In the 1960s, the thesis that dietary cholesterol contributes to blood cholesterol and heart disease risk was a rational conclusion based on the available science at that time. Fifty years later the research evidence no longer supports this hypothesis yet changing the dietary recommendation to limit dietary cholesterol has been a slow and at times contentious process. The preponderance of the clinical and epidemiological data accumulated since the original dietary cholesterol restrictions were formulated indicate that: (1) dietary cholesterol has a small effect on the plasma cholesterol levels with an increase in the cholesterol content of the LDL particle and an increase in HDL cholesterol, with little effect on the LDL:HDL ratio, a significant indicator of heart disease risk, and (2) the lack of a significant relationship between cholesterol intake and heart disease incidence reported from numerous epidemiological surveys. Over the last decade, many countries and health promotion groups have modified their dietary recommendations to reflect the current evidence and to address a now recognised negative consequence of ineffective dietary cholesterol restrictions (such as inadequate choline intake). In contrast, health promotion groups in some countries appear to suffer from cognitive dissonance and continue to promote an outdated and potentially hazardous dietary recommendation based on an invalidated hypothesis. This review evaluates the evidence for and against dietary cholesterol restrictions and the potential consequences of such restrictions.

Carbohydrate-rich foods are an essential component of the diet, providing the glucose that is continuously required by the nervous system and some other cells and tissues in the body for normal function. There is some concern that too much carbohydrate or certain types of carbohydrate such as fructose or the high glycaemic index carbohydrate foods that produce large, rapid increases in blood glucose may be detrimental to health. This review considers these issues and also summarises the public health advice currently available in Europe and the USA concerning dietary carbohydrates. The UK Scientific Advisory Committee on Nutrition is currently reviewing carbohydrates and health, and the subsequent report should help clarify some of the concerns regarding carbohydrates and health.

The human gut microbiota has been identified as a possible novel CVD risk factor. This review aims to summarise recent insights connecting human gut microbiome activities with CVD and how such activities may be modulated by diet. Aberrant gut microbiota profiles have been associated with obesity, type 1 and type 2 diabetes and non-alcoholic fatty liver disease. Transfer of microbiota from obese animals induces metabolic disease and obesity in germ-free animals. Conversely, transfer of pathogen-free microbiota from lean healthy human donors to patients with metabolic disease can increase insulin sensitivity. Not only are aberrant microbiota profiles associated with metabolic disease, but the flux of metabolites derived from gut microbial metabolism of choline, phosphatidylcholine and l-carnitine has been shown to contribute directly to CVD pathology, providing one explanation for increased disease risk of eating too much red meat. Diet, especially high intake of fermentable fibres and plant polyphenols, appears to regulate microbial activities within the gut, supporting regulatory guidelines encouraging increased consumption of whole-plant foods (fruit, vegetables and whole-grain cereals), and providing the scientific rationale for the design of efficacious prebiotics. Similarly, recent human studies with carefully selected probiotic strains show that ingestion of viable microorganisms with the ability to hydrolyse bile salts can lower blood cholesterol, a recognised risk factor in CVD. Taken together such observations raise the intriguing possibility that gut microbiome modulation by whole-plant foods, probiotics and prebiotics may be at the base of healthy eating pyramids advised by regulatory agencies across the globe. In conclusion, dietary strategies which modulate the gut microbiota or their metabolic activities are emerging as efficacious tools for reducing CVD risk and indicate that indeed, the way to a healthy heart may be through a healthy gut microbiota.

DHA is an abundant nutrient from marine lipids: its specific biological effects have been investigated in human volunteers, taking into consideration the dose effects. We report herein that, at dosages below 1 g/d, DHA proved to be effective in lowering blood platelet function and exhibited an ‘antioxidant’ effect. However, this was no longer the case following 1·6 g/d, showing then a U-shape response. The antioxidant effect has been observed in platelets as well as LDL, of which the redox status is assumed to be crucial in their relationship with atherosclerosis. Second, the oxygenated products of DHA, especially protectins produced by lipoxygenases, have been considered for their potential to affect blood platelets and leucocytes. It is concluded that DHA is an interesting nutrient to reduce atherothrombogenesis, possibly through complementary mechanisms involving lipoxygenase products of DHA.

