Proceedings of the Nutrition Society最新文献

Sleep is vital for the maintenance of physical and mental health, recovery and performance in athletes. Sleep also has a restorative effect on the immune system and the endocrine system. Sleep must be of adequate duration, timing and quality to promote recovery following training and competition. Inadequate sleep adversely impacts carbohydrate metabolism, appetite, energy intake and protein synthesis affecting recovery from the energy demands of daily living and training/competition related fatigue. Sleep's role in overall health and well-being has been established. Athletes have high sleep needs and are particularly vulnerable to sleep difficulties due to high training and competition demands, as such the implementation of the potential nutritional interventions to improve sleep duration and quality is commonplace. The use of certain nutrition strategies and supplements has an evidence base i.e. carbohydrate, caffeine, creatine, kiwifruit, magnesium, meal make-up and timing, protein and tart cherry. However, further research involving both foods and supplements is necessary to clarify the interactions between nutrition and the circadian system as there is potential to improve sleep and recovery. Additional research is necessary to clarify guidelines and develop products and protocols for foods and supplements to benefit athlete health, performance and/or recovery. The purpose of this review is to highlight the potential interaction between sleep and nutrition for athletes and how these interactions might benefit sleep and/or recovery.

It is estimated that more than one-tenth of adults aged ≥60 years are now classified as having sarcopenic obesity (SO), a clinical condition characterised by the concurrent presence of sarcopenia (low muscle mass and weakness) and obesity (excessive fat mass). Independently, sarcopenia and obesity are associated with a high risk of numerous adverse health outcomes including CVD and neurological conditions (e.g. dementia), but SO may confer a greater risk, exceeding either condition alone. This imposes a substantial burden on individuals, healthcare systems and society. In recent years, an increasing number of observational studies have explored the association between SO and the risk of CVD; however, results are mixed. Moreover, the pathophysiology of SO is governed by a complex interplay of multiple mechanisms including insulin resistance, inflammation, oxidative stress, hormonal shifts and alteration of energy balance, which may also play a role in the occurrence of various CVD. Yet, the exact mechanisms underlying the pathological connection between these two complex conditions remain largely unexplored. The aim of this review is to examine the association between SO and CVD. Specifically, we seek to: (1) discuss the definition, epidemiology and diagnosis of SO; (2) reconcile previously inconsistent findings by synthesising evidence from longitudinal studies on the epidemiological link between SO and CVD and (3) discuss critical mechanisms that may elucidate the complex and potentially bidirectional relationships between SO and CVD.

Endogenous biological rhythms synchronise human physiology with daily cycles of light-dark, wake-sleep and feeding-fasting. Proper circadian alignment is crucial for physiological function, reflected in the rhythmic expression of molecular clock genes in various tissues, especially in skeletal muscle. Circadian disruption, such as misaligned feeding, dysregulates metabolism and increases the risk of metabolic disorders like type 2 diabetes. Such disturbances are common in critically ill patients, especially those who rely on enteral nutrition. Whilst continuous provision of enteral nutrition is currently the most common practice in critical care, this is largely dictated by convenience rather than evidence. Conversely, some findings indicate that intermittent provision of enteral nutrition aligned with daylight may better support physiological functions and improve clinical/metabolic outcomes. However, there is a critical need for studies of skeletal muscle responses to acutely divergent feeding patterns, in addition to complementary translational research to map tissue-level physiology to whole-body and clinical outcomes.

