Maternal and child health are intrinsically linked. With accumulating evidence over the past two decades supporting the developmental origins of health and diseases hypothesis, it is now widely recognised that nutrition in the first 1000 d sets the foundation for long-term health. Maternal diet before, during and after pregnancy can influence the developmental pathways of the fetus and lead to health consequences later in life. While maternal and infant mortality rates have declined significantly in the past two decades, the growing burden of obesity and chronic non-communicable diseases in women of reproductive age and children is on a rapid rise worldwide, in developed and developing countries. A key contributory factor is malnutrition, which is a consequence of consuming poor quality diets. Suboptimal macronutrient balance and micronutrient inadequacies can lead to undesirable maternal body composition and metabolism, in turn influencing the health of the mother and leading to longer-term metabolic and cognitive health consequences in the infant. The GUSTO (Growing Up in Singapore Towards healthy Outcomes) study, a mother–offspring multi-ethnic cohort study in Singapore, has contributed to this body of evidence over the past 10 years. This review will illustrate how nutritional epidemiological research through a birth cohort has illuminated the importance and urgency of maternal and child nutrition and health in a modern, industrialised setting. It underscores the importance of a number of critical nutrients during pregnancy, in combination with healthy dietary patterns and appropriate meal timing, for optimal maternal and child health.

Vitamin D deficiency (25-hydroxyvitamin D; 25(OH)D) is at epidemic proportions in western dwelling South Asian populations, including severe deficiency (<12⋅5 nmol/l) in 27–60% of individuals, depending on season. The paper aimed to review the literature concerning vitamin D concentrations in this population group. Research from the UK and Europe suggests a high prevalence of South Asians with 25(OH)D concentration <25 nmol/l, with most having a 25(OH)D concentration of <50 nmol/l. In Canada, South Asians appear to have a slightly higher 25(OH)D concentration. There are few studies from the United States, South Africa and Australasia. Reasons for vitamin D deficiency include low vitamin D intake, relatively high adiposity, sun exposure avoidance and wearing of a covered dress style for cultural reasons. Possible health effects of deficiency include bone diseases such as rickets and hypocalcaemia in children and osteomalacia in adults. Vitamin D deficiency may also increase the risk of other chronic diseases. Increased fortification of food items relevant to South Asian groups (e.g. chapatti flour), as well as increased use of vitamin D supplements may help reduce this epidemic. Introducing culturally acceptable ways of increasing skin exposure to the sun in South Asian women may also be beneficial but further research is needed to assess the effectiveness of different approaches. There may be a need for a South Asian specific vitamin D dietary intake guideline in western countries. To conclude, vitamin D deficiency is epidemic in South Asians living in western countries and there is a clear need for urgent public health action.

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.

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.

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.

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.

We conducted a narrative review on the interaction between dietary patterns with demographic and lifestyle variables in relation to health status assessment. The food pattern has the advantage of taking into account the correlations that may exist between foods or groups of foods, but also between nutrients. It is an alternative and complementary approach in analysing the relationship between nutrition and the risk of chronic diseases. For the determination of dietary patterns one can use indices/scores that evaluate the conformity of the diet with the nutrition guidelines or the established patterns (a priori approach). The methods more commonly used are based on exploratory data (a posteriori): cluster analysis and factor analysis. Dietary patterns may vary according to sex, socio-economic status, ethnicity, culture and other factors, but more, they may vary depending on different associations between these factors. The dietary pattern exerts its effects on health in a synergistic way or even in conjunction with other lifestyle factors, and we can therefore refer to a ‘pattern of lifestyle’.

