Fatty acid composition of the diet may influence cardiovascular risk from early childhood onwards. The objective of the present study was to perform a systematic review of dietary fat and fatty acid intakes in children and adolescents from different countries around the world and compare these with the population nutrient intake goals for prevention of chronic diseases as defined by the WHO (2003). Data on fat and fatty acid intake were mainly collected from national dietary surveys and from population studies all published during or after 1995. These were identified by searching PubMed, and through nutritionists at local Unilever offices in different countries. Fatty acid intake data from thirty countries mainly from developed countries were included. In twenty-eight of the thirty countries, mean SFA intakes were higher than the recommended maximum of 10 % energy, whereas in twenty-one out of thirty countries mean PUFA intakes were below recommended (6–10 % energy). More and better intake data are needed, in particular for developing regions of the world, and future research should determine the extent to which improvement of dietary fatty acid intake in childhood translates into lower CHD risk in later life. Despite these limitations, the available data clearly indicate that in the majority of the countries providing data on fatty acid intake, less than half of the children and adolescents meet the SFA and PUFA intake goals that are recommended for the prevention of chronic diseases.

Observational studies have indicated that soya food consumption is inversely associated with blood pressure (BP). Evidence from randomised controlled trials (RCT) on the BP-lowering effects of soya protein intake is inconclusive. We aimed to evaluate the effectiveness of soya protein intake in lowering BP. The PubMed database was searched for published RCT in the English language through to April 2010, which compared a soya protein diet with a control diet. We conducted a random-effects meta-analysis to examine the effects of soya protein on BP. Subgroup and meta-regression analyses were performed to explore possible explanations for heterogeneity among trials. Meta-analyses of twenty-seven RCT showed a mean decrease of 2·21 mmHg (95 % CI − 4·10, − 0·33; P = 0·021) for systolic BP (SBP) and 1·44 mmHg (95 % CI − 2·56, − 0·31; P = 0·012) for diastolic BP (DBP), comparing the participants in the soya protein group with those in the control group. Soya protein consumption significantly reduced SBP and DBP in both hypertensive and normotensive subjects, and the reductions were markedly greater in hypertensive subjects. Significant and greater BP reductions were also observed in trials using carbohydrate, but not milk products, as the control diet. Meta-regression analyses further revealed a significantly inverse association between pre-treatment BP and the level of BP reductions. In conclusion, soya protein intake, compared with a control diet, significantly reduces both SBP and DBP, but the BP reductions are related to pre-treatment BP levels of subjects and the type of control diet used as comparison.

While it has been proposed, based on epidemiological studies, that whole grains may be beneficial in weight regulation, possibly due to effects on satiety, there is limited direct interventional evidence confirming this. The present cross-over study aimed to investigate the short-term effects on appetite and food intake of 48 g of whole-grain wheat (daily for 3 weeks) compared with refined grain (control). A total of fourteen healthy normal-weight adults consumed, within their habitual diets, either two whole-grain bread rolls (providing 48 g of whole grains over two rolls) or two control rolls daily for 3 weeks. Changes in food intake were assessed using 7 d diet diaries. Changes in subjective appetite ratings and food intake were also assessed at postprandial study visits. There were no significant differences between interventions in energy intake (assessed by the 7 d diet diaries and at the ad libitum test meal), subjective appetite ratings or anthropometric measurements. However, there was a significant difference between interventions for systolic blood pressure, which decreased during the whole-grain intervention and increased during the control intervention ( − 2 v. 4 mmHg; P = 0·015). The present study found no effect of whole grains on appetite or food intake in healthy individuals; however, 48 g of whole grain consumed daily for 3 weeks did have a beneficial effect on systolic blood pressure. The findings from the present study therefore do not support epidemiological evidence that whole grains are beneficial in weight regulation, although further investigation in other population groups (such as overweight and obese) would be required.

