Green tea catechins (GTC) reduce UV radiation (UVR)-induced inflammation in experimental models, but human studies are scarce and their cutaneous bioavailability and mechanism of photoprotection are unknown. We aimed to examine oral GTC cutaneous uptake, ability to protect human skin against erythema induced by a UVR dose range and impact on potent cyclo-oxygenase- and lipoxygenase-produced mediators of UVR inflammation, PGE2 and 12-hydroxyeicosatetraenoic acid (12-HETE), respectively. In an open oral intervention study, sixteen healthy human subjects (phototype I/II) were given low-dose GTC (540 mg) with vitamin C (50 mg) daily for 12 weeks. Pre- and post-supplementation, the buttock skin was exposed to UVR and the resultant erythema quantified. Skin blister fluid and biopsies were taken from the unexposed and the UVR-exposed skin 24 h after a pro-inflammatory UVR challenge (three minimal erythema doses). Urine, skin tissue and fluid were analysed for catechin content and skin fluid for PGE2 and 12-HETE by liquid chromatography coupled to tandem MS. A total of fourteen completing subjects were supplement compliant (twelve female, median 42·5 years, range 29–59 years). Benzoic acid levels were increased in skin fluid post-supplementation (P= 0·03), and methylated gallic acid and several intact catechins and hydroxyphenyl-valerolactones were detected in the skin tissue and fluid. AUC analysis for UVR erythema revealed reduced response post-GTC (P= 0·037). Pre-supplementation, PGE2 and 12-HETE were UVR induced (P= 0·003, 0·0001). After GTC, UVR-induced 12-HETE reduced from mean 64 (sd 42) to 41 (sd 32) pg/μl (P= 0·01), while PGE2 was unaltered. Thus, GTC intake results in the incorporation of catechin metabolites into human skin associated with abrogated UVR-induced 12-HETE; this may contribute to protection against sunburn inflammation and potentially longer-term UVR-mediated damage.

The gut microbiome interacts with the host in the metabolic response to diet, and early microbial aberrancies may be linked to the development of obesity and metabolic disorders later in life. Probiotics have been proposed to affect metabolic programming and blood lipid levels, although studies are lacking in infants. Here, we report on the lipid profile and global metabolic response following daily feeding of probiotics during weaning. A total of 179 healthy, term infants were randomised to daily intake of cereals with (n 89) or without (n 90) the addition of Lactobacillus paracasei ssp. paracasei F19 (LF19) 108 colony-forming units per serving from 4 to 13 months of age. Weight, length and skinfold thickness were monitored. Venous blood was drawn at 5·5 and 13 months of age for analysis of the serum lipid profile. In a subsample, randomly selected from each group, GC-time-of-flight/MS was used to metabolically characterise plasma samples from thirty-seven infants. A combination of multi- and univariate analysis was applied to reveal differences related to LF19 treatment based on 228 putative metabolites, of which ninety-nine were identified or classified. We observed no effects of probiotic feeding on anthropometrics or the serum lipid profile. However, we detected significantly lower levels of palmitoleic acid (16 : 1) (P< 0·05) and significantly higher levels of putrescine (P< 0·01) in LF19-treated infants. Palmitoleic acid is a major MUFA strongly linked to visceral obesity, while putrescine is a polyamine with importance for gut integrity. Whether the observed differences will have long-term health consequences are being followed.

Human biotin requirements are unknown and the identification of reliable markers of biotin status is necessary to fill this knowledge gap. Here, we used an outpatient feeding protocol to create states of biotin deficiency, sufficiency and supplementation in sixteen healthy men and women. A total of twenty possible markers of biotin status were assessed, including the abundance of biotinylated carboxylases in lymphocytes, the expression of genes from biotin metabolism and the urinary excretion of biotin and organic acids. Only the abundance of biotinylated 3-methylcrotonyl-CoA carboxylase (holo-MCC) and propionyl-CoA carboxylase (holo-PCC) allowed for distinguishing biotin-deficient and biotin-sufficient individuals. The urinary excretion of biotin reliably identified biotin-supplemented subjects, but did not distinguish between biotin-depleted and biotin-sufficient individuals. The urinary excretion of 3-hydroxyisovaleric acid detected some biotin-deficient subjects, but produced a meaningful number of false-negative results and did not distinguish between biotin-sufficient and biotin-supplemented individuals. None of the other organic acids that were tested were useful markers of biotin status. Likewise, the abundance of mRNA coding for biotin transporters, holocarboxylase synthetase and biotin-dependent carboxylases in lymphocytes were not different among the treatment groups. Generally, datasets were characterised by variations that exceeded those seen in studies in cell cultures. We conclude that holo-MCC and holo-PCC are the most reliable, single markers of biotin status tested in the present study.

