Advancements in image-based technologies and body composition research over the past decade has led to increased understanding of the importance of muscle abnormalities, such as low muscle mass (sarcopenia), and more recently low muscle attenuation (MA), as important prognostic indicators of unfavourable outcomes in patients with cancer. Muscle abnormalities can be highly prevalent in patients with cancer (ranging between 10 and 90 %), depending on the cohort under investigation and diagnostic criteria used. Importantly, both low muscle mass and low MA have been associated with poorer tolerance to chemotherapy, increased risk of post-operative infectious and non-infectious complications, increased length of hospital stay and poorer survival in patients with cancer. Studies have shown that systemic antineoplastic treatment can exacerbate losses in muscle mass and MA, with reported loss of skeletal muscle between 3 and 5 % per 100 d, which are increased exponentially with progressive disease and proximity to death. At present, no effective medical intervention to improve muscle mass and MA exists. Most research to date has focused on treating muscle depletion as part of the cachexia syndrome using nutritional, exercise and pharmacological interventions; however, these single-agent therapies have not provided promising results. Rehabilitation care to modify body composition, either increasing muscle mass and/or MA should be conducted, and its respective impact on oncology outcomes explored. Although the optimal timing and treatment strategy for preventing or delaying the development of muscle abnormalities are yet to be determined, multimodal interventions initiated early in the disease trajectory appear to hold the most promise.

Weight, weight change and physical activity may affect prognosis among women who are diagnosed with breast cancer. Observational studies show associations between overweight/obesity and weight gain with several measures of reduced prognosis in women with breast cancer, and some suggestions of lower survival in women who are underweight or who experience unexplained weight loss after diagnosis. Observational studies have also shown an association between higher levels of physical activity and reduced breast cancer-specific and all-cause mortality, although a dose–response relationship has not been established. The effects of purposive dietary weight loss and increase in physical activity on survival or recurrence in breast cancer are not yet established, and randomised controlled trials are needed for definitive data. This paper presents the epidemiologic evidence on weight status, weight change, and physical activity and breast cancer survival; suggests potential mediating mechanisms; summarises evidence on weight loss interventions in breast cancer survivors; describes ongoing randomised clinical trials designed to test the effects of weight loss or physical activity on breast cancer survival; and provides information on available guidelines on weight and physical activity for cancer survivors.

The burden of obesity contributes to increasing health inequality, and placing healthcare systems under huge strain. The modern society could broadly be described to support unhealthful eating patterns and sedentary behaviour; also described as obesogenic. Obesity prevention and treatment has focused on educational and behavioural interventions, with limited overall success. A sustainable approach is to address the environments that promote less healthy eating and high energy intake as well as sedentary behaviour. Approaches which modify the environment have the potential to assist in the prevention of this complex condition. The present paper focuses on food environments within the context of obesogenic environments. Takeaway and fast food, a fixture of our diet, is usually nutrient poor and energy dense. A ‘concentration effect’ has been observed, where there is a clustering of fast food and takeaway outlets in more deprived areas. Access to food and intake are associated; however, there are methodological challenges in associating the effect of the food environment on obesity. While there is an imperfect evidence base relating to the role of the food environment in terms of the obesity crisis; policy, practice, civic society and industry must work together and take action now, where current evidence suggests a change. Shaping the environment to better support healthful eating decisions has the potential to be a key aspect of a successful obesity prevention intervention.

Epidemiological studies demonstrate that poor glycaemic control is an independent risk factor for CVD. Postprandial glycaemia has been demonstrated as a better predictor of glycated Hb, the gold standard of glycaemic control, when compared with fasting blood glucose. There is a need for more refined strategies to tightly control postprandial glycaemia, particularly in those with type 2 diabetes, and nutritional strategies around meal consumption may be effective in enhancing subsequent glycaemic control. Whey protein administration around meal times has been demonstrated to reduce postprandial glycaemia, mediated through various mechanisms including an enhancement of insulin secretion. Whey protein ingestion has also been shown to elicit an incretin effect, enhancing the secretion of glucose-dependent insulinotropic peptide and glucagon-like peptide-1, which may also influence appetite regulation. Acute intervention studies have shown some promising results however many have used large dosages (50–55 g) of whey protein alongside high-glycaemic index test meals, such as instant powdered potato mixed with glucose, which does not reflect realistic dietary strategies. Long-term intervention studies using realistic strategies around timing, format and amount of whey protein in relevant population groups are required.

