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.

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.

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.

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.

In the UK 21% of pregnant women are categorised as obese(1). Women who enter pregnancy with a high body mass index (BMI) are at greater risk of gestational weight gain (GWG) above that recommended by the Institute of Medicine (IOM) and are less likely to return to their pre-pregnancy weight compared to women with a healthy BMI(2). Pregnancy can therefore alter a woman's weight gain trajectory across the life course, through retention of gestational weight gained. Given the increase in prevalence of obesity among women of reproductive age, the aim of this study was to identify antenatal and postnatal modifiable determinants associated with successful postpartum weight loss in women who participated in UPBEAT; a multi-centre randomised controlled trial comparing a lifestyle intervention of diet and physical activity to standard care during pregnancy.

710 women completed the 6-month postpartum follow-up visit, 464 (65%) of which provided complete data for the analysis. Using regression analysis, we examined the relationship between postpartum weight retention (PPWR; calculated by subtracting pre-pregnancy weight from six-month postpartum weight) and modifiable determinants including: reported glycaemic index and smoking status at baseline (15–18 weeks’ gestation), GWG within the IOM recommendations, self-reported postpartum physical activity (categorised as low, moderate or high) and mode of infant feeding (breastfed, formula or mixed). Women were excluded if they gave birth < 37 weeks gestation or they were pregnant at the 6-month visit. Results were adjusted for age, BMI, ethnicity, socio-economic status, parity and randomisation arm.

In this cohort of obese women 52% were at or below their pre-pregnancy weight by 6 months postpartum. Overall, there was a reduction in PPWR of -0.23 ± 6.7 kg [-23.5 to 23.0 kg]. In an adjusted multiple regression model, women who breastfed for ≥ 4months, had moderate or high levels of physical activity and appropriate GWG, were more likely to be at or below their pre-pregnancy weight by 6-months postpartum (all p < 0.02). In a mutually-adjusted multivariate model, for each additional factor women lost a further -1.5 kg (95%CI -2.3 to -0.68; p < 0.001) compared to their pre-pregnancy weight.

This study has shown that there is an incremental association with postpartum weight loss and the identified modifiable determinants. These findings support initiatives which target any or all these factors during the antenatal and postnatal periods to help support women with returning to their pre-pregnancy weight.

Vitamin D is a fundamentally critical nutrient that the human body requires to function properly. It plays an important role in musculoskeletal health due to its involvement in the regulation of calcium and phosphorus. Having a low level of vitamin D in the body may be detrimental for a wide range of health outcomes, including risk of osteoporotic and stress fractures, risk of CVD and some cancers, and lowering of the capability of the immune system. Vitamin D is an unusual nutrient; it is not a vitamin, in the true sense of the word but a pro-hormone. The main source of vitamin D is UV exposure, not dietary intake. Interestingly, there are two forms of vitamin D, vitamin D2 and vitamin D3, both of which are metabolised into 25-hydroxyvitamin D (25(OH)D) in the liver, the biomarker of vitamin D status. Vitamin D deficiency is a global public health problem, especially amongst older people and ethnic minority groups. The newest publication from the UK Government's Public Health England Department recommends that vitamin D intake should be 10 μg daily and this recommendation compares well (albeit lower) with other guidelines such as the Institute of Medicine recommendation of 15 μg for those aged 1–70 years and 20 μg for those 70 years or over. Few countries, however, have a specific vitamin D policy to prevent deficiency in populations. Finland leads the way, demonstrating impressive results in reducing population-level vitamin D deficiency through mandatory food fortification programmes. Collaboration between academia, government and industry, including countries from varying latitudes, is essential to identify long-term solutions to the global issue of vitamin D deficiency. This paper provides a narrative review of the evidence related to the role of vitamin D deficiency in health outcomes, outlines controversies regarding setting levels of adequacy, identifies the prevalence of vitamin D deficiency across the globe, and identifies population-level strategies adopted by countries to prevent vitamin D deficiency.

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.