Sex and gender are important factors that impact cardiometabolic traits. Men have lower life expectancy and higher prevalence of fatal chronic conditions at younger age. Lifestyle risk profiles in young men have been rarely studied in the context of cardiometabolic health. This review aimed to summarise the evidence regarding the patterns of dietary-lifestyle behaviours in a population of young men (age <40years) and their associations with cardiometabolic health. Overall, unfavourable clusters of health behaviours are more prominent in men, when compared to women and more prevalent in younger adults, when compared to older age groups. Early signs of cardiometabolic health abnormalities have been reported among men with higher adherence to patterns which consistently shared poor dietary habits as a common denominator, combined with stimulant use, inadequate sleep or insufficient physical activity. In the majority of studies, dietary assessment was limited to the investigation of one or two behaviours, most frequently fruit and vegetable intake. Since young men may engage in a mixture of explicit behaviours, the examination of a singular dietary habit may not represent the overall diet quality. To conclude, the data regarding the synergistic effects of a broad spectrum of dietary and lifestyle behaviours in the context of cardiometabolic health remain scarce in this population. The inclusion of a broader range of dietary and lifestyle variables into the multicomponent pattern analysis might have a greater potential in explaining the association with cardiometabolic health. Defining behavioural clusters can help to develop interventions, tailored to the specific needs of the targeted group.

Lifestyle intervention may be effective in reducing type 2 diabetes mellitus incidence and cardiometabolic risk. A more personalised nutritional approach based on an individual or subgroup-based metabolic profile may optimise intervention outcome. Whole body insulin resistance (IR) reflects defective insulin action in tissues such as muscle, liver, adipose tissue, gut and brain, which may precede the development of cardiometabolic diseases. IR may develop in different organs but the severity may vary between organs. Individuals with more pronounced hepatic IR have a distinct plasma metabolome and lipidome profile as compared with individuals with more pronounced muscle IR. Additionally, genes related to extracellular modelling were upregulated in abdominal subcutaneous adipose tissue in individuals with more pronounced hepatic IR, whilst genes related to inflammation as well as systemic low-grade inflammation were upregulated in individuals with primarily muscle IR. There are indications that these distinct IR phenotypes may also respond differentially to dietary macronutrient composition. Besides metabolic phenotype, microbial phenotype may be of importance in personalising the response to diet. In particular fibres or fibre mixtures, leading to a high distal acetate and SCFA production may have more pronounced effects on metabolic health. Notably, individuals with prediabetes may have a reduced response to diet-induced microbiota modulation with respect to host insulin sensitivity and metabolic health outcomes. Overall, we need more research to relate metabolic subphenotypes to intervention outcomes to define more optimal diets for individuals with or predisposed to chronic metabolic diseases.

Excessive adipose accumulation, which is the main driver for the development of secondary metabolic complications, has reached epidemic proportions and combined pharmaceutical, educational and nutritional approaches are required to reverse the current rise in global obesity prevalence rates. Brown adipose tissue (BAT) is a unique organ able to dissipate energy and thus a promising target to enhance BMR to counteract a positive energy balance. In addition, active BAT might support body weight maintenance after weight loss to prevent/reduce relapse. Natural products deliver valuable bioactive compounds that have historically helped to alleviate disease symptoms. Interest in recent years has focused on identifying nutritional constituents that are able to induce BAT activity and thereby enhance energy expenditure. This review provides a summary of selected dietary phytochemicals, including isoflavones, catechins, stilbenes, the flavonoids quercetin, luteolin and resveratrol as well as the alkaloids berberine and capsaicin. Most of the discussed phytochemicals act through distinct molecular pathways e.g. sympathetic nerve activation, AMP-kinase signalling, SIRT1 activity or stimulation of oestrogen receptors. Thus, it might be possible to utilise this multitude of pathways to co-activate BAT using a fine-tuned combination of foods or combined nutritional supplements.