Anaemia affects more than 36 % of all pregnancies globally and is associated with significant maternal and neonatal morbidity and mortality. Iron deficiency is widely recognised as the most common nutritional cause of anaemia but other nutrient deficiencies are also implicated, including the B vitamin riboflavin, albeit its role is largely under-investigated and thus typically overlooked. Riboflavin, in its co-factor forms flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), is required for numerous oxidation-reduction reactions, antioxidant function and in the metabolism of other B vitamins and iron. While clinical deficiency of riboflavin is largely confined to low-income countries, sub-clinical (functional) deficiency is much more widespread, including in high-income countries, and is particularly common among women of reproductive age and during pregnancy. Limited observational evidence from high-income populations suggests that suboptimal riboflavin status contributes to an increased risk of anaemia. Furthermore, randomised controlled trials in pregnant women from low- and middle-income countries have demonstrated beneficial effects of riboflavin on haematological status and anaemia. Various mechanisms have been proposed to explain the contribution of riboflavin deficiency to anaemia, with the strongest evidence pointing to an adverse effect on iron metabolism, given that riboflavin co-factors are required for the release of iron from storage ferritin in the production of red blood cells. Overall, this review investigates riboflavin intakes and status during pregnancy in different populations and evaluates the available evidence for the under-recognised role of riboflavin in the maintenance of haemoglobin concentrations together with its potential to protect against the development of anaemia during pregnancy.

The gastrointestinal (GI) tract plays a critical role in nutrition and the pathophysiology of disease, and there is an increasing variety of methodologies available for the assessment of various aspects of GI physiology. Advancements in assessment methods, including techniques to study gut motility, fermentation, permeability, and microbiota composition, have provided researchers with powerful tools to investigate the impact of diet on GI tract physiology and the microbiota-gut-brain axis. Mechanistic evidence from reverse translational studies, which apply findings from human studies to preclinical models in a 'bedside-to-bench' approach, have also enhanced our understanding of the bidirectional interactions and candidate signalling molecules among the diet-gut-brain relationship. Interpreting data from these advanced techniques and study designs requires a thorough understanding of their principles, applications, and limitations. This review aims to summarise the methodological advances in GI tract physiology measurements and their application in nutritional studies, focusing on gut motility, fermentation, and permeability. We will present examples of how these techniques have been utilised in recent research, discuss their advantages and limitations, and provide insights on their use and interpretation in research. Understanding the capabilities and limitations of these tools is crucial for designing robust studies and elucidating the complex interplay between diet and the GI tract. The scope of this review encompasses recent advancements in GI tract assessment methodologies and their implications for nutritional research, providing a comprehensive overview for researchers in the field.

Gestational diabetes mellitus (GDM) poses significant health concerns for women and their offspring, with implications that extend beyond pregnancy. While GDM often resolves postpartum, a diagnosis of GDM confers a greater risk of future type 2 diabetes (T2D) and other chronic illnesses. Furthermore, the intergenerational impact of GDM predisposes offspring to increased chronic disease risk. Despite the awareness of the short- and long-term consequences of GDM, translating this knowledge into prevention strategies remains challenging. Challenges arise from a lack of clarity among health professionals regarding roles and responsibilities in chronic disease prevention and women's lack of awareness of the magnitude of associated health risks. These challenges are compounded by changes in the circumstances of new mothers as they adjust to balance the demands of infant and family care with their own needs. Insights into behaviour change strategies, coupled with advances in technology and digital healthcare delivery options, have presented new opportunities for diabetes prevention among women with a history of GDM. Additionally, there is growing recognition of the benefits of adopting an implementation science approach to intervention delivery, which seeks to enhance the effectiveness and scalability of interventions. Effective prevention of T2D following GDM requires a comprehensive person-centred approach that leverages technology, targeted interventions and implementation science methodologies to address the complex needs of this population. Through a multifaceted approach, it is possible to improve the long-term health outcomes of women with prior GDM.

