An adequate intake of PUFA plays a vital role in human health. Therefore, it is important to assess PUFA intakes in different populations and validate them with biomarkers, but only a few small studies are in paediatric populations. We calculated the dietary intake of PUFA and their main food sources in children and assessed associations between PUFA intakes and plasma proportions. Dietary intakes of 7-year-old children (n 8242) enrolled in the Avon Longitudinal Study of Parents and Children were calculated from the parental-completed FFQ. Plasma PUFA were measured in 5571 children 8 months later, and 4380 children had complete dietary and plasma data. The association between dietary and plasma PUFA proportions was estimated using Spearman’s correlation coefficients, quintile cross-classification and Cohen’s κ coefficients. Mean total PUFA intake was 13·2 g/d (sd 4·2), contributing 6·5 % of total energy intake; n-6 PUFA contributed 5·2 % and n-3 PUFA 0·7 %. The n-6:n-3 ratio was 7·9:1. Mean intakes of EPA and DHA were 35·7 mg/d and 49·7 mg/d, respectively. Most n-3 and n-6 PUFA intakes were weakly correlated with their respective plasma lipids (0·07 ≤ r ≤ 0·16, P < 0·001). The correlation between dietary and plasma DHA was stronger though (r = 0·34, P < 0·001), supported by a modest level of agreement between quintiles (k = 0·32). The results indicate that the FFQ was able to reasonably rank the long-chain (LC) PUFA, DHA, in this paediatric population. Public health initiatives need to address the suboptimal ratio of n-6:n-3 PUFA and very low n-3 LC-PUFA intakes in school-age children in the UK.

The aim of this study was to investigate the effectiveness of the Hipcref (high-protein, energy-restricted, high-vitamin E and high-fibre) diet in Malaysian adults on body composition and metabolic parameters after an intervention period of 6 months. Overweight/obese Malaysian adults (n 128; BMI≥23 kg/m2) were randomised to the Hipcref (n 65) or control diet (n 63). The intervention group received Hipcref diet charts based on their personal preferences. The control group followed a generalised dietary advice based on Malaysian Dietary Guidelines, 2010. All participants were responsible for preparing their own meals. There was a significant treatment group×time effect on anthropometric parameters (P<0·05) on an intention-to-treat basis. Pairwise comparisons revealed that Hipcref diet participants had significant reduction in weight, BMI, waist circumference, fat mass and percentage body fat at months 3 and 6 compared with baseline (P<0·001). The control group had significant increase in weight and BMI at months 3 and 6 compared with baseline (P<0·05). The Hipcref diet group had higher reduction in fasting insulin, insulin resistance and C-reactive protein levels compared with the control group at month 6 (P<0·05). Post-intervention, compared with the control group, the Hipcref diet group was found to consume significantly higher percentage energy from protein, and PUFA, higher energy-adjusted vitamin E (mg) and fibre (g), and lower total energy, lower percentage energy from fat and carbohydrate (P<0·05). The success of the Hipcref diet on overweight/obese Malaysian adults may be due to the combined effect of the nutrient composition of the Hipcref diet.

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.

SFA intakes have decreased in recent years, both in Ireland and across other European countries; however a large proportion of the population are still not meeting the SFA recommendation of <10% of total energy (TE). High SFA intakes have been associated with increased CVD and type-2 diabetes (T2D) risk, due to alterations in cholesterol homoeostasis and adipose tissue inflammation. PUFA, in particular EPA and DHA, have been associated with health benefits, including anti-inflammatory effects. It is well established that dietary fat composition plays an important role in biological processes. A recent review of evidence suggests that replacement of SFA with PUFA has potential to reduce risk of CVD and T2D. The public health and molecular impact of EPA and DHA have been well-characterised, while less is known of effects of α-linolenic acid (ALA). The current dietary guideline for ALA is 0·5% TE; however evidence from supplementation trials suggests that benefit is observed at levels greater than 2 g/d (0·6–1% TE). This review highlights the gap in the evidence base relating to effects of the replacement of SFA with ALA, identifying the need for randomised controlled trials to determine the optimal dose of ALA substitution to define the efficacy of dietary fat modification with ALA.

