Obesity-related metabolic conditions such as insulin resistance (IR), type 2 diabetes and CVD share a number of pathological features, one of which is metabolic-inflammation. Metabolic-inflammation results from the infiltration of immune cells into the adipose tissue, driving a pro-inflammatory environment, which can induce IR. Furthermore, resolution of inflammation, an active process wherein the immune system counteracts pro-inflammatory states, may be dysregulated in obesity. Anti-inflammatory nutritional interventions have focused on attenuating this pro-inflammatory environment. Furthermore, with inherent variability among individuals, establishing at-risk populations who respond favourably to nutritional intervention strategies is important. This review will focus on chronic low-grade metabolic-inflammation, resolution of inflammation and the putative role anti-inflammatory nutrients have as a potential therapy. Finally, in the context of personalised nutrition, the approaches used in defining individuals who respond favourably to nutritional interventions will be highlighted. With increasing prevalence of obesity in younger people, age-dependent biological processes, preventative strategies and therapeutic options are important to help protect against development of obesity-associated co-morbidities.

Epidemiological studies have established an association between obesity, insulin resistance, type 2 diabetes and a number of cancer types. Research has focused predominantly on altered endocrine factors, growth factors and signalling pathways, with little known in man about the immune involvement in the relevant pathophysiological processes. Moreover, in an era of exciting new breakthroughs in cancer immunotherapy, there is also a need to study the safety and efficacy of immunotherapeutics in the complex setting of inflammatory-driven obesity-associated cancer. This review addresses key immune cell subsets underpinning obesity-associated inflammation and describes how such immune compartments might be targeted to prevent and treat obesity-associated cancer. We propose that the modulation, metabolism, migration and abundance of pro- and anti-inflammatory cells and tumour-specific T cells might be therapeutically altered to both restore immune balance, alleviating pathological inflammation, and to improve anti-tumour immune responses in obesity-associated cancer.

An emerging field of research in nutritional epidemiology is the assessment of several links between nutritional quality and mental health. Specifically, some studies have pointed out that several food patterns could be associated with a reduced risk of depression among adults. This association seems to be consistent across countries, cultures and populations according to several systematic reviews and meta-analyses of observational studies. Some previously described food patterns, specifically the Mediterranean Food Pattern, the Alternative Healthy Eating Index, the Prudent diet or the Provegetarian Food Pattern may be effective to reduce the future risk of depression. Among them, only the Mediterranean Food Pattern has been tested for primary prevention in a large randomised trial, but the inverse association found was not statistically significant. The scientific report of the 2015 Dietary Guidelines for Americans Advisory Committee concluded that current evidence is still limited. Notwithstanding, this field is promising and, according to large and well-conducted observational studies, food patterns potentially associated with reduced risk of depression are those emphasising seafood, vegetables, fruits and nuts. There is a need to assess whether differences in the intake of some micro or macronutrients between these dietary patterns can make a difference in their association with a lower risk of depression. Moreover, the shape of the dose–response curve and the potential existence of a nonlinear threshold effect have not yet been established.

Both the intake of fat, especially saturated trans fatty acids, and refined carbohydrates, particularly sugar, have been linked to increased risk of obesity, diabetes and CVD. Dietary guidelines are generally similar throughout the world, restrict both intake of SFA and added sugar to no more than 10 and 35 % energy for total fat and recommend 50 % energy from carbohydrates being derived from unrefined cereals, tubers, fruit and vegetables. Current evidence favours partial replacement of SFA with PUFA with regard to risk of CVD. The translation of these macronutrient targets into food-based dietary guidelines is more complex because some high-fat foods play an important part in meeting nutrient requirements as well as influencing the risk of chronic disease. Some of the recent controversies surrounding the significance of sugar and the type of fat in the diet are discussed. Finally, data from a recently published randomised controlled trial are presented to show the impact of following current dietary guidelines on cardiovascular risk and nutrient intake compared with a traditional UK diet.

The goal of preterm nutrition in achieving growth and body composition approximating that of the fetus of the same postmenstrual age is difficult to achieve. Current nutrition recommendations depend largely on expert opinion, due to lack of evidence, and are primarily birth weight based, with no consideration given to gestational age and/or need for catch-up growth. Assessment of growth is based predominately on anthropometry, which gives insufficient attention to the quality of growth. The present paper provides a review of the current literature on the nutritional management and assessment of growth in preterm infants. It explores several approaches that may be required to optimise nutrient intakes in preterm infants, such as personalising nutritional support, collection of nutrient intake data in real-time, and measurement of body composition. In clinical practice, the response to inappropriate nutrient intakes is delayed as the effects of under- or overnutrition are not immediate, and there is limited nutritional feedback at the cot-side. The accurate and non-invasive measurement of infant body composition, assessed by means of air displacement plethysmography, has been shown to be useful in assessing quality of growth. The development and implementation of personalised, responsive nutritional management of preterm infants, utilising real-time nutrient intake data collection, with ongoing nutritional assessments that include measurement of body composition is required to help meet the individual needs of preterm infants.