The intake of marine n-3 PUFA has been shown to decrease the risk of CVD in a number of studies. Since the development of CVD is often a lifelong process, marine n-3 PUFA intake early in life may also affect the development of later CVD. The aim of the present study was to investigate the association between maternal intake of marine n-3 PUFA during the second trimester of pregnancy and factors associated with cardiometabolic risk in the 20-year-old offspring. The study was based on the follow-up of the offspring of a Danish pregnancy cohort who participated in a study conducted from 1988 to 1989. A total of 965 pregnant women were originally included in the cohort and detailed information about the intake of marine n-3 PUFA during the second trimester was collected. In 2008–9, the offspring were invited to participate in a clinical examination including anthropometric, blood pressure (BP) and short-term heart rate variability measurements. Also, a fasting venous blood sample was drawn from them. Multiple linear regression modelling, using the lowest quintile of marine n-3 PUFA intake as the reference, was used to estimate the association with all outcomes. A total of 443 offspring participated in the clinical examination. No association between the intake of marine n-3 PUFA during the second trimester of pregnancy and offspring adiposity, glucose metabolism, BP or lipid profile was found. In conclusion, no association between the intake of marine n-3 PUFA during the second trimester of pregnancy and the factors associated with cardiometabolic risk in the 20-year-old offspring could be detected.

Hypertension is one of the leading causes of morbidity and mortality in Brazil. Diet may play an important role in reducing blood pressure (BP), as has been shown for diets high in fruits, vegetables and low-fat dairy products and low in salt (Dietary Approaches to Stop Hypertension (DASH)-Na). A low-glycaemic index Brazilian diet combined with the principles of the DASH-Na diet was evaluated in a randomised study of 206 individuals who were followed for 6 months. In the control group (CG), counselling was based on standard care and mainly focused on salt intake reduction. An intention-to-treat analysis showed that, after 6 months, systolic BP was reduced by 14·4 mmHg and diastolic BP by 9·7 mmHg in the experimental group (EG), compared with 6·7 and 4·6 mmHg, respectively, in the CG. After adjusting for body weight, BP at baseline and age, these changes were 12·1 and 7·9 mmHg, respectively. Urinary Na excretion was also reduced by 43·4 mEq/24 h in the EG. Food intake was modified accordingly during the intervention with an increase in the consumption of vegetables (2·97–5·85 frequency of consumption measured in three non-consecutive days), fruits (4·09–7·18), beans (1·94–3·13) and fish (1·80–2·74) by the EG. The present study showed the feasibility of a Brazilian dietary approach to treating hypertension by reducing urinary Na excretion and BP, changes that may have a great impact on public health and promote the benefits of controlling hypertension.

Paraoxonase 1 (PON1) is associated with HDL and modulates the antioxidant and anti-inflammatory role of HDL. The goals of the present study were to investigate the effect of ageing and the role of PON1 on the anti-inflammatory activity of HDL, and to determine whether extra-virgin olive oil (EVOO) consumption could improve the atheroprotective activity of HDL. HDL and PON1 were isolated from the plasma of ten young (Y-HDL and Y-PON1) and ten elderly (E-HDL and E-PON1) healthy volunteers before and after 12 weeks of EVOO consumption. Inflammation was assessed by measuring intracellular adhesion molecule 1 (ICAM-1) expression. THP-1 (human acute monocytic leukaemia cell line) monocyte chemotaxis was measured using a Boyden chamber. Oxidative damage to HDL was assessed by measuring conjugated diene formation and changes in electrophoretic migration. Y-HDL had more anti-inflammatory activity than E-HDL. The conjugated diene content and the electrophoretic mobility of E-HDL were higher than those of Y-HDL. Y-PON1 had significant anti-inflammatory activity, reducing ICAM-1 expression by 32·64 (sd 2·63) %, while E-PON1 had no significant effect. THP-1 chemotaxis measurements confirmed the ICAM-1 expression results. The 12 weeks of EVOO consumption significantly increased the anti-inflammatory activities of both HDL and PON1. The anti-inflammatory activity of HDL was modulated by PON1 and was lower in the elderly volunteers. EVOO consumption increased the anti-inflammatory effect of HDL and reduced the age-related decrease in anti-atherogenic activity.

