‘Ageing well’ has been declared a global health priority by the World Health Organisation and the role of sarcopenia and frailty in late-life health is receiving increasing attention. Frailty is the decline in an individual's homeostatic function, strength and physiologic reserves leading to increased vulnerability, while sarcopenia describes the loss of muscle mass and function with age. The conceptual definitions of these conditions have been widely agreed but there is a lack of consensus on how to measure them. We review the different operational definitions described in the literature and the evidence that, whatever definition used, the prevalence and clinical impact of these conditions is high. We also consider the commonality of low physical function to both conditions, a feature which could provide a pragmatic way forward in terms of identifying those at risk. Objective measures of physical function such as usual walking speed are simple and feasible measures, extensively validated against health outcomes. Additionally, clinical applications of sarcopenia and frailty are reviewed with particular consideration to their potential role in the management of older people undergoing surgery. Frailty appears to outperform traditional anaesthetic and surgical risk scores in terms of its association with post-operative complications, length of hospital stay, institutionalisation and mortality. However, even within this sub-specialty area there is wide variation in the approaches used to measure frailty and there is an urgent need for studies to utilise established, validated and reproducible methods to identify sarcopenia and frailty in their study participants, in order to expedite scientific development.

In 1798, Thomas Robert Malthus published ‘An essay on the principle of population’ in which he concluded that: ‘The power of population is so superior to the power of the earth to produce subsistence for man, that premature death must in some shape or other visit the human race.’ Over the following century he was criticised for underestimating the potential for scientific and technological innovation to provide positive change. Since then, he has been proved wrong, with a number of papers published during the past few decades pointing out why he has been proved wrong so many times. In the present paper, I briefly review the main changes in food production in the past that have allowed us to continue to meet ever growing demand for food, and I examine the possibility of these same innovations delivering food security in the future. On the basis of recent studies, I conclude that technological innovation can no longer be relied upon to prove Malthus wrong as we strive to feed 9–10 billion people by 2050. Unless we are prepared to accept a wide range of significant, undesirable environmental consequences, technology alone cannot provide food security in 2050. Food demand, particularly the demand for livestock products, will need to be managed if we are to continue to prove Malthus wrong into the future.

The recent developments of metagenomics permit an extremely high-resolution molecular scan of the intestinal microbiota giving new insights and opening perspectives for clinical applications. Beyond the unprecedented vision of the intestinal microbiota given by large-scale quantitative metagenomics studies, such as the EU MetaHIT project, functional metagenomics tools allow the exploration of fine interactions between food constituents, microbiota and host, leading to the identification of signals and intimate mechanisms of crosstalk, especially between bacteria and human cells. Cloning of large genome fragments, either from complex intestinal communities or from selected bacteria, allows the screening of these biological resources for bioactivity towards complex plant polymers or functional food such as prebiotics. This permitted identification of novel carbohydrate-active enzyme families involved in dietary fibre and host glycan breakdown, and highlighted unsuspected bacterial players at the top of the intestinal microbial food chain. Similarly, exposure of fractions from genomic and metagenomic clones onto human cells engineered with reporter systems to track modulation of immune response, cell proliferation or cell metabolism has allowed the identification of bioactive clones modulating key cell signalling pathways or the induction of specific genes. This opens the possibility to decipher mechanisms by which commensal bacteria or candidate probiotics can modulate the activity of cells in the intestinal epithelium or even in distal organs such as the liver, adipose tissue or the brain. Hence, in spite of our inability to culture many of the dominant microbes of the human intestine, functional metagenomics open a new window for the exploration of food–microbe–host crosstalk.

Food intake is influenced by a complex regulatory system involving the integration of a wide variety of sensory inputs across multiple brain areas. Over the past decade, advances in neuroimaging using functional MRI (fMRI) have provided valuable insight into these pathways in the human brain. This review provides an outline of the methodology of fMRI, introducing the widely used blood oxygenation level-dependent contrast for fMRI and direct measures of cerebral blood flow using arterial spin labelling. A review of fMRI studies of the brain's response to taste, aroma and oral somatosensation, and how fat is sensed and mapped in the brain in relation to the pleasantness of food, and appetite control is given. The influence of phenotype on individual variability in cortical responses is addressed, and an overview of fMRI studies investigating hormonal influences (e.g. peptide YY, cholecystokinin and ghrelin) on appetite-related brain processes provided. Finally, recent developments in MR technology at ultra-high field (7 T) are introduced, highlighting the advances this can provide for fMRI studies to investigate the neural underpinnings in nutrition research. In conclusion, neuroimaging methods provide valuable insight into the mechanisms of flavour perception and appetite behaviour.

There is increasing scientific interest in the field of vitamin D research, moving the focus beyond bone health to other disease processes. Low circulating vitamin D levels have been reported as a risk factor for several pathophysiologically divergent diseases, including cancers, diabetes, CVD, multiple sclerosis and inflammatory diseases, including rheumatoid arthritis and inflammatory bowel disease (IBD). But, therein, remains the challenge: can any single nutrient contribute to multiple complex disease mechanisms and, ultimately, have therapeutic potential? The aim of this review is to critically evaluate several strands of scientific evidence surrounding vitamin D and inflammation, primarily focusing on IBD. Epidemiological studies suggest an increased incidence of IBD and rheumatoid arthritis in countries of more northern latitudes, mirroring sunlight patterns. A considerable body of evidence supports the anti-inflammatory effects of vitamin D, at least in animal models of IBD. Although it is accepted that suboptimal vitamin D status is common in IBD, some studies suggest that this associates with more severe disease. With regard to treatment, the data are only beginning to emerge from randomised controlled trials to suggest that people with IBD may remain in remission longer when treated with oral vitamin D. In conclusion, several strands of evidence suggest that vitamin D may modify the immune response in IBD. There is a continued need for large well-designed clinical trials and mechanistic studies to determine if, and how, this emerging promise translates into tangible clinical benefits for people with chronic debilitating diseases such as IBD.

