Cardio-metabolic risk (CMR) embodies a clustering of metabolic abnormalities that increase the likelihood of developing CVD in the large arteries of the heart, peripheral tissues and brain. These abnormalities share a common origin of insulin resistance, which manifests typically as excess visceral adipose tissue in the abdominal cavity, and within cells of key metabolic tissues (ectopic fat), including the liver, pancreas, heart and skeletal muscle. As expected, the increased risk of CVD that can be attributed to CMR factors is alarmingly high in overweight and obese populations, but this risk can be reduced by reversing many of the inappropriate diet and lifestyle behaviours that underlie its development. The Nutrition Society's 2018 Winter Meeting at the Royal Society of Medicine addressed the topic of the ‘Optimal diet and lifestyle for managing cardio-metabolic risk’, with the aim of providing mechanistic insights into the impact of macronutrients, dietary patterns and meal timing in key metabolic tissues. The 2-d programme concluded with a summary of its main outcomes, and an overview of their implications for dietary policy in the UK.

Although the first description of a syndrome defined by the co-existence of atherogenic and diabetogenic metabolic abnormalities is debated in the literature, it was Gerald Reaven who proposed, in his landmark 1988 Banting award lecture, that a significant proportion of individuals (with diabetes or not) were characterised by insulin resistance causing prejudice to cardiovascular health. However, Reaven was influenced by seminal observations made more than 50 years earlier by Himsworth who proposed that there were two forms of diabetes (insulin resistant v. insulin sensitive). Reaven went further in proposing the theory that insulin resistance was the most prevalent cause of CVD associated with metabolic abnormalities that he named syndrome X. Because there was a syndrome X documented in cardiology, the term evolved to insulin resistance syndrome. As Reaven could also find insulin-resistant individuals in non-obese subjects, he did not include obesity as a feature of syndrome X. Imaging studies then revealed that excess adipose tissue in the abdominal cavity, a condition described as visceral obesity, was the form of overweight/obesity associated with insulin resistance and its related abnormalities. As obesity risk assessment and management remain largely based on body weight (BMI) and weight loss, it is proposed that our clinical approaches and public health messages should be revisited. First, patients should be educated about the importance of monitoring their waistline as a crude index of abdominal adiposity. Secondly, public health approaches focussing on ‘lifestyle vital signs’ including achieving healthy waistlines rather than healthy body weights should be developed.

CVD remains the greatest cause of death globally, and with the escalating prevalence of metabolic diseases, including type-2 diabetes, CVD mortality is predicted to rise. While the replacement of SFA has been the cornerstone of effective dietary recommendations to decrease CVD risk since the 1980s, the validity of these recommendations have been recently challenged. A review of evidence for the impact of SFA reduction revealed no effect on CVD mortality, but a significant reduction in risk of CVD events (7–17%). The greatest effect was found when SFA were substituted with PUFA, resulting in 27% risk reduction in CVD events, with no effect of substitution with carbohydrate or protein. There was insufficient evidence from randomised controlled trials to conclude upon the impact of SFA replacement with MUFA on CVD and metabolic outcomes. However, there was high-quality evidence that reducing SFA lowered serum total, and specifically LDL-cholesterol, a key risk factor for CVD, with greatest benefits achieved by replacing SFA with unsaturated fats. The exchange of SFA with either PUFA or MUFA, also produced favourable effects on markers of glycaemia, reducing HbA1c, a long-term marker of glycaemic control. In conclusion, the totality of evidence supports lowering SFA intake and replacement with unsaturated fats to reduce the risk of CVD events, and to a lesser extent, cardiometabolic risk factors, which is consistent with current dietary guidelines.

n-3 PUFA may exert favourable effects on several processes that may inhibit the atherosclerotic process. However, the role of n-3 PUFA in lowering the risk of atherosclerotic CVD (ASCVD) has been fiercely debated. In the present paper, we summarise the main findings from previous follow-up studies of intake and studies using adipose tissue as an objective biomarker to investigate exposure to n-3 PUFA in relation to ASCVD risk and discuss some perspectives for further research. The majority of previous studies investigating intake of marine- and plant-based n-3 PUFA have focused on CHD while other ASCVD such as ischaemic stroke and peripheral artery disease have been less studied. However, recent data from Danish Diet, Cancer and Health cohort suggest that marine n-3 PUFA may be inversely associated with risk of myocardial infarction, ischaemic stroke and peripheral arterial disease caused by atherosclerosis. The effect of the plant-derived n-3 PUFA α-linolenic acid on ASCVD is less clear and several gaps in the literature remain to be explored.