The aim of the present study was to investigate the possible associations between dietary energy density (ED) and the metabolic syndrome (MetS) in patients with type 2 diabetes. In the present case–control study, the dietary ED of 125 patients with type 2 diabetes (seventy-eight with (cases) the MetS and forty-seven without (controls) the MetS; mean age 62·0 (sd 9·4) years, mean diabetes duration 12·5 (sd 8·4) years and mean glycated Hb 7·2 (sd 1·3) %) was assessed by weighed diet records. The MetS was defined according to the 2009 Joint Interim Statement and ED by the amount of energy (kJ) in a given weight of food. Data are expressed as means (standard deviations) or medians (interquartile ranges). Patients with the MetS reported lower intakes of total energy and fibre, and a higher total food amount than the controls; the total ED did not differ, but the cases had a higher ED at lunch (mean 6·3 (sd 1·3) v. 5·9 (sd 0·8) kJ/g; P= 0·017). In this meal, patients with the MetS had lower intakes of beans (median 0·7 (interquartile range 0·4–1·1) v. 1·1 (interquartile range 0·6–1·6) g/kg; P= 0·020), vegetables (median 1·2 (interquartile range 0·6–1·7) v. 1·4 (interquartile range 1·0–2·0) g/kg; P= 0·046) and total meat (median 1·3 (interquartile range 1·0–1·6) v. 1·4 (interquartile range 1·2–1·8) g/kg; P= 0·034) than patients without the MetS. The associations between lunch ED (kJ/g) and food groups (g/kg) were confirmed for vegetables (r − 0·584; P< 0·001), fruits (r − 0·233; P= 0·070), beans (r − 0·189; P= 0·037) and oils (r 0·323; P< 0·001). In a multivariate logistic regression model, a high lunch ED was associated with the MetS (OR 6·89, 95 % CI 1·35, 35·15; P =0·020) after adjusting for confounders. In conclusion, a high ED at lunch increased the odds of the presence of the MetS in patients with type 2 diabetes. Beans and vegetables may be the major contributors to this association and their consumption might be considered to decrease ED.

In the present study, zebrafish (Danio rerio) were fed casein/gelatin-based diets containing either 19 % Bt (Bacillus thuringiensis)-maize or its parental non-Bt (nBt)-maize control for two generations (F0: sixty fish; F1: forty-two to seventy fish per treatment). The study focused on growth and reproductive performance, liver CuZn superoxide dismutase (SOD) enzyme activity, gene transcript levels targeting important cellular pathways in the liver and mid-intestine, histomorphological evaluation of the intestine, differential leucocyte counts, offspring larva swimming activity and global DNA methylation in offspring embryos. No significant effects were observed in the parental generation. The offspring were either fed the same diets as those fed to their parents (Bt–Bt or nBt–nBt) or switched from the Bt diet to the nBt diet (Bt–nBt). The Bt–Bt offspring exhibited a significantly higher body mass increase, specific growth rate and feed utilisation than fish fed the nBt–nBt diet and/or fish fed the Bt–nBt diet. Liver and mid-intestinal gene transcript levels of CuZn SOD were significantly higher in fish fed the nBt–nBt diet than in those fed the Bt–Bt diet. Liver gene transcript levels of caspase 6 were significantly lower for the nBt–nBt group than for the Bt–Bt group. Overall, enhanced growth performance was observed in fish fed the Bt diet for two generations than in those fed the nBt diet for one and two generations. Effects observed on gene biomarkers for oxidative stress and the cell cycle (apoptosis) may be related to the contamination of nBt-maize with fumonisin B1 and aflatoxin B1. In conclusion, it is suggested that Bt-maize is as safe and nutritious as its nBt control when fed to zebrafish for two generations.