The omega-3 index, the percentage of EPA plus DHA in erythrocytes (measured by standardised analysis), represents a human body's status in EPA and DHA. An omega-3 index is measured in many laboratories around the world; however, even small differences in analytical methods entail large differences in results. Nevertheless, results are frequently related to the target range of 8–11 %, defined for the original and scientifically validated method (HS-Omega-3 Index®), raising ethical issues, and calling for standardisation. No human subject has an omega-3 index <2 %, indicating a vital minimum. Thus, the absence of EPA and DHA cannot be tested against presence. Moreover, clinical events correlate with levels, less with the dose of EPA and DHA, and the bioavailability of EPA and DHA varies inter-individually. Therefore, the effects of EPA and DHA are difficult to demonstrate using typical drug trial methods. Recent epidemiologic data further support the relevance of the omega-3 index in the cardiovascular field, since total mortality, cardiovascular mortality, cardiovascular events such as myocardial infarction or stroke, or blood pressure all correlate inversely with the omega-3 index. The omega-3 index directly correlates with complex brain functions. Compiling recent data supports the target range for the omega-3 index of 8–11 % in pregnancy. Many other potential applications have emerged. Some, but not all health issues mentioned have already been demonstrated to be improved by increasing intake of EPA and DHA. Increasing the omega-3 index into the target range of 8–11 % with individualised doses of toxin-free sources for EPA and DHA is tolerable and safe.

PUFA of the n-3 and n-6 families are present in high concentration in the brain where they are major components of cell membranes. The main forms found in the brain are DHA (22 :6, n-3) and arachidonic acid (20:4, n-6). In the past century, several studies pinpointed that modifications of n-3 and n-6 PUFA levels in the brain through dietary supply or genetic means are linked to the alterations of synaptic function. Yet, synaptopathies emerge as a common characteristic of neurodevelopmental disorders, neuropsychiatric diseases and some neurodegenerative diseases. Understanding the mechanisms of action underlying the activity of PUFA at the level of synapses is thus of high interest. In this frame, dietary supplementation in PUFA aiming at restoring or promoting the optimal function of synapses appears as a promising strategy to treat synaptopathies. This paper reviews the link between dietary PUFA, synapse formation and the role of PUFA and their metabolites in synaptic functions.

Inflammation is a normal part of the immune response and should be self-limiting. Excessive or unresolved inflammation is linked to tissue damage, pathology and ill health. Prostaglandins and leukotrienes produced from the n-6 fatty acid arachidonic acid are involved in inflammation. Fatty acids may also influence inflammatory processes through mechanisms not necessarily involving lipid mediators. The n-3 fatty acids EPA and DHA possess a range of anti-inflammatory actions. Increased content of EPA and DHA in the membranes of cells involved in inflammation has effects on the physical nature of the membranes and on the formation of signalling platforms called lipid rafts. EPA and DHA interfere with arachidonic acid metabolism which yields prostaglandins and leukotrienes involved in inflammation. EPA gives rise to weak (e.g. less inflammatory) analogues and both EPA and DHA are substrates for the synthesis of specialised pro-resolving mediators. Through their effects on early signalling events in membranes and on the profile of lipid mediators produced, EPA and DHA alter both intracellular and intercellular signals. Within cells, this leads to altered patterns of gene expression and of protein production. The net result is decreased production of inflammatory cytokines, chemokines, adhesion molecules, proteases and enzymes. The anti-inflammatory and inflammation-resolving effects of EPA and DHA are relevant to both prevention and treatment of human diseases that have an inflammatory component. This has been widely studied in rheumatoid arthritis where there is good evidence that high doses of EPA + DHA reduce pain and other symptoms.

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.

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.

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.

Recognising the adverse outcomes that occur to obese adults over the age of 65 years with loss of muscle mass or strength, or sarcopenia is important. We will review the definitions of sarcopenic obesity, and attempt to link the epidemiological data with the molecular pathways. Upon understanding the model of sarcopenic obesity, we will discuss targeted interventions and further challenges to address this geriatric syndrome. As our understanding of this syndrome is growing, more data are emerging to help define sarcopenic obesity across different populations. We now have a better understanding of biological pathways in ageing such as changes in body composition, sex-specific hormones, pro-inflammatory markers and myocellular mechanisms. We will review a comprehensive model that shows the interactions between the different pathways leading to sarcopenic obesity. Such a model will explain the promising interventions in place and invite future ones. Sarcopenic obesity is an important geriatric syndrome with significant clinical and healthcare implications. Further research is needed to harmonise definitions, clarify mechanisms contributing to syndrome and use evidence-based interventions to target biological mechanisms in both research and clinical settings.

