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.

The 2019 Nutrition Society Spring Conference, which convened in Dundee, focused on the challenges presented by inter-individual differences in the responses to nutrition and in conducting nutritional research. The programme brought together national and international experts to discuss the collective evidence on inter-individual nutritional responses and impacts on health. Speakers and delegates from across the UK, Europe and the USA debated new methods of conducting research in nutrition and discussed the development of appropriate dietary interventions to maintain health and prevent disease in diverse populations. Symposium 1 focused on the effects of ethnicity on nutrient availability and type 2 diabetes and cardio-metabolic disease. Symposium 2 explored sex differences in nutrient availability and health and metabolism. The final symposium examined genetic and phenotypic variation, nutrition and health. The meeting ended with a panel discussion about how we take research to recommendations and concluded with a need to consider inter-individual differences in planning, conducting and analysing nutritional research.

Hypertension is a major cause of cardiovascular disease and overall mortality. High dietary salt intake is one of the key risk factors for hypertension and in 2017, it was one of the three leading dietary risk factors for death and disability adjusted life years globally. Despite the efforts to change this behaviour, salt consumption still exceeds the recommendations. One of the main determinants of food intake, and potentially salt, is taste. Taste perception may be genetically determined, however research exploring the associations between genetics, salt taste perception and salt intake is scarce. This may be of special importance in younger adult populations where increased preference for salt is suggested. Therefore, the aim of this study was to explore the associations between genetics, salt taste perception (taste threshold and preference) and salt intake in young adults.

This study was approved by the St Mary's University Ethics Sub-Committee. Forty-two participants (18–35 years, 67% female and 33% male) completed the study. Salt taste thresholds were identified using the British Standards Institution sensory analysis method (BS ISO 3972:2011) and preference for salty taste by asking participants how salty they usually prefer to eat their food using a Likert scale. Salt intake, expressed as mg sodium/1000 kcal, was measured using a five-step multiple pass 24-hour recall for one day of the week and one weekend day. Participants were genotyped for two genetic variants in the SCNN1B and TRPV1 genes, which code for ion channels expressed in taste cells. Multiple regression analysis was performed including SCNN1B and TRPV1 variants, salt taste threshold and preference as predictor variables and sodium intake (mg/1000 kcal) as the dependent variable. Statistical significance was set at p < 0.05.

Participants were normal weight (Body Mass Index 23.8 ± 3.7 kg/m2), predominantly Caucasian with salt intake 7.5 ± 2.7 g per day, reflecting current intakes in the UK. Regression model including genetics, thresholds and preference for salty taste explained 54% of the variance (p = 0.028). In this model, TRPV1 variant rs8065080 [β = 422, confidence interval (50, 794), p = 0.030] and salt preference [β = 618, confidence interval (258, 978), p = 0.004] were indicated as predictors of sodium intake. These findings suggest that genetics and preference for salty taste may be drivers of salt intake in younger populations. If replicated, this information may in the future be used in designing more personalised approaches in changing this behaviour.

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.

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.

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.

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.

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.

As the primary risk factor for cardiovascular disease (CVD), hypertension is the leading cause of preventable, premature mortality globally. Hypertension, or elevated blood pressure (BP), has a number of well-established risk factors, including genetics. A common C677T polymorphism in the gene encoding the folate metabolising enzyme methylenetetrahydrofolate reductase (MTHFR) affects 10–12% of UK and Irish populations and has been linked with 24–87% increased risk of hypertension globally. Evidence from randomised controlled trials (RCTs) conducted at this Centre has shown BP to be highly responsive (by 5–13 mmHg) to supplementation with riboflavin (MTHFR co-factor), an effect confined to homozygous individuals (TT genotype). To date, our trials have focused on peripheral BP; however, additional measures of vascular health such as central pressure are reported to be more closely correlated with CVD risk. Investigation of central BP, augmentation index (AIx) and pulse pressure amplification (PPA) may thus offer further insight into the role of this gene-nutrient interaction in blood pressure. The present study aims to investigate BP, and measures of vascular health in healthy adults stratified by MTHFR 677 genotype. Apparently healthy adults aged 18–60 years were recruited from workplaces across Northern Ireland and screened for MTHFR genotype via buccal swab. Clinic BP, anthropometry and blood sample were measured in TT individuals (n 209) and age and sex-matched CC (n 98) and CT (n 102) controls. AIx and central BP were assessed using SphygmoCor® (AtCor Medical, Australia). Preliminary results demonstrate higher BP in individuals with the MTHFR 677TT genotype compared to non-TT controls (systolic BP 134.7 ± 13.8 mmHg vs 129.7 ± 12.4 mmHg, P < 0.001; diastolic BP 81.6 ± 9.5 mmHg vs 79.7 mmHg ± 8.9 mmHg, P = 0.023, respectively). The MTHFR 677TT genotype group had significantly higher central systolic BP (119.4 ± 11.8 vs 116.7 ± 10.9 mmHg, P = 0.018), central pulse pressure (P = 0.006) and central mean pressure (P = 0.011) compared to the non-TT group. No significant differences for central diastolic BP, pulse pressure amplification, pulse pressure ratio and augmentation index were observed. This study confirms the phenotype of elevated BP in individuals with the C677T polymorphism in the gene encoding MTHFR. For the first time, this study reports that individuals with the MTHFR 677TT genotype have higher central systolic BP, central mean pressure and pulse pressure. Further investigations through RCTs investigating the effect of the MTHFR cofactor, riboflavin, on central blood pressure in these genetically at-risk adults are warranted.