Childhood obesity is an issue of public health concern globally. This review reports on levels of overweight and obesity in Irish children and examines some aspects of their diet and lifestyle proposed to promote or protect against increasing body fatness in children. While there is still some debate with regard to the most appropriate cut-off points to use when assessing body fatness in children, approximately one in five Irish children (aged 2–17 years) have been classified as overweight (including obese) according to two generally accepted approaches. Furthermore, comparison with previous data has shown an increase in mean body weight and BMI over time. On examining dietary patterns for Irish children, there was a noticeable transition from a less energy dense diet in pre-school children to a more energy dense diet in older children and teenagers, associated with a change to less favourable dietary intakes for fibre, fat, fruit and vegetables, confectionery and snacks and sugar-sweetened beverages as children got older. A significant proportion of school-aged children and teenagers reported watching more than 2 h television per day (35 % on school-days and 65 % on week-ends) compared with 13 % of pre-school children. For children aged 5–12 years, eating out of the home contributed just 9 % of energy intake but food eaten from outside the home was shown to contribute a higher proportion of energy from fat and to be less fibre-dense than food prepared at home. Improvements in dietary lifestyle are needed to control increasing levels of overweight and obesity in children in Ireland.

Assessing dietary intake in people of any age is challenging but measuring the diet of infants and children can be particularly problematic. Young children may lack the cognitive skills, writing skills and food knowledge to record their own food intake. Multiple people may be responsible for the care of the child and to collect an accurate picture of intake it may be necessary to combine parental reports with observation in school or nursery. Where interviews are conducted with the child themselves questions may need to focus on aspects of the diet which children are likely to attend to. For example, children may not be familiar with food names or brands but may be able to describe their texture, colour and images on packaging. Adolescents are likely to be more aware of the foods they consume and have the cognitive and writing skills to record their own food intake but may lack the interest or motivation. Research has focused on reducing the burden of recording intake on the participant. Developments include food photographs for assessment of portion size which remove the need for weighing each food item, and, in recent years, computer-based methods have been developed for self-completion by young people with the aim of motivating them to participate in studies by making dietary reporting more engaging. The present paper discusses methods and challenges in assessing food intake in children followed by details of two such tools developed at Newcastle University, UK, the Young Person's Food Atlas and INTAKE24.

The dramatic rise in childhood obesity has driven the demand for tools better able to assess and define obesity and risk for related co-morbidities. In addition, the early life origins of non-communicable diseases including type 2 diabetes are associated with subtle alterations in growth and body composition, including total and regional body fatness, limb/trunk length and skeletal muscle mass (SMM). Consequently improved tools based on national reference data, which capture these body components must be developed as the limitations of BMI as a measure of overweight and obesity and associated cardiometabolic risk are now recognised. Furthermore, waist circumference as a measure of abdominal fatness in children is now endorsed by the International Diabetes Federation and National Institute for Clinical and Health Excellence for diagnostic and monitoring purposes. The present paper aims to review the research on growth-related variations in body composition and proportions, together with how national references for percentage body fat, SMM and leg/trunk length have been developed. Where collection of these measures is not possible, alternative proxy measures including thigh and hip circumferences are suggested. Finally, body ratios including the waist:height and muscle:fat ratios are highlighted as potential measures of cardiometabolic disease risk. In conclusion, a collection of national references for individual body measures have been produced against which children and youths can be assessed. Collectively, they have the capacity to build a better picture of an individual's phenotype, which represents their risk for cardiometabolic disease beyond that of the capability of BMI.

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.

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.

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.