It is generally considered that the absorption of Mg is inversely related to the ingested dose. The objective of the present study was to determine if the mode of administration (bolus v. consumption throughout the day) could influence Mg bioavailability from Mg-rich natural mineral water comparing the same nutritional Mg amount (126 mg). Using a 2 d cross-over design, twelve healthy men were asked to drink 1·5 litres Mg-rich mineral water either as 2 × 750 ml or 7 × 212 ml throughout the day. Two stable isotopes (25Mg and 26Mg) were used to label the water in order to distinguish both regimens. Fractional apparent Mg absorption was determined by faecal monitoring and Mg retention was determined by measuring urinary excretion of Mg isotopes. Higher Mg absorption (50·7 (sd 12·7) v. 32·4 (sd 8·1) %; P = 0·0007) and retention (47·5 (sd 12·9) v. 29·0 (sd 7·5) %; P = 0·0008) from Mg-rich mineral water were observed when it was consumed in seven servings compared with larger servings. Thus, regular water consumption throughout the day is an effective way to increase Mg bioavailability from Mg-rich mineral water.

It is now known that health benefits associated with diets rich in fruit and vegetables may be partly derived from intake of polyphenols. Berry polyphenols may influence carbohydrate metabolism and absorption and hence postprandial glycaemia. To date, studies related to polyphenol effects on the glycaemic response have been completed only in liquids using either monosaccharides or disaccharides. It remains to be determined whether berries known to be rich in polyphenols can reduce the glycaemic response (GR) to a solid polysaccharide meal. The aim of the present study was to investigate whether berries alter postprandial hyperglycaemia and consequently the GR to a starchy food. Blood glucose was tested on seven occasions, on three occasions using a reference food and on four occasions using pancakes supplemented with either raspberries or blueberries or control pancakes containing similar amounts of fructose and glucose. Results showed that there were no differences in GR (blueberry 51·3 (sem 5·7); raspberry 54·7 (sem 5·6); blueberry control 43·9 (sem 4·2); raspberry control 41·8 (sem 6·4)), GR area under the curve or satiety index between any of the tests. The present study indicates that the ability of berries to reduce blood glucose from starch-based foods is unsubstantiated.

Hypovitaminosis D may be associated with diabetes, hypertension and CHD. However, because studies examining the associations of all three chronic conditions with circulating 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH)2D) are limited, we examined these associations in the US Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial (n 2465). Caucasian PLCO participants selected as controls in previous nested case–control studies of 25(OH)D and 1,25(OH)2D were included in this analysis. Diabetes, CHD and hypertension prevalence, risk factors for these conditions and intake of vitamin D and Ca were collected from a baseline questionnaire. Results indicated that serum levels of 25(OH)D were low ( < 50 nmol/l) in 29 % and very low ( < 37 nmol/l) in 11 % of subjects. The prevalence of diabetes, hypertension and CHD was 7, 30 and 10 %, respectively. After adjustment for confounding by sex, geographical location, educational level, smoking history, BMI, physical activity, total dietary energy and vitamin D and Ca intake, only diabetes was significantly associated with lower 25(OH)D and 1,25(OH)2D levels. Caucasians who had 25(OH)D ≥ 80 nmol/l were half as likely to have diabetes (OR 0·5 (95 % CI 0·3, 0·9)) compared with those who had 25(OH)D < 37 nmol/l. Those in the highest quartile of 1,25(OH)2D ( ≥ 103 pmol/l) were less than half as likely to have diabetes (OR 0·3 (95 % CI 0·1, 0·7)) than those in the lowest quartile ( < 72 pmol/l). In conclusion, the independent associations of 25(OH)D and 1,25(OH)2D with diabetes prevalence in a large population are new findings, and thus warrant confirmation in larger, prospective studies.

The aim of the present study was to examine the association of pre-pubertal dietary energy density (ED) with both age and body fatness at the start of the pubertal growth spurt (age at take-off, ATO). Analyses included 219 DOrtmund Nutritional and Anthropometric Longitudinally Designed Study participants with sufficient height measurements to estimate ATO who provided 3 d weighed dietary records at baseline, i.e. 2 and 3 years before ATO (mean age 6·9 (sd 1·2) years). Mean energy intakes and amounts of foods/drinks consumed at baseline were derived from the records. ED (kJ/g) was calculated based on (1) all foods and drinks (ED_all), (2) foods and energy-containing drinks (ED_energy), (3) foods and milk as a drink, but no other beverages (ED_milk) and (4) foods only, solid or liquid (ED_food). Using multiple regression analyses, the association between the ED variables and ATO was investigated. Furthermore, Z-scores of BMI and fat mass index (FMI) at ATO were considered as outcomes to reflect body fatness at puberty onset. The results showed that ED at baseline was not associated with ATO, regardless of the ED method used. For example, mean ATO in the lowest v. highest tertile of ED_food was 9·3 (95 % CI 9·0, 9·5) v. 9·4 (95 % CI 9·1, 9·7) years, Ptrend = 0·8 (adjusted for sex, maternal age, birth weight, dietary protein, dietary fibre, baseline BMI Z-score). Similarly, ED was not independently associated with BMI or FMI Z-score at ATO (Ptrend = 0·3–0·9). In conclusion, dietary ED in childhood did not influence timing or body fatness at ATO in this cohort of healthy, free-living children.

