiencies affect a high proportion of children and women. Conversely, changes in dietary habits and physical activity patterns have led to emergence of chronic diseases such as obesity, diabetes, hypertension, stroke, hyperlipidaemia, CHD and cancer. One possible explanation of weight gain and its associated health consequences is the trend of the consumption of already prepared meals and the restaurants that are in continuous development leading to high consumption of foods rich in sugar and fat. The health problems associated with NT have not spared populations in the Mediterranean area where the type of diet is reported to be healthy and to protect against cardiovascular risks. This is seen in North Africa that belongs also to the Mediterranean basin, where the nutritional situation raises the problem of traditional foods sustainability. Accurate nutritional policy and education are needed to redress the effects of malnutrition related to NT on health.

The worldwide prevalence of overweight and obesity in the adult population is estimated to be 35 %. These trends are reflected in childhood obesity prevalence, and the potential impact of early-onset obesity is of great concern. The aim of this review was to investigate the long-term implications of childhood obesity for metabolic and cardiovascular health, focusing on the independent contribution of childhood obesity to adult disease risk, as distinct from associations mediated by tracking of obesity across the lifespan. The data systematically reviewed provide little evidence to suggest that childhood overweight and obesity are independent risk factors for metabolic and cardiovascular risk during adulthood. Instead, the data demonstrate that the relationships observed are dependent on tracking of BMI between childhood and adulthood, alongside persistence of dietary patterns and physical activity. Adjustment for adult BMI uncovers unexpected negative associations between childhood BMI and adult disease, suggesting a protective effect of childhood obesity at any given level of adult BMI. Further work is required to explain these findings, both in terms of pathways and statistical artefacts. To conclude, it must be stressed that it is not suggested that childhood obesity is without negative consequence. Childhood obesity is clearly associated with a range of adverse physical and psychological outcomes. However, the data are important in supporting a positive message that the long-term consequences of childhood obesity are avoidable; and that there remains opportunity for intervention across the lifespan. This nuance in understanding long-term risk is important when considering the effectiveness of interventions at different stages of the lifespan.

Childhood obesity is of concern worldwide. The portion size (PS) and energy density (ED) of food are two major determinants of children's energy intake (EI). Trends towards increasing PS are most apparent and best documented in the USA, where PS of numerous food products have increased in the marketplace over the past three decades, particularly high-energy dense foods. Analyses of population-level dietary surveys have confirmed this trend in children for both in- and out-of-home eating, and a plethora of observational evidence positively associates PS, ED and adiposity in children. A limited number of intervention studies provide clear evidence that children, even as young as 2 years, respond acutely to increasing PS, with some studies also demonstrating the additive effects of increased ED in promoting excessive EI. However, most of the evidence is based on children aged 3–6 years and there is a paucity of data in older children and adolescents. It is unclear whether decreasing PS can have the opposite effect on children's EI but recent acute studies have demonstrated that the incorporation of lower energy dense foods, such as fruit and vegetables, into children's meals down-regulates EI. Although a direct causal link between PS and obesity remains to be established, the regular consumption of larger PS of energy dense foods do favour obesity-promoting eating behaviours in children. Further research is required to establish the most feasible and effective interventions and policies to counteract the deleterious impact of PS and ED on children's EI.

Alarmed by the sustainability of our health and social security systems, longevity has become a great societal challenge. In line with evolutionary logic we see a continuous increase of average life expectancy and maximal lifespan. Striving for a healthy old age, however, is an infelicitous expression as for human subjects the ageing process cannot be ultimately postponed. Not disregarding the huge variation in health trajectories, in old age we will all suffer from frailty and infirmity. As yet efforts of the biomedical arena are almost exclusively focused on stalling the ageing process and preventing dysfunction. Too little effort is spend on how to inspire and coach the great majority of people who still feel relatively well notwithstanding the presence of multiple age-related disorders. There is a strong rationale to separate the quest to live in good health for longer from actively and effectively negotiating the challenge of functional decline in old age. In particular, we emphasise a focus on adjusting the environment in order to correct the gene–environment mismatch that contributes to ill health. An additional strategy is to empower people to set ambitions and to realise appropriate goals, in spite of infirmity. Striving for vitality presents a striking opportunity to achieve subjective feelings of life satisfaction when ageing.

It is well established that genotype plays an important role in the ageing process. However, recent studies have suggested that epigenetic mechanisms may also influence the onset of ageing-associated diseases and longevity. Epigenetics is defined as processes that induce heritable changes in gene expression without a change in the DNA nucleotide sequence. The major epigenetic mechanisms are DNA methylation, histone modification and non-coding RNA. Such processes are involved in the regulation of tissue-specific gene expression, cell differentiation and genomic imprinting. However, epigenetic dysregulation is frequently seen with ageing. Relatively little is known about the factors that initiate such changes. However, there is emerging evidence that the early life environment, in particular nutrition, in early life can induce long-term changes in DNA methylation resulting in an altered susceptibility to a range of ageing-associated diseases. In this review, we will focus on the changes in DNA methylation that occur during ageing; their role in the ageing process and how early life nutrition can modulate DNA methylation and influence longevity. Understanding the mechanisms by which diet in early life can influence the epigenome will be crucial for the development of preventative and intervention strategies to increase well-being in later life.

The challenge of devising a set of biomarkers capable of measuring the ageing rate in human subjects was articulated long ago. In recent years, progress in the basic biology of ageing suggests the realistic possibility of preventive or restaurative interventions that may extend healthy lifespan in mammals including human subjects. Specifically, frailty is being increasingly recognised as a clinically relevant syndrome that may be therapeutically addressed. This greatly enhances the need for sensitive and specific biomarkers of healthy ageing that are validated in both experimental animals and, importantly, in human subjects over the whole age range. Here, we will discuss the present challenges and requirements for biomarker validation in human subjects. We propose the central requirements for a validated biomarker of healthy ageing as: (i) better predictive power than chronological age for multiple dimensions of ageing; (ii) identification of the age range in which the marker is informative; (iii) establishment of sensitivity/specificity as indicators of its predictive power at the level of the individual; (iv) minimisation of methodological variation between laboratories.

Protein glycation has been studied for over a century now and plays an important role in disease pathogenesis throughout the lifecycle. Strongly related to diabetic complications, glycation of Hb has become the gold standard method for diabetes diagnosis and monitoring. It is however attracting attention in normoglycaemia as well lately. Longitudinal studies increasingly suggest a positive relationship between glycation and the risk of chronic diseases in normoglycaemic individuals, but the mechanisms behind this association remain unclear. The interaction between glycation and oxidative stress may be particularly relevant in the normoglycaemic context, as suggested by recent epidemiological and in vitro evidence. In that context nutritional and lifestyle factors with an influence on redox status, such as smoking, fruit and vegetable and antioxidants consumption, may have the capacity to promote or inhibit glycation. However, experimental data from controlled trials are lacking the quality and rigour needed to reach firm conclusions. In the present review, we discuss the importance of glycation for health through the lifecycle and focus on the importance of oxidative stress as a driver for glycation. The importance of nutrition to modulate glycation is discussed, based on the evidence available and recommendations towards higher quality future research are made.