Healthy longevity is a tangible possibility for many individuals and populations, with nutritional and other lifestyle factors playing a key role in modulating the likelihood of healthy ageing. Nevertheless, studies of effects of nutrients or single foods on ageing often show inconsistent results and ignore the overall framework of dietary habits. Therefore, the use of dietary patterns (e.g. a Mediterranean dietary pattern) and the specific dietary recommendations (e.g. dietary approaches to stop hypertension, Polymeal and the American Healthy Eating Index) are becoming more widespread in promoting lifelong health. A posteriori defined dietary patterns are described frequently in relation to age-related diseases but their generalisability is often a challenge since these are developed specifically for the population under study. Conversely, the dietary guidelines are often developed based on prevention of disease or nutrient deficiency, but often less attention is paid to how well these dietary guidelines promote health outcomes. In the present paper, we provide an overview of the state of the art of dietary patterns and dietary recommendations in relation to life expectancy and the risk of age-related disorders (with emphasis on cardiometabolic diseases and cognitive outcomes). According to both a posteriori and a priori dietary patterns, some key ‘ingredients’ can be identified that are associated consistently with longevity and better cardiometabolic and cognitive health. These include high intake of fruit, vegetables, fish, (whole) grains and legumes/pulses and potatoes, whereas dietary patterns rich in red meat and sugar-rich foods have been associated with an increased risk of mortality and cardiometabolic outcomes.

Dietary restriction (DR) has been shown to extend both median and maximum lifespan in a range of animals, although recent findings suggest that these effects are not universally enjoyed across all animals. In particular, the lifespan effect following DR in mice is highly strain-specific and there is little current evidence that DR induces a positive effect on all-cause mortality in non-human primates. However, the positive effects of DR on health appear to be highly conserved across the vast majority of species, including human subjects. Despite these effects on health, it is highly unlikely that DR will become a realistic or popular life choice for most human subjects given the level of restraint required. Consequently significant research is focusing on identifying compounds that will bestow the benefits of DR without the obligation to adhere to stringent reductions in daily food intake. Several such compounds, including rapamycin, metformin and resveratrol, have been identified as potential DR mimetics. Although these compounds show significant promise, there is a need to properly understand the mechanisms through which these drugs act. This review will discuss the importance in understanding the role that genetic background and heterogeneity play in mediating the lifespan and healthspan effects of DR. It will also provide an overview of the most promising current DR mimetics and their effects on healthy lifespan.

The number of people suffering from metabolic diseases is dramatically increasing worldwide. This stresses the need for new therapeutic strategies to combat this growing epidemic of metabolic diseases. A reduced mitochondrial function is one of the characteristics of metabolic diseases and therefore a target for intervention. Here we review the evidence that mitochondrial function may act as a target to treat and prevent type 2 diabetes mellitus, and, if so, whether these effects are due to reduction in skeletal muscle fat accumulation. We describe how exercise may affect these parameters and can be beneficial for type 2 diabetes. We next focus on alternative ways to improve mitochondrial function in a non-exercise manner. Thus, in 2003, resveratrol (3,5,4′-trihydroxystilbene) was discovered to be a small molecule activator of sirtuin 1, an important molecular target regulating cellular energy metabolism and mitochondrial homoeostasis. Rodent studies have clearly demonstrated the potential of resveratrol to improve various metabolic health parameters. Here we review data in human subjects that is available on the effects of resveratrol on metabolism and mitochondrial function and discuss how resveratrol may serve as a new therapeutic strategy to preserve metabolic health. We also discuss whether the effects of resveratrol are similar to the effects of exercise training and therefore if resveratrol can be considered as an exercise mimetic.

