In this review, the relevance of selenium (Se) to viral disease will be discussed paying particular attention to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease (COVID-19). Se, the active centre in selenoproteins has an ongoing history of reducing the incidence and severity of viral infections. Host Se deficiency increased the virulence of RNA viruses such as influenza A and coxsackievirus B3, the latter of which is implicated in the development of Keshan disease in north-east China. Significant clinical benefits of Se supplementation have been demonstrated in HIV-1, in liver cancer linked to hepatitis B, and in Chinese patients with hantavirus that was successfully treated with oral sodium selenite. China is of particular interest because it has populations that have both the lowest and the highest Se status in the world. We found a significant association between COVID-19 cure rate and background Se status in Chinese cities; the cure rate continued to rise beyond the Se intake required to optimise selenoproteins, suggesting an additional mechanism. Se status was significantly higher in serum samples from surviving than non-surviving COVID-19 patients. As regards mechanism, SARS-CoV-2 may interfere with the human selenoprotein system; selenoproteins are important in scavenging reactive oxygen species, controlling immunity, reducing inflammation, ferroptosis and endoplasmic reticulum (ER) stress. We found that SARS-CoV-2 significantly suppressed mRNA expression of GPX4, of the ER selenoproteins, SELENOF, SELENOM, SELENOK and SELENOS and down-regulated TXNRD3. Based on the available data, both selenoproteins and redox-active Se species (mimicking ebselen, an inhibitor of the main SARS-CoV-2 protease that enables viral maturation within the host) could employ their separate mechanisms to attenuate virus-triggered oxidative stress, excessive inflammatory responses and immune-system dysfunction, thus improving the outcome of SARS-CoV-2 infection.

Obesity and dyslipidaemia are strongly associated with the development of cardiometabolic diseases including CVD, stroke, type 2 diabetes, insulin resistance and non-alcoholic fatty liver disease. While these conditions are preventable, they are leading causes of mortality globally. There is now overwhelming clinical and experimental evidence that these conditions are driven by chronic systemic inflammation, with a growing body of data suggesting that this can be regulated by increasing levels of physical activity and reducing sedentary time. In this review we address the role of macrophage-mediated inflammation on the development of cardiometabolic diseases in individuals with overweight and obesity and how reducing sedentary behaviour and increasing physical activity appears to lessen these pro-inflammatory processes, reducing the risk of developing cardiometabolic diseases. While loss of subcutaneous and visceral fat mass is important for reducing chronic systemic inflammation, the mediating effects of increasing physical activity levels and lowering sedentary time on the development of inflamed adipose tissue also occur independently of changes in adiposity. The message that weight loss is not necessary for the benefits of physical activity in lowering chronic inflammation and improving health should encourage those for whom losing weight is difficult. Additionally, while the health benefits of meeting the recommended physical activity guidelines are clear, simply moving more appears to lower chronic systemic inflammation. Reducing sitting time and increasing light physical activity may therefore provide an alternative, more approachable manner for some with overweight and obesity to become more active, reduce chronic inflammation and improve cardiometabolic health.

Nutrients can impact and regulate cellular metabolism and cell function which is particularly important for the activation and function of diverse immune subsets. Among the critical nutrients for immune cell function and fate, glutamine is possibly the most widely recognised immunonutrient, playing key roles in TCA cycle, heat shock protein responses and antioxidant systems. In addition, glutamine is also involved with inter-organ ammonia transport, and this is particularly important for not only immune cells, but also to the brain, especially in catabolic situations such as critical care and extenuating exercise. The well characterised fall in blood glutamine availability has been the main reason for studies to investigate the possible effects of glutamine replacement via supplementation but many of the results are in poor agreement. At the same time, a range of complex pathways involved in glutamine metabolism have been revealed via supplementation studies. This article will briefly review the function of glutamine in the immune system, with emphasis on metabolic mechanisms, and the emerging role of glutamine in the brain glutamate/gamma-amino butyric acid cycle. In addition, relevant aspects of glutamine supplementation are discussed.

Selenium is found at the active centre of twenty-five selenoproteins which have a variety of roles, including the well-characterised function of antioxidant defense, but it also is claimed to be involved in the immune system. However, due to limited and conflicting data for different parameters of immune function, intakes of selenium that have an influence on immune function are uncertain. This review covers the relationship between selenium and immune function in man, focusing on the highest level of evidence, namely that generated by randomised controlled trials (RCT), in which the effect of selective administration of selenium, in foods or a supplement, on immune function was assessed. A total of nine RCT were identified from a systematic search of the literature, and some of these trials reported effects on T and natural killer cells, which were dependent on the dose and form of selenium administered, but little effect of selenium on humoral immunity. There is clearly a need to undertake dose–response analysis of cellular immunity data in order to derive quantitative relationships between selenium intake and measures of immune function. Overall, limited effects on immunity emerged from experimental studies in human subjects, though additional investigation on the potential influence of selenium status on cellular immunity appears to be warranted.