Childhood obesity is a serious challenge for public health. The problem begins early with most excess childhood weight gained before starting school. In 2016, the WHO estimated that 41 million children under 5 were overweight or obese. Once established, obesity is difficult to reverse, likely to persist into adult life and is associated with increased risk of CVD, type 2 diabetes and certain cancers. Preventing obesity is therefore of high importance. However, its development is multi-factorial and prevention is a complex challenge. Modifiable lifestyle behaviours such as diet and physical activity are the most well-known determinants of obesity. More recently, early-life factors have emerged as key influencers of obesity in childhood. Understanding risk factors and how they interact is important to inform interventions that aim to prevent obesity in early childhood. Available evidence supports multi-component interventions as effective in obesity prevention. However, relatively few interventions are available in the UK and only one, TrimTots, has been evaluated in randomised controlled trials and shown to be effective at reducing obesity risk in preschool children (age 1–5 years). BMI was lower in children immediately after completing TrimTots compared with waiting list controls and this effect was sustained at long-term follow-up, 2 years after completion. Developing and evaluating complex interventions for obesity prevention is a challenge for clinicians and researchers. In addition, parents encounter barriers engaging with interventions. This review considers early-life risk factors for obesity, highlights evidence for preventative interventions and discusses barriers and facilitators to their success.

The aim of the present review paper is to survey the literature related to DNA methylation, and its association with cancer and ageing. The review will outline the key factors, including diet, which modulate DNA methylation. Our rationale for conducting this review is that ageing and diseases, including cancer, are often accompanied by aberrant DNA methylation, a key epigenetic process, which is crucial to the regulation of gene expression. Significantly, it has been observed that with age and certain disease states, DNA methylation status can become disrupted. For instance, a broad array of cancers are associated with promoter-specific hypermethylation and concomitant gene silencing. This review highlights that hypermethylation, and gene silencing, of the EN1 gene promoter, a crucial homeobox gene, has been detected in various forms of cancer. This has led to this region being proposed as a potential biomarker for diseases such as cancer. We conclude the review by describing a recently developed novel electrochemical method that can be used to quantify the level of methylation within the EN1 promoter and emphasise the growing trend in the use of electrochemical techniques for the detection of aberrant DNA methylation.

Globally populations are ageing. By 2050, it is estimated that there will be two billion people aged 60 years or over, of which 131 million are projected to be affected by dementia, while depression is predicted to be the second leading cause of disability worldwide by 2020. Preventing or delaying the onset of these disorders should therefore be a public health priority. There is some evidence linking certain dietary patterns, particularly the Mediterranean diet, with a reduced risk of dementia and depression. Specific dietary components have also been investigated in relation to brain health, with emerging evidence supporting protective roles for n-3 PUFA, polyphenols, vitamin D and B-vitamins. At this time, the totality of evidence is strongest in support of a role for folate and the metabolically related B-vitamins (vitamin B12, vitamin B6 and riboflavin) in slowing the progression of cognitive decline and possibly reducing the risk of depression in ageing. Future studies incorporating new technologies, such as MRI and magnetoencephalography, offer much promise in identifying effective nutrition interventions that could reduce the risk of cognitive and mental disorders. This review will explore the ageing brain and the emerging evidence linking diet and specific nutrients with cognitive function and depression in ageing, with the potential to develop strategies that could improve quality of life in our ageing population.