Osteoarthritis (OA) is a degenerative joint disease for which there are no disease-modifying drugs. It is a leading cause of disability in the UK. Increasing age and obesity are both major risk factors for OA and the health and economic burden of this disease will increase in the future. Focusing on compounds from the habitual diet that may prevent the onset or slow the progression of OA is a strategy that has been under-investigated to date. An approach that relies on dietary modification is clearly attractive in terms of risk/benefit and more likely to be implementable at the population level. However, before undertaking a full clinical trial to examine potential efficacy, detailed molecular studies are required in order to optimise the design. This review focuses on potential dietary factors that may reduce the risk or progression of OA, including micronutrients, fatty acids, flavonoids and other phytochemicals. It therefore ignores data coming from classical inflammatory arthritides and nutraceuticals such as glucosamine and chondroitin. In conclusion, diet offers a route by which the health of the joint can be protected and OA incidence or progression decreased. In a chronic disease, with risk factors increasing in the population and with no pharmaceutical cure, an understanding of this will be crucial.

Epidemiological studies, including those in identical twins, and in individuals in utero during periods of famine have provided robust evidence of strong correlations between low birth-weight and subsequent risk of disease in later life, including type 2 diabetes (T2D), CVD, and metabolic syndrome. These and studies in animal models have suggested that the early environment, especially early nutrition, plays an important role in mediating these associations. The concept of early life programming is therefore widely accepted; however the molecular mechanisms by which early environmental insults can have long-term effects on a cell and consequently the metabolism of an organism in later life, are relatively unclear. So far, these mechanisms include permanent structural changes to the organ caused by suboptimal levels of an important factor during a critical developmental period, changes in gene expression caused by epigenetic modifications (including DNA methylation, histone modification and microRNA) and permanent changes in cellular ageing. Many of the conditions associated with early-life nutrition are also those which have an age-associated aetiology. Recently, a common molecular mechanism in animal models of developmental programming and epidemiological studies has been development of oxidative stress and macromolecule damage, specifically DNA damage and telomere shortening. These are phenotypes common to accelerated cellular ageing. Thus, this review will encompass epidemiological and animal models of developmental programming with specific emphasis on cellular ageing and how these could lead to potential therapeutic interventions and strategies which could combat the burden of common age-associated disease, such as T2D and CVD.

Gait and cognitive impairments in older adults can reflect the simultaneous existence of two syndromes that affect certain brain substrates and pathologies. Nutritional deficiencies, which are extremely common among elderly population worldwide, have potential to impact the existence and rehabilitation of both syndromes. Gait and cognition are controlled by brain circuits which are vulnerable to multiple age-related pathologies such as vascular diseases, inflammation and dementias that may be caused or accentuated by poor nutrition or deficiencies that lead to cognitive, gait or combined cognitive and gait impairments. The following review aims to link gait and cognitive classifications and provide an overview of the potential impact of nutritional deficiencies on both neurological and gait dysfunctions. The identification of common modifiable risk factors, such as poor nutrition, may serve as an important preventative strategy to reduce cognitive and mobility impairments and moderate the growing burden of dementia and disability worldwide.

Influenza is a major cause of death in the over 65s. Increased susceptibility to infection and reduced response to vaccination are due to immunosenscence in combination with medical history and lifestyle factors. Age-related alterations in the composition of the gut microbiota have a direct impact on the immune system and it is proposed that modulation of the gut microbiota using pre- and probiotics could offer an opportunity to improve immune responses to infections and vaccination in older people. There is growing evidence that probiotics have immunomodulatory properties, which to some extent are strain-dependent, and are strongly influenced by ageing. Randomised controlled trials suggest that probiotics may reduce the incidence and/or severity of respiratory infections, although there is limited data on older people. A small number of studies have examined the potential adjuvant effects of selected probiotics for vaccination against influenza; however, the data is inconsistent, particularly in older people. This review describes the impact of age-related changes in the gut on the immune response to respiratory infections and evaluates whether restoration of gut microbial homoeostasis by probiotics offers an opportunity to modulate the outcome of respiratory infections and vaccination against influenza in older people. Although there is promising evidence for effects of probiotics on human health, there is a lack of consistent data, perhaps partly due to strain-specific differences and an influence of the age of the host. Further research is critical in evaluating the potential use of probiotics in respiratory infections and vaccination in the ageing population.