Non-alcoholic fatty liver disease encompasses a spectrum of conditions from hepatic steatosis through to cirrhosis; obesity is a known risk factor. The liver plays a major role in regulating fatty acid metabolism and perturbations in intrahepatic processes have potential to impact on metabolic health. It remains unclear why intra-hepatocellular fat starts to accumulate, but it likely involves an imbalance between fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver and TAG export from the liver. As man spends the majority of the day in a postprandial rather than postabsorptive state, dietary fatty acid intake should be taken into consideration when investigating why intra-hepatic fat starts to accumulate. This review will discuss the impact of the quantity and quality of dietary fatty acids on liver fat accumulation and metabolism, along with some of the potential mechanisms involved. Studies investigating the role of dietary fat in liver fat accumulation, although surprisingly limited, have clearly demonstrated that it is total energy intake, rather than fat intake per se, that is a key mediator of liver fat content; hyperenergetic diets increase liver fat whilst hypoenergetic diets decrease liver fat content irrespective of total fat content. Moreover, there is now, albeit limited evidence emerging to suggest the composition of dietary fat may also play a role in liver fat accumulation, with diets enriched in saturated fat appearing to increase liver fat content to a greater extent when compared with diets enriched in unsaturated fats.

Nutrition is a major variable factor in human environments. The composition of nutrients has changed markedly in recent decades which may contribute to the increased prevalence of metabolic diseases, such as obesity and type 2 diabetes. Fat is an important component of the diet which comes in various forms with fatty acids (FA) of different carbon chain lengths and saturation degrees. In addition to being an energy supply, FA function as potent signalling molecules and influence transcriptional activity. Among other tissues, dietary FA target white adipose tissue function, which is central in maintaining metabolic health. This review focuses on the possible role of dietary FA composition and its effect on human white adipose tissue expandability and transcriptional response. Altogether, the existing literature suggests that unsaturated fat has more benign effects on adipose tissue distribution when compared to long-chain saturated fat. However, the mechanisms of action remain poorly characterised.

This narrative review aims to critically evaluate scientific evidence exploring the therapeutic role(s) of long-chain n-3 PUFA in the context of ageing, and specifically, sarcopenia. We highlight that beyond impairments in physical function and a lack of independence, the age-related decline in muscle mass has ramifications for cardio-metabolic health. Specifically, skeletal muscle is crucial in regulating blood glucose homeostasis (and by extension reducing type 2 diabetes mellitus risk) and providing gluconeogenic precursors that are critical for survival during muscle wasting conditions (i.e. AIDS). Recent interest in the potential anabolic action of n-3 PUFA is based on findings from experimental studies that measured acute changes in the stimulation of muscle protein synthesis (MPS) and/or chronic changes in muscle mass and strength in response to fish oil-derived n-3 PUFA supplementation. Key findings include a potentiated response of MPS to amino acid provision or resistance-based exercise with n-3 PUFA in healthy older adults that extrapolated to longer-term changes in muscle mass and strength. The key mechanism(s) underpinning this enhanced response of MPS remains to be fully elucidated, but is likely driven by the incorporation of exogenous n-3 PUFA into the muscle phospholipid membrane and subsequent up-regulation of cell signalling proteins known to control MPS. In conclusion, multiple lines of evidence suggest that dietary n-3 PUFA provide an essential link between musculoskeletal and cardio-metabolic health in older adults. Given that western diets are typically meagre in n-3 PUFA content, nutritional recommendations for maintaining muscle health with advancing age should place greater emphasis on dietary n-3 PUFA intake.

It is clear that the sugars component of the diet has potentially deleterious effects on health. In the past, the dietary sugars were collectively referred to as non-milk extrinsic sugars (UK) or added sugars. The WHO first proposed a new term, free sugars, which is rather broader than added sugars, and also includes the sugars in fruit juices and purees, as well as honey and syrups. This review considers the potential problems that free sugars represent in relation to health risks, and the recent proposals that free sugars are a more appropriate focus than added or total as far as public health initiatives are concerned. This will require major activities in relation to measurement, labelling and communication to the consumer if attempts to reduce dietary free sugars content are to be successful.