Recent genome-wide association studies have identified multiple loci associated with BMI or the waist:hip ratio (WHR). However, evidence on gene–lifestyle interactions is still scarce, and investigation of the effects of well-documented dietary and other lifestyle data is warranted to assess whether genetic risk can be modified by lifestyle. We assessed whether previously established BMI and WHR genetic variants associate with obesity and weight change in the Finnish Diabetes Prevention Study, and whether the associations are modified by dietary factors or physical activity. Individuals (n 459) completed a 3 d food record and were genotyped for twenty-six BMI- and fourteen WHR-related variants. The effects of the variants individually and in combination were investigated in relation to obesity and to 1- and 3-year weight change by calculating genetic risk scores (GRS). The GRS were separately calculated for BMI and the WHR by summing the increasing alleles weighted by their published effect sizes. At baseline, the GRS were not associated with total intakes of energy, macronutrients or fibre. The mean 1- and 3-year weight changes were not affected by the BMI or WHR GRS. During the 3-year follow-up, a trend for higher BMI by the GRS was detected especially in those who reported a diet low in fibre (P for interaction = 0·065). Based on the present findings, it appears unlikely that obesity-predisposing variants substantially modify the effect of lifestyle modification on the success of weight reduction in the long term. In addition, these findings suggest that the association between the BMI-related genetic variants and obesity could be modulated by the diet.

Recent studies have suggested that dietary Ca may have beneficial effects on adiposity, insulin resistance, dyslipidaemia and blood pressure (BP). One potential mechanism underlying these benefits involves modifications in intracellular Ca concentration ([Ca2+]i). The present study aimed to evaluate the associations of dietary Ca with adiposity, erythrocyte [Ca2+]i, metabolic profile, BP, inflammatory state and endothelial function in healthy pre-menopausal women. In the present cross-sectional study, seventy-six women aged 18–50 years were submitted to the evaluation of dietary intake, anthropometric parameters, body composition, erythrocyte [Ca2+]i, biochemical variables, endothelial function and BP. A FFQ was used to assess usual dietary intake. Endothelial function was evaluated by serum concentrations of adhesion molecules and by the peripheral arterial tonometry (PAT) method, using Endo-PAT 2000®. Participants were allocated into two groups according to Ca intake: low-Ca group (LCG; n 32; < 600 mg/d) and high-Ca group (HCG; n 44; ≥ 600 mg/d). Women in the LCG compared with those in the HCG exhibited, after adjustments for potential confounders, higher values of BMI, waist circumference, waist:height ratio, percentage of body fat, insulin, homeostasis model assessment of insulin resistance, leptin, diastolic and mean BP; and lower levels of HDL-cholesterol, adiponectin and vascular cell adhesion molecule 1. Endothelial function assessed by PAT and [Ca2+]i was similar in both groups. Subjects in the HCG had lower OR for prevalent overweight, obesity, abdominal obesity, insulin resistance, HDL-cholesterol < 600 mg/l and systolic BP >120 mmHg. The findings of the present study suggest that high Ca intake is inversely associated with some cardiovascular risk factors.

Protein–energy malnutrition (PEM) causes a significant impairment of the immune system, the thymus being one of the most affected organs. It has been demonstrated that the administration of probiotic fermented milk (PFM) recovered the intestinal barrier, histological alterations and mucosal and systemic immune functions in a non-severe malnutrition model using BALB/c mice. The aim of the present study was to evaluate, in the same model of malnutrition, the effect of a PFM added to a re-nutrition diet on the recovery of the thymus, analysing histological and functional alterations caused by malnutrition. Mice were undernourished and divided into three groups according to the dietary supplement received during re-nutrition: milk, PFM or its bacterial-free supernatant (BFS). They were compared with well-nourished and malnourished mice. PFM was the most effective re-nutrition supplement to improve the histology of the thymus, decreasing cellular apoptosis in this organ and recovering the percentage of CD4+/CD8− single-positive thymocytes. Immature double-positive thymocytes were increased in the malnourished control (MC). The production of different cytokines in the thymus was increased in mice given PFM, compared with the mice that received other dietary supplements and MC. Mice given the BFS presented an improvement in the thymus similar to those that received milk. We demonstrated the importance of the whole PFM supplementation on the histological and functional recovery of the thymus in a non-severe PEM model.