This review seeks to synthesise our knowledge about changes in hunger and satiety that occur during diet-induced weight loss and during weight loss maintenance, with a particular focus on youth with obesity. Mechanisms of appetite responses to weight loss rely heavily on the adult literature. Physiological mechanisms that control appetite and satiety via the gut–brain axis have been elucidated but we have an incomplete picture of changes in gut hormones and peptides in youth with obesity. In adolescents, the role of the brain in long-term sensing of body composition and modifying appetite and satiety changes is easily over-ridden by hedonic influences for the reward of highly palatable sweet foods and encourages over-consumption. Accordingly, reward cues and hyper-responsiveness to palatable foods lead to a pattern of food choices. Different reward systems are necessary that are substantial enough to reward the continued individual effort required to sustain new behaviours, that need to be adopted to support a reduced body weight. Periods of growth and development during childhood provide windows of opportunity for interventions to influence body weight trajectory but long-term studies are lacking. More emphasis needs to be placed on anticipatory guidance on how to manage powerful hedonic influences of food choice, essential to cope with living in our obesogenic environment and managing hunger which comes with the stronger desire to eat after weight has been lost.

The influence of dietary habits on health/disease is well-established. Accurate dietary assessment is essential to understand metabolic pathways/processes involved in this relationship. In recent years, biomarker discovery has become a major area of interest for improving dietary assessment. Well-established nutrient intake biomarkers exist; however, there is growing interest in identifying and using biomarkers for more accurate and objective measurements of food intake. Metabolomics has emerged as a key tool used for biomarker discovery, employing techniques such as NMR spectroscopy, or MS. To date, a number of putatively identified biomarkers were discovered for foods including meat, cruciferous vegetables and legumes. However, many of the results are associations only and lack the desired validation including dose–response studies. Food intake biomarkers can be employed to classify individuals into consumers/non-consumers of specific foods, or into dietary patterns. Food intake biomarkers can also play a role in correcting self-reported measurement error, thus improving dietary intake estimates. Quantification of food intake was previously performed for citrus (proline betaine), chicken (guanidoacetate) and grape (tartaric acid) intake. However, this area still requires more investigation and expansion to a range of foods. The present review will assess the current literature of identified specific food intake biomarkers, their validation and the variety of biomarker uses. Addressing the utility of biomarkers and highlighting gaps in this area is important to advance the field in the context of nutrition research.

The high prevalence of maternal deficiency and the low vitamin D content of breastmilk places newborns and infants at particular risk of vitamin D deficiency. In response to an increase in the incidence of nutritional rickets, the Food Safety Authority of Ireland published an interim infant vitamin D supplementation policy in 2007, which was implemented by the Health Service Executive in Ireland in May 2010. This recommends that all infants be given a 5μg exclusive vitamin D3 supplement daily from birth to 12 months. As adherence is not monitored nationally and the policy has not been evaluated, the aim of this study was to conduct a detailed evaluation of supplementation practices across two maternal-infant cohort studies. Data from the prospective BASELINE (recruited 2008–2011) and COMBINE (recruited 2015–2017) birth cohorts, based in Cork, Ireland, were used to examine supplementation practices. After supplementation policy implementation, BASELINE collected vitamin D supplement use data (n = 1528) at 2, 6 and 12 months. In COMBINE, 7 study visits from birth to 12 months allowed continuous collection of detailed longitudinal supplementation data in 364 participants. Use of supplemental vitamin D was higher in COMBINE than BASELINE at 2 (93 vs. 49%), 6 (89 vs. 64%) and 12 (72 vs. 44%) months (all P < 0.001). In COMBINE, 92% initiated vitamin D supplementation at birth and the median supplementation duration was 51 (40, 52) weeks, although there was a wide range (3–52 weeks). 94% of COMBINE parents used a vitamin D3 only supplement and 88% used the recommended 5μg dose. Half (51%) always supplemented daily; a further 33% supplemented at least 3–6 times/week. Full policy adherence was defined as the provision of a 5μg vitamin D3 supplement daily from birth; 64% adhered fully to 2 months and 52% did so to 6 months. By 12 months, 30% had adhered fully to the policy and a further 16% gave 5μg frequently for the full 12 months. This data indicates a high level of awareness of the supplementation policy amongst new mothers, with substantially higher rates of supplementation in our current cohort compared with BASELINE. While most parents gave an exclusive 5μg vitamin D3 supplement, frequency and duration were the key barriers to full policy adherence. Given the lack of a maternal vitamin D supplementation policy in Ireland and high prevalence of low vitamin D status at birth, supplementation of infants with vitamin D remains a vital public health policy.