In 2023, the UK government announced a Major Conditions Strategy, publishing 'The case for change and our strategic framework', which set out the focus on cancers, diabetes, dementia, mental ill health, musculoskeletal disorders, CVD and chronic respiratory diseases. Together, these conditions account for 60% of total disability-adjusted life years lost to early death or ill health in England, and one in four adults has at least two (multimorbidity). This review considers some of the key dietary risks for these major conditions and population policies that may improve diets and reduce risks. UK Government dietary recommendations, based on independent risk assessment and advice from the Scientific Advisory Committee on Nutrition, are encapsulated in the national food model, the Eatwell Guide. Based on key sources of dietary data - chiefly consumption data from the National Diet and Nutrition Survey and consumer purchase data from Kantar - most people do not meet dietary recommendations. This review considers how science and evidence inform health improvement policy. This includes policies that encourage healthier food choices, such as labelling and public procurement standards to those that minimise the impact of the less healthy choice such as sugar and salt reduction and reformulation. The review also considers nutritional approaches to managing some non-communicable diseases. Given the role nutrition and excess weight play in the onset, prognosis and quality of life for those living with one or more of the major conditions, there are huge potential gains from even small dietary improvements across population groups.

Musculoskeletal disorders and age-related musculoskeletal decline are major contributors to the burden of ill health seen in older subjects. Despite this increased burden, these chronic disorders of old age receive a relatively small proportion of national research funds. Much has been learned about fundamental processes involved in ageing from basic science research and this is leading to identification of key pathways that mediate ageing which may help the search for interventions to reduce age-related musculoskeletal decline. This short review will focus on the role of reactive oxygen species in age-related skeletal muscle decline and on the implications of this work for potential nutritional interventions in sarcopenia. The key physiological role of reactive oxygen species is now known to be in mediating redox signalling in muscle and other tissues and ageing leads to disruption of such pathways. In muscle, this is reflected in an age-related attenuation of specific adaptations and responses to contractile activity that impacts the ability of skeletal muscle from ageing individuals to respond to exercise. These pathways provides potential targets for identification of logical interventions that may help maintain muscle mass and function during ageing.

The ability to manipulate brain function through the communication between the microorganisms in the gastrointestinal tract and the brain along the gut-brain axis has emerged as a potential option to improve cognitive and emotional health. Dietary composition and patterns have demonstrated a robust capacity to modulate the microbiota-gut-brain axis. With their potential to possess pre-, pro-, post-, and synbiotic properties, dietary fibre and fermented foods stand out as potent shapers of the gut microbiota and subsequent signalling to the brain. Despite this potential, few studies have directly examined the mechanisms that might explain the beneficial action of dietary fibre and fermented foods on the microbiota-gut-brain axis, thus limiting insight and treatments for brain dysfunction. Herein, we evaluate the differential effects of dietary fibre and fermented foods from whole food sources on cognitive and emotional functioning. Potential mediating effects of dietary fibre and fermented foods on brain health via the microbiota-gut-brain axis are described. Although more multimodal research that combines psychological assessments and biological sampling to compare each food type is needed, the evidence accumulated to date suggests that dietary fibre, fermented foods, and/or their combination within a psychobiotic diet can be a cost-effective and convenient approach to improve cognitive and emotional functioning across the lifespan.

The relationship between nutrition and ageing is complex. The metabolism and synthesis of micronutrients within the gut microbiome can influence human health but is challenging to study. Furthermore, studying ageing in humans is time-consuming and difficult to control for environmental factors. Studies in model organisms can guide research efforts in this area. This review describes how the nematode Caenorhabditis elegans can be used to study how bacteria and diet influence ageing and inform follow-on studies in humans. It is known that certain bacteria accelerate ageing in C. elegans. This age-accelerating effect is prevented by inhibiting folate synthesis within the bacteria, and we propose that in the human microbiome, certain bacteria also accelerate ageing in a way that can be modulated by interfering with bacterial folate synthesis. Bacterial-derived folates do not promote ageing themselves; rather, ageing is accelerated by bacteria in some way, either through secondary metabolites or other bacterial activity, which is dependent on bacterial folate synthesis. In humans, it may be possible to inhibit bacterial folate synthesis in the human gut while maintaining healthy folate status in the body via food and supplementation. The supplement form of folic acid has a common breakdown product that can be used by bacteria to increase folate synthesis. Thus, supplementation with folic acid may not be good for health in certain circumstances such as in older people or those with an excess of proteobacteria in their microbiome. For these groups, alternative supplement strategies may be a safer way to ensure adequate folate levels.