Riboflavin, or vitamin B2, as a precursor of the coenzymes FAD and FMN, has an indirect influence on many metabolic processes and determines the proper functioning of several systems, including the immune system. In the human population, plasma riboflavin concentration varies from 3·1 nm (in a moderate deficiency, e.g. in pregnant women) to 10·4 nm (in healthy adults) and 300 nm (in cases of riboflavin supplementation). The purpose of the present study was to investigate the effects of riboflavin concentration on the activity and viability of macrophages, i.e. on one of the immunocompetent cell populations. The study was performed on the murine monocyte/macrophage RAW 264.7 cell line cultured in medium with various riboflavin concentrations (3·1, 10·4, 300 and 531 nm). The results show that riboflavin deprivation has negative effects on both the activity and viability of macrophages and reduces their ability to generate an immune response. Signs of riboflavin deficiency developed in RAW 264.7 cells within 4 d of culture in the medium with a low riboflavin concentration (3·1 nm). In particular, the low riboflavin content reduced the proliferation rate and enhanced apoptotic cell death connected with the release of lactate dehydrogenase. The riboflavin deprivation impaired cell adhesion, completely inhibited the respiratory burst and slightly impaired phagocytosis of the zymosan particles. In conclusion, macrophages are sensitive to riboflavin deficiency; thus, a low riboflavin intake in the diet may affect the immune system and may consequently decrease proper host immune defence.

The risk of vitamin D insufficiency is increased in persons having limited sunlight exposure and dietary vitamin D. Supplementation compliance might be improved with larger doses taken less often, but this may increase the potential for side effects. The objective of the present study was to determine whether a weekly or weekly/monthly regimen of vitamin D supplementation is as effective as daily supplementation without increasing the risk of side effects. Participants were forty-eight healthy adults who were randomly assigned for 3 months to placebo or one of three supplementation regimens: 50 μg/d (2000 IU/d, analysed dose 70 μg/d), 250 μg/week (10 000 IU/week, analysed dose 331 μg/week) or 1250 μg/week (50 000 IU/week, analysed dose 1544 μg/week) for 4 weeks and then 1250 μg/month for 2 months. Daily and weekly doses were equally effective at increasing serum 25-hydroxyvitamin D, which was significantly greater than baseline in all the supplemented groups after 30 d of treatment. Subjects in the 1250 μg treatment group, who had a BMI >26 kg/m2, had a steady increase in urinary Ca in the first 3 weeks of supplementation, and, overall, the relative risk of hypercalciuria was higher in the 1250 μg group than in the placebo group (P= 0·01). Although vitamin D supplementation remains a controversial issue, these data document that supplementing with ≤ 250 μg/week ( ≤ 10 000 IU/week) can improve or maintain vitamin D status in healthy populations without the risk of hypercalciuria, but 24 h urinary Ca excretion should be evaluated in healthy persons receiving vitamin D3 supplementation in weekly single doses of 1250 μg (50 000 IU).

Few studies have evaluated the effects of alcohol consumption on the incidence of the metabolic syndrome (MetS). Therefore, the objective of the present study was to examine the association between alcohol consumption and incident MetS in a population of US men. This is a prospective study of 7483 Caucasian men, who were free of the MetS and CVD at baseline. Information was collected on alcohol consumption, health status and fitness level at an initial clinical examination. Additional health information and determination of incident cases of the MetS were obtained at follow-up clinical examinations between 1979 and 2005. Compared with non-drinkers, the multivariate hazard ratios of the MetS for light (1–3 drinks/week), moderate (4–7 drinks/week), moderate–heavy (8–13 drinks/week) and heavy ( ≥ 14 drinks/week) drinkers were 0·81 (95 % CI 0·68, 0·95), 0·68 (95 % CI 0·57, 0·80), 0·70 (95 % CI 0·59, 0·83) and 0·78 (95 % CI 0·66, 0·91), respectively. This association was seen across age groups, in men with one or more pre-existing MetS risk factors, and those with BMI ≥ 25 kg/m2, and in all alcohol beverage types at most levels of alcohol consumption. An inverse dose–response association between alcohol consumption and low HDL concentrations was observed, while significant associations were observed between high fasting glucose concentrations and moderate, moderate–heavy and heavy levels of alcohol consumption. Alcohol consumption was not significantly associated with central obesity, hypertriacylglycerolaemia or hypertension. All levels of alcohol consumption provided significant inverse associations with incidence of the MetS. In particular, this effect was observed in overweight and/or obese individuals, in those who had pre-existing risk factors for the MetS, and extended across all types of alcoholic beverages consumed.