A longstanding issue in the field of nutrition is the potential inaccuracy of methods traditionally used for dietary assessment (i.e. food diaries and food frequency questionnaires). It is possible to overcome the limitations and biases of these techniques by combining them with analytical measurements in human biofluids. Metabolomic technologies are gaining popularity as nutritional tools due to their capacity to measure metabolic responses to external stimuli, such as the ingestion of certain foods. This project performed both LC-MS and 1H-NMR metabolomic profiling on serum samples collected as part of the NICOLA study (Northern Irish Cohort for the Longitudinal Study of Aging) in order to discover novel dietary biomarkers. A dietary validation cohort (NIDAS) was incorporated within NICOLA, involving 45 males and 50 females, aged 50 years and over. Participants provided detailed dietary data (4-day food diary) and blood samples at two time-points, six months apart. Serum samples were processed on two analytical platforms. 1H-NMR spectra were acquired using a Bruker 600 MHz Ascent coupled to a TCI cryoprobe and processed using Bayesil (University of Alberta, Canada). A Waters TQ-S coupled with an Acquity I-class UPLC was used in combination with a targeted commercially available kit (AbsoluteIDQ p180 kit, Biocrates). Mass spectra obtained were processed with MetIDQ and verified using MassLynx (v4.1). Data were tested for normality, and metabolite concentrations were correlated with recorded dietary intake of each food type using SPSS. Additional tests (PCA, PLS-DA, ROC Curves) were performed on MetaboAnalyst 4.0 (University of Alberta, Canada). More than 50 statistically significant (P < 0.05) food-metabolite correlations were detected, 15 of which remained significant after eliminating potential confounding from sex, age and BMI. The strongest correlations were between fruit consumption and acetic acid, and between dairy consumption and certain glycerophospholipids (e.g. LysoPC aa C20:3). Stratifying the cohort by gender yielded further correlations, including PC ae C38:2 (dairy; males), PC aa C34:4 (dairy; females), PC aa C36:4 (dairy; females) and trans-4-Hydroxyproline (meat; males). A number of potential blood-based food biomarkers were detected, many of which are gender-specific, and some are corroborated by previously published studies. However, further validation work is required. For example, biological plausibility needs to be established, and the findings need to be reproduced in other cohorts to demonstrate their applicability in larger and more diverse populations. These results contribute greatly to the ongoing efforts to discover and validate reliable nutritional biomarkers as an objective and unbiased measurement of food intake.

The Nutrition Society's 1st Annual Nutrition and Cancer Networking Conference brought together scientists from the fields of Nutrition, Epidemiology, Public Health, Medical Oncology and Surgery with representatives of the public, cancer survivors and cancer charities. Speakers representing these different groups presented the challenges to collaboration, how the needs of patients and the public can be met, and the most promising routes for future research. The conference programme promoted debate on these issues to highlight current gaps in understanding and barriers to generating and implementing evidence-based nutrition advice. The main conclusions were that the fundamental biology of how nutrition influences the complex cancer risk profiles of diverse populations needs to be better understood. Individual and population level genetics interact with the environment over a lifespan to dictate cancer risk. Large charities and government have a role to play in diminishing our current potently obesogenic environment and exploiting nutrition to reduce cancer deaths. Understanding how best to communicate, advise and support individuals wishing to make dietary and lifestyle changes, can reduce cancer risk, enhance recovery and improve the lives of those living with and beyond cancer.