dl-2-Hydroxy-(4-methylthio)butanoic acid (HMTBA) is a synthetic source of dietary methionine (Met) widely used in poultry nutrition. HMTBA is transported in the intestinal epithelium by the monocarboxylate transporter 1, after which its biological utilisation relies on its conversion to l-Met. This process involves stereospecific HMTBA oxidation to 2-keto-(4-methylthio)butanoic acid (KMB) and transamination to l-Met. In the present study, we examined HMTBA conversion to l-Met, further incorporation into cellular proteins and the regulation of both processes by HMTBA supplementation in differentiated intestinal Caco-2 cells. The results showed d- and l-HMTBA oxidation in the enterocytes, this process being up-regulated by HMTBA. The data also revealed that KMB transamination is not linked to a specific amino group donor. However, the branched-chain amino acid l-leucine is the preferred amino group donor. Furthermore, transamination was not affected by HMTBA availability. The incorporation of radioactivity from HMTBA into cellular proteins was not significantly different from that of l-Met and was not affected by HMTBA supplementation. In conclusion, the results reveal the capacity of Caco-2 cells to convert HMTBA to l-Met and the up-regulation of conversion by nutritional HMTBA supplementation, thus highlighting the contribution of the intestinal epithelium in the utilisation of HMTBA as a dietary source of Met.

The present study determined whether α-ketoglutarate (AKG) might affect the expression of AMP-activated protein kinase (AMPK) and energy status in the intestinal mucosa of piglets challenged with Escherichia coli lipopolysaccharide (LPS). A total of eighteen piglets (weaned at 21 d of age) were allocated to one of three treatments: (1) non-challenged (control); (2) LPS-challenged (LPS); (3) LPS+1 % AKG (LPS+AKG). Piglets in the control and LPS groups were fed a maize- and soyabean meal-based diet, and the LPS+AKG group was fed the basal diet supplemented with 1 % AKG. On days 10, 12, 14 and 16 of the trial, piglets in the LPS and LPS+AKG groups were challenged with LPS (80 μg/kg body weight), whereas piglets in the control group received the same volume of sterile saline. Pigs were euthanised 24 h after the last administration of LPS or saline to obtain intestinal mucosae for biochemical analysis. Compared with the control group, LPS administration decreased (P < 0·05) the oxidation of AKG, oleic acid, glutamine and glucose in enterocytes, decreased concentrations of ATP in the duodenal and jejunal mucosae and decreased adenylate energy charge (AMP:ATP ratio) in the jejunal and ileal mucosae. Additionally, LPS treatment reduced (P < 0·05) mucosal concentrations of phosphorylated AMPK in the jejunum and ileum as well as acetyl-CoA carboxylase in all segments of the small intestine. The adverse effects of LPS were reversed by AKG. Collectively, these results indicate that dietary supplementation with 1 % AKG beneficially modulates the AMPK signalling pathway to improve energy status in the small intestine of LPS-challenged piglets.