Extensive research demonstrates unequivocally that nutrition plays a fundamental role in maintaining health and preventing disease. In parallel nutrition research provides evidence that the risks and benefits of diet and lifestyle choices do not affect people equally, as people are inherently variable in their responses to nutrition and associated interventions to maintain health and prevent disease. To simplify the inherent complexity of human subjects and their nutrition, with the aim of managing expectations for dietary guidance required to ensure healthy populations and individuals, nutrition researchers often seek to group individuals based on commonly used criteria. This strategy relies on demonstrating meaningful conclusions based on comparison of group mean responses of assigned groups. Such studies are often confounded by the heterogeneous nutrition response. Commonly used criteria applied in grouping study populations and individuals to identify mechanisms and determinants of responses to nutrition often contribute to the problem of interpreting the results of group comparisons. Challenges of interpreting the group mean using diverse populations will be discussed with respect to studies in human subjects, in vivo and in vitro model systems. Future advances in nutrition research to tackle inter-individual variation require a coordinated approach from funders, learned societies, nutrition scientists, publishers and reviewers of the scientific literature. This will be essential to develop and implement improved study design, data recording, analysis and reporting to facilitate more insightful interpretation of the group mean with respect to population diversity and the heterogeneous nutrition response.

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.

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.

Meta-analyses of epidemiological data report that adults who carry a common polymorphism, the MTHFR 677C→T, in the gene encoding the folate-metabolising enzyme methylenetetrahydrofolate reductase (MTHFR) have a 40% increased risk of CVD and an 87% increased risk of hypertension. Riboflavin (vitamin B2), in its co-enzymatic form flavin adenine nucleotide (FAD), is required as a co-factor by MTHFR and previous trials in hypertensive patients have shown a blood pressure lowering response to riboflavin supplementation that is specific to individuals homozygous for this polymorphism (TT genotype). Low folate status is commonly reported in adults with the TT genotype however the effect of this genetic variant on riboflavin status has not previously been investigated. The aim of this study, therefore, was to investigate dietary intake and biomarker status of riboflavin by MTHFR genotype in Irish adults using data from the National Adult Nutrition Survey (2008–2010) (www.iuna.net).

A 4-day semi-weighed food record was used to collect food and beverage intake data from a representative sample of 1500 Irish adults (18–90 years). Dietary intake data were analysed using WISP© based on UK food composition tables (modified to include recipes of composite dishes, nutritional supplements, fortified foods and generic Irish foods that were commonly consumed). Usual intakes were calculated via the NCI-method using SAS© Enterprise Guide. Blood samples (n = 1126) were collected by venepuncture by a trained professional and were processed and analysed using standard operating procedures. Biomarker status of riboflavin was determined by erthyrocyte gluthathione reductase activation coefficient (EGRac), a functional assay that measures the activity of the enzyme glutathione reductase before and after in vitro activation with its prosthetic group FAD; a lower value indicates better status.

It was found that 12% of the population had the TT genotype. As expected, there was no significant difference in riboflavin intake across the genotype (CC, CT or TT) groups. Similarly, no significant genotype differences in riboflavin status (EGRac) were observed (1.36 vs 1.37 vs 1.38 respectively). Overall, 61% of the total population had EGRac values > 1.3, indicative of low/deficient status with no significant difference observed between the genotype groups (60%,61% and 61%, respectively).

These data suggest that riboflavin status is not influenced by the C677T polymorphism in MTHFR in this cohort of nationally representative Irish adults. Further research is needed to see the impact of riboflavin status on blood pressure across the genotype groups in this nationally representative cohort of Irish adults.

Type 2 diabetes (T2D) is a global public health priority, particularly for populations of black African-Caribbean ethnicity, who suffer disproportionately high rates of the disease. While the mechanisms underlying the development of T2D are well documented, there is growing evidence describing distinctions among black African-Caribbean populations. In the present paper, we review the evidence describing the impact of black African-Caribbean ethnicity on T2D pathophysiology. Ethnic differences were first recognised through evidence that metabolic syndrome diagnostic criteria fail to detect T2D risk in black populations due to less central obesity and dyslipidaemia. Subsequently more detailed investigations have recognised other mechanistic differences, particularly lower visceral and hepatic fat accumulation and a distinctly hyperinsulinaemic response to glucose stimulation. While epidemiological studies have reported exaggerated insulin resistance in black populations, more detailed and direct measures of insulin sensitivity have provided evidence that insulin sensitivity is not markedly different to other ethnic groups and does not explain the hyperinsulinaemia that is exhibited. These findings lead us to hypothesise that ectopic fat does not play a pivotal role in driving insulin resistance in black populations. Furthermore, we hypothesise that hyperinsulinaemia is driven by lower rates of hepatic insulin clearance rather than heightened insulin resistance and is a primary defect rather than occurring in compensation for insulin resistance. These hypotheses are being investigated in our ongoing South London Diabetes and Ethnicity Phenotyping study, which will enable a more detailed understanding of ethnic distinctions in the pathophysiology of T2D between men of black African and white European ethnicity.