Living in an ‘obesogenic’ environment poses a serious challenge for weight maintenance. However, many people are able to maintain a healthy weight indicating that not everybody is equally susceptible to the temptations of this food environment. The way in which someone perceives and reacts to food cues, that is, cognitive processes, could underlie differences in susceptibility. An attention bias for food could be such a cognitive factor that contributes to overeating. However, an attention bias for food has also been implicated with restrained eating and eating-disorder symptomatology. The primary aim of the present review was to determine whether an attention bias for food is specifically related to obesity while also reviewing evidence for attention biases in eating-disorder patients, restrained eaters and healthy-weight individuals. Another aim was to systematically examine how selective attention for food relates (causally) to eating behaviour. Current empirical evidence on attention bias for food within obese samples, eating-disorder patients, and, even though to a lesser extent, in restrained eaters is contradictory. However, present experimental studies provide relatively consistent evidence that an attention bias for food contributes to subsequent food intake. This review highlights the need to distinguish not only between different (temporal) attention bias components, but also to take different motivations (craving v. worry) and their impact on attentional processing into account. Overall, the current state of research suggests that biased attention could be one important cognitive mechanism by which the food environment tempts us into overeating.

Cachexia is a clinically relevant syndrome which impacts on quality of life, morbidity and mortality of patients suffering from acute and chronic diseases. The hallmark of cachexia is muscle loss, which is triggered by disease-associated inflammatory response. Cachexia is a continuum and therefore a staging system is needed. Initially, a three-stage system (i.e. pre-cachexia, cachexia and refractory cachexia) was proposed. More recent evidence supports the use of a five-stage classification system, based on patient's BMI and severity of weight loss, to better predict clinical outcome. Also, large clinical trials in cancer patients demonstrated that cachexia emerging during chemotherapy has greater influence on survival than weight loss at baseline. Therefore, becoming widely accepted is the importance of routinely monitoring patients’ nutritional status to detect early changes and diagnose cachexia in its early phases. Although cachexia is associated with the presence of anabolic resistance, it has been shown that sustained yet physiological hyperaminoacidaemia, as well as the use of specific nutrients, is able to overcome impaired protein synthesis and revert catabolism. More importantly, clinical evidence demonstrates that preservation of nutritional status during chemotherapy or improvement of body weight after weight loss is associated with longer survival in cancer patients.

This review uses production and climate data to examine global and local production trends that can be related to events such as drought. UK grain quality data is also available and provides an overview of trends in protein content. Literature surveys show a consistent reduction in grain size due to the effects of temperature and/or drought. A review of gene expression studies showed that most genes involved in starch synthesis are down regulated under heat stress. Net protein production is also reduced under heat and/or drought stress but apparently to a lesser degree as the reduction in grain mass is larger, resulting in an increase in protein concentration. Modelling has suggested that adaptation could be achieved by moving production to more extreme latitudes but other research suggests that simply transferring germplasm from one region to another is unlikely to be successful. Another review has identified drought tolerance phenotypes that could be used to breed more drought tolerant crops. At the time of the review, the authors concluded that phenotypic selection was generally preferable to forms of marker-assisted breeding and have used the approach to produce drought tolerant wheat cultivars. Transgenic approaches have also been shown to improve drought tolerance under controlled environment conditions but there are no results to show how well these results translate into improved crop performance under field conditions. The recent advances in genomic data and detecting marker–trait associations suggest that marker-assisted breeding will play a much more important role in breeding drought tolerant cereals in the future.

The first reports of accurate skeletal muscle mass measurement in human subjects appeared at about the same time as introduction of the sarcopenia concept in the late 1980s. Since then these methods, computed tomography and MRI, have been used to gain insights into older (i.e. anthropometry and urinary markers) and more recently developed and refined methods (ultrasound, bioimpedance analysis and dual-energy X-ray absorptiometry) of quantifying regional and total body skeletal muscle mass. The objective of this review is to describe the evolution of these methods and their continued development in the context of sarcopenia evaluation and treatment. Advances in these technologies are described with a focus on additional quantifiable measures that relate to muscle composition and ‘quality’. The integration of these collective evaluations with strength and physical performance indices is highlighted with linkages to evaluation of sarcopenia and the spectrum of related disorders such as sarcopenic obesity, cachexia and frailty. Our findings show that currently available methods and those in development are capable of non-invasively extending measures from solely ‘mass’ to quality evaluations that promise to close the gaps now recognised between skeletal muscle mass and muscle function, morbidity and mortality. As the largest tissue compartment in most adults, skeletal muscle mass and aspects of muscle composition can now be evaluated by a wide array of technologies that provide important new research and clinical opportunities aligned with the growing interest in the spectrum of conditions associated with sarcopenia.