A family history of type 2 diabetes (T2D) confers a high risk of developing the disease, independent of that due to other common risk factors. Postprandial state is a pro-inflammatory condition associated with a transiently impaired endothelial function; an increased oxidative stress is considered as a mediator of such effects in T2D. We evaluated the short-term effect of a lipid meal on markers of early vascular damage in subjects at risk of developing T2D. A total of thirty-two healthy volunteers, divided according to the presence (FHD+) or absence (FHD − ) of a family history of T2D, underwent a fatty meal test. We measured the monocyte mRNA expressions of IL-6, IL-8 and IL-1β, and IL-6, soluble CD40 ligand (sCD40L), vascular cellular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1) and nitrotyrosine plasma concentrations at baseline and in the post-meal phase, relating them to the lipid profile and other biochemical parameters. The basal expression of the cytokines did not differ in FHD −  and FHD+ subjects; neither was it modified by the meal ingestion. IL-6 and sCD40L plasma levels, similar in the two groups in the fasting state, did not vary after the meal. VCAM-1 and ICAM-1 increased in FHD+ subjects but not in FHD −  subjects. Nitrotyrosine, similar between the FHD −  and FHD+ subjects at baseline, increased more in FHD+ subjects than in FHD −  subjects after the meal. In conclusion, the presence of a familial history of T2D confers an abnormal endothelial activation after an oral lipid meal, coupled with an increased oxidative stress, supporting the hypothesis of an early endothelial dysfunction already present in healthy individuals prone to develop T2D.

The present study was conducted to investigate the effect of digestion rate of dietary starch on postprandial systemic circulating glucose, insulin and lipid profiles, and the activity and gene expression of lipid metabolism-related enzymes in weaned pigs. A total of twenty-four weaned pigs, surgically fitted with a catheter in the jugular vein, were randomly assigned to three dietary treatment groups, representing the high digestion rate starch (HDRS) group, the moderate-digestion rate starch (MDRS) group and the low-digestion rate starch (LDRS) group. The amylopectin:amylose ratios in the diets of each group were 27·6:1, 27·6:8·5 and 1:27·6, respectively. The serum concentrations of glucose, TAG, total cholesterol, LDL-cholesterol and HDL-cholesterol in the HDRS group were increased to the peak point at postprandial 1·5, 2·5, 2·5, 1·5 and 1·5 h, those in the MDRS group were at postprandial 2·5, 3·5, 3·5, 3·5 and 3·5 h and those in the LDRS group were at postprandial 2·5, 3·5, 3·5, 1·5 and 3·5 h, respectively. The serum concentration of insulin in the HDRS group was higher (P < 0·05) than those in the MDRS group, and those in the MDRS group was also higher (P < 0·05) than those in the LDRS group at postprandial 0·5, 1·5 and 2·5 h, respectively. The serum concentrations of acetate, propionate and butyrate in the HDRS group were higher (P < 0·05) than those in the MDRS group, and those in the MDRS group were higher (P < 0·05) than in the LDRS group in each feeding cycle, in turn, respectively. The activity of fatty acid synthase (FAS) in the liver and abdominal adipose tissues, that of acetyl CoA carboxylase (ACC) in the myocardium and interscapular brown adipose tissues and that of the ATP-citrate lyase (ATP-CL) in the liver and interscapular brown adipose tissues in pigs of the HDRS group were higher (P < 0·05) than that of the MDRS group. The mRNA levels of FAS in the myocardium, liver and interscapular brown adipose tissues of pigs in the HDRS group were higher (P < 0·05) than those of the MDRS group. The activities and mRNA levels of FAS, ACC and ATP-CL in the myocardium, liver, abdominal and interscapular brown adipose tissues of the HDRS group were higher than those of the LDRS group. We conclude that the digestion rate of dietary starch affected not only the postprandial systemic circulating levels of glucose and insulin but also the lipid metabolism in weaned pigs. Dietary starch with higher digestion rate produces higher blood glucose and insulin response, ameliorates the blood lipid profiles and up-regulates the activity and gene expression profile of lipid metabolism-related genes in weaned pigs.