EPA and DHA appear to be the most important n-3 fatty acids, but roles for n-3 docosapentaenoic acid are now also emerging. Intakes of EPA and DHA are usually low, typically below those recommended. Increased intakes result in higher concentrations of EPA and DHA in blood lipids, cells and tissues. Increased content of EPA and DHA modifies the structure of cell membranes and the function of membrane proteins. EPA and DHA modulate the production of lipid mediators and through effects on cell signalling can alter the patterns of gene expression. Through these mechanisms, EPA and DHA alter cell and tissue responsiveness in a way that often results in more optimal conditions for growth, development and maintenance of health. DHA has vital roles in brain and eye development and function. EPA and DHA have a wide range of physiological roles, which are linked to certain health or clinical benefits, particularly related to CVD, cancer, inflammation and neurocognitive function. The benefits of EPA and DHA are evident throughout the life course. Future research will include better identification of the determinants of variation of responses to increased intake of EPA and DHA; more in-depth dose–response studies of the effects of EPA and DHA; clearer identification of the specific roles of EPA, docosapentaenoic acid and DHA; testing strategies to enhance delivery of n-3 fatty acids to the bloodstream; and exploration of sustainable alternatives to fish-derived very long-chain n-3 fatty acids.

Effective pharmaceutical treatments for age-related cognitive decline have proved elusive. There is, however, compelling evidence that nutritional status and supplementation could play crucial roles in modifying the expression of cognitive change through the lifespan. Subjective memory impairment and mild cognitive impairment can be harbingers of dementia but this is by no means inevitable. Neurocognitive change is influenced by a variety of processes, many of which are involved in other aspects of systemic health, including cardiovascular function. Importantly, many of these processes are governed by mechanisms which may be modified by specific classes of bioactive nutrients. There is increasing, converging evidence from controlled trials that nutritional interventions can improve mood and cognitive function in both clinical and healthy populations. Specific examples include selected botanical extracts such as the flavonoids. Some nutritional supplements (e.g. broad-spectrum micronutrient supplementation) appear to support improved cognitive function, possibly through redressing insufficient nutrient status (i.e. suboptimal but above the threshold for frank deficiency). Recent mechanistic research has unveiled physiologically plausible, modifiable, cognition-relevant targets for nutrition and nutraceuticals. These include processes involved in both systemic and central vascular function, inflammation, metabolism, central activation, improved neural efficiency and angiogenesis. The advent and development of human neuroimaging methodology have greatly aided our understanding of the core central mechanisms of cognitive change. Different imaging modalities can provide insights into modifiable central mechanisms which may be targeted by bioactive nutrients. The latter may contribute to slowing age-related decline through supporting neurocognitive scaffolding mechanisms.

Despite the inverse association between skin colour and efficiency of cutaneous vitamin D synthesis, in addition to the widely accepted racial disparity in vitamin D status, populations of ethnic minority are understudied in terms of setting target serum 25-hydroxyvitamin D concentrations and corresponding dietary requirements for vitamin D. In minority groups, prevention of vitamin D deficiency on a population basis is challenging due to the lack of clarity surrounding the metabolism and transport of vitamin D. Authoritative agencies have been unable to define pregnancy-specific dietary recommendations for vitamin D, owing to an absence of sufficient evidence to confirm whether nutritional requirements for vitamin D are altered during pregnancy. While the question of setting race- and pregnancy-specific dietary reference values for vitamin D has not been addressed to date, endemic vitamin D deficiency has been reported among gravidae worldwide, specifically among ethnic minorities and white women resident at high latitude. In light of the increased risk of nutritional rickets among infants of ethnic minority, coupled with growing evidence for potential non-skeletal roles of vitamin D in perinatal health, determination of the dietary vitamin D requirement that will prevent deficiency during pregnancy is a research priority. However, systematic approaches to establishing dietary requirements are limited by the quality of the available evidence and the under-representation of minority groups in clinical research. This review considers the evidence for racial differences in vitamin D status and response to vitamin D supplementation, with particular application to pregnancy-specific requirements among ethnic minorities resident at high latitudes.