Maternal obesity is a major risk factor for adverse health outcomes for both the mother and the child, including the serious public health problem of childhood obesity which is globally on the rise. Given the relatively intensive contact with health/care professionals following birth, the interpregnancy period provides a golden opportunity to focus on preconception and family health, and to introduce interventions that support mothers to achieve or maintain a healthy weight in preparation for their next pregnancy. In this review, we summarise the evidence on the association between interpregnancy weight gain with birth and obesity outcomes in the offspring. Gaining weight between pregnancies is associated with an increased risk of large-for-gestational age (LGA) birth, a predictor of childhood obesity, and weight loss between pregnancies in women with overweight or obesity seems protective against recurrent LGA. Interpregnancy weight loss seems to be negatively associated with birthweight. There is some suggestion that interpregnancy weight change may be associated with preterm birth, but the mechanisms are unclear and the direction depends if it is spontaneous or indicated. There is limited evidence on the direct positive link between maternal interpregnancy weight gain with gestational diabetes, pre-eclampsia, gestational hypertension and obesity or overweight in childhood, with no studies using adult offspring adiposity outcomes. Improving preconception health and optimising weight before pregnancy could contribute to tackling the rise in childhood obesity. Research testing the feasibility, acceptability and effectiveness of interventions to optimise maternal weight and health during this period is needed, particularly in high-risk and disadvantaged groups.

Marine n-3 fatty acids improve most of the biochemical alterations associated with insulin resistance (IR). Experimental models of dietary-induced IR in rodents have shown their ability (often at a very high dose) to prevent IR, but with sometimes a tissue specific effect. However, in a high sucrose diet-induced IR rat model, they are unable to reverse IR once installed; in other rodent models (dexamethasone, Zucker rats), they are inefficacious perhaps because of the severity of IR. The very low incidence of type-2 diabetes (T2D) in Inuits in the 1960s, which largely increased over the following decades in parallel to the replacement of their traditional marine food for a western diet strongly suggests a protective effect of marine n-3 towards the risk of T2D; this was confirmed by reversal of its incidence in intervention studies reintroducing their traditional food. In healthy subjects and insulin-resistant non-diabetic patients, most trials and meta-analyses conclude to an insulin-sensitising effect and to a very probable preventive or alleviating effect towards IR. Concerning the risk of T2D, concordant data allow us to conclude the protective effect of marine n-3 in Asians while suspicion exists of an aggravation of risk in Westerners, but with the possibility that it could be explained by a high heterogeneity of studies performed in this population. Some longitudinal cohorts in US/European people showed no association or a decreased risk. Further studies using more homogeneous doses, sources of n-3 and assessment of insulin sensitivity methods are required to better delineate their effects in Westerners.

Stress and other negative emotions, such as depression and anxiety, can lead to both decreased and increased food intake. The term ‘emotional eating’ has been widely used to refer to the latter response: a tendency to eat in response to negative emotions with the chosen foods being primarily energy-dense and palatable ones. Emotional eating can be caused by various mechanisms, such as using eating to cope with negative emotions or confusing internal states of hunger and satiety with physiological changes related to emotions. An increasing number of prospective studies have shown that emotional eating predicts subsequent weight gain in adults. This review discusses particularly three lines of research on emotional eating and obesity in adults. First, studies implying that emotional eating may be one behavioural mechanism linking depression and development of obesity. Secondly, studies highlighting the relevance of night sleep duration by showing that adults with a combination of shorter sleep and higher emotional eating may be especially vulnerable to weight gain. Thirdly, an emerging literature suggesting that genes may influence body weight partly through emotional eating and other eating behaviour dimensions. The review concludes by discussing what kind of implications these three avenues of research offer for obesity prevention and treatment interventions.

Several studies on gene–diet interactions (nutrigenetics) have been performed in western populations; however, there are only a few studies to date in lower middle-income countries (LMIC). A large-scale collaborative project called gene–nutrient interactions (GeNuIne) Collaboration, the main objective of which is to investigate the effect of GeNuIne on cardiometabolic traits using population-based studies from various ethnic groups, has been initiated at the University of Reading, UK. While South Asians with higher genetic risk score (GRS) showed a higher risk of obesity in response to a high-carbohydrate diet, South East and Western Asian populations with higher GRS showed an increased risk of central obesity in response to a high-protein diet. The paper also provides a summary of other gene–diet interaction analyses that were performed in LMIC as part of this collaborative project and gives an overview of how these nutrigenetic findings can be translated to personalised and public health approaches for the prevention of cardiometabolic diseases such as obesity, type 2 diabetes and CVD.

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.

The metabolomic profile of a biofluid can be altered by dietary intake, exercise and disease processes and, thus provides an important tool for the study of many physiological processes. However, in addition to perturbation due to disease, the metabolomic profile of urine and plasma has also been shown to vary due to many intrinsic physiological factors such as age, sex, hormonal status and diurnal variation. Characterisation of this normal degree of variation in the metabolomic profiles of human biofluids is a necessary and important step in the development of metabolomics for use in nutrition-related research. The current review focuses on the impact of sex on the metabolomic profile. A number of studies have reported that sex impacts metabolites such as amino acids, lipids, sugars and keto acids. Furthermore, we examine the effect of the menstrual cycle on the metabolomic profile. Responses to dietary interventions can also differ between the sexes and highlighting this is important for the development of the field of precision nutrition.