Accumulation of homocysteine and S-adenosylhomocysteine in bone has been shown to be associated with reduced bone quality in rats. The aim of the present study was to investigate whether high bone concentrations of homocysteine and S-adenosylhomocysteine as well as a low methylation capacity are related to an impaired bone morphology in humans. Concentrations of homocysteine and its precursors S-adenosylhomocysteine and S-adenosylmethionine were measured in femoral bone samples of eighty-two males and females (age 71 (sd 8) years) who underwent elective hip arthroplasty. Cancellous bone structure was analysed by histomorphometry. In addition, blood was sampled to measure serum concentrations of homocysteine. Results of bone and serum analyses were grouped for individuals with high or low bone concentrations of homocysteine, S-adenosylhomocysteine and S-adenosylmethionine, as well as for individuals with a high or a low methylation capacity, which is indicated by a low or a high S-adenosylhomocysteine:S-adenosylmethionine ratio (n 41, each). Histomorphometry showed a higher trabecular separation and a lower trabecular thickness, trabecular number and trabecular area in individuals with high bone concentrations of homocysteine and S-adenosylhomocysteine compared with individuals with low bone concentrations of homocysteine and S-adenosylhomocysteine. There was no association between the S-adenosylhomocysteine:S-adenosylmethionine ratio and bone morphology. It was found that 48 % of bone homocysteine was bound to the collagen of the extracellular bone matrix. Blood analyses demonstrated a significant correlation between serum and bone homocysteine. The results of the present study indicate an association between altered bone morphology and elevated bone concentrations of homocysteine and S-adenosylhomocysteine, but not between altered bone morphology and methylation capacity.

Although resveratrol has widely been studied for its potential health benefits, little is known about its metabolic effects in humans. Our aims were to determine whether the polyphenol resveratrol improves insulin sensitivity in type 2 diabetic patients and to gain some insight into the mechanism of its action. After an initial general examination (including blood chemistry), nineteen patients enrolled in the 4-week-long double-blind study were randomly assigned into two groups: a resveratrol group receiving oral 2 × 5 mg resveratrol and a control group receiving placebo. Before and after the second and fourth weeks of the trial, insulin resistance/sensitivity, creatinine-normalised ortho-tyrosine level in urine samples (as a measure of oxidative stress), incretin levels and phosphorylated protein kinase B (pAkt):protein kinase B (Akt) ratio in platelets were assessed and statistically analysed. After the fourth week, resveratrol significantly decreased insulin resistance (homeostasis model of assessment for insulin resistance) and urinary ortho-tyrosine excretion, while it increased the pAkt:Akt ratio in platelets. On the other hand, it had no effect on parameters that relate to β-cell function (i.e. homeostasis model of assessment of β-cell function). The present study shows for the first time that resveratrol improves insulin sensitivity in humans, which might be due to a resveratrol-induced decrease in oxidative stress that leads to a more efficient insulin signalling via the Akt pathway.

Chronic consumption of a Western-type diet, containing both elevated sugar and fat, results in leptin resistance. We hypothesised that fructose, as part of the sugar component of Western-type diets, is one causative ingredient in the development of leptin resistance and that removal of this component will prevent leptin resistance despite high fat (HF) content. We fed rats a sugar-free (SF), 30 % HF (SF/HF) diet or a 40 % high-fructose (HFr), 30 % HF (HFr/HF) diet for 134 d. The HFr/HF diet resulted in impaired anorexic and body-weight responses to both peripherally (0·6 mg/kg, assessed on day 65 of the diet) and centrally (1·5 μg/d, assessed on days 129–134) administered leptin, whereas SF/HF-fed rats were fully leptin responsive. At day 70, half the HFr/HF-fed animals were switched to the SF/HF diet, reversing the leptin resistance (assessed 18 d after the diet switch). The HFr/HF diet elevated serum leptin and reduced adiponectin, and levels were restored abruptly at day 3 after switching to the SF/HF diet. These data demonstrate that a diet containing both HFr and fat leads to leptin resistance, while an isoenergetic SF/HF diet does not. Moreover, removal of fructose from this diet reverses the leptin resistance and the elevated leptin, suggesting a cause-and-effect relationship. These data suggest that fructose is the bioactive component of a HF/high-sugar diet that is essential for the induction of leptin resistance.