Consumption of a high-fat diet (HFD), which is associated with chronic ‘low-grade’ systemic inflammation, alters the gut microbiota (GM). The aim of the present study was to investigate the ability of an oleic acid-derived compound (S1) and a combination of n-3 fatty acids (EPA and DHA, S2) to modulate both body weight and the GM in HFD-induced obese mice. A total of eighty mice were fed either a control diet or a HFD, non-supplemented or supplemented with S1 or S2. At week 19, faeces were collected in order to analyse the GM. Group-specific primers for accurate quantification of several major bacterial groups from faecal samples were assayed using quantitative PCR. The HFD induced an increase in body weight, which was reduced by supplementation with S1. Furthermore, S1 supplementation markedly increased total bacterial density and restored the proportions of bacteria that were increased (i.e. clostridial cluster XIVa and Enterobacteriales) or decreased (i.e. Bifidobacterium spp.) during HFD feeding. S2 supplementation significantly increased the quantities of Firmicutes (especially the Lactobacillus group). Correlation analysis revealed that body weight correlated positively with the phylum Firmicutes and clostridial cluster XIVa, and negatively with the phylum Bacteroidetes. In conclusion, the consumption of a HFD induced changes in the faecal microbiota, which were associated with the appearance of an obese phenotype. Supplementation of the HFD with S1 counteracted HFD-induced gut dysbiosis, together with an improvement in body weight. These data support a role for certain fatty acids as interesting nutrients related to obesity prevention.

We compared changes in the dietary patterns of morbidly obese patients undergoing either laparoscopic gastric bypass surgery or a comprehensive lifestyle intervention programme. The present 1-year non-randomised controlled trial included fifty-four patients in the lifestyle group and seventy-two in the surgery group. Dietary intake was assessed by a validated FFQ. ANCOVA was used to adjust for between-group differences in sex, age, baseline BMI and baseline values of the dependent variables. Intakes of food groups and nutrients did not differ significantly between the intervention groups at baseline. At 1-year follow-up, the lifestyle group had a significantly higher daily intake of fruits and vegetables (561 (sd 198) v. 441 (sd 213) g, P= 0·002), whole grains (63 (sd 24) v. 49 (sd 16) g, P< 0·001) and fibre (28 (sd 6) v. 22 (sd 6) g, P< 0·001) than the surgery group and a lower percentage of total energy intake of saturated fat (12 (sd 3) v. 14 (sd 3) %, P< 0·001). The intake of red meat declined significantly within both groups, vegetables and fish intake were reduced significantly in the surgery group and added sugar was reduced significantly in the lifestyle group. The lifestyle patients improved their dietary patterns significantly (compared with the surgery group), increasing their intake of vegetables, whole grains and fibre and reducing their percentage intake of saturated fat (ANCOVA, all P< 0·001). In conclusion, lifestyle intervention was associated with more favourable dietary 1-year changes than gastric bypass surgery in morbidly obese patients, as measured by intake of vegetables, whole grains, fibre and saturated fat.

The present study investigated the relationship between the milk protein content of a rehydration solution and fluid balance after exercise-induced dehydration. On three occasions, eight healthy males were dehydrated to an identical degree of body mass loss (BML, approximately 1·8 %) by intermittent cycling in the heat, rehydrating with 150 % of their BML over 1 h with either a 60 g/l carbohydrate solution (C), a 40 g/l carbohydrate, 20 g/l milk protein solution (CP20) or a 20 g/l carbohydrate, 40 g/l milk protein solution (CP40). Urine samples were collected pre-exercise, post-exercise, post-rehydration and for a further 4 h. Subjects produced less urine after ingesting the CP20 or CP40 drink compared with the C drink (P< 0·01), and at the end of the study, more of the CP20 (59 (sd 12) %) and CP40 (64 (sd 6) %) drinks had been retained compared with the C drink (46 (sd 9) %) (P< 0·01). At the end of the study, whole-body net fluid balance was more negative for trial C ( − 470 (sd 154) ml) compared with both trials CP20 ( − 181 (sd 280) ml) and CP40 ( − 107 (sd 126) ml) (P< 0·01). At 2 and 3 h after drink ingestion, urine osmolality was greater for trials CP20 and CP40 compared with trial C (P< 0·05). The present study further demonstrates that after exercise-induced dehydration, a carbohydrate–milk protein solution is better retained than a carbohydrate solution. The results also suggest that high concentrations of milk protein are not more beneficial in terms of fluid retention than low concentrations of milk protein following exercise-induced dehydration.