When we consume dietary fat, a series of complex metabolic processes ensures that fatty acids are absorbed, transported around the body and used/stored appropriately. The liver is a central metabolic organ within the human body and has a major role in regulating fat and carbohydrate metabolism. Studying hepatic metabolism in human subjects is challenging; the use of stable isotope tracers and measurement of particles or molecules secreted by the liver such as VLDL-TAG and 3-hydroxybutyrate offers the best insight into postprandial hepatic fatty acid metabolism in human subjects. Diet derived fatty acids are taken up by the liver and mix with fatty acids coming from the lipolysis of adipose tissue, and those already present in the liver (cytosolic TAG) and fatty acids synthesised de novo within the liver from non-lipid precursors (known as de novo lipogenesis). Fatty acids are removed from the liver by secretion as VLDL-TAG and oxidation. Perturbations in these processes have the potential to impact on metabolic health. Whether fatty acids are partitioned towards oxidation or esterification pathways appears to be dependent on a number of metabolic factors; not least ambient insulin concentrations. Moreover, along with the phenotype and lifestyle factors (e.g. habitual diet) of an individual, it is becoming apparent that the composition of the diet (macronutrient and fatty acid composition) may play pivotal roles in determining if intra-hepatic fat accumulates, although what remains to be elucidated is the influence these nutrients have on intra-hepatic fatty acid synthesis and partitioning.

Taste is a key driver of food choice and intake. Taste preferences are widely studied, unlike the diet’s taste profile. This study assessed dietary taste patterns in the Netherlands by sex, BMI, age and education. A taste database, containing 476 foods’ taste values, was combined with 2-d 24-h recalls in two study populations. The percentage of energy intake from six taste clusters was assessed in the Dutch National Food Consumption Survey (DNFCS 2007–2010; n 1351) and in an independent observational study: the Nutrition Questionnaires plus (NQplus) study (2011–2013; n 944). Dietary taste patterns were similar across study populations. Men consumed relatively more energy from ‘salt, umami and fat’ (DNFCS; 24 % energy, NQplus study; 23 %)- and ‘bitter’ (7 %)-tasting foods compared with women (21 %, P<0·001, 22 %, P=0·005; 3 %, P<0·001, 4 %, P<0·001, respectively). Women consumed more % energy from ‘sweet and fat’ (15 %)- and ‘sweet and sour’ (13 %, 12 %, respectively)-tasting foods compared with men (12 %, P<0·001, 13 %, P=0·001; 10 %, P<0·001). Obese individuals consumed more % energy from ‘salt, umami and fat’- and less from ‘sweet and fat’-tasting foods than normal-weight individuals (‘salt, umami and fat’, men; obese both studies 26 %, normal-weight DNFCS 23 %, P=0·037, NQplus 22 %, P=0·001, women; obese 23 %, 24 %, normal weight 20 %, P=0·004, P=0·011, respectively, ‘sweet and fat’, men; obese 11 %, 10 %, normal weight 13 %, P<0·05, 14 %, P<0·01, women; obese 14 %, 15 %, normal weight 16 %, P=0·12, P=0·99). In conclusion, our taste database can be used to deepen our understanding of the role of taste in dietary intake in the Netherlands by sex, BMI, age and education.

This study aimed to characterise lean and obese phenotypes according to diet and body composition, and to compare fasting and postprandial appetite and metabolic profiles following a high-fat test meal. A total of ten lean (BMI<25 kg/m2) high-fat (LHF), ten lean low-fat (LLF; >40 and <30 % energy from fat) and ten obese (BMI>30 kg/m2) high-fat consumers (OHF; >40 % energy from fat) were recruited. Before and following the test meal (4727 kJ (1130 kcal), 77 % fat, 20 % carbohydrate (CHO) and 3 % protein), fasting plasma glucose, insulin, leptin, ghrelin, peptide YY (PYY), RER, RMR and subjective appetite ratings (AR) were measured for 6 h. Thereafter, subjects consumed a self-selected portion of a standardised post-test meal (40 % fat, 45 % CHO and 15 % protein) and reported AR. Fasting (P=0·01) and postprandial (P<0·001) fat oxidation was significantly higher in LHF than in LLF but was not different between LHF and OHF. Although similar between the lean groups, fasting and postprandial energy expenditures were significantly higher in OHF compared with LHF (P<0·01). Despite similar AR across groups, LLF consumed a relatively greater quantity of the post-test meal than did LHF (7·87 (sd 2·96) v. 7·23 (sd 2·67) g/kg, P=0·013). The lean groups showed appropriate changes in plasma ghrelin and PYY following the test meal, whereas the OHF group showed a blunted response. In conclusion, the LHF phenotype had a greater capacity for fat oxidation, which may be protective against weight gain. OHF individuals had a blunted appetite hormone response to the high-fat test meal, which may subsequently increase energy intake, driving further weight gain.

Analytical expressions for the total energy derivative with respect to the magnetic moment rotations have been derived in the relativistic local-spin density functional approach and multiple scattering theory. The spin-wave stiffness constant as well as the gap in the spin-wave spectrum due to relativistic anisotropy effects is calculated in KKR-ASA approximation for bcc Fe. This is compared with other theoretical calculations and available experimental data.