Emotional eating has traditionally been defined as (over)eating in response to negative emotions. Such overeating can impact general health because of excess energy intake and mental health, due to the risks of developing binge eating. Yet, there is still significant controversy on the validity of the emotional eating concept and several theories compete in explaining its mechanisms. The present paper examines the emotional eating construct by reviewing and integrating recent evidence from psychometric, experimental and naturalistic research. Several psychometric questionnaires are available and some suggest that emotions differ fundamentally in how they affect eating (i.e. overeating, undereating). However, the general validity of such questionnaires in predicting actual food intake in experimental studies is questioned and other eating styles such as restrained eating seem to be better predictors of increased food intake under negative emotions. Also, naturalistic studies, involving the repeated assessment of momentary emotions and eating behaviour in daily life, are split between studies supporting and studies contradicting emotional eating in healthy individuals. Individuals with clinical forms of overeating (i.e. binge eating) consistently show positive relationships between negative emotions and eating in daily life. We will conclude with a summary of the controversies around the emotional eating construct and provide recommendations for future research and treatment development.

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.

Marine n-3 PUFA exert beneficial effects that might inhibit atherosclerosis and reduce vascular disease. Previous studies have, however, reported conflicting results and here we have summarised the early history and the most recent findings from follow-up studies and randomised clinical trials investigating marine n-3 PUFA in relation to the risk of atherosclerotic CVD. Most follow-up studies have suggested that the intake of marine n-3 PUFA may be associated with a lower risk of CVD. Recent studies have also shown that it is important to focus on substitution issues and dietary patterns. Further, the use of gold standard biomarkers of fatty acid exposure such as adipose tissue should be encouraged. Findings from clinical supplemental trials have shown conflicting results and findings from previous meta-analyses and guidelines have generally not supported the use of fish oil supplements for the prevention of CVD. However, a recent meta-analysis including three recent large clinical trials with fish oil supplements reported a moderate beneficial effect on cardiovascular endpoints. Interestingly, results from a large clinical trial (REDUCE-IT) have suggested that supplementation with a high dose of purified EPA ethyl ester for 4⋅9 years significantly and markedly reduced the risk of cardiovascular events in patients with CVD and mild hypertriglyceridaemia; findings that need to be confirmed. While it seems appropriate to recommend consumption of fish, particular fatty fish for prevention of CVD, an effect of fish oil supplements is probably at best marginal perhaps apart from patients with hypertriglyceridaemia.

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.

Advances in genomics generated the concept that a better understanding of individual characteristics, e.g. genotype, will lead to improved tailoring of pharmaceutical and nutritional therapies. Subsequent developments in proteomics and metabolomics, in addition to wearable technologies for tracking parameters, such as dietary intakes, physical activity, heart rate and blood glucose, have further driven this idea. Alongside these innovations, there has been a rapid rise in companies offering direct-to-consumer genetic and/or microbiome testing, in combination with the marketing of personalised nutrition services. Key scientific questions include how disparate datasets are integrated, how accurate are current predictions and how these may be developed in the future. In this regard, lessons can be learned from systems biology, which aims both to integrate data from different levels of organisation (e.g. genomic, proteomic and metabolomic) and predict the emergent behaviours of biological systems or organisms as a whole. The present paper reviews the origins and recent advancement of ‘big data’ and systems approaches in medicine and nutrition. Conclusions are that systems integration of multiple technologies has generated mechanistic insights and informed the evolution of precision medicine and personalised nutrition. Pertinent ethical issues include who is entitled to access new technologies and how commercial companies are storing, using and/or re-mining consumer data. Questions about efficacy (both long-term behavioural change and health outcomes), cost-benefit and impacts on health inequalities remain to be fully addressed.

Sarcopenic obesity is characterised by the double burden of diminished skeletal muscle mass and the presence of excess adiposity. From a mechanistic perspective, both obesity and sarcopenia are associated with sub-acute, chronic pro-inflammatory states that impede metabolic processes, disrupting adipose and skeletal functionality, which may potentiate disease. Recent evidence suggests that there is an important cross-talk between metabolism and inflammation, which has shifted focus upon metabolic-inflammation as a key emerging biological interaction. Dietary intake, physical activity and nutritional status are important environmental factors that may modulate metabolic-inflammation. This paradigm will be discussed within the context of sarcopenic obesity risk. There is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation in sarcopenic obesity. Research suggests that there may be scope for the modulation of sarcopenic obesity with alterations in diet. The potential impact of increasing protein consumption and reconfiguration of dietary fat composition in human dietary interventions are evaluated. This review will explore emerging data with respect to if and how different dietary components may modulate metabolic-inflammation, particularly with respect to adiposity, within the context of sarcopenic obesity.