Inconsistent associations between dietary glycaemic index (GI) and glycaemic load (GL) and body fatness may be partly due to differences in the underlying dietary patterns or energy under-reporting. In the present study, we examined the cross-sectional associations of dietary GI and GL with food and nutrient intake and general and central obesity, accounting for energy under-reporting. The subjects were 1487 British adults aged 19–64 years. Dietary intake was assessed using a 7 d weighed dietary record. Breads and potatoes were the positive predictive foods for dietary GI, while fruit, other cereals and dairy products were the negative predictors. These foods were similarly identified in the analysis of only acceptable reporters (AR; ratio of reported energy intake:estimated energy requirement within 0·665–1·335) and under-reporters (UR; ratio < 0·665). Dietary GL was closely correlated with carbohydrate intake. Multiple linear regression analyses showed that dietary GI was independently associated with a higher risk of general obesity (BMI ≥ 30 kg/m2) and central obesity (waist circumference ≥ 102 cm in men and ≥ 88 cm in women). Dietary GL was also associated with general (only women) and central obesity. Similarly, in the analysis of AR, the GI showed positive associations with general and central obesity, and, only in women, the GL showed positive associations with general and central obesity. Conversely, in the analysis of UR, the associations were generally weaker and many of them failed to reach statistical significance. In conclusion, we found independent positive associations of dietary GI and GL with general and central obesity in British adults.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an independent risk factor for CVD and has been proposed as a marker of vascular inflammation. Polyunsaturated n-3 fatty acids (FA) and several n-6 FA are known to suppress inflammation and may influence Lp-PLA2 mass and activity. The associations of n-3 and n-6 plasma FA with Lp-PLA2 mass and activity were analysed using linear regression analysis in 2246 participants of the Multi-Ethnic Study of Atherosclerosis; statistical adjustments were made to control for body mass, inflammation, lipids, diabetes, and additional clinical and demographic factors. Lp-PLA2 mass and activity were significantly lower in participants with the higher n-3 FA EPA (β = − 4·72, P< 0·001; β = − 1·53; P= 0·023) and DHA levels (β = − 4·47, β = − 1·87; both P< 0·001). Those in the highest quintiles of plasma EPA and DHA showed 12·71 and 19·15 ng/ml lower Lp-PLA2 mass and 5·7 and 8·90 nmol/min per ml lower Lp-PLA2 activity than those in the first quintiles, respectively. In addition, lower Lp-PLA2 mass and activity were associated with higher levels of n-6 arachidonic acid (β = − 1·63, β = − 1·30; both P< 0·001), while γ-linolenic acid was negatively associated with activity (β = − 27·7, P= 0·027). Lp-PLA2 mass was significantly higher in participants with greater plasma levels of n-6 linoleic (β = 0·828, P= 0·011) and dihomo-γ-linolenic acids (β = 4·17, P= 0·002). Based on their independent associations with Lp-PLA2 mass and activity, certain n-3 and n-6 FA may have additional influences on CVD risk. Intervention studies are warranted to assess whether these macronutrients may directly influence Lp-PLA2 expression or activity.

Dietary polyphenols, such as those from grape products, may exert beneficial effects on cardiovascular health, including anti-hypertensive effects. We investigated the effect of a specific grape seed extract (GSE) rich in low-molecular-weight polyphenolic compounds on ambulatory blood pressure (ABP) in untreated subjects with pre- and stage I hypertension. In addition, potential mechanisms that could underlie the hypothesised effect of GSE on blood pressure (BP), and platelet aggregation, were explored. The study was designed as a double-blind, placebo-controlled, randomised, parallel-group intervention study including seventy healthy subjects with systolic BP between 120 and 159 mmHg. A 1-week run-in period was followed by an 8-week intervention period, during which subjects consumed capsules containing either 300 mg/d of GSE or a placebo (microcrystalline cellulose). Before and after the intervention, daytime ABP readings, 24 h urine samples and fasting and non-fasting blood samples were taken. The mean baseline systolic BP was 135·8 (se 1·3) mmHg and diastolic BP was 81·5 (se 0·9) mmHg. BP values were modestly, but not significantly, affected by the polyphenol-rich GSE treatment v. placebo with an effect of − 3·0 mmHg for systolic BP (95 % CI − 6·5, 0·5) and − 1·4 mmHg for diastolic BP (95 % CI − 3·5, 0·6). Vasoactive markers including endothelin-1, NO metabolites and asymmetric dimethylarginine, plasma renin activity and platelet aggregation were not affected by the GSE intervention. Our findings show that consumption of polyphenol-rich GSE does not significantly lower ABP in untreated subjects with pre- and stage I hypertension.