The stark observation of the co-existence of undernourishment, nutrient deficiencies and overweight and obesity, the triple burden of malnutrition, is inviting us to reconsider health and nutrition as the primary goal and final endpoint of food systems. Agriculture and the food industry have made remarkable advances in the past decades. However, their development has not entirely fulfilled health and nutritional needs, and moreover, they have generated substantial collateral losses in agricultural biodiversity. Simultaneously, several regions are experiencing unprecedented weather events caused by climate change and habitat depletion, in turn putting at risk global food and nutrition security. This coincidence of food crises with increasing environmental degradation suggests an urgent need for novel analyses and new paradigms. The sustainable diets concept proposes a research and policy agenda that strives towards a sustainable use of human and natural resources for food and nutrition security, highlighting the preeminent role of consumers in defining sustainable options and the importance of biodiversity in nutrition. Food systems act as complex social–ecological systems, involving multiple interactions between human and natural components. Nutritional patterns and environment structure are interconnected in a mutual dynamic of changes. The systemic nature of these interactions calls for multidimensional approaches and integrated assessment and simulation tools to guide change. This paper proposes a review and conceptual modelling framework that articulate the synergies and tradeoffs between dietary diversity, widely recognised as key for healthy diets, and agricultural biodiversity and associated ecosystem functions, crucial resilience factors to climate and global changes.

This review considers evidence for a protective effect of PUFA on chronic disease. Estimates of PUFA intakes in prospective cohort studies are usually based on FFQ or biomarkers of intake. Cohort studies suggest that both linoleic and linolenic acid intake are associated with a lower risk of CHD. The intake of fish, the major source of long-chain n-3 PUFA is associated with a lower risk of both stroke and CHD, particularly sudden cardiac death. No relationship with common sites of cancer (breast and colon) and PUFA has been found. However, some recent studies suggest an association of high intakes of n-3 PUFA with risk of prostate cancer. An updated Cochrane review of dietary fat modification (replacing SFA with PUFA) randomised controlled trials to prevent CHD found a 14 % lower incidence and a non-significant 7 % lower mortality from CHD. The effects of an increased intake of n-3 PUFA on CHD incidence mortality have been tested in patients with pre-existing CHD in randomised controlled trials. Meta-analysis of these trials showed no overall benefit on total mortality or CVD incidence but a trend for lower risk of cardiac death was 0·91 (95 % CI 0·85, 0·98). At present, there is little evidence from other trials demonstrating the clear benefits or harm from increased intakes of PUFA. In conclusion, present evidence intakes benefit from partial replacement of SFA with a balanced mixture of n-6 and n-3 PUFA which may contribute to CVD prevention.

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.

Physical inactivity is an important risk factor for many chronic diseases and contributes to obesity and poor mental well-being. The present paper describes the main advantages and disadvantages, practical problems, suggested uses, and future developments regarding self-reported and objective data collection in the context of dietary surveys. In dietary surveys, physical activity is measured primarily to estimate energy expenditure. Energy expenditure surveillance is important for tracking changes over time, particularly given the debates over the role of the relative importance of energy intake and expenditure changes in the aetiology of obesity. It is also important to assess the extent of underreporting of dietary intake in these surveys. Physical activity data collected should include details on the frequency, duration and relative intensity of activity for each activity type that contributes considerably to overall activity and energy expenditure. Problems of validity and reliability, associated with inaccurate assessment, recall bias, and social desirability bias, are well-known; children under 10 years cannot report their activities accurately. However, despite such limitations, questionnaires are still the dominant method of physical activity assessment in dietary surveys due to their low cost and relatively low participant burden. Objective, time-stamped measures that monitor heart rate and/or movement can provide more comprehensive, quantitative assessment of physical activity but at greater cost and participant burden. Although overcoming many limitations of questionnaires, objective measures also have drawbacks, including technical, practical and interpretational issues.

After having participated in a weight loss trial, most participants do not stabilise the obtained weight loss but return to their initial weight. The aim of this review is to describe the main determinants of continued low weight status after weight loss, and the effectiveness of physical activity (PA), energy restriction and macronutrient composition of the diet for low long-term weight regain. Studies with intervention periods of at least 3 months duration of weight reduction measures and a follow-up at least 2 years after the intervention period were considered as eligible for the review. Owing to limited data, the studies describing the role of PA in weight management were eligible with a follow-up of 1 year only. It appears that a diet with self-regulation of dietary intake seems to be given a prominent role in the strategy of successful long-term weight loss among the obese. This measure could be combined with behaviour therapy and PA and tailored to the individual situation. However, considering available evidence it is difficult to conclude regarding unambiguous measures and to recommend a specific dietary intervention. Nevertheless, interventions should be effective in promoting intrinsic motivation and self-efficacy. The harmonisation and standardisation of data collection in the follow-up period of long-term weight loss studies is a major challenge.

Epidemiological studies fairly convincingly suggest that higher intakes of fatty fish and n-3 fatty acids are associated with reduced risk of Alzheimer's disease (AD). DHA in plasma is normally positively associated with DHA intake. However, despite being associated with lower fish and DHA intake, unexpectedly, plasma (or brain) DHA is frequently not lower in AD. This review will highlight some metabolic and physiological factors such as ageing and apoE polymorphism that influence DHA homeostasis. Compared with young adults, blood DHA is often slightly but significantly higher in older adults without any age-related cognitive decline. Higher plasma DHA in older adults could be a sign that their fish or DHA intake is higher. However, our supplementation and carbon-13 tracer studies also show that DHA metabolism, e.g. transit through the plasma, apparent retroconversion and β-oxidation, is altered in healthy older compared with healthy young adults. ApoE4 increases the risk of AD, possibly in part because it too changes DHA homeostasis. Therefore, independent of differences in fish intake, changing DHA homeostasis may tend to obscure the relationship between DHA intake and plasma DHA which, in turn, may contribute to making older adults more susceptible to cognitive decline despite older adults having similar or sometimes higher plasma DHA than in younger adults. In conclusion, recent development of new tools such as isotopically labelled DHA to study DHA metabolism in human subjects highlights some promising avenues to evaluate how and why DHA metabolism changes during ageing and AD.