Fatigue is defined as a symptom leading to the inability to continue functioning at the expected activity level. It is a highly prevalent symptom, challenging to frame into monodimensional pathophysiological mechanisms. As a result, fatigue is often underestimated in the clinical setting and is wrongly considered an unavoidable consequence of ageing. Several potential mechanisms responsible for fatigue have been proposed, including sleep patterns, autonomic nervous system abnormalities and biological complexity. Inflammation and mitochondrial dysfunction are among the most promising mechanisms through which malnutrition may cause fatigue. Not surprisingly, fatigue is highly prevalent in inflammatory conditions (e.g. COVID-19 infection). The nutritional status may also represent a critical factor in the development and presentation of fatigue, which may mimic the exhaustion of the individual's metabolic reserves. For example, the insufficient dietary intake of energy and proteins may determine the catabolism of body fat and muscles, disrupt the homeostatic balance and cause the onset of fatigue. It is necessary to conduct research on fatigue. By characterising its pathophysiological mechanisms, it will be possible to (1) support the design and development of targeted interventions, (2) improve the quality of life of many persons by acting on the symptom and (3) reduce the direct and indirect costs of a burdening condition typical of advancing age. In the present review, we provide an overview of the role that nutrition may play as a determinant of fatigue in older people, also in the context of the COVID-19 pandemic.

The incidences of both breast cancer and obesity are rising in the UK. Obesity increases the risk of developing breast cancer in the postmenopausal population and leads to worse outcomes in those of all ages treated for early-stage breast cancer. In this review we explore the multifactorial reasons behind this association and the clinical trial evidence for the benefits of physical activity and dietary interventions in the early and metastatic patient groups. As more people with breast cancer are cured, and those with metastatic disease are living longer, cancer survivorship is becoming increasingly important. Therefore, ensuring the long-term implications of cancer and cancer treatment are addressed is vital. Although there remains a lack of definitive evidence that deliberate weight loss after a diagnosis of breast cancer reduces disease recurrence, a number of studies have reported benefits of weight loss and of physical activity. However, the limited data currently available mean that clinicians remain unclear on the optimal lifestyle advice to give their patients. Further high-quality research is needed to provide this evidence base, which will be required to optimise clinical care and for the commissioning of lifestyle interventions in the UK in breast cancer survivors.

The 2nd Nutrition and Cancer Networking Meeting ‘Nutrition and Breast Cancer: Translating Evidence into Practice’ was held at Newcastle University in May 2022, with support from the Nutrition Society and British Association for Cancer Research. The first meeting in this series was held in Sheffield in 2019. The aim of this joint meeting was to bring together researchers with an interest in nutrition and breast cancer, with the programme spanning topics from risk and prevention to nutrition during treatment and beyond. Several key themes emerged, including the importance of engaging patients in the development of interventions and trials, making trials more accessible to diverse communities; training of clinical staff in nutrition and latest evidence; wider range of compounds should be considered in food composition tables; and alternative trial designs can be considered for prevention research to reduce financial burden and increase power.

Weight gain is commonly observed during and after breast cancer treatment due to chemotherapy and endocrine therapies, induced menopause, changes in metabolism and food intake and decreased physical activity. Systematic reviews show that women who are overweight or obese at diagnosis, and those who gain weight, have poorer breast cancer survival outcomes than women of a healthy weight, irrespective of menopausal status. Excess body weight after breast cancer also increases the risk of type 2 diabetes mellitus and CVD. The adverse impact of excess body weight on survival outcomes is clearly shown for women with oestrogen receptor-positive (ER+) breast cancer, which accounts for 70 % of all breast cancer cases. Higher body fat is thought to increase the risk of ER+ recurrence because of increased aromatase activity. However, this could be compounded by other risk factors, including abnormal insulin and adipokine metabolism, impaired anti-tumour immunity and chronic low-grade systemic inflammation. Observational evidence linking poorer survival outcomes with excess body fat and low physical activity in women recovering from early-stage curative-intent breast cancer treatment is reviewed, before reflecting on the proposed biological mechanisms. The issues and sensitivities surrounding exercise participation amongst overweight breast cancer patients is also discussed, before providing an overview of the co-design process involved in development of an intervention (support programme) with appropriate content, structure and delivery model to address the weight management challenges faced by overweight ER+ breast cancer patients.

Non-communicable diseases disproportionately affect African migrants from sub-Saharan Africa living in high-income countries (HICs). Evidence suggests this is largely driven by forces that include migration, globalisation of unhealthy lifestyles (poor diet, physical inactivity and smoking), unhealthy food environments, socio-economic status and population ageing. Changes in lifestyle behaviours that accompany migration are exemplified primarily by shifts in dietary behaviours from more traditional diets to a diet that incorporates that of the host culture, which promotes the development of obesity, diabetes, hypertension and CVD. The current paper presents a critical analysis of dietary change and how this is influenced by the food environment and the socio-economic context following migration. We used a food systems framework to structure the discussion of the interaction of factors across the food system that shape food environments and subsequent dietary changes among African migrant populations living in HICs.

Changing consumer behaviour has potential benefits for health, the economy and the environment. Change is possible, and behavioural change has been the purpose of much research; nevertheless we can still observe limited success, as in the case of food in public policies or individual diets. One reason is that models driving behavioural change interventions tend to neglect some important contextual factors. The three layers of components that channel behaviour (‘installations’ in the material, embodied and social realms) are described here and how this channelling can be hacked, modified and leveraged to foster behavioural change. Installations scaffold and control individual and collective behaviour at each step of the behavioural path with their three-layered and partly redundant structure. This redundancy makes the channelling resilient enough to train novices and to guide and repair behaviour. The three layers, physical affordances, embodied competences and social regulation are described in detail. To change eating behaviour, installations must be adapted at all steps of behaviour, from procurement to storage, preparation, meal and disposal. This adaptation can be done through the various layers in an opportunistic way, according to the agency of those who endeavour to change behaviour (e.g. budget, time, political power, etc.) Finally the steps necessary to design behavioural change interventions leveraging installations are listed.