Dietary fibre comprises many different, mainly plant-based, compounds that are not fully digested in the human gut. Insoluble fibres include cellulose, hemi-celluloses and lignin and soluble fibres include pectins, β-glucan and hydro-colloids. In the UK, the daily recommended amount has increased to 30 g but only 13 % of men and 4 % of women meet this recommendation. Currently the mean intake for adults is 21 g for men and 17 g for women. There is a wealth of epidemiological evidence based on systematic reviews of trials and cohorts to support the higher fibre recommendation. This includes evidence of reductions in the risk for CVD (both heart disease and stroke) and lower risk of type 2 diabetes, lower blood pressure, lower LDL-cholesterol, as well as some cancers. Beneficial effects of fibre operate via a diverse range of mechanisms throughout the digestive system including the mouth, stomach and small and large intestine; some of which are still not completely understood. The updated recommendation for fibre is a long way from a typical British diet and requires several daily portions of fruit and vegetables and wholegrain foods. Improving dietary fibre intakes will require a variety of actions and policies from stakeholders; however, there is currently more of a focus on reducing sugar than increasing fibre. In order to increase the number of adults meeting the fibre recommendation, social marketing and labelling of high-fibre foods are warranted as well as reformulation and wider availability of wholegrain versions of popular foods.

CVD are the main cause of death especially in high-income countries. Previously, research focused on single nutrients including saturated and MUFA, sodium and dietary fibre, or specific foods such as fish, fruit and vegetables, and olive oil, in the aetiology of CVD. In recent years, however, the effects of complete dietary patterns on the prevention of CVD have gained interest, to account for diet heterogeneity and food–nutrient interactions. Several dietary patterns have been investigated, such as the Paleolithic diet, the vegetarian and vegan diets, the Diet Approaches to Stop Hypertension (DASH), the Nordic and Mediterranean diets, with many contradictions remaining. The aim of this review is to give an overview of the effects of these dietary patterns on CVD risk, to discuss their overall nutrient adequacy and briefly discuss their environmental impact.

Obesity remains a major public health concern and intermittent fasting is a popular strategy for weight loss, which may present independent health benefits. However, the number of diet books advising how fasting can be incorporated into our daily lives is several orders of magnitude greater than the number of trials examining whether fasting should be encouraged at all. This review will consider the state of current understanding regarding various forms of intermittent fasting (e.g. 5:2, time-restricted feeding and alternate-day fasting). The efficacy of these temporally defined approaches appears broadly equivalent to that of standard daily energy restriction, although many of these models of intermittent fasting do not involve fed-fasted cycles every other 24 h sleep–wake cycle and/or permit some limited energy intake outside of prescribed feeding times. Accordingly, the intervention period therefore may not regularly alternate, may not span all or even most of any given day, and may not even involve absolute fasting. This is important because potentially advantageous physiological mechanisms may only be initiated if a post-absorptive state is sustained by uninterrupted fasting for a more prolonged duration than applied in many trials. Indeed, promising effects on fat mass and insulin sensitivity have been reported when fasting duration is routinely extended beyond sixteen consecutive hours. Further progress will require such models to be tested with appropriate controls to isolate whether any possible health effects of intermittent fasting are primarily attributable to regularly protracted post-absorptive periods, or simply to the net negative energy balance indirectly elicited by any form of dietary restriction.

The present paper reviews the evidence as to whether patients on lipid-lowering drugs should restrict dietary SFA intake. Premature mortality from atherosclerotic CVD has fallen dramatically in many high-income countries. This appears to be due to a combination of improved treatment following a cardiovascular event and reduced risk factors, including LDL-cholesterol. Whether this reduction is due to changes in dietary habits, or the increasing availability of highly potent cholesterol-reducing drugs remains to be firmly established. While reducing dietary SFA intake has been the cornerstone of public health nutrition policy for several decades, the efficacy of such dietary changes has been challenged in recent years. While there remains a lack of consensus in the literature, there is an emerging view that dietary advice should be specifically modified to emphasise replacing SFA with PUFA in the diet rather than carbohydrate. The advice to moderate dietary SFA intake given to the general population is usually also given to those individuals at high risk of CVD who are prescribed lipid-lowering drugs. There is limited evidence to suggest that any potential benefit of such a diet on LDL-cholesterol may be offset by a concurrent decrease in HDL-cholesterol. However, as diets rich in SFA are frequently energy-dense, and rich in red and processed meat (potential risk factors for CVD in themselves), it would seem prudent to continue to advise patients on lipid-lowering drugs to maintain a low-fat diet.

CVD is a major burden on the health system in the UK. On average, diets are not aligned with current dietary recommendations, including those for salt, saturated fat, fibre, fruit and vegetables. Obesity prevalence is high and the majority of the population is consuming more energy than required. Addressing these issues would reduce the burden of CVD and help reduce inequalities in health. There is currently a range of policy interventions in place in England designed to help improve diets and reduce obesity, which in turn should help reduce the risk of CVD. Further actions may be needed in the long term to deliver sustained improvements to diet and health.