The prevention of childhood obesity is a global priority. However, a range of complex social and environmental influences is implicated in the development of obesity and chronic disease that goes beyond the notion of individual choice. A population-level approach recognises the importance of access to and availability of healthy foods outside the home. These external food environments, in restaurants, supermarkets, and in school, or recreation and sports settings, are often characterised by energy dense, nutrient-poor food items that do not reflect the current nutritional guidelines for health. In addition, our understanding of these broader influences on nutritional intake is still limited. Particularly, lacking is a clear understanding of what constitutes the food environment, as well as robust measures of components of the food environment across different contexts. Therefore, this review summarises the literature on food environments of relevance to childhood obesity prevention, with a focus on places where children live, learn and play. Specifically, the paper highlights the approaches and challenges related to defining and measuring the food environment, discusses the aspects of the food environment unique to children and reports on environmental characteristics that are being modified within community, school and recreational settings. Results of the review show the need for a continued focus on understanding the intersection between individual behaviour and external factors; improved instrument development, especially regarding validity and reliability; clearer reported methodology including protocols for instrument use and data management; and considering novel study design approaches that are targeted at measuring the relationship between the individual and their food environment.

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.

Obesity in childhood is a very common disorder with an increasing prevalence. It is one of the most serious public health challenges. The objectives of the present paper are to increase the awareness of the problem of obesity in childhood, its serious complications and the need for prevention. Overweight and obese children are likely to remain obese into adulthood and more likely to develop serious complications including health problems such as diabetes and CVD, as well as psychological and social challenges. Overweight and obesity are largely preventable. In adults it is difficult to reduce excessive weight gain once it has become established, thus children should be considered the priority population for intervention strategies and prevention. Nutrition, exercise, weight gain in infancy, genetic and environmental factors, all contribute to the aetiology. Prevention and treatment of obesity in childhood requires education and empowerment of families relating to diet and exercise, along with the regulation and control of food marketing and clear nutritional labelling. The eating and physical activity behaviour of a child is strongly influenced by environmental and social factors. Therefore treatment will have only limited success in an environment where adequate physical activity is inhibited and the consumption of high-energy food is stimulated. Government investment in a health promotion programme addressing the issue of obesity in the population as a whole, with particular emphasis on the prevention and management of obesity in childhood is vital. The family doctor and multidisciplinary team play an important role. Regular visits to the family doctor, including growth assessment, will help motivate the family to restrict energy intake and to increase exercise. Therefore the prevention of childhood obesity needs high priority.

Research on healthy ageing lacks an agreed conceptual framework and has not adequately taken into account the growing evidence that social and biological factors from early life onwards affect later health. We conceptualise healthy ageing within a life-course framework, separating healthy biological ageing (in terms of optimal physical and cognitive functioning, delaying the onset of chronic diseases, and extending length of life for as long as possible) from changes in psychological and social wellbeing. We summarise the findings of a review of healthy ageing indicators, focusing on objective measures of physical capability, such as tests of grip strength, walking speed, chair rises and standing balance, which aim to capture physical functioning at the individual level, assessing the capacity to undertake the physical tasks of daily living. There is robust evidence that higher scores on these measures are associated with lower rates of mortality, and more limited evidence of lower risk of morbidity, and of age-related patterns of change. Drawing on a research collaboration of UK cohort studies, we summarise what is known about the influences on physical capability in terms of lifetime socioeconomic position, body size and lifestyle, and underlying physiology and genetics; the evidence to date supports a broad set of factors already identified as risk factors for chronic diseases. We identify a need for larger longitudinal studies to investigate age-related change and ethnic diversity in these objective measures, the dynamic relationships between them, and how they relate to other component measures of healthy ageing. Robust evidence across cohort studies, using standardised measures within a clear conceptual framework, will benefit policy and practice to promote healthy ageing.

Ageing is a complex multifactorial process, reflecting the progression of all degenerative pathways within an organism. Due to the increase of life expectancy, in recent years, there is a pressing need to identify early-life events and risk factors that determine health outcomes in later life. So far, genetic variation only explains ~20–25 % of the variability of human survival to age 80+. This clearly implies that other factors (environmental, epigenetic and lifestyle) contribute to lifespan and the rate of healthy ageing within an individual. Twin studies in the past two decades proved to be a very powerful tool to discriminate the genetic from the environmental component. The aim of this review is to describe the basic concepts of the twin study design and to report some of the latest studies in which high-throughput technologies (e.g. genome/epigenome-wide assay, next generation sequencing, MS metabolic profiling) combined with the classical twin design have been applied to the analysis of novel ‘omics’ to further understand the molecular mechanisms of human ageing.

Milk, meat and eggs tend not to be regarded as an important source of PUFA. They are disproportionally high in SFA compared with their PUFA content, especially those from cattle and sheep, since their rumen microbes are responsible for the loss of over 90 % of PUFA intake by livestock. This need not necessarily be the case since the relative proportion of PUFA in these foods is dictated by livestock management, especially feeding, and this can be manipulated to boost their content of crucial long-chain n-3 fatty acids and conjugated linoleic fatty acids. The present paper considers the fatty acid composition in animal-derived foods and how these can be manipulated to be more conducive for consumers’ health. The importance of recognising the effect of livestock production systems on fat composition is also highlighted along with the fact that we may have to compromise between intensive, high levels of production and this particular aspect of food quality.

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.