High amounts of time spent sedentary and low levels of physical activity have been implicated in the process of excessive adiposity gains in youth. The aim of this review is to discuss the role of physical activity, sedentary time and behaviour (i.e. television (TV)-viewing) in relation to adiposity during the first two decades of life with a specific focus on whether the association between sedentary time, and behaviour and adiposity is independent of physical activity. We identified nine cohort studies (three prospective) whether sedentary time was associated with adiposity independent of physical activity. Eight of these studies suggested that sedentary time was unrelated to adiposity when physical activity was taken into account. Results from studies (n 8) examining the independent association between TV-viewing and adiposity independent of physical activity were mixed. Those that observed a positive association between TV-viewing and adiposity independent of physical activity discussed that the association may be due to residual confounding. A few additional studies have also challenged the general notion that low levels of physical activity leads to fatness and suggested that higher baseline fatness may be predictive of a decline in physical activity. It appears unlikely that higher levels of sedentary time are associated with or predictive of, higher levels of adiposity when physical activity is controlled for in youth. Specific sedentary behaviours such as TV-viewing may be associated with adiposity independent of physical activity but the results may be explained by residual confounding.

Osteoporosis, a metabolic skeletal disease characterised by decreased bone mass and increased fracture risk, is a growing public health problem. Among the various risk factors for osteoporosis, calcium and vitamin D have well-established protective roles, but it is likely that other nutritional factors are also implicated. This review will explore the emerging evidence supporting a role for certain B-vitamins, homocysteine and the 677C→T polymorphism in the gene encoding the folate-metabolising enzyme methylenetetrahydrofolate reductase, in bone health and disease. The evidence, however, is not entirely consistent and as yet no clear mechanism has been defined to explain the potential link between B-vitamins and bone health. Coeliac disease, a common condition of malabsorption, induced by gluten ingestion in genetically susceptible individuals, is associated with an increased risk both of osteoporosis and inadequate B-vitamin status. Given the growing body of evidence linking low bone mineral density and/or increased fracture risk with low B-vitamin status and elevated homocysteine, optimal B-vitamin status may play an important protective role against osteoporosis in coeliac disease; to date, no trial has addressed this possible link.

The prevalence of osteoporosis and the incidence of age-related fragility fracture vary by ethnicity. There is greater than 10-fold variation in fracture probabilities between countries across the world. Mineral and bone metabolism are intimately interlinked, and both are known to exhibit patterns of daily variation, known as the diurnal rhythm (DR). Ethnic differences are described for Ca and P metabolism. The importance of these differences is described in detail between select ethnic groups, within the USA between African-Americans and White-Americans, between the Gambia and the UK and between China and the UK. Dietary Ca intake is higher in White-Americans compared with African-Americans, and is higher in White-British compared with Gambian and Chinese adults. Differences are observed also for plasma 25-hydroxy vitamin D, related to lifestyle differences, skin pigmentation and skin exposure to UVB-containing sunshine. Higher plasma 1,25-dihydroxy vitamin D and parathyroid hormone are observed in African-American compared with White-American adults. Plasma parathyroid hormone is also higher in Gambian adults and, in winter, in Chinese compared with White-British adults. There may be ethnic differences in the bone resorptive effects of parathyroid hormone, with a relative skeletal resistance to parathyroid hormone observed in some, but not all ethnic groups. Renal mineral excretion is also influenced by ethnicity; urinary Ca (uCa) and urinary P (uP) excretions are lower in African-Americans compared with White-Americans, and in Gambians compared with their White-British counterparts. Little is known about ethnic differences in the DR of Ca and P metabolism, but differences may be expected due to known differences in lifestyle factors, such as dietary intake and sleep/wake pattern. The ethnic-specific DR of Ca and P metabolism may influence the net balance of Ca and P conservation and bone remodelling. These ethnic differences in Ca, P and the bone metabolism may be important factors in the variation in skeletal health.