Non-communicable diseases (NCD) and atherosclerotic CVD in particular, are the most important health problems of the 21st century. Already in every world region except Africa, NCD account for greater mortality than communicable, maternal, perinatal and nutritional conditions combined. Although modifiable lifestyle factors in adults are the main determinants, substantial evidence now suggests that factors in early life also have a major role in the development of NCD; commonly referred to as the Developmental Origins of Health and Disease hypothesis. Factors in utero, early postnatal life and throughout childhood, have been shown to affect NCD by influencing risk factors for CVD such as obesity, diabetes, hypertension and dyslipidaemia. Infant nutrition (e.g. breastfeeding rather than bottle feeding) and a slower pattern of infant weight gain have been shown to be particularly protective against later risk of obesity and CVD in both low- and high-income countries. The mechanisms involved are poorly understood, but include epigenetic changes; effects on endocrine systems regulating body weight, food intake and fat deposition; and changes in appetite regulation. As a consequence, strategies to optimise early life nutrition could make a major contribution to stemming the current global epidemic of NCD. This review will consider the role of early life factors in the development of NCD, focusing on the impact of infant nutrition/growth on obesity and CVD. The review will highlight the experimental (randomised) evidence where available, briefly summarise the underlying mechanisms involved and consider the implications for public health.

The ageing process is influenced by a variety of factors, including extrinsic, malleable lifestyle variables. The present paper deals with the epidemiological evidence for the role of dietary patterns and key nutritional concerns in relation to survival and ageing-related disorders that present themselves in later life. Healthful dietary patterns appear to be most relevant in old age. Specific nutritional concerns are related to vitamin D, vitamin B12 and protein malnutrition. An important challenge to further expand the knowledge base is currently addressed by the NuAge project, acknowledging the complexity of the ageing process and integrating different dimensions of research into human healthy ageing. In the meantime, reversing poor adherence to existing guidelines for a healthy diet remains a first challenge in public health nutritional practices.

Sarcopenia, defined as loss of skeletal muscle mass and function, is associated with adverse outcomes such as physical disability, impaired quality of life and increased mortality. Several mechanisms are involved in the development of sarcopenia. Potentially modifiable factors include nutrition and physical activity. Protein metabolism is central to the nutritional issues, along with other potentially modifying nutritional factors as energy balance and vitamin D status. An increasing but still incomplete knowledge base has generated recent recommendations on an increased protein intake in the elderly. Several factors beyond the total amount of protein consumed emerge as potentially important in this context. A recent summit examined three hypotheses: (1) A meal threshold; habitually consuming 25–30 g protein at breakfast, lunch and dinner provides sufficient protein to effectively stimulate muscle protein anabolism; (2) Protein quality; including high-quality protein at each meal improves postprandial muscle protein synthesis; and (3) performing physical activity in close temporal proximity to a high-quality protein meal enhances muscle anabolism. Optimising the potential for muscle protein anabolism by consuming an adequate amount of high-quality protein at each meal, in combination with physical activity, appears as a promising strategy to prevent or delay the onset of sarcopenia. However, results of interventions are inconsistent, and well-designed, standardised studies evaluating exercise or nutrition interventions are needed before guidelines can be developed for the prevention and treatment of age-related sarcopenia.

The aim of this review is to extend present concepts of body composition and to integrate it into physiology. In vivo body composition analysis (BCA) has a sound theoretical and methodological basis. Present methods used for BCA are reliable and valid. Individual data on body components, organs and tissues are included into different models, e.g. a 2-, 3-, 4- or multi-component model. Today the so-called 4-compartment model as well as whole body MRI (or computed tomography) scans are considered as gold standards of BCA. In practice the use of the appropriate method depends on the question of interest and the accuracy needed to address it. Body composition data are descriptive and used for normative analyses (e.g. generating normal values, centiles and cut offs). Advanced models of BCA go beyond description and normative approaches. The concept of functional body composition (FBC) takes into account the relationships between individual body components, organs and tissues and related metabolic and physical functions. FBC can be further extended to the model of healthy body composition (HBC) based on horizontal (i.e. structural) and vertical (e.g. metabolism and its neuroendocrine control) relationships between individual components as well as between component and body functions using mathematical modelling with a hierarchical multi-level multi-scale approach at the software level. HBC integrates into whole body systems of cardiovascular, respiratory, hepatic and renal functions. To conclude BCA is a prerequisite for detailed phenotyping of individuals providing a sound basis for in depth biomedical research and clinical decision making.