Trichotecenes are mycotoxins produced by Fusarium sp., which may contaminate animal feeds and human food. A feeding trial was conducted to evaluate the effect of a fusarotoxin-contaminated diet, and to explore the counteracting potential of a calcium fructoborate (CFrB) additive on performance, typical health biochemistry parameters and immune response in weaned pigs. A naturally contaminated maize, containing low doses of deoxynivalenol, zearalenone, fumonisins and T-2/HT-2 toxins (1790, 20, 0·6 and 90 parts per billion), was included in a maize–soyabean meal diet, and given ad libitum to eight weaned piglets (two groups: four pigs/group) for a period of 24 d. CFrB was administered to one of the contaminated groups and to another four piglets as a daily supplement, following the manufacturer's recommendation. A decrease in performance was observed in contaminated animals at this concentration of feed toxins, which was ameliorated by the dietary CFrB supplementation. Fusarium toxins also altered the pig immune response by increasing (P < 0·05) the ex vivo peripheral blood mononuclear cell proliferation (111·7 % in comparison with control), the respiratory burst of porcine granulocytes (15·4 % for responsive cells v. 5·1 % for unstimulated cells and 70·95 v. 22·65 % for stimulated cells, respectively), the percentage of peripheral T, CD3+, CD3+CD4+ and CD3+CD8+ subsets and the synthesis of IL-1β, TNF-α and IL-8 (123·8, 217·1 and 255·1 %, respectively). The diet containing the CFrB additive reduced these exacerbated cellular immune responses induced by Fusarium toxins. However, consumption of CFrB did not counteract the effect of mycotoxins on biochemistry parameters, and increased plasma IgM and IgG of contaminated pigs.

Glucosinolates, phytochemicals found in cruciferous vegetables, are metabolised to bioactive isothiocyanates (ITC) by certain bacteria in the human gut. Substantial individual variation in urinary ITC excretion has been observed in previous cruciferous vegetable-feeding studies. We hypothesised that individual differences in gut microbial community contribute to the observed variation in glucosinolate metabolism, i.e. gut microbiota composition between high- and low-ITC excreters differs. We recruited twenty-three healthy individuals and fed them a standardised meal containing 200 g of cooked broccoli. After the meal, 24 h urinary ITC excretion was measured. Study participants with the highest (n 5) and lowest (n 5) ITC excretion provided faecal samples for ex vivo bacterial cultivation with 50 μm-glucoraphanin, the major glucosinolate found in broccoli. When grown ex vivo, faecal bacteria from the selected high-ITC excreters were able to degrade more glucoraphanin than those from the low-ITC excreters (P = 0·05). However, bacterial fingerprints of faecal and ex vivo culture microbiota revealed no statistically significant differences between the high- and low-ITC excreters in terminal restriction fragment length polymorphism analysis of the bacterial 16S ribosomal RNA gene. In conclusion, glucosinolate degradation by faecal bacteria ex vivo may be associated with in vivo bacterial glucosinolate metabolism capacity, but no direct link to specific bacterial species could be established, possibly due to the complexity and functional redundancy of the gut microbiota.

Postprandial hypotension may be influenced by the digestion of fat. The aim of the present study was to evaluate the hypothesis that products of fat digestion mediate the hypotensive response to fat. In part A of the study, nine healthy older subjects were studied on three separate occasions in randomised order. Blood pressure, heart rate (HR), plasma TAG and gastric emptying were measured following the ingestion of equivolaemic drinks: (1) 300 ml of high-fat drink (88 % fat); (2) fat drink mixed with 120 mg orlistat (lipase inhibitor); (3) water (control). In part B of the study, ten healthy older subjects were studied on two separate occasions. Blood pressure, HR, plasma TAG and superior mesenteric artery flow were measured during 90 min intraduodenal infusions of 10 % intralipid (2·7 ml/min), with and without 120 mg orlistat. Oral fat ingestion was associated with decreases in systolic and diastolic blood pressures (both P = 0·0001) that were greater when orlistat was co-administered (both P < 0·05), and an increase in HR (P = 0·0001) that was inhibited by orlistat co-administration (P < 0·03). Gastric emptying was slowed by oral fat digestion, and orlistat administration inhibited this slowing (P < 0·04). Intraduodenal fat infusion was not associated with changes in blood pressure but increased HR (P < 0·0001), an effect attenuated by orlistat (P < 0·05). In conclusion, orlistat potentiates the hypotensive response to oral fat in older adults, possibly as a result of faster gastric emptying of fat. The results do not support a role for fat digestion in lowering blood pressure.