Selenium (Se) is an essential element for human health. However, our knowledge of the prevalence of Se deficiency is less than for other micronutrients of public health concern such as iodine, iron and zinc, especially in sub-Saharan Africa (SSA). Studies of food systems in SSA, in particular in Malawi, have revealed that human Se deficiency risks are widespread and influenced strongly by geography. Direct evidence of Se deficiency risks includes nationally representative data of Se concentrations in blood plasma and urine as population biomarkers of Se status. Long-range geospatial variation in Se deficiency risks has been linked to soil characteristics and their effects on the Se concentration of food crops. Selenium deficiency risks are also linked to socio-economic status including access to animal source foods. This review highlights the need for geospatially-resolved data on the movement of Se and other micronutrients in food systems which span agriculture–nutrition–health disciplinary domains (defined as a GeoNutrition approach). Given that similar drivers of deficiency risks for Se, and other micronutrients, are likely to occur in other countries in SSA and elsewhere, micronutrient surveillance programmes should be designed accordingly.

The aim of the present paper is to review the effects of non-digestible oligosaccharides (NDO) on immunity, focusing on their microbiota-independent mechanisms of action, as well as to explore their potential beneficial role in inflammatory bowel diseases (IBD). IBD are chronic, inflammatory conditions of the gastrointestinal tract. Individuals with IBD have an aberrant immune response to commensal microbiota, resulting in extensive mucosal inflammation and increased intestinal permeability. NDO are prebiotic fibres well known for their role in supporting intestinal health through modulation of the gut microbiota. NDO reach the colon intact and are fermented by commensal bacteria, resulting in the production of SCFA with immunomodulatory properties. In disease states characterised by increased gut permeability, prebiotics may also bypass the gut barrier and directly interact with intestinal and systemic immune cells, as demonstrated in patients with IBD and in infants with an immature gut. In vitro models show that fructooligosaccharides, inulin and galactooligosaccharides exert microbiota-independent effects on immunity by binding to toll-like receptors on monocytes, macrophages and intestinal epithelial cells and by modulating cytokine production and immune cell maturation. Moreover, animal models and human supplementation studies demonstrate that some prebiotics, including inulin and lactulose, might reduce intestinal inflammation and IBD symptoms. Although there are convincing preliminary data to support NDO as immunomodulators in the management of IBD, their mechanisms of action are still unclear and larger standardised studies need to be performed using a wider range of prebiotics.

Fruit and vegetables (F&V) play an important role in the prevention of obesity and other chronic diseases and low intakes have been highlighted as one of the risk factors attributing to global mortality in adults. The childhood years are a critical period during which eating behaviours and food preferences evolve, providing an opportunity to develop and foster healthy eating practices, which carry into adulthood. This review aimed to summarise dietary guidelines relating to F&V, intakes of F&V and the contribution of F&V to energy and nutrient intakes in school-aged children in Europe. The current review showed a paucity of data in relation to guidelines specific for children for F&V consumption. Where guidelines were available, they ranged from 100 to 500 g or one to three portions of F&V daily (with variations in the categorisations). A key finding was the lack of data on estimates of F&V intakes in school-aged children across Europe. Where data were available, intakes ranged from 221 to 404 g/d and were generally below the WHO recommendation of at least 400 g/d. F&V contributed low proportions of energy intake (6–9%) but made significant contributions to intakes of dietary fibre (19–37%), vitamin A (26–46%), vitamin C (32–83%) and potassium (16–27%); however, they also contributed to intakes of total (25–50%) and free sugar (7–11%). This review has highlighted the need for more data on estimates of F&V intakes in school-aged children in Europe and a need for continued promotion of F&V consumption to increase intakes in this age group.