The concept of food addiction is currently a highly debated subject within both the general public and the scientific communities. The term food addiction suggests that individuals may experience addictive-like responses to food, similar to those seen with classic substances of abuse. An increasing number of studies have established the prevalence and correlates of food addiction. Moreover, food addiction may be associated with obesity and disordered eating. Thus, intervening on food addiction may be helpful in the prevention and therapy of obesity and eating disorders. However, controversy exists about if this phenomenon is best defined through paradigms reflective of Diagnostic and Statistical Manual of Mental Disorders (DSM-5) substance-related disorders (e.g. food addiction) or non-substance-related disorders (e.g. eating addiction) criteria. This review paper will give a brief summarisation of the current state of research on food addiction, a more precise definition of its classification, its differentiation from eating addiction and an overview on potential overlaps with eating disorders. Based on this review, there is evidence that food addiction may represent a distinct phenomenon from established eating disorders such as bulimia nervosa or binge-eating disorder. Future studies are needed to further examine and establish orthogonal diagnostic criteria specific to food addiction. Such criteria must differentiate the patterns of eating and symptoms that may be similar to those of eating disorders to further characterise food addiction and develop therapy options. To date, it is too premature to draw conclusions about the clinical significance of the concept of food addiction.

The developmental period constitutes a critical window of sensitivity to stress. Indeed, early-life adversity increases the risk to develop psychiatric diseases, but also gastrointestinal disorders such as the irritable bowel syndrome at adulthood. In the past decade, there has been huge interest in the gut–brain axis, especially as regards stress-related emotional behaviours. Animal models of early-life adversity, in particular, maternal separation (MS) in rodents, demonstrate lasting deleterious effects on both the gut and the brain. Here, we review the effects of MS on both systems with a focus on stress-related behaviours. In addition, we discuss more recent findings showing the impact of gut-directed interventions, including nutrition with pre- and probiotics, illustrating the role played by gut microbiota in mediating the long-term effects of MS. Overall, preclinical studies suggest that nutritional approaches with pro- and prebiotics may constitute safe and efficient strategies to attenuate the effects of early-life stress on the gut–brain axis. Further research is required to understand the complex mechanisms underlying gut–brain interaction dysfunctions after early-life stress as well as to determine the beneficial impact of gut-directed strategies in a context of early-life adversity in human subjects.

Food production is one of the major contributors to environmental damage. Adaptations in our food choices are needed to preserve resources for the needs of future generations. More sustainable consumption patterns have been encouraged by economic incentives, laws, education and communication campaigns. Nonetheless, consumers still find difficulties in trying to change their current food habits. This review takes a behavioural approach in encouraging sustainable food choices among consumers. From a nudging perspective, many behavioural changes can be encouraged in a non-obtrusive way by adapting the complex food environment in which consumers are operating. These interventions do not restrict consumers' choices but rather adapt the choice architecture wherein food decisions are made. Drawing on the literature from diverse theoretical perspectives, we provide an overview of the application of nudging for more sustainable food choices and highlight where more research is needed. More specifically, we discuss research that used nudging to engender cognitive impact (i.e. the use of labels or visibility enhancements), affective responses (i.e. sensorial and social influence cues) and behavioural effects (i.e. adjustments in convenience and product size). We conclude that this review only shows the tip of the iceberg of the research on nudging and sustainable consumption that is likely forthcoming in the next few years, following the successes of nudging applications in other domains. Nonetheless, each individual nudging intervention requires careful examination. Personal predispositions towards the environment should be considered when designing interventions, demonstrating the complementarity of nudging with education on sustainable consumption.

The aim of this narrative review is to assess and present evidence on the mechanisms of action of probiotics in constipation, their effectiveness and their utilisation by patients and healthcare professionals. Chronic constipation is a common bothersome disorder that has a considerable impact on patients' quality of life. Probiotics have been increasingly investigated for their effectiveness in various disorders, including chronic constipation. Probiotics may affect gut motility and constipation through their impact on the gut microbiota and fermentation, the central and enteric nervous system and the immune system. However, evidence for the effectiveness of probiotics in the management of constipation remains varied, with some strains demonstrating improvements, while others show no effect. Despite the uncertainty in evidence and the fact that the majority of healthcare professionals do not recommend probiotics for constipation, an increased prevalence of probiotic use by people with constipation has been shown. Therefore, there is a need for public health strategies to inform the public about where strong evidence of probiotic effectiveness exist, and where evidence is still weak. Education of healthcare professionals on the increased utilisation of probiotics for constipation by the public and on current evidence for the effectiveness of specific strains is also required.