Our understanding of body composition (BC) variability in contemporary populations has significantly increased with the use of imaging techniques. Abnormal BC such as sarcopenia (low muscle mass) and obesity (excess adipose tissue) are predictors of poorer prognosis in a variety of conditions or clinical situations. As a catabolic illness, a defining feature of cancer is muscle loss. Although the conceptual model of wasting in cancer is typically conceived as involuntary weight loss leading to low body weight, recent studies have shown that both sarcopenia and cachexia can be present with obesity. The combination of low muscle and high adipose tissue (sarcopenic obesity) is an emerging abnormal BC phenotype prevalent across the body weight, and hence BMI spectra. Sarcopenia and sarcopenic obesity in cancer are in most instances occult conditions, which have been independently associated with higher incidence of chemotherapy toxicity, shorter time to tumour progression, poorer outcomes of surgery, physical impairment and shorter survival. Although the mechanisms are yet to be fully understood, the associations with poorer clinical outcomes emphasise the value of nutritional assessment as well as the need to develop appropriate interventions to countermeasure abnormal BC. Sarcopenia and sarcopenic obesity create diverse nutritional requirements, highlighting the compelling need for a more comprehensive and differentiated understanding of energy and protein requirements in this heterogeneous population.

An awareness of the importance of nutritional status in hospital settings began more than 40 years ago. Much has been learned since and has altered care. For the past 40 years several large studies have shown that cancer patients are amongst the most malnourished of all patient groups. Recently, the use of gold-standard methods of body composition assessment, including computed tomography, has facilitated the understanding of the true prevalence of cancer cachexia (CC). CC remains a devastating syndrome affecting 50–80 % of cancer patients and it is responsible for the death of at least 20 %. The aetiology is multifactorial and complex; driven by pro-inflammatory cytokines and specific tumour-derived factors, which initiate an energy-intensive acute phase protein response and drive the loss of skeletal muscle even in the presence of adequate food intake and insulin. The most clinically relevant phenotypic feature of CC is muscle loss (sarcopenia), as this relates to asthenia, fatigue, impaired physical function, reduced tolerance to treatments, impaired quality of life and reduced survival. Sarcopenia is present in 20–70 % depending on the tumour type. There is mounting evidence that sarcopenia increases the risk of toxicity to many chemotherapy drugs. However, identification of patients with muscle loss has become increasingly difficult as 40–60 % of cancer patients are overweight or obese, even in the setting of metastatic disease. Further challenges exist in trying to reverse CC and sarcopenia. Future clinical trials investigating dose reductions in sarcopenic patients and dose-escalating studies based on pre-treatment body composition assessment have the potential to alter cancer treatment paradigms.

Vitamin A, retinol, circulates in blood bound to retinol-binding protein (RBP4) which, in turn, associates with another serum protein, transthyretin (TTR), to form a ternary retinol-RBP4-TTR complex. At some tissues, retinol-bound (holo-) RBP4 is recognised by a receptor termed stimulated by retinoic acid 6 (STRA6) which transports retinol into cells. This mini-review summarises evidence demonstrating that, in addition to functioning as a retinol transporter, STRA6 is also a signalling receptor which is activated by holo-RBP4. The data show that STRA6-mediated retinol transport induces receptor phosphorylation, in turn activating a Janus kinases2/signal transducers and activators of transcription (STAT)3/5 cascade that culminates in induction of STAT target genes. STRA6-mediated retinol transport and cell signalling are inter-dependent, and both functions critically rely on intracellular retinol trafficking and metabolism. Hence, STRA6 couples ‘sensing’ of vitamin A homeostasis and metabolism to cell signalling, allowing it to control important biological functions. For example, by inducing the expression of the STAT target gene suppressor of cytokine signalling 3, STRA6 potently suppresses insulin responses. These observations provide a rationale for understanding the reports that elevation in serum levels of RBP4, often observed in obese mice and human subjects, causes insulin resistance. The observations indicate that the holo-RBP4 /STRA6 signalling cascade may comprise an important link through which obesity leads to insulin resistance and suggest that the pathway may be a novel target for treatment of metabolic diseases.

Low-calorie sweeteners (LCS) are commonly used as sugar substitutes in the diet to provide a desired sweet taste without increased energy intake. The number of LCS available on the market has increased considerably over the years and despite extensive evaluation of their safety prior to approval, debate continues around the effects of consumption on health. In Europe, Member States are obligated to monitor exposure to LCS and methods currently used tend to rely on self-reported dietary intake data alongside LCS concentrations in products. However, the acquisition of accurate data can be costly in terms of resources and time and are inherently imprecise. Although LCS are intensely sweet, they are chemically diverse and a limitation of many studies investigating the health effects of consumption is that they often fail to discern intakes of individual LCS. An approach which objectively assesses intakes of individual LCS would therefore allow robust investigations of their possible effects on health. Biomarker approaches have been utilised for the objective investigation of intakes of a range of dietary components and the feasibility of any such approach depends upon its validity as well as its applicability within the target population. This review aims to provide an overview of current understanding of LCS intake and explore the possibility of implementing a biomarker approach to enhance such understanding. Several commonly used LCS, once absorbed into the body, are excreted via the kidneys; therefore a urinary biomarker approach may be possible for the investigation of short-term exposure to these compounds.