The omega-3 index, defined as the sum of EPA and DHA in erythrocyte membranes expressed as a percentage of total fatty acids, has been proposed as both a risk marker and risk factor for CHD death. A major determinant of the omega-3 index is EPA+DHA intake, but the impact of other dietary fatty acids has not been investigated. In a cross-sectional study on 198 subjects (102 men and 96 women, mean age 66 years) at high cardiovascular risk living in Spain, the country with low rates of cardiac death despite a high prevalence of cardiovascular risk factors, dietary data were acquired from FFQ and blood cell membrane fatty acid composition was measured by GC. The average consumption of EPA+DHA was 0·9 g/d and the mean omega-3 index was 7·1 %. In multivariate models, EPA+DHA intake was the main predictor of the omega-3 index but explained only 12 % of its variability (P < 0·001). No associations with other dietary fatty acids were observed. Although the single most influential determinant of the omega-3 index measured here was the intake of EPA+DHA, it explained little of the former's variability; hence, the effects of other factors (genetic, dietary and lifestyle) remain to be determined. Nevertheless, the high omega-3 index could at least partially explain the paradox of low rates of fatal CHD in Spain despite a high background prevalence of cardiovascular risk factors.

Plasma total cysteine (tCys) concentrations are associated with BMI. To study the relationship between tCys and BMI, we monitored the changes in serum concentrations of tCys and metabolically related compounds in sixty obese patients (BMI 50–60 kg/m2) from before to 1 year after either gastric bypass surgery (mean 30 % weight loss) or duodenal switch surgery (mean 41 % weight loss). A total of fifty-eight healthy persons (BMI 17–31 kg/m2) served as controls. Before surgery, obese patients had modestly (approximately 17 %) higher mean serum tCys, and markedly (>2-fold) higher glutamate concentrations, than controls (P ≤ 0·001 for both). Serial examinations after surgery revealed that gastric bypass patients had no change in tCys concentrations (P = 0·22), while duodenal switch patients showed a modest (approximately 12 %) but significant decrease in tCys (P < 0·001). Total homocysteine concentrations increased in duodenal switch patients but not in gastric bypass patients. Independent of surgery type, serum concentrations of methionine and cystathionine decreased (P < 0·05 for both), while serum glutathione and taurine remained stable. Glutamate concentrations declined, as did γ-glutamyltransferase activity (P < 0·001 for both). These results show that despite 30 % weight loss, and decreases in methionine, cystathionine and glutamate, there was no significant change in serum tCys in patients after gastric bypass surgery. The decrease in tCys in patients undergoing duodenal switch could be related to malabsorption. The present findings do not suggest that BMI is a causal determinant of plasma tCys.

As recently described, adherence to the Mediterranean diet is associated with improved asthma control. However, evidence of how specific nutrients such as fatty acids and antioxidants may affect this relationship remains largely unknown. We aimed to examine the association between dietary intake of fatty acids and antioxidants and asthma control. A cross-sectional study was developed in 174 asthmatics, mean age of 40 (sd 15) years. Dietary intake was obtained by a FFQ, and nutritional content was calculated using Food Processor Plus™ software (ESHA Research, Inc., Salem, OR, USA). Good asthma control was defined by the combination of forced expiratory volume during the first second, exhaled NO (eNO) and Asthma Control Questionnaire (ACQ) score (control: forced expiratory volume in the first second ≥ 80 %; eNO ≤ 35 ppb; ACQ < 1·0, scale 0–6 score). Multiple linear and logistic regression models were performed to analyse the associations between nutrients and asthma outcomes, adjusting for confounders. A high n-6:n-3 PUFA ratio predicted high eNO, whereas high intakes of n-3 PUFA, α-linolenic acid (ALA) and SFA were associated with low eNO. Odds for controlled asthma improved along with an increased intake of n-3 PUFA (OR 0·14, 95 % CI 0·04, 0·45; P for trend = 0·001), SFA (OR 0·36, 95 % CI 0·13, 0·97; P for trend = 0·047) and ALA (OR 0·18, 95 % CI 0·06, 0·58; P for trend = 0·005). A high n-6:n-3 PUFA ratio increased the odds for uncontrolled asthma (OR 3·69, 95 % CI 1·37, 9·94; P for trend = 0·009), after adjusting for energy intake, sex, age, education and use of inhaled corticosteroids. Higher intakes of n-3 PUFA, ALA and SFA were associated with good asthma control, while the risk for uncontrolled asthma increased with a higher n-6:n-3 PUFA ratio. The present results introduce a protective effect of ALA in asthma control, independent of marine n-3 fatty acids, and provide a rationale to dietary intervention studies in asthma.